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HEALTH  SCIENCES 
LIBRARY 


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A 

TEXT-BOOK  OF  MEDICINE 

FOR  STUDENTS   AND   PRACTITIONERS 

BY 

Dr.   ADOLF  STRUMPELL 

PROFESSOR    AND    DIRECTOR   OF/'flfHE    MEDICAL    CLINIQUE    AT 
THE    UNIVERSITY    OF   ERLANGEN 

Ublrb  Hmerican  BDition 

« 

TRANSLATED   BY  PERMISSION  FROM   THE    THIRTEENTH 
GERMAN  EDITION,  BY 

HERMAN    F.  VICKERY,   A.  B.,  M.  D. 

Instructor  in  Clinical  ^Medicine,  Harvard  University  ;  Visiting  Physician  to  the 

Massachusetts  General  Hospital ;  Member  of  the  Association  of  American 

Physicians  ;  Fellow  of  the  Massachusetts  Jledical  Society,  etc. 

AND 

PHILIP    COOMBS    KNAPP,   A.M.,  M.  D. 

Ex-President  of  the  American  Neurological  Association  ;  Chnical  Instructor 

in  Diseases  of  the  Nen'ous  System,  Han/ard  University  ;  Physician  for 

Diseases  of  the  Nervous  System,  Boston  City  Hospital ;  Fellow 

of  the  Massachusetts  Medical  Society,  etc. 

WITH  EDITORIAL   NOTES  BY 

FREDERICK    C.   SHATTUCK,   A.  M.,  M.  D. 

Jackson  Professor  of  Clinical  Medicine,  Harvard  University  ;  Visiting  Physician  to 

the  Massachusetts  General  Hospital ;  Member  of  the  Association  of  American 

Physicians  ;  Fellow  of  the  Massachusetts  Medical  Society,  etc. 


WITH    ONE    HUNDRED   AND   EIGHTY-FIVE    ILLUSTRATIONS 
IN    THE   TEXT,   AND   ONE    PLATE 


NEW     YORK 

D.    APPLETON     AND     COMPANY 

1 90 1: 


>c 


Stf/ 


Copyright,   1886,  1893,   1901, 
By  D.   APPLETON   AND    COMPANY. 

All  rights  reserved. 


Electrotyped  and  Printed 

AT  THE  ApPLETON  PreSS,  U.  S.  A. 


AUTHOR'S  PREFACE  TO  THE  THIRTEENTH  EDITION 


The  extent  to  which  my  text-book  has  been  used,  both  in  Germany  and  in 
other  countries,*  justifies  me  in  the  assumption  that  it  has  exercised  some  little 
influence  upon  the  professional  thought  and  practice  of  numerous  medical  read- 
ers, and  imposes  iipon  me  the  obligation  of  employing  everj'-  opportunity  for  the 
improvement  and  perfection  of  my  work.  Yet  I  must  confess  that  this  task  seems 
more  difficult  to  me  with  every  new  edition  of  the  book,  for  scientific  workers  are 
making  deep  and  extensive  investigations  into  the  many  subdivisions  of  internal 
medicine,  with  such  zeal  and  skill  that  it  becomes  difficult  for  any  one  man  to 
keep  step  with  the  unceasing  progress  of  investigation  in  this  wide  domain,  and 
to  maintain  that  complete  and  universal  command  of  facts  and  theories  which 
is  essential  for  a  presentation  of  the  subject,  which  shall  be  at  once  brief  and 
true  to  the  present  standpoint  of  science.  The  author  has  often  been  painfully 
sensible  of  these  limitations  of  his  personal  knowledge  and  ability,  but  he  hopes 
that  this  will  be  regarded  not  merely  as  subject  for  criticism,  but  also  as  an 
excuse  and  an  incentive  to  clemency,  in  case  a  reader  who  is  expert  in  any 
specialty  finds  here  and  there  an  omission  or  an  error.  Above  all,  I  beg  the 
reader  to  consider  that  no  text -book  such  as  the  present  one  ought  to  replace,  or 
could  replace,  the  vast  material  of  the  larger  reference  books.  My  purpose  was 
not  to  collect  all  the  facts  of  pathology  which  have  been  discovered  up  to  date, 
nor  all  the  methods  of  treatment  which  may  have  been  recommended,  wisely  or 
unwisely,  nor  all  the  theories  or  views  which  have  been  propounded.  My  wish  was 
to  give  a  complete  presentation  of  the  essentials  of  our  present  knowledge  and 
views  with  regard  to  the  various  diseases,  from  a  scientific  and  individual  stand- 
point ;  and  I  desired  particularly  to  impart  to  the  reader  an  insight  into  the  origin 
and  relation  of  the  various  morbid  phenomena.  To  this  end  I  have  brought  the 
facts  of  clinical  experience  into  the  closest  possible  relation  with  the  data  of  path- 
ological anatomy  and  of  general  pathology,  and  have  endeavored,  also,  in  discuss- 
ing therapeutics,  to  deduce  from  the  nature  of  the  symptoms  a  basis  for  rational 
medical  opinion  and  treatment,  although  I  have  not  undervalued  the  importance 

*  So  far  as  I  have  been  informed,  translations  of  my  text- book  have  appeared  in  the  following  lan- 
guages :  French,  English,  Italian,  Spanish,  Russian,  modern  Greek,  Turkish,  and  Japanese ;  and  some 
of  these  translations  have  had  several  editions. 

iii 


iy  AUTHOE'S   PEEFACE 

of  simple  experience.  A  text-book  intended  for  students  and  a  larger  circle  of 
graduate  readers  ought  not  to  incline  too  decidedly  toward  any  one  of  tlie  pre- 
vailing currents  of  scientific  opinion.  It  should,  however,  acquaint  the  reader 
to  such  an  extent  with  the  questions  at  present  under  discussion  relating  to 
internal  medicine,  as  to  give  him  at  least  a  fair  start  in  his  further  studies. 

The  author  has  made  an  honest  effort  to  bring  the  present  thirteenth  edition 
of  this  book  up  to  the  level  of  contemporary  medical  thought  and  knowledge. 
Large  portions  of  the  book  have  been  almost  completely  rewritten — in  particular, 
the  whole  doctrine  of  gastric  diseases  and  several  chapters  in  other  sections,  in- 
cluding gall-stones,  intestinal  parasites,  etc.  Almost  all  portions  of  the  book 
have  received  numerous  additions  and  improvements,  so  that  this  edition  may  be 
said  with  justice  to  be  completely  revised.  That  even  now  my  work  is  imperfect  I 
am  well  aware.  I  shall,  therefore,  be  thankful  to  any  one  who  will  inform  me  of 
the  mistakes  or  omissions  he  discovers. 

A.  Strumpell. 


TEANSLATORS'   PREFACE 


The  work  of  Professor  Striimpell  has  been  so  long  familiar  that  it  is  hardly 
necessary  for  the  translators  to  introduce  it  again  to  the  English-speaking  por- 
tion of  the  medical  profession  or  to  express  again  their  admiration  of  the  work. 
Since  the  second  edition  of  this  translation  was  published  in  1893  seven  new 
editions  have  appeared  in  Germany,  so  that  the  book  has  been  almost  wholly  re- 
written, although  it  still  retains  all  the  merits  of  the  earlier  production,  with  the 
advantage  of  being  ixdly  in  line  with  the  most  recent  medical  investigations. 
The  translators  have  kept  as  close  to  the  original  as  seemed  consistent  with  clear- 
ness. The  doses  in  the  metric  system  have  been  changed  to  the  approximate 
equivalents  in  apothecaries'  weight,  the  original  doses  being  retained  in  paren- 
theses. As  in  the  former  editions,  the  translators  have  substituted  specimens  of 
handwriting  in  English  in  the  chapter  on  general  paralysis  for  the  original  in 
German  script.  These  specimens  were  kindly  furnished  them  by  the  late  Dr. 
E.  P.  Elliot,  of  the  Danvers  Insane  Hospital.  The  translators  have  also  added  a 
chapter  upon  the  plague  and  various  notes  which  they  hope  may  prove  of  assist- 
ance to  the  American  practitioner.  These  additions  are  inclosed  in  brackets  and 
signed  by  the  initials  of  the  translators,  to  distinguish  them  from  the  (unsigned) 
additions,  also  in  brackets,  of  Dr.  Shattuck. 

Boston,  Jmie,  1901. 


00l!TTE]:^TS 


by    Separate    Organs 


Acute  General  Infectious  Diseases 

CHAPTER 

I.     Typhoid   Fever 

Phenomena  and  Complications  relating  to  the  Separate  Organs 
Peculiarities  in  the  Course  of  the  Disease 
Kelapses  of  Typhoid  Fever 
II.     Typhus  Fever     . 

III.  Relapsing   Fever 

IV.  Scarlet    Fever 
V.     Measles      . 

VI.     Rotheln      . 
VII.     Small-pox 

Variola  Vera 
Varioloid 

Course    of    the    Fever,    Symptoms    presented 
Complications 
VIII.    Varicella 
IX.     Erysipelas 

X.     Diphtheria  .  .  . 

XI.     Influenza  (Grippe) 
XII.     Dysentery 
XIII.     Cholera       .... 
XIV.     Malarial   Diseases 
Intermittent  Fever 
Pernicious  Intermittent  Fever 
Remittent  and  Continuous  Forms  of 
Chronic  Malarial  Cachexia 
Masked  Intermittent  Fever 
Typho-malarial  Fever 
XV.     Dengue      .... 
XVI.     Yellow  Fever     . 
XVn.    Plague        .... 
XVIII.     Epidemic  Cerebro-spinal  Meningi 
XIX.     Septic   and   Pysemic   Diseases 
XX.     Hydrophobia   (Rabies  canina) 
XXI.     Glanders  (Farcy) 

XXII.     Malignant  Pustule  (Anthrax.     Mycosis  intestinalis) 
XXIII.     Trichinosis 


itis 


Malarial  Fever 


and 


FA&E 

1 
9 
20 
21 
30 
33 
38 
48 
53 
54 
55 
56 

57 
62 
63 

67 
77 
81 
85 
93 
96 


99 
99 
100 
102 
104 
107 
111 
116 
122 
125 
127 
131 


Diseases  of  the  Respiratory  Organs 

SECTION    I 


DISEASES   OF   THE   NOSE 


I.     Coryza 

II.     Chronic  Rhinitis 
III.     Nose-bleed 


135 
137 
139 


VIU 


CONTEisTTS 


I. 

II. 
III. 
IV. 

V. 
VI. 


VII. 
VIII. 


SECTION   n 


DISEASES   OF   THE   LARYNX 


Acute  Laryngeal  Catarrh  (Acute  Laryngitis) 
Chronic  Laryngitis  (Chronic  Lai-yngeal  Catarrh) 
Laryngeal    Perichondritis  ..... 

CEdema  of  the  Glottis        ...... 

Tuberculosis  of  the  Larynx  (Consumption  of  the  Larynx) 
Paralyses  of  the  Laryngeal  Muscles     .... 

Paralyses  in  the  Distribution  of  the  Superior  Laryngeal  Nerve     . 
Paralyses  in  the  Distribution  of  the  Inferior  Laryngeal  or  Recurrent  Nerve 
Spasm  of  the  Glottis         ......... 

New  Growths  in  the  Larynx     ........ 

Benignant  Growths  in  the  Larynx       ....... 

Malignant  Growths.     Carcinoma  of  the  Larynx  .... 


PAGE 

.  140 

.  143 

.  145 

.  146 
.147 

.  150 

.  150 

.  150 

.  153 

.  155 

.  155 

.  155 


SECTION  III 

DISEASES  OF  THE  TRACHEA  AND  THE  BRONCHI 

I.     Acute  Catarrh  of  the  Trachea  and  the  Bronchi     . 
The  Milder  Forms  of  Acute  Bronchitis 
The  Severer  Pebrile  Forms  of  Acute  Bronchitis    . 
Catarrh  of  the  Finer  Bronchi.     Capillary  Bronchitis 
II.     Chronic  Bronchitis 
m.     Fcetid  Bronchitis  (Putrid  Bronchitis) 
rV.     Croupous  Bronchitis  (Fibrinous  Bronchitis) 
■   V.     Whooping  Cough  (Pertussis) 
VT.     Bronchiectasis    .... 
VII.     Stenosis  of  the  Trachea  and  Bronchi 
Tracheal    Stenosis 
Bronchial   Stenosis 
VIII.     Bronchial   Asthma 


156 
159 
159 
160 
162 
167 
170 
172 
176 
180 
180 
181 
181 


II. 

ni. 

IV. 
V. 


VI. 


SECTION  IV 


DISEASES   OF   THE   LUXGS 


I.     Pulmonary  Emphysema      ..........  187 

Symptoms  and  Course  of  the  Disease       .......  190 

Other  Symptoms  in  the  Lungs  and  in  Other  Organs      .  .'         .  .  .  193 

Pulmonary  Atelectasis  (Compression  of  the  Lungs.     Aplasia  of  the  Lungs)   .  195 

Pulmonary   QDdema  ..........  197 

Catarrhal  Pneumonia   (Broncho-pneumonia.     Lobular  Pneumonia)       .  .  199 

Croupous  Pneumonia  ..........  204 

Description  of  Single  Symptoms  and  Complications     .....  209 

Special  Peculiarities  and  Anomalies  in  the  Course  of  Pneumonia       .         .  218 

Tuberculosis  of  the  Lungs  (Pulmonary  Phthisis.    Pulmonary  Consumption)  226 

General  Pathology  and  etiology  of  Tuberculosis      .....  226 

etiology  of  Tiierbculosis  in  Man        ........  228 

Pathological  Anatomy  of  Tuberculosis,  especially  of  Pulmonary  Tuberculosis  231 
Clinical  History  of  Tuberculosis  in  General  and  of  Pulmonary  Tuberculosis 

in  Particular        ...........  234 


VII. 


Special  Symptoms  and  Complications 

Symptoms  on  the  Part  of  the  Lungs  . 

Symptoms  on  Physical  Examination 

General  Symptoms  in  Pulmonary  Tuberculosis 

Symptoms  and  Complications  on  the  Part  of  other  Organs 

Acute  General  Miliary  Tuberculosis     .  .  .  .  . 


237 
237 
241 
246 
248 
261 


CONTENTS 


IX 


CHAPTER 

VIII. 

IX. 

X. 

XI. 

XII. 


Gangrene  of  the  Lungs       ..........   266 

Diseases  from  the  Inhalation  of  Dust   (Pneumonoconiosis)  .  .  .   270 

Embolic  Processes  in  the  Lungs  (Hsemorrhagic  Infarction  of  the  Lungs)       .   273 
Brown  Induration  of  the  Lungs  (Lungs  of  Heart  Disease)   ....   275 

Tumors  of  the  Lungs.     Cancer  of  the  Lungs.     Echinococcus  of  the  Lungs. 

Pulmonaiy  Syphilis      ..........   276 


SECTION    V 


DISEASES   OF   THE   PLEUEA 


I.     Pleurisy     ..... 
Physical    Signs  .  ■        . 

Various  Forms  of  Pleurisy 
II.     Peripleuritis         .... 
III.     Pneumothorax 
rV.     Hydrothorax.     Hsematothorax 
V.     New  Growths   of  the  Pleura 
VI.     Mediastinal  Tumors   . 
VII.     Actinomycosis  of  the  Thoracic  Cavity 


279 
285 
288 
295 
295 
299 
300 
301 
302 


Diseases  of  the  Circulatory  Organs 
SECTION    I 


DISEASES   OF   THE   HEART 

I.     Acute  Endocarditis  (Endocarditis  verrucosa,  Endocarditis  ulcerosa)      .          .  304 

II.     Valvular   Disease    of   the   Heart          ........  308 

,    General  Pathology  of  Valvular  Disease  of  the  Heart    .....  310 

Insiifiiciency  of  the  Mitral  Valve       ........  311 

Stenosis  of  the  Mitral  Orifice  (Mitral  Stenosis)     ......  314 

Insufficiency  of  the  Semilunar  Valves  of  the  Aorta     .....  316 

Stenosis  of  the  Aortic  Orifice       .........  320 

Insufficiency  of  the  Tricuspid  Valve  ........  321 

Stenosis  of  the  Tricuspid  Orifice           ........  322 

Insufficiency  of  the  Pulmonary  Valve         .......  323 

Stenosis  of  the  Pulmonary  Orifice  (Pulmonary  Stenosis)  and  the  other  Con- 
genital Lesions  of  the  Heart       ........  323 

Combined  Valvular  Diseases  of  the  Heart    .......  325 

General  Sequelae  and  Complications  of  Valvular  Disease  of  the  Heart           .  326 

General  Course  and  Prognosis  of  Valvular  Disease  of  the  Heart         .          .  333 

Treatment  of  Valvular  Heart  Disease         .......  334 

III.  Diseases  of  the  Myocardium       .........  340 

Interstitial  Myocarditis  (Fibrinous  Degeneration  of  the  Myocardium.  Scle- 
rosis of  the  Coronary  Arteries)     ........  340 

So-called  Idiopathic  Hypertrophy  of  the  Heart    (Mechanical  Strain  of  the 

Heart) 345 

Hypertrophy  of  the  Heart,  Associated  with   Congenital   Smallness   of  the 

Systemic   Arteries         ..........  350 

Primary  Weakness  of  the  Myocardium  (Congenital  Weakness  of  the  Heart; 
Weakened  Heart;  Acute  Muscular  Strain  of  the  Heart;  Toxic  Weak- 
ness of  the  Heart)        ..........  351 

The  So-called  Fatty  Heart 353 

IV.  Cardiac  Neuroses        ...........  355 

Angina  Pectoris  (Stenocardia)     .........  355 

Nervous    Palpitation           ..........  356 

Tachycardia 357 


CONTEIs'TS 


II. 


I. 

II. 
III. 
IV. 

V. 


SECTION   II 

DISEASES   OF   THE   PERICARDIUM 

Pericarditis         .  .  .  .  .  .  .  .  . 

Special  Forms  of  Pericarditis       ....... 

Hydro-pericardium,  Hsemo-pericardium,  and  Pneumo-pericardium 

SECTION   III 

DISEASES   OF   THE   VESSELS 


PAGE 
359 

363 
369 


Arterio- sclerosis  (Endarteritis  chronica  deformans. 
Aneurism  of  the  Thoracic  Aorta 
Aneurisms  of  the  Other  Vessels  .... 
Rupture  of  the  Aorta         ..... 
Narrowing  of  the  Aorta     ..... 


Atheroma  of  the  Vessels)  370 
.374 

379 

.   380 

.  .  .380 


Diseases  of  the  Digestive  Organs 
SECTION    I 

DISEASES   OF   THE   MOUTH,   TONGUE,   AND   SALIVARY   GLANDS 

I.  Catarrhal    Stomatitis 

II.  Ulcerative   Stomatitis 

III.  Aphthous   Stomatitis 

IV.  Thrush       .... 
V.  Glossitis     .... 

Acute  Parenchymatous  Glossitis 
Glossitis  Dissecans     . 
Lingual   Psoriasis.     Leucoplacia 
VI.     Noma  .... 

VII.     Parotitis   (Mumps)      . 

Idiopathic,  Primary  Parotitis 
Secondary  Suppurative  Parotitis 
VIII.     Angina    Ludovici 

IX.     Anomalies  of  Dentition 


382 
383 
385 
386 
388 
388 
388 
388 
389 
390 
390 
391 
392 
392 


SECTION  II 

DISEASES   OF   THE   SOFT   PALATE,   TONSILS,   PHARYNX,   AND   NASO-PHARYNX 

[.     Sore  Throat  (Inflammation  of  the  Soft  Palate  and  of  the  Tonsils)         .  .  394 

Catarrhal   Sore   Throat 395 

Follicular  Tonsillitis 396 

Tonsillar  and  Peritonsillar  Abscess   (Parenchymatous  Sore  Throat)      .  .  396 

Necrotic  Tonsillitis    (Necrotic  Sore  Throat)        ......  397 

Chronic  Hypertrophy  of  the  Tonsils     ........  399 

Chronic    Pharyngitis  ..........  400 

Chronic  Catarrh  of  the  Naso-pharynx,  Chronic  Posterior  Nasal  Catarrh       .  400 

Pharyngitis  Sicca       ...........  401 

Hypertrophic  Catarrh  in  the  Pharynx  and  Naso-pharynx     ....  401 

Retropharyngeal  Abscess    ..........  403 

SECTION   III 

DISEASES   OF   THE   (ESOPHAGUS 

I.     Inflammation  and  Ulcer  of  the  CEsophagus  .......   404 

TI.     Dilatation  of  the  Oilsophagus       .........   406 


II. 
III. 


IV. 


CONTENTS 


XI 


Diffuse  Dilatation 
Diverticula 

III.  Stenosis  of  the   Oesophagus 

IV.  Cancer   of  the   CEsophagus 
V.     Rupture  of  the  CEsophagus 

VI.     Neuroses  of  the  CEsophagus 
Spasm  of  the  CEsophagus  . 
Paralysis  of  the  CEsophagus 


PAGE 

406 
406 
409 
412 
414 
414 
414 
415 


II. 
III. 
IV. 
V. 
VI. 
VII. 


VIII. 


SECTION    IV 


DISEASES   OF   THE   STOMACH 


IX. 


Brief  Preliminary  Remarks  on  the  Examination  of  the  Gastric  Contents       .  415 
Constituents   of   the   Gastric   Juice,    particularly   Free   Hydrochloric    Acid, 

Pepsine,  and  Lactic  Acid     .........  417 

Determination  of  the  Motor  Activity  of  the  Stomach         ....  419 

Estimation  of  the  Size  and  Position  of  the  Stomach     .....  420 

Testing  the  Absorptive  Powers  of  the  Stomach     ......  421 

Demonstration  of  Blood  in  the  Gastric  Contents  .....  422 

Acute  Gastric  Catarrh  (Acute  Gastritis)      .  .  .  .  .  .  .  422 

Chronic  Gastritis.     Chronic  Catarrh  of  the  Stomach  .....  425 

Phlegmonous  Gastritis        ..........  432 

Gastric  Ulcer 432 

Cancer  of  the  Stomach        ..........  444 

Anomalies  of  the  Secretion  of  Gastric  Juice       ......  452 

Anacidity  of  the  Stomach  (Achlorhydria).     Achylia  Gastrica     .  .  .  452 

Hyjjer secretion  and  Hyperacidity  of  the  Gastric  Juice  (Acid  Dyspepsia)        .  455 

Dyspepsia  with  Hypersecretion  of  the  Gastric  Juice     .....  457 

Periodical  (Intermittent)  Hypersecretion  (Gastroxynsis)      ....  459 

Abnormalities  in  the  Size  and  Position  of  the  Stomach.     Motor  Disturb- 
ances of  the  Stomach  .........  460 

Abnormalities  in  the  Size  of  the  Stomach.     Atony  of  the  Stomach         .  .  460 

Abnormal  Position  of  the  Stomach.     Gastroptosis       .....  462 

Nervous  Dysjjepsia     ...........  463 


SECTION    V 


DISEASES   OF   THE   INTESTINES 


II. 
III. 

IV. 

V. 

VI. 

VII. 

VIII. 

IX. 

X. 

XL 


XII. 


Intestinal   Catarrh      ....'... 

Appendix.     Membranous  Enteritis  and  Mucous  Colic 
Cholera  Morbus  (Cholera  Infantum)    . 
Intestinal  Catarrh  of  Children   . 
Typhlitis  and  Perityphlitis  (Appendicitis) 
Perforating  Ulcer  of  the  Duodenum     . 
Tuberculosis  of  the  Intestines 
Syphilis  of  the  Rectum       .... 

Cancer  of  the  Intestines     .... 

Heemorrhoids     ...... 

Habitual    Constipation       .... 

Stricture  and  Obstructions  of  the  Intestines 
Intestinal  Constriction        .... 

Intestinal  Obstruction         .... 

Intestinal    Parasites  .... 

Tape-worms        ...... 

Round-worms    .  .  . 

Oxyuris   vennicularis  .... 

Anchylostoma  duodenale    .... 

Trichocephalus   dispar         .  . 


474 
475 
477 
482 
488 
488 
490 
491 
493 
495 
499 
502 
503 
508 
508 
515 
516 
518 
519 


xu 


CONTE^s^TS 


SECTION    VI 

DISEASES    OF    THE    PEKITOXEUil 


CHAPTER 

I.  Acute  Peritonitis 

II.  Chronic  and.  Tubercular  Peritonitis 

III.  Ascites        ..... 

lY.  Cancer  of  the  Peritoneum  . 


PAGE 

520 
529 
533 

535 


SECTION    VII 

DISEASES   OF   THE   LIVER,   BILE-DUCTS,   A^"D   POETAL   VEEST 

I.     Catarrhal  Jaundice     ........ 

II.     Acute  Febrile  Jaundice  (Infectious  Jaundice.     Weil's  Disease) 
ni.     Biliary    Calculi 
IV.     Suppurative    Hepatitis 
V.     Cirrhosis  of  the  Liver 

VI.     Biliary  Cirrhosis  and  Hypertrophic  Cirrhosis  of  the  Liver 
VII.     Acute  Yellow  Atrophy  of  the  Liver 

Appendix.     Pernicious  Jaundice.     Cholsemia   and  Acholia 
VIII.     Icterus   Neonatorum 

IX.     Syphilis  of  the  Liver  .... 

X.     Cancer  of  the  Liver  and  Bile-ducts 
XI.     Echinococcus  of  the  Liver 
XII.     Circulatory  Disturbances  in  the  Liver 
Xm.    Atrophy,  Hypertrophy,  and  Degenerations  of  the  Liver 
XrV.     Anomalies  in  the  Shape  and  Position  of  the  Liver 
XV.     Suppurative   Pylephlebitis 
XYI.     Thrombosis   of  the  Portal  Vein 

Appendix.     Diseases  of  the  Pancreas 
Haemorrhages  into   the   Pancreas 
Atrophy  of  the  Pancreas 
Pancreatitis 
Cysts  of  the  Pancreas 
Cancer  of  the  Pancreas 
Pancreatic  Calculi 


536 

542 
543 
553 
555 

562 
565 
569 
570 
571 
572 
575 
578 
579 
581 
582 
583 
585 
585 
585 
585 
586 
586 
587 


Diseases  of  the  Kidneys,  the  Pelvis  of  the  Kidney,  and  the  Bladder 

SECTION    I 

DISEASES   OF   THE   KIDNEYS 


I.     General  Preliminary  Remarks  upon  the  Pathology  of  Renal  Disease 
Albuminuria       .......... 

Casts  and  other  Abnormal  Morphological  Constituents  of  the  Urine  in 
Disease         .  .  .  .  .  .  .  ... 

The  Dropsy  of  Renal  Disease     ....... 

Uraemia     ........... 

The  Changes  in  the  Cireulatoiy  Apparatus  in  Renal  Disease 
II.     Acute   Nephritis  ......... 

III.  The  Subchronic  and  Chronic  Forms  of  Nephritis,  with  the  Exception 

Genuine  Contracted  Kidney  ...... 

IV.  Contracted  Kidney     ......... 

V.     Amyloid   Kidney         ......... 

VI.     Purulent  Nephritis   and  Perinephritis  .  . 

Purulent  Nephritis     ......... 

Perinephritic  (Paranephritic)  Abscess  ..... 

VII.     Disturbances  of  Circulation  in  the  Kidneys  .... 


Renal 


of  the 


588 
589 

592 
594 
596 
601 
603 

618 
625 
635 
640 
640 
641 
643 


CONTEXTS 


Xlll 


VIII. 
IX. 


X. 


PAGE 

The  Congested  Kidney  '..........  643 

Embolic  Infarction  in  the  Kidneys      ........  643 

New  Growths  in  the  Kidneys     .........  644 

Parasites  of  the  Kidneys  and  of  tlie  Urinary  Passages.     Chyluria       .  .  646 

Echinococcus  of  the  Kidney         .........  646 

Distoma  Hsematobium  (Bilharzia  Heematobia)    ......  646 

Strongylus  or  Eustrongylus  Gigas      ........  647 

Filaria  Sanguinis.     Chyluria       .........  647 

Movable  Kidney  (Floating  Kidney.     Ren  Mobilis)       .....  648 

Appendix.      The   Diseases    of   the    Suprarenal    Capsules    and    Addison's 

Disease    (Bronzed  Skin)        .........  650 


SECTION    II 

DISEASES   OF   THE   PELVIS   OF   THE   KIDNEY   AND   OF   THE   BLADDER 

I.  Inflammation  of  the  Pelvis  of  the  Kidney.     Pyelitis 

II.  Nephrolithiasis  ...... 

III.  Tuberculosis  of  the  Genito-urinary  Apparatus 

IV.  Hydronephrosis  ...... 

V.  Cystitis       ........ 

VI.     New  Growths  in  the  Bladder     .... 
VII.     Enuresis  Nocturna      ...... 


654 
657 
662 
665 
667 
672 
673 


Diseases  of  the  Organs  of  Locomotion 

I.     Acute  Articular  Rheumatism      .........  675 

II.     Chronic    Articular    Rheumatism     (Chronic    Polyarthritis)     and    Arthritis 

Defonnans  ...........  688 

III.     Acute  and  Chronic  ]\Iuscular  Rheumatism  .......  694 

rV.     Acute  Polymyositis    ...........  698 

V.     Rachitis 699 

VI.     Osteomalacia      ............  704 


Diseases  affecting  the  Blood  and  Tissue-metamorphosis 

(CONSTITUTIONAL   DISEASES) 

I.     Ansemia  and  Chlorosis        ..........  708 

General  Preliminary  Remarks  as  to  the  Classification  and  etiology  of  the 

Various   Forms   of  Anaemia          ........  708 

Symptomatology  of  Anaemia      .........  711 

II.     Progressive   Pernicious   Anasmia  .  .  .  .  .  .  .  .719 

III.  Leukaemia           ............  726 

IV.  Pseudo-leukaemia 733 

V.    Haemoglobinaemia  and  Haemoglobinuria     .......  736 

Yl.     Scurvy 738 

Appendix.     Barlow's   Disease          ........  743 

VII.     Purpura.     Morbus  Maculosus  Werlhofli.     Peliosis       .....  744 

VIII.     Haemophilia 746 

IX.    Diabetes  Mellitus 748 

X.    Diabetes  Insipidus     ...........  767 

XI.     Gout 770 

XII.     Obesity 779 

XIII.     Scrofula      .         .      ' 787 


XIV 


CONTENTS 


CHAPTER 
I. 


11. 


III. 

IV. 


V. 

VI. 

VII. 


Diseases  of  the  Nervous  System 

/.     The  Diseases  op  the  Peripheral  Nerves 

SECTION    I 

DISEASES   OF   THE   SENSORY  NERVES 

General  Remarks  upon  the  Disturbances  of  Sensibility 
Sensibility  to  Contact  .... 

Sense  of  Locality  (Localization  of  Sensation) 
Sense    of   Pressure      ..... 

Sense  of  Temperature         .... 

Sensation  of  Pain      ..... 

Electro-cutaneous  Sensibility 

Delay  of  Sensation,  Summation  of  Irritation  and  After-sensations 

The  Sensibility  of  the  Muscles  and  Joints  ..... 

The  Special  Sensibility  to  Touch  (Stereognostic  Sense,  Active  Touch) 
The  Sensory  Conduction  Tracts  and  Anesthesia  of  the  Skin 
Course  of  the  Sensory  Conduction  Tracts    . 
The  General  Causes  of  Cutaneous  Anaesthesia 
The  Symptoms  of  Cutaneous  Anaesthesia     . 
Anaesthesia  of  the  Trigeminus   . 
Treatment  of  Cutaneous  Anaesthesia  . 
Neuralgia   in   General  .... 

The  Individual  Forms  of  Neuralgia     . 

Neuralgia  of  the  Trigeminus 

Occipital    Neuralgia  .  . 

Neuralgia  in  the  Region  of  the  Brachial  Plexus 

Intercostal  Neuralgia  .... 

Neuralgia  in  the  Region  of  the  Lumbar  Plexus 
Sciatica      ....... 

Neuralgia  of  the  Genitals  and  the  Rectal  Region 
Aehillodynia.     Talalgia.     Tarsalgia.     Metatarsalgia 
The  So-called  Articular  Neuralgias  (Articular  Neuroses) 
Acroparaesthesia  ..... 

Habitual  Headache     ..... 

Anomalies  of  the  Sense  of  Smell 
Anomalies  of  the  Sense  of  Taste 


PAGE 

789 
790 
790 
791 
792 
792 
793 
793 
794 
795 
796 
796 
799 
800 
802 
803 
804 
810 
810 
813 
814 
815 
816 
817 
820 
821 
821 
822 
824 
826 
827 


SECTION  II 


DISEASES   OF   THE   MOTOR   NERVES 


II. 


General  Remarks  upon  the  Disturbances  of  Motility     .....   82& 

Paralysis 829- 

Symptoms  of  Motor  Irritation   .........   835 

Ataxia        .............   837 

General  Remarks  upon  testing  the  Reflexes  and  upon  the  Condition  of  them  838 
General  Remarks  upon  the  Changes  of  Electrical  Excitability  in  the  Motor 

Nerves  and  Muscles     ..........   842 

Table  of  the  Different  Forms  of  Voluntary  Motion  and  the  Muscles  and 

Nerves  Concerned  therein     .........   851 

The  Different  Forms  of  Peripheral  Paralysis       ......   854 

Paralysis  of  the  Ocular  Muscles         .  .  .  .  .  .  .  .   854 

Paralysis  of  the  Motor  Branch  of  the  Trigeminus       .....   858 

Facial  Paralysis  ...........   858 

Paralyses  in  the  Region  of  the  Muscles  of  the  Shoulder         .      .  .  .   863 

Paralyses  of  the  Muscles  of  the  Back  and  Abdomen     .....   865 

Paralyses  in  the  Region  of  the  Upper  Extremity  ......   866 


CONTENTS 


XV 


III. 


IV. 
V. 


Paralysis  of  the  Diaphragm       .... 

Paralyses  in  the  Region  of  the  Lower  Extremity 
Toxic  Paralyses  ...... 

Lead   Paralysis  .  .  .    '      . 

Arsenical  Paralysis     ...... 

The  Different  Forms  of  Localized  Spasm     . 
Spasm  in  the  Motor  Distribution  of  the  Trigeminus 
Clonic   Facial   Spasm  ..... 

Spasm  in  the  Region  of  the  Hypoglossal  Nerve.     Lingual  Spasm 

Spasms  in  the  Muscles  of  the  Neck     . 

Spasms  in  the  Muscles  of  the  Shoulder  and  Arm 

Spasms  in  the  Muscles  of  the  Lower  Extremity  . 

Saltatory  Reflex  Spasm       ..... 

Arthrogryposis  ...... 

Spasms  in  the  Respiratory  Muscles    . 
Writer's  Cramp  and  Allied  Professional  Neuroses 
Simple  and  Multiple  Degenerative  Neuritis 
Simple  Neuritis  .... 

Primary  Simple  Neuritis     . 

Secondaiy  Simple  Neuritis 

Multiple  Degenerative   Neuritis 

Primary  Acute  and  Chronic  Multiple  Neuritis 

The  Ataxic  Form  of  Multiple  Neuritis  ("Acute  Curable  Ataxia 


VI. 


The  Acute  and  Chronic  Neuritis  of  Alcoholic  Subjects. 

(Pseudo-tabes  [Ataxia]  of  Alcoholic  Subjects) 
Beri-beri.     Endemic  Multiple  Neuritis 
New  Growths  in  the  Peripheral  Nerves       . 


Alcoholic  Paraly 


PAGE 

871 

871 
873 
873 
875 
875 
875 
876 
877 
878 
880 
,  880 
,  881 
881 
,  881 
,  882 
,  885 
.  885 
.  885 
,  885 
,  886 
.  890 
.  892 
/■sis 
.  893 
.  895 


II. 

in. 

IV. 


Raynaud's  Disease 


//.     Vasomotor  and  Trophic  Neuroses 

General  Preliminary  Remarks 

Erythromelalgia 

Symmetrical  Spontaneous  Gangrene. 

Acute  Angioneurotic  CEdema 

Myxoedema 

Cretinism  .... 

Myxoedematous   Infantilism 

Adiposis  Dolorosa 

Scleroderma         .... 

Acromegaly         .... 

Gigantism  .... 

Hyperostosis  Cranii    . 

Hydrops  Articulorum  Intermittens 

Injuries  and  Diseases  of  the  Cervical 

Migraine    ..... 

Progressive  Facial  Hemiatrophy 

Exophthalmic  Goitre 


Sympathetic 


900 
900 
900 
901 
901 
901 
902 
902 
902 
903 
904 
904 
905 
905 
908 
909 


II. 


III. 


///.  The  Diseases  of  the  Spinal  Cord 

Diseases  of  the  Spinal  Meninges         ........  915 

Acute  Inflammations  of  the  Spinal  Meninges     ......  915 

Chronic    Spinal   Leptomeningitis  ........   917 

Pachymeningitis  cervicalis  hypertrophica   .......   918 

Haemorrhage  into  the  Spinal  Meninges       .......   919 

Preliminary  Remarks  on  the  Localization  and  Topical  Diagnosis  (Segmental 

Diagnosis)  of  Diseases  of  the  Spinal  Cord     ......   920 

Disturbances  of  Circulation,  Haemorrhages,  Traumatic  Lesions,  and  Func- 
tional Disturbances  of  the  Spinal  Cord         ......   928 

Disturbances  of  Circulation        .........   928 


XVI 


CONTENTS 


Substance  of  the   Spinal   Cord.       Spinal   Apoplexy. 


929 
930 

932 
933 
934 
937 
941 
943 
946 
946 
947 
947 
948 
948 
949 
949 
950 
954 
95 


Hsemonhage  into   the 
Hsematomyelia     . 
Traumatic  Lesions  of  the  Spinal  Cord 
Diseases  of  the  Spinal  Cord  after  a  Sudden  Eeduction  of  the  Atmospheric 

Pressure  (Caisson  Disease)   . 
Functional  Disturbances  (Spinal  Irritation.     Spinal  Neurasthenia) 
IV.     The  Pressure  Paralyses  of  the  Spinal  Cord 
The  Pressure  Paralyses  in  Vertebral  Caries 
The  Pressure  Paralyses  in  Cancer  of  the  Vertebrae 
V.     Acute  and  Chronic  Myelitis 
Symptoms  of  Motor  Paralysis 
Symptoms  of  Motor  Irritation 
Ataxia        .... 

Disturbances  of  Sensibility 
Cutaneous  Reflexes     . 
Tendon  Reflexes 

Disturbances  in  the  Bladder  and  Rectum 
Trophic  Disturbances 

Disturbances  in  the  Region  of  the  Cerebral  Nerves 
VI.     Multiple  Sclerosis  of  the  Brain  and  Spinal  Cord 
Appendix.     The  So-called  Pseudo-sclerosis     . 
VII.     Tabes  Dorsalis   . 

Disturbances  of  Motility  in  the  Extremities         ......   966 

Disturbances  of  the  Cutaneous  and  Muscular  Sensibility     ....   969 

Disturbances  of  the  Reflexes       .  .  .  .  .  .  .  .  .971 

Disturbances  in  the  Eye  and  the  other  Organs  of  Special  Sense     .  .  .   972 

Disturbances  in  the  Bladder,  the  Rectum,  and  the  Sexual  Organs         .  .   973 

Symptoms  in  the  Internal  Organs       ........   973 

Trophic  Disturbances  .  .  .  .  .  .  .  .  .  .   974 

Cerebral  Symptoms    ...........   976 

VIII.     Hereditary  (Juvenile)  Ataxia  (Friedreich's  Disease)    .  .  .  .  .   981 

Appendix.     Hereditary  Cerebellar  Ataxia 984 

IX.     The  Primary  Degenerations  of  the  Motor  Tract,  including  the  Muscles  .  .   985 

Preliminary  Remarks  ..........   985 

Amyotrophic  Lateral  Sclerosis   .........   986 

Spinal  Progressive  Muscular  Atrophy         .......   990 

Neurotic  Muscular  Atrophy       .........   996 

Progressive  Muscular  Dystrophy         ...         ^  ...  .   998 

Primary  Degeneration  of  the  Pyramidal  Tracts  .....  1007 

Appendix.     Congenital  Spastic  Paraplegia  in  Children  (Spastic  Cerebral 
Paralysis.     Infantile  Spastic  Diplegia.     Little's  Disease)      .  .  .   1012 

X.     Acute  and  Chronic  Poliomyelitis      ........   1014 

Spinal  Paralysis  of  Children     .........   1014 

Acute   Poliomyelitis   of   Adults  ........   1019 

Subacute  and  Chronic  Poliomyelitis  .......   1020 

XL     The  So-called  Acute  Ascending  Spinal  Paralysis  (Landry's  Paralysis)        .  .   1021 
XII.     New  Growths  of  the  Spinal  Cord  and  of  its  Membranes     ....   1024 

XIII.  The  Syphilitic  Afi'ections  of  the  Spinal  Cord 1026 

Chronic  Gummatous  Spinal  Meningitis  and  Meningo-myelitis     .  .  .   1027 

Syphilitic  Myelitis  and  Syphilitic  Spastic  Spinal  Paralysis       .  .  .   1028 

XIV.  Syringomyelia  and  Hydromyelus       ........   1029 

J.V.     Spina  Bifida     .         .         .    ' 1032 

XVI.     Secondary  Degenerations  in  the  Spinal  Cord     ......   1033 

XVII.     Unilateral  Lesion  of  the  Spinal  Cord 1036 


IV.     The  Diseases  of  the  Medulla   Oblongata 

I.     Progressive  Bulbar  Paralysis     .........   1039 

II.     The  Rarer  Forms   of  Chronic  Bulbar  Paralysis,   Progressive   Ophthalmo- 
plegia,  and   Asthenic   Bulbar  Paralysis      ......   1045 


CONTENTS 


xvu 


III. 


IV. 


Progressive   Ophthalmoplegia    ...... 

Asthenic  Bulbar  Paralysis.     Pseudo-paralytic  Myasthenia 
Family  Periodic  Paralysis         .       '  . 
Acute  and  Apoplectiform  Bulbar  Paralysis 
Haemorrhage  into  the  Medulla  Oblongata  and  the  Pons 
Embolism  and  Thrombosis  of  the  Basilar  Artery 
Acute  Inflammatory  Bulbar  Paralysis 
Compression  of  the  Medulla     .  .  . 


PAGE 

1045 
1046 
1047 
1048 
1048 
1050 
1051 
1052 


V.     Tee  Diseases  of  the  Brain 
SECTION   I 

DISEASES   OE   THE   CEEEBKAL   MENINGES 


I.  Hsematoma  of  the  Dura  Mater 

II.  Purulent  Meningitis 

III.  Tubercular  Meningitis 

IV.  Thrombosis  of  the  Cerebral  Sinuses 


1053 
1055 
1059 
1064 


SECTION    II 


DISEASES   OF   THE   BRAIN-SUBSTANCE 

I.     Disturbances  of  Circulation  in  the  Brain     .......    1066 

II.     General  Preliminary  Remarks  upon  the  Localization  of  Cerebral  Diseases    .    1068 

The  Motor  Region  of  the  Cortex  Cerebri 1069 

The  other  Parts  of  the  Cortex  Cerebri,  except  the  Center  for  Speech     .  .   1074 

The  Centers  of  Speech  and  the  Disturbances  of  Speech  (Aphasia  and  Allied 

Conditions) 1077 

The  Centrum  Ovale,  Internal  Capsule,  Central  Ganglia,  and  Region  of  the 

Corpora   Quadrigemina        .........    1083 

The  Cerebellum 1086 

III.  Cerebral  Haemorrhage        ..........    1089 

IV.  Cerebral  Embolism  and  Tlirombosis  (Encephalo-malacia)  .  .  .    1103 
V.     Inflammation  of  the  Brain         .........    1106 

Abscess  of  the  Brain  (Suppurative  Encephalitis)         .....    1106 

Acute  and  Chronic  Non-suppurative  Encephalitis      .....    1110 

Idiopathic  (Inflammatory)   Softening  of  the  Brain     .....   1110 

Curable   Forai    of   Encephalitis  ........   1110 

Diffuse   Cerebral   Sclerosis  .........    1110 

The  Acute  Encephalitis   of  Children  .  .  .  .  .  .  .1111 

VI.     Insolation.     Sunstroke.     Heat  Prostration.     Thermic   Fever      .  .  .    1113 

VII.     Tumors  of  the  Brain .1115 

Glioma      .............    1116 

Sarcoma   .............    1116 

Gumma  and  Solitary  Tubercle  .........    1116 

Carcinoma         .  .  .  .  .  .  .  .  .  .  .  .1116 

Psammoma        ............    1116 

Cysts  of  the  Brain     .  .  .  .  .  .  .  .  .  .  .1117 

The  General  Symptoms  of  Cerebral  Tumors      ....  .    1117 

Tumors  in  the  Different  Parts  of  the  Brain  and  their  Focal  Symi)toms       .    1119 

Appendix.     Hydatids  of  the  Brain 1124 

VIJI.     Cerebral  Syphilis 1125 

IX.     Progressive  General  Paralysis  of  the  Insane  (Paralytic  Dementia)      .  .    1129 

X.     Chronic  Hydrocephalus     .  .  .  .  .  .  .  .  .  .1137 

XI.     Meniere's  Disease 1139 


XVlll 


CONTENTS 


VI.     Neuroses  without  Known  Anatomwal  Basis 


II. 


III. 

IV. 

V. 

VI. 

VII. 

VIII. 

IX. 


XI. 


Epilepsy    ............ 

Appendix.     Infantile  Convulsions  (Eclampsia  Infantum) 
Chorea       ............ 

Appendix.      Chronic    Hereditary    Chorea.      Electrical    Chorea.      Para 
myoclonus  (Myoclonia)       ........ 

Paralysis  Agitans     .......... 

Athetosis  ........... 

Tetany      .  .  .  .  .  . 

Tetanus    ............ 

Congenital  Myotonia  (Thomsen's  Disease)  ..... 

Catalepsy  ........... 

Hysteria  ........... 

The  Symptoms  and  Manifestations  of  Hysteria         .... 

The  Hysterical  Stigmata,  especially  Sensory  Anaesthesia  and  Hyperaesthesia 
Hysterical   Paralysis  ......... 

Hysterical  Contractures  ........ 

Vaso-motor    Disturbances.      Secretory    Disturbances.      Symptoms    in    the 
Internal   Organs  ......... 

General  Mental  and  Bodily  Constitution  of  the  Hysterical 
Hysterical  Attacks,  Conditions  of  Spasm,  etc.     ..... 

Neurasthenia  .......... 

Symptoms  of  Neurasthenia.     The  Mental  Symptoms 

The  Physical  Symptoms   .......... 

The  So-called  Traumatic  Neuroses  (Accident  Neuroses) 
Appendix  I.     Summary   of   the   Symptoms   and   Treatment  in   Cases   of 
Poisoning  .......... 

Appendix  II.     Table  of  Weights  and  Measures       .... 

Index   ............ 


1141 
1151 
1152 

1156 
1157 
1161 
1162 
1165 
1169 
1170 
1172 
1175 
1175 
1178 
1179 

1179 
1181 
1182 
1193 
1194 
1195 
1201 

1206 
1214 
1217 


LIST  OF  ILLUSTEATIOl^S 


FIG.  PAGE 

Table  I.  Distribution  of  the  areas  of  the  sensory  roots  upon  the  surface  of  the 

body         ..........  facing  page    924 


1. 


9. 
10. 
11. 
12. 
13. 
14. 
15. 
16. 
17. 
18. 
19. 
20. 
21, 
23. 
24. 
25. 
26. 
27. 
28. 
29. 
30. 
31. 
32. 
33. 
34. 
35. 
36. 
37. 
38. 
39. 
40. 
41. 
42. 
43. 
44. 
45. 
46. 


Typhoid  bacilli        ....... 

Temperatures  in  typhoid  fever  .  .  . 

Example  of  the  temperature  curve  in  relapsing  fever 
Spirilli  of  relapsing  fever  in  the  blood     ... 
Example  of  a  normal  scarlet-fever  curve 
Example  of  the  temperature  curve  in  measles  . 
Example  of  the  temperature  curve  in  true  small-pox 
The  cocci  of  erysipelas     ...... 

Comma  bacilli  ....... 

Different  forms  of  the  malarial  plasmodium 
Quotidian  intermittent  fever   ..... 

Tertian  intermittent  fever         ..... 

Anthrax  bacilli        ....... 

Anthrax  bacilli;  spore  formation  and  spore  germination 
Trichinae  ........ 

Paralysis  of  left  vocal  cord     ..... 

Bilateral  paralysis  of  the  posticus   .... 

Paralysis  of  both  internal  thyro-arytsenoid  muscles 
Paralysis  of  the  arytsenoideus  .... 

Paralysis  of  the  thyro-arytsenoids  and  arytaenoideus 
22.  Pediculated  fibromata         ..... 

Turpentine  pipe       ....... 

Crystals  of  fat  acids       ...... 

Asthma  crystals  and  Curschmann's  spirals 
Pneumonia  diplococci       ...... 

Example  of  the  temperature  curv'e  in  croupous  pneumonia 
Example  of  the  temperature  curve  in  "  intermitting '"  pneumon 
Cholesterine  crystals        ....... 

Influence  of  a  pulmonary  haemon-hage  upon  the  temperature 
Elastic  fibers  ....... 

Tubercle  bacilli  in  the  sputum  .... 

Sub-febrile  state  in  chronic  pulmonary  tuberculosis 
Hectic  fever  in  chronic  pulmonary  tuberculosis 
Expectoration  of  a  worker  in  graphite 
Sputum  containing  "  cells  of  heart  disease  "' 
Temperature  curve  in  pleurisy  before  and  after  tapi)in{ 
Masses  of  actinomycosis  ..... 

Pulse  cui-\'e  in  marked  mitral  stenosis 

Pulse  curve  in  aortic  insufficiency     .... 

Pulse  curve  in  stenosis  of  the  aortic  orifice 

Pulsus  bigeminus    ....... 

Pseudo-hepatic  cirrhosis  due  to  pericarditis 

Plan  of  the  dentition      ...... 

Method  of  wa.shing  out  the  stomach 

Hsemine  crystals     ....... 


1 

7 

35 

36 

40 

50 

57 

63 

86 

94 

97 

97 

127 

128 

131 

151 

152 

152 

153 

153 

155 

166 

168 

185 

206 

216 

217 

222 

239 

240 

240 

246 

246 

271 

276 

293 

302 

314 

319 

321 

328 

366 

393 

416 

422 


XX 


LIST    or   ILLUSTRATIOl^S 


FIG. 

47.  Head  of  taenia  solium 

48.  Head  of  cysticercus  of  the  brain 

49.  Tsenia  solium 

50.  Eggs  of  intestinal  parasites 

51.  Head  of  teenia  mediocanellata 

52.  Tsenia  mediocanellata 

53.  Head  of  bothriocephalus  latus 

54.  Bothrioceplialus  latus 

55.  Embryo  of  botbriocephalus  latus 

56.  Ascaris  lumbricoides 

57.  58.  Oxyuris  vermicularis 
59,  60.  Ancbylostoma  duodenale   . 

61.  Egg  of  anchylostoma  duodenale 

62.  Tricboceplialus  dispar 

63.  Leucine  and  tyrosine  crystals 

64.  Tsenia  echinococcus 

65.  66.  Ecbinococcus  scolices 

67.  Ecliinococcus  booklets 

68.  Different  forms  of  casts 

69.  Waxy  casts     . 

70.  Epithelial  cast 

71.  Distoma  hsematobium 

72.  Embryos  of  filaria 

73.  Pelvic  renal  epithelium 

74.  Crystals  of  triple  phosphate  and  amnionic  urate 

75.  Temperature  chart  in  acute  articular  rheumatism   . 

76.  Appearance  of  the  hand  in  protracted  arthritis  deforman 

77.  Chronic  arthritis  deformans  with  contracture 

78.  Puerpei'al  osteomalacia   ...... 

79.  Changes  in  the  red  blood-corpuscles  in  pernicious  anaemia 

80.  Leuksemic  blood     .... 

81.  Mixed  leukaemia  (myelaemia) 

82.  Acute  attack  of  gout  in  the  fingers  . 

83.  Changes  in  the  fingers  in  chronic  gout 

84.  Course  of  the  posterior  root-fibers  in  the  cord  and  medulla 

85.  Transverse  section  of  the  cord,  showing  the  course  of  the  posterior  root-fibers 

86.  Course  of  the  sensory  conduction  tracts  . 

87.  88.  Distribution    of   the   sensory   cutaneous   nerves   in   the    trunk    and    upper 

extremities 

89.  Detailed  distribution  of  the  nerves  to  the  dorsal  surface  of  the  fingers 

90,  91.  Distribution  of  the  sensory  cutaneous  nerves  to  the  lower  extremities 
92,  93.  Distribution  of  the  sensory  cutaneous  nerves  in  the  head     . 

94.  Sciatic  scoliosis  in  severe  sciatica     ....... 

95.  Horizontal  section  through  the  right  cerebral  hemisphere 

96.  Transverse  section  through  the  crura  cerebri  in  secondary  degeneration 

97.  Transverse  section  through  the  cer^"ical  enlargement 

98.  Transverse  section  through  the  lumbar  enlargement 

99.  Motor  points  of  face 
100,  101.  Motor  points  of  arm 844, 

102.  Motor  points  of  thigh 

103,  104.  Motor  points  of  leg  . 841 

105.  Right  facial  paralysis 

106.  Trunk  of  the  facial 

107.  Paralysis  of  the  right  serratus 

108.  Position  of  the  hand  in  paralysis  of  the  radial  nerv 

109.  Paralysis  of  the  ulnar  nerve     . 

110.  Spasm  of  the  accessory  ner\-e  . 

111.  Spasm  of  the  right  splenius  capitis 

112.  Radial  nerve  in  alcoholic  polyneuritis 


LIST    OF   ILLUSTEATIONS 


XXI 


pon 


PIG. 

113.  Acromegaly  in  a  patient  thirty  years  old  .... 

114.  Left  facial  hemiatrophy  ....... 

115.  Patient  with  Basedow's  disease   (exopjithalmus,  goitre)    . 

116.  Position  of  the  hand  in  pachymeningitis  cervicalis  hypertrophica 

117.  Distribution  of  the  sensory  root-areas  from  the  lumbo-sacral  plexus 

118.  Lesion  at  the  level  of  the  second  lumbar  segment 

119.  Lesion  at  the  level  of  the  third  lumbar  segment 

120.  Lesion  at  the  level  of  the  fifth  lumbar  segment 

121.  Lesion  of  the  first  sacral  segment     . 

122.  Lesion  of  the  second  sacral  segment 

123.  Lesion  of  the  third  sacral  segment  . 

124.  Lesion  of  the  fourth  sacral  segment 

125.  Relations  of  the  vertebrae  to  the  spinal  roots 

126.  Vertebral  displacement  in  spondylitis 

127.  Angular  kyphosis  in  vertebral  caries 

128.  Distribution  of  the  sclerosed  nodules  on  the  surface. of  the 

129.  Example  of  disease  of  the  cord  in  multiple  sclerosis 

130.  Degeneration  of  the  jjosterior  columns  in  advanced  tabes 

131.  132.  Transverse  section  of  the  cord  in  beginning  tabes  dor.'^al 

133.  Paralysis  of  the  left  oculo-motor  nerve  in  tabes 

134.  Tabetic  arthropathy  of  the  right  knee  and  left  ankle 

135.  Genu  recurvatum  in  tabes  dorsalis  .... 

136.  Attitude  of  a  patient  with  hereditary  ataxia    . 

137.  Diagram  of  the  motor  tract     ..... 

138.  Section  of  the  cervical  cord  in  amyotrophic  lateral  sclerosis 
139-141.  Atrophy  of  the  hand  in  spinal  progressive  muscular  atrophy 

142.  Atrophy  of  the  hand  and  forearm  in  spinal  progressive  muscular  atrophy 

143,  144.  Spinal  progressive  muscular  atrophy 

145.  Neurotic  muscular  atrophy 

146.  Peroneal  muscular  atrophy 

147.  Positions  of  a  child  with  pseudo-hypertrophic  paralysis  on  rising 

148.  Pseudo-hypertrophy  of  the  muscles         .... 

149.  Juvenile  myopathic  muscular  atrophy     .... 

150.  Two  brothers  with  juvenile  muscular  atrophy  . 

151.  Juvenile  muscular  dystrojjhy  ..... 

152.  Muscular  dystrophy         ....... 

153.  Juvenile  muscular  dystrophy.     Myopathic  facies 

154.  Progressive  myopathic  muscular  atrophy 

155.  Spastic  spinal  paralysis  ....... 

156.  Spastic  spinal  paralysis.     Impulsive  laughing 

157.  Family  spastic  spinal  paralysis        ..... 

158.  Position  of  the  legs  in  congenital  spastic  cerebral  paralysis 

159.  Section  of  the  cord  in  anterior  poliomyelitis     . 

160.  Old  spinal  infantile  paralysis  ..... 

161.  Deformity  of  the  hand  in  syringomyelia  .... 

162.  Secondary  descending  degeneration  of  the  pyramidal  tracts 

163.  Secondary  ascending  and  descending  degeneration    . 

164.  Course  of  the  main  tracts  in  the  cord        .... 

165.  Representation  of  the  chief  symptoms  in  unilateral  lesion 

166.  Position  of  the  nuclei  of  the  cranial  nerves 

167.  Progressive  ophthalmoplegia   ...... 

168.  Diagram  of  focal  diseases  in  the  pons       .... 

169.  170.  Lateral  aspect  of  the  brain      ..... 

171.  Aspect  of  the  median  surface  of  the  eerebnim  . 

172.  Topographical  relations  between  the  surface  of  the  brain  and  the  skull 

173.  Localization  in  the  cerebral  cortex  .... 

174.  Diagram  of  the  course  of  the  optic  fibers  in  the  chiasma 

175.  Patient  with  right  hemiplegia  .... 

176.  Cerebral  infantile  paralysis      ..... 


1009, 


PAGE 

903 

909 

911 

918 

924 

925 

925 

925 

925 

926 

926 

926 

928 

935 

938 

954 

955 

962 

963 

972 

974 

975 

983 

986 

987 

992 

993 

994 

997 

998 

1000 

1001 

1002 

1003 

1004 

1005 

1005 

1006 

1009 

1010 

1011 

1013 

1014 

1016 

1031 

1034 

1035 

1037 

1038 

1042 

1046 

1049 

1070 

1071 

1072 

1073 

1075 

1095 

1111 


xxn 


LIST  OF  illusteatio:j^s 


FIG. 

177.  Examples  of  hand"\vriting  in  general  paralysis 

178.  Characteristic  position  of  the  body  in  paralysis  agitans 

179.  Example  of  the  position  of  the  fingers  in  the  movements 

180.  Hysterical  contracture     .... 

181.  Contracture  of  the  foot  in  traumatic  hysteria 

182.  Hysterical  arc  de  cercle  .... 

183.  Hysterical  attack  with  catalepsy     . 

184.  Hysterical  abasia    ..... 

185.  Accident  case  with  hysterical  paresis 


of  athetosi 


PAGE 
1132 

1158 
1161 
1179 
1180 
1183 
1184 
1189 
1202 


ACUTE   GENERAL   INFECTIOUS   DISEASES 


CHAPTER   I 

TYPHOID    FEVER 

( Typhus  ahclominalis.     Enteric  Fever.     Ileotyphus) 

Etiology. — The  sole  cause  of  eveiy  attack  of  typhoid  fever  is  an  infection 
-of  the  body  by  a  deiinite  pathogenic  bacillus,  the  "  typhoid  bacillus  "  discovered 
by  Eberth  and  Koch,  and  later  made  better  known  by  the  researches  of  Gaffky 
and  others.  Their  length  (see 
JFig.  1)  is  about  one  third  the 
diameter  of  a  red  blood-glob- 
ule, and  their  breadth  equals 
one  third  their  length,  but 
■sometimes  they  may  grow  out 
in  long  fibers.  It  is  not  yet 
certain  whether  spore  forma- 
tion takes  place  in  their  inte- 
Tior  or  not.  The  typhoid  bacilli 
show  a  very  active  sponta- 
neous movement  in  water, 
caused  probably  by  very  fine 
filiform  threads  which  Loffler 
has  discovered  on  the  ends  of 
the  rods  and  which  he  regards 
as  the  motor  organs  of  the ' 
bacilli. 

That  these  typhoid  bacilli 
•are  specific,  is  shown,  how- 
ever, as  in  the  case  of  many 

micro-organisms,  less  by  their  external  form  than  by  their  peculiarities,  as 
observed  in  pure  cultures  of  them,  and  by  their  other  biological  peculiarities 
(virulence,  chemical  reaction,  etc.).  By  the  latter  the  pure  typhoid  bacillus 
is  distinguished  from  a  form  of  bacillus  morphologically  similar  and^perhaps 
allied  to  it,  which  often  is  found  in  the  intestine,  and  is  called  hacterium  coli 
commune  (Escherich).  The  attempt  has  even  been  made  to  regard  the  typhoid 
Taacillus  merely  as  a  virulent  form  of  the  bacterium  coli,  but  the  weight  of 
evidence  is  at  present  in  favor  of  regarding  the  typhoid  bacillus  as  an  independ- 
ent form. 

In  cultures  on  gelatine  the  typhoid  bacilli  develop  along  the  line  of  puncture 
in  little  whitish  or  yellowish  clusters,  while  a  thin  gray  pellicle  extends  slowly 
over  the  surface,  but  the  nutrient  gelatine  never  liquefies.  The  manner  of  their 
growth  on  the  cut  surface  of  boiled  potatoes  is  still  more  characteristic,  and  espe- 
cially valuable  for  their  recognition.  The  whole  cut  surface  is  covered  with  a 
1  1 


Fig.  1.— Typhoid  bacilli.    Section  from  the  spleen.    800  :  1. 
(From  FlCgge.) 


2  ACUTE  GENERAL  INFECTIOUS  DISEASES 

dense  pellicle,  scarceh^  discernible  ^n-ith  the  naked  eye,  and  forming  an  absolutely- 
pure  culture  of  typhoid  bacilli.  It  is  an  important  fact  that  typhoid  bacilli  may 
also  thrive  if  deprived  of  oxygen,  because  we  can  thus  understand  their  increase 
within  the  intestine. 

The  typhoid  bacilli  have  thus  far  been  found  chiefly  in  the  typhoidal  infiltra- 
tions in  the  intestine,  where  they  lie  between  the  cells,  and  also  in  single  foci 
in  the  mesenteric  glands,  the  spleen,  the  liver,  the  kidneys,  the  pleura,  the  me- 
ninges, in  typhoidal  foci  in  the  bones,  etc.  By  suitable  methods  of  investigation 
they  are  often  found  in  the  stools  of  typhoid  patients  and  also  in  the  fluid  ob- 
tained by  puncture  of  the  fresh  splenic  tumor,  in  the  gall  bladder,  sometimes  in 
the  urine,  and  also  in  the  blood  taken  from  a  spot  of  roseola.  As  a  rule,  they  are 
not  found  in  the  rest  of  the  blood. 

Numerous  attempts  have  been  made  to  produce  typhoid  fever  artificially  by 
introducing  pure  cultures  of  the  typhoid  bacilli  into  the  bodies  of  animals,  but  the 
results  of  these  efforts  have  not  yet  proved  perfectly  harmonious.  The  main  cause 
of  the  discrepancy  is  probably  that  animals  are  in  general  very  slightly  susceptible 
to  the  disease.  At  any  rate,  the  attempts  at  artificial  infection  up  to  this  date 
have  proved  successful  only  in  cases  when  the  animals  subjected  to  the  experiment 
(rabbits,  guinea-pigs)  have  received  large  amounts  of  the  typhoid  bacilli  directly 
into  a  vein  or  into  the  abdominal  cavity  (E.  Frankel  and  Simmonds),  or  when  the 
bacilli  have  been  introduced  into  the  duodenum  (A.  Frankel).  Probably,  how- 
ever, we  have  here  to  do  rather  Avith  the  intoxication  of  the  animals  caused  by  the 
poisonous  matters  generated  in  the  cultures  of  bacilli  than  with  an  actual  in- 
fection, for  the  pathological  changes  of  typhoid  fever  are  but  little  developed  in 
the  animals,  and  the  injected  bacilli  themselves  appear  to  be  for  the  most  part 
destroyed  within  the  body  of  the  animal  experimented  upon  (Fliigge  and 
Sirotinin,  and  others).  Attempts  to  produce  the  disease  by  mixing  the  dejecta 
of  typhoid  patients  with  the  animal's  food  have  thus  far  proved  invariably  un- 
successful. Probably  the  bacilli  are  immediately  destroyed  by  the  hydrochloric 
acid  in  the  stomach. 

Investigation  of  the  a-tiology  of  typhoid  fever  must  consequently  be  directed 
to  ascertaining  in  what  manner  and  through  what  channels  the  specific  typhoid 
bacilli  penetrate  into  the  human  body,  and  what  circumstances  are  then  essen- 
tial to  their  further  development  and  to  the  display  of  their  pathogenic  properties. 
It  must  be  confessed  that  the  ability  to  answer  these  questions  accurately  is  a  goal 
from  which  we  are  quite  distant. 

It  is  almost  universally  believed  that,  as  a  rule,  typhoid  bacilli  do  not  have  any 
permanent,  independent  existence  outside  the  human  body,  but  sometimes  under 
favorable  conditions  they  seem  to  be  able  to  remain  for  years  in  a  "  latent  condi- 
tion "  in  the  external  world  (in  moist  earth  or  stagnant  water).  Often,  however, 
the  conditions  essential  to  an  abundant  development  of  the  bacilli  arise  in  certain 
places,  and  thus  make  it  possible  for  a  greater  or  less  number  of  persons  to  absorb 
the  pathogenic  poison,  and,  as  a  result,  to  be  attacked  by  typhoid  fever.  In  this 
way  occur  the  numerous  greater  or  smaller  epidemics  of  typhoid  fever  in  contrast 
to  the  sporadic  cases,  which  are  likewise  possible,  and  are  not  infrequent.  If 
an  epidemic  of  typhoid  appears  in  a  place  till  then  entirely  free  from  the  disease, 
we  must  always  refer  it  to  an  importation  of  the  disease-germs,  and  seek  their 
source  in  some  previous  case  of  typhoid.  We  must,  therefore,  take  for  granted 
that  the  poison  of  tj-phoid  can  in  some  way  escape  from  the  body  of  the  patient 
into  the  outer  world.  If  we  believe  this,  we  shall  be  sure  to  think,  first  of  all,  of 
the  intestinal  discharges  as  the  source  of  infection.  These  discharges,  as  already 
stated,  are  known  to  contain  the  typhoid  bacilli  or  perhaps  their  spores. 

As  to  the  exact  manner  of  infection,  views  are  still  widely  different.  Up  to 
the  present  time  there  are  chiefly  two  contrasted  theories,  called,  respectively,  the 


TYPHOID  FEVER  3 

"  ground-soil  "  and  the  "  drinking-water  "  *  theories.  According  to  the  former, 
which  is  maintained  principally  by  Pettenkofer  and  his  pupils,  the  ground-soil  is 
to  be  regarded  as  the  chief  place  of  development  for  the  schizomycetic  fungus  of 
typhoid  fever.  Whether  this  will  flourish  depends  chiefly  on  the  condition  of  the 
soil  (varying  at  different  times  and  in  different  places),  and  this  alone  should  ex- 
plain all  the  peculiarities  observable  in  the  spread  of  the  disease — e.  g.,  that  single 
houses,  streets,  or  wards  of  a  city  should  suffer.  According  to  Pettenkofer,  a  soil 
that  air  and  water  easily  penetrate — e.  g.,  one  made  up  of  alluvial  or  detrital  de- 
posits— is  most  favorable  for  the  spread  of  the  disease,  while  a  firm,  rocky  bottom 
makes  its  further  development  impossible ;  and,  where  this  "  tendency  of  the 
ground-soil "  is  wanting,  the  disease  can  neither  be  introduced  nor,  if  brought  in 
by  the  sick,  spread  any  further;  for,  according  to  Pettenkofer,  the  typhoid 
poison  is  seldom  if  ever  transferred  directly  from  one  person  to  another.  The 
poison  in  the  stools  must  first  be  changed  by  the  soil  before  it  becomes  infectious. 
The  "  ground-air,"  which  is  continually  rising,  carries  the  poison  not  only  into  the 
open  atmosphere,  but  into  the  air  of  dwelling-rooms,  and,  being  then  inhaled, 
produces  infection.  We  can  thus  understand  why  Pettenkofer  regards  typhoid 
fever  as  not  directly  contagious.  The  chief  support  of  the  ground-soil  theory, 
beyond  the  results  of  comparing  the  character  of  the  soil  with  the  extent  of  the 
epidemics,  consists  in  the  proof  which  Buhl  and  Pettenkofer  have  given  (taking 
Munich  as  an  example,  and  later  Berlin  and  other  places)  that  a  relation  exists 
between  the  variations  of  the  standing  water  in  the  soil  and  the  frequency  of 
typhoid  cases.  It  appears  that,  when  the  water  stands  high  (near  the  surface), 
fewer  cases  occur,  and  when  it  falls  below  the  mean  height  cases  are  more  numer- 
ous. Pettenkofer  explains  this  relation  by  the  fact  that  the  level  of  the  ground- 
water is  certainly  an  index  of  the  moisture  and  other  conditions  of  the  soil  upon 
which  the  development  of  the  tjrphoid  bacilli  depends. 

To  be  contrasted,  or  rather  compared,  with  the  "  ground-air  "  theory  is  the  view 
held  by  most  physicians,  despite  the  vigorous  protest  of  Pettenkofer,  that  drinking- 
water  plays  an  increasingly  important  role  in  the  origin  of  many  epidemics  of 
typhoid.  In  fact,  in  the  case  of  numerous  epidemics,  whose  extent  bears  an  un- 
mistakable relation  to  the  water-supply,  we  are  forced  to  believe  that  the  typhoid 
germs  are  brought  into  the  body  by  means  of  waterused  in  drinking  or  othenvise. 
Even  then  we  are  by  no  means  wholly  to  disregard  the  character  of  the  soil,  for 
the  disease-producing  poison — not  to  speak  of  direct  pollution — is  probably  often 
communicated  to  the  well-water  from  the  soil.  The  possibility  of  this  will  be 
especially  great  if  the  wells  are  near  drains  or  cess-pools  containing  typhoid  dis- 
charges. In  epidemics  spread  by  drinking-water,  the  typhoid  bacilli  have  lately 
been  repeatedly  found  in  the  suspected  water. 

We  believe  the  idea  is  continually  gaining  ground  that  no  single  "  theory " 
can  fully  explain  all  the  facts,  and  that  the  possibility  of  infection  occurring  in 
several  different  ways  must  be  considered.  The  final  source  of  infection  is  always 
to  be  sought  for  in  a  previous  case  of  tj^phoid  fever.  From  this  patient  the 
typhoid  bacilli  reach  the  external  world  through  the  dejections,  and  may  some- 
times directly  reach  another  human  body  and  infect  it.  Hence  the  experience 
that  nurses,  laundresses  who  wash  the  soiled  linen,  etc.,  often  have  typhoid  fever; 
but  tj'phoid  fever  is  not  contagious  by  conduction  through  the  air.  In  most  hos- 
pitals typhoid  patients  are  not  isolated  from  the  rest  of  the  sick,  and  yet  out- 
breaks of  t5T)hoid  hardly  ever  occur  among  them,  provided  they  are  not  in  close 
intercourse  with  the  typhoid  cases  or  do  not  carelessly  use  the  same  dishes,  rec- 
tal thermometer,  etc.     In  the  further  extension  of  the  disease — that  is,  when 

*  Compare  with  what  follows  the  statements  concerning  the  aetiology  of  cholera,  where  the  same 
disputed  points  are  considered. 


4  ACUTE  GENERAL  INFECTIOUS  DISEASES 

there  is  an  epidemic — water  contaminated  with  typhoid  bacilli  certainly  plays  a 
frequent  and  most  important  part.  All  persons  who  indulge  directly  or  indirectly 
(rinsing  cooking  utensils,  etc.)  in  water  from  an  infected  spring  or  infected  aque- 
duct are  in  danger  of  becoming  ill.  For  example,  it  has  been  remarked  in  Eng- 
land, and  lately  in  Cologne,  that  the  fever  in  certain  epidemics  was  limited  to 
individuals  who  had  their  milk  from  one  common  source.  In  such  cases,  however, 
the  probable  cause  is  not  a  disease  in  the  cows,  but  a  pollution  of  the  milk  or  the 
milk-cans  by  water.  It  is  as  yet  doubtful  if  animals  can  have  typhoid  fever.  This 
fact  makes  it  uncertain  whether  the  illnesses  which  have  been  observed  to  follow 
the  ingestion  of  the  flesh  of  diseased  calves  (e.  g.,  the  epidemic  of  Kloten)  are 
actually  to  be  considered  typhoid  fever,  although  the  pathological  changes  are 
said  by  Huguenin  to  be  very  similar  to  those  found  in  typhoid. 

[It  is  not  probable  that  sewer-gas  in  itself  is  an  exciting  cause  of  typhoid  fever. 
Especially  in  large  cities  typhoid  dejections  are  constantly  finding  their  way  into 
the  sewers,  which  afford  all  the  conditions  favorable  to  the  further  growth  and 
development  of  the  poison.  If,  then,  the  drainage  of  any  house  is  defective,  the 
seeds  of  the  disease  can  readily  gain  access  to  the  interior  of  the  house  and  infect 
susceptible  individuals. 

One  of  the  most  instructive  epidemics  on  record  is  that  in  Plymouth,  Pennsyl- 
vania, a  town  of  eight  thousand  inhabitants.  In  the  spring  of  1885  a  disease,  at 
first  supposed  to  be  of  a  strange  character,  broke  out  in  the  place,  and,  before  it 
ceased,  affected  twelve  hundred  persons,  causing  one  hundred  and  thirty  deaths. 
It  was  soon  found  that  the  malady  was  typhoid  fever,  which  arose  from  one  case, 
briefly  in  this  wise :  In  January,  February,  and  March  there  was  a  case  of  typhoid 
in  a  house  on  a  hill  sloping  toward  a  water-supply  of  the  town.  The  dejec- 
tions were  thrown  out  on  the  snow,  under  which  the  ground  was  deeply  frozen. 
On  March  25th  a  sudden  and  great  thaw  occurred,  the  water  did  not  sink  into 
the  ground,  but  ran  immediately  into  the  natural  surface  channels,  and  on  April 
10th  the  epidemic  began.  There  were  reasons,  which  it  is  not  necessary  here  to 
detail,  why  the  above  source  of  water-supply  was  drawn  upon  to  an  unusual  de- 
gree just  at  that  time,  but  it  has  been  shown  that  those  who  derived  their  water 
from  other  sources  were  spared  by  the  disease.  The  original  case  came  from  Phil- 
adelphia.] 

In  almost  all  cases  the  intestine  seems  to  be  the  actual  gate  of  entrance  for  the 
typhoid  poison  into  the  human  system.  This  is  shown  by  the  fact  that  in  all 
cases  which  come  to  autopsy  in  early  stages  of  the  disease,  the  typhoid  bacilli  are 
mainly  confined  to  the  lymphatic  tissues  of  the  intestine.  The  typhoid  poison 
(bacilli  or  spores)  is  probably  SAvallowed,  either  directly  with  water  or  polluted 
food,  or  after  being  inhaled  or  in  some  other  way  introduced  into  the  mouth. 
[Raw  oysters  grown  in  impure  waters  may  convey  the  infection. — V.]  If 
not  destroyed  in  the  stomach,  it  passes  on  in  viable  condition  into  the  alkaline 
contents  of  the  intestine,  and  here  finds  the  conditions  essential  to  its  further 
development.  It  penetrates  at  first  into  the  lymphatic  follicles  and  Peyer's 
patches,  and  thence  goes  on  into  the  mesenteric  glands,  the  blood-current,  the 
spleen,  and  other  organs. 

As  in  the  case  of  most  other  infectious  diseases,  the  occurrence  of  infection  in 
typhoid  is  dependent  not  only  on  outward  conditions,  but  also  on  an  individual 
predisposition.  Details  of  the  circumstances  attending  this  latter  are  as  yet  not 
at  all  accurately  understood.  Even  in  the  worst  typhoid  centers,  where  the  pos- 
sibility of  infection  must  be  universal,  many  escape  the  disease. 

Age  has  an  indubitable  influence  upon  the  liability  to  the  disease.  Tj^hoid  is 
especially  a  disease  of  youthful,  vigorous  individuals,  of  fifteen  to  thirty  j^ears. 
Above  that  age  it  is  noticeably  less  frequent,  although  cases  do  occur  at  sixty  and 
even  seventy  years.     Formerly  it  was  often  said  that  young  children  were  never 


TYPHOID  FEVER  5 

attacked ;  but  this  was  because  the  disease  was  not  recognized,  for  in  reality  it  is 
only  children  under  one  year  old  who  seem  to  be  seldom  infected.  At  a  later  age, 
cases  are  by  no  means  rare. 

Sex  can  not  be  shown  with  certainty  to  have  an  especial  predisposing  influence 
upon  the  frequency  of  typhoid  fever. 

Mental  excitement  and  gross  errors  in  diet  seem  to  predispose  to  the  disease. 
On  the  other  hand,  a  certain  immunity  has  been  alleged  to  be  given  by  many  cir- 
cumstances, especially  pregnancy,  the  puerperal  state,  and  other  diseases  already 
existing  (tuberculosis,  heart  disease).  Most  of  these  statements  are  shown,  how- 
ever, by  more  extended  experience,  to  be  very  doubtful.  It  is  certain,  however, 
that  the  occurrence  of  typhoid  fever  gives  very  probable  though  not  absolute 
immunity  against  any  later  new  attack.  Recent  bacteriological  investigations 
have  suggested  a  reason  for  this  immunity.  Certain  chemical  albuminoid  sub- 
stances (protective  substance  or  "  alexine  "  of  Buchner)  probably  remain  in  the 
blood-serum  and  fluids  of  the  tissues  and  prevent  a  new  infection. 

Finally,  it  must  be  mentioned  that  the  necessary  conditions  for  an  abundant 
development  and  conveyance  of  the  typhoid  germs  are  beyond  doubt  dependent 
on  the  season.  According  to  statistics,  most  of  the  typhoid  epidemics  come  in  the 
months  from  August  to  November,  while  generally  the  number  of  cases  greatly 
diminishes  from  December  to  spring. 

General  Course  of  the  Disease. — Extended  experience  shows  that,  after  infec- 
tion with  the  typhoid  poison  has  taken  place,  a  certain  time  must  elapse  before  the 
symptoms  of  the  disease  appear.  The  length  of  this  time,  the  "  stage  of  incuba- 
tion," is,  unlike  that  of  many  other  infectious  diseases,  not  perfectly  definite.  On 
the  average,  it  lasts  two  to  three  weeks,  sometimes  less  time,  sometimes  longer. 
During  this  period  the  patient  either  feels  perfectly  well,  or  has  certain  slight 
symptoms,  to  which  he  pays  more  or  less  attention,  according  to  his  individual 
susceptibility.  These  prodromata  consist  of  langiior,  disinclination  to  exertion, 
anorexia,  slight  headache,  pain  in  the  limbs,  etc.  Often  they  last  only  a  few 
days.  Not  infrequently  the  patients  state  afterward  that  they  had  felt  the  dis- 
ease coming  on  for  weeks. 

The  transition  of  the  prodromata  into  the  regular  disease  takes  place  some- 
times so  gradually  that  it  is  utterly  impossible  to  take  any  one  day  as  the  first  of 
the  illness,  in  order  to  reckon  from  it  its  duration.  It  is  usually,  however,  the  first 
symptoms  of  a  high  temperature,  chilliness,  feverishness,  and  the  accompanying 
increase  in  general  discomfort,  which  allow  one  to  fix,  with  at  least  some  accuracy, 
the  beginning  of  the  disease.  A  decided  initial  rigor  is  certainly  exceptional.* 
After  the  fever  begins,  most  patients  soon  take  to  their  beds,  although  it  happens 
often  enough  that  the  sick  feel  either  unable  or  unwilling  to  give  up,  and  keep  on 
at  work  for  days ! 

There  have  been  manifold  attempts  to  divide  the  whole  course  of  the  disease 
into  separate  periods.  The  most  natural  division  seems  to  be  into  the  three  stages 
of  development,  height  or  fastigium,  and  decline  (stadium  incrementi,  s.  acmes,  s. 
decrementi).  Usually,  however,  physicians  reckon  according  to  the  week  of  the 
disease.  The  first  week  corresponds  to  the  developmental  stage,  the  second,  and 
in  all  severer  cases  the  third  as  well,  to  the  fastigium,  the  fourth  (in  light  cases 
the  third)  to  the  decline.  The  course  of  the  disease  is  very  variable,  however,  and 
naturally  there  is  the  greatest  diversity  in  the  departures  from  this  general  plan. 

In  the  first  week,  the  initial  period,  the  general  symptoms  augment  rapidly. 
The  patients  become,  in  severe  cases,  very  languid  and  feeble,  have  generally  an 

*  According  to  the  representations  of  many  authors,  a  marked  initial  riiror  seems  to  occur  rather 
often  in  some  places.  In  Leipsic,  and  also  in  Erlangen,  a  pronounced  rigor  at  the  beginning  of  typhoid 
is  scarcely  ever  seen. 


6  ACUTE  GENERAL  INFECTIOUS  DISEASES 

intense  headache,  and  complete  anorexia,  with  great  thirst.  The  fever,  which  is 
all  the  time  gradually  rising,  is  recognizable  subjectively  by  alternating  sensa- 
tions of  heat  and  cold,  and  objectively  by  the  hot,  dry  skin,  the  parched  lips,  and 
the  dry  and  coated  tongue.  The  sleep  is  disturbed.  For  the  most  part  there  are 
no  prominent  thoracic  or  abdominal  symptoms,  except  that  at  times  there  is  a 
sense  of  oppression  in  the  chest,  or  sorae  cough.  The  pulse  is  quickened,  some- 
times even  now  dicrotic.  There  is  often  a  temporary  epistaxis.  The  belly  is  not 
much  swollen  as  a  rule,  and  but  little  if  at  all  tender.  There  is  generally  consti- 
pation. Usually  the  spleen,  even  at  this  time,  exhibits  a  swelling  that  can  be 
easily  demonstrated. 

Generally  the  fastigium  has  begun  before  the  end  of  the  first  week.  The 
severe  general  symptoms  persist  or  even  increase.  The  fever  maintains  constant- 
ly a  considerable  elevation.  The  patients  become  more  stupid.  Often  delirium 
appears,  especially  at  night.  In  the  lungs  there  is  developed  a  more  or  less  in- 
tense and  extensive  bronchitis.  The  abdomen  becomes  more  swollen.  On  the 
skin  of  the  trunk  appear,  generally  at  the  beginning  of  the  second  week,  a  number 
of  small,  pale-red  spots,  roseolae.  Instead  of  constipation,  there  is  a  moderate 
diarrhoea.  There  are  daily  about  two  to  four  soft,  thin,  bright-yellow  dejec- 
tions. 

The  third  week,  during  which  in  the  severe  eases  the  symptoms  already  men- 
tioned persist,  is  the  chief  time  of  the  numerous  complications  and  of  especial 
clinical  events,  about  which  we  shall  speak  below  at  length.  If  the  disease 
takes  a  favorable  course,  there  comes  at  the  end  of  the  third  week  a  decline  of  the 
fever;  and  then  the  general  symptoms  also  improve  as  a  rule.  The  mind  becomes 
clearer,  the  patient  sleeps  better,  and  gains  some  appetite.  The  pulmonary  and 
digestive  symptoms  abate,  and  convalescence  gradually  begins. 

This  short  sketch  of  the  course  of  the  disease  corresponds  to  most  of  the  cases 
of  medium  severity.  There  are,  however,  besides  these,  so  many  forms  and  so 
many  variations  from  the  usual  picture,  that  it  seems  almost  impossible  to  enu- 
merate completely  all  the  events  of  typhoid  fever.  And  besides,  the  separate  epi- 
demics vary  in  their  general  character  according  to  the  time  and  place  of  their 
occurrence.  In  many  epidemics  the  cases  run  a  peculiar  course  and  have  certain 
special  complications  not  seen  in  others. 

We  will  begin  the  presentation  of  the  chief  peculiarities  by  speaking  of  the 
course  of  the  fever. 

Course  of  the  Fever. — Observation  of  the  temperature  in  typhoid  is  so  abso- 
lutely essential  for  the  estimation  of  each  individual  case  that  no  scientiiic  physi- 
cian ought  to  treat  a  case  without  regular  measurement  of  the  temperature. 
The  measurements  should  be  taken,  if  possible,  in  the  rectum.  Their  frequency 
must  of  course  be  modified  by  circumstances,  but  it  will  probably  be  possible 
to  have  three  or  four  measurements  daily.  At  night,  especially  if  the  patients  are 
asleep,  it  is  generally  not  requisite  to  take  the  temperature.  A  general  idea  of  the 
course  of  the  fever  can  be  gained  only  by  representing  the  separate  measurements 
graphically  in  a  continuous  "  temperature  curve." 

The  typical  curve  of  typhoid  fever  (see  Fig.  2)  falls  naturally  into  three  or 
four  divisions.  The  first  division  is  the  initial  period,  or  the  pyrogenetic  stage,  and 
is  seldom  observed,  since  at  this  time  the  patients  are  generally  not  yet  under  the 
doctor's  care.  The  initial  period  of  the  fever  lasts,  as  a  rule,  some  three  or  four 
days,  seldom  longer;  and  during  this  time  the  temperature  rises,  generally  by 
gradual  steps,  so  that  the  morning  as  Avell  as  the  evening  temperature  is  each  day 
2°  or  3°  (1°-1.5°  C.)  higher  than  on  the  day  before.  A  sudden  and  considerable 
rise  of  temperature,  such  as  occurs  in  many  other  diseases,  is  very  rarely  seen  in 
the  beginning  of  typhoid  fever. 

The  second  division  of  the  curve  represents  the  so-called  fastigium,  and  cor- 


TYPHOID  FEVER 


responds  to  the  height  of  the  disease.  During  this  time  the  fever  presents,  in  most 
of  the  severer  cases,  the  general  character  of  "  febris  contmua'^ — i.e.,  the  spon- 
taneous remissions  of  the  fever  seldom  exceed  2°  (1°  C).  Almost  always  the 
lower  temperatures  come  in  the  morn- 
ing hours  and  the  higher  in  the  even- 
ing. In  cases  of  average  severity  the 
morning  remissions  touch  102° -103° 
(39°-39.5°  C),  and  the  evening  ex- 
acerbations 104°-105°  (40°^0.5°  C). 
Temperatures  which  reach  or  ex- 
ceed 106°  (41°  C.)  are  seen  only  in 
very  severe  cases.  Considerable  morn- 
ing remissions  are  always  a  favorable 
symptom,  while  morning  temperatures 
of  104°  (40°  C.)  or  higher  generally 
show  the  case  to  be  severe.  The  dura- 
tion of  the  fastigium  varies  with  the 
severity  and  obstinacy  of  the  case.  It 
may  last  only  a  few  days  or  one  and  a 
half  to  two  weeks;  in  violent  cases 
still  longer. 

In  many  cases  of  slight  or  average 
severity  the  period  of  decline  follows 
directly  on  the  fastigium;  but  in 
severe  cases  there  frequently  inter- 
venes another  stage,  which  Wunder- 
lich  has  graphically  named  the  "  am- 
biguous "  period.  The  temperature- 
curve  becomes  irregular  and  more 
variable.  The  morning  remissions 
may  be  great,  even  reaching  the  nor- 
mal, while  the  evening  temperatures 
are  often  still  very  high.  This  stage 
has  accordingly  been  termed  the 
"  period  of  the  steep  curves."  It 
may  be  said  that  in  general  the 
longer  a  case  of  typhoid  lasts  the 
more  irregular  will  be  the  course  of 
the  fever. 

The  last  stage — i.  e.,  in  cases  of 
slight  or  average  severity  the  third 
stage,  and  in  severe  cases  commonly 
the  fourth — is  the  period  of  defer- 
vescence or  recovery.  The  peculiar- 
ity of  this  period  in  typhoid  fever  is 
that  the  fall  of  the  fever  is  never  by 
crisis,  but  always  gradually,  by  lysis. 
Commonly  the  temperature  descends 
by  degrees,  so  that  on  each  new  day 

the    morning    remissions    as    well    as  o^  g^  o^  °,  '^   ^ 

the  evening  exacerbations  are   l°to  ^  g?  ^  c5  '-'fa 

2°    (0.5°-l°    C.)    lower.     The   zigzag 

form  of  curve,  in  which  there  are  of  course  very  frequently  slight  irregularities, 
must  be  taken  as  the  rule.     The  duration  of  the  defervescence  generally  exceeds 


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8  ACUTE  GENERAL  INFECTIOUS  DISEASES 

that  of  the  initial  period.  It  lasts  five  to  eight  days,  often  longer.  It  is  not  very" 
seldom  that  in  defervescence  the  morning  remissions  become  from  the  first  very 
marked,  even  reaching  the  normal  temperature,  while  the  evening  exacerbations 
become  daily  less  and  less,  until  they  too  are  not  above  the  normal.  A  third  form 
of  decline  is  much  less  frequent,  in  which  the  morning  remissions  become  every 
day  greater,  while  the  evening  temperature  persists  for  some  days  at  about  the 
same  height.  Several  times  we  have  seen  the  fever  take  on  a  tertian  type  during; 
recovery. 

To  this  outline  must  be  added  a  number  of  observations  of  practical  importance. 

The  initial  period  does  not  exhibit  especial  variations  from  the  course  we  have 
stated.    Its  entire  duration  is  bounded  by  certain  relatively  narrow  limits. 

The  fastigium  presents,  as  already  mentioned,  the  greatest  varieties  in  its  dura- 
tion. In  light  cases  it  is  wholly  wanting,  so  that  these  consist  only  of  a  period  of 
gradually  rising  fever,  and  of  a  gradual  defervescence  almost  immediately  con- 
secutive to  the  rise.  The  entire  duration  of  such  light  cases  is  only  one  and  a  half 
to  two  weeks.  In  other  and  tolerably  frequent  cases,  which  are  often  tedious,  but 
still  for  the  most  part  are  light,  the  fever  is  not  continuous,  but  remittent.  Th& 
difference  between  the  morning  and  evening  temperatures  amounts  to  3°  or  4 
F.  (1.5°-2.0°  C),  but  the  absolute  height  of  the  temperature  is  often  not  very  con- 
siderable, so  that  the  temperature  curve  at  first  leads  to  error  and  excites  suspi- 
cion, for  example,  of  tuberculosis.  We  have  seen  in  Leipsic  a  number  of  cases 
in  which  the  fever  was  perfectly  intermittent  during  almost  the  entire  illness^ 
and  for  two  to  three  weeks  afternoon  elevations  reaching  104°  (40°  C.)  or  more 
daily  succeeded  normal  morning  temperatures.  These  cases  had  the  general  course 
of  light  attacks. 

Various  influences,  not  to  speak  of  therapeutic  interference,  may  produce  a. 
considerable  temporary  remission  of  temperature  in  the  course  of  the  fastigium. 
Such  a  remission  sometimes  occurs  spontaneously  from  the  seventh  to  tenth  day 
of  the  disease.  If  a  marked  intestinal  haemorrhage  happens  (vide  infra),  the  tem- 
perature generally  falls  several  degrees  centigrade,  and  the  less  frequent  instances, 
of  severe  epistaxis  have  the  same  effect.  If,  in  female  patients,  abortion  or  prema- 
ture delivery  occurs,  we  often  observe  a  similar  considerable  fall  of  temperature,, 
even  without  severe  attendant  haemorrhage.  Perforation  of  the  intestine  often 
causes  the  temperature  to  fall  rapidly.  At  times  the  occurrence  of  mental  dis- 
turbances effects  a  moderate  though  noticeable  lowering  of  temperature.  Those 
great  and  sudden  depressions  of  temperature  remain  to  be  mentioned  which  are 
accompanied  by  a  very  small  but  exceedingly  rapid  pulse  and  general  prostration. 
Every  such  collapse,  if  severe,  is  a  most  dangerous  event,  and  demands  prompt 
and  energetic  medical  treatment  (vide  infra). 

The  development  of  local  complications,  such  as  pneumonia  or  inflammation  of 
the  parotid  gland,  is  generally  accompanied  by  a  considerable  rise  of  tempera- 
ture. The  fever  in  such  cases  often  becomes  more  irregular.  This  indicates  the 
great  practical  value  of  thermometry.  Almost  every  new  rise  of  temperature  or 
any  considerable  change  in  the  ordinary  course  of  the  temperature  has  its  special 
cause,  and  is  therefore  a  warning  to  the  attending  physician  to  be  vigilant.  The 
cause  of  the  change  in  the  temperature  is  often  not  apparent  until  two  or  three 
days  later. 

The  period  of  defervescence  departs  most  frequently  from  its  typical  behavior 
by  being  lengthened  out  into  a  "  stage  of  retardation."  The  morning  tempera- 
ture is  then  generally  normal,  while  in  the  evening  slight  or  moderate  elevations 
continue.  The  reason  for  this  long  continuance  of  the  fever  may  freqviently  be 
found  in  some  not  yet  completely  healed  local  complication,  but  often  no  such 
lesion  can  be  demonstrated.  Then  we  are  commonly  inclined  to  surmise  sluggish, 
intestinal  ulcers  which  will  not  heal,  or  trouble  in  the  mesenteric  glands,  etc. 


TYPHOID  FEVER  & 

This  slow  fever  may  continue  for  weeks.  It  is  prone  to  follow  severe  cases^ 
but  lighter  attacks,  especially  in  elderly  or  feeble  patients,  may  also  take  on  this 
sluggish  character  at  a  relatively  early  period.  To  these  last-mentioned  cases 
must  finally  be  added  a  few  others  in  which  during  the  whole  course  of  typhoid 
fever  no  febrile  temperature  at  all  or  only  a  very  slight  rise  can  be  detected. 

Entrance  into  complete  convalescence  is  shown  with  far  greater  certainty  by 
the  absence  of  elevations  of  temperature  than  by  any  other  single  symptom. 
There  sometimes  come,  however,  temporary  elevations  of  temperature  during  con- 
valescence, following  some  error  in  diet,  long-continued  constipation,  or  mental 
excitement.  In  other  cases  the  new  fever  depends  on  some  local  sequela,  e.  g.,  a 
boil  or  a  glandular  abscess.  Often,  however,  the  most  accurate  investigation  fails 
to  demonstrate  a  cause.  Especially  in  the  beginning  of  convalescence  there  some- 
times comes  a  high  fever,  or  even  a  rigor,  which  may  recur  several  times,  but 
which  soon  gives  place  to  a  normal  temperature.  Generally  no  definite  cause  for 
these  brief  but  decided  elevations  of  temperature  can  be  pointed  out.  Perhaps  we 
might  consider  the  possibility  of  some  affection  of  the  mesenteric  lymph-glands. 
These  sudden  and  great  elevations  have  seldom  any  grave  significance. 

This  new  fever  which  we  have  just  described  is  best  termed  febrile  recrudes- 
cence, or  febrile  sequela,  in  contrast  with  the  proper  typhoid  relapse.  That 
is,  after  typhoid  fever  has  ended,  the  whole  process  may  be  repeated;  and  this 
occurrence  is  called  a  relapse.  Particulars  as  to  the  behavior  of  the  fever  in  such 
cases  will  be  considered  below,  in  connection  with  all  the  other  peculiarities  of 
typhoid  relapses. 

Phenomena  and  Complications  relating  to  the  Separate  Organs  * 

Before  we  undertake  a  detailed  discussion  of  the  individual  symptoms  of 
typhoid  fever,  we  must  first  make  a  brief  general  statement  which  is  of  very  great 
significance  for  the  correct  understanding  of  almost  every  infectious  disease. 
We  include  among  the  direct  typhoidal  symptoms  all  those  morbid  phenomena 
which  are  produced  immediately  by  the  typhoid  bacillus  itself  or  by  its  toxic 
chemical  action;  but,  on  the  other  hand,  every  patient  sick  with  typhoid  fever 
is  exposed  to  many  secondary  infections  (from  the  intestinal  ulcers,  from  the 
mouth,  in  the  lungs,  etc.)  whose  invasion  is  rendered  possible,  or  at  least  rendered 
easier,  by  the  pre-existing  typhoid  infection.  All  the  morbid  symptoms  arising  in 
this  way,  which  unite  with  the  pure  typhoidal  symptoms  in  making  up  the  whole 
picture  of  the  disease,  must,  strictly  speaking,  be  termed  complications  of  typhoid. 
In  the  individual  case  it  is  often  hard  to  decide  whether  a  particular  symptom 
is  of  a  typhoidal  nature  or  a  complication.  We  must,  however,  hold  fast  to  the 
essential  difference  between  these  two  kinds  of  morbid  phenomena,  if  we  would 
obtain  a  deep  insight  into  the  nature  and  origin  of  the  whole  course  of  the 
disease. 

1.  Digestive  Organs. — We  think  it  best  to  begin  our  consideration  of  the  more 
special  symptoms  with  the  phenomena  referable  to  the  intestinal  canal,  for  the 
reason  that  the  anatomical  changes  in  the  intestine  are  pathognomonic.  Indeed, 
these  alterations  may  sometimes  become  of  surpassing  import  in  a  clinical  point 
of  view,  although  in  the  majority  of  cases  the  intestinal  symptoms  are  clinically 
not  nearly  so  prominent  as  the  general  symptoms  that  result  from  the  infection 
of  the  system  as  a  whole. 

The  characteristic  typhoid  lesion  of  the  intestine  consists  of  an  affection  of 
Peyer's  patches,  most  marked  in  the  lower  part  of  the  ileum.  In  the  first  week 
the  patches  swell  gradually   (stage  of  medullary  infiltration).     The  rest  of  the 

*  To  avoid  repetition,  Ave  have  in  what  follows  united  a  description  of  the  anatomical  changes  with, 
the  presentation  of  the  clinical  symptoms. 


10  ACUTE  GENERAL  INFECTIOUS  DISEASES 

mucous  membrane  exhibits  at  the  same  tim.e  miore  or  less  marked  symptomis  of 
simple  catarrhal  inflammation.  In  the  second  week,  necrotic  crusts  form  on  the 
surface  of  the  patches,  which  are  cast  off  in  the  third  week,  leaving  behind  the 
typhoid  ulcers.  Toward  the  end  of  the  third  week  the  ulcers  clean  up,  and  then 
in  the  fourth  week,  if  the  case  takes  a  favorable  course,  the  ulcers  heal.  Smooth 
scars  are  formed,  often  diffusely  pigmented.  Experience  shows  that  these  scarcely 
ever  lead  to  stricture  of  the  intestine.  The  same  process  also  goes  on  in  a  greater 
or  less  number  of  the  solitary  follicles  as  well  as  in  the  Peyer's  patches  themselves. 
We  may  add  that  probably  in  lighter  cases  of  typhoid  (vide  infra)  there  is  often 
no  actual  ulceration.  The  swelling  of  the  lymphatic  tissue  subsides  in  this  case 
before  sloughing  occurs.  We  have  already  mentioned  the  occurrence  of  typhoid 
bacilli  in  Peyer's  patches  and  the  intestinal  follicles. 

The  number  and  size  of  the  ulcers  formed  have  no  direct  relation  whatever 
to  the  severity  of  the  case.  Although  very  extensive  lesions  in  the  intestine  are 
often  found  in  cases  that  end  fatally,  yet,  on  the  other  hand,  we  observe  fatal 
cases  in  which  only  a  few  ulcers  are  found  in  the  intestine.  In  cases  with  exten- 
sive intestinal  lesions  we  often  see  follicular  ulcers  in  the  colon  as  well  as  in  the 
small  intestine  (colo-typhoid). 

The  clinical  symptoms  referable  to  the  intestinal  canal  are,  as  we  have  said, 
prominent  only  in  exceptional  cases.  In  the  beginning  of  typhoid  fever  there  is 
usually  constipation.  This  may  last  throughout  the  illness,  so  that  the  patients 
have  but  one  dejection  in  every  two  or  three  days,  or  often  none  at  all  unless  an 
enema  be  given.  As  a  rule,  a  moderate  diarrhoea  begins  during  the  second  week. 
There  are  two  to  four  stools,  or  sometimes  more,  each  day.  These  usually  have 
a  characteristic  bright-yellow  color.  On  standing,  they  divide  into  an  upper, 
cloudy,  and  quite  liquid  layer,  and  a  lower  layer  composed  of  yellow,  crumbly 
masses.  They  have  generally  an  alkaline  reaction,  and  upon  microscopic  exami- 
nation they  are  found  to  contain,  besides  remnants  of  the  ingesta  and  granular 
detritus,  a  few  epithelial  cells,  round  cells,  many  crystals  of  triple  phosphate,  and 
numberless  bacteria.  Pfeiffer  and  other  investigators  have  been  able  frequently, 
although  not  invariably,  to  demonstrate  the  true  tjT)hoid  bacilli  in  the  dejecta 
by  means  of  special  methods  of  cultivation. 

Severe  diarrhoea  (ten  or  more  stools  daily)  is  relatively  infrequent.  In  some 
bad  cases  we  have  seen  the  stools  take  on  a  dysenteric  character.  The  autopsy 
showed  in  these  cases  unusually  severe  lesions  of  the  colon  and  a  diphtheritic 
inflammation  of  its  mucous  membrane.  They  were  probably  secondary  compli- 
cations. 

Gaseous  distention  affecting  the  intestine,  and  especially  the  colon,  is  very 
frequent ;  a  slight  but  evident  gaseous  distention,  with  a  fluctuating,  "  air-cush- 
ion "  feeling,  is  a  very  valuable  symptom  in  the  diagnosis  of  typhoid  fever,  but, 
as  a  rule,  the  meteorism  is  moderate.  Indeed,  severe  cases  of  typhoid  are  ob- 
served in  which  the  abdomen  always  remains  concave.  Marked  tympanites  is 
always  an  unpleasant  complication.  We  saw  one  case,  which  ended  fatally,  with 
very  great  tympanites,  in  which  the  lesions  were  almost  exclusively  in  the  colon, 
and  it  was  the  enormous  distention  of  its  entire  length  which  had  so  swollen 
the  abdomen.  The  noise  that«an  often  be  produced  by  pressure  in  the  ileo-cfecal 
region  (gurgling)  used  to  be  regarded,  but  probably  erroneously,  as  especially 
characteristic  of  typhoid  fever.  Abdominal  pain  is  often  entirely  absent.  Some 
patients,  however,  complain  of  abdominal  pain  during  almost  the  entire  illness. 
On  pressure,  the  belly  is  generally  somewhat  sensitive,  but  the  tenderness  is  sel- 
dom extreme.  It  is  more  apt  to  be  marked  when  there  is  constipation.  Often 
such  tenderness  is  due  to  a  participation  of  the  peritoneum  in  the  disease,  even 
when  there  is  no  perforation  (vide  infra). 

There  still  remain  two  symptoms  of  the  greatest  practical  importance,  both  of 


TYPHOID  FEVER  11 

which  have  a  direct  connection  with  the  intestinal  lesions:  they  are  intestinal 
haemorrhage  and  perforation. 

Intestinal  hsemorrhages  in  the  course  of  typhoid  are  almost  always  due  to  the 
erosion  of  the  walls  of  blood-vessels  in  connection  with  the  formation  and  throw- 
ing off  of  the  crusts  of  the  ulcers.  The  hsemorrhages  occur,  therefore,  most  fre- 
quently toward  the  end  of  the  second  and  during  the  third  week.  The  blood  pours 
out  into  the  intestine,  and  is  passed  with  the  stools.  Its  amount  may  be  small,  or 
it  may  reach  to  one  or  two  pints,  or  even  more.  Its  color  is  generally  rather  dark. 
The  later  discharges  are  generally  tarry.  Liebermeister  states  that  he  has  ob- 
served intestinal  hsemorrhages  in  7.3  per  cent,  of  typhoid  patients,  and  Griesinger 
in  5.3  per  cent.  We  have  ourselves  seen,  in  the  medical  wards  in  Leipsic,  45 
intestinal  haemorrhages  in  472  cases,  i.  e.,  in  9.5  per  cent.  In  individual  epidemics 
the  frequency  varies  greatly.     It  rose  in  1880  to  eighteen  per  cent. 

Intestinal  hsemorrhage  is  always  a  grave  symptom.  Even  slight  hsemorrhages 
deserve  consideration,  for  they  may  be  the  precursors  of  severer  ones.  Yet 
intestinal  hsemorrhage,  even  if  profuse,  is  not  necessarily  fatal.  Of  the  above 
forty-five  cases  of  typhoid  with  haemorrhage,  twenty-six  ended  in  complete  recov- 
ery. In  eight  cases,  death  occurred  as  the  immediate  result  of  the  loss  of  blood. 
Eleven  ended  fatally  after  a  time. 

After  every  considerable  intestinal  hsemorrhage,  the  symptoms  of  general 
ansemia,  often  even  of  collapse,  appear.  The  fall  of  the  bodily  temperature  has 
been  already  mentioned.  The  hsemorrhage  has  sometimes  a  favorable  influence 
on  severe  cerebral  symptoms,  for  consciousness  succeeds  to  the  previous  stupor 
or  delirium.  Often  the  haemorrhage  is  directly  followed  by  recovery  from  the 
disease. 

Much  more  ominous  than  the  intestinal  haemorrhage  is  the  occurrence  of  per- 
foration, as  a  result  of  the  breaking  through  of  a  typhoid  ulcer  into  the  abdominal 
cavity,  because,  almost  without  exception,  this  is  followed  by  a  purulent  or  even 
ichorous  peritonitis.  Peritonitis  is  never  caused  by  the  typhoid  bacillus  itself, 
but  by  pyogenic  organisms  (cocci,  perhaps  bacterium  coli?)  which  enter  the  ab- 
dominal cavity  with  the  contents  of  the  intestine.  The  amount  of  fluid  peri- 
tonitic  exudation  is,  as  a  rule,  not  very  great.  The  serous  membrane  is  often 
found  covered  merely  with  a  fibrino-purulent  or  purulent-hsemorrhagic  deposit. 
The  occurrence  of  perforation  is  sometimes  marked  by  a  violent  pain  suddenly 
felt  by  the  patient ;  but  it  may  also,  even  in  severe  cases,  take  place  insidiously. 
The  abdomen  is  generally  (not  always)  greatly  distended  and  very  tender  on 
pressure,  so  that  even  in  stupor  patients  groan  while  being  examined.  If  gas  has 
entered  through  the  opening  into  the  peritoneal  cavity,  we  often  observe  absence 
of  the  ordinary  dullness  over  the  liver ;  but  this  symptom  is  to  be  employed  cau- 
tiously as  a  factor  in  diagnosis,  for  absence  of  hepatic  dullness  may  also  result 
from  distended  intestines  lying  in  front  of  the  liver.  When  perforation  has  oc- 
curred, the  patient  soon  looks  collapsed,  with  cheeks  fallen  in  and  sharp,  cool  nose. 
Frequent  eructations  and  vomiting  often  follow.  The  pulse  becomes  small  and 
very  frequent.  The  temperature  generally  falls  as  the  peritonitis  begins,  and 
later  it  usually  undergoes  great  variations. 

Perforation  of  the  intestine  occurs  most  frequently  in  the  third  or  fourth  week 
of  the  disease,  and  much  oftener  in  men  than  in  women.  In  sluggish  cases,  how- 
ever, we  can  not  be  without  apprehensions  of  it  till  a  late  period.  The  perforation 
generally  takes  place  in  a  coil  of  the  lower  part  of  the  small  intestine,  and  with 
marked  relative  frequency  in  the  right  side  of  the  pelvis,  though  seldom  in  the  ver- 
miform appendix  or  in  the  colon.  With  few  exceptions,  death  comes  quicklj^ 
after  a  few  days  at  latest.  Only  when  the  perforation  is  small  and  the  intestines 
have  become  agglutinated  at  the  onset  is  the  course  of  the  peritonitis  slower,  so 
that  the  symptoms  are  less  violent  and  cause  death  in  a  week  or  ten  days.     Out 


12  ACUTE  GENEEAL  INFECTIOUS  DISEASES 

of  fifty-six  fatal  typhoid  cases  in  the  Leipsic  medical  clinique  we  lost  five,  or  nine 
per  cent.,  from  peritonitis  following  perforation.  Here  and  there  a  case  of  re- 
covery has  been  reported,  probably  resulting  from  a  limitation  of  the  peritonitis- 
through  sppedy  adhesion  of  the  intestines. 

It  should  be  mentioned  here  that  sometimes  in  typhoid  fever  a  local  or  general 
peritonitis  may  occur  through  direct  extension  of  the  process  to  the  serous  mem- 
brane without  actual  perforation.  We  have  seen  in  one  case,  as  the  result  of  the 
peritonitic  bands  and  false  membranes,  complete  occlusion  of  the  intestine  (ileus), 
and  death. 

Swelling  of  the  mesenteric  lymph-glands  (less  often  of  the  retro-peritoneal 
glands  as  well)  is  found  in  typhoid  almost  as  constantly  as  the  anatomical  changes. 
in  the  intestine.  Sometimes  they  break  down,  i.  e.,  suppurate.  In  cases  that  have 
passed  through  the  disease  we  often  find  considerable  deposits  of  lime  in  the 
glands.  These  changes  have  a  certain  clinical  importance;  for,  as  already  men- 
.  tioned,  we  may  often  venture  to  refer  a  more  or  less  tedious  recurrent  febrile  state 
which  has  no  other  demonstrable  cause  to  this  lesion  of  the  mesenteric  glands.. 
In  some  rare  cases  a  general  peritonitis  has  been  observed  as  a  result  of  the  burst- 
ing of  a  suppurating  gland. 

The  swelling  of  the  spleen  (acute  splenic  tumor)  is,  in  typhoid  fever  as  well  as 
in  many  other  acute  infectious  diseases,  one  of  the  most  constant  symptoms.  The 
enlargement  of  the  spleen  can  often  be  demonstrated  as  early  as  the  end  of  the 
first  week,  and  is  therefore  of  considerable  diagnostic  importance ;  but  percussion 
of  the  spleen  is  sometimes  decidedly  difiicult  and  deceptive  in  this  disease  because 
of  the  existence  of  tympanites.  The  surest  demonstration  of  splenic  enlargement 
is  therefore  always  by  means  of  palpation,  which,  after  a  little  practice,  gives  a 
positive  result  in  the  majority  of  cases.  Absence  of  splenic  tumor  is  most  fre- 
quently observed  in  elderly  typhoid  patients.  The  spleen  may  also  diminish  con- 
siderably in  size  after  severe  intestinal  haemorrhage.  Pain  in  the  splenic  region, 
resulting  from  tearing  of  the  distended  capsule,  is  comparatively  rare.  The 
splenic  infarctions  which  sometimes  occur  may,  in  exceptional  cases,  prove  the 
starting-point  of  a  peritonitis. 

Hepatic  symptoms  are  seldom  seen  in  typhoid  fever,  except  that  there  may  be  a 
moderate  swelling  of  the  organ.  The  anatomical  changes  of  "  parenchymatous, 
degeneration,"  and  the  frequent  formation  in  the  liver  of  the  small  lymphomata. 
which  Wagner  discovered,  have  no  clinical  significance.  The  bile  secreted  is  gen- 
erally pale  and  scanty.  This  is  a  partial  explanation  of  the  light  color  of  the 
stools.  A  very  rare  complication,  which  we  ourselves  observed  in  one  case,  is 
acute  yellow  atrophy  of  the  liver. 

The  stomach  presents  no  especial  anatomical  changes  in  typhoid.  Anorexia 
is  an  almost  invariable  symptom  in  the  beginning  and  during  the  course  of 
all  severer  cases.  There  is  seldom  any  desire  for  food  till  recovery  begins;  but 
then,  if  convalescence  is  undisturbed,  the  appetite  soon  attains  an  enviable  keen- 
ness. Vomiting  in  the  beginning  or  course  of  the  disease  is  an  exception,  unless 
after  some  error  in  diet.  We  have  already  mentioned  it  as  a  symptom  of  perito- 
nitis. 

The  changes  in  the  mouth  and  throat  of  typhoid  patients  deserve  the  careful 
attention  of  the  physician.  The  lips  and  tongue  are  in  severe  cases  dry  and  fis- 
sured. The  lips  are  often  covered  with  dry,  black  crusts,  sometimes  described  as 
a  "  fuliginous  coating."  The  tongue  is  apt  to  be  thickly  coated  at  first,  but  later 
cleans  off  from  the  edges  and  tip.  In  severe  cases,  especially  if  the  mouth  is  not 
.properly  cleansed,  a  rather  severe  stomatitis  may  occur  and  produce  superficial 
ulceration  of  the  buccal  mucous  membrane  and  of  the  edges  of  the  tongue.  The 
gums  sometimes  become  spongy,  and  are  apt  to  bleed,  as  if  scorbutic. 

Actual  sore  throat,  at  least  according  to  our  experience  in  Leipsic,  occurs  but 


TYPHOID  FEVER  13 

seldom  at  the  beginning  of  typhoid  fever.  The  difficulty  in  swallowing,  often 
complained  of  by  patients,  is  generally  due  to  dryness  of  the  pharynx.  In  certain 
epidemics,  however,  the  occurrence  of  sore  throat  at  the  beginning  of  the  illness 
lias  been  frequently  observed.  It  may  even  happen  that  this  early  sore  throat  is 
accompanied  by  an  erythema  diffused  over  the  body,  so  that  at  first  suspicions  of 
scarlet  fever  arise.  The  cases  are  very  interesting  and  quite  rare  (although  we  have 
repeatedly  seen  them)  in  which  disturbances  of  swallowing  exist  with  the  general 
typhoid  symptoms  from  the  beginning.  On  examining  the  fauces  we  see  on  the 
tonsils  peculiar  white,  slightly  elevated  spots,  which  later  form  superficial  ulcers. 
After  a  time  these  places  heal,  and  in  other  respects  the  disease  pursues  a  normal 
course.  The  suspicion  is  justified  that  in  these  cases  there  is  a  specific  typhoidal 
disease  of  the  tonsils  (due  to  the  typhoid  bacillus  itself),  and  such  cases  are  called 
tonsillar  or  pharyngeal  typhoid  (analogous  to  the  laryngeal  typhoid,  pneumo- 
typhoid,  and  nephro-typhoid,  to  be  mentioned  later).  In  such  cases  the  typhoid 
bacilli  have  probably  attacked  the  tonsils  at  their  first  invasion.  It  should  also 
he  mentioned  that  in  severe  cases  there  is  often  an  extensive  growth  of  thrush  in 
the  mouth  and  throat,  and  this  may  spread  quite  a  distance  down  the  oesophagus. 

The  changes  in  the  mouth  and  throat  are  of  especial  interest,  for  the  reason 
that  they  may  be  directly  propagated  to  important  neighboring  organs.  Starting 
from  the  pharyngeal  cavity,  the  pathogenic  agent,  probably  in  most  cases  the 
staphylococcus,  may  penetrate  through  the  Eustachian  tube  into  the  middle  ear. 
Thus  arise  those  inflammations  of  the  middle  ear  which  are  not  very  rare  in  severe 
cases  of  typhoid,  and  which  lead  to  perforation  of  the  membrana  tympani  and 
to  purulent  discharges  from  the  ear.  The  not  infrequent  inflammation  of  the 
parotid  gland  is  also,  as  we  believe,  occasioned  in  a  similar  way,  the  inflammatory 
agent  reaching  the  parotid  gland  from  the  mouth  by  way  of  Steno's  duct.  We  do 
not  regard  the  otitis  and  parotitis  as  especial  localizations  of  the  typhoid  poison, 
but  as  secondary  diseases,  for  the  occurrence  of  which  typhoid  fever  merely  fur- 
nishes the  occasion,  as  when  the  mouth  is  imperfectly  cleansed.  Purulent  otitis 
in  typhoid  fever  can  easily  be  overlooked  at  first,  since  stuporous  patients  only 
Tarely  complain,  of  themselves,  of  pain  in  the  ear  or  deafness.  The  parotitis 
appears  m^ost  frequently  in  the  third  week,  and  generally  on  one  side,  though 
sometimes  on  both.  It  almost  always  becomes  purulent,  and  discharges  either 
externally  or  into  the  external  auditory  meatus,  unless  there  is  a  timely  incision. 

2.  Organs  of  Respiration. — Affections  of  the  lungs  are  among  the  most  fre- 
quent and  important  complications  of  typhoid  fever,  but  are  for  the  most  part  not 
a  direct  result  of  the  typhoid  infection,  but  pure  complications.  The  bronchitis 
very  often  found  in  severe  cases,  and  especially  in  patients  who  do  not  come  till 
late  under  proper  care,  certainly  is  dependent  on  the  imperfect  expectoration  of 
the  bronchial  secretions  and  on  the  inhalation  of  inflammatory  agents  coming 
from  the  mouth  and  throat. 

ISTumerous  cases  of  typhoid  of  slight  or  average  severity,  under  proper  care, 
run  their  course  without  any  considerable  bronchitis.  In  many  other  cases,  and 
even  severe  ones,  the  bronchitis  remains  within  moderate  bounds,  especially  if 
the  patient  is  brought  promptly  under  proper  care  and  treatment ;  but  in  severe 
■cases,  when  marked  disturbances  of  the  nervous  system  arise,  and  the  patient  in 
his  stupor  expectorates  little,  swallows  things  the  wrong  way,  and  lies  all  the 
time  on  his  back,  passive  and  collapsed,  the  occurrence  of  a  severe,  diffuse  bron- 
chitis, especially  in  the  lower  lobes  of  the  lungs,  can  hardly  be  avoided.  Wor  in 
such  cases  is  there  generally  a  mere  bronchitis,  but  a  more  or  less  extensive 
catarrhal,  lobular  pneumonia,  to  be  classed  therefore  under  the  so-called  inhala- 
tion pneumonias  (cf.  chapter  on  lobular  pneumonia).  What  was  formerly 
termed  "  hypostatic  pneumonia  "  is  also  almost  invariably  to  be  put  in  this  group. 

Erom  the  way  in  which  these  pulmonary  disorders  arise,  we  can  understand 


14  ACUTE  GENERAL  INFECTIOUS  DISEASES 

why  the  bronchitis  sometimes  takes  on  a  putrid  character,  and  why  the  lobular 
infiltrations  are,  in  severe  cases,  transformed  into  genuine  gangrene.  If  such  spots 
touch  the  pleura,  they  occasion  the  development  of  a  pleurisy  which  is  almost 
always  purulent.  In  rare  cases,  pneumothorax  may  arise  as  a  sequel  to  the  perfo- 
ration of  a  gangrenous  infiltration  into  the  pleural  cavity.  Various  circumstances 
promote  the  occurrence  of  pulmonary  symptoms.  Thus  we  find  it  especially  easy 
for  a  severe  bronchitis  and  its  sequelae  to  be  developed,  in  the  case  of  elderly  per- 
sons, or  the  kyphoskoliotic,  or  the  corpulent,  or  patients  who  have  previously  suf- 
fered from  emphysema  or  cardiac  disease. 

The  subjective  thoracic  symptoms,  in  typhoid  patients  who  have  pulmonary 
complications,  are  generally  not  very  prominent.  It  is  only  occasionally  that 
patients  complain  in  the  early  stages  of  typhoid  fever  of  pain,  and  of  a  sense  of 
oppression  in  the  chest,  or  of  cough,  or  of  a  stitch  in  the  side;  and  even  when 
such  symptoms  exist,  the  physical  examination  may  give  comparatively  insignifi- 
cant results.  The  severer  pulmonary  complications  are  seen  mainly  in  those 
whose  intelligence  is  more  or  less  blunted,  and  who,  therefore,  make  little  com- 
plaint, are  not  much  disturbed  by  the  dyspnoea,  and  cough  and  expectorate  little. 
A  careful  physical  examination  alone  can  enlighten  us  as  to  their  condition.  On 
auscultation,  sibilant  rhonchi  are  the  chief  signs  observed  in  the  milder  cases.  In 
the  severer  ones  there  are  moist,  fine,  and  coarse  rales,  especially  numerous  toward 
the  base  of  the  chest.  If  there  are  abundant  moist  rales,  we  may  infer  that  there 
is  a  lobular  pneumonia,  although  this  can  not  be  demonstrated  with  certainty  till 
the  separate  islets  of  infiltration  unite  into  a  more  extensive  solidification,  so  as  to 
afford  dullness  on  percussion. 

In  addition  to  the  pulmonary  lesions  already  mentioned,  genuine  croupous  or 
lobar  pneumonia  does  occur  in  typhoid  fever.  This  is  often  an  actual  complica- 
tion, dependent  upon  a  secondary  infection  with  the  genuine  pneumonia  diplo- 
coccus.  Such  a  pneumonia  may  come  on  early  or  sometimes  during  convalescence, 
and  affect  both  the  upper  and  lower  lobes.  There  is  probably  also  a  true  typhoid 
pneumonia  caused  by  the  entrance  of  typhoid  bacilli  into  the  lungs.  Such  a 
pneumonia  can  not  at  present  be  recognized  anatomically,  but  only  by  bacterio- 
logical investigation.  Especial  interest  attaches  to  those  cases  of  typhoid  fever 
which  begin  with  a  lobar  pneumonia.  Often  there  is  at  first  not  the  slightest 
suspicion  of  a  typhoid  fever,  for  the  disease  is  regarded  as  an  ordinary  croupous- 
pneumonia;  but  it  is  usually  to  be  noticed  that  the  illness  does  not  begin  sud- 
denly with  a  rigor,  but  more  gradually,  and  that  from  its  incipiency  the  constitu- 
tional symptoms,  the  headache  and  splenic  tumor,  are  more  prominent  than  is 
usually  the  case  in  pneumonia.  At  the  end  of  the  first  week's  illness  there  is  no 
crisis,  but  persistent  fever.  Now  the  pulmonary  symptoms  often  retreat  more 
and  more  to  the  background,  while,  on  the  contrary,  diarrhoea  and  rose-spots 
appear.  The  spleen  is  enlarged.  In  short,  the  clinical  picture  of  typhoid  is 
developed.  It  is  not  unnatural  to  suppose,  although  there  is  yet  no  absolute 
proof  of  the  fact,  that  in  these  cases,  which  are  fittingly  termed  "  pneumo- 
typhoid,"  the  infection  with  the  typhoid  bacilli  has  taken  place  exceptionally  in 
the  pulmonary  tissue,  and  that,  therefore,  the  first  pathological  changes  are  devel- 
oped in  the  lungs. 

Laryngeal  Lesions. — The  same  causes  which  produce  the  bronchitis  result  alao 
in  a  simple  catarrhal  laryngitis,  with  hoarseness.  This  is  in  severe  cases  accom- 
■  panied  by  superficial  ulcers  on  the  vocal  cords  or  the  posterior  wall  of  the  larynx. 
Sometimes,  again,  the  lesion  is  due  to  mechanical  causes,  constituting  the  so-called 
"  decubitus  laryngis."  The  disorders  which  attack  the  less  superficial  structures 
of  the  larynx  are  fortunately  rare.  Chief  among  them  is  a  laryngeal  perichon- 
dritis of  the  arytenoid  cartilages.  This  complication  is  justly  regarded  as  of  bad 
omen,  and  may  lead  to  the  rapid  development  of  cedema  of  the  glottis,  with  great 


TYPHOID  FEVER  15 

laryngeal  obstruction  and  threatening  suffocation.  These  severe  laryngeal  affec- 
tions in  typhoid  are  regarded  by  some  authorities,  especially  by  Klebs,  as  always 
the  direct  effect  of  the  infecting  poison;  but  in  most  cases  they  are  probably  due 
to  an  invasion  of  staphylococci  or  some  similar  microbes.  We  have  several  times 
seen  croup  in  typhoid  fever,  and  it  is  a  very  dangerous  symptom.  In  regard 
to  their  origin  most  of  these  mild  and  severe  laryngeal  affections  in  the  course 
of  typhoid  fever  are  to  be  regarded  as  secondary  inflammations;  but  specific 
typhoid  disease  of  the  larynx  also  seems  to  exist.  The  cases  are  of  interest  where 
the  whole  morbid  process  begins  with  a  severe  laryngitis  ("  laryngeal  typhoid  ") 
and  is  followed  later  by  the  ordinary  symptoms  of  typhoid  (vide  supra,  pharyngeal 
typhoid). 

Among  symptoms  referable  to  the  mucous  membrane  of  the  nose,  epistaxis  is 
important.  It  occurs  in  the  beginning  of  typhoid  with  tolerable  frequency,  and 
is  in  one  way  not  unfavorable,  for  it  often  mitigates  the  patient's  headache.  At  a 
later  period  nose-bleed  may  become  a  most  unpleasant  complication,  as  it  is  some- 
times very  difficult  to  check.  We  have  even  seen  one  fatal  case  due  to  persistent 
nose-bleed.  Other  nasal  symptoms  are  exceptional.  There  is  an  old  saying  that 
typhoid  never  begins  with  a  coryza. 

3.  Nervous  System. — The  old  term  "  nervous  fever,"  which  is  still  used  by  the 
laity,  shows  how  frequent  and  severe  are  the  nervous  derangements  which  occur 
in  typhoid.  In  cases  of  any  severity  there  is  almost  always  a  certain  dullness  of 
intellect,  often  amounting  to  apathy  and  somnolence.  The  patients  give  mono- 
syllabic and  incomplete  answers  to  all  questions,  and  their  statements  about 
their  previous  history  are  often  disordered  and  contradictory.  There  may  even 
be  sopor  or  a  deep  coma  in  the  worst  cases.  All  cases  of  this  sort  in  which 
there  was  a  condition  of  intellectual  enfeeblement  were  termed  by  the  old 
physicians  "  fehris  nervosa  stupida,"  in  contrast  to  the  "  febris  nervosa  ver- 
satilis,"  that  form  in  which  abnormal  mental  activity  or  delirium  predominates. 
In  severe  cases  delirium  is  very  frequent.  It  is  generally  worse  at  night,  and  at 
times  when  the  patient  happens  to  be  left  alone.  Very  often  he  tries  to  leave  his 
bed,  because  of  his  delusions,  and  talks  of  persons  and  things  with  which  he  was 
fomierly  familiar;  or  he  is  very  noisy  and  restless,  sometimes  shrieking  from 
groundless  fears.  We  may  add  that  these  diverse  nervous  symptoms  frequently 
succeed  one  another,  or  appear  in  combination.  Sometimes  a  soporose  patient 
may  be  heard  softly  whispering  to  himself  in  "  muttering  delirium." 

Certain  motor  disturbances  are  often  combined  with  considerable  impairment 
of  consciousness.  There  is  a  slight  twitching  of  the  muscles  of  the  face  and  ex- 
tremities. The  old  authorities  gave  the  name  suhsultus  tendinum  to  the  sudden 
leaping  into  prominence  of  the  sinews  thus  caused.  It  is  best  seen  on  the  back 
of  the  hands.  In  severe  cases  the  patient  is  sometimes  observed  to  grind  the  teeth 
together;  this  is  due  to  a  cramp-like  condition  of  the  muscles  of  mastication,  and 
is  justly  regarded  as  ominous.  We  often  see  persistent  tremor  of  the  extremities 
and  lower  jaw;  and  it  is  especially  in  these  cases,  as  we  have  demonstrated  iipon 
numerous  patients,  that  the  tendon  reflexes  and  the  mechanical  excitability  of  the 
muscles  are  much  increased.  If  deep  coma  comes  on,  the  muscles  become  lax, 
the  motions  of  the  eye  are  not  co-ordinated,  and  reflex  excitability  diminishes,  or 
is  wholly  extinguished. 

Headache  is  one  of  the  most  constant  symptoms  in  the  beginning  of  the  dis- 
ease. It  is  usually  referred  to  the  forehead  or  temples.  The  pain  may  be  very 
violent,  and  sometimes  takes  on  almost  a  neuralgic  character.  It  almost  always 
subsides  in  the  second  week. 

If  we  seek  the  cause  of  these  nervous  symptoms,  which  are  often  so  severe,  we 
find  that  the  anatomical  changes  in  the  nervous  system,  including  the  brain,  bear 
no  relation  whatever  to  the  severity  of  the  symptoms  observed  during  life.     We 


16  ACUTE  GENERAL  INFECTIOUS  DISEASES 

sometimes  meet  with  minute  haemorrhages  in  the  cerebral  meninges,  or  meningeal 
opacity  or  oedema,  or  a  moist  condition  of  the  cerebral  parenchyma ;  but  the  con- 
nection of  these  and  similar  changes  with  the  symptoms  of  the  disease  is  often 
more  than  doubtful.  Nor  can  the  microscopic  alterations  in  the  brain,  which 
have  been  reported,  be  regarded  as  important  and  authoritative.  It  is  only  in 
very  rare  cases  that  large  cerebral  haemorrhages  or  purulent  meningitis  have 
been  found.  As  to  this  last,  we  should  always  be  very  cautious  in  making  a  diag- 
nosis, as  symptoms  which  would  seem  to  be  most  conclusively  meningeal — such 
as  stiffness  of  the  neck,  rigidity  of  the  whole  spinal  column,  and  occipital  head- 
ache— may  appear  in  typhoid  patients,  and  yet  the  autopsy  may  show  no  trace  of 
meningitis. 

One  theory,  which  has  Liebermeister  for  its  chief  supporter,  and  which  has 
won  a  tolerably  widespread  acceptance  among  physicians,  is  that  the  nervous 
symptoms  are  chiefly  a  direct  result  of  the  febrile  temperature.  It  is  impossible, 
however,  for  us  to  regard  this  view  as  universally  true.  The  unprejudiced  con- 
sideration of  a  large  number  of  personal  observations  prevents  it.  Although  it  is 
undeniable  that  elevated  temperature  has  a  harmful  influence  on  the  nervous  sys- 
tem, yet  in  numerous  cases  there  is  no  relation  between  the  height  of  the  fever 
and  the  severity  of  the  nervous  derangements.  There  are  cases  in  which  the  fever 
remains  continuously  high  for  days,  while  the  patient  feels  perfectly  comfortable 
and  presents  no  symptoms  of  any  important  cerebral  disturbance.  The  opposite 
class  of  cases  is  still  more  numerous,  in  which  from  the  very  start  there  is  always 
a  low  temperature,  and,  notwithstanding,  the  most  severe  nervous  symptoms 
arise.    Frantzel  and  others  have  published  very  striking  cases  of  this  sort. 

Hence  we  must  seek  for  some  other  special  cause  of  the  severe  nervous  symp- 
toms, and  according  to  our  present  views  this  cause  must  be  the  intoxication  re- 
sulting from  the  specific  infection.  We  know  that  all  bacteria  produce,  by  their 
own  tissue-metamorphosis  and  the  chemical  processes  which  they  excite  in  their 
neighborhood,  certain  chemical  matters  which,  especially  in  the  case  of  the 
so-called  "  pathogenic  bacteria,"  seem  to  be  similar  to  the  alkaloids  ("  ptomaines  " 
and  "toxines"),  and  exercise  a  decidedly  poisonous  influence  upon  the  body,  and 
especially  upon  the  nervous  system.  These  products  are  formed  by  the  typhoid 
bacilli,  enter  the  blood,  and  are  the  chief  cause  of  the  nervous  phenomena.  The 
difference  in  the  violence  of  the  latter  in  different  cases  probably  depends  mainly 
on  a  difference  in  the  amount,  and  perhaps  also  in  the  quality,  of  the  toxines 
produced  by  the  typhoid  bacilli,  and  probably  also  in  the  different  susceptibility  of 
individuals  to  the  poison.  The  reason  that  the  influence  of  these  poisons  is  not 
much  greater  than  it  is,  is  that  they  are  in  part  destroyed  within  the  body  and  in 
part  excreted  with  great  rapidity,  the  channel  of  exit  being  mainly  the  kidneys. 
Thus  is  explained  the  interesting  fact  observed  by  Lepine,  Bouchard,  and  others, 
that  the  urine  of  typhoid  patients  possesses  poisonous  properties  not  present  in 
normal  urine. 

That  the  appearance  of  the  nervous  symptoms  is  dependent  not  only  on  the 
material  causes,  but  also  on  the  susceptibility  of  the  individual,  is  shown  by  the 
fact  that  certain  patients  are  especially  prone  to  exhibit  marked  nervous  phe- 
nomena ;  for  example,  hard  drinkers,  "  nervous  "  individuals,  and  also  those  who 
have  suffered  violent  emotional  disturbances  shortly  before  the  onset  of  the 
disease. 

Actual  insanity  is  not  very  infrequent  during  the  course  of  typhoid,  or  in  con- 
valescence. It  generally  takes  the  form  of  melancholia.  We  have  repeatedly 
seen  patients  in  such  a  state  that  they  would  lie  almost  motionless  in  bed,  with 
eyes  open,  and  perhaps  assert  that  they  Avere  dead !  In  other  cases  there  is 
mental  excitement,  sometimes  combined  with  hallucinations,  or  there  is  confu- 
sion of  ideas.    In  one  case,  in  a  girl  who  was  evidently  predisposed  to  nervous  dis- 


TYPHOID  FEVER  17 

■orders,  we  saw  typical  hystei'ical  insanity  break  out  during  the  fever.  Sometimes 
the  mental  excitement  at  the  beginning  of  a  relapse  terminates  in  actual  insanity. 
Tew  of  the  psychoses  which  arise  during  or  at  the  end  of  typhoid  outlast  con- 
valescence. 

We  have  still  to  mention  a  number  of  nervous  diseases  that  develop  in  the 
course  of  typhoid  or  after  its  decline.  Neuralgia  is  sometimes  seen,  as  well  at  the 
beginning  as  at  the  end  of  the  disease.  It  is  most  frequent  in  the  regions  supplied 
by  the  trigeminus  and  the  occipital  nerves.  Great  hyper^esthesia  of  the  skin 
and  muscles  is  not  rare  during  convalescence.  It  attacks  the  lower  extremities 
by  preference.  Paralysis  of  single  muscles  (e.g.,  of  the  serratus  magnus),  or 
paralysis  of  a  single  extremity,  has  been  repeatedly  observed  as  a  sequela.  The 
paralysis  is  generally  of  the  atrophic  variety,  and  is  probably,  as  a  rule,  due 
to  neuritis.  Ataxia  and  spastic  paralysis  of  the  lower  extremities  are  rare  se- 
quelae. Finally,  there  are  sometimes  developed,  either  in  the  course  or  at  the 
conclusion  of  typhoid  fever,  the  symptoms  of  a  localized  cerebral  disorder  (e.  g., 
liemiplegia  and  aphasia),  the  anatomical  cause  of  which  varies.  There  may  be 
a  haemorrhage  or  an  embolism,  and  probably  in  still  other  cases  a  localized  en- 
cephalitis. 

4.  Circulatory  System. — Disturbances  of  the  heart  such  as  to  produce  striking 
-anatomical  changes  are  rare.  The  pericardium  macroscopically  almost  always 
appears  normal;  the  slight  mitral  or  aortic  endocarditis  sometimes  found  has 
no  clinical  significance.  The  disturbances  in  the  cardiac  muscle  seem  more  im- 
portant. It  is  often  more  flabby  than  normal.  The  cavities,  especially  on  the 
right  side,  are  often  dilated.  With  the  naked  eye  we  frequently  see  in  the  muscle 
itself  cloudiness  or  fatty  changes.  Microscopic  lesions  are  usually  present  and 
are  much  more  pronounced.  They  consists  usually  of  a  granular  ("  albumi- 
noid ")  or  more  rarely  of  a  fatty  or  hyaline  degeneration  of  the  fibers,  and  of 
..genuine  inflammatory  foci  of  interstitial  myocarditis  (Hayem,  Romberg).  No 
marked  disease  of  the  cardiac  ganglia  has  as  yet  been  found. 

The  clinical  significance  of  these  changes  should  not,  we  believe,  be  overesti- 
mated. In  all  probability  they  are  often  without  serious  consequences  and  dis- 
appear completely  with  recovery  from  the  disease.  Sudden  death  (heart-fail- 
ure?) occurs  in  typhoid,  but  it  is  very  rare  (see  the  chapter  on  diphtheria).  Per- 
manent disturbances  of  the  heart  after  typhoid  are  also  rare.  When  they  occur 
they  are  perhaps  due  to  the  passage  from  an  acute  myocarditis  to  a  chronic  inter- 
stitial degeneration.  [This  slowness  of  the  pulse  as  compared  with  the  fever  is 
common  enough  to  have  some  diagnostic  value,  provided  brain  trouble  is  ex- 
■cluded.  The  pulse  is  almost  always  rapid,  although  often  not  so  much  so  as  the 
Tieight  of  the  temperature  might  lead  one  to  expect. — V.] 

It  averages  from  90  to  110,  and  often  more.  When  it  keeps  at  140  or 
Tiigher,  in  adults,  it  is  always  an  unfavorable  symptom.  The  abnormal  frequency 
is  often  due  in  part  to  the  high  temperature;  but  there  are  other  factors.  Tem- 
perature and  pulse  do  not  correspond  in  all  cases.  Sometimes  the  pulse  will 
have  a  normal  or  even  subnormal  frequency  throughout  the  entire  attack,  de- 
spite the  fever.  Temporary  accelerations  are  easily  produced  by  mental  excite- 
ment or  bodily  exertion,  as  by  sitting  up  in  bed.  In  convalescence  the  rate  is  fre- 
quently subnormal. 

Slight  irregularities  of  the  pulse  are  not  rare,  either  in  the  acme  or  the  decline 
of  typhoid.  Marked  irregularity  is  always  a  grave  symptom,  although  in  many 
•cases  it  passes  off  and  the  patient  recovers. 

Dicrotism,  due  to  loss  of  tension  in  the  wall  of  the  artery,  is  so  common  that 

it  is  still  regarded  by  elderly  physicians  as  characteristic  of  typhoid,  although 

it  often  occurs  in  the  same  way  in  other  acute  diseases.    In  many  severe  cases  the 

height  and  strength  of  the  pulse  may  cause  no  alarm,  but  often  the  pulse  is 

3 


18  ACUTE  GENERAL  INFECTIOUS  DISEAS1,S 

notably  weak  and  small.  This  is  due  not  only  to  the  influence  of  the  disease, 
but  also  to  the  previous  condition  of  the  individual. 

The  diminished  cardiac  activity  may  result  in  venous  thrombosis,  especially 
in  the  lower  extremities  and  in  a  crural  vein.  This  sometimes  causes  swelling 
of  one  of  the  lower  extremities  during  the  later  stages  or  convalescence.  The 
swollen  member  generally  regains  its  normal  size  after  some  weeks.  In  other  cases 
the  thrombosis  occurs  earlier,  and  in  patients  who  are  still  too  vigorous  to  suffer 
from  cardiac  weakness,  so  that  we  are  forced  to  the  conclusion  that  there  is  some 
local  specific  cause,  a  local  thrombo-phlebitis  due  to  the  typhoid  bacillus  itself, 
or,  more  probably,  to  the  invasion  of  the  walls  of  the  vein  by  some  secondary 
infection.  A  possible,  but  fortunately  infrequent,  result  of  these  thrombi  in  the 
lower  limbs  is  pulmonary  embolism  and  sudden  death. 

In  severe  cases,  which  end  in  death,  cardiac  thrombi  are  sometimes  found,  with 
emboli  in  the  lungs,  spleen,  kidneys,  or  other  organs. 

CEdema  of  the  ankles  and  legs  is  very  often  seen  in  convalescents,  especially 
when  they  first  get  out  of  bed.  It  is  due  to  the  weakness  of  the  heart  and  changes 
in  the  vascular  walls.  Once  we  saw  a  general  dropsy  develop  at  the  end  of  a 
severe  attack  in  a  girl  of  fourteen.  The  autopsy  disclosed  no  other  possible  cause 
for  it  than  the  extreme  atrophy  and  flabbiness  of  the  heart. 

5.  Blood. — As  in  most  febrile  diseases  associated  with  great  emaciation,  so 
in  typhoid  in  severe  cases  the  number  of  red  blood-corpuscles  (and  correspond- 
ingly the  amount  of  hjemoglobin  in  the  blood)  is  much  diminished.  We  found, 
for  example,  2,800,000  to  3,200,000  in  a  cubic  millimetre.  In  milder  cases  the 
figures  do  not  differ  materially  from  normal.  It  is  a  fact  of  greater  interest  and 
also  of  distinct  diagnostic  importance  that  many  observers  have  found  that  leu- 
cocytosis  is  absent  in  typhoid  fever,  contrary  to  what  is  found  in  many  other 
acute  febrile  diseases,  pneumonia,  erysipelas,  sepsis,  etc.  We  have  often  confirmed 
this  fact  in  our  clinique.  We  sometimes  find  with  the  general  emaciation  a  de- 
crease in  leucocytes ;  for  example,  only  3,000  or  5,000  in  a  cubic  millimetre  instead 
of  the  normal  number  of  about  8,000. 

6.  Skin. — The  eruption  seen  in  typhoid  fever  is  characteristic  and  extremely 
important  in  diagnosis.  The  roseolse  or  rose-spots  (light  red,  slightly  elevated 
spots)  appear  at  the  beginning  of  the  second  week,  usually  on  the  trunk,  and 
chiefly  on  the  abdomen  and  back.  The  number  varies  greatly.  Rarely  they  are 
entirely  absent,  most  often  in  elderly  persons.  Sometimes  they  are  very  abun- 
dant, and  extend  to  the  thighs,  the  arms,  and  even  to  the  neck  and  face.  Often 
they  vanish  after  a  few  days,  but  they  may  persist  much  longer.  In  the  latter 
case  they  may  become  to  a  very  slight  degree  petechial,  so  that  they  will  not 
entirely  disappear  on  pressure.  They  often  occur  in  successive  crops.  We  have 
even  seen  several  cases  where  new  rose-spots  kept  coming  for  some  days  after  the 
fever  had  disappeared. 

As  to  other  cutaneous  eruptions,  we  may  mention  first  of  all  that  heiioes  la- 
bialis  is  so  rare  in  typhoid  that  in  cases  of  doubtful  diagnosis  it  is  a  factor  in 
excluding  that  disease.  Miliaria,  urticaria,  and  superficial  pustules  are  some- 
times observed.  Occasionally  little  bluish  spots  appear,  especially  on  the  trunk. 
These  used  to  be  called  "  laches  hleudtres  "  (pelioma  typhosum)  ;  but  later  obser- 
vations show  that  they  are  not  connected  with  typhoid  fever  particularly.  They 
are  due  to  pediculi.  We  might  use  the  term  pelioma  tj'phosum  to  designate  the 
kind  of  vesicles  which  we  have  repeatedly  seen  on  the  abdomen  in  severe  cases. 
They  are  about  the  size  of  peas,  and  have  sero-hfemorrhagic  contents.  Boils  and 
superficial  abscesses  are  frequent,  especially  as  disagreeable  sequelae  in  convales- 
cence from  severe  attacks.  There  are  often  abscesses  of  the  sweat-glands  in  the 
skin  of  the  axilla  during  convalescence.  All  these  and  similar  cases  of  suppura- 
tion in  typhoid  fever  do  not  depend,  as  a  rule,  upon  the  original  cause  of  the  dis- 


TYPHOID  FEVER  19 

ease,  but  upon  secondary  pathogenic  germs,  especially  the  staphylococcus,  for 
whose  entrance  the  typhoid  process  has  merely  prepared  the  way.  Extensive 
ecchymoses  are  very  rare,  and  are  symptomatic  of  a  general  hsemorrhagic  diath- 
esis. Petechias  are  frequent  during  recovery.  They  are  generally  seen  in  the 
follicles  of  the  skin  below  the  knee.  There  have  been  a  few  cases  of  gangrene 
in  the  lower  extremities,  especially  in  the  toes.  We  saw  in  one  patient  an  ex- 
tensive gangrene  of  the  skin  of  the  abdomen.  Its  cause  could  not  be  determined 
(ice-bag?). 

Finally,  we  must  mention  that  bed-sores  are  prone  to  develop  in  severe  or 
neglected  cases.  The  localities  most  often  attacked  are  the  nates,  the  furrow  be- 
tween them,  and  the  heels.  A  bed-sore  may  be  so  extensive,  and  accompanied  by 
such  undermining  of  the  skin,  as  to  be  a  dangerous  or  even  fatal  complication. 

The  epidermis  often  scales  oif  to  a  considerable  extent  during  convalescence 
after  a  severe  attack  of  typhoid.  Everybody  knows  how  the  hair  falls  out  after 
the  fever,  but  it  is  sure  to  grow  again.  The  nails  also  are  not  infrequently 
affected,  becoming  rough  and  brittle,  or  even  falling  off. 

7.  Muscles,  Bones,  Joints. — Zenker  has  discovered  a  degeneration  of  the  vol- 
untary muscles  which  occurs  in  typhoid  as  well  as  in  other  severe  diseases.  It  is 
called  the  "  granular  "  or  "  waxy  "  degeneration.  Whether  it  has  clinical  symp- 
toms can  not  be  determined.  Perhaps  it  may  explain  the  great  muscular  hyper- 
sesthesia  which  is  often  observed,  and  the  muscular  pains,  which  may  be  very 
trying.  Severe  cases  sometimes  have  haemorrhages  into  the  muscles,  particularly 
the  rectus  abdominis. 

Lesions  of  the  bones  and  joints  occur  but  seldom,  although  other  observers  and 
we  ourselves  have  repeatedly  seen  periostitis  and  ostitis  in  the  ribs,  tibia,  etc.,  fol- 
lowing typhoid.  It  is  an  interesting  fact  that  lately  typhoid  bacilli  have  often 
been  found  in  such  foci  of  disease,  so  that  it  is  a  true  typhoid  localization.  Swell- 
ing of  the  joints  is  rare.  When  of  a  purulent  nature  it  is  usually  due  to  secondary 
"  septic  "  infection. 

8.  Genito -urinary  Apparatus. — Genuine,  acute,  hsemorrhagic  nephritis  is  a 
very  rare  complication.  It  does  occur,  however,  and  has  even  given  rise  to  the 
establishment  of  a  special  "  renal  form  of  typhoid  fever  "  (nephro-typhoid).  This 
name  applies  especially  to  those  cases  in  which  a  severe  acute  nephritis  is  the  pre- 
dominant symptom  at  the  start,  while  at  a  later  period  the  course  of  the  fever, 
the  intestinal  symptoms,  the  rose-spots,  etc.,  show  the  disease  to  be  typhoid  fever. 
Nephro-typhoid  is  analogous  to  pneumo-typhoid  and  tonsillo-typhoid.  A  simple 
so-called  febrile  albuminuria  occurs  very  frequently  at  the  acme  of  typhoid,  and 
is  not  to  be  interpreted  unfavorably.  It  is  probably  the  result  of  that  slight  par- 
enchymatous degeneration  of  the  kidneys  which  occurs  in  typhoid  with  the  same 
frequency  as  in  most  of  the  other  severe  infectious  diseases.  There  does  not  seem 
to  be  a  direct  relation  between  the  albuminuria  and  the  fever,  although  some 
authors  assume  it  to  exist.  It  is  more  likely  that  the  renal  epithelium  is  injured 
by  the  noxious  products  which  have  been  formed  in  the  body  and  excreted  by  the 
kidneys.  In  other  respects  the  urine  in  typhoid  presents  the  same  peculiarities 
as  in  most  other  severe  febrile  diseases  :  its  amount  is  diminished ;  its  color  dark ; 
its  specific  gravity  increased;  the  excretion  of  urea  greater  than  normal.  It 
should  be  added  that  the  urine  at  the  height  of  the  disease  presents  Ehrlich's 
"  diazo-reaction  "  in  almost  all  cases.*  Cystitis  is  not  a  rare  development  toward 
the  end  of  the  illness.     It  is  probably  always  secondary. 

*  Ehrlich's  test  is  carried  out  as  follows  :  Solution  1  consists  of  strong  hydrochloric  acid,  one  part 
mixed  with  twenty  parts  of  a  one-half-per-cent.  solution  of  sulphanilic  acid.  Solution  2  is  a  one-liiilf- 
per-cent.  solution  of  sodic  nitrite  in  water. 

To  250  c.  c.  of  solution  1  is  added  6  c.  c.  of  solution  2 ;  an  equal  volume  ot  urine  is  then  added,  and, 
lastly,  about  60  c.  c.  of  ammonia.     On  shaking,  the  urine  becomes  crimson. 


20  ACUTE  GENERAL  INFECTIOUS  DISEASES 

In  men,  orchitis  is  sometimes  observed.  Women  often  have  their  catamenia 
at  the  beginning  of  typhoid.  Later  in  the  course  of  the  disease,  and  in  convales- 
cence from  severe  attacks,  the  menses  are  often  absent  for  several  periods.  In 
pregnant  women  there  is  considerable  danger  of  abortion  or  miscarriage. 

Peculiarities  in  the  Course  op  the  Disease 

The  above  statements  show  an  almost  inexhaustible  variety  in  the  possible 
symptoms  and  complications  of  typhoid.  The  course  of  the  disease  as  a  whole 
may  likewise  present  many  diverse  forms  and  peculiarities.  We  shall  attempt 
merely  to  cite  the  most  essential. 

The  numerous  light  and  rudimentary  attacks  {typhus  levissimus)  are  first  to 
be  mentioned.  It  was  not  recognized  till  lately  that  they  belonged  to  typhoid 
fever  at  all  (Griesinger).  They  used  to  have  all  sorts  of  names  applied  to  them, 
the  favorite  term  being  "  gastric  fever."  This  light  form  lasts  eight  to  fourteen 
days.  The  fever  is  moderate  and  often  decidedly  remittent.  There  is  almost  no 
proper  fastigium.  The  typhoid  symptoms  are  but  slightly  developed.  There 
is  no  severe  pulmonary  or  cerebral  disturbance.  There  is  generally  a  moderate 
diarrhoea,  the  spleen  is  plainly  enlarged,  and  often  rose-spots  can  be  found.  The 
diagnosis  of  these  cases  is  of  course  difiicult  in  proportion  to  the  scanty  develop- 
ment of  typhoid  symptoms.  It  is  best  established  by  demonstrating  an  aetiolog- 
ical  relation  between  these  cases  and  others  which  are  plainly  typhoid  fever. 

Abortive  typhoid  is  justly  distinguished  by  Liebermeister  from  typhus  levis. 
The  name  belongs  to  cases  which  begin  with  severe  symptoms  and  high  fever,  as 
if  they  were  going  to  be  grave,  but  in  which  these  violent  symptoms  disappear 
after  a  few  days  and  give  place  to  a  rapid  convalescence. 

On  the  other  hand,  there  are  cases  which  for  a  long  time  cause  so  little  subjec- 
tive discomfort  that  the  patient  does  not  even  go  to  bed  (walking  typhoid).  It  is 
not  till  quite  late  that  there  occurs  a  sudden  change  for  the  worse,  or  some  severe 
complication.  Thus  it  has  happened  that  persons  who  were  apparently  healthy 
have  suddenly  had  all  the  symptoms  of  a  severe  peritonitis  due  to  perforation  and 
have  died,  the  autopsy  disclosing  the  lesions  of  the  third  week  of  typhoid  fever; 
or  a  mild  typhoid  assumes  the  walking  type  and  is  not  detected,  but  later  a  severe 
or  dangerous  relapse  may  occur. 

The  individual  circumstances  are  very  important  in  weighing  each  case,  for 
they  may  modify  the  disease  in  many  ways. 

In  children  it  is  a  remarkable  fact  that  typhoid  ulcers  are  much  less  frequent 
than  in  adults.  This  explains  why  intestinal  haemorrhages  and  peritonitis  are 
much  rarer  in  children.  Marked  cerebral  symptoms  are,  on  the  other  hand,  very 
frequent.  In  severe  cases  children  sometimes  exhibit  the  peculiar  symptom  of 
a  continuous  penetrating  screaming.  In  other,  mild,  cases  the  children  are  sop- 
orose. 

In  the  aged  the  diagnosis  of  typhoid  is  often  very  difficult,  since  the  course  of 
the  disease  is  frequently  irregular.  Generally  the  fever  is  not  very  high,  and  it 
very  seldom  exhibits  distinctly  the  type  described  above.  The  pulmonary  or  cere- 
bral symptoms  predominate  as  a  rule. 

In  the  corpulent,  typhoid  fever  is  often  very  severe,  so  that  our  prognosis  must 
always  be  rather  grave,  especially  if  pulmonary  symptoms  arise. 

Hard  drinkers  are  also  in  especial  peril  in  this  as  in  all  other  acute  diseases. 
Dangerous  cardiac  weakness  is  prone  to  appear.  Severe  cerebral  symptoms  are 
frequent.  It  is,  however,  surprising  that  true  delirium  tremens  is  relatively  in- 
frequent, although  so  common  in  pneumonia. 

The  influence  of  previous  strong  mental  excitement  and  of  certain  already  ex- 
isting diseases  (cardiac  disease,  emphysema,  kyphoskoliosis,  etc.)  has  been  already 
mentioned.     Finally,  we  repeat  that  often  the  different  epidemics  present  certain 


TYPHOID  FEVER  21 

peculiarities.  For  instance,  in  one  the  type  of  the  disease  will  be  severe,  in 
another  mild.  In  one  epidemic  relapses  are  comparatively  frequent,  in  another 
exceptional.  The  same  is  true  with  regard  to  the  frequency  of  the  appearance  of 
certain  symptoms,  such  as  intestinal  haemorrhage,  perforation,  pneumonia,  or 
nephritis.  Indeed,  it  has  even  been  observed  that  those  cases  which  occur  during 
a  given  epidemic  in  the  same  family  or  house  or  block  sometimes  present  striking 
resemblances  to  one  another  ("  group  typhoid  "  of  E.  Wagner  and  others). 

Relapses  op  Typhoid  Fever 

Typhoid  fever  exhibits  in  many  cases  the  peculiarity  of  repeating  itself  com- 
pletely after  having  run  its  entire  course  and  disappeared.  This  process  is  called 
a  relapse.  It  is  in  all  probability  the  result,  not  of  a  fresh  infection  of  the  system 
from  without,  but  of  a  renewed  development  of  the  germs  already  present,  or  pos- 
sibly of  a  fresh  auto-infection.  A  typical  relapse  is  like  a  first  attack  in  all 
clinical  and  anatomical  particulars,  with  this  difference  that  everything  is 
more  condensed,  and  lasts  a  shorter  time  than  in  the  first  attack.  The  interval 
between  the  two,  during  which  there  is  no  fever,  lasts  seven  to  ten  days.  It  may 
be  longer,  and  is  often  shorter.  Sometimes  the  relapse  follows  immediately  upon 
recovery.  Indeed,  it  may  even  happen  that,  before  the  patient  has  completely 
recovered,  his  temperature  begins  to  rise  again  in  the  characteristic  step-like  way. 
To  such  cases  as  this  last  the  term  recrudescence  is  applied.  Except  in  the  time 
of  its  beginning,  it  may  be  just  the  same  as  a  genuine  relapse.  In  the  interval  be- 
tween the  two  attacks  many  persons  are  perfectly  comfortable,  and  appear  to  be 
fully  convalescent.  There  is  often,  however,  a  slight  evening  rise  of  temperature. 
It  is  noticeable  that  the  splenic  tumor  does  not  completely  disappear  after  the 
first  attack  in  many  cases  which  are  followed  by  a  relapse. 

The  relapse  is  generally  briefer,  as  we  have  said,  than  the  first  attack,  seldom 
lasting  more  than  fifteen  to  eighteen  days.  The  temperature  rises  more  rapidly, 
perhaps  in  two  or  three  days.  The  f  astigium  is  shorter,  the  decline  more  abrupt. 
The  absolute  height  of  the  temperature  may  be  very  considerable,  even  exceed- 
ing that  in  the  first  attack.  Rose-spots  appear  as  soon  as  the  third  or  fourth  day. 
The  stools  become  liquid,  the  spleen  enlarges  again,  and  all  sorts  of  complications 
may  arise.  The  danger  occasioned  by  a  relapse  may,  however,  be  overestimated. 
On  the  whole,  a  relapse  is  not  so  very  dangerous,  and  it  is  especially  noticeable 
that  the  subjective  symptoms,  such  as  headache,  are  often  slight.  A  severe  re- 
lapse may  follow  a  mild  case.  In  other  instances  the  relapse  may  prove  merely 
rudimentary. 

The  frequency  of  relapses  varies  considerably  in  different  epidemics.  In 
Leipsic,  we  had  relapses  in  about  nine  per  cent,  of  all  cases,  but  in  separate  years 
the  percentage  varied  between  four  and  sixteen.  Out  of  about  five  hundred  cases 
we  have  seen  three  in  which  there  were  two  successive  and  typical  relapses. 

Diagnosis. — The  diagnosis  of  typhoid  fever  may  be  perfectly  easy,  but,  if  the 
case  be  anomalous,  or  come  under  observation  at  a  late  period,  it  may  be  ex- 
tremely obscure.  Inasmuch  as  a  search  for  the  specific  bacilli  is  too  difiicult 
and  troublesome  for  the  practicing  ijhysician,  the  diagnosis  of  the  disease  must 
be  made  from  its  course  and  symptoms.  Important  factors  are  the  gradual  onset, 
then  the  height  and  course  of  the  fever,  with  no  demonstrable  localized  disease, 
and  the  rose-spots.  Less  characteristic,  but  still  of  value,  are  the  stools,  the  tym- 
panites, and  the  swelling  of  the  spleen.  Etiological  factors,  such  as  the  occur- 
rence of  undoubted  cases  of  typhoid  in  the  neighborhood,  are  of  great  diagnostic 
value  in  obscure  cases.  Sometimes  the  diagnosis  can  not  be  established  till  the 
appearance  of  certain  symptoms,  like  intestinal  haemorrhage,  a  characteristic 
mode  of  convalescence — viz.,  by  lysis — or  a  relapse.  It  is  an  important  rule  not 
to  make  a  diagnosis  of  typhoid  after  a  single  examination.     It  is  generally  neces- 


22  ACUTE  GENERAL  INFECTIOUS  DISEASES 

sary  to  observe  the  case  accurately  for  several  days  before  the  diagnosis  can  be 
established.  The  differential  diagnosis  from  other  acute  diseases,  such  as  miliary 
tuberculosis,  acute  endocarditis,  meningitis,  etc.,  will  be  considered  in  discussing 
these  diseases. 

The  diagnosis  is  usually  most  difficult  in  the  cases  with  an  imperfect  history 
which  are  first  seen  in  a  severe  "  typhoidal "  state,  with  high  fever,  disturbances 
of  consciousness,  etc.  These  are  the  cases  in  which  we  must  also  consider,  beside 
typhoid  fever,  miliary  tuberculosis,  acute  septic  or  pysemic  infection  (including 
acute  malignant  endocarditis),  meningitis,  severe  "  typhoid  pneumonia,"  etc. 
The  accurate  differential  diagnosis  between  typhoid  and  these  conditions  will  be 
spoken  of  later.  We  may  state  here  that  in  such  cases  a  careful  examination  of 
the  blood,  especially  the  absence  of  leucocytosis  in  typhoid,  may  afford  very  valu- 
able diagnostic  criteria.  The  ordinary  diagnostic  features  are  also  to  be  consid- 
ered, such  as  the  way  the  disease  began,  so  far  as  can  be  learned,  the  geti- 
ological  conditions  (i.  e.,  the  connection  with  other  cases  of  typhoid),  rose-spots, 
thin  pea-colored  stools,  meteorism,  intestinal  hemorrhage,  etc. 

Widal  has  lately  reported  a  method  for  diagnosticating  typhoid  (Widal's 
serum  reaction),  which  is  very  interesting  theoretically,  but  which,  of  course, 
can  be  used  only  in  cliniques  and  hospitals.  It  is  based  on  previous  researches 
by  Gruber  and  others.  If  we  mix  ten  or  fifteen  drops  of  a  fresh  culture  of  typhoid 
bacilli  with  a  drop  of  blood-serum  from  a  typhoid  patient,  the  bacilli  lose  their 
mobility  in  a  few  minutes,  or  at  most  in  a  quarter  to  half  an  hour,  and  come 
together  in  little  clumps  ("agglutinating"  action  of  the  serum).  If  we  add 
blood-serum  from  a  typhoid  patient  to  a  uniformly  cloudy  mixture  of  typhoid 
bacilli  in  bouillon,  the  bacilli  again  clump  together  and  sink  to  the  bottom,  while 
the  fluid  becomes  perfectly  clear.  Since  the  blood-serum  of  healthy  persons,  or 
those  not  suffering  from  typhoid,  does  not  give  this  reaction  at  all,  or  only  in  a 
slight  degree,  a  very  positive  result  from  this  test  is  quite  a  sure  diagnostic  sign. 
The  reaction  often  occurs  in  typhoid  even  in  the  first  weeks  of  the  disease,  but 
it  may  be  delayed.  It  persists  long  after  the  disease  has  subsided.  Widal's 
reaction  can  also  be  obtained  with  serum  from  a  blister  or  from  serous  inflamma- 
tory exudation  in  a  typhoid  patient.  In  otherwise  doubtful  cases  a  positive 
result  is  of  definite  diagnostic  significance. 

Prognosis.— A  perfectly  favorable  prognosis  should  never  be  made.  Cases 
which  seem  the  mildest  may  become  dangerous  (from  intestinal  perforation,  etc.). 
Yet,  if  there  are  good  nursing  and  good  treatment,  typhoid  fever  is  not  a  particu- 
larly dangerous  disease,  and  we  may  hope  for  recovery  even  in  very  severe  attacks. 
The  danger  lies,  first,  in  the  severity  of  the  infection,  as  shown  chiefly  (though 
not  wholly)  by  the  height  of  the  fever  and  the  intensity  of  the  general  symptoms. 
A  further  danger  is  the  appearance  of  the  complications  already  enumerated  and 
discussed.  Thirdly,  the  constitution  and  condition  of  the  individual  are  impor- 
tant. The  circumstances  coming  under  this  head  have  likewise  been  repeatedly 
mentioned  above.  All  these  factors  must  be  carefully  estimated  before  we  decide 
as  to  the  danger  in  each  case  and  make  our  prognosis. 

The  mortality  in  typhoid  varies  greatly  in  the  separate  epidemics.  The  severe 
cases  are  undoubtedly  more  frequent  at  some  times  than  at  others.  This  renders 
it  difficult  to  give  statistics  which  are  universally  applicable.  We  may  in  general 
reckon  on  an  average  mortality  of  about  ten  per  cent.,  and  measure  the  severity 
of  separate  epidemics  by  this  standard.  Numerous  observers  agree  that  the  treat- 
ment now  in  vogue  has  decidedly  diminished  the  mortality.  It  was  formerly  not 
rare  for  it  to  reach  twenty  or  twenty-five  per  cent. 

Treatment. — A  specific  cure  for  typhoid — i.  e.,  some  remedy  to  destroy  the 
specific  cause  of  the  disease  within  the  system,  or  to  render  it  harmless — is  as  yet 
unknown.     The  different  remedies  recommended  for  this  purpose  (carbolic  acid, 


TYPHOID  FEVER  23 

iodine,  thalline,  ergotine,  naphthaline,  etc.)  have  none  of  them  proved  their  value, 
and  we  can  not  advise  further  trial  of  them.  The  interesting  experiments  lately 
reported  of  injecting  sterilized  pure  cultures  of  typhoid  bacilli  or  the  bacillus 
pyocyaneus  into  the  patient  (Rumpf  and  Frankel)  has  as  yet  led  to  no  definite 
practical  result.  At  present  there  is  only  one  remedy,  whose  efficiency,  of  course, 
should  in  no  way  be  overrated,  which  we  would  be  unwilling  wholly  to  give  up  in 
treating  typhoid  fever,  and  that  is  calomel.  Wunderlich  noticed  that  if  a  few 
rather  large  doses  of  calomel  be  given  at  the  beginning  of  the  disease,  it  will 
on  the  average  run  a  lighter  and  more  favorable  course  than  otherwise  would 
have  been  the  case.  Wunderlich  believed  that  typhoid  fever  may  sometimes  be 
aborted  by  this  method.  Although  we  can  hardly  expect  this,  it  is  really  an 
efficient  means  of  procedure,  which  we  have  almost  always  employed,  to  give 
two  or  three  powders  of  calomel,  of  five  grains  (0.30  gramme)  each,  as  the  first 
prescription,  to  patients  who  come  under  treatment  in  the  first  week  or  the  be- 
ginning of  the  second.  As  there  is  generally  constipation,  the  laxative  effect  is 
also  beneficial.  Moreover,  it  often  lowers  the  temperature  somewhat.  A  moder- 
ate diarrhosa  is  not  a  contra-indication,  but,  if  the  bowels  be  very  loose,  the  calo- 
mel should  be  omitted. 

In  other  respects  the  treatment  of  typhoid  must  still  be  chiefly  dietetic  and 
symptomatic,  and  in  one  sense  prophylactic.  We  must  fight  the  symptoms  al- 
ready present,  and  further  seek,  as  far  as  possible,  to  defend  the  patient  from 
the  attack  of  certain  dangerous  secondary  disorders.  Starting  out  with  this 
view,  the  proper  treatment  of  typhoid  fever  is  a  task  of  the  highest  importance, 
and  by  no  means  a  thankless  one. 

We  will  begin  by  considering  the  general  treatment.  The  sick-room  must  not 
be  too  warm,  and  must  be  frequently  and  thoroughly  aired.  The  sick-bed  must 
be  well  cared  for.  If  effort  be  made  to  prevent  bed-sores,  we  shall  obviate  one 
source  of  pain  and  danger  {vide  supra),  and  save  ourselves  and  the  nurse  much 
trouble.  Those  who  are  very  ill  should  therefore  be  laid  on  an  air-cushion,  or, 
if  possible,  a  water-bed.  The  patient  should  be  told  not  to  lie  always  upon  his 
back,  but  to  change  now  and  then  upon  his  side.  The  back,  the  region  of  the  sa- 
crum, and  the  heels  are  to  be  often  bathed  with  spirits  of  camphor  or  brandy.  The 
minutest  bed-sore  is  to  be  treated  carefully.  It  should  be  cleansed  twice  a  day 
(rinsed  off  with  a  weak  solution  of  salicylic  or  carbolic  acid),  and  dressed  with  an 
ointment  containing  Peruvian  balsam,  1-30.*  If  the  bed-sore  be  extensive,  dust- 
ing with  iodoform  is  very  efficient  treatment.  We  should  be  particularly  careful 
not  to  let  the  skin  be  undermined.  If  this  has  already  occurred,  we  must  be 
prompt  in  the  use  of  the  knife  or  drainage-tube. 

We  can  not  recommend  too  strongly  that  the  mouth  should  be  kept  clean.  In 
a  light  case  the  patient  can  see  to  this  himself,  but  otherwise  the  mouth  and 
tongue  must  be  frequently  cleansed  with  a  linen  cloth  wet  in  cold  water  or  a  solu- 
tion of  borax  (1  to  30).  Perhaps  we  need  hardly  repeat  the  reason  for  this  excess- 
ive cleanliness.  It  lies  in  the  causative  relation  between  stomatitis  and  inflam- 
mation of  the  parotid  gland,  and  of  the  middle  ear.  If  the  tongue  and  lips  be 
dry,  they  may  be  touched  with  glycerine. 

The  diet  must  be  at  once  liquid  and  nourishing.  Milk  is  excellent,  and  it  should 
always  be  ordered,  but  it  can,  unfortunately,  be  taken  by  very  few  patients  continu- 
ously. It  is  often  better  borne  if  coffee  or  a  little  brandy  be  added  to  it.  Cocoa 
made  with  milk  may  also  be  given  for  a  change.  In  severe  cases  ISTestle's  food 
(Kindermehl)  has  been  often  employed  by  us  with  benefit.  Broths  and  soups,  thick- 
ened with  sago  or  rice,  are  also  good.     They  may  be  made  more  nourishing  by 

*  The  unguentum  balsami  peruviani  is  made  by  mixing  one  part  of  balsam  very  thoroughly  with 
thirty  parts  of  the  glycerite  of  starch  (B.  P.).    It  is  not  officinal  in  Germany. — Trans. 


24  ACUTE  GENERAL  INFECTIOUS  DISEASES 

adding  an  egg  to  them.  If  the  patient  is  very  anxious  to  have  more  solid  food^ 
as  often  happens,  we  need  not  hesitate  to  give  him  a  roll  or  rusk  (Zwieback) 
that  has  been  softened  by  soaking.  If  a  patient  becomes  exceedingly  enfeebled 
we  should  give  him  fine  shavings  of  raw  beef,  regardless  of  the  fever.  A  little 
dilute  hydrochloric  acid  might  be  given  with  the  meat.  Beef -tea  would  be  still 
better  than  the  raw  meat,  and  is  to  be  strongly  recommended.  The  various  prep- 
arations of  meat  which  are  now  made  (meat-juice,  meat-peptones,  etc.)  may  be 
useful.  When  the  fever  takes  a  sluggish  course,  we  must  often  begin  to  give 
stronger  nourishment  before  the  fever  has  ended.  The  best  drink  is  cold  Avater, 
which  must  be  offered  to  the  patient  even  when  he  does  not  ask  for  it.  Lem- 
onade and  similar  preparations  generally  become  distasteful  in  time.  Drinks 
containing  carbonic  dioxide  are  to  be  avoided,  because  they  increase  the  me- 
teorism.  Cold  tea  with  milk  is  good.  In  severer  cases  we  should  give  some 
good  strong  wine,  such  as  port,  Malaga,  or  Hungarian  wine,  but  it  is  not  necessary 
to  force  the  patient  to  take  wine  if  he  does  not  care  for  it.  If  the  patient  desires 
beer,  we  need  not  hesitate  to  give  it  in  moderate  amount.  During  convalescence 
we  should  be  very  careful  about  diet,  since  errors  often  have  disagreeable  conse- 
quences. We  must  wait  till  there  has  been  no  fever  at  all  for  seven  to  ten  days 
before  we  allow  a  solid,  animal  diet,  and  return  by  degrees  to  common  sorts  of 
food. 

The  general  and  dietetic  treatment  which  we  have  thus  far  discussed  is  very 
important.  Outside  of  this,  it  is  our  opinion  that  there  is  only  one  method  of 
treatment  to  be  chiefly  considered — at  least  under  the  present  limitations  of  our 
therapeutic  ability.  This  method  consists  in  the  persistent  use  of  cool  baths,  as 
first  practiced  by  Brand  in  Stettin.  We  do  not  indeed  believe  that  the  indica- 
tions for  this  method  of  treatment  are  exactly  what  its  original  promoter  held 
them  to  be,  and  we  think  some  of  the  minutiae  of  the  treatment  should  be  changed. 
Yet  there  is  at  present  no  other  single  method  of  treating  typhoid  fever  which  has 
so  numerous  and  evident  advantages  for  the  patient  when  properly  and  moder- 
ately used.  To  carry  it  out  in  private  practice  may  often  be  more  difficult  than 
in  a  well-appointed  hospital.  However,  even  in  private  houses  it  will  generally  be 
possible  to  manage  it,  and  we  regard  it  as  the  duty  of  every  physician  who  under- 
takes to  treat  a  severe  case  of  typhoid  to  try  his  best  to  have  the  baths  employed, 
y^  The  great  advantages  of  the  treatment  by  baths  are :  1.  Thejjaths  diminish 
^  (I  the  JBYer.  if  Ih&ir  temperature  bfi_j[inly  sufficient! v  low,  by  djrect  jLbsorption  _of 
•  I  heat.  The  baths  thus  obviate,  as  far  as  possible,  all'"tKi~Bad  effects  which  might 
result  from  a  rise  of  temperature.  2.  The  direct  influence  of  the  baths  upon  the 
nervous  system  is  still  more  important.  The  intellect  becomes  clearer,  the  apathy 
and  dullness  diminish.  In  fact,  if  baths  be  used,  we  do  not  see  nearly  so  often  as 
formerly  the  grave  "  typhoid  condition."  It  is  thus  evident  that  bathing  not  only 
causes  an  improvement  in  the  subjective  sensations  of  the  patient,  but  brings  in 
its  train  many  other  beneficial  effects.  The  patient  takes  his  nourishment  better, 
does  not  so  often  swallow  the  wrong  way,  coughs  more  effectively,  is  easier  to 
move,  and  his  body  and  his  mouth  can  be  better  cleansed.  3.  The  influence  of 
the  baths  upon  the  respiratory  organs  is  of  the  greatest  importance.  We  refer 
especially  to  the  stimulation  to  deeper  inspiration,  and  the  promotion  of  expec- 
toration. The  best  proof  of  the  benefit  of  this  influence  is  the  circumstance 
that  if  patients  are  subjected  to  baths  from  the  start,  it  is  comparatively  a  rare 
thing  for  severe  bronchitis,  atelectasis,  and  catarrhal  pneumonia  to  develop.  4. 
The  good  care  of  the  skin,  which  the  bathing  makes  possible,  is  not  to  be  despised. 
Since  this  treatment  has  been  introduced,  bed-sores  are  much  rarer  in  typhoid 
than  before.  5.  Lastly,  the  baths  are  sometimes  observed  to  have  a  diuretic 
effect. 

What  has  been  said  shows  that  the  height  of  the  fever  is  by  no  means  the  sole 


TYPHOID  FEVER  25- 

indication  for  the  employment  of  baths,  at  least  in  our  opinion.  The  condition 
of  the  nervous  system  and  of  the  respiratory  organs  is  also  to  be  considered.  It  is 
true  that  numerous  mild  cases  run  a  favorable  course  without  a  single  bath;  but 
we  should  always  remember  that  this  treatment  is  not  only  directed  against  the 
symptoms  already  existing,  but  has  also  a  prophylactic  importance,  since  it  tends- 
to  prevent  any  severe  cerebral  or  pulmonary  manifestations. 

We  will  pass  on  to  the  special  method  of  carrying  out  balneo-therapeutics  in 
typhoid.  Full  baths  are  generally  employed,  immersing  the  patient  to  his  neck. 
The  tub  must  stand,  if  possible,  by  the  bedside.  In  hospitals,  where  there  are  beds- 
on  rollers,  it  is  a  better  way  to  wheel  the  patients  into  the  bathroom.  All  who 
are  severely  ill  should  be  lifted  into  the  bath  and  there  held  and  supported,  to 
avoid  any  bodily  fatigue.  During  the  bath  the  skin  should  be  gently  rubbed. 
This  averts  unpleasant  sensations  of  chilliness.  The  temperature  of  the  water 
should  not  be  set  too  low,  especially  for  the  first  baths.  We  begin  at  85°  to  90° 
(24°  to  26°  R.),  or,  if  the  individual  be  elderly  or  sensitive  and  timid,  at  even 
warmer  temperatures.  When  the  patient  has  become  accustomed  to  the  tempera- 
ture of  the  water,  we  can  cool  off  the  bath  still  further.  Baths  below  73°  (18°  to 
20°  R.)  have  scarcely  ever  been  used  by  us,  and  we  believe  that  they  are  seldom 
needed.  A  very  satisfactory  average  temperature  is  80°  to  85°  (20°  to  24°  R.). 
A  bath  lasts  on  the  average  ten  minutes.  If  the  patient  feels  very  cold  or  very 
uneasy  in  the  bath,  it  must  be  cut  short.  After  the  bath  the  patient  is  at  once 
lifted  into  bed,  wrapped  up  in  a  sheet  previously  made  ready,  and  wiped  dry,  with 
rather  vigorous  rubbing  of  the  extremities  and  back.  The  moist  sheet  is  then 
removed.  The  patient  is  covered  up  rather  warmly,  and  is  given  some  hot  brotK 
or  a  sip  of  good  strong  wine.  The  effect  of  the  bath  upon  the  temperature  is 
measured  about  half  an  hour  later  by  the  rect-um.  If  the  temperature  be  2°  to  3° 
(1°  to  2°  C.)  lower  than  before,  the  result  is  deemed  satisfactory.  Often  the  dif- 
ference is  greater,  but  in  severe  cases  the  fever  may  be  so  obstinate  that  the  tem- 
perature remits  only  a  small  fraction  of  a  degree.  In  such  cases  it  is  sometimes 
permissible  to  lower  the  temperature  of  the  bath  still  more,  or  continue  it  a  little 
longer.  If  cool  baths  are  ill-borne,  protracted  baths  of  lukewarm  water  are  some- 
times very  efficient  (Riess,  and  others). 

In  so  far  as  the  height  of  the  fever  furnishes  an  indication  for  baths,  we  m.ay 
accept  103.6°  (39.8°  C.)  in  the  rectum,  as  the  temperature  calling  for  a  bath, 
but  spontaneous  variations  of  the  temperature  of  the  body  are  always  to  be  re- 
garded. In  cases  which  show  a  low  morning  temperature  without  special  inter- 
ference, the  height  of  the  evening  temperature  is  seldom  an  indication  for  a  cold 
bath.  We  regard  it  as  ver-f  important  that  the  baths  be  not  given  too  frequent- 
ly, since  their  advantages  may  thus  be  overbalanced  by  their  incontestable  evil 
consequences.  At  present  we  rarely  prescribe  more  than  two  to  four  baths  a  day. 
At  night  we  have  given  baths  only  very  seldom,  when  forced  to  by  extremely 
high  temperatures  or  other  bad  symptoms.  It  must  be  a  mistake  to  wake  a  pa- 
tient who  is  quietly  sleeping,  and  put  him  into  cold  water,  even  if  his  tempera- 
ture is  above  104°  (40°  C).  On  the  other  hand,  even  if  the  temperature  be  not 
excessive,  or  even  if  it  be  normal,  there  is,  as  we  have  said,  no  better  remedy  than 
the  baths  for  severe  pulmonary  or  cerebral  symptoms.  In  such  cases  we  often 
raise  the  temperature  of  the  baths  a  little,  and  during  them  we  have  colder  water 
poured  upon  the  head  and  back.  If  we  do  this,  the  ears  must  be  stopped  with 
cotton-wool,  lest  the  cold  water  find  its  way  into  them. 

Advantageous  as  the  bath  treatment  of  typhoid  generally  is,  it  must,  how- 
ever, like  every  other  therapeutic  method,  be  used  with  wise  moderation  and  with 
constant  regard  to  individual  conditions.  If  the  patients  are  very  weak,  show  a 
strong  aversion  to  the  baths,  or  feel  dull  and  exhaiasted  instead  of  refreshed  after 
them,  it  is  well  to  consider  whether  we  really  do  good  by  continuing  their  employ- 


26  ACUTE  GENERAL  INFECTIOUS  DISEASES 

ment.  In  such  cases  we  liave  of  late  years  often  advised  cold  wet  packs  of  the 
whole  body  in  bed,  instead  of  the  baths,  and  we  consider  such  a  use  of  cold 
as  very  advisable  in  these  cases.  The  antithermic  action  of  the  pack  is,  of 
course,  much  less  than  that  of  the  bath,  but  it  can  easily  be  aided  by  the  exhibi- 
tion of  antipyretics  internally.  The  respiration  and  the  nervous  system,  how- 
ever, are  almost  always  most  favorably  affected.  Most  patients  readily  consent 
to  the  packs  and  lie  quiet  for  an  hour  or  two  in  the  wet  envelope.  We  would 
urgently  recommend  the  more  frequent  use  of  jjacks,  especially  in  private  prac- 
tice, where  the  bath  treatment  often  meets  with  greater  difficulties  than  in 
hospitals.  We  should  here  always  begin  with  higher  temperatures,  and  only 
gradually  go  on  to  cold  packs.  There  are  a  number  of  contra-indications  to 
the  use  of  baths  which  can  not  be  disregarded.  First,  the  occurrence  of  intes- 
tinal haemorrhage,  however  slight,  and  likewise  the  suspicion  that  peritonitis 
is  developing,  prohibit  bathing.  In  these  cases  quiet  is  the  very  first  re- 
quirement of  the  patient,  and  the  baths  must  be  at  once  discontinued.  The 
onset  of  otitis,  severe  laryngeal  affections,  and  acute  nephritis  are  also  complica- 
tions in  which  we  should  properly  omit  the  baths  entirely  or  employ  them  very 
cautiously,  giving  them  warmer  and  less  frequently.  Sometimes  rheumatic 
pains  in  the  limbs  or  an  attack  of  boils  render  the  continued  use  of  baths  difficult. 
In  short,  we  see  that  nothing  could  be  more  foolish  than  to  try  to  establish  a 
general  rule  for  the  bath  treatment  of  typhoid. 

Passing  to  the  consideration  of  the  further  symptomatic  treatment  of  typhoid, 
the  first  important  question  is  about  giving  drugs  to  reduce  the  fever.  The  one- 
sided point  of  view  which  considered  that  the  chief  task  of  the  physician  in  the 
treatment  of  acute  febrile  disease  was  to  lower  the  temperature  has  been  grad- 
ually abandoned.  In  describing  the  bath  treatment  of  typhoid  we  have  em- 
phasized the  fact  that  the  action  of  the  bath  in  reducing  the  temperature  was 
only  one  factor,  and  perhaps  neither  the  most  efficient  nor  the  most  impor- 
tant factor,  in  the  curative  action  aimed  at.  In  giving  antipyretics  inter- 
nally their  antifebrile  action  is  of  chief  importance,  but  some  of  them  also  have 
a  certain  sedative  action  on  the  nervous  system.  The  important  influence  of 
the  bath  on  the  respiration  and  skin  they  do  not  possess.  If  we  had  to  decide 
whether  to  treat  typhoid  exclusively  by  baths  or  exclusively  by  antipyrine  and 
similar  drugs  we  should  decidedly  prefer  the  former.  We  would  not  wholly 
exclude  the  use  of  antipyretics  internally  in  the  treatment  of  typhoid,  but  we 
would  limit  their  use  more  than  is  often  the  case.  In  our  opinion  they  are  indi- 
cated only  when  with  existing  high  fever  baths  are  for  any  reason  impossible  or 
contra-indicated  (vide  supra),  or  when,  in  spite  of  the  baths,  the  fever  remains 
constantly  high.  In  such  cases  the  baths  can  often  be  judiciously  combined  with 
the  use  of  antipyretics  internally  if  the  patient  bears  the  drug  well  and  feels 
better  subjectively  after  the  reduction  of  temperature  than  before.  We  often 
treat  typhoid  patients  by  baths  in  the  day.  and,  if  the  fever  be  high,  by  a  dose  of 
antipyrine  (fifteen  to  thirty  grains,  grammes  1-2)  at  night.  With  severe  head- 
ache, nervous  restlessness,  etc.,  this  remedy  is  especially  indicated;  but  we 
regard  it  as  at  least  useless  and  often  improper  to  give  a  patient  with  moderate 
fever  large  doses  of  an  antipyretic  without  any  sufficient  reason,  as  unfortu- 
nately is  often  the  case  in  practice;  the  only  permanent  result  is  to  make  the 
patient  feel  worse  and  upset  his  stomach. 

In  regard  to  the  different  antipyretics  so  frequently  brought  forward  and 
recommended  of  late,  we  are  of  the  opinion  that  antipyrine  is  most  to  be  rec- 
ommended. It  was  introduced  by  L.  Knorr  and  first  recommended  by  Filehne. 
In  doses  of  fifteen  to  thirty  grains  (grammes  1-2).  best  given  in  wafers, 
it  usiially  reduces  the  temperature  considerably,  although  we  may  find  that 
the  height  and  the  obstinacy  of  the  fever  are  not  identical  terms.     We  do  not 


TYPHOID  FEVER  27 

often  see  unpleasant  effects  from  antipyrine  (such  as  vomiting,  profuse  sweat- 
ing with  defervescence,  a  chill  when  the  temperature  rises  again,  and  some- 
times a  measles-like  eruption).  The  patient  often  feels  better  than  before  while 
under  the  influence  of  antipyrine,  since  the  drug,  as  we  have  said,  also  acts  favor- 
ably on  the  nervous  symptoms  (headache,  restlessness).  The  dose  of  fifteen  to 
thirty  grains  (grammes  1-2)  can  in  severe  cases  be  repeated  several  times  a  day, 
but,  as  a  rule,  we  should  not  exceed  eighty  or  ninety  grains  (grammes  5-6)  in  the 
twenty-four  hours.  One  or  two  doses  a  day  are  usually  all-sufficient.  Lactophe- 
nine  is  also  much  recommended  and  even  held  as  a  specific  in  typhoid.  In  doses 
of  seven  to  fifteen  grains  (gramme  0.5-1)  it  reduces  the  temperature  considerably 
and  usually  causes  a  marked  improvement  in  the  general  condition.  A  total  of 
eighty  or  ninety  grains  (grammes  5-6)  can  be  used  in  a  day.  Of  the  many  other 
antipyretics  which,  of  course,  have  often  been  tried  in  typhoid,  we  may  first  men- 
tion antifebrine  (acetanilide),  which  in  doses  of  four  to  seven  grains  (gramme 
0.25-0.5)  has  a  similar  action  to  antipyrine  (Cahn  and  Hepp),  and  it  should  be 
used  in  practice  among  the  poor  because  it  is  much  cheaper.  If  we  avoid  too 
large  doses  we  seldom  see  unpleasant  results.  The  appearance  of  a  pale-cyanotic 
hue  of  the  skin  is  the  only  disturbing  feature;  this,  as  in  aniline  poisoning,  is 
probably  due  to  a  change  in  the  coloring  matter  of  the  blood,  and  therefore  warns 
us  to  be  cautious.  Other  new  antipyretics  are  phenacetine  (fifteen  grains, 
gramme  1,  at  a  dose),  salipyrine,  etc.,  which  have  no  special  advantages.  Qui- 
nine in  doses  of  fifteen  to  thirty  grains  (grammes  1-2)  and  salicylate  of  soda  in 
doses  of  seventy-five  grains  (grammes  5)  are  now  little  used  as  antipyretics,  and 
properly,  since  their  unpleasant  action  (vomiting,  tinnitus,  sweating,  etc.)  is 
much  greater  than  that  of  the  other  drugs  mentioned  above. 

[Water  or  an  acid  drink  should  be  given  frequently  by  the  nurse  without  wait- 
ing for  the  patient  to  ask  for  it,  unless  the  mind  is  unusually  clear.  Phenacetine 
seems  to  have  proved  itseK  less  depressing  to  the  heart  than  its  predecessors.  The 
antipyretic  dose  usual  in  this  country  is  five  grains.  A  strong  protest  should  be 
entered  against  the  routine  or  frequent  use  of  any  of  these  internal  antipyretics. 
If  the  temperature  seems,  in  itself,  to  cause  restlessness  and  discomfort,  an  occa- 
sional dose  may  be  given.  When  used  early  in  the  course  of  the  disease,  anti- 
pyretics may  seriously  embarrass  the  diagnosis  in  doubtful  cases.  The  method  of 
Brand  has  been  slowly  working  its  way  in  America  of  late  years,  and  perhaps 
would  have  spread  more  widely  and  rapidly  were  it  not  that  we  have  long  been  in 
the  habit  of  frequently  sponging  our  typhoid  patients  with  alcohol  and  water.] 

Another  important  symptom  which  needs  special  treatment  is  intestinal 
haemorrhage.  It  has  been  already  mentioned  that  if  this  occurs,  the  baths  should 
cease  at  once.  Further  than  this,  the  chief  remedies  are  ice  and  opium.  Flat 
ice-bags  are  laid  upon  the  abdomen.  They  should  not  be  too  heavy,  and  should, 
if  possible,  be  suspended  from  a  hoop.  Internally,  the  patient  is  given  every  two 
hours  fifteen  or  twenty  drops  of  laudanum  or  a  powder  of  one-half  grain  or  one 
grain  (gramme  0.03  to  0.05)  of  opium,  either  pure  or  combined  with  acetate  of 
lead  (opii,  gr.  ss.,  grm.  0.03;  plumbi  acetatis,  gr.  j,  grm.  0.05;  sacchari  albi,  gr. 
j,  grm.  0.05).  The  object  of  the  opium  is  to  check  peristalsis,  and  thus  promote 
the  formation  of  a  clot  in  the  bleeding  vessel.  In  severe  cases  we  may  tiy  injec- 
tions of  ergotine  or  fluid  extract  of  hydrastis,  twenty  drops  three  or  four  times. 
Liquor  ferri  chloridi  (five  to  ten  drops  in  water  eveiy  hour)  is  often  employed, 
but  is  of  extremely  doubtful  value.  The  baths  can  not  be  resumed  till  there  has 
been  no  bleeding  for  at  least  three  or  four  days — and  then  only  cautiously. 

If  peritonitis  occurs,  the  treatment  is  much  the  same.  Above  all,  opium  must 
be  used  in  still  larger  doses,  but,  unfortunately,  as  a  rule,  in  vain.  The  surgical 
treatment  of  peritonitis  has  rather  more  of  a  future  and  more  success,  but  experi- 
ence of  this  is  still  scanty. 


28  ACUTE  GENERAL  INFECTIOUS  DISEASES 

If  there  is  considerable  diarrhoea,  we  can  give  mistura  gummosa  [P.  G.,  gunt 
arabic  and  sugar,  each  15  parts;  water,  170  parts],  or  small  doses  of  opiiun,  th& 
latter  sometimes  combined  with  tannin,  tannigen,  etc.  In  general  it  is  certainly 
proper  not  to  check  the  ordinary  moderate  diarrhoea  of  typhoid.  Persistent  con- 
stipation is  always  to  be  avoided.  Constipation  at  the  beginning  of  the  disease 
is  overcome  by  calomel  {vide  supra).  In  later  stages  we  always  try  enemata  first, 
to  produce  an  operation.  If  this  does  not  succeed,  then  we  must  employ  rhubarb 
or  castor-oil.  Great  tympanites  may  be  diminished  by  laying  cold  wet  cloths  or 
ice-bags  upon  the  belly.  Considerable  amounts  of  gas  may  often  be  removed  by 
introducing  a  long  rectal  tube.  As  to  puncturing  the  greatly  inflated  intestines, 
a  method  practiced  by  some  physicians,  we  have  no  personal  experience. 

If  there  are  severe  pulmonary  symptoms,  baths  or  wet  packs  are,  as  we  have 
said,  the  best  remedies.  Internally  we  may  try  liquor  anamonii  anisatus  [P.  G., 
olei  anisi,  1  part ;  aquae  destillatee,  24  parts ;  aquse  ammoniae,  5  parts]  and  benzoic 
acid  (grains  ij  to  iij,  gramme  0.1  to  0.2,  in  powder).  If  the  pulse  be  very  rapid,^ 
we  may  put  an  ice-bag  over  the  heart.  If  at  the  same  time  the  pulse  is  small 
and  weak,  we  give  stimulants.  Of  late  we  have  most  frequently  given  tincture  of 
strophanthus  (ten  to  fifteen  drops  several  times)  with  the  best  results.  We  only 
rarely  use  digitalis  in  typhoid.  If  symptoms  of  severe  cardiac  weakness — so-called 
collapse — suddenly  occur  a  rapid  and  energetic  interference  is  urgently  demanded. 
Subcutaneous  stimulation,  injections  of  ether  or  camphorated  oil,*  should  be 
given,  with  wine,  stropanthus,  etc.,  internally.  If  the  respiration  stops  it  can 
sometimes  be  started  up  again  by  douches  of  cold  water  on  the  back  of  the  neck, 
or  we  may  often  restore  it  by  artificial  respiration.  Digitalis  (one-half  grain  of 
the  leaves,  gramme  0.03,  two  or  three  times  daily)  may  also  be  employed  if  the 
pulse  be  rapid;    but  it  should  be  used  with  great  caution. 

For  nervous  symptoms  the  baths  and  douching  are  the  most  effective  rerae- 
dies.  The  head  is  meanwhile  covered  by  an  ice-bag.  Antipyrine  sometimes  acts 
favorably  on  the  nervous  symptoms.  If  there  be  great  excitement,  as  shown  by 
excessive  restlessness  or  delirium,  small  doses  of  morphine  internally,  or,  better, 
subcutaneously,  are  often  very  useful. 

The  numerous  other  complications  and  sequelse  which  may  occur,  but  which 
can  not  all  be  mentioned  here,  should  be  treated  on  general  principles. 

The  prophylactic  measures  to  avoid  the  spreading  of  the  disease  can  be  only 
briefly  referred  to.  Of  chief  importance  is  careful  disinfection  of  the  excreta. 
The  best  means  for  this  purpose  is  a  two-per-cent.  solution  of  corrosive  sublimate 
or  a  five-per-cent.  solution  of  carbolic  acid.  We  may  also  pour  on  milk  of  lime 
until  the  reaction  becomes  alkaline,  or  use  concentrated  mineral  acids.  We 
should  take  care  that  bed-pans,  bed-clothes,  linen,  the  rectal  thermometer,  etc., 
should  be  handled  by  other  persons  as  little  as  possible,  and  should  be  care- 
fully disinfected.  If  there  seems  reason  to  suspect  that  the  disease  was  due  to 
bad  water,  of  course  the  source  of  siich  suspected  water  must  be  cut  oif. 

[Eecent  experiments  tend  to  show  that  the  above  solution  of  carbolic  acid  does 
not  kill  spores  except  after  prolonged  contact. 

The  following  are  the  measures  of  disinfection  recommended  by  the  American 
Public  Health  Association.  It  will  be  observed  that  they  apply  to  all  infectious 
diseases,  and  it  seems  well  to  give  them  here  nearly  in  extenso,  as  the  directions 
for  disinfection  in  most  text -books  are  far  too  vague. 

Disinfection  of  Excreta,  etc. — The  infectious  character  of  the  dejections  of 
patients  suflering  from  cholera  and  from  typhoid  fever  is  well  established;  and 
this  is  true  of  mild  cases  and  of  the  earlier  stages  of  these  diseases  as  well  as  of 

*  One  part  of  camphor  to  four  of  olive-oil  in  doses  of  seven  to  fifteen  minims  (gramme  0.5  to  1) 
every  hour  or  two. 


TYPHOID  FEVER  29 

severe  and  fatal  eases.  It  is  probable  that  epidemic  dysentery,  tuberculosis,  and 
perhaps  diphtheria,  yellow  fever,  scarlet  fever,  and  typhus  fever,  may  be  trans- 
mitted by  means  of  the  alvine  discharges  of  the  sick.  In  cholera,  diphtheria, 
yellow  fever,  and  scarlet  fever,  all  vomited  material  should  be  looked  upon  as 
infectious;  and  in  tuberculosis,  diphtheria,  scarlet  fever,  and  infectious  pneu- 
monia, the  sputa  of  the  sick  should  be  disinfected  or  destroyed  by  fire.  It  seems 
advisable  also  to  treat  the  urine  of  patients  sick  with  an  infectious  disease  with 
one  of  the  disinfecting  solutions  below  recommended. 

Chloride  of  lime,  or  bleaching  powder,  is,  perhaps,  entitled  to  the  first  place 
for  disinfecting  excreta,  on  account  of  the  rapidity  of  its  action.  The  following 
standard  solution  is  recommended: 

Standard  Solution  ISTo.  1 

Dissolve  chloride  of  lime,  of  the  best  quality,*  in  pure  water,  in  the  proportion 
of  four  ounces  to  the  gallon.  Use  one  quart  of  this  solution  for  the  disinfection 
of  each  discharge  in  cholera,  typhoid  fever,  etc.  Mix  well  and  leave  in  vessel  for 
at  least  one  hour  before  throwing  into  privy-vault  or  water-closet.  The  same 
directions  apply  for  the  disinfection  of  vomited  matters. 

Standard  Solution  ITo,  2 

Dissolve  corrosive  sublimate  and  permanganate  of  potash  in  pure  water,  in  the 
proportion  of  two  drachms  of  each  salt  to  the  gallon.  This  is  to  be  used  for  the 
same  purposes  and  in  the  same  manner  as  Standard  Solution  No.  1.  It  is  equally 
effective,  but  it  must  be  left  a  longer  time  in  contact  with  the  material  to  be  dis- 
infected— at  least  four  hours.  The  only  advantage  this  solution  has  over  ISTo.  1 
consists  in  the  fact  that  it  is  odorless.  It  costs  about  two  cents  a  gallon.  It  is 
very  poisonous,  and  will  injure  lead  pipes  if  passed  through  them  in  considerable 
quantities.  Solutions  of  corrosive  sublimate  should  not  be  placed  in  metal  re- 
ceptacles. 

Disinfection  of  the  Person. — The  surface  of  the  body  of  a  sick  person,  or  of 
his  attendants,  when  soiled  with  infectious  discharges,  should  be  at  once  cleansed 
•with  a  suitable  disinfecting  agent.  For  this  purpose  solution  of  chlorinated  soda, 
diluted  with  three  parts  of  water,  or  Standard  Solution  ISTo.  1,  diluted  with  three 
parts  of  water,  may  be  used.  A  two-per-cent.  solution  of  carbolic  acid  is  also 
suitable  for  this  purpose,  and,  under  proper  supervision,  the  use  of  a  solution  of 
corrosive  sublimate  (1-1,000)  is  to  be  recommended. 

In  diseases  like  small-pox  and  scarlet  fever,  in  which  the  infectious  agent  is 
given  oif  from  the  entire  surface  of  the  body,  occasional  ablutions  with  solution 
of  chlorinated  soda,  diluted  with  twenty  parts  of  water,  will  be  more  suitable  than 
the  stronger  solution  above  recommended. 

In  all  infectious  diseases  the  body  of  the  dead  should  be  enveloped  in  a  sheet 
saturated  with  Standard  Solution  N'o.  1,  or  with  a  five-per-cent.  solution  of  car- 
bolic acid,  or  a  1-500  solution  of  corrosive  sublimate. 

Disinfection  of  Clothing. — Boiling  for  half  an  hour  will  destroy  the  vitality 
of  all  known  disease-germs,  and  there  is  no  better  way  of  disinfecting  clothing  or 
bedding  which  can  be  washed  than  to  put  it  through  the  ordinary  operations  of 
the  laundry.  ISTo  delay  should  occur,  however,  between  the  time  of  removing 
soiled  clothing  from  the  person  or  bed  of  the  sick  and  its  immersion  in  boiling 
water,  or  in  one  of  the  following  solutions;  and  no  article  should  be  permitted 
to  leave  the  infected  room  until  so  treated. 


*  Good  chloride  of  lime  should  contain  at  least  twenty-five  per  cent,  of  available  chlorine.    The  cost 
of  the  solution  is  less  than  one  cent  a  gallon.     The  sediment  does  no  harm. 


30  ACUTE  GENERAL  INFECTIOUS  DISEASES 


Standard    Solution  No.  3 

Dissolve  four  ounces  of  corrosive  sublimate  and  one  pound  of  sulphate  of 
copper  in  a  gallon  of  water.  Two  fluid  ounces  of  this  standard  solution  to  the 
gallon  of  water  will  make  a  suitable  solution  for  the  disinfection  of  clothing. 
The  articles  to  be  disinfected  must  be  thoroughly  soaked  with  the  disinfecting 
solution,  and  left  in  it  for  at  least  two  hours,  after  which  they  may  be  wrung  out 
and  sent  to  the  wash. 

Clothing  may  also  be  disinfected  by  immersing  it  for  four  hours  in  a  two-per- 
cent, solution  of  carbolic  acid.  Soiled  mattresses,  pillows,  feather  beds,  and 
articles  of  this  nature  can  not  be  eifectually  disinfected  by  sulphur  fumigation, 
owing  to  the  fact  that  the  gas  does  not  penetrate  to  their  interior  in  sufficient 
amount.  For  articles  of  this  kind,  and  in  general  for  articles  of  little  value, 
which  have  been  soiled  by  the  discharges  of  the  sick,  destruction  by  fire  will  be 
advisable. 

Disinfection  of  the  Sick-Boom. — No  disinfectant  can  take  the  place  of  free 
ventilation  and  cleanliness,  and  it  is  impracticable  to  disinfect  an  occupied  apart- 
ment.    Neutralizing  bad  odors  is  not  disinfection. 

All  surfaces  should  be  thoroughly  washed  with  Standard  Solution  No.  1,  diluted 
with  three  parts  of  water,  or  with  a  1-1,000  solution  of  corrosive  sublimate. 
Standard  Solution  No.  3,  diluted  in  the  proportion  of  four  ounces  to  the  gallon  of 
water,  may  be  used. 

The  walls  and  ceiling,  if  plastered,  should  be  brushed  over  with  one  of  these 
solutions,  and  subsequently  washed  over  with  a  lime-wash. 

Especial  care  must  be  taken  to  wash  away  all  dust  from  window  ledges  and 
other  places  where  it  may  have  settled,  and  thoroughly  to  cleanse  crevices  and 
out-of-the-way  places.  After  this  application  of  the  disinfecting  solution,  and  an 
interval  of  twenty-four  hours  or  longer  for  free  ventilation,  the  floors  and  wood- 
work should  be  well  scrubbed  with  soap  and  hot  water,  and  this  should  be  followed 
by  a  second  more  prolonged  exposure  to  fresh  air,  admitted  through  open  doors 
and  windows. 

As  an  additional  precaution,  fumigation  with  sulphur-dioxide  gas  is  to  be 
recommended,  especially  for  rooms  which  have  been  occupied  by  patients  with 
small-pox,  scarlet  fever,  diphtheria,  typhus  fever,  and  yellow  fever.  All  apertures 
into  the  room  should  be  carefully  closed,  and  not  less  than  three  pounds  of  sul- 
phur for  each  thousand  feet  of  air-space  should  be  burned.  To  secure  complete 
combustion,  the  sulphur,  in  powder  or  small  fragments,  and  moistened  with 
alcohol,  should  be  placed  in  a  shallow  iron  pan,  and  this  should  be  placed  on 
bricks  in  a  tub  partly  filled  with  water  to  guard  against  fire. — Editor.] 

[Formaldehyde  gas  is  superior  to  sulphur  dioxide,  because  of  its  greater 
efficiency  and  rapidity  of  action,  and  because  it  does  less  harm  to  household  goods. 
Both  gases  have  merely  a  superficial  action. — V.] 


CHAPTER  IT 

TYPHUS   FEVER 

(Spotted  Fever.     Ship  Fever) 

Typhus  fever  is  an  acute  infectious  disease,  perfectly  distinct  from  typhoid 
fever,  but  formerly  often  confounded  with  it.  The  similarity  of  the  two  diseases, 
which  led  to  their  similar  names,  consists  only  in  the  grave  general  condition  with 


TYPHUS  FEVER  31 

fever,  and  in  a  number  of  complications  which  may  appear  in  both.  There  is, 
however,  an  essential  difference  in  the  whole  course  of  the  two  diseases,  and  espe- 
cially in  the  circumstance  that  the  intestinal  lesion  which  is  characteristic  of 
typhoid  is  never  seen  in  typhus.  The  chief  distinction  between  the  two  affections, 
which  must  undoubtedly  lie  in  the  difference  in  their  causes,  can  not  yet  be  dem- 
onstrated. We  do  not  yet  know  the  organized  pathogenic  agents  of  typhus  fever, 
although  it  must  be  presupposed  that  they  exist. 

.Sltiology. — As  to  the  way  in  which  infection  occurs,  we  have  much  less  infor- 
mation even  than  in  relation  to  typhoid.  We  know  nothing  as  yet  as  to  the 
supposed  specific  agents  which  produce  typhus,  although  micro-organisms  have 
been  repeatedly  found  in  the  blood.  It  is  an  incontestable  fact  that  the  appear- 
ance of  typhus  in  a  place  previously  free  from  the  disease  is  always  to  be  referred 
to  an  importation  of  the  pathogenic  poison  from  without.  It  is  likewise  deter- 
mined, through  numerous  observations,  that  typhus  is  one  of  the  contagious  dis- 
eases— that  is,  that  the  specific  poison  can  be  directly  transferred  from  the  patient 
to  others  around  him.  How  it  is  transferred  we  have  no  certain  knowledge.  Per- 
haps the  poison  is  contained  in  the  expired  air;  or,  as  is  still  more  probable,  in 
the  scales  of  epidermis ;  or,  perhaps,  in  the  other  excretions  and  secretions  of  the 
patient.  We  are  equally  ignorant  through  what  channel  the  infectious  agent 
enters  the  system — whether  it  is  inspired  or  swallowed.  It  is  certain  that  the 
poison  may  be  transferred  in  the  clothes,  etc.,  of  the  patient  (fomites). 

Favorable  hygienic  surroundings  decidedly  diminish  the  contagiousness  of 
typhus  fever.  For  example,  in  the  well-ventilated  pavilions  of  the  Leipsic  hos- 
pital there  have  rarely  been  cases  of  transfer  of  the  disease  to  physicians,  nurses, 
or  other  patients.  On  the  other  hand,  if  the  hygienic  influences  be  unfavorable, 
typhus  fever  may  appear  in  very  widespread  epidemics.  Those  terrible  epidemics 
which  have  been  described  under  the  names  of  "  famine  fever,"  "  camp  fever " 
(Hungertyphus,  Kriegstyphus),  etc.,  were  for  the  most  part  typhus  fever.  In  the 
smaller  epidemics  it  is  often  possible  to  trace  the  disease  to  some  wretched,  over- 
filled tenement-house. 

At  present  typhus  fever  appears  constantly  in  Great  Britain.  Ireland  has  been 
notorious  for  many  years  as  a  breeding-place  of  the  disease.  It  is  also  frequent  in 
the  eastern  part  of  Germany  (Posen,  East  Prussia  and  West  Prussia,  Silesia),  in 
Poland,  Galicia,  Russia,  and  in  parts  of  southern  Europe.  The  isolated  cases 
which  occur  every  year  here  and  there  in  central  Germany,  though  more  or  less 
numerous,  are,  almost  without  exception,  to  be  referred  to  an  importation  of  the 
disease. 

Typhus  fever  attacks  by  preference  young  adults  of  twenty  to  forty  years ;  but 
it  occurs  in  children,  and  is  comparatively  frequent  in  elderly  persons.  There  is 
no  marked  dependence  of  the  epidemics  upon  any  particular  season  of  the  year. 
As  in  the  case  of  typhoid  fever,  a  person  who  has  once  had  the  disease  seems  to 
enjoy  immunity  from  any  fresh  attack. 

[The  practical  acquaintance  of  American  physicians  with  typhus  fever  is,  for- 
tunately, limited.  Many  of  the  outbreaks  which  have  occurred  were  traceable  to 
immigrants,  especially  from  Ireland. 

During  our  civil  war  the  disease  broke  out  neither  among  the  armies  in  the 
field  nor  among  the  prisoners  of  war.  A  number  of  cases  were  reported  at  the 
time,  but  great  doubt  has  since  been  thrown  upon  the  correctness  of  the  diagnosis.] 

Course  and  Symptoms  of  the  Disease.— If  we  try  to  sketch  the  characteristic 
behavior  of  typhus  fever,  especially  as  contrasted  with  typhoid,  we  may  say  that 
the  disease  begins  much  more  abruptly  and  rapidly,  and  that  the  fever  quickly 
becomes  very  high  and  the  general  disturbance  very  severe,  but  the  illness  lasts 
a  shorter  time,  seldom  more  than  two  weeks,  and  generally  passes  by  crisis  into 
recovery. 


32  ACUTE  GENERAL  INFECTIOUS  DISEASES 

The  length  of  incubation  seems  to  vary.  Murchison  thinks  it  is  usually 
xaore  than  nine  days.  Sometimes,  though  not  invariably,  slight  prodromata 
precede  by  some  days  the  actual  outbreak  of  the  disease.  These  are  languor, 
anorexia,  headache,  and  pain  in  the  limbs.  Then  the  regular  illness  begins,  as  a 
Tule,  rather  suddenly,  and  often  with  a  pronounced  rigor.  With  this  the  tem- 
perature rises  quickly,  and  may  on  the  very  first  evening  reach  104°  or  105° 
(40°-40.5°  C).  Vomiting  is  not  rare,  and  may  be  repeated.  A  grave  general 
■condition,  with  fever,  is  developed  in  a  few  days.  The  patient  feels  exhausted. 
There  is  often  violent  pain  in  the  loins  and  extremities.  Nervous  symptoms 
soon  appear:  persistent  and  intense  headache,  vertigo,  spots  before  the  eyes, 
ringing  in  the  ears,  and  in  many  cases  quickly  increasing  stupor  and  delirium. 
In  severe  cases  the  fever  often  reaches  106°  (41°  C),  and  may  be  even  higher,  and 
it  is  almost  constant,  with  but  slight  morning  remissions.  The  skin  is  hot  and 
■dry,  the  tongue  dry  and  thickly  coated,  the  respiration  moderate,  the  pulse  very 
•rapid.  We  very  frequently  find  in  the  chest  the  signs  of  an  extensive  bronchitis. 
ISTasal  catarrh  and  conjunctivitis  also  occur.  Serious  intestinal  symptoms  are 
generally  absent,  although  there  may  be  slight  tympanites  or  diarrhoea.  The 
spleen  is  almost  always  greatly  enlarged.  Only  in  a  few  epidemics  is  the  splenic 
tumor  said  to  have  been  wanting  ( ?).  The  urine  is  concentrated  and  scanty,  and 
sometimes  has  a  trace  of  albumen. 

On  the  third  to  the  seventh  day  of  the  disease  the  characteristic  eruption  ap- 
pears. To  this  the  disease  owes  its  name  of  "  spotted  fever."  The  eruption  con- 
sists of  rose-spots,  generally  very  numerous  and  widespread,  upon  the  trunk  and 
extremities,  often  also  on  the  face.  Sometimes  the  spots  are  larger,  and  may  then 
I)ear  great  resemblance  to  a  fresh  eruption  of  measles.  The  skin  between  the  sep- 
-arate  rose-spots  is  not  infrequently  diffusely  reddened.  After  two  or  three  days 
"the  roseolse  become  hsemorrhagic,  and  change  into  lighter  or  darker  petechise. 
It  is  commonly  only  in  the  lighter  cases  that  the  rose-spots  fade  away  without 
:first  becoming  petechial.  In  rare  though  well-substantiated  cases  the  eruption  has 
been  scanty,  or  even  wholly  wanting.     Herpes  does  occur,  but  only  seldom. 

The  fever  begins  to  abate  in  light  cases  as  early  as  the  second  week,  coin- 
■cidently  with  an  improvement  in  the  general  symptoms.  Often  this  change  is 
indicated  about  the  seventh  day  by  a  considerable  remission  in  the  temperature. 
On  the  other  hand,  in  severe  cases,  all  the  symptoms  grow  worse.  The  weakness 
increases.  The  nervous  derangement  reaches  the  extreme  of  a  severe  "  typhoidal 
•state,"  expressed  either  by  marked  stupor,  which  sometimes  passes  into  complete 
<3oma,  or  by  violent  delirium.  Lobular  pneumonia  attacks  the  lungs,  and  the 
fever  continues  with  unabated  violence.  These  symptoms  may  end  with  death, 
I)ut  in  favorable  cases  they  decline  rapidly.  Sometimes  this  decline  is  preceded 
I)y  a  great  rise  in  temperature  (perturhatio  critica),  especially  about  the  seven- 
teenth day,  rarely  a  few  days  earlier  or  later.  In  such  cases  the  temperature  is 
apt  to  fall  by  crisis,  sinking  in  a  day  or  two,  with  but  slight  interruption,  down  to 
the  normal  level.  Even  in  those  cases  in  which  the  descent  is  by  gradations  it  is 
always  decidedly  more  abrupt  than  in  typhoid.  The  eruption  quickly  fades,  the 
patients  gradually  improve,  and,  as  a  rule,  become  completely  and  permanently 
convalescent.  It  is  true  that  some  observers  have  seen  relapses,  but  they  are,  at 
least  in  our  present  epidemics,  extreriiely  rare. 

Complications  and  Varieties  in  the  Course  of  the  Disease. — From  what  we 
Tiave  said  of  its  course,  it  is  evident  that  the  symptoms  are  essentially  those  of  an 
intense  general  infection  of  the  system.  The  sole  demonstrable  local  lesion  which 
is  almost  invariably  present  is  the  characteristic  eruption,  and  this  has  evidently 
no  causal  relation  to  the  severe  symptoms  of  the  disease.  It  is  likewise  extremely 
probable  that  most  of  the  complications,  which  not  infrequently  arise  in  severe 
•cases,  are  secondary,  and  occur  in  the  way  already  described  with  considerable 


RELAPSING  FEVER  33 

detail  in  the  preceding  chapter.  They  are  just  such  complications  as  are  possible 
in  every  severe  general  disease,  and  embrace  otitis,  parotitis,  extensive  lobular 
pneumonia,  more  rarely  gangrene  of  the  lungs,  and  pleurisy;  also  furunculosis, 
jDurulent  cellulitis,  bed-sores,  dysentery,  icterus,  etc.  Whether  some  of  the  local 
lesions  which  are  observed  may  not  be  direct  results  of  the  pathogenic  poison, 
we  can  not  at  present  decide.  Among  these  would  come,  first  of  all,  the  rare 
cases  of  lobar  pneumonia  and  nephritis.  Sequelae  are,  on  the  whole,  rare,  though 
sometimes  there  is  a  tedious  ansemic  condition,  or  neuralgia,  paralysis,  etc. 

The  separate  epidemics  of  typhus  present  considerable  variety,  not  only  as 
regards  the  occurrence  of  individual  complications,  but  more  especially  in  the 
general  course  and  character  of  the  cases.  For  instance,  some  epidemics  are  dis- 
tinguished by  the  greater  frequency  of  light  attacks  {typhus  exanthematicus 
levissimus,  unsuitably  termed  by  some  "  febricula  ").  Here  the  entire  attack  runs 
its  course  in  five  to  eight  days.  The  fever  is  generally  comparatively  moderate; 
there  are  no  severe  general  symptoras,  and  complications  are  exceptional. 

Diagnosis. — It  may  be  very  difficult  for  a  time  to  distinguish  typhus  from 
typhoid.  The  following  factors  are  of  chief  importance :  1.  The  onset  is  much 
more  abrupt  in  typhus  than  in  typhoid,  and  is  often  accompanied  by  a  pronounced 
rigor.  2.  In  typhus,  the  nervous  disturbances  usually  appear  earlier  and  are  more 
severe  than  in  typhoid.  3.  The  rash  is  seldom  so  extensive  in  typhoid  as  in  ty- 
phus, and  in  typhoid  it  hardly  ever  becomes  petechial.  4.  In  typhus  the  pains  in 
the  loins  and  limbs  are  generally  much  more  pronounced.  5.  If  we  still  find  it 
hard  to  decide,  the  manner  of  recovery  will  almost  always  settle  the  question. 
Recovery  in  severe  cases  of  typhoid  is,  on  the  average,  much  more  tardy  and 
gradual,  by  lysis.  In  typhus  it  occurs  generally  by  the  seventeenth  day,  and  by 
crisis. 

The  prognosis  is  chiefly  determined  by  the  severity  of  the  fever  and  of  the 
nervous  symptoms.  Extensive  lobular  pneumonia  is  the  most  frequent  dangerous 
complication.  The  mortality  varies  greatly  in  the  separate  epidemics.  It  is  some- 
times only  six  or  seven  per  cent.,  but  may  rise  to  twenty  per  cent. 

Treatment  is  based  on  the  same  principles  as  in  typhoid  fever.  There  is  no 
specific  remedy.  Besides  good  nursing,  a  judicious  employment  of  baths  is  cer- 
tainly our  chief  reliance  for  lessening  the  severity  of  many  of  the  symptoms,  such 
as  febrile,  nervous,  and  pulmonary  disturbances,  as  well  as  for  averting  many 
dangerous  complications.  For  all  details  of  treatment  we  may  refer  to  the  pre- 
ceding chapter. 


CHAPTER   III 

RELAPSING    FEVEB 

{Relapsing   Typhus — Febris  Tecwrens) 

.aitiolog-y. — This  disease  was  first  named  by  English  pathologists  relapsing 
fever,  and  by  Griesinger  feliris  recurrens.  It  has  a  peculiar  course,  made  up  of 
separate  attacks,  and  is  further  of  great  interest  because  it  is  one  of  the  first  infec- 
tious diseases  in  which  the  specific  pathogenic  organisms  became  known,  and, 
being  easily  demonstrable  in  each  separate  case,  were  utilized  for  the  speedy 
and  certain  diagnosis  of  the  disease.  Obermeier  discovered  in  Berlin,  in  the  year 
1873,  that  in  relapsing  fever  the  blood,  at  certain  times,  invariably  contains 
peculiar  thread-like  micro-organisms.  This  discoveiy  has  since  been  universally 
confirmed;   and  it  may  be  maintained  that  if  once  the  presence  of  these  "  spirilli  " 


34  ACUTE  GENERAL  INFECTIOUS  DISEASES 

be  demonstrated  in  the  blood,  we  are  justified  in  making  an  absolute  diagnosis  of 
relapsing  fever. 

In  Germany  the  disease  did  not  become  epidemic  till  the  year  1868.  In  1S72 
and  1873  there  were  considerable  epidemics  in  Breslau  and  Berlin.  Its  last  exten- 
sive appearance  was  in  1879  and  1880,  when  it  spread  over  most  of  northern  and 
central  Germany,  and  was  accurately  studied  by  numerous  observers.  People  of 
the  poorer  classes  were  almost  exclusively  attacked,  and  especially  the  "  tramps." 
The  uncleanly  dens  where  these  people  lodge  were  found  everywhere  to  be  the 
chief  centers  of  infection. 

The  precise  manner  of  infection  is  as  yet  almost  wholly  unknown.  All  ob- 
servers agree  that  the  disease  is  directly  contagious ;  but  it  can  not  be  very  con- 
tagious if  the  hygienic  influences  be  good.  At  least  the  results  of  our  late  epi- 
demics would  imply  this.  In  the  Leipsic  hospital,  where  at  that  time  over  two 
hundred  and  fifty  cases  were  treated,  and  isolation  could  not  be  at  all  perfectly 
carried  out,  not  one  case  of  infection  occurred.  It  is  certain  that  the  disease  can 
be  transmitted  by  direct  inoculation  with  the  blood  of  patients.  This  has  been 
established  by  a  Russian  physician,  by  the  experimental  inoculation  of  healthy 
persons.  Doctors  have  been  repeatedly  inoculated  at  the  autopsy  of  those  who 
have  died  of  relapsing  fever.  The  disease  may  likewise  be  transferred  by  inocula- 
tion to  monkeys,  while  other  mammals  seem  to  enjoy  an  immunity  from  it. 

[The  first  cases  of  relapsing  fever  observed  in  this  country  were  in  Irish  immi- 
grants coming  over  in  the  same  vessel  in  the  year  1844.  At  several  periods  since 
then  more  or  less  limited  outbreaks  traceable  to  immigration  have  occurred,  but 
the  disease  has  never  acquired  any  foothold  with  us,  and  comparatively  few  physi- 
cians have  ever  seen  it.  So  far  as  I  can  learn,  only  one  case  has  ever  been  seen  in 
Boston,  and  that  was  in  the  person  of  a  physician  from  another  city,  who  brought, 
the  disease  with  him  and  passed  through  it  in  the  Massachusetts  General  Hos- 
pital.] 

Clinical  History. — The  stage  of  incubation  lasts  about  five  to  eight  days.  It  is. 
only  exceptionally  that  some  slight  prodromal  symptoms  present  themselves  just 
before  the  outbreak  of  the  disease  proper.  As  a  rule,  it  begins  suddenly,  with  a 
more  or  less  pronounced  chill  and  intense  constitutional  symptoms.  There  are 
violent  headache,  great  languor,  anorexia,  and  especially  marked  pains  in  the 
loins  and  extremities.  The  temperature  rises  rapidly,  reaching  generally  106° 
(41°  C.)  or  higher  as  early  as  the  first  or  second  day.  The  skin  is  hot  and  dry, 
and  usually  quickly  assumes  a  very  characteristic  dirty-yellowish  color.  In  Leip- 
sic, we  often  saw  herpes  labialis,  which  seems,  however,  to  have  been  rarer  in 
epidemics  elsewhere.  The  tongue  becomes  dry  and  thickly  coated.  Sometimes  there 
is  vomiting.  The  bowels  are  constipated,  or  there  is  a  slight  diarrhoea.  The 
spleen  becomes  rapidly  enlarged,  being,  as  a  rule,  even  larger  than  in  typhoid  or 
typhus.  The  liver  is  slightly  enlarged.  The  chest  presents  the  signs  of  a  bron- 
chitis, generally  moderate,  but  in  exceptional  instances  severe.  The  pulse  is 
much  quickened.  It  is  seldom  that  there  are  severe  cerebral  symptoms  beyond  a 
certain  apathy  and  stupor.  We  have  seen  delirium  tremens  sometimes,  in  drunk- 
ards. A  very  characteristic  symptom,  already  mentioned,  is  the  marked  hyperses- 
thesia  of  the  muscles,  especially  in  the  calves. 

After  these  symptoms,  accompanied  by  persistent  and  generally  very  high 
fever,  have  lasted  five  days  to  a  week,  there  is  a  critical  decline  of  temperature, 
with  profuse  sweating.  The  patient  now  improves  so  rapidly  and  decidedly  that 
he  thinks  himself  completely  cured,  and  generally  gives  little  credence  to  the 
physician's  prophecy  of  a  relapse.  In  rare  but  well-attested  cases  there  has  been 
really  but  one  attack.  The  rule  is  that,  after  about  a  week,  a  second  attack  occurs, 
often  a  third  after  that,  and,  infrequently,  even  a  fourth  and  fifth.  In  each  of 
these,  the  above-mentioned  symptoms  are  repeated  more  or  less  completely  and  vio- 


RELAPSIls^G   FEVER 


35 


lently.  As  the  only  certain  and  constant  sign  of  the  recurring  attacks  (the 
so-called  relapses)  is  a  fresh  rise  of  temperature,  it  will  be  well  to  consider  their 
peculiarities  at  the  same  time  that  we  describe  the  course  of  the  fever.^  During 
the  intervals  of  normal  temperature  the  other  objective  symptoms  of  disease  are 
usually  absent,  except  an  evident  splenic  tumor,  and,  not  infrequently,  the  peculiar 
pale-yellow  hue. 

Course  op  the  Fever  (see  Fig.  3). — The  beginning  of  the  fever  in  the  first 
attack  is,  as  we  have  said,  almost  always  sudden,  so  that  it  may  even  in  a  few 
hours  reach  a  considerable  height.  The  fever  lasts,  as  a  rule,  five  to  seven  days, 
but  not  infrequently  as  short  a  time  as  three  or  four  days,  or  as  long  as  ten  or 


2    3 


5      6      7      8     9     10     11    12     13     14    15    16     17    18    19    20    21    22    23    24 


Fig.  3. — Example  of  the  temperature  curve  in  relapsing  fever. 

twelve  days.  During  this  time  it  may  keep  a  tolerably  uniform  height,  but 
oftener  there  are  considerable  remissions,  which  may  even  come  to  deserve  the 
name  of  pseudo-crises.  In  such  cases  the  temperature  sinks  in  the  morning  to 
normal  or  even  lower,  so  that  we  might  believe  the  fever  ended ;  but  in  the  even- 
ing the  temperature  rises  again  to  its  former  level.  These  pseudo-crises  are  most 
frequent  toward  the  end  of  the  attack,  but  do  occur  sometimes  in  the  very  first 
days.  The  absolute  height  of  the  fever  is,  as  a  rule,  very  considerable.  Tempera- 
tures between  105.5°  and  106.5°  (41°  and  41.5°  C.)  are  very  often  observed,  and 
in  themselves  are  not  especially  ominous  in  relapsing  fever.  The  highest  tempera- 
ture we  have  observed  was  107.9°  (42.2°  C).  Sometimes  the  temperature  is  more 
moderate  (between  102°  and  104°,  39°  and  40°  C).  The  fever  almost  always 
ends  at  the  close  of  the  attack  by  crisis,  only  rarely  by  a  rapid,  gradual  decline. 
The  crisis  is  often  preceded  by  an  especially  great  rise  the  evening  before  {per- 
turhatio  critica) ;  so  that  the  subsequent  fall  of  temperature  is  very  considerable. 
It  generally  occurs  at  night,  and  is  accompanied  by  profuse  perspiration.  The 
fall  may  amount  to  9°  or  10°  (5°  to  6°  C).  The  temperature  sinks  almost 
always  below  normal,  often  as  low  as  95°  (35°  C.)  or  thereabouts.  Once  we  saw 
it  fall  to  92.1°  (33.4°  C). 

To  the  first  attack  succeeds  an  interval  during  which  there  is  no  fever  (a py- 
rexia), which  lasts  on  the  average  about  a  week,  sometimes  a  less  time,  and  often 
a  greater.  The  longest  interval  we  have  ever  observed  lasted  seventeen  days. 
During  this  interval  the  temperature,  which,  as  a  rule,  is  at  first  subnormal,  rises 
to  normal,  and  then  generally  remains  there.  Exceptionally  there  are  slight 
evening  exacerbations  to  above  100.5°  (38°  C).  These  may  have  no  demon- 
strable cause,  or  may  result  from  some  complication,  such  as  otitis,  or  a  furun- 
cle.    Then  comes  another  change,  and  generally  a  sudden  one,  ushered  in  with  a 


36 


ACUTE    GEIsTEEAL   INFECTIOUS    DISEASES 


chill,  and  a  new  rise  of  temperature,  the  beginning  of  the  second  attack  or  first 
relapse.  During  this  attack  the  fever  has  the  same  general  peculiarities  as  in  the 
first  attack.  Generally  the  first  relapse  is  briefer  by  a  day  or  two  than  the  first 
attack ;  but  the  reverse  is  sometimes  true.  We  will  add  that  we  have  observed 
not  infrequently  a  rather  high  evening  temperature  (101.5°,  38.5°  C.)  for  one 
or  two  days  before  the  second  attack  began,  as  also  before  the  third. 

Relapsing  fever  seems  in  many  epidemics  to  have  been  made  up  of  two  attacks, 
so  that  not  more  than  one  tenth  of  the  cases  had  a  third  attack.  On  the  other 
hand,  the  majority  of  the  cases  in  the  last  epidemic  had  two  relapses.  In  these 
cases  the  rule  was  for  the  interval  between  the  second  and  third  attacks  to  be 
one  or  two  days  longer  than  the  first  apyrexia;  but  earlier  epidemics  seem  to 
have  had  the  second  apyrexia,  if  there  was  one  at  all,  briefer  than  the  first.  The 
third  attack  is  set  down  in  all  reported  cases  as  decidedly  shorter  than  either  of  its 
predecessors.  It  lasts  generally  two  or  three  days.  Exceptionally  we  have  seen 
it  persist  for  four  or  even  six  days. 

A  fourth  and  even  a  fifth  attack  may  occur,  but  only  exceptionally.  If  they 
do  happen,  they  are  usually  imperfectly  developed,  and  often  are  limited  to  a 

fever  of  one  day's  duration.  The  more  ac- 
curately and  persistently  we  take  the  tem- 
perature during  convalescence,  the  oftener 
do  we  find  slight  rises  of  temperature  oc- 
curring at  intervals  late  in  the  history  of 
the  case.  These  are  probably  to  be  inter- 
preted as  final,  rudimentary  attacks. 

The  Spirilli. — The  number  of  cases  of 
relapsing  fever  in  which  no  spirilli  can 
be  demonstrated  in  the  blood,  if  the  exami- 
nation be  accurate,  has  become  so  small 
that  it  can  be  disregarded,  when  we  com- 
pare it  with  the  much  greater  number  of 
cases  where  such  demonstration  is  made 
with  ease  and  certainty.  The  best  way  is 
to  get  a  drop  of  blood  by  pricking  the 
skin,  and  examine  it  as  it  is,  without  mix- 
ing anything  with  it.  Staining  (with  the 
basic  aniline  colors)  is  easy  but  unneces- 
sary. With  any  good  dry  lens  of  400  to  500  diameters  the  spirilli  are  seen  with 
perfect  distinctness.  It  requires  a  little  practice  to  make  them  out ;  but  this  is 
easily  obtained.  Often  the  attention  is  first  caught  by  little  jogglings  and  mo- 
tions of  the  red  blood-corpuscles,  and  then  we  see  the  delicate,  narrow  threads. 
Their  length  equals  about  three  to  six  times  the  diameter  of  the  red  globules  (Fig. 
4).  They  exhibit  an  active  and  almost  continuous  motion,  like  snakes.  Often 
the  whole  thread  bends  upon  itself,  and  then  stretches  out  again.  They  are 
partly  separate  and  partly  tied  up  in  knots  composed  of  four  to  twenty  individ- 
uals. The  whole  number  visible  in  one  field  varies  greatly  in  individual  cases, 
and  has  no  direct  relation  to  the  severity  of  the  case.  Often  it  requires  long 
searching  to  find  a  few,  while  in  other  eases  there  may  be  twenty  or  more  in  the 
field  at  once.  A  very  interesting  fact  is  that  their  appearance  in  the  blood  de- 
pends upon  the  attacks  of  fever.  On  the  first  day  of  the  attack  we  rarely  find 
spirilli,  and  then  only  one  or  two.  Upon  succeeding  days  their  number  increases. 
Shortly  before  the  end  of  the  attack — that  is,  before  the  crisis — they  generally 
disappear  entirely ;  but  even  after  the  crisis  they  have  been  found,  exceptionally 
and  in  very  small  numbers.  They  have  very  often  been  found  by  the  author  as 
well  as  other  observers  during  the  pseudo-crisis  described  above,  so  that,  after  the 


Fig.  4.— Spirilli  of  relapsing  fever  in  the  blood. 


KELAPSING   FEVER  37 

temperature  has  become  normal,  the  presence  of  spirilli  makes  it  very  probable 
that  another  rise  of  temperature  is  impending.  The  spirilli  have  thus  far 
been  found  in  the  blood  only,  in  the  catamenia,  in  bloody  urine,  or  in  blood 
coughed  up  from  the  lungs,  and  never  in  the  organs  or  secretions  (urine,  milk, 
sweat,  contents  of  herpetic  vesicles).  There  can  hardly  be  any  doubt  that  the 
spirilli  which  appear  in  the  separate  attacks  are  to  be  regarded  as  separate  gener- 
ations. As  to  their  manner  and  place  of  development  we  have  as  yet  no  knowl- 
edge. In  the  final,  rudimentary  attacks,  we  find  few  if  any.  If  the  patient  dies 
during  an  attack,  they  are  to  be  found  in  the  blood  after  death.  Artificial 
cultivations  have  not  been  very  successful;  nor  have  pure  cultures  of  them, 
to  our  knowledge,  ever  succeeded.  Albrecht  states  that  they  will  subsequent- 
ly develop  in  blood  taken  from  a  patient  during  the  ioiterval  when  he  has  no 
fever. 

The  blood  is  otherwise  modified  during  relapsing  fever.  "We  very  often  find  a 
slight  increase  in  the  white  corpuscles.  There  is  often  a  noticeable  abundance  of 
very  small  bodies,  so-called  granular  elements  (Kornchenbildungen).  The  signifi- 
cance of  these  (the  remains  of  white  corpuscles?)  is  still  doubtful.  There  are, 
finally,  peculiar  cells,  rather  large,  with  fat-granules.  They  were  demonstrated 
by  Ponfick  in  the  venous  blood,  and  are  said  to  come  from  the  spleen.  We  also 
find  fatty-degenerated  endothelium  in  the  blood. 

Complications  are  on  the  whole  rare,  and  mostly  secondary.  Important 
among  these  are  troublesome  ophthalmic  disturbances,  especially  iritis  and  irido- 
choroiditis.  Sometimes  parotitis,  laryngitis,  or  pneumonia  occur.  Epistaxis  is 
a  not  infrequent  complication.  It  is  usually  profuse  and  persistent,  and  it  may 
even  be  dangerous.  Sometimes  there  has  been  rather  severe  dysenteric  trouble. 
In  one  case  which  ended  fatally  we  observed  a  very  peculiar  intestinal  lesion, 
consisting  of  hsemorrhagic-necrotic  foci  in  the  colon  and  lower  ileum.  In  severe 
cases  acute  hsemorrhagic  nephritis  occurs  with  comparative  frequency.  At  the 
autopsy  an  important  and  characteristic  phenomenon  is  the  wedge-shaped  white 
spots  which  occur  in  the  spleen,  like  infarctions.  They  have  a  clinical  interest, 
as  they  may  become  the  starting-point  of  pygemic  conditions  or  of  peritonitis. 
Splenic  abscesses  have  been  observed  in  a  few  cases. 

Variations  in  the  course  of  the  disease  occur  in  this,  as  in  all  other  acute 
infectious  diseases.  First  there  are  mild,  abortive  cases,  in  which  the  attacks 
are  few  and  brief.  Then  cases  have  been  described  resembling  intermittent  fever. 
Of  chief  importance  is  that  severe  variety  of  relapsing  fever  first  observed  in 
Egypt  by  Griesinger,  and  described  as  "  bilious  typhoid."  There  is  no  longer  any 
doubt  about  the  proper  classification  of  this  disease,  for  spirilli  have  been  proved 
to  appear  in  it,  and  it  has  even  been  shown  that  its  inoculation  upon  another 
person  (  !)  produces  an  ordinary  case  of  relapsing  fever.  Bilious  typhoid  fever  oc- 
casions successive  attacks,  like  those  of  relapsing  fever.  The  type  is  much  more 
severe.  As  a  rule,  there  appear  marked  icterus,  grave  nervous  symptoms,  hfemor- 
rhages  into  the  skin  and  mucous  membranes;  and  the  termination  is  frequently 
fatal.  The  autopsy  shows  a  greatly  enlarged  spleen,  often  containing  infarctions 
and  abscesses,  and  in  some  cases  hepatic  abscesses,  septic  nephritis,  and  similar 
lesions. 

The  prognosis  of  ordinary  relapsing  fever  is  on  the  whole  very  favorable.  In 
the  last  epidemics  the  usual  mortality  was  only  two  to  four  per  cent.  The  fatal 
cases  could  some  of  them  be  laid  to  wretched  nursing.  In  the  remaining  portion 
death  resulted  from  complications,  such  as  pneumonia  and  nephritis. 

The  treatment  must  as  yet  be  purely  symptomatic.  Antipyretic  treatment  is 
generally  needless,  since  the  fever  is  relatively  brief  and  often  quite  intermittent. 
Moreover,  most  patients  can  not  well  endure  cold  baths,  because  the  muscles  are 
so  painful.     As  a  rule,  good  nursing  and  proper  food  amply  suflSce.     If  the  mus- 


38  ACUTE   GENERAL   INFECTIOUS   DISEASES 

cular  pains  are  very  violent,  we  may  order  chloroform  liniment  as  an  embroca- 
tion.    Complications  are  to  be  treated  on  general  principles. 

We  are  not  acquainted  with  any  remedy  that  can  influence  the  disease  itself 
or  avert  the  relapses.  Large  doses  of  quinine,  salicylic  acid,  etc.,  have  been  fre- 
quently employed  for  this  purpose,  but  never  with  success.  Lately  there  has 
been  ascribed  to  calomel  a  favorable  influence  upon  the  general  course  of  the  dis- 
ease, and  its  use  is  said  to  diminish  the  number  of  attacks.  We  must  await  fur- 
ther evidence  in  support  of  this  statement. 


CHAPTEE   IV 

SCABLET    TEVEE 

{Scarlatina) 

We  now  begin  the  consideration  of  those  acute  infectious  diseases  which  are 
usually  embraced  under  the  name  of  the  "  acute  exanthemata."  In  this  group 
are  reckoned,  besides  scarlet  fever,  measles,  rotheln,  small-pox,  and  varicella.  The 
point  which  these  diseases  have  in  common  i^  that  in  all  of  them  is  developed  a 
characteristic  eruption,  of  slight  clinical  signiflcance  in  itself,  in  most  cases, 
but  of  thoroughly  characteristic  appearance  in  each  disease,  and  hence  of  essen- 
tial importance  in  diagnosis.  A  number  of  the  acute  exanthemata  have  this 
further  point  of  mutual  resemblance  that  they  appear  chiefly  in  children.  These 
diseases  are  scarlet  fever,  measles,  rotheln,  and  varicella. 

.Etiology. — Infection  with  the  specific  scarlatinal  poison  occurs  almost  always 
by  contagion,  which  takes  place  very  readily.  A  single  approach  to  a  patient  ill 
with  scarlet  fever  may  suffice  to  communicate  the  disease.  There  is  no  doubt  that 
the  disease  may  be  transferred  by  objects  which  the  patient  has  touched,  such  as 
linen,  clothing,  furniture,  or  toys.  Persons  who  have  been  with  the  sick  may  be 
the  means  of  transmitting  the  disease,  although  themselves  unaffected.  In  Eng- 
land it  has  been  thought  that  the  contagium  may  be  carried  by  milk. 

Numerous  observations  show  that  the  scarlatinal  poison  is  with  great  difficulty 
destroyed,  and  that  it  may  keep  its  contagious  powers  for  months  ("tenacity"). 
We  can  thus  see  how  difficult,  how  impossible,  it  may  be  in  an  individual  case  to 
point  out  the  source  of  contagion.  Scarlet-fever  patients  can  communicate  the 
disease  certainly  as  late  as  the  end  of  the  desquamative  period,  or  perhaps  some- 
what longer. 

Details  as  to  the  manner  of  contagion,  or  as  to  the  specific  poison  itself,  are  as 
yet  unknown.  All  statements  made  in  regard  to  finding  alleged  specific  micro- 
organisms of  scarlet  fever  are  extremely  doubtful.  The  exciting  agent  of  scarlet 
fever  must,  however,  be  contained  in  the  blood  and  in  the  contents  of  the  miliary 
vesicles  of  scarlet-fever  patients,  for  the  disease  has  repeatedly  been  artificially 
produced  in  healthy  persons  by  inoculation  with  these  fluids. 

Predisposition  to  scarlet  fever  is  far  less  universal  than  is  pi'edisposition  to 
measles  or  small-pox.  In  families  with  several  children  often  only  one  or  two  fall 
sick,  while  the  rest  escape,  although  equally  exposed.  As  age  increases,  liability 
to  the  disease  greatly  diminishes,  although  there  are  cases  of  scarlet  fever  among 
adults.  The  majority  of  patients  are  between  two  and  ten  years  of  age.  Scarlet 
fever  is  rare  during  the  first  year  of  life.  It  is  an  interesting  fact  that  children 
with  fresh  wounds,  either  accidental  or  surgical,  are  especially  liable  to  scarlet 
fever.     An  analogous  and  familiar  fact  is  that  women  after  delivery  have  a  strong 


SCARLET  FEVER  39 

tendency  to  the  disease.*  As  a  rule,  a  person  is  attacked  but  once,  so  that,  after 
the  disease  is  over,  an  immunity  from  contagion  is  enjoyed;  but  there  are  excep- 
tions to  this  rule. 

Scarlet  fever  is  now  spread  over  the  entire  globe.  In  Germany  there  are 
almost  always  some  sporadic  cases  in  the  larger  towns,  while  from  time  to  time, 
especially  in  autumn,  there  are  more  or  less  extensive  epidemics  in  one  place  or 
another.  There  is  considerable  variation  in  the  different  epidemics  of  scarlet 
fever,  as  in  many  other  infectious  diseases,  in  the  general  character  of  the  disease, 
and  above  all  in  the  prevailing  mildness  or  severity  of  the  cases  and  the  frequency 
of  certain  complications  (nephritis,  diphtheria),  etc. 

Clinical  History. — The  period  of  incubation  is  not  definitely  known.  Many 
observations  seem  certainly  to  indicate  a  short  period  of  two  to  four  days,  but  the 
incubation  stage  is  perhaps  often  somewhat  longer — four  to  seven  days.  There 
are  hardly  ever  any  decided  prodromata.  The  disease  begins  rather  suddenly, 
with  fever,  often  introduced  by  chilliness,  and  sometimes  by  a  well-marked  rigor. 
There  is  almost  invariably  a  painful,  scarlatinal  sore  throat.  A  further  symp- 
tom, in  all  cases  of  any  severity,  is  cerebral  disturbance,  generally  rather  intense. 
There  may  be  headache,  dullness,  uneasy  sleep,  delirium,  and,  in  smaller  chil- 
dren, sometimes  even  convulsions.  A  very  frequent  and  characteristic  early 
sjTQptom  is  vomiting,  which  raay  be  repeated. 

The  characteristic  rash  usually  appears  as  soon  as  the  close  of  the  first  day,  or 
on  the  second,  and  begins  on  the  neck  and  on  the  chest  and  face,  quickly  becoming 
almost  universal.  The  eruption  consists  at  first  of  numberless  small  red  points, 
crowded  thickly  together  and  soon  united  into  a  diffuse,  intense,  scarlet-colored 
erythema.  The  small  and  somewhat  elevated  points  almost  always  correspond  to 
the  swollen  hair-follicles.  The  diffuse  redness  is  the  result  of  an  excessive  hyper- 
emia of  the  skin,  and  vanishes  completely  on  pressure.  The  skin  as  a  whole 
seems  slightly  swollen  and  thickened.  The  back  usually  presents  the  most  vivid 
tint.  In  the  face  there  is  generally  pallor  of  the  lips  and  chin,  presenting  a  very 
striking  and  characteristic  contrast  to  the  bright-red  cheeks.  If  some  object 
like  the  end  of  a  pen-holder  be  drawn  over  the  red  skin,  there  soon  arise  corre- 
sponding white  lines,  due  to  contraction  of  the  blood-vessels.  It  is  possible  thus 
to  make  letters  or  pictures  upon  the  back  of  the  patient.  We  should  add,  how- 
ever, that  this  is  not  a  peculiarity  of  the  scarlatinal  eruption,  being  seen  in  other 
erythematous  eruptions. 

The  rash  persists  for  some  three  or  four  days,  at  first  even  increasing  somewhat 
in  vividness.  It  often  appears  more  intense  by  artificial  light  than  in  the  day- 
time. Meanwhile  the  severe  general  symptoms  continue — the  fever,  the  usually 
excessively  rapid  pulse,  the  cerebral  sjonptoms,  and  the  throat  trouble.  The  spleen 
is  often  somewhat  swollen,  though  seldom  very  large.  Then  the  eruption  begins 
to  fade,  the  fever  gradually  ceases  by  lysis,  the  general  condition  and  the  difficulty 
in  swallowing  improve.  With  the  end  of  the  first  week  or  the  beginning  of  the 
second,  the  cases  which  run  the  tjTDical  course  become  fully  convalescent.  When 
the  rash  disappears,  the  epideraiis  usually  begins  to  peel  off,  in  a  very  character- 
istic way,  in  pieces  of  considerable  size.  The  exfoliation  upon  the  hands  and 
feet  is  especially  pronounced,  and  the  little  convalescents  often  amuse  them- 
selves by  peeling  off  the  epidermis  in  strips.  Cases  which  are  apparently  the 
mildest  and  most  benign  may  have  their  convalescence  interrupted  by  the  oc- 
currence of  a  secondary  scarlatinal  nephritis.  There  is  no  sure  prophylaxis 
against  this. 

We  will  now  pass  on  from  this  general  summary  to  a  more  complete  considera- 

*  In  puerperal  cases  genuine  scarlet  fever  and  septic  diseases  were  formerly  often  confounded. 
(See  Chapter  XVIII.) 


40 


ACUTE  GENERAL  INFECTIOUS  DISEASES 


41.0° 


40.0' 


39.0° 


38.0 


37.0° 


Mwmmmmm 


■■■■■■■■BnnBIHB 

■iBBssaaffii 


Fig.  5. 


Eruption. 
-Example  of  a  normal  scarlet-fever  curve. 


tion  in  detail  of  general  and  local  symptoms;  and  we  shall  see  how  manifold 
are  the  clinical  phenomena  presented  by  scarlet  fever. 

1.  Fever  (see  Fig.  5). — Although  in  a  few  undeveloped  cases  there  is  no  fever, 
or  scarcely  any,  almost  all  cases  of  any  severity  have  high  fever.  It  is  only  ex- 
ceptionally that  severe  cases  are  observed  in  which  the  bodily  temperature  is  little 
if  at  all  elevated.  As  a  rule,  the  fever  rises  rapidly  upon  the  very  first  day,  cor- 
responding to  the  sudden  onset  of  all 
the  symptoms,  to  about  104°  or  105° 
(40°-40.5°  C).  The  next  day  it  often 
becomes  a  little  higher  still,  and  then 
persists  with  but  slight  variations,  as 
a  rule,  so  long  as  the  eruption  is  at  its 
height.  During  this  period  a  tempera- 
ture of  105°  or  more  (40.5°^1°  C.)  is 
not  infrequently  observed.  When  the 
eruption  fades,  and  the  other  symp- 
toms decline,  defervescence  occurs. 
This  happens  but  rarely  by  crisis,  and 
that  in  the  slight  attacks.  It  is  almost 
always  by  prolonged  lysis,  as  in  ty- 
phoid, only  more  irregularly  and  more 
rapidly.  If  the  fever  lasts  into  the  sec- 
ond week  of  the  disease,  it  is  almost 
always  (though  not  without  excep- 
tions) caused  by  demonstrable  complications.  The  most  frequent  causes  are  the 
persistence  of  a  severe  sore  throat,  the  occurrence  of  inflammatory  changes  in  the 
cervical  glands,  or  a  purulent  otitis  media.  In  closing  what  we  have  to  say  about 
the  fever  in  this  disease,  we  would  emphasize  the  fact  that  the  pulse  is  often  very 
rapid  (140  to  160  a  minute),  even  in  comparison  with  the  height  of  the  tem- 
perature. 

2.  The  Throat. — The  throat  presents  the  most  constant  local  lesion  of  scarlet 
fever.  Sore  throat  is  only  in  the  rarest  cases  wholly  absent ;  *  but  its  form  and 
intensity  may  vary  extremely.  The  mildest  variety  is  a  simple,  erythematous 
catarrh,  without  much  swelling,  but  exhibiting  usually  a  vivid  and  often  punctate 
reddening  of  the  soft  palate  and  tonsils,  the  pharynx,  and  also  the  mucous  mem- 
brane of  the  hard  palate,  frequently  associated  with  enlargement  of  the  little 
mucous  follicles.  Sometimes  minute  haemorrhages  take  place  into  the  mucous 
membrane.  In  other  cases  the  scarlatinal  affection  of  the  throat  is  from  the  start 
associated  with  considerable  swelling  of  the  parts,  and  especially  of  the  tonsils, 
justifying  the  term  "  parenchymatous  sore  throat."  Not  infrequently  small 
abscesses  form  in  the  lacunae  of  the  tonsils ;  or  superficial  spots  of  necrosis  develop 
which  leave  behind  them  larger  or  smaller  ulcers,  and  sometimes  occasion  con- 
siderable haemorrhage.  There  may  even  be  a  circumscribed  gangrene  of  the 
tonsils. 

The  most  important,  because  it  is  also  the  most  dangerous,  of  the  affections 
of  the  throat  resulting  from  scarlet  fever  is  the  so-called  scarlatinal  diphtheria 
— that  is,  a  diphtheritic  inflammation  of  the  tonsils  and  soft  palate.  This  usually 
develops  on  the  third,  fourth,  or  fifth  day  of  the  disease,  replacing  a  simple  in- 


*  Absence  of  sore  throat  has  been  noted  by  others  and  by  myself,  especially  in  the  scarlet  fever  of 
women  in  childbed.  I  suspect  that  the  reason  for  this  is  that  the  infection  does  not  enter  in  the  usual 
■way  through  the  mouth,  but  from  some  wound  due  to  parturition.  On  the  other  hand,  it  is  to  be  noted 
that  in  the  scarlet  fever  from  wounds,  when  the  infection  follows  an  injury  to  the  finger,  etc.,  a  sore 
throat  occurs. 


SCAELET  FEVER  41 

flammatory  condition  of  the  parts.  Whitish,  dirty-colored  spots  develop  on  the 
tonsils,  the  arches  of  the  palate,  and  the  uvula.  These  rapidly  increase  in  size, 
and  cause  a  dry  necrosis  of  the  mucous  membrane  and  subsequent  ulceration. 
The  process  is  a  truly  diphtheritic  one — that  is,  there  is  an  inflammation  com- 
bined with  an  extension  into  the  diseased  tissues  of  a  fibrinous  exudation. 

It  is  especially  characteristic  of  scarlatinal  diphtheria  that  there  is  almost 
invariably  a  considerable  swelling  of  the  cervical  lymph-glands,  except  in  those 
cases  which  die  very  quickly.  It  is  true  that  the  glands  are  usually  somewhat 
enlarged  in  the  milder  forms  of  pharyngitis  accompanying  scarlet  fever,  but  they 
seldom  attain  the  size  observed  in  the  true  diphtheritic  process.  In  this  there  is 
an  inflammatory  and  oedematous  infiltration  affecting  often  not  only  the  glands 
themselves,  but  also  the  surrounding  connective  tissue,  so  that  in  severe  cases  the 
whole  cervical  region  and  the  floor  of  the  buccal  cavity  presents  a  firm  and 
usually  a  very  painful  enlargement.  It  should  be  added  that  the  severity  of  the 
throat  symptoms  and  the  extent  of  the  glandular  swelling  are  not  always  com- 
mensurate. Almost  always  the  scarlatinal  diphtheria  is  associated  with  a  marked 
stomatitis,  and  very  often  also  with  a  severe  purulent  or  even  diphtheritic  rhinitis, 
although  an  invasion  of  the  larynx  (vide  infra)  is  only  exceptionally  seen. 
At  the  alse  of  the  nose  and  the  corners  of  the  mouth  there  are  often  superficial 
ulcers  from  this  cause.  Otitis  is  also  a  frequent  complication  of  scarlatina  (vide 
infra) . 

The  infiuence  of  the  scarlatinal  diphtheria  upon  the  general  condition  of  the 
patient  is  always  considerable.  Apart  from  the  marked  local  discomfort,  there 
is  often  a  severe  general  septic  condition.  Grajre  signs  of  cardiac  weakness  (a 
very  rapid,  small  pulse)  are  very  apt  to  appear  early.  Moreover,  cases  of  scarlet 
fever  associated  with  pharyngeal  diphtheria  often  show  at  the  same  time  other 
severe  septic  complications  (inflammation  of  several  joints,  simple  or  purulent 
inflammation  of  the  serous  membranes,  nephritis,  etc.).  Many  cases  end  fatally 
in  a  few  days,  while  others  pursue  a  more  tedious  course,  lasting  perhaps  several 
weeks  before  death  comes.  These  are  often  associated  with  pysemic  processes  in 
other  parts  of  the  body. 

With  regard  to  the  pathogenesis  of  the  throat  troubles  seen  in  scarlet  fever,  the 
more  simple  forms  are  in  all  probability  directly  associated  with  the  scarlatinal 
process — that  is,  they  are  direct  sequences  of  the  affection.  In  regard,  however, 
to  the  severer  forms,  and  especially  to  the  diphtheritic  variety,  it  is  almost  cer- 
tain that  these  are  not  a  direct  result  of  the  scarlatinal  poison,  but  are  due  to 
some  secondary  infection  which  occurs  on  the  soil  furnished  by  the  primary  scar- 
latinal angina.  The  severe  necrotic  disease  of  the  mucous  membranes  and  the 
secondary  changes  in  the  lymph-glands  and  other  septic  complications  are  due 
chiefly  to  streptococci  (Loffler)  ;  but  we  are  almost  compelled  to  suppose  that  there 
is  some  intimate  connection  between  the  two  varieties  of  infection,  else  why 
should  this  peculiar  secondary  disease,  the  scarlatinal  diphtheria,  be  so  often  con- 
joined with  scarlet  fever  ?  It  seems  to  us  certain  that  "  scarlatinal  diphtheria  " 
should  not  without  further  evidence  be  identified  with  true  diphtheria,  in  spite  of 
the  similarity  of  the  anatomical  ("  diphtheritic  ")  changes.  From  a  purely  clin- 
ical standpoint  the  two  present  several  important  points  of  difference.  In  partic- 
ular the  scarlatinal  diphtheria,  in  contrast  with  the  primary  form  of  the  disease, 
seldom  spreads  to  the  larynx.  Laryngeal  croup  is  therefore  but  rarely  seen  in 
scarlet  fever.  The  severe  dyspntea  which  sometimes  develops  in  the  course  of  scar- 
let fever  is  probably  caused  by  an  inflammatory  cedema  of  the  glottis.  Another 
important  clinical  distinction  between  genuine  and  scarlatinal  diphtheria  is  that 
paralysis  of  the  soft  palate,  the  ocular  muscles,  and  other  parts  is  scai'cely  ever 
a  sequel  of  scarlatinal  diphtheria.  On  the  other  hand,  however,  it  is  easily  con- 
ceivable  that  many   similarities   between   the   two   diseases   should   exist,   since 


42  ACUTE  GENERAL  INFECTIOUS  DISEASES 

severe  secondary  septic  streptococcus  infection  may  occur  both  in  scarlatinal 
angina  and  in  true  diphtheria.  It  is  also  possible  that  in  some  cases  an  actual 
true  diphtheria  should  appear  as  a  secondary  infection  in  scarlatinal  angina.  The 
reported  cases  of  laryngeal  croup  after  scarlet  fever  may  thus  be  explained.  All 
these  conditions,  which  have  been  ranch  discussed,  will  be  made  wholly  plain 
when  the  accurate  bacteriological  investigations  of  individual  cases  become  more 
numerous. 

3.  We  proceed  by  a  natural  sequence  'to  the  consideration  of  the  affections  of 
certain  parts  adjacent  to  the  throat,  troubles  which  must  be  regarded  as  chiefly 
the  result  of  direct  extension,  or  of  a  conveyance  of  the  inflammatory  process 
from  the  throat. 

The  stomatitis  we  have  already  mentioned,  as  well  as  the  disturbance  in  the 
neighboring  lymph-glands  and  the  surrounding  tissue.  Parotitis  is  not  rare  in 
severe  cases.  Of  especial  importance  is  the  scarlatinal  inflammation  of  the  middle 
ear,  which  often  results  in  permanent  deafness. 

This  inflammation  usually  arises  at  the  time  of  desquamation,  but  it  may  occur 
earlier.  It  is  either  a  simple  catarrh,  a  purulent  otitis  media,  or,  in  severe  cases, 
an  actual  diphtheritic  process.  The  deafness  and  earache  are  easily  overlooked, 
as  the  other  symptoms  of  the  patient  occupy  the  attention,  so  that  the  ear  trou- 
ble is  first  recognized  by  the  occurrence  of  perforation  of  the  tympanum  and  sub- 
sequent purulent  otorrhoea.  After  this  declines  there  very  often  remains  behind, 
as  we  have  said,  permanent  deafness.  Statistics  have  shown  that  four  or  five  per 
cent,  of  all  cases  of  deafness  are  referable  to  an  attack  of  scarlet  fever  in  child- 
hood. The  otitis  is  seldom  immediately  dangerous,  but  yet  cases  of  purulent 
meningitis  have  been  observed  to  follow  it. 

We  have  already  spoken  of  the  purulent  or  even  diphtheritic  rhinitis  which 
almost  always  accompanies  the  scarlatinal  sore  throat.  In  rare  cases  there  may 
also  occur  a  purulent  conjunctivitis,  which  is  most  probably  the  result  of  a  direct 
conveyance  of  inflammatory  secretions. 

The  tongue  in  scarlet  fever  deserves  special  mention.  The  first  coating  cleans 
off,  and  then  the  tongue  usually  presents  a  very  characteristic  appearance.  It  is 
diffusely  reddened  and  covered  with  little  elevations  corresponding  to  swollen 
papillae  (strawberry  tongue,  scarlatinal  tongue). 

4.  The  characteristic  eruption,  as  developed  in  the  great  majority  of  cases,  has 
been  described  above.  It  remains  to  describe  certain  variations  from  the  usual 
appearances. 

First,  the  eruption  may  be  rudimentary.  It  is  then  not  pronounced,  and  visi- 
ble only  on  a  limited  portion  of  the  body  (face,  trunk,  or  extremities). 

Variations  from  the  type  are  not  rare ;  sometimes  the  papules  are  more  strongly 
develoi)ed  (scarlatina  papulosa)  ;  very  frequently  there  are  little  vesicles  {scarla- 
tina miliaris).  This  latter  form  of  the  eruption  appears  by  preference  upon  the 
trunk,  but  it  may  come  also  upon  the  extremities,  and  is  often  brought  out  by  ex- 
cessive perspiration,  or  by  wrapping  up  the  patient  too  warmly.  Many  epidemics 
are  noticeable  from  the  frequent  appearance  of  this  miliary  form.  More  rarely 
the  rash  has  a  spotted  look,  resembling  the  eruption  of  measles  {scarlatina  varie- 
gata).  There  may  be  minute  ecchymoses,  which  are  not  very  rare  and  not  omi- 
nous. Well-developed  cases  of  hemorrhagic  scarlatina  are,  however,  very  danger- 
ous, because  here  the  general  infection  of  the  system  is  almost  always  exceedingly 
severe,  and  probably  due  to  secondary  sepsis;  and  there  is  besides,  as  a  rule,  a 
general  ha^morrhagic  diathesis.  Other  cutaneous  lesions,  especially  herpes  and 
urticaria,  are  not  so  very  unusual  in  connection  with  the  scarlatinal  eruption. 
Furunculosis  has  been  repeatedly  observed  after  the  rash  fades. 

Desquamation  generally  begins  as  soon  as  the  rash  has  completely  disappeared, 
but  it  may  not  occur  till  a  few  days  or  even  one  or  two  weeks  later.    Its  extent 


SCAELET  FEVER  43 

corresponds  in  general  to  the  severity  of  the  eruption,  although  extensive  desqua- 
mation may  follow  a  rudimentary  eruption.  It  is  seldom  bran-like  or  furfura- 
ceous,  as  in  measles.  The  rule  is  for  it  to  be  in  lamellae,  so  that,  as  we  have  stated, 
quite  large  strips  of  epidermis  may  be  detached  entire. 

In  rare  cases  an  cedema  of  the  skin  appears  after  scarlet  fever,  which  can  not 
be  shown  to  depend  upon  nephritis  {vide  infra),  but  which  may  perhaps  be  due  to 
an  abnormal  permeability  of  the  walls  of  the  cutaneous  blood-vessels  following 
the  eruption  (hydrops  scarlatinosus  sine  nephritide) . 

6.  Kidneys. — Next  to  the  severer  forms  of  throat  trouble,  the  most  important 
and  dangerous  complications  are  located  in  the  kidneys.  They  may  appear  as 
early  as  the  acme  of  the  disease,  as  in  many  other  infectious  diseases.  The  urine 
has  a  trace  of  albumen.  In  rare  cases  the  amount  of  albumen  may  be  consider- 
able. The  appearance  of  the  urine  is  generally  not  much  changed,  and  the  micro- 
scope reveals  but  few  abnormal  constituents.  There  are  some  white  and  red  blood- 
globules,  a  few  hyaline  casts,  sometimes  one  or  two  renal  epithelial  cells.  This 
initial  albuminuria  very  rarely  gives  cause  for  alarm. 

The  genuine  scarlatinal  nephritis  scarcely  ever  develops  much  before  the  end 
of  the  second  or  the  beginning  of  the  third  week.  Sometimes  it  comes  even  later. 
In  one  case  under  our  own  observation  it  did  not  begin  till  the  thirty-third  day  of 
the  disease.  It  may  therefore  be  regarded  to  a  certain  degree  as  a  localized  re- 
lapse. It  may  be  so  mild  as  to  cause  no  subjective  symptoms  whatever,  so  that  it 
would  be  unnoticed  if  the  urine  were  not  carefully  examined.  On  the  other 
hand,  it  may  be  accompanied  by  the  gravest  symptoms,  and  may  soon  terminate 
fatally.  It  may  follow  either  severe  cases  or  the  mildest,  so  that  the  rule  should 
be  to  examine  the  urine  in  every  case  of  convalescence  from  scarlet  fever  as  often 
and  as  carefully  as  possible.  No  exact  statement  can  be  made  as  to  the  fre- 
quency of  this  complication,  for  it  is  much  more  common  in  some  epidemics  than 
in  others. 

The  development  of  nephritis  is  often  marked  by  a  fresh  rise  of  temperature. 
The  elevation  may  be  slight  or  it  may  reach  104°  (40°  C).  According  to  our  own 
experience,  the  fever  often  comes  a  day  or  two  earlier  than  the  changes  in  the 
urine.  As  the  nephritis  goes  on,  it  is  very  often  accompanied  by  a  moderate 
fever  with  remissions.  This  fever  may  be  almost  wholly  absent,  especially  in 
mild  cases.  The  pulse  generally  becomes  harder,  and  is  sometimes  quickened; 
but  in  many  cases  it  will  be  slow,  and  it  is  sometimes  irregular.  Among  other 
objective  symptoms,  the  first  to  excite  notice  is  generally  a  slight  pufiiness  of  the 
face,  which  is  usually  pale.  The  eyelids,  particularly,  present  an  evident  oedema. 
In  the  milder  cases  this  oedema  remains  limited,  while  in  others  it  gradually 
increases  in  extent  and  degree,  involving  first,  as  a  rule,  the  dependent  parts  of 
the  trunk,  and  later  the  extremities.  Severe  cases  develop  a  pronounced  ana- 
sarca. There  are  then,  usually,  effusions  into  the  serous  cavities,  especially  ascites 
and  hydrothorax.  The  latter  is  dangerous  chiefly  through  disturbance  of  the 
respiration,  particularly  if  it  be  associated  with  severe  bronchitis  or  pneumonia 
(vide  infra).  Although  in  general  the  development  of  a  universal  dropsy  is 
characteristic  of  scarlatinal  nephritis,  oedema  may  at  times  be  wholly  absent. 
On  the  other  hand,  it  is  noteworthy  that  the  oedema  may  occasionally  show  a 
peculiar  localization,  especially  in  the  mucous  membranes  (oedema  of  the  con- 
junctiva;, oedema  of  the  ary-epiglottic  folds  with  symptoms  of  laryngeal  stenosis, 
oedema  of  the  uvula  and  soft  palate,  etc.). 

The  urine  exhibits  the  most  important  changes  (vide  the  section  on  renal 
diseases).  These  may  be  insignificant  in  the  milder  cases,  but  they  are  very  pro- 
nounced in  the  severe  ones.  The  amount  is  much  diminished.  Sometimes  there 
will  be  for  several  days  almost  complete  anuria.  In  cases  of  any  severity  the  urine 
is  turbid,  dark,  often  evidently  bloody,  with  increased  specific  gravity  (about  1015 


44  ACUTE  GENERAL  INFECTIOUS  DISEASES 

to  1025),  and  containing  a  large  amount  of  albumen.  The  sediment  is  generally 
abundant,  and  exhibits  numerous  hyaline  easts  of  various  lengths  and  diameters. 
To  these  may  be  attached  red  or  white  blood-corpuscles,  detritus,  granules  of 
hsematoidin,  or  bacteria.  In  cases  of  some  duration  the  casts  are  often  moderately 
fatty.  Very  frequently  there  are  found  noticeably  long  and  broad  waxy  [fibrin- 
ous] casts,  which  are  opaque  and  yellow.  In  many  cases  of  scarlatinal  nephritis 
the  urine  is  peculiar  in  having  very  many  white  blood-corpuscles,  either  isolated 
or  adhering  to  the  casts.  These  undoubtedly  originate  for  the  most  part  in  the 
kidneys.  Red  globules,  some  of  them  in  the  form  of  colorless  rings,  are  found. 
They  are  usually  present  in  small  numbers,  but  may  become  more  abundant, 
especially  for  a  day  at  a  time.  We  have  seen  a  very  h^emorrhagic  urine  after  the 
special  albuminuria  had  disappeared.  Renal  epithelium  is  frequently  seen,  but 
not  invariably  nor  in  very  large  amount. 

Ur^emic  symptoms  often  develop  in  scarlatinal  nephritis.  They  may  be  of  all 
degrees  of  severity.  They  will  be  described  in  detail  under  diseases  of  the  kidney 
(vide  infra).  The  uraemia  may  be  so  severe  as  to  cause  convulsions,  coma,  and 
death;  but  it  is  remarkable  how  often  children  recover  from  what  seems  to  be  the 
most  pronounced  uraemia. 

The  duration  of  scarlatinal  nephritis  varies  greatly  according  to  its  severity.  ' 
In  cases  which  run  a  favorable  course,  the  urine  is  generally  abnormal  for  two  to 
four  weeks,  or  even  longer.  There  is  sometimes  a  very  slight  albuminuria  present 
for  months  without  causing  any  symptoms.  Death  may  be  due  to  uraemia  or 
more  frequently  it  may  come  on  with  severe  dyspncea.  The  latter  is  due  partly  to 
dropsical  conditions  (hydrothorax,  ascites),  or  often  to  a  severe  diffuse  bronchitis 
or  pneumonia  accompanying  the  nephritis.  Cardiac  insufficiency  also  may  be  the 
cause  of  death.  The  transition  of  acute  scarlatinal  nephritis  into  chronic  nephri- 
tis, especially  into  chronic  contracted  kidney,  is  rare,  but  it  has  certainly  been 
seen  both  by  ourselves  and  others.  It  is  worthy  of  note  that,  after  the  nephritis 
has  lasted  some  four  to  six  weeks,  beginning  hypertrophy  of  the  left  ventricle  can 
be  detected  by  the  displacement  and  strengthening  of  the  apex-beat.  Friedlander 
has  demonstrated  this  early  h^i^ertrophy  at  autopsy. 

The  anatomical  changes  of  scarlatinal  nephritis  can  be  mentioned  only  briefly 
here.  The  forms  vary.  We  often  find  the  "  large  white  kidney  " — that  is,  a  dif- 
fuse acute  nephritis  with  fatty  degeneration  of  the  epithelium — and  usually  also 
more  or  less  numerous  hsemorrhages.  In  other  cases  the  kidneys  macroscopically 
are  apparently  little  altered,  but  we  see  in  the  cortex  the  gray,  prominent,  blood- 
less glomeruli,  in  which  the  microscope  shows  very  marked  changes  ("  glomerulo- 
nephritis "  of  Klebs  and  others). 

6.  Joints. — When  desquamation  begins,  or  even  earlier,  pain  and  swelling 
may  attack  a  certain  number  of  the  joints.  This  trouble  was  formerly  called 
scarlatinal  rheumatism,  but  now  it  is  usually  known  as  scarlatinal  synovitis.  It 
is  generally  mild  and  quite  temporary,  but,  exceptionally,  it  may  be  severe  and 
even  purulent.  Then  it  is  usually  a  part  of  a  secondary  sepsis  or  a  general 
pyEemia,  as  evinced  by  such  other  lesions  as  empyema,  subcutaneous  abscesses, 
jaundice,  splenic  tumor,  nephritis,  etc.;  and  they  all  seem  to  be  caused  by  a  sec- 
ondary infection  with  streptococci,  etc. 

We  have  seen  a  few  instances  of  excessive  pain  in  the  muscles  of  the  thighs, 
accompanied  by  a  moderate,  diffuse  swelling. 

7.  Another  important  complication  of  scarlet  fever  is  pneumonia.  In  severe 
cases  lobular  pneumonia  sometimes  appears  as  early  as  the  first  stage  of  the  dis- 
ease; but  it  occurs  more  frequently  in  connection  with  the  nephritis,  when  it 
may  have  the  significance  of  so-called  nephritic  pneumonia  (vide  infra).  The 
respiration  may  be  very  seriously  embarrassed  by  it.  Inflammations  of  serous 
membranes  in  the  chest — viz.,  endocarditis,  pericarditis,  and  pleurisy — are  more 


SCAELET  FEVER  45 

rare.  They  may  or  may  not  be  accompanied  by  disturbances  in  the  joints 
{vide  supra).  Pericarditis,  endocarditis,  and  myocarditis  sometimes  develop 
during  scarlet  fever,  but  it  is  usually  hard  to  decide  whether  they  are  due 
to  the  direct  action  of  the  scarlatinal  poison  itself  or  to  secondary  septic  com- 
plications. We  refer  the  tendency  to  tachycardia  or  bradycardia,  irregularity 
of  the  heart-beat,  etc.  (which  sometimes  last  long  after  the  scarlet  fever),  to 
myocarditic  changes.  Endocarditis  may  result  in  permanent  valvular  disease. 
Quite  severe  intestinal  symptoms,  such  as  diarrhoea,  may  appear.  These 
are  generally  the  result  of  a  catarrhal  inflammation  of  the  intestinal  follicles. 
Dysentery  is  less  frequent.  The  enlargement  of  the  spleen  has  been  already 
mentioned.  The  liver  is  sometimes  found  to  be  considerably  enlarged.  A  general 
moderate  swelling  of  the  lymph-glands  (neck,  axillae,  groins)  is  usually  present 
in  scarlet  fever  at  the  time  of  the  eruption.  We  usually  find  in  the  blood  a 
pronounced  leucocytosis  which  sometimes  lasts  long  after  the  other  morbid 
symptoms. 

Variations  in  the  Course  of  the  Disease. — The  diversities  of  the  clinical  pic- 
ture in  different  cases  of  scarlatina  will  be  understood  when  we  consider  the 
variety  and  number  of  the  disturbances  thus  far  cited.  It  is  to  be  added  that  the 
general  course  of  the  disease  may  exhibit  numerous  peculiarities,  of  which  it  is 
hardly  possible  to  give  an  exhaustive  presentation.  We  will  content  ourselves 
with  a  cursory  statement  of  the  most  important  deviations  from  the  typical 
course. 

1.  Rudimentary  Forms. — To  this  class,  in  which  the  disease  does  not  reach  a 
perfect  development,  belong  first  the  cases  of  simple  sore  throat  with  no  erup- 
tion, or  at  most  an  extremely  faint  and  partial  one  {scarlatina  sine  exanthe- 
mate).  Soraetimes  even  the  sore  throat  is  hardly  to  be  seen,  and  there  is  noth- 
ing but  a  brief  and  slight  fever  with  mild  symptoms  of  general  disturbance.  The 
recognition  of  these  cases  as  scarlatinal  is  possible  only  when  we  consider  their 
setiological  relation  to  other  undoubted  cases  of  scarlet  fever.  We  had  an  excel- 
lent opportunity  to  observe  them  when  the  disease  broke  out  in  the  children's 
wards  of  the  hospital  at  Leipsic.  The  diagnosis  is  sometimes  confirmed  by  a 
slight  though  evident  desquamation,  affecting  the  hands,  feet,  legs,  and  back,  or 
by  an  acute  nephritis,  which  may  follow  the  mildest  attacks  of  this  sort.  Many 
cases  of  acute  nephritis,  though  apparently  wholly  spontaneous  and  primary, 
must  be  regarded  as  setiologically  scarlatinal. 

2.  Rudimentary  hut  Pernicious  Forms. — Under  this  head  belong  those  attacks 
of  scarlet  fever  in  which  the  eruption  is  scanty  or  absent,  while  from  the  very 
start  the  most  violent  general  symptoms  appear.  There  is  a  very  high  fever,  enor- 
mously rapid  pulse,  and  delirium.  Such  cases  must  be  the  result  of  an  uncom- 
monly severe  general  infection.  They  usually  end  in  speedy  death.  Other  cases, 
ending  fatally  in  a  few  days,  have  a  well-developed  rash  without  other  localized 
disturbances. 

3.  Severe  Forms  with  a  more  Protracted  Course. — In  these  cases  the  long- 
duration  is  not  the  exclusive  result  of  especial  complications,  but  is  likewise  due 
to  the  severity  of  the  intoxication.  One  variety  is  the  so-called  typhoidal  form  of 
scarlatina,  with  persistent  high  fever  and  severe  constitutional  symptoms.  An- 
other variety  is  the  hsemorrhagic  form  briefly  mentioned  above,  in  which  there 
are  extensive  haemorrhages  into  the  skin  and  into  the  mucous  and  serous  mem- 
branes. This  form  may  run  an  extremely  acute  course.  Further,  in  all  per- 
nicious forms,  there  may  be  severe  local  complications,  particularly  diphtheritic 
or  gangrenous  sore  throat,  inflammations  of  serous  membranes,  etc.  Attacks 
of  this  sort  are  often  not  produced  by  the  poison  of  scarlet  fever  alone,  but  by 
secondary  complicating  processes.  While  speaking  of  scarlatinal  diphtheria  it 
has  already  been  pointed  out  that  secondary  infection  of  the  system  may  result, 


46  ACUTE  GENERAL  INFECTIOUS  DISEASES 

principally  orig-inating  from  the  diseased,  throat,  and  occasioning  sometimes 
grave  septic  conditions  of  the  whole  body,  sometimes  local  disease  of  different 
parts. 

4.  In  extremely  rare  cases  Relapses  do  occur.  After  the  first  illness  a  fresh 
eruption  breaks  out  with  all  the  other  symptoms. of  scarlet  fever.  In  anomalous 
cases,  running  a  severe  course,  there  is  sometimes,  at  an  advanced  stage,  a  fresh, 
imperfect  eruption  (generally  in  spots),  which  Thomas  has  termed  a  pseudo- 
relapse.     Probably  this  is  usually  a  septic  eruption. 

Diag^nosis. — The  diagnosis  of  scarlet  fever  is  made  in  most  cases  from  the 
characteristic  eruption  taken  in  connection  with  the  other  symptoms.  We 
should,  however,  bear  in  mind  that  exceptionally  other  eruptions  appear  which 
exhibit  the  closest  resemblance  to  that  of  scarlet  fever.  1.  After  the  use  of 
certain  drugs,  especially  atropine  (belladonna),  quinine,  antipyrine,  morphine, 
chloral;  and  likewise  after  the  ingestion  of  crabs,  fish,  etc.  2.  As  a  symptom 
of  other  infectious  diseases,  such  as  typhoid  fever,  small-pox;  and,  above  all, 
in  septic  diseases  {vide  infra).  In  an  uncertain  or  anomalous  case,  factors  of 
importance  for  diagnosis  are  the  aetiology  (connection  with  other  well-defined 
cases),  the  initial  sore  throat,  and  the  eventual  occurrence  of  desquamation  or  of 
a  secondary  nephritis. 

The  prognosis  must  in  every  case  be  guarded.  From  what  has  been  said  of  the 
course  of  the  disease,  it  is  evident  that,  even  in  cases  which  are  at  first  appar- 
ently the  most  favorable,  dangerous  complications  may  appear.  The  commonest 
dangerous  complication  during  the  height  of  the  disease  is  scarlatinal  diph- 
theria, the  commonest  dangerous  sequel  is  nephritis. 

Treatment. — The  majority  of  those  cases  of  scarlet  fever  which  take  a  typical. 
course  will  recover  completely  without  our  aid.  In  these  the  task  of  the  physi- 
cian, so  far  as  treatment  is  concerned,  consists  in  arranging  the  details  of  hygiene 
and  the  general  care  of  the  patient.  The  sick-room  should  be  cool  and  well  ven- 
tilated and  the  diet  rather  strict,  consisting  mainly  of  milk.  Broths  and  eggs 
may  also  be  allowed.  We  should  see  that  the  skin  and  the  mouth  are  kept  clean. 
To  change  the  linen  frequently,  if  done  with  proper  precaution,  is  not  only 
permissible,  but  very  desirable.  Rubbing  the  skin  with  olive-oil,  vaseline,  etc., 
has  some  merit,  and  is  especially  to  be  recommended  if  the  skin  be  harsh  and  dry 
after  the  eruption  has  faded. 

[From  the  moment  that  the  disease  is  declared  the  patient  should  be  thor- 
oughly anointed  daily  with  carbolized  vaseline,  lard,  or  the  like;  and  this  should 
be  kept  up  until  desquamation  has  ceased.  Not  only  is  the  comfort  of  the 
patient  promoted,  but  the  danger  of  the  spread  of  the  infection  is  thereby 
greatly  lessened.] 

The  scarlatinal  disease  of  the  throat  must  be  treated  with  the  greatest  atten- 
tion, the  main  duty  of  the  physician  in  this  regard  being  to  prevent,  if  possible, 
the  ingress  of  the  above-mentioned  secondary  infection.  It  is  therefore  our 
opinion  that  in  every  case  of  scarlet  fever  the  greatest  pains  should  be  taken' 
from  the  very  commencement  of  the  disease  to  maintain  complete  disinfection 
of  the  mouth  and  throat.  Larger  children  may  use  a  gargle  (two-per-cent.  solu- 
tion of  chlorate  of  potash,  one-  or  two-per-cent.  solution  of  carbolic  acid).  In- 
halations of  carbolic-acid  spray,  dilute  lime-water,  etc.,  are  also  to  be  recom- 
mended where  practicable.  If  there  is  prostration,  or  if  the  child  be  young  or 
willful,  we  must  cleanse  the  mouth  and  throat  at  short  intervals,  by  means  of  a 
spray-apparatus,  with  disinfectants,  such  as  boracic  acid  or  permanganate  of  potash 
in  solution.  Sometimes  it  is  a  good  plan  to  let  the  patient  swallow  slowly  a  half- 
teaspoonful  of  a  solution  of  potassic  chlorate  (about  1  to  40),  every  half-hour  or 
oftener,  with  the  object  of  contributing  to  the  local  disinfection  of  the  throat.  If 
scarlatinal  diphtheria  nevertheless  develops  and  the  cervical  lymph-glands  begin- 


SCARLET  FEVER  47 

to  increase  further  in  size,  there  is  reason  to  hope,  according  to  the  experience  of 
Taube  and  Heubner,  that  parenchymatous  injections  into  the  tissue  of  the  tonsils 
or  the  palatine  arches  may  yet  check  the  spread  of  the  secondary  infection.  About 
6  miniuis  (a  Pravaz  syringe  half  full)  of  a  three-per-cent.  solution  of  carbolic 
acid  may  be  injected  twice  daily  upon  each  side  by  means  of  a  long  hollow  needle 
and  a  subcutaneous  syringe.  Catti  recommends  painting  the  affected  parts  with 
a  l-to-1,000  solution  of  corrosive  sublimate.  Of  the  many  other  remedies  ad- 
vised, we  may  add  that  the  insufflation  or  dusting  of  the  tonsils  with  powdered 
sugar  is  of  advantage.  In  ordinary  scarlatinal  diphtheria  we  can  expect  no 
benefit  from  Behring's  serum-therapy,  but  if  there  is  a  complication  with  true 
diphtheria  a  serum-injection  is  most  advisable. 

If  the  nose  be  likewise  affected,  the  chief  thing  to  do  is  frequent  cleansing 
and  syringing  while  the  head  is  bent  forward.  We  should  be  on  the  watch  for 
the  possible  occurrence  of  otitis.  In  this  particular  the  physician  is  often  guilty 
of  sins  of  omission.  Much  harm  may  be  averted  by  a  prompt  syringing  of  the 
ears,  or,  if  need  be,  by  insufflation  of  air  into  the  middle  ear,  or  paracentesis  of 
the  membrana  tympani. 

Inflammation  of  the  glands  in  the  neck,  if  severe,  is  prone  to  pass  on  to  sup- 
puration, and  it  must  then  be  treated  surgically.  When  the  swelling  has  just  begun, 
or  is  still  moderate,  we  may  try  to  cure  it  by  rubbing  in  iodoform  ointment  (1  to 
15)  two  or  three  times  a  day.  Ice  is  generally  not  so  well  borne  as  warm  applica- 
tions (poultices  or  warm  bran-cushions). 

If  there  be  continuous  high  fever,  accompanied  by  rather  severe  constitutional 
symptoms,  a  moderate  employment  of  the  cold-water  treatment  in  scarlet  fever 
is  strongly  to  be  recoramended.  The  baths  seldom  need  to  be  cooler  than  81°  to 
88°  (22°-25°  R.),  and  are  to  be  employed  two  or  three  times  daily,  or  oftener 
in  severe  cases.  If  the  nervous  disturbance  be  serious,  or  if  the  respiration 
be  impaired,  the  patient  should  be  douched  with  cold  water  during  the  bath. 
Instead  of  baths,  wet  packs  may  be  used  to  advantage.  Internal  antipyretics, 
such  as  antipyrine,  may  usually  be  dispensed  with,  although  in  private  practice 
we  may  be  obliged  to  employ  them. 

We  must  watch  the  condition  of  the  heart  carefully.  When  the  pulse  is  very 
rapid  we  may  use  an  ice-bag  on  the  heart.  When  the  heart  begins  to  grow 
weak  we  may  prescribe  tincture  of  strophanthus,  wine,  etc.,  and  the  most  efficient 
remedy  for  threatening  collapse  is  injections  of  camphor.  With  mild  scarla- 
tinal arthritis  salicylate  of  sodium  and  antipyrine  act  well  as  palliatives,  but  in 
severe  cases  they,  of  course,  do  little  good. 

We  know  of  no  means  to  avert  the  nephritis.  In  justice  to  himself,  the  physi- 
cian must  always  at  the  start  point  out  the  possibility  of  its  occurrence,  and  must 
avoid  as  far  as  possible  errors  in  diet  or  exposure  to  cold  on  the  part  of  his  pa- 
tient. He  may  thus  escape  blame.  The  treatment  of  the  nephritis  and  its 
results  is  fully  described  in  the  section  on  renal  diseases.  The  most  important 
remedies  are  a  mild  diet  and  the  use  of  warm  or  hot  baths  and  packs.  The  other 
complications  of  scarlet  fever  must  be  treated  symptomatically  in  the  ordi- 
nary way. 

The  patient  must,  as  a  rule,  keep  his  bed  three  or  four  weeks,  even  if  convales- 
cence be  uninterrupted. 

[This  injunction  is  rather  extreme.  Xephritis  is  as  likely  to  follow  a  mild  as  a 
severe  case,  and  occurs  sometimes  in  spite  of  every  precaution.  The  physician 
should  use  his  discretion  as  to  the  length  of  time  the  patient  is  kept  in  bed.  care- 
fully guarding  against  exposure  to  cold  and  imprudence  in  diet.] 

After  desquamation  is  completed  the  skin  should  be  thoroughly  cleaned  by 
warm  baths.  The  disease  is  so  dangerous  that,  whenever  a  case  occurs  in  a  fam- 
ily, isolation  is  absolutely  demanded,  and,  if  possible,  all  the  other  children  should 


48  ACUTE  GENERAL  INFECTIOUS  DISEASES 

be  sent  away.  If  this  advice  be  disregarded,  we  can  reject  all  responsibility  for 
any  further  cases  and  their  results. 

[Scarlet  fever  is  a  disease  at  once  so  highly  contagious  and  so  common  that  it 
may  be  taken  as  the  type  of  its  class.  Its  hygienic  treatment  and  the  measures 
needful  to  prevent  its  spread  consequently  deserve  more  minute  detail. 

The  sick-room  should  be  at  the  top  of  the  house,  if  possible,  and  exposed  to  the 
south;  every  unnecessary  article  of  furniture  and  all  ornaments  should  be  re- 
moved beforehand,  carpets,  curtains,  and  stuffed  or  upholstered  furniture  being 
included.  A  window  should  be  kept  open  constantly,  top  and  bottom;  in  cool 
weather  a  fire  should  be  burning;  in  warm  weather  ventilation  is  furthered  by 
placing  a  gas-burner  or  large  kerosene  lamp  near  the  throat  of  the  chimney. 
Outside  the  door  of  the  sick-room  a  sheet  moistened  with  a  disinfectant  solution 
should  be  carefully  hung.  Only  those  whose  presence  is  absolutely  necessary  are 
to  be  allowed  in  the  sick-room,  and  the  physician,  when  his  visit  is  completed, 
should  pass  directly  out  of  the  house. 

A  convalescent  should  be  kept  away  from  all  who  are  liable  to  contract  or  con- 
vey the  disease  until  desquamation  has  entirely  ceased.  Several  warm  soap-baths 
should  be  given  before  the  child  emerges  into  every-day  life,  and  it  should  finally 
be  dressed  in  uncontaminated  clothing. 

For  further  directions  as  to  the  disinfection  of  the  room,  the  clothing,  and  the 
excreta,  see  pages  28-30.] 


CHAPTER   V 

MEASLES 

(Morbilli) 


iEtiology. — In  contrast  with  the  malignancy  of  scarlet  fever  is  the  compara- 
tively benign  nature  of  measles,  a  disease  of  childhood  which  is  but  little  feared 
even  by  mothers.  It  is  so  widespread,  and  the  susceptibility  to  it  is  so  universal, 
that  measles  passes  for  an  almost  unavoidable  but  comparatively  insignificant  an- 
noyance. Indeed,  few  escape  it;  and  probably  the  reason  why  adults  have  mea- 
sles so  much  less  frequently  than  children  is  simply  that  most  adults  have  already 
suffered  from  it  in  childhood.  A  second  attack  of  measles  in  the  same  individual 
may  occur,  but  it  is  certainly  extremely  rare. 

[In  highly  civilized  countries  measles  has  prevailed  so  long  that  it  would  seem 
that  a  relative  resistance  against  the  poison  has  been  acquired.  The  frightful 
ravages  of  the  disease  when  it  was  planted  in  virgin  soil,  as  among  the  Fiji  Is- 
landers not  many  years  ago,  apparently  bear  out  this  view.  The  susceptibility  to 
measles  is  greater  and  more  widespread  than  is  that  to  scarlet  fever — that  is  to 
say,  fewer  individuals  reach  adult  life  without  having  experienced  an  attack  of 
the  former  than  of  the  latter.] 

Measles  generally  comes  in  epidemics.  Sporadic  cases  are  exceptional.  In 
this  respect  measles  differs  decidedly  from  scarlet  fever.  The  rapid  spread  of  the 
disease  when  it  has  once  broken  out  is  a  result  of  its  great  contagiousness.  If  one 
child  in  a  family  is  attacked,  the  others  almost  always  take  the  disease.  The  in- 
fection may  be  transmitted  even  by  well  persons  and  by  means  of  articles  with 
which  the  sick  have  come  in  contact,  although  this  is  not  often  the  case.  We  are 
not  yet  acquainted  with  the  specific  poison  of  measles — although  its  existence 
is  to  be  taken  for  gTanted — nor  with  the  details  of  its  transmission.  Still  it 
seems  most  probable  that  the  poison  is  inhaled  through  the  mouth  and  nose, 
iand  that  this  is  the  reason  why  its  effects  are  usually  first  developed  in  the 


MEASLES  49 

respiratory  passages  (vide  infra).  The  disease  can  be  artificially  produced  by  in- 
oculation of  healthy  children  with  the  blood  or  liquid  secretions  of  those  suffer- 
ing from  it. 

Clinical  History. — The  length  of  the  stage  of  incubation  is  tolerably  uniform. 
It  is  ten  days  to  the  beginning  of  the  first  symptoms,  and  thirteen  or  fourteen 
days  to  the  breaking  out  of  the  eruption.  These  figures  have  been  established  by 
the  observations  of  Panum,  the  opportunity  having  been  afforded  upon  the  first 
introduction  of  the  disease  into  the  Faroe  Islands.  As  a  rule,  there  are  no  espe- 
cial prodromata  during  the  period  of  incubation  except  some  slight  elevations  of 
temperature.  At  the  end  of  ten  days  the  initial  stage  *  begins,  generally  sudden- 
ly, and  with  an  abrupt  rise  of  temperature  to  102°  or  104°  (39°-40°  C).  At  the 
same  time  the  characteristic  catarrhal  symptoms  appear:  nasal  catarrh  (coryza), 
to  be  recognized  by  the  abundant  nasal  secretion,  the  frequent  sneezing,  and 
sometimes  also  by  nose-bleed;  more  or  less  severe  conjunctivitis,  characterized  by 
photophobia,  reddening  of  the  eyes,  and  increased  flow  of  tears;  and,  lastly, 
symptoms  of  a  catarrh  of  the  upper  part  of  the  respiratory  tract,  usually  mod- 
erate, but  nevertheless  causing  hoarseness  and  a  slight  cough.  With  all  this 
the  general  condition  is  disturbed,  the  children  are  restless,  have  headache,  and 
eat  little.  Symptoms  of  a  mild  sore  throat  are  not  infrequent,  but  are  very  far 
from  being  so  prominent  as  in  scarlet  fever. 

These  initial  symptoms  last,  as  we  have  said,  three  or  four  days.  Then  the 
eruption  begins  (stage  of  eruption).  This  is  very  often  preceded  for  a  day  or 
two  by  a  peculiar,  usually  spotted,  reddening  of  the  hard  and  soft  palates,  termed 
"  eruption  upon  the  mucous  membrane."  [Koplik,  in  1898,  called  attention  to 
an  eruption  of  bluish-white  specks,  surrounded  by  a  reddish  area,  upon  the  mu- 
cous membrane  of  the  cheek  and  lips,  occurring  twenty-four  to  seventy-two  hours 
before  the  cutaneous  exanthem.  Others  confirm  his  observations  and  regard 
"  Koplik's  spots  "  as  a  great  aid  in  early  diagnosis. — V.]  The  true  eruption  of 
measles  begins  almost  always  in  the  face,  on  the  cheeks,  forehead,  and  around  the 
mouth  (contrasting  with  the  characteristic  pallor  of  the  chin  in  scarlet  fever), 
and  spreads  from  there  rapidly  downward  over  all  the  rest  of  the  body.  The  erup- 
tion consists  at  first  of  little  papillae,  corresponding  to  the  follicles.  These  are 
soon  surrounded  by  a  pale-red,  slightly  elevated  border,  and  in  many  cases  become 
confluent.  Perfectly  flat  elevations,  of  various  sizes  and  of  extremely  irregular, 
dentated,  roundish,  or  angular  shape,  develop.  They  are  often  so  thickly  crowded 
together  as  to  touch  one  another,  but  usually  limited  portions  of  normal  skin 
intervene  between  them.  Within  each  raised  spot  the  little  follicular  papillae 
remain  visible. 

With  the  beginning  of  the  eruption  the  fever  rises,  having  been,  as  a  rule, 
slight  during  the  last  days  of  the  initial  stage.  It  attains  about  104°  or  105° 
(40°-40.5°  C).  In  thirty-six  to  forty-eight  hours  the  eruption  reaches  its  full 
development  and  its  greatest  extent.  The  fever  and  the  catarrhal  symptoms  also 
persist  for  the  same  length  of  time.  Sometimes  we  find  a  slight  swelling  of  all  the 
lymph-glands.  Then  follows  a  decline  in  the  fever,  usually  rapid,  and  indeed 
almost  by  crisis,  while  the  eruption  after  a  short  period  of  full  development  begins 
gradually  to  fade  during  the  two  or  three  days  following.  At  the  same  time  the 
catarrhal  symptoms  diminish.  A  more  or  less  extensive  desquamation  of  the 
epidermis  begins,  scarcely  ever  in  large  pieces  as  in  scarlet  fever,  but  in  little 
scales,  like  bran.  In  eight  or  ten  days,  if  the  disease  runs  a  normal  course,  the 
patient  is  fully  convalescent. 

*  We  consider  the  term  "initial  stage"  more  correct  than  "prodromal  stage."     The  "larodromal 
symptoms"  are  the  first  slight  symptoms  which  occur  during  the  time  of  incubation  of  an  infectious 
disease,  while  the  symptoms  presented  by  measles  before  the  breaking  out  of  the  eruption  are  a  part 
of  the  already  developed  disease. 
4 


50 


ACUTE  GENERAL  INFECTIOUS  DISEASES 


After  this  brief  description  of  the  usual  course,  we  must  consider  more  closely 
some  of  the  symptoms  and  possible  complications. 

The  fever  (see  Fig.  6)  of  measles  exhibits,  as  has  been  already  implied,  a  toler- 
ably typical  course.  It  begins  with  a  rather  marked  and  rapid  rise  upon  the  com- 
mencement of  the  disease.  On  the  morning  of  the  second  day  there  is  usually  a 
marked  remission,  often  to  normal.     In  the  last  two  days  of  the  initial  stage  the 

fever  is  moderate,  very  rarely  being  so 
high  as  at  the  beginning.  With  the 
eruption  there  is  a  new,  rapid  rise,  usu- 
ally higher  than  the  initial  one,  so  that 
we  may  well  divide  the  fever  into  two 
periods^ — the  prodromal  fever  and  the 
eruptive  fever.  This  latter  is  but  brief 
and  does  not  persist,  as  in  scarlet  fever, 
during  the  entire  duration  of  the  erup- 
tion. It  falls  by  crisis  when  the  rash  has 
attained  full  development.  There  may, 
to  be  sure,  be  slight  elevations  of  tem- 
perature during  the  next  day  or  two; 
but,  if  the  fever  is  considerable  and  per- 
sistent, it  is  always  a  sign  that  complica- 
tions have  arisen,  probably  in  the  respir- 
atory apparatus. 


39.0' 


38.0= 


37.0° 


36.0° 


Initial  Fever. 


Eruptive  Fever. 
Eruption. 

Fig.  6.— Example  of  the  temperature  curve  in 
measles. 


The  eruption  usually  assumes  the 
form  described  above,  but  may  present 
manifold  varieties.  Sometimes  its  de- 
velopment is  rudimentary.  Sometimes 
it  does  not  begin  on  the  face,  but  on  some  other  part  of  the  body.  This  is  generally 
regarded  as  a  sign  that  the  case  will  be  anomalous  in  other  ways  as  well.  The 
individual  spots  may  be  smaller  than  usual,  and  may  remain  entirely  separate 
from  each  other  {morhilli  papulosi).  In  other  cases  the  eruption  is  so  confluent 
(morhilli  confluent es)  that  it  resembles  the  eruption  of  scarlatina.  The  forma- 
tion of  vesicles  {morhilli  vesiculosi)  also  occurs,  but  much  more  rarely  than  in 
scarlet  fever.  Hsemorrhagic  measles  is  also  observed,  but  usually  only  in  the 
form  of  small,  capillary  bleeding,  and  in  cases  that  otherwise  run  a  perfectly 
favorable  course.  Very  rare  cases  have  indeed  been  described,  with  a  general 
haemorrhagic  diathesis  and  severe  symptoms,  resembling  hsemorrhagic  scarlatina. 
It  is  doubtful  whether  the  "  black  measles  "  of  the  old  writers  was  actually  mea- 
sles at  all.  In  addition  to  the  proper  eruption  of  measles,  other  eruptions  some- 
times develop — such  as  vesicles,  wheals,  and  pustules. 

The  pulse  is  generally  not  so  rapid  in  measles  as  in  scarlet  fever.  Enlarge- 
ment of  the  spleen  can  be  made  out  only  to  a  slight  degree,  if  at  all.  As  a  rule, 
we  find  no  pronounced  leucocytosis  in  the  blood. 

The  complications  of  measles  are  for  the  most  part  exaggerations  or  abnormal 
varieties  and  extensions  of  those  troubles  which  are  observed  during  the  usual 
mild  course  of  the  fever.  As  in  scarlet  fever  (vide  supra),  we  often  have  to  deal 
with  the  effects  not  of  the  original,  but  of  secondary  infection.  Compared  with 
the  great  majority  of  mild  attacks  taking  the  typical  course,  cases  presenting  com- 
plications of  any  severity  are  rare,  and  much  less  frequent  than  in  scarlet  fever. 
Epidemics  are  only  now  and  then  distinguished  by  unusual  severity. 

Often  quite  serious  eye-diseases  are  developed,  particularly  blennorrhagic  con- 
junctivitis, keratitis,  and  iritis. 

Marked  inflammation  of  the  mucous  membrane  of  the  nose,  throat,  and  lar- 
ynx may  prolong  the  course  of  the  disease.     This  is  often  merely  an  exaggera- 


MEASLES  51 

tion  of  the  usual  catarrh.  Otitis  media  likewise  sometimes  occurs.  A  laryngitis 
of  marked  intensity,  with  considerable  swelling  of  the  parts  involved,  may  pro- 
duce much  discomfort,  or  even  symptoms  of  stenosis  ("false  croup")-  Actual 
croupous  and  diphtheritic  lesions  of  the  throat  and  larynx  also  occur  (diphtheria 
of  measles).  This  last  is  indeed  much  rarer  than  scarlatinal  diphtheria,  but  it 
may  have  the  same  unhappy  termination.  It  is  worth  mentioning  that  sometimes 
genuine  laryngeal  croup  is  observed  in  measles,  unaccompanied  by  lesions  of  the 
pharynx.  In  all  these  affections  secondary  infection  plays  the  chief  part,  as  it 
does  in  scarlet  fever  (vide  supra,  page  41). 

It  is,  however,  in  the  lungs  that  the  most  frequent  and  important  of  all  compli- 
cations in  measles  occur.  The  usual  mild  bronchitis  becomes  very  intense,  ex- 
tends into  the  bronchioles  (capillary  bronchitis),  and  then  results,  for  the  most 
part,  in  a  more  or  less  extensive,  lobular,  catarrhal  pneumonia  (q.  v.).  Accord- 
ing- to  Koster,  measles  pneumonia  rises  from  an  inflammatory  proliferation  of 
nuclei  about  the  small  bronchi,  and  it  usually  invades  the  neighboring-  alveoli  by 
continuity  along  the  small  branches  of  the  pulmonary  artery.  It  is  then  a  "  small 
nodular,"  but  not  strictly  a  lobular  pneumonia.  Measles  pneumonia  is  to  be 
diagnosticated  when  moist  rales  are  heard  in  abundance  over  a  large  part  of  the 
chest,  and  when  there  is  at  the  same  time  persistent  fever  and  pronounced  diffi- 
culty in  respiration,  with  cough  or  dyspnoea.  We  get  decided  dullness  on  per- 
cussion only  when  the  separate  centers  of  infiltration  are  more  than  usually  con- 
fluent. Genuine  lobar,  croupous  pneumonia  appears  much  less  often  than  the 
lobular  variety.  It  attacks  one  lobe,  or  several,  is  attended  by  high  fever,  and 
may  end  with  a  well-marked  crisis. 

The  foregoing  pulmonary  symptoms  usually  appear  at  the  height  of  the  dis- 
ease, and  persist  after  the  eruption  fades.  They  may  delay  convalescence  for 
weeks.  In  other  cases  measles  will  be  seen  at  the  start  to  run  a  normal  course,  the 
temperature  will  have  already  fallen,  and  then  come  new  fever  and  the  appear- 
ance of  decided  pulmonary  disturbance.  This  is  always  to  be  regarded  as  a  grave 
complication;  and  especially  in  feeble  children  it  may  lead  to  death,  with  the 
symptoms  of  impaired  respiration  or  of  constitutional  exhaustion.  At  present 
we  can  not  definitely  state  how  far  in  measles  pneumonia  we  have  to  do  with  the 
direct  action  of  the  measles  poison  itself  or  with  secondary  infection  (strepto- 
cocci, diplococci,  etc.). 

Marked  intestinal  symptoms  sometimes  appear,  particularly  an  excessive  diar- 
rhoea, due  to  intestinal  catarrh.  It  is  characteristic  of  measles  that  in  severe 
cases  such  a  diarrhoea  may  assume  a  pronounced  dysenteric  character,  indicated  by 
blood  and  slime  in  the  dejections,  symptoms  which  usually  depend  upon  the  devel- 
opment of  follicular  colitis  with  ulcerations. 

IvTow  and  then  still  other  complications  may  present  themselves,  of  which  a  full 
enumeration  is  impossible.  Nephritis  does  occur,  but  far  less  often  than  in  scar- 
let fever.  A  simple  albuminuria  during  the  acme  of  the  disease  is  not  infrequent, 
but  as  a  rule  it  has  no  especial  clinical  significance.  We  should  mention  gangrene 
of  the  cheek,  the  so-called  noma,  as  a  complication,  which  is  very  rare  but  appar- 
ently characteristic. 

Peculiarities  in  the  course  of  the  disease  are  much  rarer  in  measles  than  in 
scarlet  fever.  Yet  we  see,  on  the  one  hand,  unusually  mild  or  rudimentary 
cases,  in  which  either  the  rash  or  the  other  local  symptoms  are  remarkably  slight, 
and  on  the  other  hand,  abnormally  severe  cases.  These  latter  are  distinguished 
by  the  unusual  height  or  persistence  of  the  fever,  by  the  severe  constitutional  and 
nervous  sjanptoms,  and  further  by  the  early  appearance  of  complications.  Such 
cases  have  been  termed  "  typhoid  measles."  We  have  already  mentioned  the 
severe  form  of  hsemorrhagic  measles. 

We  should  notice  the  clinical  relation  which  measles  bears  to  two  other  in- 


62  ACUTE  GENERAL  INFECTIOUS  DISEASES 

fectious  diseases — to  whooping-cough  and  tuberculosis.  Measles  and  pertussis 
(q.  V.)  may  follow  each  other  in  the  same  individual  at  a  short  interval,  some- 
times one  and  sometimes  the  other  taking  the  initiative ;  epidemics  of  the  two  dis- 
eases prevail  with  comparative  frequency  at  the  same  time.  Tuberculosis  is  like- 
wise to  be  mentioned  as  an  important  sequela  of  measles.  In  these  cases  it  is 
probable  that  the  children  have  a  tubercular  focus  smoldering  somewhere  in 
the  body  (lymph-glands,  lungs)  before  the  attack  of  measles  which  kindles  it  and 
aids  its  further  extension.  The  measles  may  also,  of  course,  excite  a  predisposi- 
tion to  infection  with  tubercle  bacilli. 

The  diagnosis  of  measles,  as  of  the  other  acute  exanthematous  diseases,  is 
based  chiefly  upon  the  eruption,  but  we  must  also  regard,  of  course,  other  symp- 
toms which  may  be  present  (fever,  catarrhal  symptoms).  Personal  experience  does 
more  to  sharpen  the  perception  than  can  the  fullest  descriptions.  We  can  merely 
suspect  the  disease  during  the  initial  stage  unless  an  epidemic  prevails.  If, 
beside  the  characteristic  catarrhal  symptoms,  the  above-mentioned  eruption  on 
the  mucous  membrane  of  the  palate  exists,  the  diagnosis  becomes  tolerably  cer- 
tain. We  should  consider  that  eruptions  similar  to  that  of  measles  appear  in 
other  diseases,  more  especially  in  rotheln,  scarlet  fever,  typhus  fever,  in  the  begin- 
ning of  small-pox,  and  sometimes  in  secondary  syphilis.  Furthermore,  we  need  to 
exclude  eruptions  due  to  drugs,  especially  antipyrine,  and  also  turpentine,  balsam 
of  copaiba,  etc.  In  doubtful  cases  we  shall  be  enabled  to  form  a  decided  opinion 
by  the  other  symptoms,  and,  above  all,  by  the  further  course  of  the  disease. 

Prognosis. — We  have  already  remarked  how  favorable  in  general  the  prog- 
nosis is,  but  we  must  here  repeat  that  all  epidemics  do  not  exhibit  the  same 
benign  character,  and  that  in  every  case  the  physician  must  bear  in  mind  the  pos- 
sibility of  complications,  and  particularly  the  danger  of  severe  pulmonary  dis- 
turbances. 

Treatment. — The  patient  should  in  general  be  kept  somewhat  warmer  than  in 
scarlet  fever.  Even  in  what  seem  to  be  the  mildest  cases  the  child  should  be 
kept  in  bed  till  desquamation  is  over.  The  sick-chamber  is  to  be  somewhat  dark- 
ened, on  account  of  the  photophobia  which  usually  exists  at  first.  In  this  way, 
normal  cases  run  on  favorably  without  any  especial  therapeutic  interposition. 
The  catarrhal  symptoms,  however,  should  always  be  heeded,  since  to  disregard 
them  may  lead  to  their  becoming  aggravated.  The  chief  requisite  is  cleanliness. 
At  regular  intervals  the  eyes,  the  nasal  cavity,  and  the  mouth  should  be  washed 
out  with  lukewarm  water. 

If,  despite  all  this,  certain  disturbances  appear  in  a  worse  form  than  usual,  or 
if  complications  develop,  these  must  receive  especial  attention.  Severe  eye  trou- 
bles should  be  treated  according  to  the  usual  ophthalmological  practice.  The 
treatment  of  croupous  trouble  in  the  throat  or  larynx  will  be  fully  described  in  a 
later  chapter.  For  the  pulmonary  complications,  lukewarm  baths,  combined  if 
need  be  with  rather  cool  douches,  constitute  the  most  effectual  remedy.  Cold 
packs  are  also  very  efiicient.  These  we  shall  speak  of  later  in  more  detail  in  the 
chapter  on  catarrhal  pneumonia.  The  chief  task  of  the  physician  in  the  treat- 
ment of  measles  is,  however,  to  hinder  as  far  as  possible  the  appearance  of  compli- 
cations. We  are  not  acquainted  with  any  internal  remedies  for  the  hmg  troubles 
which  are  at  all  trustworthy.  In  rare  instances  the  excessive  accumulation  of 
mucus  in  the  bronchi  requires  the  administration  of  an  emetic.  As  expectorants 
we  may  try  ipecac,  liquor  ammonii  anisatus,  etc.  If  considerable  intestinal  dis- 
turbance arises,  we  must  employ  small  doses  of  opium,  calomel,  tannalbin,  or  sub- 
nitrate  of  bismuth.  We  hardly  need  to  say  that,  whatever  else  is  done,  the 
strength  of  the  patient  should  be  kept  up  as  much  as  possible  by  giving  wine, 
broths,  milk,  eggs,  etc.  For  at  least  two  or  three  weeks  after  the  disease  has 
ended,  the  child  must  be  very  carefully  watched. 


ROTHELN  53 

As  the  disease  is  usually  so  raild,  prophylaxis  is  not  very  strenuously  at- 
tempted. If  one  child  in  a  family  is  attacked,  it  is  probably  already  too  late  to 
isolate  the  others,  and  it  is  even  an  advantage  to  the  family  to  have  all  the  chil- 
dren finish  at  once  what  they  will  hardly  be  able  eventually  to  avoid.  We  would 
make  an  exception  in  favor  of  isolation  if  the  disease  prevailed  in  a  severe 
form. 

[It  is  not  customary  with  us  to  insist  so  strongly  upon  isolation  and  thorough 
disinfection  as  in  scarlet  fever,  but  the  tendency  of  the  present  day  is  toward  a 
wide  application  of  the  principles  of  preventive  medicine.  It  is  certainly  of  no 
advantage  to  a  child  to  contract  measles.  Delicate  children,  especially  those 
with  tubercular  predisposition,  should  be  carefully  guarded  against  it ;  and,  even 
if  it  is  decided  that  it  is  not  worth  while  to  attempt  to  confine  the  disease  to  one 
member  of  a  family,  every  precaution  should  be  taken  against  infecting  other 
families.  Under  suspicious  circumstances,  consequently,  children  are  to  be  kept 
away  from  school  and  from  contact  with  others. 

If  there  is  any  reason  to  fear  the  development  of  tuberculosis,  every  possible 
hygienic  means  should  be  employed  in  order  that  full  vigor  may  be  regained.] 


CHAPTER   VI 

ROTHELIT 

{German  Measles) 

EoTHELN  is  a  disease  similar  to  measles,  but  distinct  from  it,  although  formerly 
often  confounded  with  it,  and  perhaps  with  scarlet  fever  as  well.  The  observa- 
tions of  Steiner,  Thomas,  and  others  leave  now  no  room  to  doubt  that  these  dis- 
eases are  distinct,  for  epidemics  occur  in  which  all  cases  present  the  characteristic 
peculiarities  ascribed  to  rotheln.  But  the  best  proof  is  that  children  who  have 
had  rotheln  are  not  infrequently  attacked  by  genuine  measles  later.  It  may  in- 
deed be  very  difficult  in  an  individual  case  to  decide  which  disease  is  present ;  but 
that  rotheln  does  exist,  as  an  independent  form  of  disease,  can  be  denied  by  those 
alone  who  have  never  seen  it. 

After  an  incubation  of  about  two  or  three  weeks  the  disease  begins  with 
the  appearance  of  the  eruption,  which  is  usually  noticed  first  in  the  face. 
Initial  symptoms  (cough,  sneezing,  etc.),  preceding  the  eruption,  either  are 
wholly  absent  or  at  most  last  for  half  a  day.  The  eruption  is  decidedly  like 
that  of  measles,  but  its  individual  spots  are  smaller.  They  are  seldom  larger 
than  small  peas  and  circular,  being  only  exceptionally  as  dentated  and  irregular 
in  outline  as  are  the  maculae  of  measles.  They  appear  on  the  whole  face,  the 
head,  the  trunk,  and  the  extremities,  are  pale  red  (sometimes  deep  red),  only 
slightly  elevated,  and  are  not  apt  to  become  confluent.  In  rare  instances, 
small  vesicles  develop  upon  the  macules.  The  soft  palate  sometimes  exhibits, 
as  in  measles,  a  faint  macular  eruption  at  the  beginning  of  the  disease. 
After  two  to  four  days  the  eruption  fades.  There  is  usually  no  decided  desquama- 
tion. 

Other  symptoms  of  disease  than  this  eruption  are  slight.  Fever  in  many 
cases  appears  to  be  entirely  absent.  As  a  rule,  there  is  for  a  day  or  two  a  little 
elevation  of  temperature,  reaching  102°  (39°  C.)  at  most.  Tokens  of  a  moderate 
catarrh  of  the  conjunctiva,  the  nasal  mucous  membrane,  the  throat,  and  the 
larynx  are  also  observed — viz.,  photophobia,  nasal  discharge,  and  cough.  Often, 
the  cervical  lymph-glands  are  more  or  less  swollen.     The  constitutional  disturb- 


54:  ACUTE    GENEEAL   INFECTIOUS    DISEASES 

ance  is  generally  so  slight  that  the  child  can  hardly  be  kept  in  bed.     Important 
complications  hardly  ever  occur. 

The  prognosis  of  rotheln  is  therefore  perfectly  favorable,  and  the  employment 
of  any  special  treatment  is  needless. 


CHAPTER   VII 

SMALL-POX 

( Variola.     Varioloid) 

.ffitiology. — Small-pox  has  been  known  for  centuries,  although  formerly  often 
confounded  with  other  diseases.*  It  is  one  of  the  most  dreaded  acute  infectious 
diseases,  and  in  earlier  times  it  has  destroyed  thousands  in  its  pestilential  prog- 
ress. It  was  the  discovery  of  the  possibility  of  prophylactic  inoculation,  and  the 
ever-increasing  spread  of  this  precautionary  measure,  which  first  robbed  the  dis- 
ease of  some  portion  of  its  terrors. 

Numerous  statements  have  been  made  about  the  occurrence  of  micro-organ- 
isms in  the  variolous  eruptions  on  the  skin  and  mucous  membranes,  but  we  are 
compelled  to  say  that  we  are  not  yet  acquainted  with  the  specific,  organized  poison 
of  small-pox,  however  strongly  justified  we  may  be  in  assuming  its  existence. 
Bacteria  can  in  fact  easily  be  demonstrated  in  the  eruption  of  variola,  but  most 
of  them  come  from  the  surrounding  atmosphere,  and  have  no  relation  to  the  spe- 
cific variolous  processes.  The  foci  of  bacteria  found  in  the  internal  organs  (liver, 
spleen,  kidneys)  are  also  due,  as  their  discoverer,  Weigert,  himself  supposed,  to  the 
secondary  ingress  of  other  varieties  of  micro-organisms,  and  are  not  directly  asso- 
ciated with  the  variolous  process,  the  diseased  condition  of  the  skin  furnishing  a 
ready  entrance  for  infectious  matter. 

Predisposition  to  variola,  except  as  diminished  by  vaccination  (vide  infra),  is 
universal.  The  disease  may  appear  at  any  age,  even  in  utero.  Women  are 
believed  to  be  especially  liable  to  it  during  pregnancy  and  child-bed.  It  is  said 
that  persons  ill  with  another  acute  infectious  disease,  such  as  scarlet  fever, 
measles,  or  typhoid  fever,  are,  for  the  time  being,  tolerably  secure  from  infection 
with  small-pox;  but  this  rule  certainly  has  exceptions.  The  same  individual 
rarely  takes  the  disease  a  second  time. 

A  case  of  variola  is  always  the  result  of  transmission  of  the  poison  to  a  healthy 
person  from  one  who  is  already  ill  with  it.  The  specific  poison  is  most  abundant 
in  the  diseased  portions  of  the  body  and  in  the  pus  of  the  suppurating  pocks, 
as  well  as  the  crusts  and  scales  which  are  left  when  these  have  dried  up;  but 
the  disease  is  also  contagious  in  its  earlier  stages,  before  the  pustules  develop, 
and  even,  according  to  a  few  observations,  during  the  stage  of  incubation.  Cer- 
tainly the  variolous  poison  is  very  volatile — that  is,  it  is  prone  to  disseminate 
itself  through  the  air  in  the  neighborhood  of  the  patient.  In  order  to  catch  the 
disease  it  is  not  necessary  to  touch  the  patient,  but  merely  to  remain  in  his  vicin- 
ity. In  many  cases  we  can  not,  however,  determine  with  exactness  the  mode  of 
transmission,  since  the  contagion  may  either  be  direct  or  by  means  of  objects  and* 
utensils  with  which  a  patient  has  come  in  contact — for  example,  the  soiled  linen. 
The  dead  body  also  is  capable  of  transmitting  the  disease.  In  general,  numerous 
instances  point  to  a  considerable  "  tenacity  "  in  the  poison.     The  precise  manner 


*  The  very  name  small-pox  (petite  verole)  is  significant  of  its  confusion  with  syphilis,  which  was 
termed  the  "  great  pox." 


SMALL-POX  55 

of  infection  is  not  yet  known.  It  is  most  probable  that  the  poison  is  drawn  into 
the  lungs  with  the  inspired  air. 

It  has  been  demonstrated  that  the  disease  can  be  transmitted  to  healthy  per- 
sons by  direct  inoculation  of  the  contents  of  the  variolous  pustules.  It  is  stated 
that  monkeys  and  other  animals  may  be  successfuly  inoculated  in  the  same  way. 
Whether  inoculations  with  the  blood  of  the  sick  will  reproduce  the  disease  is  not 
yet  settled.  The  secretions  (saliva,  sweat,  urine,  and  milk)  do  not  apparently 
contain  the  infectious  matter. 

Course  of  the  Disease.  Variola  and  Varioloid.— The  stage  of  incubation  lasts 
as  a  rule  thirteen  to  fourteen  days,  sometimes  a  somewhat  shorter  time.  During 
this  period  prodromal  symptoms  are  absent  or  insignificant. 

The  disease  itself  begins  suddenly  with  what  are  usually  very  characteristic 
initial  symptoms — rigor,  fever,  headache,  and  intense  pain  in  the  loins.  It  is  only 
in  comparatively  few  cases  that  one  or  another  of  these  symptoms  is  slight  or 
wanting.  The  constitutional  symptoms  may  be  very  severe — a  dry  tongue,  stupor, 
wakefulness,  delirium.  The  fever  continues  intense  for  some  days.  The  pulse  is 
much  quickened.  There  is  almost  total  anorexia,  and  often  there  is  vomiting. 
There  is  constipation,  or,  more  rarely,  diarrhoea.  Frequently  there  is  a  slight  sore 
throat,  and  sometimes  a  slight  bronchitis.  The  spleen  is  enlarged  in  most  of  the 
severe  cases,  and  the  urine  often  has  a  trace  of  albumen.  In  women,  menstrua- 
tion occurs  in  a  remarkably  large  number  of  cases.  The  proper  variolous  eruption 
does  not  at  once  appear,  but  from  the  second  day  other  characteristic  efflores- 
cences are  not  rare.  These  are  termed  the  initial  rash  of  small-pox.  We  may 
&id  either  a  diffuse  or  macular  erythema,  extending  in  varying  degree  over  the 
trunk  and  extremities  (especially  on  the  extensor  surface),  or  a  h^emorrhagic 
eruption  with  small  spots,  appearing  by  preference  upon  the  hypogastrium  and 
the  inner  surface  of  the  thighs  (in  the  so-called  femoral  triangle  of  Simon)  or  on 
the  lateral  surface  of  the  trunk  and  on  the  upper  arm.  The  erythema  soon  dis- 
appears, but  the  hsemorrhagic  spots  can  be  seen  longer.  Both  forms  of  the  initial 
eruption  may  be  combined. 

The  initial  stage,  just  pictured,  lasts  usually  three  days.  Severe  symptoms 
occurring  at  this  time  do  not  exclude  the  possibility  that  the  further  course  of  the 
disease  may  prove  favorable,  while  mild  symptoms  are  of  good  omen. 

At  the  end  of  the  third  or  on  the  fourth  day  the  temperature  makes  a  decided 
fall,  and  the  regular  variolous  eruption  begins  to  be  developed  upon  the  skin — the 
stadium  eruptionis.  During  this  period  an  evident  difference  among  the  separate 
cases  becomes  manifest.  This  distinction  can  not  indeed  be  always  drawn  with  a 
narrow  line,  but  it  is  noticeable  enough  to  justify  the  establishment  of  two  types 
of  variolous  disease.  We  refer  to  the  division  into  a  severe  form  (variola  vera), 
and  another,  mild  form  (varioloid).  The  variola  proper  has  a  well-developed 
eruption  with  many  pustules,  and,  as  a  result  of  this,  a  second  stage  of  fever 
(stadium  suppurationis).  Varioloid  has  a  much  more  scanty  eruption,  and  little 
or  no  suppurative  fever.     We  must  now  discuss  these  two  forms  separately. 

Variola  Vera 

The  eruption  almost  always  begins  in  the  face  and  upon  the  hairy  scalp,  ap- 
pearing somewhat  later  on  the  trunk  and  arms,  and  last  of"  all  upon  the  legs. 
It  begins  in  the  form  of  little  red  dots  and  spots,  which  develop  in  about  two  days 
to  small  papules  (stadium  floritionis) .  If  the  hand  be  passed  over  thickly  set  and 
well-developed  papules  of  variola,  a  peculiar  soft,  satin-like  feeling  is  perceived. 
On  the  points  of  these  papilla  a  little  vesicle  forms.  This  keeps  growing  larger 
and  larger,  its  contents  becoming  turbid  and  purulent,  till  at  last,  on  the  sixth  day 
of  the  eruption  and  the  ninth  of  the  disease,  the  development  of  the  genuine  pus- 
-tule  of  variola  is  complete  (stadium  suppurationis) .    The  pustule  usually  presents 


56  ACUTE   GENERAL   INFECTIOUS   DISEASES 

upon  its  summit  a  little  dimple  (umbilication),  and  is  surrounded  by  a  red 
border  or  "  halo."  Where  the  pocks  are  especially  close  together,  as  in  the  face, 
the  skin  between  them  is  diffusely  swollen,  and  the  consequent  burning  and  pain 
are  excessive.  The  countenance  becomes  much  disfigured.  Often  the  eyes  can 
not  be  opened  because  of  the  oedema.  The  hands  also  are  apt  to  be  intensely 
affected,  especially  the  back  of  the  hands,  and  also  all  parts  which  have  previously 
been  injured  in  any  way  (pressure  or  friction  of  clothing,  etc.).  On  the  trunk 
the  pustules  are  very  rarely  as  close  together  as  on  the  face  and  hands.  It  is 
worthy  of  note  that  often  new  eruptions  of  pustules  keep  appearing  for  two  or 
three  days. 

At  the  same  time  with  the  eruption  upon  the  skin,  or  even  somewhat  earlier,  a 
perfectly  analogous  efflorescence  develops  upon  the  mucous  membranes.  The 
chief  places  for  its  appearance  are  the  mouth  and  throat,  the  tongue,  the  soft  pal- 
ate, the  nasal  cavity,  also  the  larynx,  the  trachea,  and  the  upper  part  of  the  oesopha- 
gus. In  the  vagina  and  rectum  it  is  rare  and  scanty.  In  this  mucous  efflores- 
cence, however,  there  are  no  proper  pustules,  but  small,  superficial  ulcers.  These 
result  from  the  maceration  of  the  uppermost  layers  of  the  mucous  membrane. 
They  sometimes  become  confluent.  The  annoyance  produced  by  this  eruption  in 
the  mouth  and  throat  is,  of  course,  very  great.  The  pocks  in  the  larynx  manifest 
themselves  by  hoarseness,  and  occasionally  by  symptoms  of  stenosis. 

As  we  have  said,  the  beginning  of  the  eruption  is  the  signal  for  a  noticeable 
fall  in  the  temperature;  but  in  true  variola  the  fall  does  not  reach  the  normal, 
or  only  temporarily.  The  other  symptoms  likewise  remit,  especially  the  head- 
ache and  lumbar  pain.  When,  however,  the  suppuration  begins,  the  fever  rises 
once  more,  and  there  are  fresh  symptoms  of  constitutional  disturbance.  This  is 
the  time  for  the  dreaded  attacks  of  delirium,  during  which  the  patient  must  be 
vigilantly  watched,  lest  some  untoward  event  happen.  Now,  too,  complications 
may  arise  (vide  infra). 

On  the  twelfth  or  thirteenth  day  of  the  disease  the  pustules  begin  to  dry  up 
(stadium  exsiccationis) .  The  purulent  contents  of  the  pustules,  part  of  which 
have  burst,  form  yellow  crusts,  the  swelling  of  the  skin  subsides,  and,  a  few 
days  later,  the  crusts  and  scabs  begin  to  fall  off.  With  the  beginning  of  desic- 
cation, the  fever  declines;  the  local  as  well  as  the  constitutional  symptoms 
become  daily  slighter,  and  convalescence  follows.  The  healing  of  the  pustules  is 
frequently  accompanied  by  an  extremely  troublesome  itching.  After  the  scabs 
have  been  cast  off,  the  skin  presents  pigmented  spots,  which  persist  for  months. 
Wherever  the  cutis  vera  has  itself  been  destroyed  by  the  suppuration,  a  scar  is 
inevitable.  Thus  arise  the  familiar  scars  (pitting)  of  small-pox,  which  continue 
visible  through  life.  Yery  often,  after  the  end  of  the  disease,  there  is  almost 
complete  alopecia.    The  hair  often  grows  again,  but  not  always. 

Varioloid 

The  distinction  between  varioloid  and  variola  vera  is  not  in  kind,  but  in  de- 
gree. Varioloid  is  only  a  milder  form  of  variola.  There  is,  as  we  have  already 
said,  no  sharp  boundary-line  between  the  two.  Varioloid  is  most  often  observed 
in  those  whose  susceptibility  to  the  variolous  poison  has  been  diminished  by 
vaccination  (vide  infra). 

As  above  mentioned,  the  behavior  of  the  disease  during  its  initial  stage  will 
not  permit  us  to  decide  positively  whether  variola  or  varioloid  will  be  developed. 
It  is  true  that  if  the  symptoms  be  especially  mild,  we  may  guess  that  it  will  be 
varioloid ;  and,  likewise,  the  appearance  of  the  initial  erythema  already  spoken  of 
is  regarded  as  a  favorable  omen. 

Shortly  after  the  pocks  begin  to  appear,  the  decision  can  almost  always  be 
made  with  certainty.     In  varioloid  the  eruption  is  rather  scanty.     It  is  often 


SMALL-POX 


57 


irregular,  and  does  not  by  any  means  always  begin,  like  that  of  variola,  in  the 
face,  but  often  on  the  trunk.  The  individual  pocks  are  in  no  way  different  from 
those  of  variola ;  but  it  often  happens  that  they  do  not  pass  through  all  the  regu- 
lar stages  to  full  suppuration,  but  ^mdergo  resolution  before  this  occurs.  Such 
cases,  in  which  there  is  nothing  beyond  papillae  or  vesicles,  are  sometimes  spoken 
of  as  variolois  verrucosa  seu  miliaris.  The  scantiness  of  the  eruption  and  the 
limited  amount  of  suppuration  have  for  their  corollary  an  absence,  or  at  least  a 
very  slight  development,  of  the  suppurative  fever. 

When  the  eruption  appears  the  temperature  usually  falls  by  crisis  to  the 
normal  level  and  remains  there.  The  desiccation  may  begin  as  early  as  the 
eighth  or  tenth  day  of  the  disease,  so  that  the  whole  duration  of  varioloid  is  con- 
siderably shorter  than  that  of  variola.  Grave  complications  are  very  exceptional. 
The  pocks  may  develop  upon  the  mucous  membranes,  but  here,  too,  they  are 
scanty  and  not  very  vigorous. 

Course  of  the  Fever,  Symptoms  presented  by  Separate  Organs,  and 

Complications 

1.  Fever  {vide  Fig.  7). — In  the  initial  stage,  as  we  have  said,  the  temperature 
rises  rapidly  as  a  rule,  with  a  pronounced  rigor ;  and  during  the  first  days  it  very 
often  reaches  104°  to  106°  (40°-41°  C).  It  sinks  on  the  third  to  the  sixth  day, 
when  the  first  papillae  develop,  and  then,  in  the  case  of  varioloid,  falls  rapidly  to 
normal,  and  remains  there.  In  variola  the  decline  is  slower  and  less  complete; 
and  with  the  beginning  of  suppuration  the  temperature  begins  to  rise  again.  The 
violence  of  this  suppur-ative  fever  is  usually  in  direct  proportion  to  the  severity  of 
the  eruption.     It  has  manifold  fluctuations,  but  seldom  lasts,  in  severe  cases,  less 


3         3         4         5  fi 


«  9         10        11       12        13        14        15        16        \7        18 


40.0° 


39.0° 


38.0° 


37.0° 


— iBimymi 

iBHIIinillllSISSBHB 


Initial  Fever  Suppurative  Fever. 

Eruption. 

Fig.  7. — Example  of  the  temperature  curve  in  true  small-pox. 

than  a  week.  Temperatures  of  104°  (40°  C.)  and  higher  are  common.  The  fever 
declines  by  lysis.  In  case  of  approaching  death,  the  temperature  may  be  ex- 
tremely high,  even  reaching  108°  or  109°  (42°-43°  C). 

2.  Shin. — We  have  already  described  the  macroscopic  appearance  of  the  erup- 
tion. It  remains  to  mention  briefly  the  histological  phenomena.  The  first  de- 
monstrable changes  are  in  the  cells  of  the  deeper  layers  of  the  rete  Malpighii.  As 
a  result  of  the  variolous  infection,  the  cells  perish,  are  swollen  by  the  lymph 
which  escapes  from  the  papillary  blood-vessels,  and  transformed  into  flaky, 
homogeneous  masses  without  nuclei  ("coagulation  necrosis"  of  Weigert).  The 
lymph  becomes  more  and  more  abundant,  and  crowds  the  cells  farther  and  far- 
ther apart.     These  are  thereby  finally  changed   into   threads   and   membranes. 


58  ACUTE   GENERAL   INFECTIOUS   DISEASES 

forming  a  distinct  net-work  in  the  vesicle.  This  explains  why,  if  such  a  vesicle 
be  pricked,  its  entire  contents  are  never  discharged  at  once.  Great  numbers  of 
white  corpuscles  escape,  along  with  the  lymph,  from  the  blood-vessels,  and  finally 
render  the  contents  of  the  original  vesicle  purulent.  Proliferative  processes  occur 
in  the  surrounding  epithelial  cells,  which  are  still  intact,  and  thus  the  margin  of 
the  vesicle  becomes  elevated,  while  the  dead  portion  in  the  center  sinks  in.  Thus 
the  pock  becomes  umbilicated.  If  a  portion  of  the  papilla  itself  suppurates,  a  scar 
must  be  left  on  healing.  If  the  process  remains  limited  to  the  epithelium,  com- 
plete regeneration  takes  place,  and  the  skin  reassumes  its  normal  appearance. 

Certain  secondary  complications,  which  sometimes  attack  the  skin,  remain  to 
be  mentioned :  abscess,  phlegmon,  erysipelas,  gangrene,  and  bed-sores.  None  of 
these  are  due  directly  to  the  specific  variolous  intoxication. 

3.  Respiratory  Organs. — The  disturbances  here  are  in  part  symptoms  of  the 
specific  process  of  the  disease,  and  in  part  secondary.  The  frequent  occurrence  of 
secondary  symptoms  in  small-pox  is  easy  to  understand  (compare  the  chapter  on 
lobular  pneumonia).  Of  the  primary  symptoms,  we  should  mention  genuine 
pocks  in  the  larynx,  the  trachea,  and  the  larger  bronchi.  As  sequels  to  these, 
naore  or  less  severe  secondary  disorders  are  very  frequent :  laryngeal  ulcerations, 
which  may  even  lead  to  laryngeal  perichondritis  and  oedema  of  the  glottis ;  diffuse 
bronchitis;  lobular  pneumonia,  often  of  great  extent,  due  to  the  inhalation  of 
solid  matter  into  the  lungs,  and  frequently  accompanied  by  pleurisy.  It  should 
be  especially  noticed  that  lobar,  croupous  pneumonia  is  not  rare.  Whether  this 
be  likewise  secondary,  or  a  direct  result  of  the  variolous  poison,  is  not  yet  known. 

4.  Digestive  System. — The  genuine  pocks  often  develop,  as  stated,  in  the 
mouth  and  pharynx,  and  likewise  in  the  upper  part  of  the  oesophagus.  They  are 
not  observed  in  the  mucous  membrane  of  the  stomach  or  intestines.  The  active 
diarrhoea  sometimes  seen  depends  upon  catarrh  of  the  intestine.  Dysentery  is 
rare.  The  eruption  in  the  mouth  and  throat  may  result  in  severe  secondary  trou- 
bles, purulent  otitis,  parotitis,  pharyngeal  diphtheria,  etc.  The  spleen  is  almost 
always  considerably  enlarged,  and  often  the  liver  also,  but  in  a  less  degree. 

5.  Circulatory  System. — Pathological  changes  in  the  heart  are  rare,  if  we 
except  the  slight  parenchymatous  degeneration  of  its  muscular  fibers,  common  to 
almost  all  severe  infectious  diseases.  Sometimes  there  is  a  slight  endocarditis 
(^q.v.),  which  is  probably  secondary.     Pericarditis  is  rather  more  frequent. 

6.  Organs  of  Special  Sense. — Genuine  variolous  pustules  occur  upon  the  eye- 
lids and  the  conjunctiva.  Later  in  the  disease  there  may  be  keratitis,  iritis,  or 
choroiditis. 

We  have  already  mentioned  the  relative  frequency  of  aural  disturbances,  par- 
ticularly purulent  otitis  media. 

7.  Articular  swelling  may  appear  in  the  suppurative  stage.  The  shoulders  and 
knees  are  most   apt  to  be  attacked.     Periostitis  also   occurs. 

8.  Nervous  System. — We  find  no  pathological  changes  corresponding  to  the 
severe  nervous  derangements  manifested  during  the  disease.  After  the  small-pox 
is  over,  spinal  diseases  sometimes  occur,  with  either  paralysis  or  ataxia.  Westphal 
has  shown  that  they  are  caused,  in  some  cases,  by  numerous  disseminated  centers 
of  inflammation  in  the  spinal  cord.  .  Encephalitic  processes  have  also  been  ob- 
served in  small-pox,  and  in  some  cases  neuritic  paralysis. 

9.  Albuminuria  is  quite  common  in  severe  attacks,  but  genuine  nephritis  is  a 
very  rare  complication.  In  pregnant  women  attacked  by  small-pox  abortion  or 
premature  labor  is  very  apt  to  occur.  If  a  living  child  be  born,  it  usually  dies 
soon  after  birth. 

Anomalies  in  the  course  of  the  disease  are  manifold.  We  will  not  speak  of 
the  two  typical  forms  already  considered.  There  are  abnormally  mild  cases,  with 
scarcely  any  initial  symptoms,  or  with  an  obscure  eruption,  or  with  no  eruption  at 


SMALL-POX  59 

all  (fehris  variolosa  sine  exanthemate).  In  such  cases  a  correct  diagnosis  is  pos- 
sible only  at  the  time  an  epidemic  prevails,  and  by  the  aid  of  the  attendant  setio- 
logical  circumstances.  There  are  also  abortive  cases  in  which  the  first  symptoms 
are  severe,  but  which  recover  with  remarkable  rapidity. 

The  abnormally  severe  cases  are  more  important.  First,  there  is  the  confluent 
variety.  This  is  merely  the  typical  process  in  its  completest  development.  The 
initial  symptoms  are  themselves  generally  very  severe,  and  are  followed,  without 
any  considerable  remission  of  the  fever,  by  the  eruption  of  hundreds  of  pustules. 
The  skin  of  the  face  and  hands  is  one  continuous  area  of  suppuration.  The  local 
discomfort  is  extreme,  as  is  also  the  intensity  of  the  fever  and  of  the  constitu- 
tional symptoms.  The  nervous  system  suffers  most.  There  is  at  the  same  time 
an  unusually  abundant  eruption  upon  the  mucous  membranes.  The  occurrence 
of  the  above-mentioned  complications  affecting  the  various  organs  of  the  body  is 
frequent.  Death  is  a  common  result;  or,  if  recovery  takes  place,  it  may  be 
delayed  by  tedious  sequelae. 

Hsemorrhagic  small-iDox  is  the  worst  anomalous  form.  The  name  is  applied 
to  several  different  varieties.  In  the  first  place,  any  variolous  eruption  may  be- 
come more  or  less  hsemorrhagic,  and  yet  the  general  course  of  the  disease  not  be 
essentially  altered.  Such  cases  are  more  common  among  elderly  people,  cachec- 
tic persons,  and  drunkards.  Secondly,  there  is  a  very  severe  form  of  small-pox, 
which  is  generally  quickly  fatal.  The  initial  stage  is  marked  by  the  unusual 
severity  of  the  symptoms.  The  abundant  eruption  soon  becomes  hsemorrhagic, 
and  there  are  also  ecchymoses  in  the  mucous  membranes  and  the  internal  organs. 
This  has  been  called  black  small-pox,  and  by  Curschmann  variola  hcemorrhagica 
pustulosa. 

There  is  another  form  of  hsemorrhagic  variola,  different  from  these  but  linked 
to  them  by  transitional  varieties.  In  it  the  acute  hsemorrhagic  diathesis  develops 
during  the  initial  stage.  Death  almost  always  occurs  before  the  regular  variolous 
eruption.  This  most  frightful  form  is  usually  termed  purpura  variolosa.  That 
it  is  small-pox  is  proved  by  its  setiological  relations  alone.  Otherwise  it  would  be 
impossible  to  distinguish  it  from  certain  other  acute  septic  disorders.  It  is  prone 
to  attack  the  youthful  and  vigorous.  Chills,  headache,  and  pain  in  the  loins  are 
the  first  symptoms,  just  as  in  ordinary  cases.  Cutaneous  ecchymoses  appear  as 
early  as  the  second  or  third  day.  They  increase  in  area  so  rapidly  that  one  can 
almost  see  them  grow.  They  are  most  extensive  in  the  hypogastric  region.  There 
are  also  ecchymoses  in  the  eyelids,  the  conjunctiva,  the  mouth  and  pharynx,  and, 
as  the  autopsy  discloses,  many  in  the  internal  viscera.  The  constitutional  symp- 
toms are  most  severe,  and  the  patient  seldom  survives  the  fifth  or  sixth  day  of  the 
disease. 

Diagnosis. — The  certainty  with  which  we  can  make  the  diagnosis  of  small-pox 
in  any  well-developed  case  is  equaled  by  the  difficulty  of  deciding  about  it  during 
the  beginning  of  the  disease,  or  even  during  the  beginning  of  the  eruption.  At 
this  period  diagnosis  may  be  impossible.  When  the  variolous  eruption  is  in  pro- 
cess of  development,  it  may  be  qonfounded  with  typhus  fever,  with  that  form  of 
measles  in  which  the  papillae  are  prominent,  with  syphilitic  eruptions,  and  with 
certain  forms  of  erythema  exsudativum,  just  breaking  out.  We  can  not  here 
fully  discuss  all  the  factors  which  should  be  considered  in  making  this  diagnosis. 
It  is  important  not  to  regard  the  cutaneous  appearances  alone,  but  to  note  all  the 
other  symptoms  besides.  But  it  is  often  necessary  to  watch  a  doubtful  case  for 
some  time  before  a  diagnosis  can  be  established. 

Prog-nosis. — The  facts  which  are  of  greatest  weight  in  prognosis  have  already 
been  emphasized.  We  may  repeat  tliat  during  the  initial  stage  the  prognosis  of 
any  individual  case  can  seldom  be  determined.  If  the  first  symptoms  are  mild, 
or  if  the  initial  erythema  appears,  the  case  is  regarded  hopefully.    The  abundance 


60  ACtTTE   GENERAL   INFECTIOUS   DISEASES 

of  the  eruption  has  an  influence  upon  the  severity  of  the  disease.  Circumstances 
peculiar  to  the  individual  are  also  important — e.  g.,  age,  constitution,  or  alcoholic 
habits.  We  have  already  called  attention  to  the  danger  of  confluent  small-pox, 
and  to  the  almost  absolutely  fatal  prognosis  in  the  genuine  hsemorrhagic  variety. 
The  mortality  varies  greatly  in  different  epidemics;  on  the  average  it  may  be 
taken  at  about  fifteen  to  thirty  per  cent.  Beyond  doubt,  the  introduction  of 
vaccination  has  decidedly  lessened  the  fatality  of  the  disease  by  diminishing- 
the  frequency  of  the  severe  forms. 

Treatment. — 1.  Prophylaxis — Vaccination. — As  in  all  contagious  diseases, 
isolation  is  of  little  avail  unless  complete.  This  fact  has  led  to  the  erection  in 
late  years  of  small-pox  hospitals.  All  utensils  used  by  the  patient,  and  his  cloth- 
ing, bedding,  and  the  like,  should  be  most  carefully  disinfected.  The  best  method 
is  to  employ  a  high  degree  of  heat— viz.,  240°  to  250°  (115°-120°  C). 

These  precautionary  measures  are  employed  in  many  other  diseases  as  well, 
but  for  small-pox  we  are  acquainted  with  a  special  method  of  prophylaxis.  It  is. 
founded  upon  a  fact  which  is  the  most  remarkable  within  the  domain  of  the  infec- 
tious diseases.  We  refer  to  prophylactic  vaccination.  It  must  long  ago  have 
been  remarked  that  a  person  who  has  had  the  disease  once,  enjoys,  to  a  large 
degree,  immunity  from  any  fresh  infection.  This  suggested  the  idea  of  exposing- 
children  purposely  to  contagion,  so  as  to  insure  them  from  small-pox  for  the  rest 
of  their  lives.  The  actual  inoculation  of  small-pox  is  said  to  have  been  long 
practiced  in  India  and  China.  In  the  year  1717  it  was  employed  by  Lady  Mary 
Wortley  Montagu,  of  England,  upon  her  own  son,  and  with  success.  Unfortu- 
nately, however,  the  inoculated  small-pox  proves  fatal  in  many  instances;  and, 
being  itself  contagious,  it  serves  to  spread  the  disease  still  further.  Then  ap- 
peared an  article  written  by  the  English  surgeon,  Edward  Jenner,  in  1798.  This 
informed  the  medical  profession  of  a  fact  already  known  to  the  rural  population 
of  his  native  place,  but  which  Jenner  first  established  scientifically,  and  recognized 
in  all  its  importance.  There  sometimes  occurs  a  disease  similar  to  small-pox  upon 
the  teats  and  udder  of  the  cow,  called  variola  vaccina.  It  is  apparently  a  local 
trouble,  and  it  can  easily  be  inoculated  upon  the  skin  of  human  beings.  Vaccine 
pustules  will  be  developed  upon  the  spot  inoculated.  These  almost  invariably 
heal  without  any  great  constitutional  disturbance ;  but  the  person  vaccinated  pos- 
sesses the  same  immunity  from  small-pox  as  if  he  had  had  small-pox  itself.  This 
statement  of  Jenner's  was  soon  confirmed  upon  every  side.  The  result  is  the  con- 
tinually spreading  custom  of  prophylactic  vaccination.  In  some  countries  it  is 
enforced  by  law,  and  it  can  be  opposed  only  by  ignorance  or  by  lamentable 
prejudice. 

To  explain  exactly  how  vaccination  can  protect  against  small-pox  in  this  way 
is  still  beyond  our  powers ;  but  vaccination  has  at  present  lost  much  of  its  former 
enigmatical  character,  since  we  know  that  a  similar  immunity  can  be  produced 
in  almost  all  infections  by  inoculation  with  attenuated  or  altered  virus  (see  the 
chapters  on  malignant  pustule,  diphtheria,  tetanus,  pneumonia,  etc.).  This  anal- 
ogy has  become  the  more  certain  since  there  is  no  longer  any  doubt,  according  to 
recent  observations  (Fischer  and  others),  that  vaccinia  is,  in  fact,  only  a  form  of 
small-pox  rendered  milder  and  modified  by  transmission  to  animals.  If  we  in- 
oculate a  calf  with  the  contents  of  a  fresh  small-pox  vesicle  from  man,  typical  vac- 
cinia is  produced.  With  the  contents  of  this  vaccine  vesicle  children  can  be 
inoculated  without  any  danger,  and  they  are  no  longer  susceptible  either  to  vac- 
cinia or  small-pox. 

We  can  mention  only  the  most  important  of  the  details  relating  to  vaccination 
and  the  method  of  its  performance.  Only  exceptionally  do  we  vaccinate  with 
the  contents  of  a  human  vaccine  vesicle  ("humanized  lymph"),  but  we  almost 
invariably  use  animal  lymph  from  vaccine  vesicles  of  calves.     This  is  now  ob- 


SMALL-POX  61 

-tained  in  large  quantities  and  put  on  the  market.  The  process  of  vaccination  is 
to  make  three  shallow  incisions,  3  or  4  centimetres  apart,  in  the  skin  of  the  upper 
arm,  and  to  introduce  the  vaccine-lymph  into  them.  The  surrounding  tissue 
hecomes  swollen  in  three  or  four  days.  In  seven  or  eight  days  the  vaccine  vesicles 
are  well  developed,  if  the  disease  takes  its  normal  course.  Next  they  become 
purulent,  and  then  dry  up,  and  finally,  on  healing,  leave  the  familiar  scar  behind. 
The  whole  process  occupies  about  three  weeks.  If  the  vaccination  fails,  or  is  but 
partially  successful,  it  must  be  repeated  after  a  few  months.  The  protective 
power  of  vaccination  does  not  last  indefinitely,  and  therefore  re-vaccination  is 
necessary  every  five  or  six  years.  The  first  vaccination  of  children  usually  takes 
place  when  they  are  three  or  four  months  old.  If  they  are  feeble  we  wait  longer, 
unless  small-pox  is  prevalent. 

It  must  be  confessed  that  vaccination  is  not  without  its  dangers.  The  little 
cutaneous  wound  made  by  it  may  lead,  like  any  other,  to  sepsis  or  to  erysipelas. 
The  latter  has  been  called  vaccination-erysipelas.  But  such  misfortunes  are  ex- 
tremely rare.  The  not  uncommon  "  vaccine  roseola  "  deserves  especial  mention. 
It  appears  first  upon  the  arm  vaccinated,  and  spreads  over  the  rest  of  the  body; 
but  it  is  not  a  serious  matter.  It  is  of  course  possible,  by  especially  bad  luck  in 
the  use  of  human  lymph,  that  other  diseases,  among  which  syphilis  is  of  chief 
importance,  may  be  inoculated  along  with  vaccinia ;  but  this  is  a  very  rare  occur- 
rence— much  more  so  than  the  enemies  of  vaccination  pretend.  If  the  physician 
exercise  proper  care  in  the  selection  of  the  person  from  whom  to  take  humanized 
virus,  it  can  be  entirely  avoided. 

[The  incubation  stage  of  vaccinia  being  shorter  than  that  of  small-pox,  the 
prompt  vaccination  of  an  unprotected  individual  who  has  been  exposed  to  infec- 
tion should  always  be  practiced,  if  possible;  oftentimes  the  severe  disease  may 
thus  be  prevented.] 

2.  The  treatment  of  small-pox  is  purely  symptomatic.  When  the  disease  has 
once  begun  it  is  too  late  for  vaccination  to  have  any  influence  upon  its  further 
course.  During  the  initial  period  we  may  advantageously  employ  cool  baths  to 
diminish  the  fever  and  alleviate  the  constitutional  symptoms.  An  ice-bag  will 
relieve  the  headache.  We  must  not  let  the  lumbar  pains  lead  us  to  any  but  a 
cautious  use  of  local  irritants,  for  the  pocks  come  out  in  greater  abundance  upon 
such  portions  of  the  skin  as  have  been  in  any  way  irritated.  If  the  disease  proves, 
during  the  stage  of  eruption,  to  be  varioloid,  there  will  be  no  further  need  of 
special  treatment.     Good  nursing  and  proper  food  will  suffice. 

The  true  small-pox,  on  the  other  hand,  demands  the  interposition  of  the  physi- 
cian. He  must  strive  to  guard  the  regular  course  of  the  disease  in  the  skin  and  in 
those  portions  of  the  mucous  membrane  which  are  accessible  from  being  disturbed 
by  secondary  inflammations;  for  we  have  no  doubt  that  the  ruptured  pustules 
furnish  a  most  easy  ingress  to  septic  impurities  from  the  surrounding  atmosphere, 
so  that  later,  when  there  is  extensive  suppuration  of  the  skin,  or  analogous  and 
severe  disturbance  in  the  mucous  membrane,  it  is  impossible  to  discriminate 
between  the  effects  of  the  small-pox  itself  and  those  due  to  the  secondary  suppura- 
tion. If  we  were  able  to  have  the  whole  process  go  on  "  antiseptically "  we 
should  certainly  have  made  an  important  advance  in  therapeutics.  Indeed,  the 
methods  of  treatment  which  have  been  up  to  this  time  recommended  fulfill  this 
indication  up  to  a  certain  point,  e.  g.,  painting  the  skin  with  tincture  of  iodine,  or 
with  a  strong  solution  of  nitrate  of  silver — methods  formerly  much  in  vogue. 
Schwimmer's  suggestion  seems  still  better.  He  recommends,  from  the  beginning 
of  the  eruption,  the  use  of  a  paste  made  as  follows :  Acid,  carbol.,  parts  4  to  10 ; 
ol.  olivse,  40;  crette  prseparat.,  60.  M.  et  ft.  pasta  mollis.  This  is  spread  on  pieces 
of  old  linen  and  laid  upon  those  parts  where  the  eruption  is  apt  to  be  worst — ^viz., 
the  forearm,  hand,  and  leg.     The  face  is  covered  with  a  mask,  having  holes  corre- 


62  ACUTE   GENERAL   INFECTIOUS   DISEASES 

sponding  to  the  mouth,  nose,  and  eyes.  The  applications  are  changed  every 
twelve  hours.  Under  this  treatment  the  local  distress  is  said  to  be  diminished, 
suppuration  slight,  and  healing  comparatively  rapid.  The  pain  and  sense  of  ten- 
sion in  the  skin  are  often  relieved  by  cold  applications,  or  by  simple  ointment  or 
oil.  Under  Hebra,  in  Vienna,  continuous  warm  baths  were  employed  in  severe 
cases  with  great  success. 

The  treatment  of  the  affected  mucous  membrane  in  small-pox  must  also  meet 
the  indication  above  mentioned.  The  most  thorough  disinfection  of  the  mouth 
and  pharynx  must  be  aimed  at.  The  means  to  be  used  are  careful  washing  and 
gargling  with  solutions  of  chlorate  of  potash  (1  to  30),  carbolic  acid,  borax,  per- 
manganate of  potash,  or  liquor  ferri  chloridi.  The  eyes,  if  they  need  it,  must  also 
be  appropriately  treated.  As  to  all  other  complications,  cool  baths  are  relatively 
the  most  useful  remedy.  They  can  be  given  without  difficulty.  The  chief  indica- 
tions for  them  are  severe  pulmonary  or  nervous  symptoms,  or  continuous  high 
fever.  Internal  antipyretics,  such  as  quinine  or  antipyrine,  are  also  employed. 
Violent  nervous  disturbances,  such  as  delirium,  sometimes  require  the  cautious 
use  of  narcotics.  There  is  nothing  to  add  as  to  the  treatment  of  malignant  hsem- 
orrhagic  small-pox,  for,  as  we  have  said,  such  cases  are  unfortunately  almost 
hopeless. 


CHAPTER   VIII 

VARICELLA 

( Chicken-pox) 

Varicella  is  truly  one  of  the  diseases  of  childhood.  Adults  very  rarely  have  it. 
It  is  contagious,  and  often  conies  in  epidemics. 

The  stage  of  incubation  does  not  last  over  thirteen  to  seventeen  days.  The 
disease  begins  with  the  appearance  of  vesicles,  the  size  of  a  pea  or  a  little  larger, 
usually  having  a  small  red  areola,  and  varying  in  number  from  ten  to  one  hun- 
dred or  more.  The  trunk  usually  bears  the  greater  part  of  the  vesicles,  while  the 
extremities  have  few.  The  face  is  frequently  the  seat  of  a  considerable  number, 
and  sometimes  there  are  a  few  upon  the  hairy  scalp.  There  may  be  a  vesicle  here 
and  there  upon  the  mucous  membrane  of  the  mouth  or  palate.  There  are  seldom 
any  prodromata.  Slight  symptoms  of  fever  may  attend  the  eruption  itself.  The 
eruption  is  usually  over  in  a  few  days,  although  there  may  be  repeated  crops,  so 
that  we  often  see  fresh  vesicles  by  the  side  of  others  which  are  drying  up.  Each 
individual  vesicle  heals  quickly,  and  the  pustulation  seen  in  small-pox  is  here  ex- 
ceptional. The  course  of  the  disease  is  completed  in  a  week  or  ten  days.  Most 
children  feel  perfectly  well  the  whole  time,  although  there  may  be  in  rare  cases 
pain  in  the  limbs,  anorexia,  and  a  slight  coryza.  A  severe  complication  is  hardly 
ever  seen.     An  unusual  event  is  a  mild  nephritis. 

Exceptionally,  the  disease  may  be  rudimentary,  with  a  varicelloid  roseola  and 
no  formation  of  vesicles.  On  the  other  hand,  some  cases  present  quite  severe  con- 
stitutional symptoms  and  a  high  fever,  even  reaching  105°  (41°  C.)  temporarily. 
In  most  cases,  however,  as  we  have  said,  the  child  is  so  slightly  disturbed  that  a 
physician  is  hardly  thought  necessary. 

The  diagnosis  is  almost  always  easy.  Formerly  varicella  was  often  con- 
founded with  small-pox,  and  to  this  day  the  followers  of  Hebra,  in  Vienna,  for 
some  inconceivable  reason,  maintain  the  identity  of  the  two.  That  they  are  essen- 
tially distinct  is  shown  (1)  by  the  epidemics  of  the  two  appearing  entirely  separate 
from  each  other,  (2)  by  the  fact  that  having  one  does  not  give  immunity  from  the 


ERYSIPELAS 


63 


other,  and  (3)  by  the  uniform  failure  of  attempts  to  produce  variola  by  inoculat- 
ing varicella,  or  vice  versa.  Still,  we  must  bear  in  mind,  in  order  to  avoid  mis- 
takes, that  many  dermatologists  class  the  mildest  cases  of  small-pox  as  varicella. 
Those  who  devote  themselves  to  general  diseases  are  probably  all  now  convinced 
that  varicella  is  a  separate  disease. 

The  prognosis  is  perfectly  good.    There  is  usually  no  special  treatment  neces- 
sary, but  young  children  should  be  kept  in  bed  till  the  eruption  has  dried  up. 


CHAPTER  IX 


ERYSIPELAS 

(.b'i.  Anthony'^s  Fire) 

.Sitiology. — Erysipelas  is  a  peculiar  inflammation  of  the  skin,  recognized  by 
redness,  swelling,  and  pain.  It  has  the  peculiarity  of  spreading  gradually,  by 
direct  extension,  from  its  point  of  origin  over  a  larger  or  smaller  portion  of  the 
body.  The  cause  of  this  inflammation,  as  was  first  shown  by  Fehleisen,  is  a  local 
infection  by  the  streptococcus  pyogenes  and  its  further  extension  in  the  skin. 
The  exciting  agent  of  erysipelas  is  then  bacteriologically  identical  with  the  strep- 
tococcus which  is  the  cause  of  phlegmonous  suppuration,  severe  septic  infection, 
etc.     The  reason  why  in  the  individual  case 

erysipelas  develops,  and  not  some  other  strep-  ----iV^^^tAifSiSpij^^ 

tococcus  disease,  is  the  special  variety  of  in-  :  ;;;'/'    ;'    - 

fection  and  the  further  spread  of  the  strepto-  ^^^^'^/(^  y/  /^ 

cocci   in  the  deeper  lymphatics   of   the  skin,  jff^Mi  "^^^^m 

and  in  part  perhaps  the  special  "  virulence  "  #3^RSf3||jr--     '^^-^S 

of  the  infecting  germs.  ^^Mf>^^^^0^^ '''^^^ifflWXS 

The    former    distinction    between    "  trau-  "  "? /I?^^^:" '•:'■^■p^^^^^5^ 

matic  "     and    "  idiopathic  "     or    "  exanthe- 

matic  "   erysipelas   can   no   longer   be   rigidly        ^^^^m----:-  '•  ■•'.■^-^Ip-  - 
maintained.     Every  erysipelas  is  in  a  certain        Wrf^M,  '    -'l^^M^i^f"'^' 
sense  traumatic,  since  infection  with  strepto- 
cocci can  not  occur  through  the  unbroken  skin. 
The  so-called  "  idiopathic  "  erysipelas  is  dis-        'W^i^'fiMi- 
tinguished     from     "  wound     erysipelas "     (in        W0''^^^--^^ 
which,  of  course,  we  include  puerperal  erysipe-  ?^^Va" 

las,  erysipelas  of  the  newborn  starting  from  -v/^i-:^"-' 

the  umbilical  wound,  etc.)    only  by  the  fact      fig.  8.-The  cocci  of  erysipelas.    x700. 

that  in  the  former  the  infection  takes  place  in  Section  through  a  lymph-vessel  in  the  skin, 
small,  insignificant  wounds  of  the  skin  which 

are  easily  overlooked.  Such  an  erysipelas  occurs  chiefly  in  the  face  and  head,  and 
the  following  description  of  the  symptoms  refers  chiefly  to  this  facial  erysipelas. 
Most  of  these  cases  of  erysipelas  arise  from  little  excoriations,  cracks,  and  scratches 
about  the  nose  or  ears,  or  more  rarely  about  other  parts  of  the  face  or  scalp.  A 
previous  coryza,  by  the  accompanying  slight  erosions  about  the  nose,  sometimes 
gives  the  opportunity  for  an  attack  of  erysipelas,  but  sometimes  the  infection  oc- 
curs in  the  mucous  membrane  of  the  nose  or  pharynx;  then  we  have  a  primary 
erysipelas  of  the  mucous  membrane,  which  extends  through  the  nasal  passages  and 
finally  appears  on  the  external  surface  of  the  nose.     . 

Facial  erysipelas  is  most  apt  to  attack  the  young,  and  seems  to  be  somewhat 
more  frequent  in  women  than  in  men.    The  laity  erroneously  regard  catching  cold 


64  ACUTE   GEKEEAL   INFECTIOUS   DISEASES 

and  getting  frightened  as  frequent  causes  of  the  disease.  If  we  except  the  pre- 
disposing causes  above  mentioned — viz.,  coryza,  slight  scratches,  cuts,  etc. — we 
usually  find  no  cause  of  which  we  can  feel  certain.  Often  endemic  influences  are 
important.  It  has  been  long  known  that  traumatic  erysipelas  can  get  so  secure 
a  footing  in  particular  hospitals  or  wards  that  every  wounded  person  treated  in 
them  is  in  danger  of  this  disease;  but  the  apparently  idiopathic  variety  is  some- 
times remarkably  frequent  in  particular  places  (barracks,  etc.).  Several  mem- 
bers of  one  family  may  likewise  have  facial  erysipelas  simultaneously.  In  nearly 
all  such  cases  the  sufferers  are  infected  from  some  common  source,  for  direct 
contagion  is  certainly  exceptional;  but  patients  with  open  wounds  should  never 
be  put  near  erysipelas  cases,  because  here  the  risk  of  infection  can  not  be  wholly 
excluded.  Direct  inoculation  can,  however,  as  has  been  proved,  convey  the  dis- 
ease from  a  patient  to  other  persons  or  to  animals. 

In  contrast  with  the  behavior  of  many  other  infectious  diseases  (typhoid 
fever,  measles,  scarlet  fever,  small-pox,  etc.),  erysipelas  is  peculiarly  apt  to  attack 
the  same  individual  over  and  over  again.  There  are  persons  who  have  facial 
erysipelas  about  every  one  or  two  years,  and  ten  to  fifteen  times.  Often  the 
explanation  of  this  apparently  lies  in  some  chronic  disease — e.  g.,  chronic 
oza;na,  chronic  eczema  of  the  nostrils  or  ears — which  makes  infection  easy, 
but  in  other  cases  no  cause  can  be  discovered.  Of  course  when  erysipelas 
afilicts  the  same  person  a  number  of  times  the  individual  attacks  gradually  be- 
come milder.  Marasmus  seems  to  predispose  to  erysipelas.  At  least  we  have 
observed  that  erysipelas  occurred  with  relative  frequency,  in  the  Leipsic  hos- 
pital, in  patients  suffering  from  the  last  stages  of  phthisis  or  cancer,  or  similar 
diseases. 

Clinical  History, — In  many  cases  the  first  subjective  symptoms  ai'e  simultane- 
ous with  the  cutaneous  swelling,  and  these  are  chiefly  local.  There  is  pain  and  a 
sense  of  tension  in  the  skin.  Soon  subjective  symptoms  of  fever  also  appear,  such 
as  general  malaise,  anorexia,  headache,  and  sometimes  vomiting.  In  other  cases 
the  disease  starts  with  more  violent  constitutional  symptoms :  there  is  an  initial 
rigor,  with  violent  headache  and  great  languor.  The  local  erysipelatous  swelling 
appears  almost  at  the  same  time  with  these  general  symptoms  or  sometimes  a  few 
days  later,  either  because  the  local  inflammation  is  at  first  slight  or  because 
it  is  not  noticed,  as  in  the  scalp  when  the  hair  is  very  thick.  In  rare  instances  the 
disease  begins  with  sore  throat.  We  saw  three  almost  simultaneous  cases  of  facial 
erysipelas  in  one  family,  in  which  a  severe  sore  throat  lasted  for  four  or  five  days 
preceding  the  appearance  of  the  cutaneous  disorder.  We  have  seen  a  number  of 
similar  cases  since  and  believe  that  they  are  due  to  a  true  erysipelatous  angina — 
that  is,  to  an  erysipelas  of  the  soft  palate  which  extends  through  the  nostrils  to 
the  external  skin.  In  cases  of  erysipelas  which  follow  a  coryza  we  may  assume, 
as  stated  above,  that  there  is  an  erysipelas  of  the  nasal  mucous  membrane  pre- 
ceding the  erysipelas  of  the  skin. 

The  erysipelatous  process  in  the  skin  is  almost  always  circumscribed  at  first. 
It  usually  starts  on  the  nose,  less  often  upon  the  cheek,  the  ears,  or  the  hairy  scalp. 
The  skin  becomes  considerably  swollen,  grows  red,  smooth,  and  shiny,  and  feels 
hot.  The  redness  and  swelling  keep  spreading.  There  is  usually  a  sharp,  elevated 
ridge,  perceptible  to  sight  and  touch,  separating  the  diseased  from  the  still  healthy 
portion  of  the  skin.  As  long  as  the  erysipelas  is  spreading,  we  see  stretching  out 
from  its  border,  or  somewhat  removed  from  it,  small  red  streaks  and  spots  which 
gradually  increase  in  area  and  intensity,  and  finally  coalesce.  Any  decided  fold  in 
the  skin  may  hinder  for  a  time  the  extension  of  the  disease.  The  naso-labial  folds 
are  particularly  apt  to  limit  it.  The  border  of  the  hairy  scalp  frequently  forms  a 
terminal  line;  but  the  whole  scalp  may  be  attacked,  the  inflammation  stopping 
only  when  it  reaches  the  nape  of  the  neck.    The  boundary  of  the  erysipelas  in  the 


ERYSIPELAS  65 

hairy  scalp  can  usually  be  quite  accurately  deteiinined  by  palpation  (swelling  and 
local  tenderness). 

It  is  only  in  a  relatively  small  number  of  cases  that  it  spreads  farther  yet, 
attacking  the  back,  the  arms,  and -the  anterior  surface  of  the  trunk,  or  even 
extending  to  the  feet.  This  is  known  as  erysipelas  migrans.  The  facial  erysipelas 
may  be  healed  long  before  the  disease  ceases  to  extend  over  the  other  parts  of 
the  body.  When  the  spreading  process  is  about  to  cease,  the  inflammation 
usually  becomes  decidedly  milder,  appears  only  in  isolated  spots,  and  finally 
stops  completely.  In  most  cases,  only  the  face,  the  ears,  and  a  part  of  the  scalp 
are  attacked. 

It  is  not  a  rare  thing  for  vesicles  or  bullse  to  form  in  the  portions  of  skin 
attacked.  Such  cases  are  called  erysipelas  vesiculosum  or  erysipelas  hullosum. 
The  serum  may  change  to  pus  in  these  blisters,  and  then  we  have  erysipelas 
pustulosum.  Exceptionally  the  infiltration  of  the  skin  becomes  so  intense  as  to 
result  in  a  localized  necrosis  or  gangrene — erysipelas  gangrcenosum.  The  parts 
most  apt  to  be  attacked  by  this  are  the  eyelids,  where  abscesses  sometimes  form. 

Microscopic  examination  of  the  skin  shows  a  marked  hypersemia  of  all  the 
blood-vessels  and  a  very  considerable  infiltration  of  both  the  skin  and  the  subcu- 
taneous connective  tissue  with  serum  and  cells.  In  those  parts  where  vesicles  are 
formed  there  are  many  dead  and  disintegrated  epithelial  cells  in  the  rete  Mal- 
pighi.  In  the  parts  where  most  streptococci  develop  there  may  also  be  necrosis 
of  the  deeper  layers  of  the  skin.  We  have  already  said  that  there  may  be  many 
streptococci  in  the  lymphatics  of  the  skin,  but  they  are  found  only  in  the  first 
fresh  stages  of  the  inflammation.  When  the  inflammatory  exudation  has  reached 
its  full  height,  the  streptococci  have  usually  wholly  disappeared.  As  a  rule  we 
find  only  a  few  or  no  streptococci  in  the  contents  of  erysipelas  vesicles. 

The  inflammation  in  any  one  spot  usually  ends  four  or  five  days  after  it  has 
made  its  appearance  there.  There  is  apt  to  be  much  attendant  desquamation. 
The  face  is  often  left  with  a  finer  complexion  than  it  had  before. 

The  other  symptoms,  of  which  the  constitutional  disturbance  and  the  fever  are 
chief,  correspond  pretty  closely  to  the  severity  and  extent  of  the  cutaneous  lesion. 
It  is  comparatively  seldom  that  this  correspondence  does  not  exist. 

The  fever  in  facial  erysipelas  usually  rises  rapidly  at  first,  and  to  a  considerable 
height.  We  have  seen  but  few  cases  where  the  high  fever  was  delayed  till  a  day 
or  two  after  the  skin  was  attacked.  The  temperatures  observed  in  erysipelas  are 
often  extreme:  106°  (41°  C.)  is  not  at  all  rare.  The  highest  we  ever  saw  was 
107.2°  (41.8°  C).  While  the  erysipelas  continues  or  is  spreading,  the  fever  is  sel- 
dom continuous,  nor  are  the  remissions  insignificant.  Pronounced  intermissions, 
even  down  to  normal,  are  very  frequent,  but  are  followed  again  by  a  rapid  and 
great  rise  of  temperature.  The  fever  may  terminate  with  a  genuine  crisis.  In 
intense  cases  of  considerable  extent,  or  in  erysipelas  migrans,  the  termination 
is  more  apt  to  be  by  a  more  or  less  gradual  lysis.  We  have  seen  the  cutaneous 
inflammation  in  erysipelas  migrans  still  extend  itself  a  little,  in  a  rudimentary 
form,  after  the  fever  had  completely  ceased. 

The  headache  is  often  intense,  and  seems  to  result  not  merely  from  the  inflam- 
mation of  the  scalp  but  from  disturbances  of  the  circulation  in  the  underlying 
parts,  or  more  probably  from  the  action  of  a  toxine.  Other  severe  cerebral 
symptoms  are  also  relatively  frequent.  The  patient  may  be  very  restless,  excited, 
and  wakeful.  At  night  there  may  be  mild  or  even  violent  delirium;  or  there 
may  be  decided  stupor.  All  these  sjanptoms  are  in  chief  part  due  to  the  general 
intoxication  caused  by  the  infection ;  but  they  also  justify  a  surmise,  as  we  have 
said,  that  there  is  a  circulatoiy  derangeraent  in  the  meninges  and  the  brain  itself, 
resulting  from  the  inflammation  of  the  scalp.  In  drunkards,  delirium  tremens  is' 
not  infrequent. 
5 


m  ACUTE    GENERAL   IXEECTIOUS    DISEASES 

One  of  the  most  constant  symptoms  in  facial  erysipelas  is  gastric  and  intestinal 
disturbance.  There  is  usually  complete  anorexia.  The  tongue  is  thickly  coated. 
Vomiting  is  frequent,  not  only  at  the  beginning  but  during  the  course  of  the  dis- 
ease. There  is  constipation ;  or  there  may  be  quite  severe  diarrhoea.  There  is  no 
pathological  lesion  known  corresponding  to  these  clinical  symptoms.  The  spleen 
is  usually  moderately  swollen.  In  all  severe  cases  we  find  in  the  blood  a  pro- 
nounced leucocytosis  (16,000  to  18,000  leucocytes  in  a  cubic  millimetre).  Strep- 
tococci are  not  found  in  the  blood. 

The  entire  duration  of  the  disease  varies  greatly  in  different  cases.  A  very 
light  case  may  get  well  in  a  few  days.  Most  cases  of  average  severity  last  a  week 
or  ten  days.  Erysipelas  migrans  may  continue  for  many  weeks.  We  have  sev- 
eral times  seen  a  relapse  come  on  after  a  number  of  days  of  complete  apyrexia. 
Either  the  face  would  be  once  more  attacked,  or  some  portion  of  the  skin  which 
had  previously  escaped. 

Local  complications  are  comparatively  rare  and  insignificant  in  erysipelas. 
The  lymphatic  glands  of  the  throat  and  back  of  the  neck  are  very  frequently 
somewhat  swollen,  but  seldom  attain  great  size.  Bronchitis  and  lobular  pneu- 
monia may  develop  in  severe  cases,  but  are  not  at  all  characteristic.  Some  ob- 
servers call  attention  to  the  occurrence  of  pleurisy,  endocarditis,  and  pericarditis ; 
but  these  complications  also  are  very  rare.  The  spleen  is  usually  slightly  swollen. 
Sometimes  there  is  an  icteroid  hue.  The  urine  frequently  contains  a  small 
amount  of  albumen,  and  in  severe  cases  of  erysipelas  acute  hsemorrhagic  nephritis 
is  not  so  very  rare,  but  it  almost  always  disappears  entirely.  The  albuminuria 
usually  disappears  a  few  days  after  the  fever.  Swelling  of  the  joints  has  been 
repeatedly  observed.  It  is  more  frequent  in  the  severe  surgical  forms  of  erysipelas, 
which  are  combined  with  universal  septic  and  pysemic  conditions  of  the  system. 
Purulent  meningitis  may  complicate  an  erysipelas  located  in  the  head,  but  it  is 
very  rare.  We  should  be  exceedingly  cautious  about  asserting  its  existence  even 
when  the  cerebral  symptoms  are  very  pronounced. 

Cutaneous  complications  are  relatively  frequent.  We  have  seen  herpes  labialis 
quite  often,  and  a  number  of  cases  of  urticaria.  Of  much  greater  importance  are 
the  cutaneous  abscesses  which  occur  in  severe  cases.  These  are  due  to  a  phleg- 
monous or  even  gangrenous  inflammation  of  the  connective  tissue.  Their  most 
frequent  seat  in  the  face  is  the  eyelids,  as  already  stated;  and  in  that  case  the  eye 
may  itself  be  endangered.  At  the  close  of  severe  cases  of  erysipelas  migrans, 
numerous  abscesses  may  develop  in  the  skin  of  the  trunk  and  extremities,  delay- 
ing convalescence.  Since,  as  we  have  said,  the  streptococcus  of  erysipelas  is  abso- 
lutely identical  with  the  streptococcus  pyogenes,  all  purulent  inflammatory  com- 
plications of  erysipelas  are  to  be  referred  to  the  local  or  metastatic  action  of 
the  original  infectious  germs,  but  erysipelatous  nephritis  is  probably  of  purely 
toxic  origin. 

The  diagnosis  of  erysipelas  is  almost  always  easy  when  once  the  cutaneous 
lesion  has  developed.  Phlegmonous  inflammation  of  the  skin  and  lymphangitis 
are  to  be  eliminated ;  but  this  is  always  possible,  with  proper  care.  After  a  single 
examination,  we  may  confound  it  with  acute  facial  eczema  of  great  severity,  or 
even  with  a  marked  urticaria.  Chief  attention  should  be  paid  to  the  characteristic 
border  of  erysipelas  and  to  its  manner  of  extension.  In  erysipelas  beginning  in 
the  hairy  scalp  the  local  inflammation  may  easily  be  overlooked,  being  completely 
masked  by  the  severe  general  symptoms. 

The  prognosis  of  facial  erysipelas,  when  it  attacks  a  healthy  person,  is  very 
favorable.  In  drunkards  a  severe  case  may  be  complicated  by  delirium  tremens, 
and  the  issue  be  unfavorable.  We  saw  one  case  end  fatally  because  of  gangrene 
of  the  eyelids,  followed  by  purulent  inflammation  of  the  orbital  connective  tissue. 
Erysipelas  migrans  may  so  exhaust  the  powers  of  feeble  patients  as  to  become 


DIPHTHEEIA  67 

dangerous.  The  prognosis  of  surgical  erysipelas  is  relatively  more  unfavorable, 
but  it  can  not  be  considered  here. 

Treatment. — The  treatment  of  ordinary  erysipelas  of  the  head  and  face, 
which  is  the  main  question  here,  is  purely  symptomatic.  The  large  number  of 
remedies  recommended  (tincture  of  iodine,  nitrate  of  silver,  iodoform,  ichthyol, 
carbolic  acid,  collodion,  etc.)  shows  that  they  can  not  any  of  them  materially 
influence  the  morbid  process.  It  is  easy  to  be  deceived  about  their  efiicacy,  as  most 
cases  are  relatively  benign.  We  therefore  usually  content  ourselves  with  powder- 
ing the  affected  skin  or  covering  it  with  oil  or  vaseline  to  relieve  the  tension,  and 
also  with  putting  on  an  ice-bag  if  the  patient  likes  it.  We  have  found  no  proof 
that  we  can  limit  the  advance  of  the  disease  mechanically  by  applying  firm  ad- 
hesive plaster  to  the  boundary  of  the  erysipelas,  etc.  We  can  expect  no  specific 
action  from  internal  remedies  (Pirogoff's  camphor  cure,  liquor  ferri  sesquichlo- 
rati,  etc.). 

Apart  from  alleviating  the  local  discomfort,  some  other  symptoms  occasionally 
demand  special  consideration.  Severe  headache  and  other  severe  nervous  symp- 
toms may  be  relieved  by  the  local  use  of  cold  or  by  antipyrine  and  similar  remedies. 
With  high  temperature  cool  baths  or  antipyretics  internally  may  be  used  with 
benefit,  but  in  general  the  fever  does  not  often  demand  energetic  treatment,  since 
in  erysipelas,  as  we  have  said,  considerable  spontaneous  remissions  of  temperature 
often  occur.  When  there  are  marked  gastro-intestinal  symptoms  we  may  pre- 
scribe hydrochloric  acid,  opium,  etc. 

Only  when  there  is  a  true  migrating  erysipelas  and  the  disease  spreads  over  the 
body  should  we  try  more  energetic  methods.  Heuter  recommended  subcutaneous 
injections  of  a  two-per-cent.  solution  of  carbolic  acid  a  little  way  from  the  edge 
of  the  erysipelas.  Although  this  method  is  certainly  rational,  we  have  usually 
seen  no  striking  results  from  it.  It  seems  more  effective  to  scarify  the  erysipela- 
tous skin  and  then  wash  it  with  a  corrosive-sublimate  solution,  as  lately  recom- 
mended. In  the  severe  cases  the  main  point,  after  all,  is  to  maintain  the  patient's 
strength  by  nursing  and  food.  If  cutaneous  abscesses  form,  they  should  be  opened 
promptly,  when  they  usually  soon  heal. 


CHAPTEE   X 


DIPHTHEEIA 

{Diplitheritis.     Croup.     C'ynanche  contagiosa) 

.ffitiology  and  General  Pathology. — Clinically,  "diphtheria"  means  a  certain 
well-characterized,  specific,  acute,  infectious  disease,  the  chief  visible  lesion  of 
which  is  a  croupous-diphtheritic  inflammation  of  the  pharynx  and  upper  air-pas- 
sages. In  a  purely  pathological  sense,  however,  the  terms  "  croupous  "  and  "  diph- 
theritic "  have  a  broader  meaning.  They  denote  a  certain  form  of  inflammation 
which  may  occur  in  the  mucous  membrane  of  almost  any  part  of  the  body.  It  is 
frequent  in  the  intestine  and  bladder.  There  is  great  diversity  in  the  causes 
which  may  produce  it. 

The  pathological  characteristic  of  every  croupous-diphtheritic  inflammation 
consists  in  the  formation  of  a  fibrinous  exudation.  This  may  either  be  a  croupous 
membrane,  which  is  grayish  white,  rather  firm  and  elastic,  and  which  can  be  lifted 
off  with  comparative  ease  from  the  mucous  membrane  upon  which  it  rests,  or  it 
may  be  a  diphtheritic  infiltration  with  necrosis  of  the  tissues.  Here  the  exudation 
is  more  or  less  deeply  imbedded  within  the  proper  structure  of  the  mucous  mem- 


68  ACUTE   GENERAL  IISTFECTIOUS   DISEASES 

brane  itself.  There  is  no  essential  difference  between  croup  and  diphtheria ;  diph- 
theritic inflammation  is  the  severer  form  of  the  disease,  croupous  inflammation  the 
milder.  In  diphtheria  the  fibrinous  exudation  is  preceded  by  a  necrosis  of  the 
epithelium  and  of  the  underlying  tissues  of  the  mucous  membrane  as  ^vell,  while 
in  the  case  of  croupous  exudation  the  necrosis  is  limited  to  the  epithelium.  The 
croupous  membrane  never  rests  upon  an  intact  mucous  surface,  but  replaces  the 
epithelium,  which  has  already  been  totally  or  in  very  large  part  destroyed.  Flaky 
remnants  of  the  epithelium,  no  longer  nucleated,  are  sometimes  found  in  the 
meshes  of  the  fibrine.  The  preceding  destruction  of  the  epithelium  is  essential  to 
the  occurrence  of  fibrinous,  croupous  inflammation.  The  fibrinous  exudation  can 
be  formed  in  those  places  only  where  the  cause  which  excites  the  inflammation 
kills  the  epithelium  at  the  same  time.  It  is  still  undecided  whether  or  in  what 
degree  the  epithelium  takes  part  in  the  formation  of  the  croupous  membrane. 
Most  pathologists  hold  that  the  material  for  the  fibrine  comes  from  the  fibrinogen 
of  the  infiammatory  matter  which  transudes  through  the  walls  of  the  vessels,  and 
also  from  the  disintegrated  migratory  white  blood-globules.  These  last  are 
abundant  throughout  the  deposit  itseK,  and  still  more  numerous  in  the  entire 
tissue  of  the  mucous  membrane  beneath  the  croupous  or  diphtheritic  exudation. 
If  recovery  takes  place  in  croup,  all  that  is  needed  after  the  exudation  has  been 
cast  off  is  the  renewal  of  the  epithelium,  which  can  be  accomplished  through  the 
exclusive  agency  of  the  remnants  of  epithelium  left  along  the  borders  of  the  dis- 
eased spot.  In  diphtheria,  however,  the  entire  necrotic  portion  of  mucous  mem- 
brane must  slough  off,  a  line  of  demarkation  being  formed,  and  cicatricial  tissue 
replaces  the  necrosed  portion. 

The  above  is  a  bare  outline  of  the  present  views  about  croupous  and  diph- 
theritic inflammations.  They  have  been  reached  gradually  through  the  labors  of 
E,  Wagner,  Weigert,  and  others.  We  have  not  yet  touched  upon  the  setiological 
factors;  but  what  precedes  renders  it  evident  how  manifold  they  may  be,  for 
many  causes  which  destroy  the  epithelial  layer  of  the  mucous  membrane,  and  at 
the  same  time  promote  inflammation,  may  excite  croup.  We  have  mechanical 
causes,  such  as  impacted  f eeces,  gall-stones,  renal  calculi ;  chemical  irritants, 
caustics,  like  ammonia  and  the  acids;  and,  fijially,  a  number  of  specific,  infec- 
tious, disease-producing  poisons.  Among  these  is  the  specific  poison  of  diphtheria 
proper. 

There  has  been  no  doubt  for  a  considerable  period  that  true  pharjTigeal  diph- 
theria could  be  produced  only  by  a  specific  organized  cause.  To  demonstrate  this, 
however,  has  been  thus  far  extremely  difficult,  for  there  are  in  the  diseased  parts 
a  great  number  of  diverse  micro-organisms,  originating  in  the  mouth  and  throat, 
and  really  secondary  to  the  diphtheritic  process;  and,  although  they  of  course  are 
entirely  different  from  the  specific  "  diphtheritic  bacteria,"  it  is  very  hard  to 
separate  them.  Nevertheless  Loffler  has  of  late  succeeded  in  solving  the  ques- 
tion of  the  origin  of  diphtheria  in  an  apparently  decisive  way.  From  numerous 
investigations  by  Roux  and  Yersin,  Heubner,  and  others,  there  can  scarcely  be 
a  doubt  at  present  that  the  specific  diphtheria  bacillus  is  a  form  of  bacillus  char- 
acterized by  a  definite  and  particular  granular  formation,  a  club-like  swelling  at 
the  ends,  and  special  methods  of  growth  on  blood-serum.  The  diphtheria  bacilli 
are  found  only  on  the  diseased  portion  of  the  mucous  membrane  or  the  point 
of  inoculation,  and  never  in  the  blood  or  the  internal  organs.  This  fact  is  of  the 
greatest  pathological  significance,  and  it  has  been  established  not  only  for  diph- 
theria in  man,  but  also  for  experimental  diphtheria  in  animals.  In  pharyn- 
geal diphtheria  they  are  found  chiefly  on  the  under  surface  of  fresh  false  mem- 
brane. The  severe  general  symptoms  of  diphtheria,  however,  except  when  due  to 
secondary  infection  (vide  infra),  depend  upon  the  poisonous  chemical  action  of 
certain  substances  produced  by  processes  of  metabolism  in  the  bacilli.     Little 


DIPHTHEEIA  69 

that  is  definite  is  known,  however,  as  to  the  precise  chemical  nature  of  these 
"  toxines." 

We  may  accept  it  as  a  fact  that  the  diphtheria  bacilli  or  their  spores  reach 
the  pharyngeal  cavity  directly  through  the  inspired  air  or  in  some  other  way, 
and  there,  in  case  they  attach  themselves  to  the  mucous  membrane  and  increase,, 
produce  diphtheria.  In  a  few  rare  cases  they  seem  to  be  inhaled  into  the  larynx 
at  once,  and  to  excite  there  a  "  primary  laryngeal  croup "  (vide  infra) .  The 
source  of  the  infection  is  always  to  be  referred  ultimately  to  another  case  of 
diphtheria,  but  the  way  in  which  the  disease  spreads  can  not  always  be  traced  in 
detail.  In  many  cases,  of  course,  a  direct  ("  contagious  ")  transmission  of  the 
poison  is  evident,  as  from  coughing,  or  the  many  cases  of  the  disease  in  physi- 
cians and  nurses  from  sucking  the  croupous  membrane  out  of  the  tracheotomy 
tube  in  children,  etc.  If  several  children  in  one  house  fall  sick,  as  often  hap- 
pens, we  may  here  suspect  a  direct  transmission  of  the  disease,  although  it  is 
also  possible  that  in  such  an  event  several  cases  may  arise  from  the  same  source 
of  infection.  We  do  not  yet  know  positively  how  far  the  diphtheria  bacilli  can 
lead  an  independent  existence  outside  of  the  human  body  (the  earth,  the  floors 
of  dwellings,  etc.).  It  seems  certain  that  the  infection  can  be  carried  from  one 
person  to  another  by  some  intermediary,  by  clothing,  linen,  toys,  and  other  objects 
to  which  the  diphtheria  poison  clings.  The  resistance  of  the  latter  to  external  in- 
fluences— temperature,  drying,  etc. — is  very  considerable.  After  complete  recov- 
ery from  diphtheria,  virulent  diphtheria  bacilli  may  be  found  in  the  oral  cavity 
for  a  considerable  time.  This  is  particularly  to  be  noted  on  account  of  its  prac- 
tical importance.  We  must  mention,  in  conclusion,  that  attention  has  lately  been 
called  to  the  possibility  of  the  transmission  of  diphtheria  from  sick  animals 
(hens,  doves,  calves,  [cats] )  to  man,  since  diseases  resembling  diphtheria  undoubt- 
edly occur  in  the  domestic  animals  mentioned. 

Diphtheria,  as  is  well  known,  is  a  disease  chiefly  of  childhood,  but  some 
cases,  and  even  very  severe  ones,  may  occur  in  adults.  In  advanced  life  the  dis- 
ease is  very  rarely  seen.  In  large  cities  sporadic  cases  occur  from  time  to  time, 
but  the  disease  often  takes  on  an  epidemic  character.  At  such  times  some  places 
appear  to  be  much  more  subject  to  the  disease  than  others. 

[While  it  seems  in  the  highest  degree  probable  that  the  poison  is  usually  purely 
local  at  the  start,  cases  occur  which  suggest  that  constitutional  infection  through 
the  pulmonary  blood-vessels  may  precede  the  local  manifestations.  Infection 
through  the  alimentary  canal  is  not  probable,  though  its  occurrence  can  not  be 
positively  denied. 

There  are  still  points  in  the  etiology  and  pathology  of  this  affection  which  are 
involved  in  obscurity.  Much  has  been  said  and  written  in  this  country  and  in 
England  about  the  relations  of  filth  and  diphtheria.  That  filthy  surroundings 
contribute  a  soil  favorable  to  the  development  of  the  poison,  and  at  the  same  time 
diminish  the  resisting  power  of  the  human  organism,  can  not  be  doubted ;  but,  as 
long  as  the  parasitic  theory  of  infectious  diseases  prevails,  sewer-gas  and  the  like 
must  be  classed  among  the  predisposing  or  accessory  causes. 

Some  of  the  frightfully  virulent  epidemics  of  diphtheria  in  sparsely  settled 
country  districts  and  on  the  Western  plains  are  difiicult  to  explain  under  the 
theory  that  each  case  is  mediately  or  immediately  the  result  of  a  previous  case; 
these  difficulties  will,  however,  doubtless  be  cleared  away  in  time.] 

Clinical  History. — The  incubation  is  rather  brief,  seldom  exceeding  two  to  five 
days.  The  disease  itself  almost  always  begins  with  general  malaise,  headache, 
fever,  and  pain  on  swallowing.  Little  children,  however,  often  do  not  complain 
of  this  last  symptom,  and  in  older  children  the  sore  throat  may  not  be  very 
troublesome  at  first.  It  is  therefore  a  very  important  rule  for  the  physician  to 
examine  the  throat  carefully  in  every  child  who  presents  ill-defined  general  symp- 


70  ACUTE    GENEEAL   INFECTIOUS    DISEASES 

toms.  If  diphtheria  is  beginning,  we  find  redness  of  the  soft  palate,  and  more  or 
less  swelling  of  the  tonsils.  Upon  the  inner  surface  of  the  latter,  and  perhaps 
upon  the  arch  of  the  palate  and  the  uvula  also,  are  spots  covered  with  a  grayish- 
white  coating,  which  is  quite  firmly  adherent  to  the  mucous  membrane.  They  are 
less  frequent  at  first  upon  the  posterior  wall  of  the  pharynx  and  the  hard  palate. 
Their  extent  varies  greatly  in  different  cases.  In  the  mildest  they  are  chiefly 
confined  to  the  tonsils,  attacking  the  soft  palate  or  the  tonsillar  surface  of  the 
uvula  but  little  if  at  all.  In  severer  attacks  the  spread  of  the  false  membrane 
during  the  first  days  of  illness  is  rapid.  Almost  invariably  there  is  a  very  early 
and  considerable  swelling  of  the  lymph-glands  at  the  angle  of  the  jaw.  The  con- 
stitutional symptoms  persist.  The  children  are  restless.  There  is  complete  an- 
orexia, and  frequently  vomiting.  The  temperature-curve  is  not  typical.  It  is 
irregular,  but  is  often  rather  elevated.  In  true  diphtheria  such  high  tempera- 
ture, 104°-105°  (40°-41°  C),  as  is  common  in  follicular  tonsillitis,  is  certainly 
exceptional.  On  the  other  hand,  fever  may  be  slight  or  almost  absent,  even  in 
the  worst  cases.  The  pulse  is  very  rapid.  The  urine  may  have  a  trace  of 
albumen. 

In  mild  eases  the  local  and  constitutional  symptoms  remain  moderate ;  and  at 
the  end  of  a  week  or  ten  days  there  is  decided  improvement,  with  rapid  convales- 
cence. In  severe  cases,  however,  dangerous  symptoms  appear,  perhaps  early ;  the 
croupous  inflammation  involves  neighboring  organs,  or  a  severe  constitutional 
condition  is  developed. 

The  diphtheria  very  frequently  extends  into  the  nose.  This  "diphtheritic 
eoryza,"  though  not  in  itself  dangerous,  is  usually  a  sign  that  the  case  is  a  severe 
one.  The  inflammation  of  the  nasal  mucous  membrane  may  be  simply  muco- 
purulent (from  secondary  infection  with  streptococci?),  but  it  may  also  be 
croupous.  It  is  betrayed  by  the  abundant  purulent  discharge.  Excoriations  and 
superficial  ulcers  are  usually  soon  produced  at  the  edge  of  the  nostrils.  There 
may  be  nose-bleed. 

A  much  more  dangerous  complication  is  the  extension  of  the  croupous  infiam- 
mation  into  the  larynx.  This  creates  a  mechanical  hindrance  to  respiration, 
which  proves  fatal  in  a  great  many  cases,  as  the  child's  larynx  is  so  small.  For- 
merly "  croup  " — i.  e.,  croupous  inflammation  of  the  larynx — was  regarded  as  a 
different  disease  from  diphtheria.  Many  specialists  in  children's  diseases  still 
maintain  this  view ;  but  it  is  in  direct  opposition  to  all  anatomical,  clinical,  and 
aatiological  facts.  We  grant  that  there  are  cases  where  the  pharynx  is  slightly 
affected,  while  the  croupous  inflammation  of  the  larynx  is  extreme ;  and  once  in 
a  great  while  the  diphtheritic  infection  results  in  croupous  laryngitis  and  trache- 
itis alone,  the  pharynx  escaping  disease'.  Still  the  proposition  that  there  are  two 
distinct  diseases,  "croup"  and  "diphtheria,"  is  absolutely  untenable.  In  the 
overwhelming  majority  of  cases  the  throat  is  first  affected  and  then  the  larynx. 
We  should  also  consider  how  easily  slight  lesions  in  the  phai-ynx  may  be  over- 
looked, especially  if  located  upon  the  posterior  surface  of  the  soft  palate  or  upon 
the  epiglottis.  Cases  of  what  is  called  "  ascending  croup,"  in  which  the  laryngeal 
affection  precedes  the  appearance  of  the  disease  in  the  pharynx,  are,  to  say  the 
least,  very  exceptional. 

Hoarseness  is  usually  the  first  indication  that  the  diphtheria  has  attacked  the 
larynx.  Then  follows  the  peculiar,  harsh,  ringing,  "  croupy  cough,"  so  dreaded  by 
the  parents,  and,  finally,  there  are  signs  of  beginning  laryngeal  stenosis.  Kespira- 
tion  is  not  much  accelerated,  but  is  labored,  and  the  accessory  muscles  of  respira- 
tion are  called  more  and  more  into  action.  The  child  becomes  more  restless  and 
anxious.  Its  face  grows  pale  and  livid.  Even  in  children  who  can  make  no 
definite  statement  as  to  their  subjective  sensations  these  symptoms  which  we 
have  mentioned  are  very  noticeable.     The  chief  cause  of  the  dyspna?a  is  undoubt- 


DIPHTHEEIA  Tl 

edly  the  mechanical  stenosis  due  to  the  croupous  deposit.  Paralysis  of  the  laryn- 
geal muscles  may  perhaps  be  a  factor.  If  portions  of  the  false  membrane  become 
partially  detached,  they  may  act  like  valves,  being  sucked  in  at  each  inspira- 
tion, and  pushed  aside  by  the  current  of  expired  air.  If  greater  stenosis  occurs, 
respiration  becomes  noisy,  resembling  snoring.  Inspiration,  particularly,  is  pro- 
longed and  "  sawing,"  and  is  attended  by  marked  depression  of  the  larynx  toward 
the  sternum.  An  important  diagnostic  point  is  the  drawing  in  during  inspiration 
of  the  supra-sternal  region,  the  epigastrium,  and  the  lower  part  of  the  sides  of  the 
thorax.  This  is  the  direct  result  of  the  obstructed  flow  of  air  into  the  lungs.  As 
the  lungs  do  not  expand  enough  to  correspond  to  the  inspiratory  dilatation  of  the 
thorax,  the  parts  mentioned  are  forced  in  by  atmospheric  pressure.  The  degree  of 
dyspnoea  may  vary  at  different  times.  The  false  membrane  may  be  loosened  and 
coughed  up,  rendering  respiration  easier  for  a  time,  till  fresh  exudations  or  dis- 
placements of  membrane  cause  renewed  distress.  Recovery  is  still  possible.  The 
membrane  may  be  expectorated  and  no  more  be  formed.  Unfortunately,  this 
happy  termination  rarely  occurs.  In  most  cases  the  symptoms  of  suffocation  in- 
crease more  and  more,  respiration  grows  quicker  and  more  superficial,  and  the 
child  becopies  more  and  more  stupefied  by  the  excess  of  carbonic  dioxide  in  the 
blood.  The  pulse  gets  very  small,  rapid,  and  irregular.  There  are  mild  convul- 
sions and  then  death. 

The  autopsy  in  these  cases  usually  discloses  that  the  croupous  infiammation 
has  extended  into  the  larger  bronchi  or  even  into  the  smaller.  The  lumen  of  the 
bronchioles  may  be  almost  completely  occluded  by  false  membrane.  This  croup- 
ous bronchitis  gives  rise  to  no  especial  auscultatory  phenomena  during  life, 
so  that  often  we  suspect  it  rather  than  diagnosticate  it.  Its  clinical  signifi- 
cance, however,  is  very  great,  since,  even  in  adults,  it  may  cause  death  by  suffoca- 
tion without  any  especial  stenosis  of  the  larynx.  If  it  is  present,  respiration  may 
not  be  materially  relieved  in  spite  of  tracheotomy. 

Beside  the  dangers  attendant  upon  the  local  extension  of  the  diphtheritic 
inflammation,  the  general  intoxication  of  the  body  must  be  regarded  as  the  second 
most  important  circumstance  in  our  general  estimate  of  the  disease.  As  men- 
tioned above,  the  diphtheria  bacilli  produce  an  extremely  poisonous  toxine,  which 
enters  the  circulation  and  which  may  give  rise  to  the  severest  symptoms.  Our 
knowledge  of  human  diphtheria  is  not  yet  so  far  advanced  that  we  can  state  posi- 
tively what  particular  symptoms  are  due  to  this  intoxication,  but  special  attention 
must  be  called  to  the  fact  that  the  general  symptoms  are  often  very  slight,  in  spite 
of  extensive  local  croupous  inflammation.  On  the  other  hand,  where  the  local  dis- 
ease is  relatively  slight,  severe  general  symptoms  sometimes  occur  which  may 
justly  be  referred  to  this  diphtheritic  intoxication.  Among  these  severe  general 
symptoms  are  somnolence,  which  may  increase  to  complete  sopor,  an  increase  in 
the  pulse  to  120  or  140,  progressive  cardiac  weakness,  and  collapse.  The  con- 
ditions are  different  in  those  cases  which  are  termed  septic  diphtheria.  Here 
the  local  disease  in  the  pharynx  usually  has  a  special  appearance :  instead  of  the 
croupous  deposits  we  see  a  deeper-seated  necrotic  destruction  of  mucous  mem- 
brane covered  with  a  foul-smelling,  greasy,  purulent  deposit  ("  gangrenous  diph- 
theria"). In  such  cases  the  lymph-glands  in  the  neck  are  almost  always  much 
swollen.  The  tongue  is  dry  and  fissured,  and  a  stinking  secretion  runs  from  the 
nose.  The  temperature  is  usually  not  very  high,  but  the  pulse  is  very  rapid  and 
small.  In  these  cases  there  is  certainly  a  secondary  septic  infection,  probably 
in  most  cases  from  streptococci,  as  in  scarlatinal  diphtheria  (vide  supra).  Gen- 
eral septic  intoxication  and  secondary  septic  inflammation  are  now  mixed  with 
the  original  disease,  and,  as  we  have  said,  it  is  often  hardly  possible  to  trace  in 
an  individual  case  the  precise  origin  of  the  morbid  condition. 

These  considerations  must  also  be  borne  in  mind  in  our  study  of  the  symptoms 


72  ACUTE   GEl^EEAL   INEECTIOUS   DISEASES 

manifested  in  other  organs  in  diphtheria.  We  must  iirst  mention  the  direct  local 
extension  of  the  original  specific  diphtheritic  process  to  the  neighboring  parts.  "We 
have  already  said  that  the  nose,  larynx,  trachea,  and  bronchi  are  often  involved, 
but  the  dense  squamous  epithelium  of  the  oesophagus  and  the  mucous  membrane 
of  the  stomach,  which  is  protected  by  its  secretion,  are  very  rarely  affected.  We 
must  add,  however,  that  diphtheria  often  extends  to  the  Eustachian  tube  and  mid- 
dle ear,  and  also  to  the  anterior  part  of  the  oral  cavity  (gums,  lips),  and  through 
the  nose  to  the  lachrymal  canal  and  the  conjunctiva.  The  latter  may  also  be 
affected  by  the  direct  conveyance  of  the  infectious  matter  by  the  finger,  etc. 
In  a  similar  way  diphtheria  may  sometimes  involve  the  external  genitals  (in 
girls)  or  any  accidental  wounds  or  injuries  of  the  skin,  such  as  blistered  sur- 
faces, etc. 

Of  the  internal  organs,  the  lungs,  heart,  and  kidneys  demand  chief  attention. 
In  the  lungs,  beside  croupous  bronchitis,  pneumonia  often  develops  in  severe  cases. 
This  is  usually  a  lobular  catarrhal  pneumonia,  more  rarely  lobar  croupous  pneu- 
monia. Although  we  can  not  absolutely  deny  that  the  pneumonia  may  some- 
times be  of  a  true  diphtheritic  nature,  the  majority  of  cases  of  pneumonia  de- 
veloping in  diphtheria  must  certainly  be  classed  as  secondary  affections,  due  to 
the  inhalation  and  development  of  secondary  agents  (probably  streptococci), 
which  may  readily  take  place.  After  the  original  diphtheria  has  disappeared  the 
secondary  lobular  pneumonia  may  long  prevent  recovery  or  even  cause  a  fatal 
termination  of  the  illness.  The  condition  of  the  heart  in  diphtheria  is  of  especial 
importance,  because  severe  functional  impairment,  probably  of  toxic  origin,  is 
common.  Even  when  the  fever  is  slight  the  pulse  may  sometimes  be  very  rapid, 
small,  and  often  irregular.  An  abnormal  slowness  of  beat  is  much  rarer.  It  is 
especially  to  be  borne  in  mind  that  even  in  apparently  mild  cases  there  may  be 
^ery  dangerous  cardiac  weakness.  Even  during  convalescence  we  repeatedly  see 
sudden  death  which  must  be  regarded  solely  as  "  heart-failure."  The  autopsy 
shows  that  gross  disease  of  the  heart  is  very  exceptional  in  diphtheria,  but  degen- 
eration of  the  muscular  fibers  and  little  interstitial  myocarditic  foci  of  secondary 
origin  are  often  found  in  severe  cases.  It  is  at  present  quite  impossible  to  esti- 
mate the  actual  clinical  significance  of  these  anatomical  changes,  since  it  is  at 
least  probable  that  disturbances  of  the  innervation  of  the  heart  cause  the  car- 
diac weakness  as  much  as  these  lesions  of  the  cardiac  muscle. 

Since  nephritis  is  especially  common  in  septic  diphtheria,  it  is  hard  to  decide 
whether  it  is  due  to  the  primary  disease  or  is  to  be  considered  a  secondary  compli- 
cation. Its  clinical  significance  is  not  very  great,  since  it  neither  materially 
modifies  the  general  picture  nor  has  any  definite  bearing  on  the  result  of  the 
disease.  (Edema,  ursemia,  etc.,  are  only  rarely  seen  in  diphtheritic  nephritis. 
The  macroscopic  changes  in  the  kidney  are  usually  very  slight.  Microscopically 
we  find  the  various  degenerative  conditions  of  acute  nephritis  (vide  infra). 

The  Nervous  Sequelae  of  Diphtheria. — The  convalescent  from  diphtheria  is 
liable  to  be  attacked  by  certain  nervous  sequelae.  Of  these,  diphtheritic  paralysis 
is  the  most  important.  It  appears  about  one  or  two  weeks  after  the  throat  trouble 
ceases,  or  perhaps  earlier,  and  it  is  quite  as  likely  to  follow  mild  cases  as  severe 
ones.  It  attacks  the  soft  palate  by  preference.  The  voice  becomes  nasal  and 
deglutition  difficult.  The  naso-pharynx  is  imperfectly  cut  off  during  the  act  of 
swallowing,  and  with  each  attempt  liquid  regurgitates  through  the  nose.  Usually 
the  pharyngeal  mucous  membrane  is  hyposesthetic  at  the  same  time,  and  de- 
prived of  its  reflex  excitability.  There  may  also  be  paralysis  of  the  vocal  cords 
upon  one  or  both  sides,  and  this  again  is  frequently  combined  with  angesthesia  of 
the  mucous  membrane  of  the  throat.  There  may  be  paralysis  of  the  ocular  mus- 
cles, of  which  those  controlling  accommodation  are  most  apt  to  be  affected,  render- 
ing the  vision  for  near  objects  imperfect.     Paralysis  of  the  muscles  of  the  trunk 


DIPHTHEEIA  73 

and  extremities  is  least  frequent,  but  it  may  be  very  extensive.  Sometimes  sev- 
eral of  these  parts  are  paralyzed  simultaneously.  Thus  we  see  quite  often  paral- 
ysis of  the  soft  palate  and  of  the  rauscles  of  accommodation  combined.  In  some 
cases  there  is  well-marked  ataxia  of  the  lower  limbs  with  or  without  paresis. 
This  renders  the  gait  very  uncertain  and  tottering,  the  tendon  reflex  is  almost 
always  abolished,  while  sensation  is  affected  slightly  if  at  all.  Very  rarely  diph- 
theria is  followed  by  contracture  of  the  hands  or  other  parts,  by  difficulty  in  artic- 
ulation and  paresis  of  the  bladder.  A  paralysis  of  the  pharynx  is  sometimes  left 
behind,  so  that  the  children  have  to  be  fed  for  weeks  through  an  o3Sophageal  tube. 
It  is  a  remarkable  fact  that  not  only  in  almost  every  case  of  the  nervous  dis- 
orders which  we  have  mentioned,  but  often  also  in  individuals  who  have  entirely 
escaped  them,  there  may  be  no  patellar  reflex  after  diphtheria  for  weeks  or  even 
months.  With  regard  to  the  pathological  state,  it  is  probably  a  degenerative  con- 
dition of  the  corresponding  peripheral  nerves,  not  only  in  the  post-diphtheritic 
paralysis,  bvit  also  in  the  cases  of  post-diphtheritic  ataxia  (see  the  chapter  on  mul- 
tiple neuritis).  These  degenerations  are  probably  due  to  the  poisonous  chemical 
action  of  certain  toxines  which  are  produced  directly  by  the  vital  processes  of 
the  diphtheria  bacilli.  It  is  therefore  of  great  interest  to  note  that  paralysis 
has  been  produced  experimentally  in  animals  by  the  action  of  diphtheritic  toxine 
by  Roux  and  Yersin  and  others.  The  prognosis  of  all  the  nervous  sequelae  of  diph- 
theria is  very  favorable,  and  even  in  severe  cases  complete  recovery  usually  takes 
place  in  the  course  of  a  few  weeks  or  months.  This  is  in  harmony  with  the  periph- 
eral nature  of  the  disease.  But  there  is  one  paralysis  which  is  highly  dangerous — 
that  of  the  heart,  as  already  mentioned.  It  may  occur  suddenly  during  convales- 
cence. Probably  it  is  analogous  to  the  other  nervous  derangements,  and  the 
result  of  degeneration  in  the  [nuclei  or]  fibers  of  the  pneumogastric. 

Diag'nosis. — The  physician  will  seldom  fail  to  recognize  a  case  of  actual  diph- 
theria if  he  pays  proper  attention.  The  characteristic  patches  and  the  severe  gen- 
eral and  local  symptoms  make  the  diagnosis  certain.  It  is  much  more  common  to 
mistake  other  forms  of  sore  throat,  particularly  in  adults,  for  diphtheria.  The 
most  deceptive  are  follicular  and  necrotic  tonsillitis  {vide  infra).  We  must  not 
suppose  that  every  white  spot  upon  the  tonsils  is  diphtheritic,  and  we  must  speak 
of  "  diphtheria  "  only  when  there  is  an  actual  croupous  inflammation  in  the  phar- 
ynx with  a  true  membranous  deposit.  The  practiced  eye  can  usually  distinguish 
at  the  first  glance  the  plugs  of  pus  limited  to  the  follicles  of  the  tonsils,  which  are 
usually  multiple,  and  also  the  slight  and  superficial  necrosis  of  mucous  membrane 
limited  to  the  tonsils  in  necrotic  angina.  Of  late,  it  has  often  been  proved  by 
bacteriological  examination  that  in  these  tonsillar  affections  there  are  no  diph- 
theria bacilli,  and  that  they  therefore  are  not  true  diphtheria. 

We  must  add,  however,  that  there  are  light  forms  of  true  diphtheria  in  which 
the  pathological  changes  assume  a  milder  form,  resembling  the  tonsillar  affections 
just  mentioned.  In  such  cases  we  are  therefore  certainly  justified,  especially 
in  dealing  with  children,  in  bearing  in  mind  the  necessary  precautions,  but  in  our 
opinion  the  physician  should  never  alarm  the  family  by  the  justly  dreaded  word 
"  diphtheria  "  without  sufficient  reason. 

An  absolutely  definite  diagnosis  between  diphtheria  and  the  other  tonsillar 
diseases  can  be  made  only  by  bacteriological  examination.  This  is  at  present 
still  too  difficult  a  matter  in  diphtheria  to  be  within  the  scope  of  every  physician, 
but  the  constantly  increasing  number  of  good  bacteriological  laboratories  renders 
it  possible  for  almost  every  physician  to  obtain  bacteriological  examination  of 
the  suspected  deposit  in  doubtful  or  important  cases.  An  experienced  clinician 
can  usually  make  a  correct  diagnosis  and  prognosis  even  without  a  "  culture." 

[When  the  membranes  are  confined  to  the  nose,  the  diagnosis  may  be  more  or 
less  difficult;  but  it  is  especially  in  cases  in  which  the  nasal  mucous  membrane  is 


Y4  ACUTE   GENERAL   INFECTIOUS    DISEASES 

involved  that  we  encounter  great  swelling  of  the  glands  at  the  angles  of  the  jaw. 
There  is  also  apt  to  be  a  thin,  acrid,  bloody,  or  sero-purulent  discharge. 

Jacobi  states  that  while  diffuse  pharyngeal  injection  may  or  may  not  point  to 
imminent  diphtheria,  marked  local  congestion  is  either  traumatic  or  diphtheritic. 
An  examination  of  the  urine  should  never  be  neglected  in  doubtful  cases :  in  diph- 
theria a  trace  of  albumen  is  very  common;  in  simple  or  follicular  sore  throat 
albumen  is  very  rare,  if  indeed  it  occurs  at  all.] 

Prognosis. — The  dubious  prognosis  of  true  diphtheria  is  universally  known, 
even  by  the  laity.  The  very  fact  that  the  best-developed  and  healthiest  children 
so  often  fall  victims  to  it  associates  the  name  diphtheria  with  the  saddest  mem- 
ories. There  are  indeed  many  mild  cases  which  recover  in  a  week  or  two,  and 
severer  ones  which  end  happily  in  three  or  four  weeks;  but  in  most  cases,  where 
the  process  extends  into  the  larynx,  or  the  symptoms  of  a  severe  constitutional  in- 
fection occur,  the  prognosis  must  be  regarded  as  very  serious.  Only  recently, 
however,  since  the  introduction  of  the  serum  treatment,  has  the  prognosis  even 
of  severe  diphtheria  become  considerably  more  favorable.  Formerly,  before  the 
serum  treatment,  it  was  regarded  as  a  relatively  favorable  result  if  one  half  of  the 
children  with  diphtheria  in  the  hospitals,  on  whom  tracheotomy  was  done,  re- 
covered !  Sixty  or  seventy  per  cent,  of  the  children  operated  on  often  died.  At 
present,  however,  the  mortality  of  the  tracheotomy  cases,  treated  at  the  same 
time  with  serum,  has  fallen  to  about  twenty-five  per  cent.,  and  these  are  only  the 
severe  cases  in  which  the  serum  treatment  was  begun  late.  The  improved  prog- 
nosis under  the  serum  treatment  appears  much  more  favorable  if  we  compare  the 
whole  number  of  cases  and  the  death-rate  of  diphtheria  before  and  after  the  in- 
troduction of  this  treatment  (Heubner,  Widerhofer,  Baginsky,  etc.). 

In  general,  diphtheria  is  to  be  regarded  as  the  more  serious  the  younger  the 
child  is.  In  later  childhood,  after  the  eighth  or  tenth  year,  the  number  of  dan- 
gerous cases  is  much  less.  The  description  of  the  symptoms  shows  sufficiently 
what  the  dangers  of  the  disease  are,  and  how  they  are  to  be  recognized.  We 
would  state  once  more  that,  even  in  apparently  mild  cases,  the  danger  of  sudden 
paralysis  of  the  heart,  though  fortunately  rare,  always  demands  the  greatest 
caution. 

Treatment. — Up  to  a  short  time  ago  it  was  impossible  to  say  anything  in  re- 
gard to  any  generally  recognized  treatment  of  diphtheria  which  was  really  effect- 
ive, but  very  recently  a  method  of  treatment  has  been  discovered,  chiefly  by 
the  important  and  interesting  investigations  of  Behring  and  Roux,  which  de- 
serves to  be  called  an  actual  specific.  If  further  observations  confirm  the  pres- 
ent results,  this  treatment  is  one  of  the  most  brilliant  and  triumphant  medical 
acquisitions. 

Behring  found,  in  continuing  the  important  discoveries  of  Pasteur,  Buchner, 
and  others,  that  certain  protective  matter  ("  antitoxine  ")  was  formed  in  the 
blood-serum  of  those  animals  (sheep,  goats,  horses,  etc.)  which  had  been  infected 
with  artificially  weakened  cultures  of  diphtheria  bacilli.  If  the  animal  survive 
the  milder  infection,  it  is  less  sensitive  to  a  severer  infection,  and,  finally,  by 
continued  inoculation,  it  may  even  become  completely  immune  to  the  severest  in- 
fection. The  blood-serum  of  such  immune  animals  can  now  be  used  in  the  treat- 
ment of  diphtheria  in  man.  The  treatment  is  simple,  and  consists  in  injecting 
the  serum  under  the  skin  of  the  child  who  has  diphtheria  by  means  of  a  carefully 
disinfected  syringe.  The  best  places  for  injection  are  the  anterior  chest  wall  or 
the  thigh.  Since  the  amount  of  serum  to  be  injected  is  usually  about  five  cubic 
centimetres,  we  should  use  a  special  syringe  which  is  not  too  small.  The  best  are 
made  like  a  Pravaz  syringe  with  an  asbestos  packing.  It  is  to  be  understood  that 
the  injections  must  be  made  with  the  strictest  aseptic  precautions.  There  are 
three  different  preparations  of  serum  in  the  market,  varying  according  to  the 


DIPHTHEEIA  75 

strength  of  their  immunizing  action.  In  fresh  and  milder  cases  we  inject  Serum 
I  ("  600  units  of  antitoxine  "),  in  severer  and  more  advanced  cases,  especially  if 
there  be  any  signs  of  disease  in  the  larynx,  we  use  at  once  Serum  II  ("  1,000  units 
■of  antitoxine")?  or  even  Serum  III.  According  to  the  severity  of  the  case,  or 
according  to  its  course,  we  repeat  the  same  injection  or  a  weaker  dose  of  the  same 
once  in  the  next  twelve  to  twenty-four  hours.  In  many  cases  of  moderate  severity 
a  single  injection  of  Serum  II  suffices.  The  favorable  action  of  the  serum  is 
shown  chiefly  by  the  fact  that  the  affection  does  not  extend  after  the  injection. 
The  existing  croupous  deposit  is  thrown  off  in  the  course  of  the  next  four  or 
five  days. 

The  serum  injections  have  no  injurious  action.  Urticaria  sometimes  occurs 
after  an  injection,  but  it  has  no  serious  significance.  There  is  no  proof  that 
albuminuria  and  post-diphtheritic  paralysis  are  seen  oftener  in  cases  treated 
with  serum  than  in  other  cases.  We  need  not  explain  further  that  the  serum  must 
be  ineffectual  in  severe  septic  diphtheria.  Taking  everything  into  consideration, 
it  is  therefore  the  duty  of  the  physician,  in  accordance  with  our  present  knowl- 
edge, to  use  the  serum  in  every  case  of  true  diphtheria  in  children.  At  present 
it  is,  of  course,  impossible  to  pronounce  a  final  judgment  on  the  whole  question; 
but  it  seems  beyond  a  doubt  that  we  physicians  are  standing  on  the  threshold  of 
an  entirely  new  era  in  the  treatment  of  infectious  diseases. 

It  is  of  the  greatest  practical  importance  that  the  serum  treatment  be  begun  as 
early  as  possible.  The  most  favorable  results  are  seen  in  children  treated  on  the 
very  first  days  of  the  disease.  [In  merely  suspicious  cases,  therefore,  it  would 
seem  wise  to  administer  the  antitoxine  at  once,  and  thus  give  the  patient  the 
benefit  of  the  doubt.- — V.]  Local  treatment  of  the  affected  places  in  the  phar- 
ynx at  the  same  time  is  unnecessary.  We  would,  however,  emphasize  the  impor- 
tance of  a  general  cleansing  and  disinfection  of  the  whole  oral  cavity  by  gargling 
and  rinsing  with  dilute  solutions  of  potassic  chlorate,  salicylic  acid,  corrosive  sub- 
limate (1  to  3,000),  etc.  Inhalations  naay  also  be  used,  with  caution,  for  the  same 
purpose.  It  is  also  very  important  to  watch  the  child's  nutrition  carefully  in 
order  to  keep  up  the  strength.  Milk,  eggs,  meat  juice,  small  quantities  of  wine, 
etc.,  are  most  advisable. 

Since  the  introduction  of  serum-therapy  all  the  former  methods  of  treatment 
have  been  quite  superseded.  This  is  especially  true  of  the  many  previous  attempts 
to  limit  the  morbid  process  and  cause  it  to  disappear  by  local  disinfection.  The 
practical  difficulties  in  carrying  out  any  really  effective  local  treatment  have 
always  prevented  the  general  recognition  of  the  value  of  caustics,  i^ainting,  etc. 
Nevertheless  some  remedies,  even  up  to  the  present  time,  are  still  recommended 
as  efficient,  especially  liquor  ferri  sesquichlorati  (pure  or  diluted),  dabbing  with 
a  l-to-1,000  sublimate  solution,  etc. 

Of  the  many  internal  remedies  which  were  formerly  tried  we  can  mention 
only  chlorate  of  potassium  and  iodide  of  potassium.  The  former  remedy  may  still 
be  recommended  and  may  be  given  in  teaspoonful  doses  of  a  solution  containing 
1  part  to  30  or  40  of  water. 

[The  tincture  of  the  chloride  of  iron  is  much  used  in  this  country  in  the  treat- 
ment of  diphtheria,  and  appears  to  be  of  real  service ;  but  it  must  be  given  in  large 
doses.  The  following  prescription  is  recommended  by  Jacobi,  whose  experience 
has  been  very  large,  for  a  child  of  two  years : 

]^   Tinct.  ferri  chloridi oij ; 

Potas.  chlorat gr.  xx ; 

Glycerin,  pur ,^j ; 

Aquae  ^r. 

M.  S. :  Teaspoonful  every  fifteen,  twenty,  or  thirty  minutes. 


76  ACUTE    GENEEAL  IJ^FECTIOUS   DISEASES 

Turpentine  is  better  as  an  inhalation  than  by  the  stomach;  a  teaspoonful  or  two 
of  the  oil  can  be  poured  in  water  kept  at  the  boiling  point  by  an  alcohol-lamp. 
The  whole  air  of  the  room  is  thus  charged  with  the  remedy.  ITo  drug  should  be 
used  with  disorders  the  stomach.  Tablet  triturates  containing  one  one-thou- 
sandth of  a  grain  of  corrosive  sublimate  can  be  allowed  to  melt  in  the  mouth  with 
the  greatest  freedom,  and  seem  sometimes  to  exert  a  distinctly  beneficial  local 
action.  The  dose  is,  however,  too  small  to  secure  the  systemic  effects  of  the  drug 
unless  the  case  is  a  mild  one  and  free  from  notable  dysphagia.] 

If  the  larynx  is  attacked,  and  if,  in  spite  of  the  serum  treatment,  the  conse- 
quent laryngeal  stenosis  threatens  to  cause  suffocation,  tracheotomy  is  our  only 
resort.  It  is  never  indicated  by  the  disease  itself  nor  by  the  severity  of  the  case^ 
but  only  by  persistent  obstruction  of  the  larynx.  It  is  therefore  not  invariably 
easy  to  decide  whether  tracheotomy  is  called  for  in  any  particular  case.  If  the- 
general  condition  be  bad  and  respiration  already  impaired,  it  is  often  very  diffi- 
cult to  determine  whether  laryngeal  stenosis  exists.  Tracheotomy  will  be  of  no 
avail  if  the  croup  has  already  extended  to  the  bronchi,  or  if  the  dangerous  condi- 
tion of  the  patient  is  due  to  the  severity  of  the  constitutional  infection  or  to 
incipient  paralysis  of  the  heart.  We  have  already  said  that,  since  the  introduc- 
tion of  the  serum  treatment,  the  prognosis  of  diphtheria  has  become  better  even 
in  the  tracheotomy  cases.  How  tracheotomy  is  performed,  and  in  what  the  after- 
treatment  consists,  must  be  learned  in  the  text-books  on  surgery,  where  we  will 
also  find  the  necessary  description  of  the  so-called  intubation  of  the  larynx. 

Intubation,  as  devised  by  Dr.  O'Dwyer,  is  a  procedure  which  makes  a  distinct 
advance  in  the  treatment  of  laryngeal  stenosis.  In  permitting  the  free  access  of 
air  to  the  trachea,  intubation  may  save  life  without  resort  to  the  serious  operation 
of  tracheotomy ;  or  it  may  tide  over  a  time  until  tracheotomy  becomes  absolutely 
necessary  or  until  the  consent  of  the  parents  can  be  obtained  to  the  use  of  the 
knife.    In  hopeless  cases  it  may  promote  euthanasia.    " 

If  severe  pulmonary  symptoms  occur  in  diphtheria,  we  should  use  first  of  all 
wet  packs  of  the  whole  body  or  tepid  baths  with  cool  affusions.  Such  cutaneous 
stimulation  refreshes  and  enlivens  the  whole  nervous  system,  and  we  should  there- 
fore try  it  also  in  the  severe  cases  with  secondary  septic  infection.  In  septic 
diphtheria  we  must  also  pay  especial  attention  to  the  condition  of  the  heart.  So 
far  as  is  possible  we  should  try  to  avert  the  threatening  cardiac  paralysis  by  stimu- 
lants, such  as  wine,  camphor,  and  strophanthus. 

The  nervous  sequelae  of  diphtheria  are  best  treated  with  the  constant  current. 
As  an  internal  remedy,  iron  is  good,  and  also  nux  vomica  or  strychnine.  The  last 
may  be  given  subcutaneously,  if  desired,  in  doses  of  gv.-io-^o  (grm.  0.001-0.002). 

The  prophylaxis  of  diphtheria  demands  that  every  child  with  diphtheria  be 
absolutely  isolated  from  healthy  children.  Behring  [and  many  othe*-s]  believe 
that  a  healthy  child  may  be  positively  protected  from  infection  by  diphtheria  for 
two  or  three  weeks  by  the  injection  of  a  small  dose  of  serum — the  whole  or  one 
half  of  Dose  I — that  is,  about  three  hundred  units  of  antitoxine.  It  is,  of  course, 
very  hard  to  judge  of  this,  and  for  the  present,  therefore,  it  must  be  left  to  the 
individual  judgment  of  the  physician  in  what  cases  he  will  try  prophylactic  injec- 
tions of  serum. 

[Diphtheria  is  a  disease  which  involves  commonly  much  exhaustion,  and  too 
much  stress  can  hardly  be  laid  on  the  importance  of  administering  the  maximum 
amount  of  nourislnnent  in  the  most  assimilable  and  easily  swallowed  forms  from 
the  start. 

It  is  also  important  to  give  stimulants  early  in  most  cases,  not  waiting  for 
signs  of  exhaustion.  Enormous  quantities  of  brandy  can  often  be  given  to  small 
children  without  the  slightest  toxic  effect.  ISTo  general  rule  can  be  laid  down; 
the  requirements  of  each  case  miist  be  studied  and  met. 


INFLUENZA  7Y 

When  painful  deglutition  interferes  with  nutrition,  peptonized  milk,  eggs, 
brandy,  and  the  like,  must  be  given  by  the  rectum.  Rectal  alimentation  and 
stimulation  and  feeding  with  the  oesophageal  tube  are  also  to  be  resorted  to  in 
cases  of  post-diphtheritic  paralysis  o_f  the  oesophagus.] 


CHAPTER   XI 

INFLUENZA 

{La  Gri])pe) 

Influenza  is  a  specific,  acute,  infectious  disease  which  is  especially  distin- 
guished by  the  occasional  enormous  extent  of  its  epidemics.  While  often  years 
and  decades  pass  without  any  especial  attention  being  called  to  the  disease,  sud- 
denly cases  of  it  will  appear  with  such  frequency  that  the  largest  part  of  the 
population  is  attacked,  and  the  disease  may  better  be  described  as  pandemic  than 
■epidemic.  Pandemics  of  influenza  can  be  traced  back  with  certainty  into  the  six- 
teenth century.  In  the  present  century  the  influenza  during  the  years  1830-33 
traversed  almost  all  of  Asia  and  of  Europe,  then  later  there  appeared  numerous 
smaller  epidemics,  but  these  aroused  general  attention  so  little  that  the  disease, 
upon  its  last  pandemic  appearance  in  the  winter  of  1889-90,  was  almost  unknown 
to  many  physicians.  Since  that  time  the  disease  seems  never  to  have  wholly 
■disappeared,  as  a  few  cases,  and  occasionally  small  groups  of  cases,  are  constantly 
seen. 

.Etiology. — The  organized  agents  of  influenza  are  still  not  positively  known, 
but  R.  Pfeiffer  has  invariably  found  in  the  bronchial  secretion  of  patients  with 
the  "  catarrhal  form "  of  influenza  {^vide  infra)  a  definite  form  of  very  small 
bacilli  with  rounded  ends  which  stain  darker  than  the  central  portion.  These 
bacilli,  which  are  either  free  in  the  mucus  or  in  the  pus-cells,  are  very  probably 
of  significance  as  a  cause  of  the  disease.  The  influenza  bacilli  very  soon  die  if 
•dried,  and  also  if  put  in  water. 

In  all  probability  the  infection  is  usually  due  to  inhaling  the  germs.  The 
bacilli  seem  to  appear  at  certain  times  over  an  immense  territory,  so  that  they 
or  their  spores  are  scattered  everywhere  through  a  large  extent  of  country. 
Many  observations  upon  the  appearance  of  the  disease  in  isolated  institutions 
(convents  and  the  like)  render  it  very  probable  that  the  poison  may  also  be 
carried  by  a  person  suffering  from  the  influenza  to  another  in  regions  pre- 
viously unaffected.  Nevertheless,  this  contagious  manner  of  spreading  plays  no 
great  role  in  comparison  with  the  direct  infection  from  the  outer  world,  this  latter 
mode  being  everywhere  possible  during  an  epidemic  of  influenza. 

There  is  scarcely  any  reason  for  speaking  of  especial  predisposing  causes  of 
influenza,  inasmuch  as  at  the  time  of  a  well-marked  epidemic  the  overwhelm- 
ing majority  of  the  population  are  attacked,  both  the  healthy  and  the  diseased,  the 
vigorous  and  the  feeble.  Sex  certainly  makes  no  difference,  and  age  only  to  this 
extent,  that  the  disease  is  seen  more  rarely  in  little  children  under  one  year  of  age 
than  in  older  children  and  adults.  That  catching  cold  has  no  special  astiological 
significance  is  evident  from  the  fact  that  influenza  often  appears  in  patients  who 
are  already  sick  in  bed. 

It  should  finally  be  mentioned  that  animals  also,  and  in  particular  horses,  may 
be  attacked  by  the  influenza ;  but,  nevertheless,  it  is  as  yet  a  doubtful  question 
whether  all  the  diseases  in  animals  which  are  described  under  this  name  are  actu- 
ally identical  with  genuine  influenza. 

Symptoms  and  Clinical  History. — The  best  general  idea  of  the  extremely 
manifold  symptoms  of  the  disease  will  be  obtained  if  we  bear  in  mind  that  the 


78  ACUTE    GENERAL   Il^EECTIOUS    DISEASES 

influenza  causes  both,  a  marked  infectious  (or  toxic)  general  constitutional  dis- 
turbance of  the  body,  and  also  certain  local  lesions  with  local  symptoms.  The 
clinical  picture  therefore  varies  greatly  according  to  the  predominance  of  one  or 
the  other  group  of  symptoms,  and  also  according  to  the  special  form  of  the  local 
disease.  ^ 

The  onset  of  influenza  is  generally  rather  sudden.  As  a  rule  the  marked  cases 
begin  with  rather  high  fever,  ushered  in  with  a  chill,  violent  headache,  marked 
constitutional  depression,  and  usually  considerable  pain  in  the  back  and  loins. 
The  weakness  of  the  patient  may  be  so  great  that,  even  if  a  vigorous  individual, 
he  will  at  once  take  to  his  bed.  Severe  nervous  symptoms,  such  as  stupor  and  de- 
lirium, are  exceptional.  Sometimes,  but  not  very  often,  there  is  initial  vomiting. 
The  backache  is  often  associated  with  pains  in  the  muscles  and  joints.  Oppressive 
pain  in  the  eyes  is  quite  characteristic  also.  This  is  particularly  felt  upon  moving 
the  eyeballs,  and  therefore  is  probably  located  in  the  external  muscles.  The  spleen 
is  occasionally  somewhat  swollen,  but  any  great  increase  in  its  size  is  excep- 
tional. 

If  the  clinical  symjDtoms  as  the  case  progresses  are  mainly  limited  to  the  above- 
named  constitutional  symptoms — fever,  languor,  headache,  pain  in  the  muscles — 
we  may  speak  of  a  "  typhoidal  form  "  of  the  disease.  Usually,  however,  certain 
local  symptoms  put  in  an  early  appearance,  and  it  is  especially  the  respiratory 
apparatus  which,  is  attacked.  The  precise  symptoms  vary  considerably  in  different 
cases.  Sometimes  the  upper  portion  of  the  respiratory  tract,  the  nose,  larynx,  and 
trachea  are  involved ;  sometimes,  from  the  start,  the  smaller  bronchi.  In  the  first 
instance  there  is  marked  coryza  or  hoarseness,  in  the  other  case  there  is  cough, 
due  to  a  dry  bronchitis,  which  can  be  easily  detected  upon  auscultation,  and  which 
involves  especially  the  lower  portion  of  the  lungs.  If  these  local  symptoms  out- 
weigh the  constitutional,  the  case  is  described  as  belonging  to  the  "  catarrhal 
f  onn  "  of  influenza. 

Sometimes  the  influenza  is  localized  in  the  digestive  apparatus.  This  "  gas- 
tro-intestinal  form  "  is  much  rarer  than  the  catarrhal.  In  this  case,  in  addition 
to  the  more  or  less  strongly  characterized  constitutional  symptoms,  there  is 
marked  disturbance  of  the  stomach  and  intestines,  as  shown  particularly  by 
nausea  with  persistent  vomiting,  diarrhoea,  abdominal  pain,  etc.  In  one  case 
we  observed  jaundice.  We  may  also  mention  in  this  connection  the  appearance 
of  an  initial  pharyngitis. 

The  pains  in  the  back,  loins,  and  extremities  already  mentioned  may  persist 
with  unusual  violence,  and  this  peculiar  form  of  the  disease  is  known  as  the 
"  rheumatoid."  The  muscles  and  the  muscular  attachments  are  probably  the  chief 
seat  of  these  pains,  which  may  be  so  violent  that  the  patient  is  unable  to  lie  com- 
fortably, and  sometimes  keeps  up  a  continual  moaning.  The  loins,  in  particular, 
may  be  the  seat  of  most  acute  pain,  also  the  upper  arms,  the  knees,  the  thighs,  and 
the  eyes.  Objective  changes  in  the  jjainful  parts,  such  as  swelling  of  the  joints, 
are  scarcely  ever  seen,  nor  are  the  nerve-trunks  as  a  rule  especially  sensitive  to 
pressure.     The  painful  muscles  are  usually  weaker  than  normal. 

The  grouping  of  the  clinical  varieties  of  influenza  under  the  four  forms  al- 
ready named  affords  a  general  idea  of  the  manifold  symptoms  of  the  disease,  but 
this  division  into  separate  forms  must  not  be  carried  out  too  strenuously,  for  in 
reality  many  cases  of  the  disease  occur  which  present  transition  fonns  and  com- 
binations of  the  various  groups  of  symptoms.  Moreover,  in  all  the  forms  a  dis- 
tinction must  be  made  between  mild  and  severe  attacks,  for  in  influenza,  just  as 
in  most  other  infectious  diseases,  there  are  many  rudimentary  and  mild  cases  as- 
well  as  the  fully  developed  ones,  and  some  could  not  be  properly  interpreted  but 
for  the  presence  of  the  epidemic. 

The  duration  of  the  disease  is  best  determined  by  the  duration  of  the  fever. 


INFLUENZA  T9 

In  the  very  mildest  cases  there  may  be  no  fever  whatever,  or  simply  a  slight 
evening  rise  of  temperature.  As  a  rule,  there  is  a  moderate  fever,  between 
101.5°  and  103°  F.  (38.5°  and  39.5°  C),  although  higher  temperatures  even  to 
104°  F.  (40°  C.)  and  more  are  not  infrequent.  In  the  beginning  of  every  severe 
attack  the  fever  rises  abruptly.  After  a  duration  of  several  days  (four  to  seven) 
it  may  fall  again  in  a  manner  approaching  a  crisis.  More  frequently,  espe- 
cially when  there  exists  diffuse,  catarrhal  trouble  in  the  lungs,  the  fever  ends  by 
lysis.  With  comparative  frequency  there  are  found  to  be  noticeable  deviations 
in  the  temperature  curve ;  thus,  for  example,  the  high  fever  of  the  onset  sinks  on 
the  second  or  third  day,  to  be  followed  by  an  almost  afebrile  period  of  one  or  two 
days,  whereupon  a  marked  rise  of  temperature  ensues.  With  this  change  in  the 
temperature  there  are  usually  also  corresponding  variations  in  other  symptoms. 

We  see,  then,  that  the  duration  of  simple,  uncomplicated  influenza  is  in  the 
mild  eases  about  three  or  four  days,  in  the  severer  cases  about  seven  to  ten  days. 
To  be  sure,  we  should  also  consider  in  this  connection  that  convalescence  is  often 
surprisingly  slow,  so  that  the  after-pains  (as  it  were)  of  the  disease  are  felt  for 
weeks.  These  consist,  for  instance,  in  a  certain  degree  of  debility,  and  in  pain- 
fulness  of  the  muscles.  Sometimes  also  there  are  complete  relapses,  so  that  di- 
rectly or  a  short  time  after  the  disease  has  ended  the  symptoms  begin  anew.  The 
special  form  of  the  disease  may  change  in  this  case,  so  that,  for  example,  the  re- 
lapse of  an  influenza  with  predominant  constitutional  symptoms  assumes  the  pro- 
nounced catarrhal  form.  Again,  during  the  same  epidemic  it  is  not  very  rare  for 
a  patient  to  suffer  from  two  attacks  of  influenza  separated  by  a  considerable  inter- 
val of  time. 

Complications  and  Sequelae. — While  all  the  symptoms  of  influenza  which  we 
have  thus  far  described  are  the  direct  effects  of  the  original  pathogenic  cause,  the 
majority  of  the  frequent  complications  are  undoubtedly  dependent  upon  the  in- 
gress of  secondary  infection.  The  system  when  attacked  by  influenza  is  greatly 
exposed  to  these  secondary  influences,  and  almost  all  the  dangerous  and  tedious, 
cases  of  influenza  become  such  only  because  of  a  mixed  infection  of  this  sort. 
This  is  particularly  true  of  the  lungs,  in  which  secondary  disease  occurs  most  fre- 
quently— sometimes  even  in  the  flrst  days  of  illness,  but  also  in  other  cases  later. 
The  conditions  here  are  similar  to  those  seen  in  measles  and  whooping-cough. 
The  simple,  mild  catarrh  belongs  to  the  original  disease;  the  severe  pulmonary 
affections  are,  however,  invariably  secondary  complications  occasioned  by  new 
pathogenic  influences.  These  influences  are  not  always  the  same.  According  to 
the  investigations  of  Ribbert,  Finkler,  and  others  it  is  chiefly  the  pneumonia  dip- 
lococcus  and  the  streptococcus  which  are  the  true  excitants  of  the  secondary  pneu- 
monia seen  in  influenza.  These  cases  of  pneumonia  are  either  extensive  catarrhal 
pneumonia  especially  affecting  the  lower  lobes,  or  more  rarely  croupous  pneu- 
monia with  its  characteristic  sputum.  We  must  also  add  that  the  influenza 
bacilli  themselves  may  excite  a  lobular  pneumonia,  which  shows  a  marked  puru- 
lent character.  If  pneumonia  be  added  to  influenza,  the  former  overshadows  the 
whole  picture.  The  patient  is  oppressed  for  breath,  has  a  severe  cough  with  pro- 
fuse expectoration,  looks  pale  or  cyanotic,  and  suffers  from  high  fever.  These 
symptoms  persist  for  two  or  three  weeks,  and  then  gradually  abate.  It  is  in  this 
way  that  influenza  becomes  dangerous  for  elderly  and  feeble  or  sickly  persons. 
With  noticeable  frequency,  pleurisy  with  effusion  is  conjoined  with  the  influ- 
enza pneumonia.  The  exudation  is  generally  serous,  but  exceptionally  it  is  puru- 
lent. 

Complications  in  other  organs  are  less  frequent.  We  would  make  especial 
mention  of  purulent  otitis  media  and  keratitis  and  other  severe  diseases  of  the 
eye.  We  haVe  several  times  observed  acute  nephritis,  but  this  has  always  pursued 
a  mild  course.    Among  cutaneous  eruptions  herpes  labialis  is  a  frequent  phenome- 


80  ACUTE    GE^^ERAL  INFECTIOFS    DISEASES 

non  in  all  forms  of  influenza,  even  the  milder.  Other  exanthems,  such  as  urticaria 
and  roseola,  are  much  less  frequent.  Many  of  the  complications  named  may  con- 
tinue even  after  the  fever  and  all  other  symptoms  have  ceased,  so  that  they  must 
be  regarded  as  sequelse.  This  is  particularly  true  of  the  diseases  of  the  ear  and 
eye  and  of  persistent  bronchitis,  but  only  rarely  of  a  pneumonia  assuming  the 
chronic  form.  An  important  and  for  the  patient  a  troublesome  and  painful 
sequel  is  furunculosis,  especially  if  some  of  the  boils  are  located  in  the  axilla  or 
near  the  anus.  Very  often  neuralgic  pains  in  the  distribution  of  the  trigeminus 
or  in  the  course  of  the  sciatic  or  other  nerves  will  persist  for  a  considerable  time 
after  the  influenza  has  ceased;  but  these  pains  may  sometimes  be  located  in  the 
muscles;  thus,  for  example,  the  frequent,  persistent,  and  troublesome  pain  in  the 
eyes.  In  a  few  cases  more  severe  nervous  sequelse,  such  as  spinal  symptoms  and 
psychoses,  have  been  seen  after  infltienza.  A  special  form  of  acute  hsemorrhagic 
encephalitis  (vide  infra)  has  been  thought  to  have  a  relation  to  influenza. 

Diagnosis. — The  diagnosis  of  influenza  is  in  general  not  difiicult  if  one  has  to 
deal  with  a  w^ell-marked  case  at  the  time  of  an  influenza  epidemic.  The  charac- 
teristic initial  symptoms  of  fever,  headache,  and  pain  in  the  loins  are  to  be  con- 
sidered flrst  of  all.  Their  onset  is  much  more  rapid  than,  for  example,  in  typhoid 
fever.  Later  on  the  pain  in  the  various  muscles  as  well  as  the  catarrhal  symp- 
toms are  the  most  characteristic  phenomena. 

Uncertainties  and  errors  in  diagnosis  may  arise  from  the  fact  that,  on  the  one 
hand,  we  are  disposed  at  the  time  of  an  epidemic  to  call  almost  all  the  catarrhal 
and  indefinite  mild  affections  we  see  "  influenza,"  while,  on  the  other  hand,  when 
there  is  no  epidemic,  we  can  not  positively  distinguish  the  sporadic  "  cases  like 
influenza  "  from  the  ordinary  acute  febrile  bronchitis,  etc.  It  is  indeed  very 
possible,  a  priori,  that  different  morbid  agents  may  produce  similar  mild  acute 
diseases  of  the  accessible  mucous  membranes.  In  such  cases,  with  pronounced 
general  symptoms,  high  fever,  etc.,  we  must  often  be  content  with  the  diagnosis 
of  "infectious"  laryngitis,  bronchitis,  etc.,  without  being  able  to  decide  defi- 
nitely whether  the  case  is  to  be  classed  setiologically  with  influenza  or  not.  At 
any  rate  in  practice  we  should  not  abuse  the  diagnosis  of  influenza. 

Prognosis. — For  an  individual  who  is  healthy  and  vigorous,  influenza  is  not  a 
dangerous  disease,  even  in  its  severer  forms;  for  elderly  persons  or  invalids  it 
may,  however,  be  a  serious  affection.  Patients  with  heart  disease  or  pulmonary 
disease,  or  those  suffering  from  chronic  nervous  troubles,  sometimes  succumb  to  it ; 
so  that  the  general  mortality  at  the  time  of  a  great  epidemic  of  influenza  is 
always  considerably  increased.  The  above-enumerated  pulmonary  complications 
are  by  far  the  most  dangerous ;  less  often  is  a  fatal  termination  caused  by  general 
or  cardiac  weakness.  The  above-mentioned  nervous  sequelse  are  also  to  be  con- 
sidered in  prognosis. 

Treatment. — IsFo  specific  remedy  for  the  disease  is  known.  Many  physicians 
maintain  that  the  exhibition  of  calomel  at  the  beginning  of  the  attack  decidedly 
shortens  its  course,  but  confirmatory  experience  is  wanting.  In  general  we  must, 
therefore,  pursue  a  purely  symptomatic  method  of  treatment.  For  the  initiatory 
fever,  the  headache,  and  the  pain  in  the  loins,  antipyrine  is  sometimes  a  good 
remedy,  and  the  same  may  be  said  also  of  phenacetine,  antefebrine,  and  especially 
salipyrine.  These  drugs  are  also  prescribed  for  the  persistent  pains  in  the  mus- 
cles which  come  on  later.  Soothing  liniments  and  ointments  may  be  employed, 
with  friction,  for  the  same  purpose.  The  treatment  of  the  pulmonary  complica- 
tions is  according  to  the  established  methods.  Morphine  is  mainly  used  for  the 
troublesome  cough.  Apomorphine,  senega,  and  other  expectorants  may  be  em- 
ployed, and,  if  indicated,  external  remedies  such  as  an  ice-bag  or  dry  cupping. 
If  the  patient  becomes  very  feeble,  stimulants  such  as  [strychnine],  champagne, 
and  strophanthus  are  demanded. 


DYSENTEEY  81 

CHAPTEE   XII 
DYSENTERY 

jSltiology. — By  "  dysentery  "  is  meant  a  disease  of  the  colon,  which  appears 
sporadically,  but  more  often  in  epidemics;  it  is  excited  by  infection  with  an 
organized  pathogenic  poison,  about  which  we  have  as  yet  no  definite  knowledge ; 
and  the  infection  is  probably  at  first  a  local  one.  From  the  investigations  of 
various  men,  especially  Kartulis,  it  seems  very  probable  that  a  certain  form  of 
amoeba  must  be  regarded  as  the  cause  of  "  endemic  tropical  dysentery."  At  least 
in  endemic  dysentery  we  almost  invariably  find,  both  in  the  stools  and  in  the 
walls  of  the  dysenteric  intestinal  ulcers  and  in  the  dysenteric  abscesses  of  the 
liver,  many  amoebae  (amoeba  coli),  which  are  never  found  in  any  other  intes- 
tinal affection.  Dysentery  may  also  be  artificially  produced  in  cats  by  means  of 
f  seces  containing  amoebse.  In  dysentery  as  it  occurs  in  Germany,  however,  we  do 
not  apparently  find  amcebse  in  the  stools  as  a  rule,  although  even  in  Germany 
Quincke  and  others  have  described  certain  cases  of  "  acute  enteritis  "  ("  amoebic 
enteritis  ")  in  which  there  were  a  large  number  of  amoebse.  The  question  of 
the  excitants  of  dysentery  therefore  needs  further  investigation,  and  it  is  not 
impossible  that  several  intestinal  affections  with  different  aetiology  have  thus 
far  been  included  under  the  name  of  dysentery,  especially  in  the  tropics.  The 
true  home  of  dysentery  is  in  warmer  and  tropical  countries,  where  the  disease  is 
much  more  violent  and  widespread  than  here.  For  example,  the  mortality 
among  the  soldiers  of  the  Anglo-Indian  army  due  to  dysentery  is  said  to  be  at 
times  thirty  per  cent,  of  the  entire  number  of  deaths.  In  our  climate  most  of 
the  epidemics  occur  at  the  end  of  summer  and  in  autumn.  Endemic  influences 
are  certainly  important.  The  special  conditions  in  some  places  are  evidently 
very  favorable  for  the  development  and  dissemination  of  dysenteric  germs,  and 
there  are  other  places  equally  unfavorable.  There  can  be  no  other  explanation 
of  the  immunity  of  some  localities  contrasting  with  the  great  prevalence  of  the 
disease  in  others.  How  infection  occurs  we  do  not  yet  know.  Many  observations, 
especially  in  southern  countries,  support  the  idea  that  the  germs  may  be  taken 
into  the  system  by  drinking  water.  Dysentery  does  not  seem  to  be  directly 
contagious;  but  that  it  can  be  spread  through  the  medium  of  the  fsecal  dejections 
of  the  sick — e.  g.,  from  privies,  chamber-vessels,  and  bed-linen — is  very  probable. 
Many  cases  were  formerly  referred  to  catching  cold  or  to  some  error  in  diet ;  but 
we  must,  of  course,  regard  these  merely  as  predisposing  influences. 

The  objective  pathological  lesion  of  the  colon,  in  all  severe  cases,  consists  in 
a  pronounced  croupous-diphtheritic  inflammation.  The  remarks  as  to  the  general 
pathology  of  such  inflammations  made  in  the  preceding  chapter  are  equally  ap- 
plicable to  the  analogous  dysenteric  inflammation.  In  this  case,  too,  there  is  first 
a  destruction  of  the  epithelium  and  then  the  formation  of  a  fibrinous  exudation 
occupying  its  place,  and  penetrating  down  into  the  tissue  of  the  mucous  mem- 
brane itself.  At  the  same  time  there  is  an  intense  purulent  infiltration  of  the 
mucous  and  submucous  tissue,  accompanied  by  extensive  ecchymoses.  In  the 
most  virulent  cases  the  macroscopic  appearances  are  marked  thickening  of  the 
whole  wall  of  the  intestine,  congestion  of  the  serous  layer,  and  the  conversion  of 
the  inner  surface  into  a  mottled,  dark-red,  irregularly  roughened  area  of  ulcera- 
tion. The  disease  may  be  confined  to  the  rectum  and  the  sigmoid  flexure,  but  in 
severer  cases  it  involves  the  entire  colon  as  far  as  the  ileo-cascal  valve,  or  even 
extends  to  the  lower  portion  of  the  ileum.  Besides  this  severe  form  of  diph- 
theritic or  even  gangrenous  dysentery,  there  is  a  milder  variety,  termed  catarrhal 
dysentery.  In  this  the  mucous  membrane  is  found  in  a  state  of  intense  purulent 
6 


82  ACUTE    GENERAL   INFECTIOUS    DISEASES 

inflammation,  with  ecchymoses.  Even  here  little  masses  of  croupous  exudation, 
which  can  be  torn  off,  have  replaced  the  epithelium;  but  they  never  form  con- 
tinuous layers  of  great  extent.  There  is  no  sharp  boundary-line  between  the  two 
forms,  the  milder  catarrhal-croupous  and  the  severer  diphtheritic  dysentery. 
ISTumerous  transitional  and  combined  varieties  exist. 

We  must  remark,  in  conclusion,  that  precisely  the  same  anatomical  changes 
as  are  presented  in  true  dysentery  may  result  from  other  causes.  Important 
among  these  is  persistent  faecal  impaction  in  the  rectum,  which,  by  a  purely 
mechanical  effect  upon  the  epithelium,  may  excite  a  diphtheritic  inflammation  in 
the  mucous  membrane.  And  any  severe  constitutional  disease  whatsoever,  such  as 
typhoid  fever,  measles,  small-pox,  septicaemia,  or  phthisis,  may  be  attended  by  a 
so-called  "  secondary  dysentery."  This  is  most  frequent  in  hospitals.  Whether 
it  has  the  same  aetiology  as  genuine  dysenteiy  is  uncertain. 

Clinical  History. — Throughout  the  entire  illness  the  most  prominent  symp- 
toms are  intestinal.  There  may  be  first  of  all  some  slight  irregularity  of  the 
bowels  for  a  few  days,  and  then  appears  a  moderate  diarrhoea.  The  stools  are  at 
first  feculent,  although  thin,  and  number  two  to  six  daily.  After  a  few  days 
the  discharges  increase  in  frequency,  and  become  extremely  characteristic. 

The  stools  are  very  frequent,  occurring  ten  to  twenty,  and  even  sixty  or  more, 
times,  in  twenty-four  hours.  In  severe  cases  there  may  be  a  distressing  and  almost 
constant  desire  to  evacuate  the  bowels.  After  every  operation,  and  to  some  extent 
during  it,  there  is  tenesmus  attended  by  intense  burning  pain  in  the  anus.  The 
stools  soon  lose  their  usual  feculent  character  in  great  part  if  not  entirely.  They 
become  scanty,  so  that  not  more  than  about  half  an  ounce  is  evacuated  each 
time.  For  the  most  part  they  usually  consist  of  a  sero-mucous  fluid,  in  which 
are  suspended  numerous  shreds  and  particles  of  varying  size.  These  are  blood- 
stained bits  of  mucus,  little  coagula  of  blood,  and  necrosed  pieces  of  mucous  mem- 
brane. One  or  another  of  these  constituent  parts  may  predominate,  so  that  there 
may  be  slimy,  purulent,  or  bloody  stools,  or  all  sorts  of  combinations  of  these 
varieties.  We  often  find,  besides,  a  few  small  masses  of  faeces,  usually  covered 
with  mucus.  We  sometimes  see  numerous  clumps  of  mucus,  resembling  sago  or 
frog's  spawn ;  they  are  probably  mucous  casts  of  the  follicles.  Under  the  micro- 
scope the  greater  part  of  the  dysenteric  discharge  is  seen  to  consist  of  pus-corpus- 
cles and  blood.  There  are  also  cylinder  epithelium  and  an  enormous  amount  of 
detritus,  and  the  bacteria  of  putrefaction.  A  purely  dysenteric  stool  has  no  bad 
odor,  except  that  in  the  worst  cases  of  gangrenous  dysentery  the  discharges  become 
blackish  and  extremely  offensive. 

The  rectal  tenesmus  may  be  accompanied  by  a  cramp-like  pain  during  micturi- 
tion. There  are  often  violent  attacks  of  colic.  The  abdomen  is  usually  rather 
tense,  aud  tender  on  pressure  along  the  line  of  the  colon,  but  without  tympanites. 
The  anus  may  be  red,  inflamed,  and  excoriated.  Gastric  symptoms  are  on  the 
whole  infrequent,  if  we  except  the  complete  anorexia  which  exists  in  all  severe 
cases.  Sometimes  there  is  repeated  vomiting.  Occasionally  hiccoughs  prove  dis- 
tressing.    The  tongue  usually  has  a  dry,  greasy  coating. 

The  symptoms  just  depicted  last  about  a  Aveek  or  ten  days.  If  the  case  is  of 
much  intensity,  the  general  condition  is  also  greatly  affected.  The  patient  seems 
much  collapsed,  and  is  very  languid  and  feeble,  with  a  small  and  rapid  pulse. 
The  skin  becomes  cool  and  rough,  the  voice  weak  and  hoarse.  There  is  pain  in 
the  muscles.  The  patient  wastes  away.  The  temperature  has  little  that  is  char- 
acteristic or  typical.  In  many  cases  there  is  no  fever  at  all,  and  the  temperature 
may  even  be  subnormal.  In  most  cases,  however,  there  is  an  irregular  fever 
seldom  exceeding  104°  (40°  C),  and  having  remissions. 

In  the  worst  cases  the  general  weakness  may  increase  more  and  more,  and 
death  occur;   but  with  us  a  favorable  termination  is  much  more  frequent.     The 


DYSEi^TERT  83 

distress  gradually  diminishes,  the  stools  assume  more  and  more  of  a  feculent  char- 
acter, the  patient  becomes  stronger,  and  after  one  and  a  half  to  three  weeks  con- 
valescence is  established.  It  may  be  a  long  while,  however,  before  a  patient  com- 
pletely recovers  from  a  severe  attack.  A  third  possibility  is  the  transition  of  the 
acute  into  a  chronic  dysentery.  In  this  the  symptoms  of  a  chronic  colitis,  usually 
attended  with  cachexia,  may  persist  for  months  and  years. 

Mild,  rudimentary  forms  of  dysentery  also  occur,  presenting  no  severe  intes- 
tinal symptoms,  and  recovering  at  the  end  of  a  few  days.  In  these  cases,  too, 
great  sensitiveness  of  the  intestine  to  disturbing  influences  frequently  persists  for 
quite  a  long  time  after  the  illness.  There  may  be  exacerbations  of  the  disease,  and 
relapses. 

Complications  of  dysentery,  localized  in  other  organs,  are  rare,  at  least  in 
epidemics  here.  In  tropical  dysentery  abscess  of  the  liver  is  comparatively  com- 
mon. It  is  dependent  upon  metastatic  processes  from  the  portal  radicals.  In 
some  cases  abscesses  of  the  lungs  and  of  the  brain  may  follow  abscess  of  the  liver. 
Inflammation  of  the  serous  membranes  or  of  one  or  more  joints  may  also  occur. 
If  paraplegia  follows  it  may  be  referred  either  to  secondary  myelitis  or  to  poly- 
neuritis. Dysentery  is  also  said  to  occur  in  connection  with  a  "  general  scorbutic 
diathesis,"  but  to  all  appearances  this  is  usually  a  "  septic  "  complication.  The 
dysenteric  ulcers  rarely  lead  to  perforation  and  consequent  peritonitis. 

The  diagnosis  is  seldom  very  difiicult.  It  is  based  exclusively  upon  the  intes- 
tinal symptoms  and  the  character  of  the  stools.  It  is  only  the  cases  of  secondary 
dysentery  which  occur  in  the  course  of  other  severe  diseases  that  are  likely  to 
escape  observation. 

The  prognosis  is  mainly  influenced  by  the  character  of  the  epidemic,  which,  as 
we  have  said,  is  in  our  climate  usually  benign.  There  may  be  danger,  particu- 
larly to  elderly  people,  from  bodily  weakness  and  collapse. 

Treatment. — Prophylaxis  demands  that  the  isolation  of  the  patient  and  the 
disinfection  of  the  stools  be  as  complete  as  possible.  The  healthy  must  be  very 
careful  during  an  epidemic  not  to  catch  cold,  and  to  avoid  errors  in  diet,  for 
experience  shows  that  an  opposite  course  predisposes  to  the  disease. 

The  patient  must  be  kept  warm,  and  must  not  leave  his  bed,  even  if  the  attack 
be  mild.  The  diet  must  be  rigorous.  If  the  strength  is  fair,  thin  porridge,  milk, 
and  broths  sufiice  for  some  days.  To  a  feebler  person  we  should  give  somewhat 
stronger  nourishment  from  the  start,  e.  g.,  eggs,  peptonized  meat,  and  wine.  Most 
patients  bear  liquids  that  are  lukewarm  better  than  those  which  are  cold. 

As  to  drugs,  the  habit  of  almost  all  experienced  physicians  is  to  give  at  first  a 
mild  laxative.  Although  opiura  does  not  usually  control  the  diarrhoea  and  tenes- 
mus at  all,  it  is  the  rule  for  decided  improvement  to  follow  the  exhibition  of  the 
laxative.  During  the  first  days,  or,  if  need  be,  later,  we  give  two  to  four  table- 
spoonfuls  of  castor-oil  daily.  If  this  medicine  is  very  disagreeable  to  the  patient, 
we  can  replace  it  by  a  strong  infusion  of  rhubarb  (10-100).  In  southern  countries 
large  doses  of  calomel  (gr.  x  to  xv,  grm.  0.5-1)  are  customary,  and  are  highly 
praised  by  the  physicians  there.  Further  on  in  the  disease  we  may  content  oi;r- 
selves  with  giving  mistura  amygdalae ;  or  we  may  administer  bismuth  in  the  fol- 
lowing mixture:  Bismuthi  subnit.  vel  salicylat.,  grm.  5;  mucilaginis  acaciae, 
syrupi  simpl.,  aa  15;  aquse  destil.,  120 — to  be  shaken  before  taking.  If  the  dis- 
ease should  get  worse  again,  however,  we  should  always  try  a  laxative. 

Emetics  at  the  beginning  of  the  disease  are  often  employed  in  the  tropics,  but 
seldom  with  us.  Ipecacuanha  (radix  antidysenterica) ,  given  in  large  doses  of  fif- 
teen to  thirty  grains  (grm.  1-2),  is  even  regarded  by  many  as  a  specific.  Among 
antiparasitic  remedies,  naphthalin  (gr.  viij,  grm.  0.5,  thrice  daily)  and  salol  (one 
to  two  drachms,  grm.  4.0-8.0,  a  day)  have  been  especially  recommended.  ISTumer- 
ous  attempts  have  been  made  at  local  treatment  by  enemata.    No  brilliant  results. 


84  ACUTE    GEls^EEAL   INFECTIOUS    DISEASES 

however,  can  be  claimed  for  any  of  these  methods  or  medicines.  A  decided  pallia- 
tive effect  can  be  obtained  from  the  injection  of  thin  starch  to  which  twenty  or 
thirty  drops  of  laudanum  have  been  added.  Suppositories  of  cocoa  butter  con- 
taining extract  of  opium  often  mitigate  the  tenesmus.  Other  injections  are  recom- 
mended, each  to  measure  §ij  to  iijss.  (grm.  60-100),  and  to  contain  either  argenti 
nitrat.,  gr.  j  to  vj  (grm.  0.05-0.30),  or  plumbi  acetat.,  gr.  ij  to  viij  (grm.  0.1-0.5), 
or  potassii  chlorat.,  gr.  xv  to  xx  (grm.  1-1.5),  and  especially  tannin  (three  in- 
jections a  day  of  a  warm  0.5-per-cent.  solution).  In  severe  cases  we  may  also  try 
high  injections  of  solutions  of  tannin  as  in  cholera  (vide  infra).  Many  other 
solutions  are  used.  The  success  of  this  treatment  is,  however,  dubious.  In  all 
cases  the  margins  of  the  anus  must  be  protected  from  inflammation  by  frequently 
washing  and  anointing  the  skin. 

The  treatment  of  weakness  and  collapse  is  by  the  usual  stimulants — ^wine, 
ether,  camphor,  and  the  like.  In  chronic  dysentery  the  main  point  is  to  persevere 
in  a  strict  control  of  the  diet.  We  may  exhibit  astringents,  such  as  tannin  and 
columbo.  Subnitrate  of  bismuth  is  also  given,  and  nitrate  of  silver  and  acetate  of 
lead.  And  in  these  chronic  cases  a  long-continued  and  thorough  use  of  rectal 
irrigation  with  fluids  containing  some  mild  astringent  or  disinfectant  may  have  a 
good  effect. 

[Sporadic  dysentery  is  a  self -limited  disease,  and,  as  has  been  shown  by  Flint, 
runs  its  course  within  ten  days  without  medication.  Treatment,  however,  adds  to 
the  comfort  of  the  patient  and  shortens  the  course.  It  is  not  customary  with  us 
to  use  daily  laxatives.  If  there  is  any  doubt  as  to  whether  the  intestines  have 
been  emptied,  a  saline  should  be  given,  the  action  of  which  should  be  followed  by 
opium  in  sufficient  doses  to  allay  pain  and  tenesmus.  Subsequent  action  of  the 
bowels  is  best  obtained  by  simple  large  enemata.  In  weak  persons  castor-oil  is  to 
be  preferred  to  salines. 

In  epidemic  dysentery  active  treatment  is  much  more  important.  Laxatives 
are  contra-indicated  by  sero-sanguinolent  dejections  or  by  asthenia,  but  enemata 
can  be  freely  used.  Stimulation  is  often  required;  nutrition  must  be  carefully 
looked  after,  such  articles  being  chosen  as  are  digested  and  absorbed  by  the 
upper  portions  of  the  intestinal  tract,  leaving  as  little  residue  as  possible  to  pass 
on  to  the  inflamed  colon.  Opium  is  often  demanded  and  tolerated  in  large  doses, 
and  astringents,  such  as  the  acetate  of  lead,  gallic  acid,  and  the  pernitrate  of  iron, 
are  of  service. 

In  acute  dysentery  the  patient  should  be  instructed  not  to  yield  to  the  desire  to 
go  to  stool  if  he  can  help  it,  and  tenesmus  can  often  be  much  diminished  by 
simple  irrigation  of  the  lower  bowel  with  water,  which  may  be  warm  or  cold, 
whichever  the  patient  finds  more  agreeable. 

Chronic  dysentery  is  one  of  the  most  difficult  maladies  with  which  we  have 
to  deal.  In  its  treatment  a  sea  voyage,  or  removal  for  at  least  some  months  to  a 
climate  other  than  that  in  which  the  disease  originated,  is  of  far  more  value  than 
drugs. 

Am(ebic  Dysentery 

The  amoeba  coli,  first  found  by  Losch  in  the  stools  of  a  dysenteric  patient,  has 
received  very  careful  study  at  the  Johns  Hopkins  Hospital,  and  forms  the  subject 
of  a  most  exhaustive  and  valuable  monograph  by  Councilman  and  Lafleur. 

The  living  organism  is  readily  seen,  and  recognized  especially  by  its  active 
amoeboid  movements  on  the  warm  stage  of  the  microscope.  If  the  imees  contain 
small  gelatinous  masses,  these  will  be  found  to  provide  the  most  fruitful  field 
for  search.  The  numbers  of  the  organisms  vary  widely  in  different  cases,  and  even 
in  the  same  case,  from  day  to  day.  They  are  said  to  be  present  in  this  form  of 
dysentei-y  alone,  and  have  been  found  in  secondary  abscesses  of  the  liver  and  the 


CHOLERA  85 

lung,  alike  after  death  and  during  life.    They  should  be  sought  for  in  all  obstinate 
cases  with  dysenteric  symptoms. 

The  prognosis  is  uncertain,  and  the  cases  are  apt  to  drag  along  with  exacerba- 
tions and  remissions  of  the  symptoms;  but  recovery  does  take  place.  There  is 
notable  danger  of  the  formation  of  secondary  abscesses,  in  which  event  re- 
covery is  hardly  to  be  hoped  for.  The  only  treatment  which  seems  to  have  been 
of  much  service — beyond  a  general  hygienic  and  supportive  regimen — consists  in 
the  use  of  copious  injections  into  the  intestinal  canal  of  solutions  of  quinine, 
in  the  strength  of  one  to  one  thousand  or  even  five  thousand.  Losch  found  that 
contact  with  a  solution  of  the  latter  strength  for  one  minute  sufiices  to  kill  the 
amoebae.] 


CHAPTER  XIII 

CHOLERA 

(Asiatic  Cholera) 

Historical  Remarks. — The  home  of  genuine  Asiatic  cholera  is  India.  The  first 
epidemic  in  that  country  with  which  we  are  accurately  acquainted  occurred  in 
1817.  This  was  very  widespread.  The  disease  was  probably  endemic  there  at  an 
earlier  period.  In  the  next  few  years  the  cholera  extended  in  all  directions,  and 
reached  Astrakhan  by  way  of  Persia.  Between  1830  and  1832  the  disease  made  its 
first  great  epidemic  progress  over  Europe.  Invading  all  European  Russia,  it 
reached  Germany  in  1831,  and  France  and  England  in  1832.  Then  came  many 
smaller  epidemics  up  to  1838,  when  there  was  a  complete  cessation  till  1846,  in 
which  year  the  disease,  again  starting  from  Asia,  overspread  Europe.  There  have 
in  later  years  been  epidemics  in  many  places,  but  we  can  not  here  enter  into  the 
particulars  of  them.  During  the  war  of  1866  there  were  many  cases  of  cholera  in 
Germany,  and  from  1883  to  1886  Italy,  France,  and  Spain  were  visited  by  the  dis- 
ease. In  August,  1892,  cholera  broke  out  suddenly  and  very  unexpectedly  in 
Hamburg,  where  within  three  months  about  18,000  persons  were  attacked  by  the 
disease,  and  over  7,600  died  of  it. 

.ffitiology. — Some  time  ago  it  had  become  evident  that  the  real  cause  of  cholera 
consists  in  the  infection  of  the  system  by  a  specific  micro-organism.  Koch  was, 
however,  the  first  to  succeed  in  the  search  for  the  poisonous  agent.  He  was  in 
charge  of  the  scientific  expedition  sent  out  by  the  German  Government  in  1883  to 
Egypt  and  India  for  the  purpose  of  investigating  the  disease.  Koch  found  in  the 
intestines  of  all  the  victims  of  cholera  whose  bodies  he  examined  a  certain  kind 
of  micro-organism  which  he  named  the  comma  bacillus.  It  is  shorter  than  the 
bacillus  of  tuberculosis,  but  somewhat  thicker,  and  it  is  usually  bent  in  the  shape 
of  a  comma,  or  even  like  a  semicircle  (see  Fig.  9).  In  pure  cultures  the  comma 
bacilli  grow  into  long  spiral  threads,  resembling  the  spirilli  of  recurrent  fever. 
Examined  in  a  liquid,  the  individual  bacilli  are  seen  to  make  vigorous  move- 
ments. This  mobility  is  probably  dependent  upon  the  thin,  filiform  fibers  at  the 
ends  of  the  comma  bacilli  discovered  by  LofSer. 

The  comma  bacilli  flourish  best  at  a  temperature  between  86°  and  104°  (30° 
and  40°  C).  Below  61°  (16°  C.)  they  cease  to  grow,  but  they  are  not  killed  even 
by  a  greater  degree  of  cold.  The  free  access  of  oxygen  is  desirable  but  not  abso- 
lutely indispensable  to  their  growth.  They  multiply  veiy  rapidly  in  liquids — e.  g., 
broth  or  milk — and  they  may,  under  favorable  circumstances,  retain  their  vitality 
for  many  weeks,  while  they  can  be  readily  destroyed  by  desiccation.  In  this  again 
they  resemble  the  genuine  spirilli,  which  can  maintain  their  existence  only  in 


86  ACUTE    GENERAL   USTFECTIOTJS   DISEASES 

fluids.  It  is  necessary  that  the  nutrient  material  have  an  alkaline  reaction.  On 
neutral  or  acid  material  the  growth  of  the  comma  bacilli  ceases  entirely.  The 
characteristic  features  of  pure  cultures  can  not  be  described  in  detail  here,  but 
we  may  observe  that  the  nutrient  gelatin  is  slowly  liquefied  by  the  bacilli.  JSToth- 
ing  definite  is  yet  known  as  to  the  occurrence  and  the  formation  of  permanent 
spores. 

There  can  now  be  no  doubt  that  the  sole  cause  of  cholera  is  infection  by  the 
comma  bacilli.  It  has  been  shown  that  in  every  case  of  genuine  Asiatic  cholera 
the  comma  bacilli  are  present  in  the  intestine,  and  that  they  are  never  found 
under  any  other  circumstances.  Even  the  last  postulate  which  was  needed  to 
show  their  pathogenic  significance  has  been  fulfilled.  Rietsch  and  ISTicati,  followed 
by  Koch  himself  and  others,  have  succeeded  in  producing  cholera  in  a  guinea-pig 
by  introducing  into  its  duodenum  or  into  the  contents  of  the  stomach  previously 
made  alkaline,  pure  comma  bacilli. 

Investigation  as  to  the  origin  of  cholera  must,  therefore,  now  meet  this  culmi- 
nating question:    Under  what  circumstances  and  through  what  channel  do  the 

comma    bacilli   penetrate   into    the   human 
system,  and  in  what  raanner  do  they  there 
excite   the   characteristic  processes   of   the 
f'l^i''^'' ,^,\{   /''^//  disease?  There  can  be  no  doubt  that  among 

/"J-  ji''  •z;;^' |'^^'_^'  '/  Europeans,  and  probably  everywhere  except 

*'''  ''  '     jr'>J  f- — " — "^     i^^  India,,  the  cholera  is  invariably  imported. 
'  It  is  equally  certain  that  the  dejections  of 

''  /-V,!    '->  '^/'     ,  }k)i'' ,  II  cholera  patients,  which  are  rich  in  comma 

I  ,',v/j>^''/    ^  1/    jPj'Jf  //I  I  bacilli,  are  the  chief  if  not  the  only  agent 

\''A    -  ~  /i    /,.-  r.i     1^   \  j^y  which  the  disease  is  spread.     The  bacilli 


n  -/■:>' 


Avhich  escape  into  the  outer  world  with  the 
stools  find  abundant  means  to  prolong  their 
'W-'.'ff!'''','  ,'0^/'    '' 1  existence.       They    continue    their    growth 

"  'I   '     \  ^i'  'f"  J   )   \\  upon   moistened   bed-clothes,    or    in   water 

''  ',1       lu* 't  j'f^i  which  contains  a  sufficient  amount  of  or- 

■  -        /     ///'/'  // /  '  ganic  substances,  or  in  food,  such  as  fruit  or 

/I  ''        !    ''  milk,  or  in  moist  earth;  and  the  ways  by 

Fig.  9.— (From  Koch.)     Comma  bacilli  from  which  they  Can  in  turn  enter  the  system  of 

a  cholera  deiection  which  had  lain  for  two         i       i.i      "^i  i     •  •    e.    •  j.      • 

days  on  a  wet  cloth.    The  s-shaped  bacilli    a  healthy  human  being  are  infinite  m  num- 
are  at  a.    600  diameters.  hox.     It  is  easy  to  understand  why  certain 

persons — e.  g.,  laundresses  and  nurses — are 
more  liable  to  infection  than  others;  and  it  is  equally  intelligible  that  the  spread 
of  the  disease  should  often  bear  a  relation  to  certain  outward  circumstances. 
The  fact  has  long  been  a  familiar  one,  that  the  cholera  almost  always  progresses 
along  the  world's  most  frequented  highways,  and  that  it  never  travels  faster  than 
the  means  of  human  intercommunication  render  possible.  This  is  important, 
because  it  shows  plainly  that  the  germs  of  the  disease  are  not  disseminated  by 
currents  of  air.  It  is  easy  to  understand  that  the  distribution  of  the  disease 
should  sometimes  correspond  with  that  of  water  destined  for  personal  use.  The 
experience  of  the  last  few  years  has  again  proved  most  clearly  that  the  drinking- 
water  is  the  chief,  although  of  course  not  the  only,  source  for  the  dissemination 
of  cholera.  If  an  extensive  water-supply  is  contaminated  by  comma  bacilli,  as 
was  the  case  in  Hamburg,  the  disease  may  suddenly  break  out  in  a  place  with  great 
severity.  Sporadic  cases  usually  arise  from  the  use  of  a  contaminated  stream 
which  is  used  for  drinking  only  by  a  small  number  of  men  (sailors,  etc.). 

A  man  falls  sick  with  cholera,  of  course,  not  simply  from  swallowing  the 
cholera  bacilli,  but  because  the  bacilli  remain  in  the  intestine  and  multiply.  It 
is  safe  to  assume  that  many  men  swallow  comma  bacilli  at  the  time  of  a  cholera 


CHOLEEA  87 

epidemic  without  falling  sick  at  all,  or  without  any  but  the  slightest  disturb- 
ance, because  the  comma  bacilli  are  at  once  destroyed  by  the  acid  gastric  juice 
or  they  develop  in  the  intestine  only  in  small  numbers  or  perhaps  in  an  attenuated 
form.  In  the  last  epidemic  at  Hamburg  comma  bacilli  were  sometimes  found  in 
the  solid  stools  of  healthy  men,  who  were  in  close  contact  with  cases  of  cholera, 
and  also  in  the  stools  of  men  who  had  a  very  mild  "  cholera  diarrhoea."  These 
facts  are  extremely  important.  They  lead  to  a  correct  estimate  of  the  infection 
experiments  repeatedly  practiced  of  late  on  human  beings,  and,  on  the  other 
hand,  they  have  a  great  practical  significance  in  regard  to  the  danger  of  trans- 
mitting cholera. 

These  theories  may  be  brought  into  harmony  with  the  observations  collected 
by  Pettenkofer,  which  go  to  show  a  connection  between  the  dissemination  of 
cholera  and  the  character  of  the  soil.  The  character  of  the  soil  can  evidently 
influence  the  dissemination  of  the  cholera  bacilli  in  various  ways.  The  conditions 
of  the  water  in  springs,  etc.,  may  depend  very  materially  upon  the  character  of 
the  surrounding  soil.  The  epidemiological  facts  especially  emphasized  by  Petten- 
kofer are :  1.  Certain  places  are  immune,  especially  those  lying  in  a  rocky  terrain. 
2.  The  frequency  of  cholera  (as  of  typhoid  fever,  vide  supra)  corresponds  with 
variations  in  the  ground-v/ater. 

Most  cholera  epidemics  happen  in  the  summer  months.  Liability  to  the  dis- 
ease is  very  widespread,  although  some  remarkable  exceptions  are  seen.  Sex  is 
unimportant.  Age  has  more  influence.  The  disease  occurs  in  sucklings,  but,  as 
a  rule,  is  more  rare  among  children  than  among  adults.  Elderly  people  are 
very  apt  to  take  the  disease,  while  of  typhoid  fever  the  opposite  is  true.  Most 
authors  lay  great  stress  upon  predisposing  causes.  Among  these,  taking  cold 
is  not  so  important  as  are  errors  in  diet  and  mild  attacks  of  gastro-intestinal 
catarrh,  which  are  shown  by  numerous  observations  to  predispose  strongly  to  the 
disease,  because  the  acidity  of  the  gastric  contents  is  thus  diminished,  and  the 
retention  of  comma  bacilli  in  the  intestine  is  thus  facilitated.  The  stage  of  incu- 
bation seldom  lasts  over  one  to  three  days  at  most. 

Clinical  History. — In  cholera,  as  in  most  acute  infectious  diseases,  the  inten- 
sity of  the  illness  varies  between  the  extremes  of  mildness  and  severity,  so  that 
usually  a  correct  interpretation  of  the  mildest  cases  is  rendered  possible  only  by 
the  fact  that  an  epidemic  exists  and  by  the  discovery  of  comma  bacilli.  These 
insignificant  cases  are  called  simple  choleraic  diarrhoea.  The  symptoms  are 
those  of  a  violent  acute  intestinal  catarrh;  the  dejections  are  watery,  rather 
large,  painless,  and  number  about  three  to  eight  in  twenty-four  hours.  There 
is  considerable  malaise,  complete  anorexia,  and  thirst,  and  there  may  already  be 
indications  of  severer  choleraic  symptoms — vomiting,  slight  pains  in  the  calves 
of  the  legs,  and  diminished  secretion  of  urine.  Many  cases  recover  after  a  few 
days  or  a  week,  but  in  others  the  first  mild  diarrhoea  is  succeeded,  at  the  end  of 
about  one  to  three  days,  or  rarely  later  still,  by  a  severe  attack  of  cholera.  In 
such  cases  we  speak  of  a  "  premonitory  diarrhoea  of  cholera." 

The  mild  form  is  succeeded  in  a  gradual  transition  by  the  cases  designated 
as  "  cholerine."  Cholerine  exhibits  the  symptoms  of  a  violent,  rather  sudden 
cholera  morbus.  It  often  begins  at  night.  To  the  diarrhoea,  which  now  and  then 
displays  even  at  this  time  the  characteristics  of  pronounced  cholera,  vomiting  is 
soon  added.  The  accompanying  constitutional  symptoms  are  rather  severe. 
There  is  great  languor  and  depression.  The  voice  grows  weak,  the  extremities  are 
cool,  the  pulse  is  small  and  accelerated,  painful  cramps  occur  in  the  calves  of  the 
legs,  the  urine  grows  scanty  and  perhaps  albuminous.  The  whole  attack  lasts 
about  a  week  or  two,  before  recovery  is  complete.  The  course  of  the  disease  is 
not  infrequently  varied  by  repeated  improvements  and  relapses. 

From  these  cases  of  medium  severity  there  is  again  a  continuous  line  of  tran- 


88  ACUTE    GENEEAL   INFECTIOUS   DISEASES 

sition  to  the  pronounced  severe  form  of  cholera.  Statistics  as  to  the  frequency 
of  the  separate  forms  can  not  be  given,  since  many  of  the  milder  cases  escape 
observation. 

The  true  attack  of  cholera  may  begin  suddenly  with  the  severest  symptoms. 
As  a  rule,  however,  it  is  preceded,  as  already  stated,  by  a  first  stage  of  brief  pre- 
monitory diarrhoea.  This,  after  one  to  three  days,  is  replaced  with  equal  sudden- 
ness by  the  severe  symptoms  of  the  second  or  "  algid  stage,"  or  "  cholera  asphyxia."^ 
Its  first  symptoms  are  the  abrupt  appearance  of  great  bodily  weakness,  chilliness,, 
and  vertigo.  The  characteristic  gastro-intestinal  symptoms  soon  declare  them- 
selves. 

The  diarrhcea  grows  very  violent.  At  short  intervals  there  are  copious  painless 
dejections,  which  at  first  retain  somewhat  of  a  feculent  character,  but  very  soon 
present  a  characteristic  resemblance  to  rice-water,  gruel,  or  whey.  A  single 
stool  will  measure  a  little  less  than  half  a  pint  (grammes  200).  The  stools 
have  no  color  and  almost  no  odor.  They  are  watery,  and  usually  deposit  a  finely 
granular,  grayish-white  sediment  upon  standing.  Their  reaction  is  neutral  or 
alkaline.  Only  one  or  two  per  cent,  is  solid  matter,  with  a  little  albumen  and 
a  relatively  large  amount  of  sodic  chloride.  In  many  severe  cases  the  dejections, 
contain  more  or  less  blood.  The  microscope  reveals  epithelium,  triple  phosphate, 
and  numerous  micro-organisms.  Of  these  last  a  part  are  the  comma  bacilli,, 
and  a  part  are  bacteria  of  putrefaction,  etc. 

These  excessive  evacuations  are  but  very  rarely  absent.  They  are  more  apt 
to  fail  if  death  occurs  at  the  end  of  a  few  hours — cholera  sicca. 

[In  cholera  sicca  the  intestines  after  death  contain  the  characteristic  rice- 
water  material  which,  perhaps  owing  to  paralysis  of  the  muscular  coat,  was  not 
expelled  during  life.] 

The  appearance  of  the  diarrhoea  is  soon  followed  by  frequent  though  rarely 
distressing  vomiting.  The  vomitus  consists  in  part  of  ingested  liquids  and  in  part 
of  an  actual  transudation  through  the  mucous  membrane  of  the  stomach  and 
intestine.     Hiccoughs  may  accompany  and  follow  the  emesis. 

In  addition  to  these  prominent  digestive  symptoms  of  vomiting  and  profuse 
diarrhoea  there  are  complete  anorexia  and  excessive  thirst.  The  tongue  has  a 
thick,  dry  coat.  The  abdomen  is  usually  flat  and  soft,  or  it  may  be  concave  and 
hard.  Sometimes  we  may  feel  fluctuation  in  the  intestines,  due  to  their  being- 
filled  with  fluid.  There  is  not  much  real  abdominal  pain;  what  there  is,  is  de- 
scribed as  a  "  feeling  of  heat  and  pressure  "  around  the  umbilicus. 

At  the  same  time  very  severe  symptoms  develop  in  other  organs.  The  circu- 
latory system  is  chiefly  affected. 

The  action  of  the  heart  may  be  stimulated  at  the  beginning  of  the  attack. 
The  patient  complains  of  palpitation  and  great  precordial  anxiety.  After  a  brief 
time,  however,  cardiac  weakness  appears,  and  continually  increases.  The  action 
of  the  heart  becomes  very  weak,  and  the  heart-sounds  feebler  and  feebler.  The 
pulse  at  the  wrist  grows  very  small,  and  is  usually  somewhat  accelerated.  In  a 
severe  case  the  pulse  vanishes  completely  after  a  few  hours. 

This  collapse  of  circulation  makes  itself  quickly  evident  in  the  appearance  of 
the  patient.  The  face  and  extremities  grow  cool,  and  then  ice-cold ;  the  complex- 
ion becomes  partly  livid  and  partly  a  bluish  gray;  the  lips  are  almost  black.  The 
surface  temperature  may  fall  below  95°  (35°  C),  while  in  the  rectum  febrile  tem- 
peratures may  often  be  observed,  reaching  102°  (39°  C.)  and  higher.  The  eye  and 
cheek  grow  very  hollow,  the  skin  becomes  wrinkled,  and  loses  all  its  elasticity. 
The  voice  grows  hoarse  and  feeble  (voice  of  cholera).  Respiration  is  laborious 
and  superficial.  The  mind  may  remain  unclouded  to  the  end,  but  usually  there  is 
great  apathy,  and  all  acuteness  of  perception  is  destroyed.  Only  a  few  patients  are 
restless  and  excited.     Reflex  action  is  much  impaired. 


CHOLEEA  89 

One  characteristic  symptom  is  the  cramps  in  the  muscles.  These  are  usually 
very  painful,  and  consist  in  tonic  contractions  of  the  muscles,  particularly  those 
of  the  calf  of  the  leg,  but  also  those  of  the  toes,  thighs,  arms,  and  hands.  The 
cramps  occur  spontaneously  or  upon  the  least  provocation,  last  a  few  minutes,  and 
recur  at  short  intervals.  The  precise  reason  of  their  occurrence  is  not  yet  known. 
It  may  be  the  effect  of  poison  (vide  infra).  They  can  be  observed  in  other  severe 
acute  diseases,  although  most  marked  in  cholera.  They  sometimes  occur  in  chol- 
era morbus. 

In  a  well-developed  attack  of  cholera  there  is  almost  invariably  oliguria  or 
anuria.  The  urine,  if  any  be  secreted,  is  concentrated,  with  abundant  sediment, 
and  it  very  often  contains  albumen.  In  many  cases  not  one  drop  of  urine  reaches 
the  bladder  for  days,  and  this  condition  persists  till  death  or  recovery. 

The  symptoms  thus  far  depicted,  if  taken  as  a  whole,  represent  the  algid  stage, 
which  seldom  lasts  more  than  one  or  two  days.  In  many  cases  death  occurs 
during  this  period.  It  is  ushered  in  by  the  tokens  of  extreme  general  prostration, 
and  may  take  place  after  a  few  hours,  or  more  frequently  in  the  second  half  of  the 
first  day.  But  in  other  cases  the  "  stage  of  reaction  "  succeeds.  This  may  be  a 
true  compensatory  period,  leading  directly  to  convalescence.  The  evacuations 
become  less  frequent  and  more  feculent,  and  the  vomiting  ceases.  The  pulse 
becomes  stronger,  the  cyanosis  and  coolness  of  the  extremities  diminish,  and  an 
abundant  perspiration  is  not  infrequent.  After  a  few  days  urine  is  again  ex- 
creted. This  is  almost  invariably  quite  albuminous,  and  usually  contains  casts 
and  red  blood-globules.  If  convalescence  be  uninterrupted,  however,  the  urine 
very  soon  becomes  perfectly  normal,  and  after  a  week  or  two  recovery  is  to  be 
regarded  as  complete. 

Departures  from  this  favorable  course  of  the  stage  of  reaction  are  frequent. 
Eecovery  may  be  interrupted  by  repeated  relapses  into  the  previous  condition, 
sometimes  with  a  fatal  result;  instead  of  convalescence,  there  is  developed  a 
severe  third  stage,  usually  with  fever.  This  stage  ordinarily  bears  the  generic 
name  of  cholera  typhoid,  although  it  is  subject  to  manifold  variations  in  its  clin- 
ical symptoms  as  well  as  its  exciting  causes. 

Cholera  typhoid  may  present  an  actually  typhoidal  general  condition  with 
severe  fever.  There  is  a  considerable  elevation  of  temperature,  headache,  and 
dullness.  The  pulse  is  full  and  rapid,  the  face  flushed.  The  skin,  particularly 
that  of  the  extremities,  sometimes  presents  the  so-called  choleraic  eruption,  in  the 
form  of  an  erythema,  roseola,  urticaria,  or  the  like.  This  variety  of  cholera 
typhoid  ends  after  a  few  days  in  recovery,  or  else  passes  into  one  of  the  following 
conditions. 

A  second  form  of  cholera  typhoid  is  distinguished  by  the  development  of  the 
most  diverse  local  inflammations.  Thus,  there  may  be  a  severe  dysenteric  or  diph- 
theritic inflammation  of  the  small  and  large  intestine,  attended  by  offensive  puru- 
lent and  bloody  stools.  Pneumonia  is  also  possible,  as  well  as  purulent  bronchitis, 
diphtheritic  inflammation  of  the  larynx,  pharynx,  bladder,  and  female  genitals, 
parotitis,  and  sometimes  erysipelas  and  pyaemia.  And  when  we  consider  that, 
besides  all  these  conditions,  the  usual  intestinal  symptoms,  or  those  of  choleraic 
nephritis,  may  exist  also,  it  is  evident  how  varied  the  clinical  picture  may  be. 
The  development  of  these  local  affections  frequently  lays  the  foundation  for 
numerous  sequelae. 

Choleraic  nephritis  gives  rise  to  the  third  or  ura-mic  variety  of  cholera  typhoid. 
The  secretion  of  urine  is  almost  suspended.  The  region  of  the  kidneys  is  some- 
times sensitive  on  pressure.  The  little  urine  that  is  still  passed  contains  numer- 
ous casts,  albumen,  and  frequently  renal  epithelium  and  white  and  red  blood-glob- 
ules. Somewhere  toward  the  end  of  the  first  week,  or  possibly  earlier,  there  are 
grave  nervous  symptoms,  to  be  regarded  as  uraemic :  first  there  is  headache  and 


90  ACUTE    GENERAL   IAtEECTIOUS    DISEASES 

vomiting,  then  sopor  and  coma,  or  delirium  and  convulsions.  Most  of  these  cases 
are  fatal. 

Patholog-y  and  Pathogenesis. — We  are  now  acquainted  with  the  manifold 
symptoms  and  varieties  of  the  disease.  If  we  seek  for  the  pathological  changes 
which  control  the  process,  and  endeavor  to  find  some  correspondence  between 
them  and  the  symptoms,  we  shall  be  disappointed.  At  least,  in  its  early  stages, 
cholera  is  merely  a  severe  local  disease  of  the  intestine.  We  find  the  serous  layer 
of  the  coils  of  the  small  intestine  rose-red  from  congestion.  The  mucous  mem- 
brane is  in  a  state  of  catarrhal  inflaramation :  it  is  swollen,  reddened,  and  at  first 
covered  with  a  layer  of  tough,  transparent  mucus;  but  very  soon  an  abundant 
transudation  flows  into  the  canal,  so  that  the  intestinal  coils  are  filled  with  a  large 
amount  of  clear  fluid,  looking  like  rice-water  or  gruel,  and  so  devoid  of  bile 
as  to  indicate  the  suspension  of  its  secretion.  The  signs  of  inflammation  of 
the  mucous  membrane  now  grow  more  pronounced.  The  solitary  follicles  and 
Peyer's  patches  become  swollen,  with  edges  of  a  vivid  red,  and  frequently  there 
are  many  small  ecchymoses  in  the  mucous  membrane.  The  extensive  desquama- 
tion of  the  epithelial  lining  of  the  intestine  has  also  been  regarded  as  important, 
because  it  was  regarded  as  in  part  the  cause  of  the  copious  transudation.  Still 
it  may  be  questioned  whether  the  desquamation  is  not,  at  least  to  some  extent, 
a  post-mortem  change.  In  yet  later  stages  of  the  disease  the  intestinal  trouble 
very  frequently  assumes  a  croupous-diphtheritic  character.  The  surface  is  ne- 
crosed and  ulcerated  in  many  places,  and  the  contents  of  the  intestine  are  no 
longer  colorless,  but  sanious  and  bloody,  with  a  foul  odor. 

Otherwise  most  of  the  post-mortem  lesions  correspond  to  what  was  obvious 
at  the  bedside.  The  muscles  exhibit  an  early  and  persistent  rigor  mortis,  and  fre- 
quently contract  in  such  a  way  as  to  throw  the  corpse  into  some  unusual  posture. 
All  the  internal  organs  are  remarkably  dry,  pale,  and  anemic.  The  left  ventricle 
is  contracted.  The  blood  lies  mostly  in  the  large  veins,  the  right  side  of  the 
heart,  and  the  cerebral  sinuses.  It  is  thickened,  is  but  little  clotted,  and  is  said  to 
resemble  the  juice  of  bilberries  or  huckleberries.  The  spleen  is  not  enlarged — an 
exception  to  the  rule  in  infectious  diseases.  The  kidneys  present  marked  passive 
congestion,  most  pronounced  in  the  cortex.  The  microscope  reveals  a  greater  or 
less  degree  of  parenchymatous  nephritis,  with  great  destruction  of  the  epithelium. 
If  death  takes  place  at  a  rather  advanced  stage  of  the  disease,  the  tissues  have  lost 
their  characteristic  dryness,  and  the  most  diverse  local  lesions,  including  nephri- 
tis, may  be  found  to  have  occasioned  death. 

If  we  search  for  the  connection  between  the  pathological  changes  just  de- 
scribed and  the  cause  of  the  disease,  or  again  between  these  lesions  and  the  clin- 
ical symptoms,  the  first  point  to  guide  us  is  that  the  comma  bacilli  are  found 
only  in  the  lumen  of  the  intestine,  and  never  in  the  blood  or  in  other  parts  of 
the  body.  The  intestinal  symptoms  are  satisfactorily  explained  by  this  abnor- 
mal state  of  the  intestine,  but  for  all  the  other  grave  symptoms  we  have  to 
seek  some  special  cause.  The  desiccation  which  the  body  undergoes  as  a  result 
of  the  excessive  liquid  dejections  can  not  fail  to  affect  the  tissues,  but  can  not 
fully  explain  the  symptoms,  for  the  circulatory  disturbances  and  the  cardiac 
failure  at  least  may  develop  before  large  evacuations  have  occurred.  It  has  also 
been  settled  beyond  question  by  means  of  the  newer  investigations  that  precisely 
the  worst  symptoms  of  cholera — namely,  the  muscular  cramps,  the  subnormal  tem- 
perature, and  the  changes  in  the  blood^are  occasioned  by  the  chemical  results  of 
tissue  metamorphosis  in  the  comma  bacilli,  that  is,  by  the  so-called  toxines.  Some 
of  these  have  been  already  isolated  chemically  by  Brieger  and  others.  It  is  an 
interesting  circumstance  that  the  amount  and  virulence  of  the  toxines  formed 
by  the  comma  bacilli  seem  to  depend  on  the  physical  characteristics  of  the  nutrient 
material  on  which  the  culture  grows. 


CHOLEKA  91 

As  to  the  complications  which  occur  in  the  later  stages  of  the  disease  and 
which  are  embraced  under  the  generic  name  of  cholera  typhoid,  we  regard  them  as 
mainly  secondary.  The  choleraic  process  itself  does  not  cause  them,  but  is  merely 
the  occasion  for  their  appearance.  The  examination  of  the  intestine  in  such 
cases  shows  that  numerous  other  varieties  of  bacteria  follow  closely  upon  the 
comma  bacillus,  gaining  entrance  to  the  system  by  treading  in  its  footsteps. 
Cholera  nephritis  is  probably  due  to  various  causes.  Some  forms  of  nephritis  seem 
to  be  caused  by  specific  cholera  toxines  (in  analogy  with  scarlatinal  nephritis), 
while  others  are  probably  of  a  secondary  septic  nature. 

Diagnosis. — A  positive  diagnosis  of  cholera  can  be  made  only  by  finding  the 
comma  bacilli  in  the  stools.  When  an  epidemic  prevails  it  is  often  neither  neces- 
sary nor  possible  to  make  the  search  in  each  individual  case.  Sporadic  cases  or 
the  first  cases  of  a  beginning  epidemic  can  and  must  be  diagnosticated  only  in 
this  way,  which  gives  absolute  certainty.  We  can  not  give  here  a  detailed  account 
of  the  bacteriological  diagnosis,  but  we  may  state  briefly  that,  when  cholera  exists, 
the  simple  microscopical  examination  of  a  smear  preparation  sometimes  makes 
the  diagnosis  extremely  probable.  For  this  purpose  a  small  clump  of  mucus  is 
taken  from  a  stool  as  fresh  as  possible,  spread  on  a  cover-glass  as  thinly  as  possi- 
ble, fixed  by  passing  it  carefully  through  the  flame  several  times,  and  stained  with 
an  aqueous  solution  of  methylene  blue  or  carbol-fuchsine.  In  actual  cholera  we 
then  find  the  comma  bacilli  sometimes  in  large  amount  (almost  a  pure  culture) 
or  especially  arranged  in  characteristic  small  groups.  To  render  our  diagnosis  un- 
assailable we  must  employ  gelatine  or  agar  plate  cultures,  etc.,  the  details  of 
which  are  to  be  found  in  the  text-books  of  bacteriology. 

All  those  affections  whose  symptoms  are  like  those  of  cholera  may  be  con- 
founded with  true  cholera,  especially  cholera  morbus  (vide  mfra) ;  and  also  cer- 
tain cases  of  poisoning,  especially  acute  arsenical  poisoning,  may  give  rise  to 
symptoms  wonderfully  like  cholera. 

The  prognosis  should  always  be  guarded  at  the  beginning,  even  if  the  symp- 
toms be  mild,  for,  as  already  mentioned,  a  simple  diarrhoea  may  prove  to  be 
'■^  premonitory  "  of  a  severe  attack  of  cholera.  During  the  real  attack  the  prog- 
nosis grows  graver  in  proportion  as  the  case  presents  the  characteristics  of  as- 
phyxia and  cyanosis.  The  mortality  in  many  epidemics  is  frightful.  All  the 
inhabitants  of  a  house  or  street  may  in  a  brief  period  be  swept  away.  Accurate 
statistics  are  difficult  to  give.  If  we  count  the  typical  cases  alone,  the  mortality 
is  not  infrequently  fifty  to  seventy  per  cent.  In  about  two  thirds  of  the  fatal 
cases  death  occurs  during  the  first  days  of  the  stage  of  asphyxia,  and  in  about  one 
third  during  the  second  period,  known  as  "  cholera  tyiAoid."  The  influence  of 
the  diet  and  the  hygienic  surroundings  of  the  patient  before  his  illness  is  impor- 
tant. A  greater  proportion  of  children  and  old  people  perish  than  of  the  mid- 
dle-aged. 

Prophylaxis  and  Treatment.— The  measures  to  be  taken  to  prevent  the  spread 
of  the  disease,  when  it  has  once  started  in  a  place,  can  be  only  briefly  discussed 
here.  The  chief  things  are  the  quickest  isolation  possible  of  the  first  cases  that 
occur,  the  disinfection  of  the  stools  and  all  linen,  objects,  etc.,  soiled  by  the  stools', 
and  finally  the  determination  of  the  source  of  infection  (drinking-water,  etc.), 
in  order  to  prevent  further  infection.  The  evacuations  (stools  and  vomitus)  can 
be  best  disinfected  with  a  five-per-cent.  solution  of  carbolic  acid  or  with  milk  of 
lime,  chloride  of  lime,  etc. ;  the  linen  and  other  objects  should  be  disinfected  in  a 
special  disinfecting  apparatus.  It  is  veiy  important  to  keep  a  strict  oversight  of 
the  drinking-water,  milk,  and  all  articles  of  food  eaten  in  an  uncooked  con- 
dition. 

In  regard  to  individual  prophylaxis,  we  must  remember  especially  that  any 
slight  gastric  or  intestinal  catarrh  increases  the  liability  to  the  disease.     Hence, 


92  ACUTE   GEIsTEEAL   nsTFECTIOUS   DISEASES 

at  the  time  of  a  cholera  epidemic,  careful  dietetic  restrictions  are  imperatively 
necessary  and  every  disturbance  of  the  stomach  or  the  intestines,  even  the  slight- 
est, needs  the  promptest  and  most  careful  treatment.  It  is  best  wholly  to  avoid 
the  use  of  water  that  has  not  been  boiled,  raw  vegetables,  etc. 

[Various  efforts  have  been  made  to  render  human  beings  immune  to  choleraic 
infection.  The  best  results  seem  to  have  been  attained  by  inoculating  Haffkine's 
attenuated  virus. — V.] 

In  the  treatment  of  the  cholera  attack  itself  many  physicians  even  now  use 
opium  (laudanum  or  pure  opium  in  powder,  gr.  ss.-j,  grm.  0.03-0.05),  while  others,, 
especially  at  the  beginning  of  the  disease,  prefer  large  doses  of  calomel  (gr.  v-x^ 
grm.  0.3-0.5,  several  times),  and  during  the  subsequent  course  they  give  con- 
tinued small  doses  of  calomel  (gr.  ss.-j,  grm.  0.03-0.05,  every  two  hours).  In 
the  algid  stage  warmth  is  especially  advisable.  Hot  baths,  hot  packs,  sweat- 
boxes  with  dry  or  moist  hot  air,  embrocations  of  hot  oil,  an  abundant  supply 
of  hot  drinks  (coffee,  tea,  mulled  wine,  broths)  are  praised  by  all  physicians, 
and  they  must  certainly  be  used.  The  remaining  treatment  is  symptomatic; 
morphine  or  ice  for  the  vomiting  and  embrocations  of  chloroform  oil  or  sub- 
cutaneous injections  of  morphine  for  the  painful  cramps  in  the  calves.  The 
weaker  the  heart  becomes,  the  more  energetically  must  we  give  stimulants  (injec- 
tions of  camphor  or  ether,  champagne). 

Among  the  newer  methods  of  treatment  tried  during  the  last  epidemic  we  may 
mention  subcutaneous  infusions  of  warm  "normal"  (0.6  per  cent.)  salt  solution 
in  the  infraclavicular  region  or  under  the  skin  of  the  abdomen.  By  uninter- 
rupted infusion  by  means  of  an  irrigator  or  a  funnel  two  or  three  quarts  (litres) 
of  salt  solution  can  be  infused  in  twenty-four  hoi;irs.  Intravenous  injections  have 
given  still  better  results,  and  injections  into  the  abdominal  cavity  have  also  been 
tried.  Cantani  strongly  recommends  intestinal  injections  ("  enteroclysis  ")  with 
warm  tannin  solutions  at  a  temperature  of  100°  to  10i°  F.  (38°-40°  C).  The 
fluid  contains  5  to  10  parts  of  tannic  acid,  50  parts  of  gum  arable,  and  2  or  3 
parts  of  laudan-um  to  2,000  parts  of  water.  All  these  methods  are  believed  to 
have  shown  some  favorable  results,  but  none  of  them  has  been  able  to  attain  gen- 
eral recognition  and  iise.  After  many  experiments  most  physicians  have  finally 
gone  back  to  the  old  forms  of  treatment. 

[The  vital  importance  of  the  serious  treatment  of  a  beginning  diarrhoea  dur- 
ing a  cholera  epidemic  can  not  be  too  strongly  insisted  on.  Rest,  simple  diet,  and 
a  little  medication  will,  in  the  vast  majority  of  instances,  entirely  prevent  grave 
consequences.  The  apparently  trifling  character  of  the  symptoms  is  apt  to  lead 
people  into  a  false  security.  Those  who  can  leave  an  infected  district  should  do- 
so  without  delay. 

With  reference  to  the  prevention  of  an  epidemic,  a  pure  water  supply  and 
strict  cleanliness  in  its  broad  sense  possess  far  more  vii*tue  than  cordons  of  troops 
or  measures  of  quarantine.  It  is  more  practicable  to  destroy  the  soil  than  to  keep 
out  the  seed  in  these  days  of  constant  and  rapid  international  communication^ 
The  systematic  disinfection  of  all  cholera  discharges  or  articles  soiled  by  them 
should  be  a  matter  of  course.] 

Great  caution  must  be  exercised  about  the  diet,  not  merely  during  the  attack 
itself,  but  for  a  considerable  time  afterward.  At  first  we  can  allow  only  thin  por- 
ridge, milk,  broths,  and  toast  or  rusks.  It  is  advisable  to  administer  dilute 
hydrochloric  acid  with  the  food. 

The  treatment  of  cholera  typhoid  varies  greatly,  of  course,  according  to 
the  kind  of  attack.  The  separate  complications  should  receive  their  customary 
treatment. 

[In  the  first  stage,  absolute  rest,  opium,  and  lumps  of  ice  by  the  mouth  ad  libi- 
tum are  the  chief  measures  on  which  reliance  is  to  be  placed.     It  should  be  remem- 


MALAEIAL   DISEASES  93 

Lered  that  the  entire  function  of  the  intestinal  tract  is  reversed;  thus,  instead  of 
an  absorbing-,  it  has  become  an  excreting  surface. 

In  the  stage  of  coHapse  the  nervous  system  is  more  or  less  paralyzed,  the  blood 
is  damaged  by  the  loss  of  its  watery  constitutents,  and  the  circulation  of  that  fluid 
is  greatly  impeded.  The  subcutaneous  or  gastric  absorption  of  drugs  is  conse- 
<iuently  delayed  or  suspended.  The  utility  of  any  active  internal  treatment  dur- 
ing this  stage  is  very  questionable.  Certainly  narcotism  by  opium  is  highly  un- 
desirable. Mild  external  stimulation  and  the  tentative  administration  of  ice  and 
small  quantities  of  champagne  or  food  are,  at  all  events,  not  likely  to  do  harm. 
iN'ature  sometimes  reasserts  herself  when  the  conditions  are  seemingly  desperate, 
and  the  third  stage,  or  that  of  reaction,  comes  on.  In  this  stage,  careful  nursing 
and  a  sensible  symptomatic  but  in  no  way  meddlesome  treatment  are  most  like- 
ly to  be  followed  by  good  results.] 


CHAPTEE  XIV 

MALARIAL   DISEASES 

{Intermittent  Fever.     Fever  and  Ague.     Sivarnp  Fever) 

.Etiology  and  Pathological  Anatomy. — Malarial  poisoning  is  the  best  exam- 
ple of  a  purely  "  miasmatic  "  affection.  The  poison  which  produces  the  disease  is 
without  doubt  localized  in  certain  places,  in  which  every  human  being  is  liable  to 
become  its  victim;  but  if  an  infected  person  comes  to  a  place  free  from  malaria 
and  not  naturally  favorable  to  its  development,  there  is  no  danger  that  he  will 
cause  the  disease  in  others.  The  disease  is  never  caught  through  contact  with  the 
patient.  It  is  not  at  all  contagious ;  the  malarial  poison,  after  it  has  once  pene- 
trated into  the  body,  has  practically  no  opportunity  to  escape  again  in  an  efficient 
form  from  the  diseased  system  into  the  outer  world;  but  the  blood  of  a  patient 
injected  into  a  healthy  person  may  transfer  the  disease  (Gerhardt  and  others). 

If  we  except  the  polar  zones,  there  are  few  regions  where  malaria  is  not  en- 
demic in  certain  parts,  at  least  from  time  to  time,  if  not  constantly.  There  is, 
however,  great  variation  in  the  virulence  as  well  as  in  the  number  of  cases.  While 
the  common  forms  of  intermittent  fever  are  very  frequent  in  Germany,  in  numer- 
ous places,  especially  on  the  shores  of  the  North  and  Baltic  Seas,  and  also  in 
the  alluvial  lands  of  the  Vistula,  Oder,  Elbe,  etc.,  yet  the  grave  forms  of  the  dis- 
ease are  very  rare.  Other  lands  are  notorious  for  the  severe  malarial  diseases, 
€.  g.,  Hungary,  the  lands  lying  on  the  lower  Danube,  the  Roman  Campagna,  the 
Pontine  marshes,  Sicily,  and  numerous  districts  in  other  parts  of  the  world, 
chiefly  tropical.  Numerous  observations  have  only  served  to  confimi  the  opinion 
that  the  soil  is  the  true  home  and  cradle  of  the  malarial  poison,  and  that  the 
virus,  escaping  thence  into  the  lower  strata  of  the  atmosphere,  may  be  taken  into 
the  system,  probably  during  inspiration.  Permanent  dampness  of  the  soil  is  essen- 
tial to  the  development  of  the  malarial  poison.  This  explains  why  marshy  dis- 
tricts are  so  often  malarial.  The  ground  must  not  be  covered  by  a  great  amount 
of  water,  but  must  during  the  dry  season  lie  exposed  to  the  atmospheric  air.  The 
access  of  air  to  the  moist  soil  seems  to  be  a  second  essential  condition  for  the  devel- 
opment of  the  malarial  germs.  A  third  influential  factor  is  the  temperature  of 
the  air,  as  proven  by  the  great  prevalence  of  the  disease  in  southern  countries  and 
in  the  summer  season. 

The  special  agent  which  causes  malaria  was  flrst  described  by  Laveran  in  1881, 
and  soon  after  by  Marchiafava  and  Celli.    Since  then  many  other  observers,  espe- 


94 


ACUTE    GENERAL   INFECTIOUS    DISEASES 


cially  in  Italy,  have  investigated  the  subject  and  have  given  us  very  interesting 
information  about  these  peculiar  parasites.  Besides  the  writers  named  we  may 
refer  to  the  studies  of  Golgi,  Guarnieri,  Canalis,  etc.  The  parasite  belongs  to 
the  protozoa  (whether  to  the  sporozoa  or  rhizopoda  is  still  uncertain),  and  is  now 
generally  called  the  Plasmodium  malarice.  The  organisms  are  found  in  the  blood 
of  men  sick  with  malaria,  in  unstained  specimens  or  in  specimens  stained  with 
methylene  blue,  and  are  -at  first  inclosed  in  the  red  blood-corpuscles.  Here  they 
appear  as  delicate  protoplasmic  bodies  with  an  indication  of  a  nucleus ;  at  rest  they 
have  a  rounded  form,  but  they  may  assume  various  shapes  through  their  amoeboid 
movenients  (see  Fig.  10).  These  movements  probably  have  some  relation  to  the 
nutrition  of  the  parasite,  which  takes  place  at  the  expense  of  the  red  blood-corpuscle 


Fig.  10.— Different  forms  of  the  malarial  Plasmodium  according  to  Marchiafava  and  Celli.  «,  6,  c,  or- 
dinary Plasmodia  without  pigment,  d,  e.  spore  formation  in  Plasmodia.  /,  g,  pigmented  Plasmodia 
'^^''th  fl'^^'Tl      '™  *'  °^^^    ^°*'^  crescentic  forms   of  Plasmodia,     fc,  pigmented  Plasmodium 

that  shelters  it.  The  ha3moglobine  taken  up  by  the  Plasmodium  is  thus  changed  to 
melanine,  which  probably  contains  no  iron,  and  the  black  granules  of  this  mela- 
nine  can  easily  be  seen  in  the  body  of  the  adult  parasite.  The  second  phase  in 
the  life  of  the  Plasmodium  now  begins  and  serves  for  its  propagation  and  in- 
crease. The  amo3boid  movements  cease,  the  pigment  granules  collect  in  a  ring 
about  the  periphery,  in  radiating  stripes,  or  in  the  center  of  the  parasite,  while 
the  rest  of  the  mass  in  a  few  hours  breaks  up  into  a  number  of  rounded  spores. 
Their  inclosing  capsule  disappears,  the  spores  are  set  free  in  the  blood  and  pene- 
trate other  red  blood-corpuscles. 

Besides  these  chief  forms  of  the  malarial  plasmodium  just  described,  there 
are  also  other  forms  (crescentic  form,  flagellated  foma)  whose  relations  to  one 
another  and  to  the  ordinary  type  are  still  obscure.  This  fact  alone  seems  to  be 
certain  that  the  different  clinical  forms  of  malaria — tertian,  quartan,  pernicious, 
etc. — correspond  to  different  biological  forms  of  the  plasmodium.  By  inocula- 
tion of  the  blood  into  another  human  being  we  can  therefore  produce  nothing  but  a 
tertian  from  a  tertian  or  a  quartan  from  a  quartan.  The  quotidian  fever  is  due  to 
two  tertians  co-existing  in  the  same  person,  each  individual  tertian  owing  its  origin 
to  a  special  generation  of  the  plasmodium.  The  continuous  and  pernicious 
malarial  fevers  are  characterized  by  the  presence  of  many  of  the  crescentic  forms 
of  development. 

Although  no  one  has  yet  been  successful  in  establishing  this  view  of  the  plas- 


MALARIAL   DISEASES  95 

modia  by  means  of  pure  cultures  and  inoculation  of  the  same,  yet  the  relation 
of  the  Plasmodium  to  malaria  seems  evident  from  the  fact  that  in  every  patient 
with  malaria  the  plasmodia  can  be  easily  demonstrated  in  the  blood,  while  these 
same  forms  are  never  detected  in  the  blood  except  in  malaria.  The  way  in  which 
the  Plasmodia  enter  the  human  body  is  not  yet  known.  It  may  be  by  inhalation 
or  by  the  stings  of  insects. 

[It  has  now  been  proved  that  malarial  organisms  can  be  communicated  by 
certain  varieties  of  mosquito  (anopheles  claviger  and  a.  pictus)  to  man,  and  also 
by  man  to  the  mosquito.  The  obvious  deduction  is  that  a  healthy  man  should 
guard  himself  from  mosquitoes  for  his  own  sake  and  an  already  infected  man  for 
the  sake  of  others. — V.] 

The  investigations  with  regard  to  the  plasmodium  of  malaria  have  also  ex- 
plained the  long-recognized  fact  that  in  chronic  malaria  large  amounts  of  pig- 
ment collect  in  the  internal  viscera.  These  deposits  are  most  abundant  in  the 
spleen,  which  in  the  chronic  varieties  of  the  disease  develops  into  a  firm,  hard 
tumor;  but  they  are  also  found  in  the  bone-marrow,  liver,  brain,  and  kidneys, 
leading  finally  in  the  liver  and  the  kidneys,  in  frequent  instances,  to  processes  of 
chronic  degeneration  and  inflammation.  It  is  especially  noteworthy  that  in 
those  patients  who  present  the  most  marked  cerebral  disturbances  (pernicious 
comatose  fever,  vide  infra),  the  cerebral  capillaries  are  found  to  be  completely 
occluded  with  pigmented  plasmodia. 

[Periodical  fever  is  very  widely  distributed  in  the  United  States,  and  in  the 
southern  portions  occurs  in  severe  though  not  in  the  severest  forms.  Some  regions 
which  were  formerly  free  from  it  are  no  longer  so,  and,  vice  versa,  some  regions 
which  were  greatly  subject  to  it  are  now  exempt;  these  changes  are  closely  con- 
nected with  the  clearing  and  upturning  of  virgin  soil  largely  impregnated  with 
decaying  vegetable  matter,  and  with  the  subsequent  cultivation  of  the  same  for 
considerable  periods  of  time.  The  poison  does  not  extend  far  above  the  surface  of 
the  ground,  as  is  shown  by  the  relative  safety  of  sleeping  in  the  upper  as  compared 
with  the  lower  story  of  a  house ;  during  the  night  the  poison  seems  to  exist  in 
greater  intensity  than  during  the  day.  Attacks  are  more  liable  to  occur  diiring 
the  spring  and  autumn  than  at  other  seasons. 

The  hopes  which  have  been  entertained  in  some  quarters  that  malarial  regions 
might  be  rendered  healthy  by  large  plantations  of  the  Australian  eucalyptus  glob- 
ulus, a  rapidly  growing  tree  which  absorbs  immense  quantities  of  water,  do  not 
seera  likely  to  be  realized  in  the  light  of  French  experience  in  Africa,  and  in  that 
of  the  Trappist  monks  in  Italy.] 

Klebs  and  Tommasi-Crudeli  have  made  extensive  investigations  as  to  the 
nature  of  the  malarial  poison.  We  must  regard  it  as  organic.  The  authorities 
just  named  state  that  the  true  cause  of  malaria  is  a  specific  variety  of  bacillus. 
They  found  peculiar  bacilli  and  their  spores  both  in  the  earth  of  malarial  regions 
and  in  the  adjacent  strata  of  the  atmosphere;  and,  by  infecting  rabbits  with 
these,  they  were  able  to  induce  attacks  of  fever,  swelling  of  the  spleen,  and  the 
characteristic  formation  of  pigment  matter  (vide  infra).  Before  this,  bacilli  and 
spores  had  been  found  in  the  blood  and  spleen  of  patients  suffering  from  malaria. 
It  can  not  yet  be  said  just  how  much  significance  these  discoveries  have. 

[To  Laveran  really  belongs  the  credit  for  the  discovery  and  accurate  descrip- 
tion of  the  Plasmodium.  His  work  in  Algiers  has  been  substantiated  by  observers 
in  widely  separated  malarial  regions,  and,  at  the  same  time,  no  very  important 
additions  have  been  made  to  it. 

It  is  difficult  to  overrate  the  diagnostic  and  therapeutic  importance  of  this  dis- 
covery. The  ordinary  intermittents  are  usually  easy  of  diagnosis,  but  the  remit- 
tent forms  often  simulate  typhoid  fever,  while  the  pernicious  form  may  resemble 
uraemia  or  intracranial  disease.    Especially  in  pernicious  cases  life  may  be  saved 


S6  ACUTE   GEXEEAL   IISTFECTIOUS   DISEASES 

by  prompt  and  appropriate  treatment,  which  must  be  based,  of  course,  on  accurate 
diagnosis.  The  following  details  mar  be  of  use  to  those  who  are  not  familiar  with 
the  method  of  blood  examination.  The  finger  tips  should  fii-st  be  scrubbed  with  a 
nail-brush,  and  soap  and  water,  and  then  washed  in  alcohol  or  ether,  to  obviate  the 
danger  of  mistaking  minute  particles  of  dirt  for  the  pigment-granules  derived  from 
the  destruction  of  red  blood-corpuscles.  A  portion  of  a  drop  of  blood  is  then  to  be 
received  on  a  scrupulously  clean  object-  or  cover-glass,  and  squeezed  out  between 
the  two,  so  that  a  thin  layer  of  blood  with,  separation  of  the  individual  corpuscles 
is  secured.  The  amoeboid  forms  of  the  Plasmodium  retain  their  movements  for  a 
niunber  of  minutes  in  a  warm  room,  much  longer,  of  course,  with  a  warm  stage. 
The  presence  of  pigment-granules  in  the  red  corpuscles  may  be  the  readiest  indi- 
cation of  the  presence  of  the  organism.  The  erescentic  forms  are  found  more 
especially  in  chronic  cases  which  have  been  under  treatment  by  quinine,  as  is 
stated  by  Osier.  Many  of  the  other  forms  can  be  found  in  the  blood  only  during 
a  paroxysm.  The  editor  has  seen  them  in  abundance  in  a  cachectic  malarial 
patient  from  Panama,  and  failed  to  find  them  ag'ain  after  a  single  large  dose  of 
quinine,  which  terminated  the  chills. 

In  dried  and  stained  specimens  it  is  also  possible  to  detect  the  organisms,  but 
amoeboid  movement  is,  of  course,  lost.] 

Liability  to  the  disease  is  very  widespread.  Xo  race,  no  age,  no  sex,  enjoys 
immunity.  It  is  a  noticeable  fact  that  those  who  have  had  the  disease  once  are 
all  the  more  apt  to  have  it  again.  Former  patients,  although  they  feel  perfectly 
well  in  a  non-malarious  region,  are  very  liable  to  fresh  attacks,  or  at  least  much 
discomfort,  as  soon  as  they  re-enter  an  infected  district.  The  time  of  incubation 
does  not  seem  to  be  constant.  It  is  put  at  from  six  to  twenty  days,  but  may  be 
shorter.  We  shall  consider  below  chiefly  the  common  forms  of  intermittent,  such 
as  appear  in^Germany,  contenting  ourselves  with  a  very  brief  description  of  the 
severer  forms. 

Varieties  of  ]\Ialaeial  Disease 

1.  Intermittent  Fever.— This  is  the  simplest  form,  and  has  for  its  especial 
characteristic  the  relative  brevity  of  the  febrile  attacks,  which  almost  always 
exhibit  a  remarkably  uniform  type.  A  febrile  attack  of  this  kind  is  frequently 
the  very  first  symptom  of  the  disease.  In  other  cases  the  paroxysm  of  fever  is 
preceded  by  a  prodromal  stage  lasting  several  days,  during  which  the  patient  feels 
languid,  has  no  real  appetite,  complains  of  headache  and  pain  in  the  back  of  the 
neck  and  in  the  limbs,  and  often  even  thus  early  presents  a  slig-htly  yellowish 
complexion  and  an  enlarged  spleen. 

In  the  typical  attack  of  intermittent  fever  there  are  three  stages.  The  attack 
begins  with  a  chill.  There  is  pronounced  malaise,  attended  by  intense  chilliness 
and  more  or  less  shivering.  The  skin  is  cool  and  pale,  the  face  may  be  somewhat 
livid.  The  temperature  of  the  interior  of  the  body  is  elevated,  and  rapidly  rises 
higher.  In  by  far  the  greater  nxunber  of  cases  the  attack  occurs  in  the  morning, 
or  at  least  before  noon,  and  but  seldom  later  in  the  day.  This  cold  stage  varies 
greatly  in  length,  usually  lasting  an  hour  or  two. 

The  chilliness  is  followed  by  the  hot  stage.  The  skin  grows  burning  hot,  the 
face  flushes,  the  pulse,  which  was  before  small,  becomes  full,  and  the  action  of  the 
heart  is  excited.  At  first  the  temperature  continues  to  increase,  and  reaches  in 
this  stage  its  maximum  for  the  attack.  It  is  exceptional  for  it  to  remain  under 
104°  (40°  C),  and  by  no  means  rare  for  it  to  touch  106°,  or  even  107°  (41°-41.5° 
C).  This  stage  almost  always  lasts  longer  than  the  preceding,  generally  about 
three  to  five  hours.  The  temperature  may  begin  to  fall  as  early  as  the  latter  part 
of  the  hot  stage,  but  may  persist  till  the  beginning  of  the  third  stage. 

In  this  sweating  stage  the  skin  grows  moist,  and  there  is  soon  a  profuse  gen- 


MALARIAL   DISEASES 


97 


eral  perspiration.  The  patient  begins  to  feel  much  better.  In  a  few  hours  the 
temperature  usually  becomes  normal,  and,  after  lasting  in  all  about  eight  to  twelve 
hours,  the  attack  is  over.  It  may  be  shorter  or  rarely  longer.  Usually,  however, 
the  temperature  keeps  on  sinking  slowly,  so  as  to  be  still  subnormal  even  on  the 
next  morning,  perhaps  not  above  97°   (36°  C). 

There  are  certain  peculiarities  in  the  temperature-curve  which  we  have  our- 
selves observed.  The  elevation  of  temperature  is  almost  invariably  more  rapid 
than  its  decline.  The  rise  is  most  abrupt  during  the  first  hours  of  the  cold  stage, 
and  slower  during  the  first  portion  of  the  hot  stage.  The  ascent  is  but  very  sel- 
dom interrupted.  During  the  hot  stage,  w^hen  the  fever  is  highest,  in  the  neigh- 
borhood of  106°  F.  (41°  C),  there  are  not  infrequently  two  little  summits  to  the 
fever-curve,  if  the  temperature  be  taken  at  short  intervals.  But  the  temperature 
may  for  hours  remain  the  same.  The  temperature  generally  begins  to  fall  some 
little  time  before  the  perspiration  is  evident.  The  decline  is  slow.  It  may  be  per- 
fectly continuous,  or  it  may  be  interrupted  by  fresh  elevations,  which  are  some- 


40.0° 


38.0° 


37.0° 


36.0= 


41.0° 


40.0° 


39.0° 


38.0° 


37.0° 


36.0' 


■niBHjBijnn 


Fig.  11. — Quotidian  inter- 
mittent fever. 


Fig.  1:2, — Tertian  intermittent  fever. 
[Chinin  3.0  =  Quinine  30  grains.] 


times  slight  and  sometimes  considerable.  In  many  cases  the  descent  is  by  steps, 
the  temperature  remaining  the  same  for  half  an  hour  or  an  hour,  and  then 
abruptly  falling  a  couple  of  degrees  and  remaining  for  a  time  at  this  new  level. 
The  chief  characteristic  is  not,  however,  the  nature  of  the  single  attacks,  but 
the  peculiar  manner  of  their  repetition.  If  the  case  is  not  under  treatment,  the 
single  attacks  keep  recurring  for  a  time,  either  daily,  as  in  the  quotidian  variety, 
or  every  second  day.  This  latter  type  of  tertian  intermittent  fever  (cf.  Figs.  11 
and  12)  is  probably  the  most  frequent.  There  may  exceptionally  be  still  longer 
afebrile  intervals.  Thus  we  have  quartans,  quintans,  etc.  If  there  are  two  attacks 
in  one  day,  a  rare  event  among  us,  we  have  a  double  quotidian.  If  there  is 
a  violent  attack  every  second  day,  and  on  the  intervening  days  there  are  milder 
attacks,  it  is  a  case  of  double  tertian.  Very  often  the  attacks  do  not  recur  at  just 
the  same  time  of  day,  but  a  few  hours  earlier  each  time.  Less  frequently  they 
are  later.  This  peculiarity  is  expressed  by  the  term  "  anticipating  "  or  "  retard- 
ing," as  the  case  may  be — e.  g.,  a  retarding  tertian  ague.  In  cases  of  long  stand- 
ing, the  paroxysms  may  finally  lose  all  regularity,  so  that  the  fever  is  described  as 
*'  erratic." 

7 


98  ACUTE    GENEEAL   EN"FECTIOUS    DISEASES 

Xext  to  the  febrile  attacks,  the  swelling  of  the  spleen  is  the  most  constant  and 
important  symptom.  It  is  usually  considerable  and  capable  of  demonstration  by 
percussion  and  palpation.  At  first  the  tumor  increases  with  every  fresh  attack, 
and  diminishes  but  little  during  the  intervals.  After  the  patient  is  freed  from  his 
attacks  of  fever  the  spleen  naay  continue  enlarged  for  some  time.  It  is  tender  on 
pressure.  [Certainly  in  many  cases  tenderness  is  absent. — V.]  The  liver  may 
likewise  be  swollen,  but  this  is  less  constant  and  also  less  important. 

Certain  changes  in  the  skin  are  very  characteristic,  chief  among  which  is  a 
peculiar  yellowish-brown  discoloration.  This  is  due  to  an  abnormal  deposition  of 
pigment  in  the  skin.  Herpes  on  the  lips  or  nose  is  seen  very  frequently  during 
the  attacks.  We  have  seen  one  case  of  herpes  on  the  cornea.  Mention  has  also 
been  made  of  urticaria,  purpura,  and  other  eruptions. 

Other  internal  organs  than  those  already  spoken  of  are  rarely  much  disturbed. 
One  symptom  should  be  mentioned,  which  we  have  ourselves  seen  several  times, 
viz.,  a  quite  marked  acute  dilatation  of  the  heart  during  the  attack.  There  were 
no  bad  results,  and  the  normal  condition  was  soon  re-established.  We  may  hear 
during  the  attack  functional  cardiac  murmurs  of  a  blowing  character.  Thoracic 
examination,  particularly  if  made  during  the  attack,  may  afford  the  signs  of  a 
dry  bronchitis.  Sometimes  there  is  considerable  diarrhoea,  or  other  evidence  of 
intestinal  derangement.  Catarrhal  jaundice  is  confined  to  the  severer  cases. 
Sometimes  the  urine  has  a  moderate  amount  of  albumen.  Genuine  nephritis  is 
met  with  only  in  the  graver  varieties  of  the  disease.  The  increased  excretion  of 
urea  on  the  days  of  the  fever  results,  as  in  any  fever,  from  the  increased  destruc- 
tion of  albimaen.  Severe  pain  in  the  cervical  and  upper  dorsal  vertebraB  is  re- 
garded as  characteristic  of  intermittent. 

Besides  the  typical  attacks,  rudimentary  and  modified  ones  are  not  rare,  in 
which  the  separate  stages  are  ill  defined,  or  in  part  wanting.  We  are  most  apt  to 
see  this  in  cases  which  have  been  already  treated  with  quinine.  Children  do  not 
have  a  true  rigor.  They  merely  become  pale  or  livid.  They  may  present  marked 
nervous  symptoms. 

2.  Pernicious  Intermittent  Fever. — This  dangerous  form  occurs  only  in  the 
true  malarial  districts,  and  is  often  preceded  by  a  few  attacks  of  a  milder  charac- 
ter. Then  appear,  in  addition  to  the  more  or  less  perfectly  marked  stages  of  the 
febrile  attack,  other  graver  symptoms  which  not  infrequently  end  in  death. 
Severe  nervous  symptoms  are  most  frequent.  There  may  be  unconsciousness, 
coma,  delirium,  or  epileptiform  or  tetanic  convulsions,  ^one  of  these  symptoms 
persist  longer,  as  a  rule,  than  does  the  common  sort  of  an  attack,  and  in  a  favor- 
able case  vanish  completely  when  the  sweating,  which  is  usually  profuse,  begins. 
The  great  danger  comes  from  the  recurrence  of  the  attacks.  A  second  form  of 
pernicious  intermittent  fever  causes  violent  gastro-intestinal  symptoms,  which 
may  almost  exactly  imitate  the  algid  stage  of  cholera,  with  vomiting,  diarrhcea, 
and  collapse;  or  there  may  be  severe  cardialgia,  dysentery,  and  the  like.  In  the 
so-called  pernicious  intennittent  with  jaundice,  intense  jaimdice  appears  during 
the  attack,  with  vomiting  and  diarrhoea,  and  sometimes  the  gravest  nervous  symp- 
toms. There  are  certain  very  peculiar  fonns,  in  which  local  disorders,  such  as 
pleurisy  or  pneumonia,  can  be  demonstrated  during  every  attack,  but  vanish 
wholly  or  in  part  when  the  temperature  declines,  only  to  appear  again  during  the 
next  attack. 

[The  pernicious  form  occurs  in  isolated  cases  wherever  the  ordinary  variety  of 
the  disease  prevails,  but  is  much  more  common  in  the  Southern  and  Western 
States,  and  there  varies  in  frequency  in  different  years.  Periodicity  in  the  attack 
is  not  always  obseiwed.  The  pernicious  character  is  not  always  manifested  in  the 
first  attack,  one  or  more  mild  paroxysms  being  often  precedent.  In  this  country 
the  algid  form  of  pernicious  periodic  fever  is  often  called  "  congestive  chills,"' 


MALAEIAL   DISEASES  99 

and  this  f onu  is  more  common  than  the  comatose  or  another  form  mentioned  below 
by  the  author — the  hemorrhagic.  In  the  latter  the  blood  escapes  from  the  kid- 
neys, and  less  constantly  from  the  mucous  membrane.  During  the  late  civil  war 
the  mortality  among  the  white  soldiers  of  the  United  States  army  from  pernicious 
malarial  fever  was  23.91  per  cent.] 

3.  Remittent  and  Continuous  Forms  of  Malarial  Fever. — These  are  generally 
severe,  and  are  seen,  like  the  preceding,  only  in  the  worst  haunts  of  malaria.  The 
proof  that  they  have  the  same  etiology  as  intermittent  fever  lies  in  the  fact  that 
they  are  sometimes  developed  out  of  the  milder  forms ;  but  it  is  to  be  noticed  that 
many  types  of  disease  which  physicians  in  the  tropics  describe  as  malarial  affec- 
tions have  not  yet  been  proved  to  our  satisfaction  to  have  an  actual  identity  of 
origin  with  the  common  intermittent  fever.  A  positive  diagnosis  can  be  made 
only  by  examining  the  blood  for  the  plasmodia.  The  symptoms  of  this  variety  are 
likewise  those  of  a  severe  constitutional  infection.  Gastro-intestinal  symptoms 
may  predominate;  or  there  may  be  such  grave  nervous  symptoms  as  coma,  deliri- 
um, and  convulsions;  or  there  may  be  jaundice,  hsematuria,  and  even  a  general 
hemorrhagic  diathesis;  or  various  local  disorders  may  exist,  such  as  pneumonia, 
nephritis,  and  hepatic  and  splenic  abscesses.  The  fever  is  high,  but  without  any 
sort  of  regular  intermissions,  maintaining  for  one  or  two  weeks  a  remittent  or  a 
tolerably  continuous  type.  Milder  forms  may  end  in  recovery  after  eight  to  four- 
teen days,  but  often  death  ensues  at  this  time,  or  even  earlier. 

[The  remittent  form  apparently  shows  a  greater  intensity  of  the  poison  or  a 
greater  susceptibility  of  the  individual.  In  the  United  States  army,  from  1861  to 
1866,  its  mortality  was  twelve  times  as  great  as  that  from  the  intermittent  form.] 

4.  Chronic  Malarial  Cachexia. — This  occurs  in  the  true  malarial  regions,  and 
affects  not  only  persons  who  have  had  frequent  attacks  of  pronounced  intermittent 
or  remittent  fever^  but  also  those  who  have  never  had  acute  attacks.  The  condi- 
tion is  chronic.  It  may  exhibit  a  genuine  intermittent  character.  The  patient 
usually  has  a  decidedly  yellowish,  malarial  complexion,  and  almost  always  the 
spleen  is  evidently  enlarged.  There  are  no  regular  febrile  attacks,  but  merely 
symptoms  of  general  debility,  anorexia,  tendency  to  diarrhoea,  or,  more  rarely, 
constipation,  vertigo,  wakefulness,  frequent  perspiration,  pain  in  the  muscles  and 
joints,  dyspncea,  and  palpitation.  There  may  be  such  nervoiis  symptoms  as  trem- 
bling, paralysis,  and  mental  disturbance  [or  multiple  neuritis,  q.  v.'\  ;  or  we  may 
see  intestinal  symptoms  and  jaundice.  Dropsy  occurs;  also  epistaxis,  cutaneous 
ecchymoses,  and  other  signs  of  a  scorbutic  condition.  The  spleen  and  liver  gradu- 
ally become  greatly  hypertrophied  and  melanotic.  At  the  same  time  there  may 
be  an  irregular  fever,  approaching  either  an  intermittent  or  a  remittent  in  type. 
Finally,  secondary  diseases  are  possible — e.  g.,  tuberculosis,  amyloid,  or  dysentery 
— and  these  may  prove  the  immediate  cause  of  death.  The  milder  forms  may 
be  cured,  but  seldom  unless  the  patient  abandons  forever  the  malarial  district. 

5.  Masked  Intermittent. — This  is  the  designation  of  cases  in  which,  although 
there  is  no  fever,  certain  other  disturbances  arise  in  regular  intennittent  attacks. 
Chief  among  these  is  neuralgia.  Its  favorite  seat  is  the  supra-orbital  branch  of 
the  trigeminus.  It  may  occur  in  the  other  branches  of  the  same  nerve,  or  in  the 
sciatic,  the  anterior  crural,  the  nerves  of  the  brachial  plexus,  and  elsewhere.  Car- 
dialgia  and  enteralgia  may  occur  in  the  same  way.  These  attacks  last  from  thirty 
minutes  to  several  hours,  and  are  frequently  associated  with  all  sorts  of  constitu- 
tional symptoms,  but,  as  we  have  said,  are  afebrile.  There  may  be  a  splenic  tumor, 
which  aids  diagnosis ;   but  this  sign  may  be  wanting. 

Numerous  other  intermittent  disorders  besides  neuralgia  have  been  described 
as  masked  intermittent.  The  list  includes  anaesthesia,  convulsions,  and  paralysis; 
also  intermittent  hemorrhage,  oedema,  cutaneous  affections,  and  intestinal  symp- 
toms.   We  must  add,  however,  that  those  who  have  described  diseases  of  this  sort, 


100  ACUTE   GENEEAL  rN"FECTIOUS   DISEASES 

some  of  whicli  seem  strange  enough,  have  not  always  been  as  critical  as  they 
ought,  and  that  the  connection  between  many  cases  of  "  masked  intermittent  "  and 
true  malaria  is  more  than  doubtful. 

[6.  Typho-Malarial  Fever. — This  is  a  term  which  was  formerly  in  use,  but  it 
is  not  a  distinct  disease.  It  expresses  a  combination  in  the  same  individual 
at  the  same  time  of  the  effects  of  the  special  poison  causative  of  each  affection. 
Typhoid  being  a  continued  fever,  its  complication  with  malaria  results  in  a 
pyrexia  of  a  remittent  type.  The  combination  of  the  two  occurs  in  malarial  re- 
gions, especially  in  the  Southern  States,  and  may  be  seen  in  non-malarial  regions 
in  the  persons  of  those  in  whom  malaria,  contracted  elsewhere,  is  in  a  more  or  less 
active  state. 

The  characteristic  symptoms  of  the  two  diseases  are  intermingled,  those  of 
typhoid,  the  graver  disease,  usually  predominating.  The  history  of  the  case  and 
careful  observation  of  the  symptoms  will  generally  clear  up  any  doubts  felt  as 
to  the  diagnosis  in  the  early  stages.  It  would  naturally  be  supposed  that  the 
combined  affections  must  produce  an  illness  more  severe  in  character  and  more 
unfavorable  as  regards  prognosis  than  belongs  to  simple  typhoid.  Such  does  not, 
however,  seem  to  be  the  case.  Woodward's  statistics  show  that  the  mortality  of 
uncomplicated  typhoid  was  far  greater  among  the  white  and  colored  troops  alike 
during  our  late  civil  war  than  was  the  mortality  of  typho-malarial  fever. 

The  treatment  as  regards  the  typhoid  fever  differs  in  no  way  from  that  suitable 
for  cases  of  the  ordinary  affection;  the  periodic  element  demands  the  manage- 
ment appropriate  to  simple  intermittent  or  remittent  fever.] 

Diagnosis. — ^It  is  often  very  difficult  to  diagnosticate  a  case  of  intermittent 
fever  at  the  first  visit,  particularly  in  a  place  where  malarial  poisoning  is  infre- 
quent. The  history  of  the  case  is  by  no  means  always  enough  to  put  one  on  the 
right  track;  and  a  single  examination  of  the  patient  may  prove  equally  negative 
in  its  practical  results,  whether  it  is  made  during  the  febrile  stage  or  in  the  inter- 
val. Continued  observation,  however,  will  almost  always  disclose  the  regularity  of 
the  febrile  attacks,  the  splenic  tumor,  the  characteristic  complexion,  and  the 
herpes;  and  our  diagnosis  becomes  evident.  Still  it  is  not  very  exceptional  for 
an  intermitting  fever  to  be  taken  at  first  for  an  intermittent  malarial  one,  while 
eventually  some  quite  different  disease  is  found  to  produce  the  symptom.  Pyaemia 
may  give  rise  to  mistakes  of  this  kind;  also  purulent  phlebitis,  acute  vilcerative 
endocarditis,  and  even  tuberculosis.  We  should  be  very  cautious  in  making  a 
hasty  diagnosis  of  "  irregular  intermittent  fever."  Our  own  experience  has  taught 
us  that  almost  invariably  the  case  turns  out  to  be  something  else.  Where  there  is 
doubt  we  may,  in  addition  to  a  careful  consideration  of  all  the  symptoms  and  a 
thorough  physical  examination,  be  aided  by  the  therapeutic  action  of  qui- 
nine (vide  infra).  If  a  high  fever  of  intermitting  type  is  affected  by  large 
doses  of  quinine  but  temporarily  if  at  all,  then  a  diagnosis  of  malarial  intermit- 
tent fever  is  rendered  doubtful.  An  absolutely  certain  diagnosis  can  be  made 
only  by  finding  the  plasmodia  in  the  blood  under  the  microscope.  We  have 
already  said  that  the  greatest  skepticism  is  requisite  in  the  diagnosis  of  "  masked 
intermittent." 

Treatment. — Malarial  poisoning  is  one  of  the  few  diseases  upon  which  we  can 
make  a  direct  attack  with  assured  success.  In  quinine  we  possess  a  remedy  which 
probably  acts  upon  the  veiy  cause  of  the  disease,  and  its  therapeutic  efficacy 
is  undisputed.  Quinine  is  therefore  the  sovereign  remedy  in  all  forms  of 
malarial  poisoning,  and  is  often  the  only  drug  employed.  In  the  mild  cases, 
which  are  the  only  kind  that  occur  in  Germany,  we  do  not  usually  give  the  remedy 
upon  the  instant  that  the  patient  comes  under  treatment.  It  is  best  to  wait  for 
one  or  two  attacks,  partly  to  make  sure  of  our  diagnosis,  and  partly  to  learn  what 
the  type  of  the  fever  is,  whether  quotidian,  tertian,  anticipating,  or  recurring  at 


MALAEIAL   DISEASES  101 

the  same  hour;  and  in  most  cases  this  delay  works  no  hann  to  the  patient.  Dur- 
ing the  attack  itself  there  is  seldom  any  use  in  special  treatment.  Of  course, 
the  patient  must  stay  in  bed  and  be  kept  warm  during  the  cold  stage,  and  have 
lighter  coverings  during  the  hot  stage.  During  the  afebrile  interval  the  patient 
may  be  up  if  he  feels  strong  enough  and  is  careful.  Quinine  (hydrochlorate  or 
sulphate)  is  given  about  five  or  six  hours  before  the  next  attack  is  due.  It  is 
best  to  administer  one  large  dose  of  twenty  to  thirty  grains  (1.5-2  grm.),  either 
in  solution  or  in  capsules  of  seven  grains  (0.50  grm.)  each.  If  the  quinine  be 
given  in  powder  or  capsules,  it  is  a  good  way  to  follow  it  with  a  few  drops  of 
muriatic  acid,  to  promote  its  solution  in  the  stomach.  Often  one  large  dose  pre- 
vents the  next  attack.  In  other  cases  it  does  occur,  but  with  less  subjective  dis- 
turbance, no  chill,  and  more  moderate  fever.  We  must  then  give  another  large 
dose  before  the  second  attack  is  expected.  If  the  attack  does  not  take  place,  then 
we  may  give  for  several  days  quinine  to  the  arhount  of  eight  grains  (0.5  grm.) 
per  diem.  After  all,  relapses  are  possible,  even  at  the  end  of  several  weeks;  but 
they  yield  readily  to  quinine. 

In  the  treatment  of  pernicious  intermittent  fever,  of  the  masked  forms,  of  the 
remittent  and  continued  fevers,  and  of  malarial  cachexia,  the  chief  remedy  is  like- 
wise quinine,  given  in  sufficient  doses.  Baccelli  has  shown  that  sometimes  in 
pernicious  fever  the  direct  injection  of  quinine  into  a  vein  may  save  life.  In  all 
cases  of  considerable  duration  it  is  also  of  the  greatest  importance  to  remove  the 
patient  from  the  malarial  region,  if  it  can  possibly  be  done.  This  often  proves  to 
be  the  only  way  to  avoid  relapses  and  attain  a  perfect  cure. 

In  cases  of  longer  standing,  quinine  sometimes  loses  its  power.  Then  we  resort 
to  arsenic.  It  is  frequently  employed  in  malarial  cachesfia  and  in  intermittent 
neuralgia,  either  alone  or  combined  with  iron.  We  give  gtt.  v  to  viij  of  Fowler's 
solution  two  or  three  times  a  day  in  water.  It  is  still  better  to  give  pills  of  arseni- 
ous  acid  containing  gr.  ^  -  5V  (grm.  0.002-0.003)  and  gradually  increasing  to  a 
daily  dose  of  gr.  I  -A  (grm.  0.010-0.012).  It  may  be  added  that  arsenic  is  also  said 
to  have  a  prophylactic  virtue :  a  long-continued  use  of  it  is  stated  to  render  a  per- 
son proof  against  malarial  poisoning.  We  will  not  speak  of  the  numerous  other 
remedies  recommended,  such  as  eucalyptus,  piperine,  pilocarpine,  berberine,  and 
many  others,  for  they  can  be  entirely  dispensed  with. 

The  management  of  the  severe  varieties  of  malarial  disease  involves  symptom- 
atic treatment  as  well  as  the  administration  of  quinine.  We  can  not  enter  into 
the  particulars.  In  combating  the  grave,  nervous,  intestinal,  pulmonary,  and  renal 
symptoms,  the  dropsy  and  the  angemia,  the  physician  must  conf  oi-m  to  the  general 
rules  of  treatment. 

[There  is  nothing  to  be  gained  by  allowing  a  patient  to  have  an  unnecessary 
chill.  If  there  is  a  reasonable  probability  that  his  paroxysms  are  due  to  malaria, 
a  prompt  effort  should  be  made  to  cut  them  short.  Four  hours  is  the  shortest 
time  that  it  is  safe  to  allow  for  quinine  by  the  stomach  with  probability  that  the 
expected  chill  will  be  prevented.  The  drug  acts  much  more  promptly  when 
given  hypodermically.  The  hydrobromate  is  preferred  by  some  to  the  sulphate 
for  subcutaneous  use  on  account  of  the  necessity  of  using  acid  to  dissolve  the 
latter,  and  the  consequent  risk  of  abscess.  Such  a  risk  should  have  no  weight  if 
the  physician  has  any  suspicion  that  he  has  to  deal  with  the  pernicious  form  of 
the  disease.  If  the  stomach  is  irritable,  the  remedy  can  be  given  by  enema. 
Quinine  can  also  be  given  by  suppository,  though  it  may  thus  produce  some  irri- 
tability of  the  rectum;  but  the  impossibility  of  disguising  the  bitter  taste  of  the 
remedy  or  of  making  children  swallow  capsules  renders  this  a  valuable  means  of 
treatment  sometimes  in  infants  and  young  children. 

Warburg's  tincture  is  an  antiperiodic  which  does  good  service  in  cases  which 
do  not  yield  to  the  ordinary  methods  of  treatment. 


102  ACUTE   GENEEAL   INFECTIOUS    DISEASES 

The  hypodermic  injection  of  pilocarpine  is  reported  to  abort  an  impending 
chill. 

Some  prefer  divided  and  smaller  to  the  single  and  large  dose  of  quinine  or  one 
of  its  substitutes,  a  difference  of  view  which  is  of  minor  importance. 

In  the  remittent  forms  boldness  in  the  use  of  quinine  is  required.  Cinchonism 
should  be  induced  as  promptly  as  may  be,  and  maintained  to  a  mild  degree  for 
several  days;    the  quantity  of  the  drug  can  then  be  gradually  diminished. 

The  treatment  of  the  pernicious  forms  of  periodic  fever  presents  itself  under 
three  main  heads : 

1.  The  prevention  of  pernicious  paroxysms. 

2.  The  treatment  of  the  paroxysm  when  present. 

3.  The  prevention  of  a  recurrence. 

1.  We  have  seen  that  very  frequently  the  pernicious  character  is  manifested 
after  the  occurrence  of  one  or  more  mild  attacks ;  consequently,  in  localities  and 
seasons  marked  by  the  occurrence  of  grave  cases  it  is  an  imperative  duty  to  treat 
every  mild  case  promptly  and  energetically,  a  course  which  unquestionably  saves 
many  a  life. 

2.  The  management  of  the  paroxysm  differs  according  to  the  form  which  it 
assumes ;  in  other  words,  is  largely  symptomatic.  Bemiss  (Pepper's  "  System  of 
Medicine  ")  says :  "  The  cure  of  a  congestive  chill  is  one  of  the  most  difficult  prob- 
lems the  physician  can  possibly  encounter."  Heat  externally,  opium  and  chloro- 
form by  the  mouth,  and  moi-phine  and  atropine  subcutaneously,  nutrition  by  the 
stomach  or  rectum,  according  to  circumstances,  and  alcoholics  if  the  action  of  the 
heart  is  feeble,  are  the  measures  of  widest  application. 

Whatever  the  type  of  the  attack,  a  weak  heart  calls  for  alcoholic  stimulation. 
Cinchonism  is  always  to  be  induced  as  rapidly  as  possible. 

In  the  comatose  form  it  is  to  be  remembered  that  the  cerebral  and  other  nervous 
symptoms  are  not  due  to  congestion,  but  probably  to  a  combination  of  the  malarial 
and  secondary  blood-poisons.  To  quote  Bemiss  again :  "  Efforts  to  nourish  the 
patient  must  never  be  relaxed.  One  must  see  many  of  these  cases  before  he  can 
realize  how  often  they  recover  from  conditions  apparently  hopeless  when  promptly 
treated  and  properly  nourished." 

The  hsemorrhagic  form,  like  the  others,  demands  cinchonism  and  careful  nutri- 
tion, but  also  haemostatics.  Purgative  doses  of  calomel  are  indicated  in  some  cases 
of  each  form,  but  should  not  be  given  in  a  routine  manner. 

3.  Prompt  cinchonism  is  the  chief  means  of  attaining  the  third  aim  of  treat- 
ment. Removal  to  a  healthy  locality  should  be  secured  if  possible,  and  the  general 
condition  of  the  patient  requires  careful  attention. 

It  remains  to  add  that  those  going  to  a  malarial  region  can  often  avoid  con- 
tracting the  disease  by  taking  advice  of  a  local  physician  as  to  hygienic  precau- 
tions, and  by  moderate  divided  doses  of  quinine.] 


CHAPTEE  XV 
DENGUE 

[This  affection  has  never  appeared  in  Germany,  and  hence,  doubtless,  was 
omitted  by  the  author.  The  name  "  dengue  "  is  supposed  to  be  a  Spanish  corrup- 
tion of  dandy,  the  term  dandy  fever  having  been  applied  to  the  disease  by  the 
West  India  negroes  on  account  of  the  stiff  carriage  of  those  affected  by  it.  An- 
other name  is  "  break-bone  fever." 


DENGUE  103 

The  disease  generally  appears  in  epidemics,  and  is  almost  exclusively  confined 
to  tropical  and  semi-tropical  countries.  In  1870  an  epidemic  supposed  to  be 
dengue  prevailed  in  Philadelphia,  and  outbreaks  have  occurred  repeatedly  in  the 
Southern  States  in  the  last  hundred  years.  In  1880  Charleston,  Savannah,  New 
Orleans,  and  other  Southern  cities  were  visited  by  it.  There  are  those  who  main- 
tain that  dengue  and  epidemic  influenza  are  identical,  a  view  which  the  facts  do 
not  seera  to  the  editor  to  bear  out. 

.ffitiology. — As  to  the  causation  but  little  is  known.  Those  who  have  had 
opportunities  of  studying  the  disease  consider  it  both  contagious  and  infectious, 
and  the  inference  that  it  depends  on  a  specific  gerra  is  readily  suggested.  It 
seems  to  prefer  low  lands  along  the  sea-shore,  and  to  be  influenced  by  meteoro- 
logical conditions  in  that  it  generally  prevails  during  the  summer  and  disappears 
as  cold  weather  comes  on.  Neither  age,  sex,  nor  condition  affords  any  protection 
from  the  disease;  it  was  thought  by  Dickson  that  one  attack  generally  confers  im- 
munity for  life. 

Pathology. — The  disease  is  so  rarely  fatal  that  few  opportunities  have 
been  afforded  for  its  post-mortem  study.  So  far  as  is  known,  it  has  no  pecul- 
iar lesions.  The  prominence  and  the  character  of  the  muscle  and  joint  pains 
have  led  some  observers  to  think  the  affection  related  in  some  way  to  rheu- 
matism. 

Symptoms  and  Course. — The  onset  is  usually  sudden,  but  a  pronounced  chill  is 
said  never  to  occur.  Prodromata  similar  to  those  of  other  infectious  diseases  are 
sometimes  observed,  but  the  first  symptom  is  very  often  pain  and  stiffness  in  the 
muscles  and  joints,  with  frequent  swelling  of  the  latter.  The  large  and  small 
joints  are  equally  affected,  and  the  pain  is  increased  by  motion.  With  the  pain 
there  is  a  rise  in  temperature  and  in  the  frequency  of  the  pulse.  The  pain  is  apt 
to  increase  during  the  first  two  or  three  days  and  disapiDcar  on  the  fifth,  but  irreg- 
ular remissions  are  liable  to  occur.  As  the  thermometer  falls  the  pain  and  other 
symptoms  diminish,  but  reappear  in  full  force  with  any  subsequent  rise.  During 
the  later  days  of  the  disease  a  skin  eruption  appears  on  the  upper  part  of  the  body, 
and  in  severe  cases  becomes  general  in  about  two  days.  This  eruption  is  very 
variable  in  character ;  it  may  appear  simply  as  an  erythema,  or  simulate  the  erup- 
tions of  scarlet  fever,  rubeola,  lichen,  or  urticaria ;  it  is  apt  to  be  associated  with 
well-marked  heat  and  itching  of  the  skin.  In  mild  cases  the  eruption  is  evanes- 
cent or  absent.  Swelling  of  the  lymphatic  glands  is  not  uncommon ;  in  severe 
cases  the  mucous  membrane  of  the  mouth,  throat,  and  nose  is  reddened,  and  haem- 
orrhage from  the  outlets  of  the  body  has  been  observed.  Pregnant  women  are 
apt  to  miscarry.  Delirium  is  rare  in  adults,  but  common  in  children ;  the  face  is 
generally  flushed,  and  the  eyes  are  injected;  the  tongue  becomes  increasingly 
coated  as  the  disease  progresses,  the  appetite  is  lost,  nausea  is  not  uncommon, 
vomiting  is  rare.  The  bowels  and  the  kidneys  present  no  constant  or  distinctive 
symptoms. 

In  mild  cases  recovery  is  sometimes  rapid;  sometimes,  and  especially  after 
severe  cases,  convalescence  is  very  tedious,  the  muscular  and  articular  pain  and 
stiffness  passing  off  gradually,  and  the  glandular  swelling  lasting  for  weeks. 
Copious  skin  eruptions  are  followed  by  desquamation. 

Diagnosis  and  Prognosis. — As  to  diagnosis  there  can  seldom  be  any  difficulty 
during  the  prevalence  of  an  epidemic.  The  first  cases  are  the  only  ones  which  are 
liable  to  be  mistaken,  and  even  their  nature  can  not  remain  long  in  doubt.  The 
prognosis  is  tinif  ormly  good. 

Treatment. — We  are  acquainted  with  no  agent  capable  of  aborting  or  cutting 
short  the  disease;  nor  is  there  any  known  measure  of  prophylaxis  except  for  an 
individual  to  keep  away  frora  those  places  in  which  the  affection  is  known  to 
prevail. 


104  ACUTE    GE^TEEAL   INTECTIOUS   DISEASES 

The  treatment  of  the  attack  is  simply  symptomatic;  notable  pain  calls  for 
opium  in  some  form.  Quinine  has  not  seemed  to  be  of  service.  Debility  follow- 
ing the  attack  demands  suitable  alimentation  and  tonics.] 


CHAPTEE  XVI 
YELLOW    FEVER 

[This  disease  is  not  a  visitant  of  Germany,  but  its  consideration  can  not  be 
omitted  from  a  text-book  on  the  practice  of  medicine  for  use  in  America.  In  the 
following  description  the  aim  will  be  to  bring  out  the  more  important  features  of 
the  disease,  while  for  fuller  details  the  reader  is  referred  to  larger  works  and 
monographs. 

.^Itiology. — Yellow  fever  is  an  acute  infectious  disease,  confined  within  cer- 
tain geographical  limits,  and  occurring  chiefly  in  epidemics  of  greater  or  less  ex- 
tent. In  certain  localities,  notably  Havana  and  jSTew  Orleans,  a  season  rarely 
passes  without  some  sporadic  cases.  The  influence  of  temperature  is  well  estab- 
lished ;  the  disease  prevails,  namely,  during  the  summer  or  the  warm  season,  and 
is  abruptly  arrested  by  one  or  two  decided  frosts;  dampness  is  favorable  to  it. 
That  it  depends  ultimately  on  a  special  cause  and  does  not  originate  de  novo  are 
undisputed  facts.  [Sanarelli  claims  to  have  found  the  specific  germ  in  a  minute 
bacterium,  occurring  in  pairs  and  with  rounded  ends,  which  he  calls  the  bacillus 
icteroides.  Other  authorities  do  not  as  yet  admit  that  this  bacillus  is  certainly  the 
cause  of  yellow  fever. — V.]  The  poison  appears  to  be  more  active  at  night  than 
during  the  day,  prefers  low-lying  districts,  and  in  them  hugs  the  ground  to  a  cer- 
tain extent.  Bad  sanitary  conditions  are  most  important  accessory  causes  of  the 
disease,  furnishing  the  soil  for  the  multiplication  of  the  poison.  There  can  be 
little  doubt  that,  under  the  observance  of  strict  personal  and  public  cleanliness, 
yellow  fever  visitations  might  be  made  simply  a  matter  of  history.  The  trans- 
mission of  the  poison  may  take  place  through  the  atmospheric  air,  thus  finding  its 
way  to  the  blood  through  the  lungs ;  conclusive  evidence  is  lacking  that  it  gains 
entrance  to  the  system  through  the  alimentary  canal.  [Eecent  investigations 
seem  to  indicate  that  it  may  be  transmitted  by  mosquitoes. — V.]  While  the  air 
may  be  the  medium  of  transmission,  the  distance  to  which  the  poison  can  be  car- 
ried by  the  air  alone  is  very  short ;  it  can,  however,  be  transported  to  an  indefinite 
distance  by  f  omites,  especially  if  inclosed  in  trunks,  packing-cases,  letters,  and  the 
like.  Its  vitality  may  thus  be  maintained  for  very  long  periods.  It  is  a  remark- 
able fact  that  in  large  cities  the  infection  may  be  of  great  virulence,  but  confined 
to  a  limited  district  or  districts,  by  carefully  shunning  which  unprotected  persons 
are  comparatively  safe.  An  infected  area  is  apt  to  extend  itself,  but  the  progress 
is  slow,  and  is  interrupted  by  streams  of  water,  high  walls,  or  simply  streets. 

That  the  disease  is  not,  strictly  speaking,  contagious  is  the  nearly  unanimous 
opinion  of  those  competent  to  form  one.  In  other  words,  the  poison  is  not  thrown 
off  in  a  matured  state  from  the  body  of  an  individual  suffering  from  the  disease; 
but,  after  being  so  thrown  off,  remains  in  the  atmosphere  or  lodges  on  solid  bodies, 
and  then  undergoes  changes  which  render  it  active  for  evil.  One  attack  of  the 
disease  renders  the  system  of  that  person  insusceptible  forever  after;  the  natives 
of  a  yellow-fever  district  are  far  less  liable  to  contract  the  disease  than  are  those 
who  move  into  the  district  from  elsewhere;  until  these  have  passed  through  an 
attack  they  can  not  consider  themselves  as  acclimated.  The  negro  race  is  sus- 
ceptible to  the  disease,  though  in  a  less  degree  than  the  whites,  and  in  the  colored 


■       YELLOW    TEYER  105 

the  affection  is  far  less  fatal.  Xeither  age  nor  sex  has  any  special  bearing  on  sus- 
ceptibility. That  fear,  anxiety,  worry,  or  anything  which  tends  to  depress  the 
nervous  system  increases  the  individual  liability  is  highly  probable.  The  stage 
of  incubation  is  very  variable,  ranging  from  one  day  to  three  weeks  or  even 
more. 

Pathological  Anatomy. — The  disease  involves  no  constant  and  peculiar  le- 
sions. In  rapidly  fatal  cases,  congestion  and  often  hemorrhage  are  found,  espe- 
cially in  the  nervous  system,  liver,  kidneys,  and  digestive  tract.  In  fatal  cases 
of  longer  duration  more  or  less  parenchymatous  degeneration  is  found.  A  fatty 
degeneration  of  the  liver  is  quite  common,  and  imparts  a  yellow  coloration  to  the 
organ,  giving  rise  to  the  terms  cafe  au  lait,  or  box-wood  liver.  Jaundice  of  the 
skin  and  tissues  generally  is  also  observable  after  death,  and  depends  upon  causes 
in -no  way  connected  with  mechanical  obstruction  to  the  flow  of  bile  into  the  intes- 
tine during  life.     Splenic  enlargement  is  conspicuous  by  its  absence. 

Course  and  Symptoms. — The  onset  of  the  disease  is  generally  sudden,  but  it 
may  be  preceded  for  a  few  days  by  malaise  and  other  signs  of  general  constitu- 
tional disturbance;  the  initial  chill  is  seldom  severe,  reaction  following  soon  and 
the  thermometer  rising  to  102°-105°  ;  hypei'pyrexia  is  rare.  The  pulse-rate  does 
not  increase  proportionately  with  the  fever.  The  face  becomes  flushed  and  the 
eyes  injected  and  watery;  headache  and  pain  in  the  back  are  early  and  usually 
very  prominent  symptoms.  The  bowels  are  confined ;  the  tongue  is  apt  to  be  clean 
if  it  was  so  before  the  disease  came  on ;  the  stomach  is  usually  somewhat  irritable, 
and  there  may  be  vomiting;  moderate  epigastric  tenderness  is  common;  the  mind 
remains  clear,  as  a  rule,  but  delirium  is  not  very  uncommon,  and  in  children  a 
convulsion  may  usher  in  the  attack  as  in  other  acute  infectious  diseases;  the  con- 
dition of  the  urine  is  at  first  not  remarkable,  but  albumen  may  soon  appear.  This 
hot  or  febrile  stage  may  last  from  twelve  hours  to  several  days.  The  pulse  gen- 
erally declines  in  frequency  before  the  disease  has  reached  its  maximum.  As  the 
fever  disappears  the  other  symptoms  vanish  also,  and  the  second,  or  "  stage  of 
calm,"  begins.  From  this  point  recovery  may  be  rapid  and  uninterrupted,  the 
whole  disease  consisting  of  but  a  single  febrile  paroxysm  of  greater  or  less  inten- 
sity and  of  short  duration. 

In  grave  cases,  and  gravity  is  often  foreshadowed  in  the  first  stage  by  marked 
capillaiy  congestion  of  the  surface  of  the  body  irrespective  of  the  intensity  of  the 
other  symptoms,  and  after  a  stage  of  calm  lasting  for  sorae  hours,  but  rarely  ex- 
ceeding twenty-four,  more  distinctive  symptoms  appear.  The  pulse  is  very  com- 
pressible, the  surface  of  the  body  is  cool,  vomiting  occurs  or  becomes  more  promi- 
nent, and  haemorrhage  is  now  apt  to  take  place.  The  escape  of  blood  into  the 
stomach,  its  retention  and  the  changes  which  it  there  undergoes,  and  its  susbse- 
quent  expulsion,  explain  the  dreaded  and  characteristic  symptom  know  as  "  black 
vomit."  Tarry  stools  sometimes  are  observed.  Haemorrhage  elsewhere  is  also 
common,  occurring  from  the  gums,  the  nose,  eyes,  uterus,  kidneys,  into  the  skin, 
etc.  Albuminuria  with  casts  is  very  common.  Jaundice,  sometimes  of  a  lemon- 
yellow  hue,  comes  on,  and  is  rarely  lacking  in  severe  cases.  From  this  symptom 
the  name  of  the  disease  is  derived. 

In  cases  marked  by  more  or  less  complete  suppression  of  urine,  coma  and  con- 
vulsions, probably  largely  urfemic,  come  on.  Some  severe  cases  are  of  the  "  walk- 
ing "  type,  the  patients  going  about  while  the  malady  is  far  advanced,  or  even  up 
to  the  time  of  death.     As  a  rule,  however,  muscular  prostration  is  marked. 

If  the  disease  does  not  prove  fatal  in  this  third  stage,  convalescence  comes  on 
more  or  less  gradually,  and  is  followed  by  complete  recovery;  relapses,  however, 
occasionally  occur. 

The  duration  of  the  affection  is  variable,  but,  on  the  whole,  short,  usually 
being  less  than  a  week. 


106  ACUTE   GENEEAL  INEECTIOUS   DISEASES 

Diagnosis. — In  mild  cases  the  symptoms  are  not  distinctive,  and  the  diagnosis 
at  the  commencement  of  an  epidemic  is  not  likely  to  be  reached  except  by  an 
experienced  observer,  and  even  by  him  more  or  less  con jectur ally.  During  an 
epidemic  the  severe  lumbar  pain,  the  headache,  the  suffusion  of  the  eyes,  and  the 
moderate  gastric  irritability,  are  all-sufficient  for  diagnostic  purposes.  Severer 
cases  are  also  marked  by  capillary  congestion  of  the  surface  of  the  body,  and  the 
third  stage  with  the  black  vomit,  haemorrhage,  jaundice,  slow  pulse,  scanty  urine, 
and  prostration  is  characteristic.  Of  course,  all  the  above  symptoms  are  not  pres- 
ent in  every  case.  The  only  disease  which  can  well  give  rise  to  confusion  is  remit- 
tent fever  with  jaundice.  This  affection  has  a  different  temperature-curve,  is  not 
confined  to  the  yellow-fever  zone,  is  controlled  by  quinine,  and  is  not  accompanied 
by  black  vomit. 

Prognosis. — This  varies  in  any  given  locality  with  the  character  of  the  preva- 
lent epidemic.  The  death-rate  is  sometimes  very  high,  sometimes  moderate ;  it  is 
greater  in  hospital  than  in  private  practice. 

In  the  first  stage  of  the  disease  the  chief  element  in  the  formation  of  the  prog- 
nosis seems  to  be  the  presence  of  marked  and  general  capillary  congestion  of  the 
skin,  a  symptom  which  foretells  a  severe  attack.  The  absence  of  this  symptom  is 
rather  less  important  than  its  presence.  Cases  may  turn  out  to  be  severe  in  which 
it  is  lacking.  The  frequent  deceptiveness  of  the  stage  of  calm  is  to  be  remem- 
bered. 

Yellowness,  black  vomit,  and  suppression  of  urine  are  symptoms  denoting  the 
greatest  gravity,  but  do  not  justify  the  complete  abandonment  of  hope. 

Treatment. — There  are  no  means  in  our  power  of  aborting  the  disease.  Pre- 
vention is  to  be  attained  by  cleanliness  in  its  large  sense,  and  by  careful  quaran- 
tine against  things  rather  than  persons.  Individuals  from  infected  localities  may 
safely  be  admitted  into  non-infected  localities,  provided  that  they  and  their  cloth- 
ing and  effects  are  thoroughly  disinfected.  Merchandise,  the  mails,  and  the  like, 
must  be  excluded  or  disinfected.  So  also  vessels  and  all  other  means  of  commu- 
nication. 

The  earlier  proper  treatment  can  be  instituted,  the  better.  Absolute  rest  and 
good  ventilation  are  the  first  requisites.  Emetics  and  cathartics  are  not  indicated 
by  the  disease  itself ;  the  condition  of  the  stomach  and  bowels  should  be  inquired 
into,  and  indigestible  food  or  an  accumulation  of  faeces  should  be  removed  if 
present.  A  hot  mustard  foot-bath  early  in  the  attack  is  useful.  For  the  lumbar 
pains,  opium  or  morphine  are  indicated.  Sinapisms,  or  other  similar  external 
counter-irritants,  with  ice  internally,  and  hydrocyanic  acid  or  chloroform,  are 
serviceable  against  gastric  irritability.  High  fever  is  to  be  combated  by  cold 
spongings,  the  wet  pack,  and  the  cold  bath.  Eor  haemorrhage,  styptic  remedies 
may  be  used,  though  it  is  doubtful  whether,  when  given  internally,  they  are  really 
of  much  benefit.  Of  course,  no  medication  is  to  be  resorted  to  which  is  likely  to 
heighten  a  tendency  to  emesis. 

[Much  work  has  been  done  with  antitoxines  for  yellow  fever,  but  with  no 
settled  results,  as  yet.  Sternberg's  f ormiala  for  internal  use  is  said  to  be  valuable 
for  quieting  the  stomach  and  promoting  diuresis.  It  is  as  follows:  Sod.  bicarb., 
gr.  cl;  hydrarg.  chlorid.  corros.,  gr.  J;  aquas  purse,  O  ij.  M.  S.  Three  table- 
spoonfuls  ice-cold  hourly. — V.] 

Suppression  of  urine  is  to  be  met  by  dry  cups  to  the  loins,  diuretic  remedies 
internally  if  the  condition  of  the  stomach  allows,  or  the  hot-air  bath.  The  results 
of  pilocarpine  are  disappointing  according  to  Bemiss,  who  states  that  he  has  seen 
good  effects  from  large  enemata  of  water,  preferably  cold,  if  there  be  notable  fever 
in  these  cases.  Prostration  is  an  indication  for  the  use  of  alcoholic  stimulants, 
among  which  iced  dry  champagne  ranks  high.  It  will  be  seen  that  the  treatment 
is  entirely  symptomatic.     The  disease  is  self -limited,  has  a  short  course,  and  the 


PLAGUE  107 

patient  will  recover  if  he  can  be  kept  alive  until  the  poison  is  exhausted.  During 
the  attack  and  until  convalescence  is  thoroughly  established  the  management  of 
the  diet  is  all-important.  Small  quantities  of  the  most  easily  assimilable  food 
may  be  given  at  short  intervals  if  they  are  tolerated  by  the  stomach ;  if  not,  ali- 
mentation must  be  by  the  rectum,  and  the  lower  bowel  in  this  disease  is  generally 
in  a  fair  condition  for  this  method  of  nutrition. 

Courage  and  hopefulness  on  the  part  of  the  physician  may  do  much  good,  and 
the  sei-vices  of  a  skillful  and  experienced  nurse  are  of  the  utmost  importance.  I 
am  told  that  in  New  Orleans,  and  perhaps  elsewhere,  it  is  customary,  for  those 
who  are  not  protected  and  can  afford  this  course,  to  secure  in  advance  a  nurse  as 
soon  as  an  epidemic  breaks  out.  They  then  take  to  their  beds  at  the  first  sign  of 
illness.] 


CHAPTEE   XYII 

PLAGUE 

{Byhonic  Plague.     Malignant  Adenitis.     Black  Death) 

[Definition. — Plague  is  an  acute,  febrile,  infectious  disease,  occurring  endem- 
ically  and  epidemically,  somewhat  contagious,  and  occasioned  by  the  hacillus 
pestis  hubonicce. 

Historical  Remarks. — Although  it  is  difficult  to  identify  diseases  from  the 
descriptions  of  ancient  authors,  Hirsch  believes  that  the  first  historical  account 
of  the  plague  relates  to  an  epidemic  affecting  Libya,  Egypt,  and  Syria,  at  the 
end  of  the  third  or  the  beginning  of  the  second  century  before  Christ.  Pan- 
demics occurred  in  the  sixth  century  of  our  era ;  the  fourteenth,  when,  under  the 
name  of  the  "  Black  Death,"  it  is  estimated  to  have  destroyed  twenty-five  million 
of  the  inhabitants  of  Europe ;  and  the  seventeenth  century.  The  great  plague  of 
London  in  1665  destroyed  seventy  thousand  out  of  a  population  of  four  hundred 
and  sixty  thousand. 

Erom  the  end  of  the  seventeenth  century  the  disease  gradually  yielded  to  the 
march  of  sanitary  improvement.  Like  leprosy,  it  is  now  unknown  in  countries 
where  it  foi*merly  was  a  terrible  scourge.  It  remains  endemic  in  northern  Africa, 
southwestern  Arabia,  India,  southern  China,  and  a  large  district  in  the  neigh- 
borhood of  the  Caspian  Sea  (Payne).  At  the  present  writing  the  disease  is  ex- 
tended widely  over  the  habitable  globe,  but  the  immunity  from  its  ravages  which 
civilized  races  now  enjoy  well  illustrates  the  prophylactic  value  of  modern 
hygiene. 

Plague  became  active  in  south  China  in  1894,  afflicted  Hong-Kong  from  1895 
to  1898,  and  has  occurred  there  within  a  year.  In  three  years,  ending  September, 
1899,  there  were  319,040  cases  in  the  Bombay  presidency,  and  of  these.  250,677 
were  fatal.  It  appeared  in  Egj^pt  in  1899;  also  in  Oporto,  Algiers,  and  South 
Africa.  In  the  year  1900  there  were  cases  in  the  Chinese  quarter  of  San  Fran- 
cisco, Honolulu,  Manila,  Australia,  and  Glasgow. 

-ffitiology. — The  plague  is  due  to  a  minute  organism,  known  as  the  bacillus 
pestis  bubonicse.  This  organism  is  constantly  found  in  those  suffering  from 
the  disease  and  in  their  bodies  after  death,  and  a  piire  culture  of  it  will  cause 
in  animals  a  disease  unquestionably  like  that  seen  in  men.  In  1898,  an  assistant 
in  a  pathological  laboratory  in  Vienna  came  down  with  the  disease,  while  occu- 
pied with  infected  animals — there  being  no  possibility  of  human  contagion.  The 
attack  was  fatal  and  entailed  the  fatal  illness  of  the  attending  physician.  There 
are  three  cases  on  record  of  successful  inociilation,  one  by  a  physician,  Whyte, 


108  ACUTE   GEXEEAL   IXFECTIOFS   DISEASES 

upon  himself  in  1802,  and  fatal,  and  two  upon  condemned  criminals,  who  took 
the  disease  but  survived.  These  three  eases,  however,  occurred  at  times  when 
the  disease  was  epidemic. 

The  mode  of  growth  of  the  bacillus  is  characteristic.  It  stains  readily  with 
the  ordinary  aniline  dyes — e.  g.,  Loeffler's  blue  or  weak  carbol-fuchsine.  It  is  de- 
colorized by  Gram's  method.  Its  ends  stain  more  deeply  than  the  central  portion, 
giving  it  somewhat  the  appearance  of  a  diplococcus.  It  has  no  spores.  Like  other 
micro-organisms,  its  virulence  varies  greatly  under  varying  circumstances  of  cul- 
ture and  transmission  through  animals.  When  an  epidemic  is  imminent,  the 
first  cases  are  often  mild,  then  the  intensity  of  the  poison  increases  rapidly, 
abating  again  toward  the  end  of  the  visitation.  Lower  animals  and  even  insects 
are  liable  to  infection.  The  list  includes  rats,  mice,  dogs,  and  also  flies,  fleas, 
lice,  mosquitoes,  ants,  and  bugs.  The  external  circumstances  which  most  favor 
the  spread  of  the  disease  are  overcrowding,  poverty,  and  filth.  Great  extremes  of 
temperature  are  unfavorable  to  its  development;  a  certain  degree  of  moisture, 
on  the  other  hand,  fosters  its  growth.  The  geological  character  of  a  place,  or 
the  elevation  above  the  sea,  has  little  influence.  The  immense  practical  impor- 
tance of  proper  social  and  hygienic  conditions  is  illustrated  by  the  percentage  of 
deaths  among  the  different  races  in  Hong-Kong  during  the  late  epidemic :  Chi- 
nese, 90.4;  Hindoos,  77;  Japanese,  60;  Europeans,  18.2.  These  figures  indicate 
very  fairly  the  relative  hygienic  conditions  of  the  classes  eniunerated.  It  is  un- 
doubtedly lack  of  a  favorable  soil  that  has  freed  Europe  and  the  civilized  parts 
of  America  from  the  disease. 

The  mode  of  infection  varies.  It  is  believed  that  most  cases  are  due  to  the 
entrance  of  the  germ  through  some  trauma,  or  fissure  of  the  skin — e.  g.,  through 
the  bite  of  insects  or  the  scratches  occasioned  by  the  same.  In  support  of  this 
view,  the  fact  has  been  emphasized  that  the  characteristic  buboes  are  mainly  in 
the  groin,  and  among  barefooted  people ;  but  against  it  is  the  experience  of  Euro- 
peans, who,  with  their  lower  extremities  protected,  also  have  a  preponderance  of 
inguinal  adenitis.  In  cases  with  pulmonary  localization  the  sputum  is  danger- 
ous, either  if  it  is  projected  upon  the  conjunctivge,  or  presumably  if  it  is  inhaled 
when  suspended  in  the  air  mixed  with  minute  particles  of  moisture.  Localities 
and  houses  seem  to  hold  and  transmit  the  infection,  persons  in  the  lowest  part 
of  the  house,  nearest  the  soil,  being  most  apt  to  suffer.  It  seems  very  difiicult  to 
disinfect  a  dwelling  by  ordinary  methods,  the  poison  sometimes  surviving  a 
deluge  of  liquid  disinfectants.  On  the  other  hand,  soldiers  wisely  directed  can 
engage  in  the  purification  of  a  dangerous  locality  with  impunity. 

Certain  articles  are  capable  of  transmitting  the  infection.  The  Sanitary 
Conference  at  Venice,  in  1898,  enumerated  in  this  class :  used  .body  linen,  cloth- 
ing, bedding,  and  other  personal  effects,  rags,  bagging,  carpets,  old  embroidery, 
green  hides  and  skins,  raw  silk  and  wool,  animal  and  human  hair. 

Animals  fed  upon  the  infected  viscera  acquire  the  disease,  but  it  has  not  been 
proved  that  man  becomes  infected  through  the  ingesta,  althougli  the  bacilli  are 
found  in  the  dejections.  At  any  rate,  during  an  epidemic  it  would  be  wise  to 
have  all  drinking  water  boiled,  and  to  eat  no  raw  fruit  or  other  uncooked  food. 

Course  and  Symptoms. — The  period  of  incubation  is  usually  three  to  five 
days.  It  may  be  as  short  as  thirty-six  hours,  or,  exceptionally,  extend  to  fourteen 
days.  The  Conference  at  Venice  settled  upon  ten  days,  for  quarantine  purposes. 
During-  incubation  the  symptoms  are  uncharacteristic,  if  any  at  all  appear.  The 
onset  of  the  disease  is  usually  abrupt,  with  rigors  or  chilliness,  intense  headache, 
and  general  pains.  The  temperature  may  be  104°-105°  F.  (40°^1°  C.)  on  the 
first  day,  but  is  more  apt  to  reach  such  a  height  by  the  third  day.  The  pulse  is 
somewhat  characteristic,  being  rapid,  out  of  proportion  to  the  general  condition, 
ranging  from  100  to  120  or  even  140.     It  soon  becomes  feeble,  dicrotic,  hard  to 


PLAGFE  109 

count,  and,  toward  death,  intermittent.  The  heart  is  weak,  and  its  first  sound 
gradually  becomes  indistinct,  and  its  right  side  dilated.  The  condition  of  the 
tongue  is  regarded  as  important  for  diagnosis.  It  has  a  white,  moist  coat  at  first, 
later  becoming  dry  and  brownish.  Exceptionally,  it  may  be  brown  from  the  start. 
Quite  constantly  the  edges  and  tip  and  often  the  median  furrow  are  clean. 

The  throat  and  tonsils  are  red  and  congested.  Sometimes  the  tonsils  seem  to 
be  the  gate  of  entrance  for  the  poison,  and  in  such  cases  the  cervical  glands  are 
apt  to  be  much  enlarged.  The  eyes  are  congested  and  sunken,  with  a  dark  ring- 
around  them. 

The  general  appearance  of  the  patient  gives  the  impression  of  sepsis.  The 
countenance  may  have  a  "  fatuous,  listless,  unconcerned  "  expression,  or  may  be 
"  pain-drawn  and  haggard."  In  children  the  onset  in  this,  as  in  other  infectious 
diseases,  may  be  marked  by  convulsions.  Delirium  is  common;  this  may  be 
quiet  or,  exceptionally,  maniacal.  The  gait  is  early  affected,  becoming  feeble  and 
staggering,  and  suggesting  alcoholic  intoxication.  The  speech  is  thick  and  husky, 
due  to  lingual  paresis,  and  is  quite  characteristic. 

Adenitis  is  present  in  sixty-five  to  one  hundred  per  cent,  of  the  cases.  It  is 
this  circumstance  which  has  given  rise  to  the  name  bubonic  plague.  The  change 
in  the  glands  usually  becomes  apparent  by  the  third  day,  but  it  may  precede  the 
constitutional  symptoms  or  may  be  delayed  to  the  sixth  day.  At  first  an  enlarged 
gland  is  felt,  varying  in  size  from  a  walnut  to  a  small  orange.  This  is  tender 
and  often  extremely  painful;  soon  there  is  a  collateral  oedema,  making  a  large 
swelling  in  the  neighborhood.  The  favorite  location  of  the  adenitis  is  the  fem- 
oral or  inguinal  region.  It  is  usually  unilateral.  Other  points  of  development 
are  the  axilla,  neck,  and  less  often  the  back  of  the  knee  and  the  elbow.  The 
parotid  gland  also  may  be  afl^ected.  Sometimes  more  than  one  group  of  glands 
are  affected  at  the  same  time,  and  post  mortem  there  may  be  found  enlargement 
of  every  gland  in  the  body.  The  buboes  may  remain  hard  until  death;  in  other 
cases  they  suppurate,  which  is  regarded  as  favorable.  On  the  other  hand,  if  they 
soften  or  disappear  during  the  height  of  an  attack,  death  may  be  expected.  By 
the  eighth  or  tenth  day  the  skin  over  a  bubo  may  slough;  and  if  a  patient  sur- 
vives, convalescence  may  be  prolonged  for  weeks  by  the  adenitis  with  its  compli- 
cations. There  are  apt  to  be  subcutaneous  hsemorrhages  in  the  skin  over  buboes, 
as  well  as  petechise  in  various  other  parts  of  the  surface,  or  more  extensive  hsem- 
orrhagic  stains.  Exceptionally,  there  may  be  a  rash  resembling  that  seen  in 
severe  exanthematic  typhus.  Haemorrhage  is  a  sign  of  severity;  it  may  occur 
from  the  nose,  mouth,  stomach,  lungs,  intestine,  kidneys,  or  womb.  A  pregnant 
woman  is  almost  certain  to  miscarry. 

Boils  and  abscesses  may  occur  in  the  disease.  Certain  lesions  called  carbun- 
cles sometimes  appear.  They  are  really  areas  of  moist  gangrene,  extending  hori- 
zontally instead  of  deeply  into  the  tissues,  and  they  may  attain  a  diameter  of  sev- 
eral inches. 

The  urine  is  scanty,  and  is  often  retained  or  actually  suppressed.  Apart  from 
renal  haemorrhage  it  shows  merely  acute  congestion,  as  in  other  infectious  dis- 
eases. The  liver  is  enlarged  and  tender;  the  spleen  is  always  very  much  en- 
larged, up  to  three  or  four  times  its  usual  size.  There  may  be  persistent  vomit- 
ing at  the  onset  of  the  disease.  Constipation  is  present,  as  a  rule,  but  there  may 
be  severe  diarrhoea.     In  ordinary  cases  respiration  is  somewhat  hurried. 

Fluid  withdrawn  from  a  bubo  in  its  early  stages  shows  the  characteristic  ba- 
cillus. When  suppuration  has  occurred  the  organism  may  not  be  found,  having 
probably  been  destroyed  by  the  agents  of  suppuration.  The  circulating  blood 
contains  the  organisms,  but  they  are  isolated  from  it  with  some  difficulty.  After 
death  the  viscera,  particularly  the  spleen,  are  found  to  contain  great  numbers  of 
the  germs. 


110  ACUTE   GEKEEAL   INEECTIOUS   DISEASES 

In  the  pneiunonic  cases  of  plague  the  disease  is  septicsemic  in  its  characteris- 
tics and  fatality;  hence,  cough  is  a  very  important  symptom.  The  signs  in  the 
chest  are  remarkably  slight.  There  may  be  a  small  lobule  of  consolidation  found, 
particularly  in  the  lower  part  of  the  back  or  at  the  apex.  The  signs  vary  from 
one  day  to  another.  The  expectoration  may  be  scanty  or  absent,  and  if  present 
may  seem  merely  bronchitic.  It  is  more  apt  to  be  sero-mucous  than  muco-puru- 
lent.  Often  the  sputum  is  almost  a  pure  culture  of  the  specific  organisms. 
Pneumonic  cases  are  almost  invariably  fatal  before  the  end  of  the  third  day. 
As  a  rule,  they  are  not  associated  with  enlargement  of  the  glands  in  any  part  of 
the  body. 

A  third  variety  of  plague  is  the  septicsemic,  in  which  death  occurs  by  the  sec- 
ond or  third  day.  There  is  delirium,  merging  into  coma;  all  the  glands  are 
enlarged  but  not  prominent;  haemorrhage  is  frequent  and  apyrexia  not  un- 
common. 

Pestis  Minor. — At  the  beginning  of  an  epidemic  there  may  be  cases  of  very 
little  severity,  but  with  bubonic  manifestations  of  a  mild  type.  This  form  almost 
always  runs  a  favorable  course,  and  lasts  about  two  weeks.  Its  importance  in 
the  way  of  prophylaxis  and  public  hygiene  may  be  very  great. 

Diagnosis. — The  general  picture  of  the  disease  is  that  of  a  profound  sepsis, 
plus  the  peculiar  adenitis.  Sometimes  the  changes  in  the  glands  are  attended 
with  no  subjective  symptoms,  and  the  physician  is  in  danger  of  regarding  the 
case  as,  for  instance,  typhoid  or  typhus  fever.  Typhoid  fever  has  a  more  grad- 
ual onset,  a  relatively  slower  pulse,  rose-spots,  and  eventually  a  Widal  reaction. 
Typhus  fever  runs  fourteen  days  instead  of  a  week,  is  more  regularly  associated 
with  an  eruption,  and  has  different  setiological  relations.  The  enlarged  glands 
might  be  mistaken  for  tuberculosis  or  syphilis,  and  the  sjmiptomatic  parotitis  has 
been  regarded  as  mumps,  but  due  care  would  make  mistakes  of  this  sort  infre- 
quent. Diphtheria  has  been  suspected  in  a  ease  attended  by  such  changes  in  the 
cervical  glands  that  the  mouth  could  not  readily  be  inspected.  Cases  with  ingui- 
nal adenitis  have  been  regarded  as  gonorrhoea,  in  both  sexes  (Hossack  and 
Colvin). 

Malaria  has  been  confoianded  with  plague,  but  the  temperature  curve,  the 
efficacy  of  quinine,  and  the  discovery  of  plasmodia  in  the  blood  should  enable 
one  to  recognize  it.  So  much  cedema  is  sometimes  associated  with  the  buboes 
as  to  simulate  erysipelas.  Cases  of  severe  influenza  and  of  pneumonic  plague 
greatly  resemble  each  other  in  everything,  except  prognosis  and  the  micro-organ- 
isms of  the  sputum.  Other  diseases  which  have  been  simulated  by  plague  ar© 
puerperal  fever,  septico-pysemia,  eerebro-spinal  meningitis,  cerebral  embolism, 
epilepsy,  uraemic  coma,  diarrhcea,  debility,  marasmus,  and  alcoholic  poisoning 
(Hossack). 

Prognosis. — When  at  its  height,  the  disease  is  fatal  in  perhaps  ninety  per  cent, 
of  the  cases.  The  average  fatality  of  epidemics  has  been  stated  as  from  thirty-five 
to  fifty  per  cent.  Death  may  occur  as  early  as  the  second  or  third  day;  if  life  is 
preserved  beyond  the  sixth  there  is  hope  of  recovery.  Petechias,  haemorrhages, 
and  pulmonary  signs  are  of  fatal  omen. 

Treatment.- — ^With  the  present  ease  of  human  intercommunication  we  can 
not  hope,  with  the  strictest  quarantine,  to  exclude  every  infectious  germ,  but  we 
can  render  the  exposed  locality  unsuitable  for  its  growth.  This  is  well  illustrated 
by  the  recent  experience  of  Glasgow,  where  the  disease  has  now  ceased  after  a 
minimum  loss  of  life  (27  cases  and  8  deaths).  Major  Edie.  United  States  health- 
officer  at  Manila,  says :  ^  "  The  opinion  I  have  formed  of  plague  from  the  experi- 
ence of  the  past  six  months  is  that  little  difficulty  will  be  found  in  controlling  it 

*  Surgeon-Generars  report,  1900. 


EPIDEMIC    CEEEBKO-SPI^^AL   MENINGITIS  ill 

in  any  intelligent  community  with  modern  sanitary  conditions."  The  physi- 
cians, nurses,  and  visitors  at  well-regulated  plague  hospitals  do  not  catch  the 
disease. 

Therapeutic  measures  have  been,  until  recently,  mainly  symptomatic  and 
apparently  futile.  Two  forms  of  specific  treatment  have  been  introduced.  Yersin 
has  prepared  an  antitoxic  serum  from  the  horse,  precisely  analogous  to  the  anti- 
diphtheritic  serum  obtained  from  the  same  animal.  This  preparation  keeps 
well,  is  harmless,  painless,  and  confers  imraediate  immunity  to  the  disease,  last- 
ing about  fourteen  days.  It  is  to  a  certain  extent  curative  in  cases  already 
diseased,  the  more  so  the  earlier  it  is  given.  Haffkine  has  prepared  a  vaccine 
fluid  by  subjecting  a  culture  of  the  bacilli,  in  broth,  to  a  temperature  of  70°  C. 
for  one  hour.  This  sterilized  fluid  contains  the  dead  germs,  and  also  the  toxines 
developed  incidentally  to  their  growth.  It  confers  immunity  to  infection,  begin- 
ning the  seventh  day  after  inoculation.  The  injection  is  best  repeated  two  or 
three  times,  at  intervals  of  eight  days.  The  local  reaction  from  this  is  consider- 
able, but  does  not  last  more  than  two  or  three  days,  and  the  person  treated  re- 
mains immune  for  months.  Haffkine's  fluid  is  said  to  aggravate  an  impending 
attack,  if  it  is  given  during  the  period  of  incubation,  so  that  a  person  who  might 
otherwise  have  survived  the  disease  may  lose  his  life.  The  most  recent  writers 
on  the  treatment  of  the  plague  are  not  in  full  accord  as  to  the  value  of  these 
injections  just  described.  Major  Edie  (already  quoted)  says:  "A  thorough  test 
has  not  been  given  to  either  the  Haffkine  material  or  the  Yersin  serum,  but  we 
have  not  been  favorably  impressed  with  either."  The  reports  from  India  are 
more  encouraging.^V.] 


CHAPTER   XVIII 

EPIDEMIC    CEREBRO-SPINAL    MENINGITIS 

(Spotted  Fever.     Certhro-spinal  Fever) 

.31tiology. — The  epidemic  form  of  cerebro-spinal  meningitis  has  been  known 
only  since  the  beginning  of  the  nineteenth  century.  The  first  epidemics  were  ob- 
served in  southern  France  and  in  Geneva.  Smaller  ones  occurred  in  Germany  in 
1822  and  1853;  but  it  was  not  till  1863  that  the  disease  became  at  all  frequent 
among  us.  Since  that  date  there  have  been  more  or  less  extensive  epidemics  almost 
eveiy  year.  The  southern  and  central  portions  of  Germany  are  particularly  liable 
to  them.     Sporadic  cases  may  occur  at  any  time. 

Most  of  the  epidemics  appear  in  the  winter  and  spring.  We  do  not  know  any 
particular  factors  which  promote  the  disease.  It  often  seems  to  be  decidedly 
endemic.  Barracks,  work-houses,  and  the  like  have  been  marked  by  tolerably 
extensive  epidemics.  Whether  the  disease  can  be  carried  by  patients  to  places 
previously  free  from  it  is  still  uncertain.  It  is  not  directly  contagious.  Children 
and  young  adults  are  the  most  frequent  victims;  but  now  and  then  elderly  per- 
sons are  attacked.     Sex  can  not  be  shown  to  have  much  influence. 

That  the  disease  is  infectious  is  clearly  shown  not  o\\\j  by  its  epidemic  and  en- 
demic character,  but  by  its  whole  course.  The  peculiar  pathogenic  organisms 
and  the  manner  of  infection  have  not  yet,  however,  been  positively  ascertained. 
Diplococci  are  usually  found  in  the  purulent  exudation  in  the  meninges,  which 
are  so  much  like  Frankel's  pneumonia  diplococci  that  many  authors  have  consid- 
ered the  germs  of  croupous  pneumonia  and  of  epidemic  meningitis  as  identical. 
It  is  confirmatory  of  this  that  many  clinical  facts  suggest  a  relationship  between 
the  two  diseases :  the  appearance  of  herpes,  the  comparative  frequency  of  sec- 


112  ACUTE    GENEEAL   INFECTIOUS    DISEASES 

ondary  purulent  meningitis  in  pneumonia,  the  occasional  co-existence  of  epidem- 
ics of  pneumonia  and  meningitis,  etc.  On  the  other  hand,  we  must  not  overlook 
the  clinical  differences,  especially  the  atypical  course  of  epidemic  meningitis, 
which  almost  never  ends  by  crisis.  The  chief  point  is  that,  assuming  that  pneu- 
monia and  epidemic  meningitis  are  due  to  identical  germs,  we  can  not  explain 
why  the  same  germ  at  certain  times  finds  its  way  to  the  lungs,  and  at  other  times 
and  in  other  localities  goes  to  the  cerebral  meninges.  In  the  separate  epidemic 
occurrence  of  cerebro-spinal  meningitis  we  find  a  strong  argimient  for  the  specific 
individuality  of  the  disease.  Weichselbaum  and  others  have  recently  found  in 
epidemic  meningitis  another  peculiar  diplococcus  which  is  called  the  diplococcus 
intracellularis  meningitidis.  This  diplococcus,  arranged  in  pairs  or  tetrads,  is 
found  chiefly  within  the  pus  cells,  and  externally  closely  resembles  the  gonococcus. 
Further  research  is  necessary  to  determine  the  significance  and  constancy  of  its 
presence.  [Later  researches  seem  to  show  that  this  coccus  is  the  actual  cause  of 
the  disease. — K.] 

With  regard  to  the  gate  of  entrance  of  infection  in  primary  epidemic  menin- 
gitis, perhaps  the  specific  poison  may  enter  through  the  nostrils  and  the  cribriform 
plate  to  the  otherwise  so  well  protected  envelopes  of  the  central  nervous  system. 

[Sanitary  conditions  seem  to  play  a  less  important  role  in  this  than  in  many 
other  infectious  diseases.  During  the  epidemic  which  visited  New  England  in 
1873  the  writer  was  interne  at  the  Massachusetts  General  Hospital,  and  there  saw 
a  number  of  cases.  The  disease  was  also  prevalent  among  horses  at  the  same 
time,  and  it  is  curious  to  note  that  a  like  association  of  the  affection  in  men  and 
animals  was  observed  in  Vermont  in  1811,  and  in  New  York  city  in  1871.  During 
the  year  1873,  216  deaths  were  returned  as  due  to  this  malady  in  the  city  of 
Boston.] 

Pathological  Anatomy. — The  autopsy  discloses  an  acute  purulent  cerebro- 
spinal leptomeningitis.  It  is  only  in  rapidly  fatal  cases  that  slight  and  incipient 
lesions  have  been  met  with.  As  a  rule,  the  extent  and  intensity  of  the  objective 
lesions  correspond  to  the  severity  of  the  symptoms.  In  the  brain  the  purulent 
inflammation  attacks  the  convexity  as  well  as  the  base.  It  is  usually  most  marked 
along  the  larger  blood-vessels  and  in  the  fissures  of  the  cortex.  Of  the  spinal 
cord  the  posterior  surface  suffers  most.  Frequently  the  lumbar  portion  is  more 
affected  than  the  parts  above.  It  is,  however,  exceptional  for  the  disease  to  be 
limited  to  the  meninges;  it  is  prone  to  extend  into  the  underlying  parenchyma. 
The  microscope  reveals  clumps  of  pus-corpuscles  about  the  blood-vessels,  where 
they  penetrate  into  the  tissues,  and  not  infrequently  there  are  numerous  centers 
of  genuine  encephalitis.  These  latter  may  be  visible  to  the  naked  eye.  Excep- 
tionally there  may  even  be  cerebral  abscesses  of  considerable  size.  The  vessels  are 
distended  with  blood,  clear  into  the  central  ganglia,  and  ecchymoses  are  frequent. 
The  cerebral  ventricles  are  usually  enlarged,  and  filled  with  a  cloudy  serum,  or 
even  with  pus.  It  is  plain  that  these  lesions  of  the  cerebro-spinal  parenchyma 
greatly  modify  the  clinical  picture,  and  that  they  must  frequently  have  more  to 
do  with  the  severity  of  the  symptoms  than  has  the  leptomeningitis  itself. 

Clinical  History. — Prodromata  are  relatively  rare,  and  if  present  they  are  not 
severe,  being  confined  to  general  malaise,  with  slight  headache,  and  pain  in  the 
limbs.  Usually  the  disease  begins  rather  suddenly;  there  is  intense  headache, 
often  felt  mainly  in  the  occiput,  pain  and  stiffness  in  the  back  of  the 
neck,  and  great  general  discomfort.  It  is  not  rare  for  vomiting  to  occur  at  first. 
Very  often  there  are  among  the  early  symptoms  such  important  mental  disturb- 
ances as  stupor  or  delirium.  There  is  usually  fever  from  the  first.  An  initial 
rigor  may  occur,  but  it  is  not  the  rule. 

The  intensity  of  these  first  symptoms  is  not  always  the  same.  Subsequently  to 
them  the  course  of  the  disease  may  vary  greatly.    First  there  are  very  acute,  vio- 


EPIDEMIC    CEEEBRO-SPINAL  MENINGITIS  113 

lent  forms,  termed  "  explosive  "  (meningitis  cerehro-spinalis  siderans,  meningite 
foudroyante),  in  which  the  cerebral  symptoms  are  very  severe,  and  the  patient 
survives  only  a  few  days  or  even  hours.  Again,  there  are  abortive  cases.  These 
begin  with  equally  threatening  symptoms,  but  after  a  few  days  completely  recover 
with  remarkable  rapidity.  The  majority  of  cases  last  about  two  to  four  weeks. 
In  severe  cases  death  may  come  as  early  as  the  first  week.  The  disease  is  often 
protracted  to  six  or  eight  weeks'  duration,  or  even  longer,  and  may  end  in  death 
aftler  all.  Cases  that  last  a  good  while  sometimes  exhibit  a  remarkably  inter- 
mittent character.  Finally,  there  are  a  considerable  number  of  mild  cases  in  which 
none  of  the  symptoms  are  very  pronounced,  and  recovery  is  relatively  early. 

The  symptoms  of  the  disease  may  be  divided  into  (1)  the  severe  general  symp- 
toms, referable  to  the  brain  and  spinal  cord ;  (2)  the  more  localized,  nervous  symp- 
toms; and  (3)  the  results  of  the  constitutional  infection,  including  fever  and 
symptoms  in  other  parts  of  the  body. 

1.  Among  the  less  definite  cerebral  symptoms  headache  is  important.  It  is 
usually  terribly  severe.  It  is  chiefly  occipital,  but  sometimes  is  frontal  or  tem- 
poral. Like  most  of  the  symptoms  of  meningitis,  the  headache  undergoes  very 
frequent  changes  in  intensity  during  the  course  of  the  disease.  For  a  time  it  may 
remit,  only  to  recur  with  fresh  severity.  Marked  vertigo  and  a  sense  of  fullness 
in  the  head  may  accompany  it. 

The  pain  in  the  head  is  re-enforced  by  intense  pain  in  the  nape  of  the  neck  and 

'rrck,  due  to  the  spinal  meningitis.     There  is  almost  always  considerable  tender- 

•S3  along  the  whole  spinal  column.     The  erector  spinse  is  contracted,  making 

tlie  back  straight  and  rigid,  or  even  producing  opisthotonos;  and  the  head  is 

I'cnt  backward  by  the  reflex  contraction  of  the  neighboring  muscles. 

In  most  of  the  severe  cases  intelligence  is  blunted ;  we  find  all  degrees  of  dis- 

u'bance,  from  slight  drowsiness  to  delirium  on  the  one  hand,  or  deep  coma  on  the 

:her.     Some  cases  begin  with  marked  raaniacal  excitement.     These  symptoms 

likewise  may  undergo  frequent  variation  in  their  intensity.     General  convulsions 

occur  in  very  severe  cases  alone,  and  are  of  evil  omen. 

The  vomiting  is  also  to  be  regarded  as  of  cerebral  origin.  It  frequently  is  an 
early  symptom,  but  may  be  deferred. 

2.  Symptoms  referable  to  the  individual  cerebral  nerves  are  manifold  and 
variable.  The  most  frequent  disturbances  are  in  the  nerves  that  supply  the  muscles 
of  the  eye.  They  include  strabismus;  nystagmus,  or  slow  movements  independ- 
ent of  volition;  unilateral  or  bilateral  ptosis;  slow  reaction  of  the  pupils,  or 
inequality  of  them,  or  myosis  or  mydriasis.  In  the  area  of  distribution  of  the 
facial  there  is  often  a  noticeable  contraction  of  the  muscles,  giving  the  face  a 
peculiar,  painfully  distorted  look.  Trismus,  or  tetanus  of  the  masseters,  is  rare, 
and  usually  a  bad  sign. 

Disturbance  of  the  nerves  of  special  sense  is  frequent.  Deafness  may  be 
due  to  the  stupor,  but  is  often  the  result  of  an  extension  of  the  inflammation 
to  the  acoustic  nerve.  The  purulent  inflammation  may  be  propagated  as  far  as 
the  labyrinth,  or  even  into  the  middle  ear.  Tinnitus  aurium  is  also  frequent. 
Disturbances  of  vision  are  far  less  frequently  observed,  but  optic  neuritis  has 
been  repeatedly  found  by  the  ophthalmoscope.  Severe  purulent  irido-choroiditis 
has  been  also  observed.  It  is  probably  due  to  extension  of  the  inflammation 
along  the  .sheath  of  the  optic  nerve.  Conjunctivitis  and  keratitis  sometimes 
occur;  but  they  are  probably  caused  by  external  injuries  rendered  possible  by  the 
imperfect  closure  of  the  lids,  or  the  diminished  sensitiveness  of  the  parts.  We 
have  several  times  found  the  sense  of  smell  diminished. 

Disturbances  in  the  area  of  distribution  of  the  spinal  nerves  are,  on  the  whole, 
less  frequent.  The  only  one  of  value  in  diagnosis  is  the  cutaneous  hyperassthesia. 
It  is  apt  to  be  particulnrly  severe  in  the  extremities,  and  it  may  be  so  extreme  that 
8 


114  ACUTE    GEl^ERAL   rNTFECTIOUS   DISEASES 

the  light  touch  of  a  finger  or  a  needle  causes  great  pain.  Sometimes  there  is  a 
slight  twitching  in  the  muscles  of  the  extremities.  This  has,  however,  no  special 
significance.  There  is  often  rigidity  and  stiffness  of  the  muscles.  Kernig  has 
called  attention  to  the  frequent  appearance  of  flexure  contractions  in  the  lege;- 
and  sometimes  also  in  the  arms,  if  the  patients  are  caused  to  sit  up  or  if  the- 
thigh  is  passively  bent  upon  the  trunk.  As  might  be  expected,  there  is  no  in- 
variable rule  about  the  reflexes.  The  cutaneous  reflexes  are  usually  well  marked,, 
and  the  tendon  reflexes  may  be;  but  in  some  cases  we  have  found  the  tendon 
reflexes  markedly  diminished  or  even  abolished.  Such  a  condition  is  probably 
due  to  some  lesion  of  the  fibers  of  the  posterior  nerve-roots. 

All  of  the  nervous  symptoms  above  enumerated  result  from  one  of  two  causes 
— either  the  roots  of  the  nerves  are  affected  by  the  purulent  exudation,  or  the 
inflammation  extends  inward  to  the  central  organs  themselves.  This  extension  is 
the  explanation  also  of  other  symptoms  sometimes  observed — ^viz.,  hemiplegia, 
paraplegia,  partial  convulsions,  and  aphasia. 

3.  In  addition  to  all  these  nervous  disturbances,  we  see  also  symptoms  refer- 
able to  other  parts  of  the  body.  Of  this  class  there  is  one  cutaneous  affection 
which  is  a  very  valuable  aid  to  diagnosis.  Herpes  labialis  or  herpes  facialis  is  apt 
to  appear  soon  after  the  beginning  of  the  meningitis.  It  is  seen  in  more  than  half 
the  cases,  and  as  frequently  in  severe  as  in  mild  attacks.  Other  eruptions  occur 
now  and  then— e.  g.,  roseola,  urticaria,  or  petechise.  Sometimes  they  are  so  sym- 
metrically distributed  upon  the  two  halves  of  the  body  as  to  suggest  the  idea  of  a 
nervous  origin. 

The  digestive  system  seldom  displays  severe  symptoms  beyond  the  vomiting- 
already  mentioned.  Anorexia  and  constipation  are,  indeed,  usually  present,  as 
in  many  grave  diseases.  We  have  seen  mild  dysentery  a  few  times.  "Now  and 
then  a  slight  jaundice  has  been  noticed.  The  spleen  is  often  somewhat  swoller., 
but  very  rarely  attains  great  size. 

Swelling  of  the  joints  has  been  observed  quite  often;  it  is  much  more  frequent 
in  some  epidemics  than  in  others.  The  enlargement  may  be  an  early  or  a  later 
symptom.     It  does  not  usually  prove  serious. 

The  urinary  apparatus  is  seldom  affected.     The  urine  may  contain  some  albi 
men  and  a  few  casts.     Polyuria  is  an  interesting  symptom,  probably  of  nervo  :■ 
origin.     It  is  more  apt  to  occur  in  the  latter  part  of  the  disease.     In  a  number     ■ 
cases  sugar  has  been  found  in  the  urine.     Cystitis  is  a  secondary  disorder  whicL 
is  not  very  rare,  particularly  in  severe  cases  when  the  catheter  has  been  used. 

Pulmonary  and  bronchial  symptoms  are  likewise  secondary.  They  occur  very 
often  in  bad  cases.  It  is  evident  how  easily  the  stupor  of  the  patient  may  lead  to 
the  inhalation  of  solid  matter,  with  consequent  bronchitis  and  lobular  pneu- 
monia. 

Lesions  of  the  circulatory  system  are  rare.  Acute  endocarditis  has  been  ob- 
served only  a  few  times.  The  pulse  is  usually  somewhat  accelerated,  seldom 
rendered  slow.  Yery  frequently  the  pulse-rate  is  remarkably  variable,  un- 
doubtedly because  of  variation  in  the  supply  of  nervous  force.  Slight  irregu- 
larities in  the  pulse  are  also  common.  In  the  blood  we  flnd  quite  a  marked 
leucocytosis. 

4.  The  fever  in  epidemic  meningitis  conforms  to  no  single  type.  It  does  not 
correspond  at  all  to  the  severity  of  the  other  symptoms ;  the  worst  cases  may  run 
their  course  with  little  or  no  fever.  In  most  instances  the  fever  has  irregular  re- 
missions. It  seldom  exceeds  104°  (40°  C).  Sometimes  the  fever  exhibits  a  decid- 
edly intermittent  character.  It  is  in  these  cases  particularly  that  we  find  the 
variation  in  the  intensity  of  all  the  symptoms  of  which  mention  has  been  made 
repeatedly.  The  variations  in  the  temperature  do  not,  however,  always  run  par- 
allel with  the  changes  in  the  other  symptoms.     In  mild  cases  the  fever  is  usually 


EPIDEMIC    CEREBRO-SPINAL   MENINGITIS  115 

moderate  and  brief.  The  abortive  attacks  may  present  high  temperatures  at 
first,  but  these  quickly  abate.  In  case  of  a  fatal  issue  there  is  sometimes  hyper- 
pyrexia before  death,  reaching  108°  to  109°  (42°-43°  C).  In  the  severer  but 
not  fatal  cases  the  fever  declines  slowly  but  irregularly.  The  fever  may  be  over, 
long  before  the  other  symptoms  disappear. 

It  is  impossible  to  portray  all  the  forms,  symptoms,  and  courses  the  disease 
may  have.  The  chief  varieties  have  been  already  mentioned;  but  in  reality  these 
are  only  types  which  run  into  one  another  without  sharply  defined  border-lines. 
It  is  in  itself  a  characteristic  of  epidemic  meningitis  that  most  of  the  more 
tedious  cases  have  a  variable,  uncertain  course.  We  may  even  meet  with  a  com- 
plete intermission  of  all  the  symptoms,  lasting  for  quite  a  while,  so  that  the  return 
of  the  trouble  may  fairly  be  called  a  relapse. 

Sequelae  are  not  rare  after  severe  cases.  Persistent  deafness  is  the  most  fre- 
quent. It  results  from  the  complications,  already  mentioned,  which  affect  the 
labyrinth  and  the  middle  ear.  Little  children  may  become  deaf  and  dumb. 
Again,  vision  may  be  deranged,  because  of  retinitis,  atrophy  of  the  optic  nerve, 
or  corneal  opacities,  etc.  It  is  not  very  rare  for  meningitis  to  leave  grave  nerv- 
ous disorders  behind  it.  These  are  frequently  the  symptoms  of  a  chronic  hydro- 
cephalus. We  may  observe  headache,  sudden  unconsciousness,  or  even  convul- 
sions, mental  impairment,  and  weakness  of  the  extremities.  Or  there  may  be 
localized  disturbances  due  to  permanent  injury  of  limited  portions  of  the  brain  or 
spinal  cord,  such  as  hemiplegia,  paraplegia,  and  aphasia.  From  many  of  these 
conditions  there  may  be  a  gradual  recovery,  but  others  prove  incurable. 

The  diagnosis  of  cerebro-spinal  meningitis  is  not  difficult  in  a  well-developed 
case,  particularly  if  the  prevalence  of  an  epidemic  puts  us  in  mind  of  the  disease. 
Diagnosis  is  more  difficult  in  sporadic  cases,  and  most  difficult  of  all  when  the 
patient  does  not  come  under  observation  till  he  is  very  ill  and  when  we  can  not 
obtain  the  previous  history.  Important  factors  are  the  abrupt  onset,  the  speedy 
appearance  of  grave  cerebral  symptoms,  the  characteristic  headache  and  pain  in 
the  back,  the  stiffness  of  the  neck,  and  the  herpes  labialis. 

If  we  find  evident  symptoms  of  meningitis,  we  have  still  to  decide  whether  the 
case  is  one  of  primary  epidemic  disease,  or  secondary,  due  perhaps  to  extension 
from  some  other  part.  Bearing  this  last  possibility  in  mind,  we  should  examine 
the  ears  carefully ;  for,  as  is  well  known,  chronic  otitis  media  may  set  up  a  puru- 
lent meningitis.  Again,  it  may  be  very  difficult  to  exclude  a  tubercular  menin- 
gitis. Here  we  should  consider  other  circumstances  that  might  render  tuberculosis 
probable,  such  as  the  general  condition  of  the  patient,  heredity,  previous  pleurisy, 
the  results  of  thoracic  examination,  or  scrofulous  disease  of  the  bones  or  joints. 
The  existence  of  herpes  points  toward  epidemic  meningitis,  for  it  is  exceptional 
in  the  other  forms  of  the  disease.  It  is  sometimes  difficult  to  distinguish  between 
meningitis  and  severe  cases  of  other  acute  infectious  diseases — e.  g.,  typhoid 
fever  and  septic  diseases.  Here  we  must  weigh  all  the  circumstances  carefully. 
Lumbar  puncture  has  greatly  aided  the  diagnosis  of  meningitis.  This  was 
recently  introduced  by  Quincke,  and  it  has  often  been  performed  since.  As 
Quincke  first  showed,  we  can  usually  reach  the  subarachnoid  space  of  the  Cauda 
equina  without  difficulty  between  the  third  and  fourth  lumbar  vertebrte  with 
an  aspirating  needle  about  eight  centimetres  long.  The  patient  should  lie  on  one 
side.  In  this  way  we  can  obtain  more  or  less  of  any  meningitic  exudation  that 
may  be  present.  In  epidemic  meningitis  we  often  obtain  a  sero-purulent  or 
purulent  exudation  which  can  be  examined  bacteriologically.  [The  discovery  of 
the  diplococcus  intracellularis  in  the  fluid  withdrawn  by  lumbar  puncture  is  of 
extreme  importance  in  the  diagnosis  of  doubtful  or  sporadic  cases. — K.] 

This  is  a  good  opportunity  to  mention  the  secondary  meningitis  which   is 
said  to  occur  with  relative  frequency  just  at  the  time  of  an  epidemic.     The  com- 


116  ACUTE    GEl^ERAL   lis'FECTIOUS   DISEASES 

bination  of  croupous  pneumonia  (q.  v.)  and  purulent  meningitis  has  been 
repeatedly  observed.  Still,  it  is  not  easy  to  determine  whether  the  cause  of  this 
secondary  meningitis  is  actually  identical  with  that  of  the  epidemic  form  {vide 
supra).  In  other  acute  diseases,  such  as  typhoid  and  articular  rheumatism,  when 
they  occur  at  the  time  of  an  epidemic,  the  "  tendency  to  meningitis  "  is  potent 
enough  to  make  meningeal  symptoms  more  frequent  than  usual.  It  has  not  been 
clearly  demonstrated,  however,  that  this  fact  is  actually  due  to  the  epidemic  men- 
ingitis. 

The  prognosis  depends  chiefly  upon  the  severity  of  the  cerebral  symptoms. 
Yet  we  should  be  guarded  in  our  utterances,  even  when  the  case  seems  mild,  or 
has  apparently  made  the  first  steps  toward  convalescence.  The  disease  sometimes 
changes  for  the  worse  at  a  late  period.  In  general  the  mortality  is  about  thirty 
to  forty  per  cent.  Probably  this  estimate  does  not  take  into  account  many  very 
mild  cases. 

Treatment  is  purely  symptomatic.  There  is  no  specific  for  meningitis.  A 
valuable  remedy  is  cold  applications.  Ice-bags  are  placed  upon  the  head,  and,  if 
possible,  along  the  spine.  There  are  long  and  narrow  rubber  bags  for  the  latter 
purpose.  These  applications  a.re  borne  well  by  most  patients  and  afford  decided 
relief.  The  local  abstraction  of  blood  has  also  an  undeniably  beneficial  infiuence, 
however  difficult  this  may  be  to  explain.  Leeches  are  put  behind  the  ears,  and 
cupping-glasses  on  the  back  of  the  neck  and  along  the  spine.  Mercurial  ointment 
is  often  rubbed  in,  not  only  locally  but  also  in  the  same  way  as  in  treating  syphi- 
lis. Its  efficacy  is  doubtful.  The  narcotics  are  of  great  value.  The  best  is  mor- 
phine given  subcutaneously.  It  lessens  the  pain,  and  often  affords  the  uneasy  and 
delirious  patient  rest  and  sleep.  Chloral  and  bromide  of  potash  may  also  be  em- 
ployed. Iodide  of  potash  is  often  given  internally,  to  the  amount  of  twenty  to 
thirty  grains  (grammes  1.5-2)  in  a  day,  especially  in  cases  with  a  slow  course. 
The  evacuation  of  a  part  of  the  meningitic  exudation  by  lumbar  puncture  (vide 
supra)  is  sometimes  followed  by  a  temporary  improvement  of  the  sjTuptoms,  but 
no  actual  and  permanent  therapeutic  result  has  yet  been  obtained  by  lumbar  punc- 
ture. 

The  fever  hardly  ever  requires  special  treatment.  Quinine  exerts  no  influence 
in  the  intermittent  type.  Antipyrine  is  better  borne,  and  it  also,  like  the  other 
nervines,  sometimes  relieves  the  nervous  symptoms.  Cool  baths  are  not  to  be 
recommended,  but  hot  baths  or  hot  packs  sometimes  seem  to  be  of  decided  benefit. 
Later,  warm  baths  are  often  beneficial.  Local  complications — e.  g.,  affecting  the 
eye  or  the  ear — require  special  treatment.  The  swelling  of  the  joints  which  some- 
times occurs  we  have  thought  to  be  somewhat  relieved  by  salicylic  acid. 


CHAPTER   XIX 

SEPTIC    AND    PYEMIC    DISEASES 

( S2}07itaneozis  Septicopycemia) 

The  septic  and  pyemic  processes  Avhich  follow  serious  injiiries  or  operations 
belong  to  surgery;  but  analogous  diseases  occur  in  persons  who  are  apparently  in 
perfect  condition.  They  take  the  form  of  an  extremely  severe  acute  infectious 
disease,  usually  fatal.  There  can  scarcely  be  a  doubt  that  in  almost  all  these 
cases  there  is  some  small  break  in  the  continuity  of  the  external  skin  or  the 
mucous  membrane  which  affords  an  entrance  for  the  infectious  material;  but, 
since  the  infection  itself  is  wholly  unnoticed,  the  general  disease  seems  a  primary 


SEPTIC    AND    PY.EMIC    DISEASES  117 

affection,  and  its  correct  interpretation  often  occasions  the  physician  considerable 
difficulty.  Even  if  the  septic  infection  be  correctly  recognized,  it  is  sometimes 
impossible  to  determine  the  point-  of  origin.  For  such  cases  Leube  has  intro- 
duced the  name  of  "  cryptogenic  "  septicopysemia.  We  must  add,  however,  that 
in  many  cases  at  least,  a  careful  inquiry  and  examination  will  reveal  the  origin 
of  the  infection.  In  many  cases,  however,  a  complete  explanation  of  the  occur- 
rence of  the  infection  is  given  only  by  the  autopsy,  and  the  origin  of  some  cases 
remains  obscure  even  after  a  careful  autopsy. 

The  causes  of  pysemic  and  septic  affections  are  chiefly  the  same  pus  cocci 
which  produce  many  circumscribed  inflammations  and  suppurations,  especially  the 
streptococcus  pyogenes,  the  staphylococcus  pyogenes  albus,  and  the  staphylococcus 
pyogenes  aureus.  We  can  not  make  any  definite  clinical  distinction  in  the  septic 
affections  according  to  the  special  cocci  that  produce  them;  but,  in  general,  it  is 
the  rule  that  the  severe,  fatal  pysemic  and  septicsemic  affections  are  most  often 
due  to  streptococci — for  example,  many  cases  of  pytemia,  of  puerperal  sepsis,  of 
severe  ulcerative  endocarditis,  etc.  The  staphylococci  seem  on  the  whole  to  cause 
more  benign  forms  of  suppurative  or  septic  disease.  As  we  shall  see  later,  it  is 
not  improbable  that  acute  articular  rheumatism  must  be  regarded  as  such  a 
staphylococcus  infection.  Mixed  infections  with  streptococci  and  staphylococci 
also  occur,  and,  finally,  other  micro-organisms  (pneumonia  diplococci,  gonococci) 
may  sometimes  cause  forms  of  disease  which  have  many  points  of  similarity  to 
the  other  septic  diseases. 

The  essential  thing  in  all -septic  infections  is  the  general  disease  of  the  body 
caused  by  the  entrance  of  the  germs  into  the  circulation  and  their  increase 
therein.  The  form  and  severity  of  the  disease  thus  caused  depends  probably 
in  part  upon  the  special  variety  and  in  part  upon  the  varying  specific  "  viru- 
lence "  of  the  bacteria  that  have  entered  the  system,  but  the  form  and  severity 
also  depend  upon  the  greater  or  less  resistance  of  the  body,  which  varies  in  indi- 
viduals. If  the  micrococci  enter  the  general  circulation  only,  they  cause  a  large 
number  of  intoxication  symptoms,  due  to  the  action  of  different  "toxines"  formed 
by  the  chemical  changes  in  the  micrococci.  The  micrococci,  however,  may  collect 
in  the  smaller  blood-vessels  ("micrococcus  foci,"  "micrococcus  emboli"),  and  in 
this  way  may  cause  circumscribed  or  extensive  suppuration  in  the  various  organs. 
In  prevailing  parlance  we  call  this  multiple  abscess  formation  pyaemia,  and  the 
cases  with  severe  (toxic)  general  symptoms,  haemorrhage,  etc.  (vide  infra),  but 
without  suppuration,  we  call  septicaemia  or  sepsis.  Since,  however,  the  two 
groups  of  symptoms  may  be  associated  with  each  other  in  many  ways,  we  often 
speak  of  septicopyaemia. 

It  is  very  important  for  the  correct  understanding  of  all  these  conditions  to 
bear  in  mind  that,  in  different  cases,  different  organs  or  parts  of  the  body  may 
become  the  chief  seat  for  the  localization  of  the  micrococci.  Hence  severe  local 
disorders  may  arise,  which,  of  course,  may  give  diverse  aspects  to  the  clinical 
picture  according  to  the  special  localization.  This  is  the  reason  why  many  of 
these  affections  were  formerly  regarded  as  separate  diseases,  although  in  reality 
they  were  only  different  localizations  and  forms  of  the  same  infectious  process. 
Among  these  affections  were  the  so-called  "  acute  osteomyelitis  "  almost  always 
caused  by  the  staphylococcus  jjyogenes  aureus,  "  malignant  endocarditis,"  certain 
forms  of  "  malignant  erysipelas,"  etc.  In  their  clinical  aspect  these  differences 
are,  of  course,  still  of  great  importance,  but  the  Eetiological  connection  of  all 
these  cases  must  always  be  emphasized,  because  only  by  putting  a  proper  stress  upon 
this  point  can  we  obtain  a  correct  understanding  of  all  the  combinations  mani- 
fested in  the  clinical  course  of  the  disease. 

Before  we  consider  the  details  of  the  anatomical  changes  in  septic  affections, 
we  would  mention  those  circumstances  (exciting  causes),  which,  we  know  by  ex- 


118  ACUTE   GEl^EEAL   nsTj^ECTIOUS   DISEASES 

perience,  most  commonly  cause  or  render  possible  the  occurrence  of  septic  infec- 
tion. In  each  individual  case  it  must  be  our  task,  as  we  have  said,  either  during 
the  patient's  life  or  at  the  autopsy,  to  determine  if  possible  the  point  of  origin  of 
the  infection.  The  following  are  chiefly  to  be  considered :  1.  The  puerperal  pro- 
cesses take  the  first  place.  Both  after  delivery,  and  still  more  frequently  after 
abortion,  the  raw  surface  of  the  uterus  may  be  the  door  of  entrance  for  the  septic 
poison,  but  a  gross  pathological  change  is  not  necessarily  to  be  seen  in  the  uterus 
itself  or  in  its  appendages.  We  do  find,  often  enough,  diphtheritic  and  gan- 
grenous inflammation  at  the  place  where  the  placenta  was  inserted,  or  purulent 
thrombi  in  the  veins  of  the  uterms  and  of  the  pelvis,  etc. ;  but  in  other  cases  the 
uterus  is  merely  a  gate  of  entrance  for  the  poison,  remaining  itself  normal. 
2.  The  septic  poison  may  also  be  absorbed  through  slight  abrasions  of  the  skin, 
injuries,  felons,  whitlows,  etc.;  and  these  may  be  almost  completely  healed  by 
the  time  the  severe  symptoms  of  disease  are  developed.  Bed-sores  belong  in  this 
category.  3.  Ulcers  of  the  mucous  membranes  may  give  rise  to  infection.  This 
is  the  explanation  of  those  cases  of  sepsis  which,  in  rare  instances,  follow  all  sorts 
of  intestinal  ulcers  (simple  intestinal  ulcers,  typhoid,  dysentery,  etc.),  diphthe- 
ritic processes  in  the  pharynx,  even  mild  tonsillar  affections,  etc.  In  the  descrip- 
tion of  scarlet  fever  and  pharyngeal  diphtheria  we  have  already  considered  this 
important  form  of  secondary  sepsis  in  detail.  4.  Lastly,  we  sometimes  find  no 
other  source  for  the  pyaemia  than  a  suppurating  disease  of  the  bones,  joints,  or 
other  parts,  previously  existing.  We  must  here  suppose  that  some  connection  was 
formed  between  the  original  pus  cavity  and  the  blood  or  lymph  channels,  and  that 
thus  the  micrococci  entered  the  general  circulation  and  were  enabled  rapidly 
to  increase. 

The  above  enumeration  by  no  means  exhausts  all  the  possibilities;  still,  it 
will  be  found  to  explain  most  cases.  The  more  minutely  we  search  for  a  place 
of  entrance  for  the  septic  virus,  the  rarer  will  the  "  cryptogenic  "  cases  be  in 
which  the  starting-point  of  the  infection  remains  unknown.  [The  editor  has 
seen  two  clear  cases,  one  confirmed  by  autopsy,  of  general  septic  infection  and 
malignant  endocarditis  as  a  sequel  of  gonorrha^a.] 

Pathological  Anatomy.- — The  most  striking  feature  at  the  autopsy  of  such 
cases  is  that  there  is  never  found  a  lesion  of  one  organ  exclusively.  Several,  or 
it  may  be  almost  all  of  the  organs,  exhibit  numerous  limited  foci  of  disease.  The 
lesions  sometimes  consist  for  the  most  part  of  multiple  abscesses,  sometimes  of 
numerous  ecchymoses,  and  sometimes  of  combinations  of  the  two.  The  abscesses 
are  found  chiefly  in  the  lungs,  kidneys,  liver,  spleen,  muscles,  heart,  brain,  and 
thyroid  gland.  Quite  extensive  purulent  inflammation  is  also  found.  This  at- 
tacks the  joints  or  causes  phlegmon  of  the  muscles  or  skin  by  preference,  but  it 
also  attacks  the  pleura,  the  meninges,  and  the  eye,  where  it  causes  purulent 
choroiditis,  panophthalmitis,  and  purvilent  degeneration  of  the  vitreous.  Puru- 
lent phlebitis  also  occurs.  The  ecchymoses  are  most  frequent  upon  the  surface 
of  the  body,  the  serous  membranes  (pericardium,  pleura),  the  retina,  the  conjunc- 
tiva, the  brain,  the  pelvis  of  the  kidney,  etc.  Beside  these  multiple  abscesses  and 
ecchymoses,  there  is  frequently  another  disorder,  which  seems  to  be  the  very 
focus  of  the  disease,  viz.,  acute  ulcerative  endocarditis  (cf.  the  appropriate 
chapter).  This  usually  attacks  the  mitral  valve,  more  rarely  the  valves  of  the 
aorta,  and  quite  exceptionally  the  valves  of  the  right  side  of  the  heart.  Finally 
come  a  number  of  changes  common  to  all  severe  constitutional  infectious  diseases 
— acute  splenic  tumor,  "  cloudy  swelling  "  of  the  liver  and  kidneys,  a  dryness  and 
dark-red  color  of  the  muscles,  etc. 

In  regard  to  the  special  origin  of  all  these  symptoms  we  may  certainly 
refer  the  abscesses,  the  purulent  inflammation,  and  the  endocarditis  to  the 
immediate  presence   of   the   micrococci   themselves,   while   the   parenchymatous 


SEPTIC   A:ND   pyemic    diseases  119 

degenerations  of  different  organs,  the  hgemorrhages,  and  ijrobably  the  splenic  en- 
largement and  the  diffuse  acute  nephritis,  are  to  be  regarded  as  due  to  toxic 
action.  Microscopic  examination  of  the  internal  organs  gives  us  a  very  instruc- 
tive insight  into  the  morbid  process.  This  often  reveals  the  presence  of  many 
tiny  foci  of  disease,  in  the  center  of  which  we  often  see  a  little  blood-vessel  com- 
pletely filled  with  micrococci  ("micrococcus  embolus")-  As  Weigert  first  found, 
the  primary  action  of  a  little  focus  of  micrococci  upon  the  surrounding  tissues 
consists  of  a  circumscribed  cell  necrosis,  a  small  focus  of  "  coagulation-necrotic  " 
•cells  without  nuclei.     This  may  be  followed  later  by  circumscribed  suppuration. 

Clinical  History. — It  is  our  intention  to  discuss  below  those  cases  chiefly 
which  are  of  interest  to  the  physician  rather  than  the  surgeon^ — i.  e.,  where  the 
septicopygemia  is  an  apparently  primary,  acute,  and  grave  disease.  Many  of  the 
■essential  traits  of  this  type  of  disease  are  identical  with  those  of  the  pytemia 
which  complicates  the  effects  of  serious  wounds  or  the  inflammation  subsequent 
to  childbirth ;  but  it  is  precisely  because  no  cause  at  all  presents  itself  that  many 
■cases  of  this  form  of  sepsis  seem  so  obscure,  and  are  so  often  wrongly  diagnosti- 
cated. Besides,  the  patient  may  be  very  ill  indeed  before  the  physician  sees  him ; 
and  this  adds  greatly  to  the  difficulties  of  a  correct  diagnosis. 

The  beginning  of  the  disease  is  usually  rather  abrupt.  An  apparently  healthy 
person  is  attacked  with  febrile  sjTuptoms,  headache,  and  "  rheumatic  "  pains 
in  the  muscles,  joints,  and  loins.  There  may  also  be  gastro-intestinal  symptoms 
of  considerable  severity,  including  vomiting  and  diarrhoea.  Usually  the  patient 
feels  ill  enough  to  take  speedily  to  his  bed.  The  symptoms  now  increase  rapidly, 
and  develop  into  a  severe  illness  which  may  resemble  either  a  bad  case  of  typhoid 
fever  or  miliary  tuberculosis.  Or  the  cerebral  symptoms,  such  as  headache, 
stupor,  and  delirium,  m-ay  become  so  prominent  that  the  attack  seems  like  menin- 
gitis. If  the  trouble  in  the  joints  (vide  infra)  predominates  and  there  are  signs 
of  endocarditis,  the  disease  may  at  first  be  taken  for  a  violent  attack  of  acute 
articular  rheumatism. 

Taking  up  the  separate  symptoms,  we  shall  first  name  those  which  belong  to 
every  severe  acute  infectious  disease  and  have  nothing  characteristic  about  them. 
In  this  list  belong  the  general  prostration,  the  anorexia,  the  mental  disturbance, 
the  stupor  and  delirium,  the  headache,  the  subjective  symptoms  of  fever,  the  dry- 
ness of  the  tongue,  and  finally  the  acute  splenic  tumor  which  can  often  be  made 
•out.  There  are,  however,  other  and  more  characteristic  symptoms;  and  it  is 
chiefly  upon  these  that  the  diagnosis  rests,  provided  we  can  make  one  at  all. 
These  are : 

1.  The  Course  of  the  Fever. — In  many  cases  it  must  be  confessed  that  this 
is  not  at  all  characteristic.  It  may  even  be  so  like  that  of  typhoid  fever,  at 
least  for  some  time,  as  to  lead  to  a  wrong  diagnosis.  In  other  cases,  however,  the 
temperature-curve  does  aid  us  greatly,  viz.,  when  it  represents  an  intermitting 
fever  with  marked  elevations,  reaching  106°  (41°  C.)  and  higher,  and  often 
accompanied  by  a  chill,  and  with  subsequent  deep  depressions.  The  curve  may 
thus  come  to  resemble  closely  that  of  a  quotidian  or  even  tertian  intermittent 
fever.  This  true  "  pyajmic  "  fever,  in  which  the  rise  in  temperature  is  usually  asso- 
ciated with  a  severe  chill,  occurs  chiefly  in  the  cases  with  multiple  abscesses. 
Sometimes,  again,  the  course  of  the  fever  is  made  up  of  similar  paroxysmal  eleva- 
tions, separated  by  periods  of  ordinary  remitting  fever. 

2.  Cutaneous  Symptoms. — These  are  very  frequent,  and  a  great  aid  to  diag- 
nosis. The  hemorrhages  into  the  skin  are  of  chief  importance.  They  may  be 
either  punctiform  petechice  or  more  extensive  ecchymoses.  Of  other  cutaneous 
appearances,  the  first  in  relative  frequency  is  an  erythema  resembling  scarlatina. 
It  is  not  improbable,  as  W'e  have  already  said,  that  many  cases  which  have  been 
■described  as  severe  scarlet  fever  occurring  during  childbed  were  in  reality  septic 


120  ACUTE   GENEEAL   INFECTIOUS   DISEASES 

disease.  We  also  sometimes  see  eruptions  resembling  erythema  exsudativum 
multiforme  or  erythema  nodosum,  and  also  in  some  cases  roseola,  pustular  erup- 
tions, and  herpes.  Extensive  inflammations  of  the  skin  like  erysipelas  are  espe- 
cially characteristic  of  certain  cases.  They  are  seen  on  the  lateral  surfaces  of 
the  thorax,  the  back,  the  thighs,  etc.,  and  often  end  in  phlegmonous  suppuration. 
When  they  occur  we  can  usually  make  a  very  positive  diagnosis  of  septic  in- 
fection. 

3.  Circulatory  Disturbances. — An  ability  to  recognize  the  cardiac  lesions 
would  be  very  desirable;  but  often  this  is  impossible  before  death.  Endocardial 
murmurs  are  often  wanting,  even  in  cases  where  the  autopsy  discloses  abundant 
exudation  and  ulcers  upon  the  valves.  Still,  in  some  cases  of  this  sort  we  have 
found  the  heart-sounds  noticeably  deficient  in  clearness.  Sometimes  we  hear 
very  loud  or  low,  blowing  sounds.  The  cardiac  dullness  is  often  quite  normal,  in 
other  cases  somewhat  increased.  In  some  cases  fibrinous  or  purulent  pericarditis 
develops.  Functional  disturbances  of  the  heart's  action  are  almost  always  pres- 
ent. The  heart's  action  is  excited  and  very  rapid  (120  to  140  or  more),  or  in  rare 
cases  abnormally  slow.  Irregularity  and  inequality  of  the  pulse  are  common. 
The  tension  of  the  pulse  is  usually  low,  and  the  frequent  pallor  and  mild  cyanosis 
of  the  patient  point  to  a  diminished  energy  in  the  heart's  action.  In  the  blood 
we  find  almost  invariably  a  more  or  less  pronounced  leucocytosis.  The  presence 
of  micrococci  in  the  blood  would  naturally  be  of  the  greatest  significance.  They 
have,  in  fact,  been  repeatedly  found  in  septic  affections  during  life,  but  more 
extensive  clinical  bacteriological  investigations  are  still  needed  in  regard  to  this 
point. 

4.  The  grave  cerehral  symptoms  are  for  the  most  part  quite  analogous  to  those 
of  other  severe  acute  infectious  diseases.  They  may  be  present,  and  yet  no 
marked  objective  lesions  may  be  found  after  death.  In  other  cases  they  have  an 
anatomical  basis — in  purulent  meningitis,  hsemorrhagic  pachymeningitis,  cere- 
bral haemorrhage,  or  abscess.  These  conditions,  just  enumerated,  may  excite 
localized  cerebral  symptoms,  e.  g.,  hemiplegia. 

5.  Affections  of  the  joints  are  comparatively  frequent,  and  of  great  value  in 
diagnosis.  We  may  find  serous,  or  more  likely  purulent  inflammation,  or  even  peri- 
articular abscesses.  If  they  appear  early  in  the  attack,  they  may,  as  we  have 
said,  lead  to  an  erroneous  diagnosis  of  acute  articular  rheumatism.  Suppurative 
processes  affecting  the  periosteum  and  the  marrow  of  the  bones  not  infrequently 
accompany  the  joint  affections.  Only  in  rare  cases  do  the  bones  remain  wholly 
unaffected,  as  is  evident  from  the  frequent  occurrence  of  pain  in  the  long  bones. 
If  there  is  decided  suppuration  in  the  bones  we  speak  of  an  acute  osteomyelitis. 
This  is  seen  especially  in  the  lower  extremities.  It  is  almost  always  occasioned 
by  the  staphylococcus  aureus.  In  earlier  times  such  cases  were  termed  bone- 
typhoid.  Finally,  abscesses  and  extensive  phlegmonous  suppuration  in  the  mus- 
cles are  not  uncommon. 

6.  Renal  changes  are  very  frequent,  but  abscesses  and  haemorrhages  may  be 
numerous  in  the  kidneys,  or  haemorrhages  in  the  mucous  membrane  of  the  pelvis 
of  the  kidney,  without  materially  altering  the  character  of  the  urine.  In  most 
cases,  however,  an  acute  septic  nephritis  is  conjoined  with  the  infarctions  and 
abscesses,  and  then  the  urine  exhibits  all  the  characteristics  of  acute  Bright's 
disease,  having  a  small  or  large  amount  of  albumen,  red  and  white  blood-corpus- 
cles, epithelium,  and  casts. 

7.  The  pulmonary  symptoms  are  in  part  secondary.  Bronchitis  and  lobular 
pneumonia  develop  as  in  all  other  severe  constitutional  diseases.  The  pulmonary 
abscesses  of  themselves  give  rise  usually  to  no  objective  symptoms-^or,  at  most,  to 
a  marked  dyspnoea,  out  of  all  proportion  to  the  scanty  physical  signs.  Empyema 
is  a  not  infrequent  result  of  infection  of  the  pleura,  due  to  the  foci  of  disease 


SEPTIC   AND   PYEMIC   DISEASES  121 

which  are  situated  upon  the  outer  surface  of  the  lungs,  or  perhaps  sometimes  to 
the  condition  of  the  blood.  If  the  aspirating-needle  shows  the  actual  existence  of 
empyema,  this  fact  may  make  the  .diagnosis  of  the  constitutional  disease  much 
easier.  A  fibrinous  pleurisy  of  slight  degree  is  often  found  at  the  autopsy,  and  it 
may  be  diagnosticated  during  life  by  the  detection  of  a  slight  pleuritic  friction-rub. 

8.  Of  the  abdominal  symptovis  we  have  already  mentioned  the  acute  splenic 
tumor.  It  is  almost  impossible  to  diagnosticate  infarctions  and  abscesses  in  the 
spleen.  If  the  spleen  is  enlarged  and  noticeably  painful,  we  may  suspect  their 
existence.  There  are  sometimes  quite  severe  intestinal  symptoms,  such  as  a  pro- 
fuse "  septic  diarrhoea,"  in  cases  where  the  autopsy  does  not  show  any  particularly 
grave  lesions.  Still  intestinal  ecchymoses  and  intestinal  diphtheria  have  some- 
times been  observed.  We  should  mention  that  often  the  skin  has  a  faint  jaun- 
diced hue.  This  is  sometimes  the  result  of  duodenal  catarrh,  but  more  frequently 
it  is  to  be  regarded  as  a  "  hepato-hsematogenous  "  jaundice  due  to  a  decomposition 
of  the  blood. 

9.  Ocular  Disturbances. — The  purulent  inflammations  of  the  eye,  which  are 
probably  of  embolic  origin  and  which  may  develop  into  diffuse  septic  panoph- 
thalmitis, have  been  known  for  some  time.  Lately,  Litten  and  others  have  called 
attention  to  more  minute  changes  in  the  fundus  of  the  eye.  These  are  revealed 
through  the  ophthalmoscope,  and  have  great  diagnostic  value.  Chief  among 
them  is  retinal  haemorrhage,  which  is  sometimes  accompanied  by  a  white  spot  in 
the  center,  corresponding  to  a  necrosis  of  the  retina  in  that  place;  but  there  may 
be  similar  white  spots  without  haemorrhage. 

Course  of  the  Disease  and  Prognosis. — In  severe  general  septic  infection 
death  sometimes  occurs  in  a  few  days.  In  other  cases  the  disease  continues 
longer,  the  symptoms  lasting  two  or  three  weeks  or  even  more.  Improvement 
sometimes  takes  place,  followed  by  a  relapse.  Here,  too,  the  result  is  often  fatal, 
although  the  infection  may  finally  be  completely  overcome.  We  may  also  accept 
as  certain  that  there  are  mild,  curable  forms  of  septic  disease.  In  these  the 
signs  of  general  infection  may  predominate,  such  as  fever  with  general  intoxica- 
tion, cardiac  weakness,  pains  in  the  joints,  albuminuria  or  exanthemata,  or,  in 
other  cases,  the  chief  symptoms  may  be  due  to  a  special  localization  of  the  germs 
or  their  toxines  (acute  endocarditis,  septic  nephritis,  septic  inflammation  of  the 
serous  membranes,  septic  enteritis,  etc.).  As  we  shall  see  later,  acute  articular 
rheumatism  (polyarthritis  acuta)  is  probably  nothing  but  a  benign  septic 
infection. 

Diagnosis. — It  is  self-evident  that  a  disease  which  combines  symptoms  so 
manifold  and  so  ambiguous  must  be  very  difficult  to  recognize.  We  will  re- 
capitulate the  chief  diseases  to  be  excluded.  A  case  may  greatly  resemble  typhoid 
fever  when  there  is  persistent  prostration,  diarrhoea,  an  eruption  like  roseola,  and 
an  enlarged  spleen.  In  discriminating,  we  should  consider  with  great  care  the 
possible  aetiology — e.  g.,  external  injuries,  etc. ;  we  should  remember  that  most 
septic  affections  begin  rather  more  rapidly;  and  we  should  look  for  swelling  of 
the  joints,  cutaneous  ecchymoses,  nephritis,  phlegmonous  suppurations,  an  inter- 
mitting form  of  fever,  and  septic  disease  of  the  retina.  We  have  repeatedly 
found  that  leucocytosis  was  a  very  valuable  sign,  since  it  is  almost  always  absent 
in  typhpid  fever,  but  a  positive  result  from  Widal's  serum  reaction  (vide  page 
22)  renders  a  diagnosis  of  typhoid  very  probable.  It  is  all  the  more  possible 
for  the  disease  to  resemble  meningitis,  because,  as  we  have  said,  meningeal  dis- 
turbance may  be  one  of  the  symptoms  of  the  sepsis  and  color  the  whole  pic- 
ture. Here  the  characteristic  symptoms  of  septic  poisoning  already  mentioned 
would  be  of  some  value  in  diagnosis,  and  the  physical  signs  of  endocarditis  or 
of  a  greatly  enlarged  spleen  would  be  worth  still  more.  There  may  be  much 
difficulty  in  the  differential  diagnosis  between  acute  sepsis  and  acute  miliary 


122  ACUTE    GENEEAL   IK"FECTIOUS    DISEASES 

tuberculosis.  Here  we  should  consider  carefully  each  separate  symptom,  and, 
above  all,  the  Eetiology,  searching  for  something  that  would  explain  the  occur- 
rence of  sepsis  on  the  one  hand,  or  of  acute  miliary  tuberculosis  (q.  v.)  on  the 
other.  If  we  found  miliary  tubercles  in  the  choroid  by  means  of  the  ophthal- 
moscope, or  tubercle  bacilli  in  the  sputum  or  in  the  blood  (which  is,  of  course, 
not  always  possible),  all  doubt  would  vanish.  At  the  beginning  of  a  septic 
attack  the  rigors  may  arouse  suspicions  of  intermittent  fever.  Usually  the  early 
appearance  of  other  symptoms  corrects  this  idea;  but,  if  not,  the  powerless- 
ness  of  quinine  will.  If  a  severe  acute  nephritis  has  developed  itself  in  a  septic 
case,  all  the  symptoms  may  be  erroneously  referred  to  ursemia;  but  persistent 
observation  will  usually  lead  us  to  the  right  conclusion.  As  to  the  conditions 
of  great  prostration  resembling  acute  sepsis,  which  occur  in  acute  (primary) 
ulcerative  endocarditis  and  in  severe  articular  rheumatism,  see  the  appropriate 
chapters. 

In  general  the  diagnosis  of  acute  sepsis  can  i-arely  be  settled  during  the  first 
days  of  the  disease,  but  on  further  observation  and  with  due  attention  a  toler- 
ably definite  diagnosis  can  often  be  made.  The  chief  elements  for  diagnosis  are 
a  careful  consideration  of  the  aetiology,  attention  to  the  whole  clinical  picture, 
and  to  any  individual  symptoms  especially  characteristic  of  septic  infection 
(purulent  infiammation,  chills  and  fever,  cutaneous  and  retinal  haemorrhages, 
nephritis,  marked  leucocytosis,  etc.). 

We  must  refer  the  reader  to  the  appropriate  chapters  for  the  morbid  condi- 
tions allied  to  acute  sepsis,  such  as  "  primary  acute  endocarditis,"  "  acute  articu- 
lar rheumatism,"  "  purpura  hsemorrhagica,"  etc. 

The  treatment  is  merely  symptomatic.  Of  course  we  try  again  and  again 
to  cut  short  the  attacks  of  fever  by  large  doses  of  quinine  or  antipyrine,  but 
never  with  any  but  temporary  success.  With  marked  swelling  of  the  joints  we 
may  try  salicylic  acid.  Of  other  remedies,  cardiac  stimulants  are  most  fre- 
quently employed,  and  narcotics  if  necessary.  Great  stress  is  to  be  laid  on  keep- 
ing up  the  physical  strength  by  careful  nourishment.  Circumscribed  suppura- 
tion (empyema,  phlegmon,  etc.),  when  it  exists,  of  course  requires  the  proper 
surgical  treatment. 


CHAPTEE   XX 

HYDROPHOBIA 

(Babies  caniiia.     Lyssa) 

Etiology.  Habies  in  Dogs. — A  peculiar  infectious  disease  sometimes  occurs 
in  dogs,  and  more  rarely  in  some  other  animals — ^viz.,  the  wolf,  fox,  cat,  etc. 
Men  who  are  bitten  by  the  animal  may  catch  the  disease,  and  thus  suffer  from 
very  severe  symptoms  originating  in  the  central  nervous  system. 

Two  forms  of  madness  are  distinguished  in  dogs — the  raving  madness  and  the 
quiet  madness.  Bollinger  describes  the  raving  form  as  beginning  with  prodro- 
mata,  the  melancholy  stage,  lasting  one  to  three  days.  The  animal  is  low-spirited, 
timorous,  and  without  appetite.  Then  comes  the  stage  of  irritation  or  of  mania, 
in  which  the  animal  is  possessed  with  an  impulse  to  bite.  It  seems  determined  to 
run  away  and  rove  about,  and  it  utters  a  peculiar  howl.  The  dog  will  not  touch 
his  ordinary  food,  but  he  often  swallows  straw,  hair,  earth,  bits  of  wood,  etc.  In 
the  third  or  paralytic  stage  paralysis  appears.  The  dog  looks  lean  and  wretched, 
and  always  dies  on  the  tenth  day  at  the  latest.  In  what  is  called  the  quiet  mad- 
ness there  is  no  maniacal  stage.  The  symptoms  of  paralysis,  affecting  chiefly  the 
hind  limbs  and  the  lower  jaw,  occur  earlier  and  are  sooner  fatal.    Marked  patho- 


HYDEOPHOBIA  123 

logical  changes  are  not  found.  There  are  pulmonary  and  intestinal  catarrh  and 
jjassive  congestion  of  the  viscera,  and  the  stomach  often  contains  foreign  bodies 
in  place  of  the  usual  partially  digested  food. 

[On  the  Western  plains  hydrophobia  is  said  not  infrequently  to  follow  skunk 
bites.  The  bite  is  inflicted  during  sleep  on  persons  passing  the  night  in  the  open 
air  or  in  tents  to  which  the  animal  can  gain  access.] 

Rabies  is  transferred  to  the  human  being  almost  invariably  by  the  bite  of  some 
raving  animal,  and  this  animal  is  almost  always  a  dog;  much  more  rarely  a  wolf 
or  cat.  It  is  of  practical  importance,  and  it  has  been  repeatedly  confirmed,  that 
the  bite  of  such  an  animal,  although  still  in  the  incubation  period  of  hydrophobia, 
can  convey  the  disease  to  man.  The  poison,  which  is  not  yet  known  in  its  pure 
form,  is  evidently  contained  in  the  saliva  or  slaver  and  in  the  blood  of  mad  ani- 
mals, and  can,  by  means  of  these  substances,  be  successfully  inoculated  in  other 
animals.  Pasteur  has  discovered  another  way  to  produce  the  disease  experi- 
mentally. He  takes  minute  portions  of  the  brain,  medulla  oblongata,  or  some 
other  internal  viscus  of  a  mad  dog,  and  either  injects  them  into  the  veins  of  a 
healthy  animal,  or  trephines,  and  then  inserts  them  beneath  the  meninges.  The 
virulence  of  the  rabic  poison  when  thus  manipulated  undergoes,  under  special  con- 
ditions, very  peculiar  alterations,  which  will  be  detailed  at  the  close  of  this 
chapter. 

About  one  half  of  those  who  are  bitten  by  mad  animals  exhibit  no  subsequent 
symptoms.  Still  this  can  scarcely  be  due  to  inherent  immunity  from  the  dis- 
ease, and  it  must  result  chiefly  from  imperfect  infection.  Experience  has  shown 
that  infection  is  especially  apt  to  follow  when  a  nerve  has  been  injured  by  the 
bite;  and  infection  occurs  more  readily  the  larger  and  the  nearer  the  brain  the 
wound  is.  Wounds  of  the  head  are  therefore  the  most  dangerous.  The  dura- 
tion of  incubation  until  rabies  finally  breaks  out  seems  to  vary  greatly.  As  a  rule 
it  is  about  three  to  six  months,  but  observers  have  reported  instances  both  of 
shorter  and  of  much  longer  duration. 

Clinical  History. — The  disease  begins  with  a  general  feeling  of  indisposition, 
anorexia,  headache,  and  uneasiness.  This  last  is  partially  explained,  to  be  sure, 
by  a  dread  of  what  is  impending.  If  the  bite  was  in  the  face,  frequent  convulsive 
sneezing  may  occur.  Even  now,  in  this  prodromal  stage,  a  marked  aversion  to 
liquids  is  a  usual  and  early  symptom.  The  attempt  to  swallow  excites  slight  con- 
vulsive disturbances.  Painful  sensations  may  arise  once  more  in  the  bitten  place, 
although  this  has  usually  been  cicatrized  long  before,  and  the  neighboring  lymph- 
glands  are  often  found  to  be  swollen. 

Only  a  day  or  two  later  the  second,  hydrophobic  stage  begins.  The  especial 
characteristic  of  this  consists  in  the  peculiar  attacks  of  tonic  convulsions.  The 
pharynx  suffers  most,  but  convulsions  also  attack  the  muscles  of  respiration  and 
those  of  the  trunk  and  extreiuities.  A  terrible  feeling  of  anxiety  and  oppression 
accompanies  these  attacks,  so  that  one  who  has  once  witnessed  the  sight  can  never 
forget  it.  The  convulsions  always  seem  to  be  reflex,  and  are  prodviced  by  the 
slightest  causes,  particularly  by  any  attempt  to  swallow,  or  sometimes  by  the  mere 
sight  of  water.  They  recur  at  gradually  diminishing  intervals,  and  last  from  a 
few  minutes  to  half  an  hour.  The  excitement  of  the  patient  may  reach  the  pitch 
of  delirium  or  mania.  The  pulse  is  at  first  full  and  rapid,  but  later  it  is  small 
and  irregular.  The  temperature  is  usually  only  slightly  elevated,  but  it  may  be 
high.  There  is  great  thirst,  accompanied  by  burning  pain  in  the  throat.  Usu- 
ally there  is  marked  salivation. 

This  condition  lasts  one  to  three  days.  Then  death  occurs,  ushered  in  by  vio- 
lent convulsions.  Death  may  also  be  preceded  by  a  brief  third  stage  of  paralysis, 
during  which  there  are  no  convulsive  attacks.  Cases  of  recovery  in  man,  if  they 
ever  happen,  are  extremely  rare. 


124  ACUTE    GENEEAL   liTEECTIOUS   DISEASES 

The  autopsy  shows  very  little.  The  brain  and  medulla  especially  show  no 
gross  changes,  so  that  we  may  conclude  that  hydrophobia  is  chiefly  the  effect  of  a 
toxine.  The  microscope  has  repeatedly  detected  very  minute  haemorrhages,  clus- 
ters of  lymph-cells  around  the  blood-vessels,  etc.  There  have  been  only  a  few 
investigations  of  the  finer  microscopical  changes  in  the  motor  ganglion  cells  of 
the  medulla,  etc.  The  throat  may  present  the  signs  of  catarrh.  The  lungs  are 
congested,  and  often  oedematous.  The  blood  is  dark,  with  few  clots.  The  heart, 
liver,  and  spleen  are  apparently  normal. 

The  diagnosis  is  usually  easy,  particularly  if  we  know  of  the  possibility  of 
infection.  We  are  guided  by  the  convulsions  following  attempts  to  swallow,  as 
well  as  by  the  whole  group  of  symptoms.  Hydrophobia  is  distinguished  from 
traumatic  tetanus  by  the  absence  of  trismus  and  of  the  characteristic  tension  of 
the  muscles  of  the  back  and  abdomen,  by  the  convulsions  coming  in  separate 
attacks,  and  by  the  usually  greater  length  of  incubation.  There  is  only  one 
form  of  tetanus  which  bears  very  great  resemblance  to  rabies,  viz.,  the  so-called 
hydrophobic  tetanus  {vide  infra).  It  should  be  mentioned  that  the  mere  dread 
of  hydrophobia  may  cause  an  easily  excited  person  to  have  the  nervous  symp- 
toms of  the  disease  ("hysterical  hydrophobia"),  but  of  course  without  disastrous 
results.  Hysteria,  also,  may  give  rise  to  convulsions  on  swallowing  somewhat 
resembling  those  of  hydrophobia. 

However  hopeless  treatment  seems,  we  must  at  least  try  to  mitigate  the  pa- 
tient's suffering.  JSTarcotics  accomplish  this  best — e.  g.,  opium  or  chloral,  or,  most 
useful  of  all,  the  inhalation  of  chloroform.  Curare  has  been  administered  repeat- 
edly, and  does  seem  to  lessen  the  violence  of  the  attacks.  The  attempt  to  find  a 
serum-therapy  for  hydrophobia  has  unfortunately  not  been  thus  far  successful. 

Prophylaxis  is  extremely  important.  We  can  not  consider  in  detail  the  regu- 
lations (muzzling)  which  the  government  should  make  in  order  to  prevent  the 
spread  of  the  disease.  As  to  individual  prophylaxis,  every  suspicious  bite  should 
be  very  thoroughly  disinfected,  and  then  cauterized  either  with  carbolic  acid, 
caustic  potash,  or  the  red-hot  iron.  It  has  also  been  recommended  that  the  entire 
wound  or  scar  should  be  excised,  along  with  any  swollen  lymphatic  glands  which 
may  be  found  in  the  neighborhood.  Internal  remedies  to  prevent  the  outbreak 
of  the  disease  are  probably  quite  useless. 

On  the  other  hand,  Pasteur  has  recently  made  a  series  of  extremely  remarkable 
observations  which  have  led  to  a  special  method  of  prophylactic  inoculation 
against  rabies  in  human  beings.  If  a  bit  of  the  spinal  marrow  taken  from  a  mad 
dog  (an  emulsion  of  the  substance  of  the  cord  rubbed  up  in  salt  solution  or 
bouillon)  is  introduced  beneath  the  dura  mater  of  a  rabbit  by  means  of  trephining, 
the  animal  exhibits  the  symptoms  of  rabies  after  fourteen  days'  incubation.  If 
in  the  same  way  a  second  rabbit  is  inoculated  from  the  first,  and  so  on,  the  viru- 
lence of  the  inoculated  material  increases  gradually  with  every  inoculation,  while 
the  period  of  incubation  grows  shorter  and  shorter,  tiU  it  lasts  but  seven  days. 
Beyond  this  point  the  period  of  incubation  does  not  seem  to  diminish.  If,  on  the 
other  hand,  the  same  series  of  inoculations  are  made  on  apes,  the  virulence 
of  the  poisonous  matter  does  not  increase,  but  diminishes.  If  dogs  are  inocu- 
lated with  material  artificially  attenuated  in  this  manner,  the  animals  remain 
in  good  health,  and  furthermore  acquire  an  immunity  against  more  virulent 
inoculations,  so  that  they  may  be  bitten  by  mad  dogs  without  becoming  infected. 

Pasteur  has  also  published  a  still  more  simple  and  valuable  method  of  artifi- 
cial attenuation  of  the  virus.  He  removes  small  portions  of  the  spinal  marrow  of 
rabbits  which  are  suffering  from  rabies  in  its  most  violent  form  produced  by  the 
above-detailed  method,  and  these  bits  of  marrow  he  exposes  to  air  which  has 
been  wholly  deprived  of  moisture.  In  this  way  the  poison  contained  in  the  spinal 
marrow  gradually  and  progressively  loses  its  virulence,  imtil  it  finally  becomes 


GLANDEES  125 

inert.  A  portion  of  spinal  marrow  which  by  long  drying  has  completely  lost  its 
original  virulence  is  then  rubbed  up  in  sterilized  bouillon  and  injected  into  some 
animal — for  instance,  a  dog — and  then  in  regular  succession  pieces  of  marrow 
which  have  been  dried  for  shorter  and  shorter  periods  and  so  contain  more  and 
more  of  the  poison,  until  finally  the  point  is  reached  when  it  is  possible  to  use  for 
the  injection  pieces  which  are  perfectly  fresh  and  extremely  poisonous,  without 
affecting  the  animal's  health.  That  is,  the  animal  has  attained  immunity  from 
the  disease. 

This  second  method  has  now  been  employed  by  Pasteur  on  several  thousands 
of  human  beings  who  were  said  to  have  been  bitten  by  mad  dogs.  According  to 
the  reports,  so  small  a  number  of  these  inoculated  persons  (about  one  per  cent.) 
have  actually  been  attacked  later  by  hydrophobia  that  we  can  no  longer  doubt 
the  prophylactic  value  of  Pasteur's  protective  inoculations,  especially  as  we  have 
to  do  with  observations  which  are  by  no  means  unique  in  bacteriology.  The  dan- 
ger that  hydrophobia  may  perhaps  be  excited  by  such  a  "  protective  inoculation  " 
can  not  be  wholly  excluded,  but  it  will  certainly  grow  less  and  less. 

Prophylactic  inoculation  for  hydrophobia  can  at  present  be  practiced  only 
in  special  institutes.  In  most  civilized  countries,  therefore,  such  institutions 
have  already  been  established  on  the  plan  of  the  Pasteur  Institute  in  Paris. 


CHAPTEE   XXI 

GLANDERS 

{Farcy) 

Etiology. — Glanders  is  a  disease  of  the  horse  and  some  animals  allied  to  it — 
viz.,  the  ass  and  mule.  It  can,  however,  be  transferred  to  man.  It  is  character- 
ized by  peculiar  new  growths,  either  like  nodes  ("farcy-buds"),  or  more  rarely 
diffuse.  These  are  very  prone  to  suppurate  and  break  down.  Such  nodes,  and 
the  ulcers  which  they  leave  behind  them,  occur  most  frequently  in  the  mucous 
membrane  of  the  nose.  In  horses  the  purulent  nasal  discharge  is  one  of  the 
earliest  and  most  important  symptoms  of  the  disease.  Similar  nodes  are  found 
in  the  larynx,  lungs,  liver,  spleen,  and  kidneys,  and  often  also  in  the  skin.  The 
cutaneous  swellings  and  deep,  crater-like  ulcers  belong  to  that  form  of  the  dis- 
ease which  is  called  "  farcy."  The  corresponding  lymphatic  vessels  and  glands 
are  usually  much  swollen.  The  animal  has  fever,  grows  weaker  and  weaker,  and 
almost  invariably  dies  at  the  end  of  one  to  three  weeks. 

Glanders  in  man  is  always  referable  to  infection  from  a  diseased  animal, 
although  in  certain  instances  it  is  impossible  to  demonstrate  the  source.  The 
disease  is  therefore  commonest  among  persons  who  have  much  to  do  with  horses 
■ — e.  g.,  hostlers,  coachmen,  farmers,  and  cavalrymen.  The  virus  is  usually  con- 
veyed by  the  pus  and  nasal  secretions  of  the  diseased  animals.  A  little  of  this 
falls  upon  some  excoriation  on  the  hand  or  some  crack  in  the  skin,  and  is  absorbed. 
Man  does  not  seem  very  liable  to  the  disease ;  it  is  of  rare  occurrence. 

Loffler  and  Schiitz  have  discovered  the  specific  disease-producing  agent.  These 
investigators  were  able  to  demonstrate  in  all  the  products  of  glanders  delicate 
bacilli  about  the  size  of  the  bacilli  of  tuberculosis.  These  bacilli  can  be  reared 
artificially,  and,  if  inoculated  upon  horses  and  other  animals,  they  give  rise  to  a 
typical  attack  of  glanders  in  every  instance.  The  bacilli  of  glanders  can  scarcely 
ever  be  detected  in  the  blood.  It  is  also  very  interesting  that  they  rapidly  lose  their 
virulence  in  purified  cultures  outside  of  the  living  body.    This  is  one  more  proof  of 


126  ACUTE    GENERAL   INFECTIOUS   DISEASES 

the  fact,  which  is  lately  coming  more  and  more  into  prominence,  that  the  external 
influences  surrounding  the  life  of  bacteria  modify  greatly  their  biological  pecul- 
iarities. By  repeated  inoculations  of  glanders  in  the  horse  the  virulence  of  the 
bacilli  rapidly  diminishes,  while,  on  the  other  hand,  by  repeated  inoculation  in 
the  weasel  the  virulence  is  very  considerably  increased. 

Clinical  History. — The  period  of  incubation  lasts  about  three  to  five  days,  and 
sometimes  longer.  The  first  symptoms  are  local,  if  the  infection  has  resulted 
from  a  visible  injury.  There  is  considerable  swelling  and  pain  in  this  spot,  and 
usually  considerable  lymphangitis  in  its  neighborhood.  In  other  cases,  however, 
the  disease  begins  with  indefinite  constitutional  symptoms,  such  as  fever,  head- 
ache, and  pain  in  the  limbs,  so  that  there  may  be  some  resemblance  to  beginning 
typhoid  fever.  The  local  and  general  disturbances  increase,  and  the  disease  soon 
attacks  other  parts  of  the  body.  In  the  skin  we  see  small  macules  or  papules, 
singly  or  in  groups,  which  soon  change  to  pustules  like  those  of  small-pox,  or  to 
larger  abscesses.  These  abscesses  burst  and  discharge  offensive  pus,  leaving  be- 
hind them  irregular,  deep  ulcers.  'Not  infrequently  the  joints  are  swollen.  The 
mucous  membranes  are  also  attacked;  chief  among  these  troubles  are  ulcers  in 
the  nose.  The  nose  swells  as  if  with  erysipelas,  and  there  is  a  purulent,  foul- 
smelling  discharge.  The  nose  rarely  escapes.  The  conjunctivae,  throat,  mucous 
membrane  of  the  mouth,  and  the  larynx  also  undergo  inflammation  and  ulcera- 
tion. A  violent,  diffuse  bronchitis  develops.  Sometimes  there  is  considerable 
disturbance  of  the  stomach  and  intestines,  giving  rise  to  vomiting  and  diarrhoea. 
At  the  same  time  the  constitutional  symptoms  become  more  and  more  severe. 
The  patient  grows  stupid  or  delirious.  In  some  few  cases  the  severe  cerebral 
symptoms  are  due  to  a  purulent  meningitis,  perhaps  through  extension  of  the 
inflammation  by  contiguity  f rora  the  nose.  The  fever  is  high,  and  sometimes  it  is 
quite  continuous.  More  rarely  there  are  chills  and  great  elevations  of  tempera- 
ture, as  in  the  fever  of  pyaemia.  '  The  pulse  is  rapid  and  small.  The  spleen  is 
seldom  much  enlarged.     The  urine  may  contain  a  trace  of  albumen. 

In  these  severe  acute  cases  the  termination  is  almost  always  fatal.  Death 
occurs  at  the  end  of  two  to  four  weeks.  There  are  cases  with  a  more  chronic 
course,  with  tedious  persistence  of  the  troubles  in  the  skin  and  mucous  mem- 
branes, and  milder  febrile  and  constitutional  symptoms.  Such  attacks  appear  at 
first  tolerably  favorable,  but  they  may  end  fatally  with  persistent  fever  and 
increasing  physical  weakness,  or  they  may  run  on  for  months,  and  at  last  end 
in  complete  recovery. 

The  autopsy  reveals  a  condition  greatly  resembling  that  in  pyaemia.  We  find 
abscesses  in  many  parts,  particularly  the  muscles  and  the  lungs,  and,  next  in  fre- 
quency to  them,  the  spleen,  brain,  and  other  viscera.  In  the  mucous  membrane  of 
the  nasal  cavities,  the  pharynx,  and  the  larynx,  are  found  nodes  and  ulcers,  such 
as  occur  in  the  horse.  As  in  septicaemia,  there  are  often  numerous  hasmorrhages 
into  the  serous  and  mucous  membranes.  It  has  already  been  mentioned  that  the 
specific  bacilli  of  glanders  are  present  in  the  abnormal  secretions. 

Diagnosis. — Without  the  aid  of  aetiological  factors  the  diagnosis  of  glanders 
is  often  very  difficult.  Indeed,  until  recently  there  have  been  instances  where 
even  the  autopsy  did  not  suffice  to  exclude  pyaemia;  but  now  that  the  specific 
bacilli  have  been  discovered  we  can  clear  up  all  doubts.  We  can  not,  however, 
enter  into  a  particular  description  of  the  distinguishing  characteristics  of  these 
bacilli.  Their  demonstration  requires  pure  cultures.  At  the  bedside  also  aeti- 
ology is  all-important  in  diagnosis — e.  g.,  exposure  to  infection,  or  occupation. 
Experience  with  a  limited  number  of  cases  renders  it  probable  that  in  the  future 
we  shall  be  able  to  demonstrate  the  bacilli,  during  the  life  of  the  patient,  in 
the  nasal  secretions  or  the  contents  of  the  abscesses.  The  most  characteristic 
symptoms  are  the  nasal  and  cutaneous.     In  a  case  that  takes  a  chronic  course 


MALIGNANT   PUSTULE 


127 


there  is  a  possibility  of  mistaking-  the  cutaneous  ulcers  for  syphilitic  or  tubercu- 
lar sores. 

Ivalning  has  discovered  a  very  interesting  fact,  which,  so  far  as  we  know,  has 
not  been  applied  to  man.  A  substance  can  be  obtained  from  cultures  of  glanders 
bacilli,  the  so-called  malleine.  If  this  be  injected  in  small  amounts  in  horses  sick 
with  glanders  it  causes  high  fever,  while  the  injection  has  no  effect  in  any  other 
animal.  Malleine,  therefore,  has  the  same  significance  in  the  diagnosis  of  glan- 
ders as  tuberculine  has  in  the  diagnosis  of  tuberculosis. 

We  have  already  implied  that  the  treatment  of  acute  cases  is  almost  hopeless. 
We  must  do  all  we  can  in  the  way  of  cleanliness  and  disinfection  to  improve  the 
local  condition  of  the  skin,  the  nose,  and  the  throat.  All  abscesses  and  nodules 
m.ust  be  opened  as  soon  as  possible  and  curetted  and  disinfected.  Appropriate 
agents  are.  carbolic  and  salicylic  acids.  Further  treatment  should  be  in  accord- 
ance with  the  general  rules  for  the  care  of  severe  acute  infectious  diseases.  An 
inunction  treatment  with  unguentum  cinereum  (gr.  xxx-xlv.,  grm.  2-3,  daily) 
has  a  very  favorable  effect.  Iodide  of  potassium,  arsenic,  etc.,  have  also  been 
recommended.  [Malleine  has  been  employed  subcutaneously  in  chronic  glanders, 
with  "  marked  improvement." — V.] 


CHAPTEE   XXII 

MALIGNANT    PUSTULE 

{AntJirax.     Charlov.     Splenic  Fever.     Mycosis  intestinalis,     Carlunculus  contagiosus) 

.ffitiology. — The  cause  of  malignant  pustule  is  the  infection  of  the  body  with  a 
specific  kind  of  bacilli,  the  bacillus  anthracis.  This  organism  was  discovered  by 
Pollender  in  1849,  and  a  few  years  later,  independently,  by  Brauell. 

These  bacilli  are  very  minute  cylinders,  about  as  long  as  the  diameter  of  a 
red  blood-corpuscle.  They  are  found  in  enormous  numbers  in  the  blood  and 
organs  of  animals  which  die  of  anthrax.  Aniline-staining  makes  them  more 
easily  visible.  By  means  of  blood  containing  the  bacilli,  Davaine  (1863)  and 
others  have  inoculated  many 
animals  with  the  disease,  in- 
cluding mice,  rats,  guinea- 
pigs,  cows,  sheep,  goats,  and 
birds.  The  bacilli  can  also 
be  isolated  and  cultivated, 
and  then  produce  infection. 
This  is  proof  positive  that 
they  are  the  actual  carriers 
of  contagion.  The  rapid  in- 
crease of  the  anthrax  bacilli 
in  the  blood  goes  on  by  sub- 
division. In  the  artificial 
cultivations,  however,  the 
bacilli  grow,  as  Koch  has 
shown,      into      quite      long' 

threads,  in  which  shortly  appear  minute,  brilliant  egg-shaped  bodies  (cf.  Figs. 
13  and  14).  The  threads  become  disintegrated,  setting  free  the  little  shining 
ovoids,  the  spores  of  anthrax,  to  grow  into  bacilli.  The  bacilli  can  live  only  a 
relatively  brief  time;  but  the  spores  have  unusual  tenacity  of  existence.     They 


\ 


® 


Fig.  13 


Anthrax  bacilli.  (From  Koch.)  6.50  diameters.  »4,  from 
the  blood  of  a  guinea-pig.  B.  from  the  spleen  of  a  mouse 
after  three  hoiu's''  culture  in  the  aqueous  humor. 


128 


ACUTE    GENEEAL   INEECTIOUS    DISEASES 


may  remain  dried  up  for  years,  and  then  be  brought  to  further  development  if 
placed  in  favorable  conditions  of  heat  and  moisture.  If  the  spores  are  trans- 
ferred to  animals,  they  develop  into  bacilli,  and  there  is  scarcely  room  to  doubt 
that  men  and  animals  are  quite  as  often  infected  by  spores  as  by  full-grown 
bacilli.  There  are  facts  which  render  it  not  improbable  that  the  anthrax  bacilli 
exist  in  other  places  than  the  bodies  of  men  or  animals,  and  may  there  complete 
their  circle  of  development.  Such  places  are  marshes,  the  banks  of  streams,  and 
the  like.  If  it  is  possible  for  them  to  be  carried  by  high  water  to  the  pasture  lands, 
we  have  an  explanation  of  those  sudden  endemic  appearances  of  anthrax  which 
sometimes  occur  in  places  previously  free  from  the  disease. 

Anthrax  in  animals  is  of  great  practical  importance,  because  its  favorite 
victims  are  the  herbivorous  domestic  animals — viz.,  the  cow,  sheep,  and  horse. 
Among  these  it  is  terribly  destructive.  It  is  remarkable  that  the  carnivora  enjoy 
almost  complete  immunity.  The  disease  usually  runs  a  very  acute  course  in  ani- 
mals. Indeed,  it  often  seems  like  apoplexy;  the  apparently  healthy  animal  sud- 
denly falls,  suffers  for  a  few  minutes  from  convulsions  and  dyspnoea,  and  dies. 


Fig.  14.— Anthrax  bacilli ;  spore  formation  and  spore  germination.  (From  Koch.)  A,  from  the  spleen 
of  a  mouse  after  twenty-four  hours'  culture  in  the  aqueous  humor,  spores  arranged  like  strings  of 
beads  in  the  filaments.  650  diameters.  B,  germination  of  the  spores.  650  diameters.  C.  the  same, 
with  a  higher  power.    1650  diameters. 

Other  cases  have  a  somewhat  longer  and  more  intermittent  course,  but  in  these 
also  recovery  is  very  rare. 

Human  beings  are  probably  infected  in  most  cases  by  direct  inoculation. 
Shepherds,  farmers,  butchers,  and  others  who  come  in  contact  with  animals  suffer- 
ing from  anthrax,  are  liable  to  infection  through  any  little  wound  or  scratch 
upon  the  hands.  Very  often  the  disease  is  caught  from  hides,  hair,  or  other  parts 
of  dead  animals.  In  workshops  and  factories  where  wool  and  hides  have  been 
used  which  came  from  diseased  animals,  anthrax  has  repeatedly  occurred.  Cur- 
riers, rope-makers,  paper-makers,  hatters,  furriers,  brush-workers,  and  those  who 
handle  horse-hair  and  wool,  are  all  exposed.  Anthrax  has  also  acquired  the  name 
of  "  rag-pickers'  disease."  Another  way  of  infection,  supposed  to  happen  among 
animals  as  well  as  men,  is  through  the  sting  of  insects — e.  g.,  flies — bringing  the 
poison  from  diseased  animals.  It  is  not  likely  that  the  virus  can  be  absorbed 
through  the  unbroken  skin.  It  is  certain,  however,  that  the  intestine  may  some- 
times afford  ingress  to  the  infectious  matter.  Koch  has  proved  this  by  putting 
spores  in  the  food  of  sheep.  Intestinal  mycosis  in  man  (vide  infra)  may  very 
possibly  be  due  to  a  similar  mode  of  infection.  Many  cases  of  poisoning  from  eat- 
ing meat  have  been  referred  to  the  ingestion  of  the  flesh  of  animals  who  died  from 
anthrax.  Some  observations  on  pulmonary  anthrax  seem  to  favor  the  idea  that 
the  poison  may  be  inhaled  with  dust  and  develop  primarily  in  the  lungs. 


MALIGNANT   PUSTULE  129 

Clinical  History. — Anthrax  in  man  has  two  distinct  forms.  These  may  ap- 
pear in  combination.  The  first  begins  with  a  local  disorder  of  the  skin  at  the 
point  of  infection — viz.,  the  malignant  pustule,  or  anthrax  carbuncle.  The  sec- 
ond and  rarer  form  presents  the  symptoms  of  a  severe  acute  constitutional  infec- 
tion. An  accompanying  cutaneous  disorder  or  other  local  disease  is  sometimes 
observed. 

1.  The  malignant  pustule  usually  comes  on  the  hand,  the  arm,  or  the  throat, 
and  appears  from  three  to  seven  days  after  infection.  A  vesicle  forms  at  the 
infected  spot,  grows  rapidly,  becomes  excoriated,  and  usually  takes  on  a  charac- 
teristic appearance,  being  of  a  dark-bluish  or  black  color.  The  surrounding 
parts  become  diffusely  swollen  and  red.  Secondary  vesicles  may  surround  the 
original  one.  The  swelling  becomes  more  and  more  extensive.  Inflamed  lymph- 
vessels  or  veins  radiate  in  red  lines  from  the  pustule,  and  the  neighboring  glands 
are  also  affected.  These  appearances  are  accompanied  by  fever,  and  more  or  less 
prostration.  In  a  favorable  case  the  swelling  subsides,  the  scab  falls  off,  and 
there  is  at  last  complete  recovery.  But  in  other  cases  the  constitutional  infection 
becomes  more  and  more  prominent,  and  eclipses  the  local  disorder.  The  fever  and 
prostration  increase.  Severe  intestinal  symptoms  appear,  or  else  stupor,  delirium, 
and  other  nervous  disturbances ;  and  death  may  ensue  after  a  few  days'  illness. 

The  so-called  anthrax  oedema  (malignant  oedema,  cedeme  charhonneux,  charhon 
blanc)  is  a  form  of  primary  anthrax  of  the  skin  differing  from  malignant  pus- 
tule. It  is  seen  chiefly  in  the  eyelids,  lips,  and  mucous  membrane  of  the  mouth 
and  tongue,  and  also  in  other  parts  of  the  skin.  In  this  form  we  see  a  circum- 
scribed, doughy,  oedematous  swelling,  in  which  small  bullse  with  sero-sanguineous 
contents  often  develop.  These  bullse  may  become  gangrenous.  On  the  neck  and 
back  the  anthrax  cedema  may  sometimes  be  of  considerable  extent.  The  other 
symptoms  are  similar  to  those  of  malignant  pustule.  We  can  not  make  an  abso- 
lute separation  of  the  two  forms. 

2.  Intestinal  Anthrax  {"Intestinal  Mycosis"). — A  quite  different  picture  is 
presented  by  this  second  form,  which  is  called  intestinal  anthrax  (formerly  intes- 
tinal mycosis)  from  the  marked  intestinal  lesions.  In  this  the  cutaneous  dis- 
order, if  it  exists  at  all,  is  insignificant  compared  with  the  severe  constitutional 
disturbance.  It  is  only  within  a  few  years  that  the  labors  of  Buhl,  Waldeyer,  E. 
Wagner,  Leube,  and  others  have  shown  that  attacks  of  this  kind  have  any  connec- 
tion with  anthrax. 

In  cases  of  this  sort  the  attack  is  usually  rather  sudden,  beginning  with  chilli- 
ness, vomiting,  headache,  and  languor.  The  diagnosis  is  usually  very  obscure  at 
first,  unless  the  calling  of  the  patient  suggests  the  possibility  of  anthrax.  On 
careful  examination,  we  may  find  some  places  where  the  skin  is  broken,  or  pos- 
sibly a  small  characteristic  pustule.  In  a  case  which  came  under  our  own  obser- 
vation a  pustule  had  existed  on  the  back  of  the  right  hand  for  some  weeks  before 
severe  symptoms  appeared,  but  had  not  attracted  the  attention  of  the  patient  at 
all.  In  this  case,  therefore,  the  constitutional  infection  seems  to  have  come  from 
the  local  disease.  But  in  other  cases  cutaneous  troubles,  in  the  form  of  small  car- 
buncles, may  occur  secondarily  in  the  course  of  the  disease.  Haemorrhages  into 
the  skin  and  mucous  membranes  (especially  on  the  gums)  also  occur. 

Of  other  symptoms,  the  gastro-intestinal  deserve  to  be  mentioned  first.  Vom- 
iting occurs  frequently,  and  also  a  moderate,  painless,  and  sometimes  bloody  diar- 
rhoea. There  is  usually  severe  dyspnoea,  and  a  marked  sense  of  oppression  in  the 
thorax,  but  without  objective  puhnonary  signs.  Very  soon  there  is  collapse;  the 
nose  and  extremities  grow  cool ;  the  pulse  is  rapid,  but  small ;  and  there  is  livid- 
ity.  In  a  few  instances  tetanic  or  epileptiform  convulsions  have  been  observed. 
(Edematous  swelling  of  the  eyelids  is  sometimes  seen.  The  temperatui*e  is  sel- 
dom much  elevated.  It  may  be  subnormal.  In  a  few  days  the  prostration  be- 
9 


130  ACUTE    GE^TEEAL  INFECTIOUS   DISEASES 

conies  complete,  and  death  ensues.  Sometimes  these  severe  general  symptoms  are 
associated  Tvith  the  signs  of  a  circumscribed  pneumonia  (vide  infra). 

Milder  forms  apparently  occur,  but  here  the  diagnosis  maj  not  be  absolutely 
certain.  We  have  seen  a  few  such  cases  originating  in  a  rope-walk  where  Russian 
hair  was  used.  The  constitutional  s^^mptoms  were  only  moderately  severe,  the 
fever  was  mild,  and  recovery  occurred  after  two  or  three  weeks. 

3.  Pulmonary  Anthrax. — Pulmonary  anthrax  probably  arises,  as  we  have  said, 
from  the  inhalation  of  dust  containing  anthrax  spores.  The  disease  runs  its 
course  as  a  broncho-pneumonia,  usually  bilateral  and  associated  with  high  fever, 
pleurisy,  severe  dyspnoea,  cardiac  weakness,  and  great  general  prostration.  The 
anthrax  bacilli  can  be  found  in  the  sputum  and  the  pleuritic  exudation,  and 
sometimes  in  the  blood.     Most  cases  of  this  type  terminate  fatally  in  a  few  days. 

Pathology. — In  the  fatal  cases  of  anthrax  the  intestinal  lesions  are  the  most 
characteristic.  Besides  the  signs  of  catarrhal  inflammation,  we  find  peculiar 
lesions  in  the  mucous  membrane  of  the  small  intestine,  and  sometimes  in  the 
upper  portion  of  the  colon.  These  consist  of  dark,  infiltrated  spots,  with  haem- 
orrhages, the  spots  being  somewhat  larger  than  a  silver  dime.  The  microscope 
reveals  numerous  collections  of  anthrax  bacilli,  situated  chiefly  in  the  lumen  of 
the  blood-vessels.  The  spleen  is  usually  only  moderately  enlarged,  but  dark  and 
congested.  There  may  be  ecchymoses  in  the  kidneys,  the  brain,  and  the  serous 
membranes.  Often  there  is  swelling  of  the  lymph-glands.  In  one  case  which  we 
saw,  with  slight  intestinal  lesions,  the  mesenteric  glands  were  considerably  en- 
larged, and  the  bronchial  lymph-glands  were  perfectly  enormous.  The  bacilli 
are  found  in  all  the  organs  mentioned. 

The  diagnosis  of  malignant  pustule  is  seldom  difiicult,  particularly  if  atten- 
tion be  directed  to  the  aetiology.  All  doubt  is  over  if  we  find  the  bacilli.  The 
cases  of  intestinal  and  pulmonary  anthrax  may  be  more  obscure.  The  chief 
point  is  that  the  attention  be  directed  to  the  possibility  of  anthrax  by  the  patient's 
occupation,  the  severe  general  symptoms,  and  any  pustule  on  the  skin.  For  a 
positive  diagnosis  we  need,  of  course,  to  find  the  bacilli  in  any  pustule  on  the 
skin  or  in  the  blood. 

Treatment. — 1.  Prophylactic  inoculation.  Toussaint  and  Pasteur  were  the 
first  to  show  that  the  virulence  of  anthrax  bacteria  can  be  artificially  diminished 
by  certain  external  influences.  If  the  bacilli  are  kept  under  cultivation  for  sev- 
eral weeks  at  an  unchanging  temperature  of  106°  to  107.5°  (42°-43°  C),  they 
preserve  their  external  appearance  completely,  as  well  as  their  ability  to  grow, 
but  gradually  lose  their  power  of  infection.  Inoculations  made  with  this  "  vac- 
cine virus  "  produce  at  most  an  insignificant  disturbance.  But  what  is  especially 
remarkable  is  that  the  animals  thus  vaccinated  are  protected  thereafter  from  in- 
fection with  actual  anthrax.  Pasteur  was  the  first  to  make  this  assertion;  and 
he  proposed  that  the  prophylactic  inoculation  of  sheep  and  other  animals  liable 
to  anthrax  should  be  undertaken  on  a  large  scale,  promising  the  farmers  that  very 
great  benefit  would  result.  So  far  as  experience  has  thus  far  gone,  the  mortality 
of  anthrax  in  sheep  and  cattle  seems  actually  to  have  been  considerably  dimin- 
ished by  the  many  protective  inoculations  which  have  been  performed  in  France 
and  Hungary. 

French  investigators  have  lately  made  known  new  methods  of  producing  an 
artificial  diminution  of  the  growth  and  virulence  of  anthrax  bacilli,  and  also  of 
other  varieties  of  bacteria.  Chauveau  has  found  that  cultures  of  anthrax  bacilli 
exposed  for  several  days  to  an  atmospheric  pressure  of  three  to  twelve  atmos- 
pheres, or  to  compressed  oxygen,  lose  a  portion  of  their  virulence ;  and  that  ani- 
mals inoculated  with  bacilli  thus  attenuated  gain  an  immunity  to  inoculations 
with  the  original  anthrax  poison.  The  statements  of  Arloing  are  very  remark- 
able.    He  says  that  the  direct  play  of  sunlight,  or  even  of  a  concentrated  artificial 


TEICHIi^OSIS 


131 


light,  upon  the  cultures  exercises  a  restraining  influence  upon  the  growth  and 
poisonous  properties  of  the  bacilli,  and  that  inoculation  material  weakened  in  this 
way  may  be  emploj'ed  to  render  animals  immune. 

2.  The  treatm.ent  of  malignant  pustule  is  surgical.  Cauterization  is  often 
tried  with  such  agents  as  caustic  potash,  nitric  acid,  or  carbolic  acid;  but  it 
should  always  be  borne  in  mind  that  such  manipulations  may  easily  contribute  to 
a  local  extension  of  the  anthrax  poison.  For  the  same  reason  one  should  hesitate 
to  incise  or  to  excise  the  pustules.  We  are  therefore  usually  obliged  to  confine 
ourselves  to  the  prescription  of  a  suitable  position  for  the  affected  member,  and 
the  application  of  an  ice-bag  over  the  diseased  spot. 

The  treatment  of  intestinal  and  pulmonary  anthrax  must  be  purely  sjonp- 
tomatic.  In  intestinal  anthrax  the  use  of  calomel  (gr.  ij-iij,  grm.  0.1-0.2,  several 
times  a  day)  is  most  to  be  recommended.  Quinine  (gr.  vij,  grm.  0.5,  four  times  a 
day)  and  carbolic  acid  (gr.  xv,  grm.  1.0,  a  day  in  pills  or  subcutaneously)  seem  also 
to  have  a  favorable  influence  on  the  general  infection. 

CHAPTER   XXIII 

TRICHINOSIS 

(  Tridiiiiatous  Bistase) 

The  Natural  History  of  Trichinae. — The  trichina 
spiralis,  one  of  the  class  of  round  worms  or  nematoda, 
has  long  been  known  to  occur  occasionally  in  the  mus- 
cles of  men  and  certain  animals;  but  it  was  not 
until  1860  that  Zenker  showed  that  trichinge  are  capa- 
ble of  exciting  in  man  a  dangerous  and  sometimes  fatal 
disease.  Since  then  numerous  individual  cases  and 
quite  extensive  epidemics  have  been  reported  ;  and  the 
labors  of  Virchow,  Levickart,  and  others  have  taught 
us  the  anatomy  and  mode  of  development  of  this  pecul- 
iar parasite. 

The  trichina  appears  in  two  shapes — as  intestinal 
trichina  and  as  muscular  trichina.  The  intestinal 
form  is  a  small  white  worm,  visible  to  the  naked  eye. 
The  female  is  3-4  mm.  long,  the  male  only  1-1.5  mm. 
They  have  well-developed  digestive  and  sexual  organs. 
The  male  is  disting-uished  by  two  little  processes  at 
the  tail.  The  muscular  trichina  (vide  Fig.  15)  is  a 
small  worm  0.7-1  mm.  long.  It  is  found  coiled  up 
among  the  muscular  fibers,  inside  a  connective-tissue 
capsule,  which  is  often  calcified. 

The  events  in  the  life  of  the  trichina  are  remark- 
able. If  living  muscular  trichinae  reach  the  human 
stomach  through  the  eating  of  trichinatous  pork,  the 
capsules  are  dissolved,  and  the  trichinae,  thus  set  free, 
grow  in  two  or  three  days  into  sexually  perfect  intes- 
tinal trichinae.  In  the  uterus  of  the  impregnated 
female  the  eggs  develop  into  embryos,  which  are  born  already  hatched.  The 
birth  of  embryos  begins  seven  days  after  the  ingestion  of  the  muscular  trichinas, 
and  seems  to  continue  for  some  time.     A  single  female  is  said  to  produce  more 


mwmi 


Fig  n  — (Fioin  Helleh  )  An 
isolated  piiniitne  bundle 
with  two  free  trichina"  iu 
the  sheath  of  the  sarco- 
lemnia.     Mneh  enlarged. 


132  ACUTE   GENEEAL   INFECTIOUS    DISEASES 

than  one  thousand  embryos.  These  latter  begin  their  travels  soon  after  birth, 
and  reach  the  voluntary  muscles.  As  to  the  routes  they  choose  we  are  still 
somewhat  in  doubt.  Some  authorities  state  that  the  trichinae  penetrate  through 
the  walls  of  the  intestine  and  the  abdominal  cavity  into  the  connective  tis- 
sue. Others  affirm  that  they  enter  the  lymphatic  vessels,  or  exceptionally  the 
blood-vessels.  They  penetrate  into  the  primitive  fibers  of  the  muscles,  and  cause 
them  to  disintegrate.  Finally,  they  coil  themselves  up,  attain  the  size  of  mus- 
cular trichinae  in  about  fourteen  days,  and  become  encapsulated.  Each  capsule 
usually  contains  but  one,  although  it  may  inclose  as  many  as  four.  The  capsule 
is  formed  partly  by  an  excretion  from  the  trichina,  and  partly  from  the  reflex 
hyperplasia  of  the  surrounding  connective  tissue.  The  process  of  development  is 
now  complete.  The  muscular  trichinse  seem,  unlike  the  intestinal  form,  to  have 
a  very  long  lease  of  life,  and  usually  endure  till  the  death  of  their  host.  They 
are  often  found  accidentally  at  autopsies.  They  are  most  abundant  in  the  dia- 
phragm, the  intercostal  muscles,  the  muscles  of  the  larynx  and  throat,  and  the 
biceps. 

.Sltiology  of  Trichinosis. — The  only  cause  yet  known  for  trichinatous  disease 
in  man  is  the  ingestion  of  trichinatous  raw  or  underdone  pork — e.  g.,  smoked  ham. 
Swine  are  pre-eminently  subject  to  trichinae.  They  probably  become  infected  in 
various  ways,  e.  g.,  from  the  faeces  of  human  beings  and  swine  suffering  from 
trichinosis,  or  through  the  ingestion  of  the  trichinatous  flesh  of  other  swine.  The 
waste  of  slaughter-houses  is  often  fed  out  to  swine,  and  the  disease  thus  dissemi- 
nated. Many  affirm  that  swine  are  also  infected  by  eating  rats  infested  with 
trichinae,  but  the  contrary  condition,  whereby  rats  become  trichinatous  from  eat- 
ing the  flesh  of  diseased  hogs,  seems  more  in  accordance  with  the  facts. 

Clinical  History. — The  symptoms  in  man  correspond  in  general  to  the  devel- 
opmental and  vital  processes  of  the  trichinae,  as  above  depicted.  In  individual 
cases,  however,  the  separate  stages  are  quite  often  obscured,  probably  because 
all  the  parasites  do  not  develoio  simultaneously,  or  because  there  are  relapses.  The 
first  symptoms  are  gastro-intestinal.  At  the  commencement  there  is  a  feeling  of 
pressure  in  the  epigastrium,  with  nausea  and  vomiting.  Later,  diarrhoea  is  prom- 
inent, becoming  in  some  cases  so  violent  as  to  remind  one  of  cholera.  It  is  not 
impossible,  although  rare,  to  find  intestinal  trichinse  in  the  stools.  Sometimes 
there  is  constipation  instead  of  diarrhoea.  In  some  cases  the  initial  gastro-intes- 
tinal symptoms  are  but  slight.  Frequently,  even  in  the  beginning  of  the  disease, 
there  is  complaint  of  pain  and  stiffness  in  the  muscles,  too  early  for  it  to  be  due 
to  the  migrations  of  the  trichinae. , 

The  genuine  severe  muscular  sjTnptoms,  due  to  the  myositis  produced  by  the 
trichinae  in  the  muscles,  do  not  begin  till  the  second  Aveek,  or  even  later.  In  many 
cases,  where  the  invading  parasites  seem  to  be  relatively  few  in  number,  the 
muscular  symptoms  are  slight,  or  wholly  absent.  In  the  more  severe  cases,  how- 
ever, they  may  be  extremely  violent  and  distressing.  The  muscles  become 
swollen,  firm  and  hard,  very  tender  on  pressure,  and  very  painful.  The  patient 
avoids  all  movements  and  contraction  of  the  muscles  as  much  as  possible,  lying 
motionless  in  bed,  with  flexed  arms  and  with  legs  either  extended  or  likewise  flexed. 
The  patellar  reflex  almost  always  disappears,  and  on  testing  the  electrical  re- 
actions there  is  found  a  considerable  diminution  of  muscular  excitability  to 
both  the  galvanic  and  faradic  currents,  sometimes  associated  with  delayed  con- 
tractions, and  abnormally  long  duration  of  the  same  after  the  stimulus  ceases 
(Eisenlohr).  The  masseters  and  the  pharyngeal  and  laryngeal  muscles  are  at- 
tacked, so  that  there  is  difficulty  in  mastication  and  deglutition,  and  hoarseness. 
The  involvement  of  the  ocular  muscles  causes  pain  in  the  eyes.  The  condition 
of  the  diaphragm,  intercostals,  and  abdominal  muscles  causes  serious  difficulty 
in  respiration.     There  is  distressing  dyspnoea,  and  expectoration  is  so  hampered 


TRICHINOSIS  133 

that  secretions  accumulate  in  the  air-passages.  In  some  fatal  cases  of  trichinosis 
death  is  due  principally  to  this  impairment  of  respiration.  The  condition  may 
be  aggravated  by  diffuse  bronchitis  or  lobular  pneumonia. 

Third  in  the  list  of  important  symptoms  comes  oedema.  It  appears  toward  the 
end  of  the  first  week  in  the  eyelids.  Somewhat  later  it  involves  the  upper  and 
lower  extremities.  What  produces  it  is  not  quite  clear.  It  has  been  regarded  as 
in  part  inflammatory  and  in  part  the  result  of  occlusion  and  thrombosis  of  the 
smaller  lymphatics.  Cutaneous  eruptions  also  develop — e.  g.,  vesicles,  wheals, 
petechige,  and  pustules.  Frequently  there  is  profuse  perspiration,  consequent 
upon  which  abundant  crops  of  miliaria  or  sudamina  may  appear. 

In  well-marked  cases  there  may  be  quite  high  fever  and  other  severe  constitu- 
tional symptoms  in  addition  to  the  local  disturbances  already  discussed.  The 
temperature  may  for  a  time  reach  104°  to  106°  (40°-41°  C.) ;  but  the  fever  is 
seldom  continuous  for  any  length  of  time,  being  usually  interrupted  by  fre- 
quent and  considerable  intermissions.  There  are  also  a  rapid  pulse,  headache, 
stupor,  and  other  symptoms  suggesting  typhus  or  typhoid  fever.  In  fact,  the  first 
case  in  which  trichinosis  was  recognized  at  the  autopsy  (by  Zenker  of  Dresden) 
had  been  regarded  before  death  as  typhoid.  The  urine  may  be  albuminous ;  and, 
in  rare  instances,  nephritis  is  seen. 

[The  blood  shows  a  leucocytosis,  with  a  great  relative  and  absolute  increase  in 
polymorphonuclear  eosinophilic  cells. — Y.] 

The  duration  of  the  disease  varies  widely.  There  are  mild  cases  often  unrec- 
ognized, which  get  well  after  slight  symptoms  have  lasted  two  or  three  weeks. 
More  pronounced  cases  occupy  six  to  eight  weeks,  or  even  a  much  longer  time.  Of 
the  more  severe  cases  about  one  third  prove  fatal,  usually  from  the  fourth  to  the 
sixth  week.  Sometimes  death  is  caused  by  the  severity  of  the  constitutional  dis- 
turbance,'but  usually  from  disabled  respiration.  Even  if  the  case  ends  favorably, 
recovery  is  often  very  tedious. 

Pathology. — The  autopsy  reveals  little  that  is  characteristic  excepting  the 
changes  in  the  muscles.  There  are  sometimes  the  signs  of  hsemorrhagic  catarrhal 
inflammation  of  the  small  intestine.  The  spleen  is  not  enlarged.  Very  often 
the  liver  is  decidedly  fatty.  What  should  cause  this  in  trichinosis  has  not  yet 
been  determined.  The  lungs  often  present  islets  of  lobular  pneumonia,  or  some- 
times even  of  gangrene.  The  trichinae  are  found  in  the  muscles,  beginning  with 
the  fifth  week.  They  can  be  recognized  by  the  naked  eye  as  little  whitish  lines. 
We  have  already  named  the  muscles  chiefly  infested.  Under  the  microscope  we 
see  the  fibers  in  which  the  trichinae  lie  transformed  into  a  fine  granular  mass. 
The  nuclei  of  the  muscular  fibrillse  are  greatly  increased  in  number  in  the 
neighborhood  of  the  coiled-up  parasite.  Finally,  the  sarcolemma  collapses,  and 
becomes  greatly  thickened  upon  its  external  surface  by  a  hyperplasia  of  con- 
nective tissue.  The  muscles  also  present  many  other  degenerative  changes,  such 
as  a  flaky  disintegration,  waxy  degeneration,  and  the  formation  of  vacuoles. 
There  is  furthermore  a  marked  increase  of  nuclei  in  the  interstitial  tissue  of  the 
muscles.  Within  the  intestines  are  sometimes  to  be  found,  even  after  several 
weeks'  illness,  numerous  living  intestinal  trichinae — a  fact  of  importance  from  a 
therapeutic  point  of  view. 

Diag'nosis. — The  diagnosis  of  trichinosis  is  generally  not  difiicult,  since  the 
peculiar  symptoms  of  the  disease,  especially  the  extensive,  painful  inflammation 
of  the  muscles  and  the  oedema,  occur  in  this  way  in  only  one  other  rare  disease, 
primary  acute  polymyositis  (q.  v.).  Trichinosis  is  distinguished  from  this  partly 
by  the  peculiar  aetiology  (affecting  several  people,  the  use  of  raw  pork,  etc.),  and 
partly  by  the  initial  gastro-intestinal  symptoms.  Trichinosis  may  also  be  con- 
founded with  multiple  neuritis  and  perhaps  with  acute  articular  rheumatism,  but 
careful  observation  of  the  patient  will  usiially  make  the  diagnosis  clear.    An  abso- 


134  ACUTE    GEXEEAL  INEECTIOUS    DISEASES 

lutely  certain  diagnosis  may  be  arrived  at  by  finding  intestinal  trichinae  in  the 
dejections,  but,  as  we  have  said,  this  is  not  an  easy  matter. 

Treatment. — The  trichinae  may  still  be  alive  in  pork  that  has  been  smoked 
or  salted  or  half -cooked — e.  g.,  many  sausages  are  unsafe.  The  only  possible 
prophylaxis,  therefore,  as  far  as  the  individual  is  concerned,  is  to  avoid  all  such 
food.  A  real  protection  for  the  public  against  the  disease  is  also  afforded  by 
governmental  microseoiDic  inspection  of  meat,  as  already  established  in  many 
places. 

When  an  individual  has  become  infected  with  trichinae,  if  it  is  possible  that 
intestinal  trichinas  still  are  present,  the  treatraent  must  always^  begin  with  the 
exhibition  of  purgatives,  such  as  corapound  infusion  of  senna,  calomel,  or  castor- 
oil.  Since  trichina  may  be  found  in  the  intestines  as  long  as  eight  weeks  after 
the  beginning  of  the  first  symptoms,  we  should  not  neglect  local  action  on  the 
intestinal  contents  even  in  the  later  stages  of  the  disease.  Of  the  remedies  which 
are  calculated  to  destroy  the  intestinal  trichinae,  glycerine,  which  was  first  recom- 
mended by  Fiedler,  seems  to  be  the  most  efficient.  It  must  be  given  in  rather 
large  doses,  say  a  tablespoonful  every  hour.  Other  drugs  are  much  less  reliable, 
but  we  will  uame  among  them  benzine  in  the  total  daily  dose  of  one  to  two 
drachms  (grm.  4  to  8)  in  capsules,  and  picric  acid  in  pills — the  daily  dose  being 
five  to  eight  grains  (grm.  0.3-0.5). 

Treatment  is  unfoi'tunately  almost  wholly  powerless  against  the  myositic 
symptoms  of  trichinosis  and  their  sequelee.  The  muscular  pains  can  be  alleviated 
by  narcotics,  particularly  moi*phine  sxibcutaneously,  poultices,  and  chloroform-oil 
as  an  embrocation.*  Protracted  warm  baths  are  excellent.  Antipyrine  and 
salicylic  acid  are  also  said  to  do  good  in  many  cases. 

*  Generally  one  part  of  chloroform  to  ten  of  olive-oil.     It  is  not  officinal  in  Germany,  but  is  weaker 
than  the  linimentum  chloi'oformi  (U.  S.  P.). — Teans. 


DISEASES   OF   THE   RESPIRATORY   ORGANS 


SECTION  I 

Diseases  of  the  Nose* 

CHAPTEE  I 

CORYZA 

(Snuffles.     Wi  in  it  is.     Cold  in  the  Head) 


etiology. — The  well-known  symptoms  of  coryza  depend  upon  a  catarrhal 
inflammation  of  the  nasal  mucous  membrane.  Although  this  catarrh  may  often 
be  due  to  infectious  influences,  still  we  can  not  deny  that  it  is  one  of  those  dis- 
eases which  may  be  caused  by  taking  cold.  Daily  experience  teaches  us  how  often 
coryza  follows  an  evident  exposure  to  cold,  such  as  wetting  the  feet,  but  it  is  of 
course  possible  that  exposure  to  cold  may  merely  favor  infection.  We  may  men- 
tion its  contagiousness  as  an  argument  in  favor  of  its  infectious  character,  and 
this  may  be  illustrated  by  the  fact  that  it  may  be  conveyed  by  handkerchiefs, 
kissing,  etc.,  but  an  experimental  transmission  of  common  coryza  has  not  yet  been 
successful. 

Coryza  may  also  arise  from  the  action  of  chemical  irritants  or  mechanical 
irritants,  such  as  dust,  on  the  nasal  mucous  membrane.  The  iodine  coryza,  which 
occurs  from  the  internal  use  of  iodine,  is  especially  noteworthy.  In  this  form 
iodine  can  easily  be  detected  in  the  nasal  secretion.  The  idiosyncrasy  of  many 
people  to  ipecacuanha  is  also  well  known,  the  very  smell  of  it  setting  up  a  coryza. 
A  severe  coryza  is  the  chief  symptom,  too,  in  hay  fever,t  which  is  probably  due 

*  Special  treatises  on  the  pathology  and  thei-apeutics  of  nasal  diseases  are  to  be  found  in  the  follow- 
ing works  :  Michel,  "  Krankheiten  der  Nasenhohle."  Fraenkel,  "  Diseases  of  the  Nose,"  in  "  Ziems- 
sen's  Cyclopedia."  Stork,  "Kliuik  der  Krankheiten  des  Kehlkopfes,  der  IS'ase,  und  des  Eachens." 
Schech,  "  Krankheiten  der  Mundhohle,  des  Kachens,  und  der  Nase."  Moldenhauer,  "  Krankheiten  der 
Nasenhohlen."  C.  Rosenthal,  "Die  Erkrankungen  der  Nase  und  des  Kehlkopfes."  W.  Kiesselbach 
in  Penzoldt  and  Stintzing's  "  Handbuch  der  Therapie,"  vol.  iii,  etc.  [Bosworth,  "  Diseases  of  the  Nose 
and  Throat."  Burnett,  "Diseases  of  the  Ear,  Nose,  and  Throat."  Ingals,  "Diseases  of  the  Chest, 
Throat,  and  Nasal  Cavities."] 

t  The  disease  called  hay  fever  (catarrJi'us  astivus)  is  of  frequent  occurrence  in  England  and  North 
America,  although  rare  with  us  in  Germany.  It  usually  affects  men  in  middle  life,  less  often  women. 
Some  individuals  are  peculiarly  liable  to  the  disease.  For  them  an  attack  may  be  produced  merely 
by  walking  across  a  meadow  or  near  a  grain-field  at  that  season  when  the  grasses  are  in  bloom,  i.  e., 
about  May  to  July.  As  already  intimated,  it  is  supposed  that  the  grains  of  pollen  excite  the  disease, 
being  difl'used  in  the  air  and  thus  drawn  into  the  nostrils.  At  any  rate,  they  have  repeatedly  been 
found  in  the  nasal  secretion  and  also  in  the  tears  of  affected  persons.  The  si/?nptoms  consist  in  a  very 
severe  coryza,  with  burning  of  the  nose  and  violent  sneezing.  The  erectile  tissue  of  the  nose  is  prob- 
ably acutely  swollen.  Usually  these  symptoms  are  accompanied  by  a  well-marked  conjunctivitis  with 
oedema  of  the  eyelids.  In  severer  cases  there  is  furthermore  a  catarrh  of  the  larynx  and  bronchi. 
There  is  frequently  a  tendency  to  violent  attacks  of  asthma  ("hay-asthma"),  especially  at  night  (see 
the  chapter  on  bronchial  asthma ).     The  treatment  consists  first  in  avoiding  the  cause  by  change  of 

135 


136  DISEASES    OF   THE   EESPIEATOEY   OEGAI^S 

to  the  action  of  the  pollen  of  certain  grasses  on  the  respiratory  mucous  mem- 
brane. Finally,  we  must  bear  in  mind  that  coryza  may  often  be  only  a  symptom 
of  some  other  disease  such  as  measles,  syphilis,  or  glanders,  and  that  severe  purulent 
inflammation  of  the  nasal  mucous  membrane  may  be  excited  by  the  presence  of 
the  secretion  from  a  gonorrhoeal  or  blennorrhosal  conjunctivitis. 

The  symptoms  of  coryza  are  in  most  of  the  milder  cases  of  a  local  nature  only. 
The  secretion  is  troublesome ;  at  first  it  is  scanty  and  mucous,  but  later  it  becomes 
more  abundant  and  watery;  and  sometimes  it  is  purulent.  The  nasal  passages 
are  not  infrequently  closed  from  the  swelling  of  the  mucous  membrane.  The 
patient  necessarily  has  to  breathe  through  the  mouth,  which  explains  the  well- 
known  nasal  speech.  This  closure  of  the  nares  may  give  rise  to  dangerous  attacks 
of  dyspnoea  in  children,  especially  in  infants,  who  have  to  breathe  through  the 
nose  when  sucking  at  the  breast.  The  sense  of  smell  is  always  diminished.  The 
local  sensations  of  pain  and  burning  are  due  chiefly  to  a  mild  inflammation  of  the 
skin  of  the  nostrils  and  upper  lip  set  up  by  the  irritation  of  the  secretion.  The 
irritated  condition  of  the  inflamed  mucous  membrane  occasions  a  feeling  of 
tickling  and  itching  in  the  nose,  and  frequently  by  a  reflex  action  violent  sneez- 
ing. The  symptoms  are  more  severe  if  the  cavities  adjacent  to  the  nose  are 
attacked  by  catarrh,  and  if  in  them  accumulations  of  secretion  occur.  Marked 
pain  in  the  forehead  occurs  in  catarrh  of  the  frontal  sinuses.  The  sinuses  of  the 
ethmoid  and  sphenoid  bones,  and  the  antrum  of  Highmore,  may  also  be  impli- 
cated. Much  more  frequently  a  severe  coryza  sets  up  inflammation  in  adjacent 
mucous  membranes.  Thus  we  find,  following  coryza,  conjunctivitis,  affection  of 
the  ear,  sore  throat,  or  laryngitis.  In  persistent  coryza  eczema  is  not  infrequently 
excited  on  the  skin  of  the  upper  lip,  and  mention  has  already  been  made  of  the 
fact  that  coryza  may  sometimes  act  as  the  exciting  cause  of  erysipelas. 

In  severe  coryza  we  may  sometimes  have  quite  a  marked  general  disturbance, 
and  often  slight  elevations  of  temperature.  The  "  feverish  cold  "  of  children,  for 
instance,  is  well  known. 

Treatment. — Special  treatment  is  usually  unnecessary,  for  most,  cases  recover 
of  themselves  in  a  few  days.  It  seems  doubtful  whether  the  internal  use  of 
quinine  in  fresh  coryza  is  of  service,  as  is  claimed.  With  abundant  secretion, 
especially  in  fresh  cases,  Hager's  "  coryza  remedy  "  (as  an  inhalation)  is  worthy  of 
trial;  this  consists  of  ten  parts  each  of  alcohol  and  carbolic  acid,  and  five  parts 
of  ammonia-water.  Painting  the  nasal  mucous  membrane  with  a  solution  of 
cocaine  (two  to  five  per  cent.)  is  also  greatly  praised  [but  it  may  lead  to  the 
formation  of  the  cocaine  habit. — K.]  When  the  secretion  forms  abundant  dry 
scabs,  an  attempt  should  be  made  to  wash  them  out  by  injections  of  warm  fluids, 
such  as  warm  milk.  The  upper  lip  and  the  nostrils  should  be  smeared  with 
vaseline  or  simple  ointment  to  protect  the  skin  from  the  action  of  the  secre- 
tion. Only  in  the  rare  cases  of  a  severe  purulent  catarrh  can  energetic  local 
treatment  of  the  nasal  mucous  membrane  be  necessary.  Here  we  may  use  douches 
or  sprays  of  astringents  like  tannin  or  alum,  or  let  the  patient  snuff  them  up,  or 
we  may  apply  caustics  like  nitrate  of  silver.  In  children  who  can  not  blow  the 
nose,  it  is  advisable  to  cleanse  the  nose  frequently  with  a  small  sponge  and  a  one- 
per-cent.  solution  of  boracic  acid. 

residence,  as  by  going  to  the  sea-shoi-e.  For  the  nasal  catarrh  douches  are  most  to  be  recommended, 
such  as  a  solution  of  1  part  of  quinine  to  500-1,000  parts  of  water,  or  a  solution  of  carbolic  acid.  The 
administration  of  iodide  of  potassium  might  be  tried,  particularly  where  there  is  asthma. 


CHEONIC   RHINITIS  137 

CHAPTER  II 

CHRONIC    RHINITIS 

{Rhinitis  chronica  hypcrtropMca  et  atrophica.     Oscena) 

1.  Chronic  Hypertrophic  Rhinitis. — It  is  in  many  cases  impossible  to  deter- 
mine the  causes  of  liypertrophic  rhinitis.  Sometimes  the  condition  seems  to 
develop  as  a  sequel  to  frequently  repeated  nasal  catarrh,  although  in  this  case  the 
relation  is  often  reversed — it  being  the  chronic  rhinitis  which  occasions  a  pre- 
disposition to  the  frequent  acute  exacerbations  of  the  catarrh.  Certain  diatheses 
(anaemia,  scrofula)  appear  to  iniluence  the  development  of  the  disease.  This  is 
also  true  of  occupations  which  expose  the  individual  to  dust  or  smoke,  and  some- 
times true  of  malformation  of  the  nose  (for  instance,  deviation  of  the  septum) 
and  perhaps  also  of  hereditary  predisposition. 

The  anatomical  changes  consist  of  a  slow  but  progressive  swelling  and  hyper- 
trophy of  the  mucous  membrane.  This  seems  spongy,  and  of  a  red  or  reddish- 
gray  color.  The  greatest  change  is  almost  always  found  over  the  inferior  turbi- 
nated bone,  and  next  to  that  over  the  middle  turbinated.  In  advanced  cases  the 
mucous  membrane  presents  rough,  uneven  swellings,  and  even  polypi.  These 
changes  are  often  visible  upon  inspection  of  the  nostrils  anteriorly,  but  they  may 
escape  discovery  until  a  rhinoscopic  examination  of  the  posterior  choanae  is  made. 

The  disturbance  occasioned  by  chronic  hypertrophic  rhinitis  may  be  very  con- 
siderable. Respiration  through  the  nose  is  obstructed,  the  voice  becomes  nasal, 
the  senses  of  smell  and  taste  are  impaired.  The  nasal  secretion  is  for  the  most 
part  increased,  but  it  may  be  diminished.  Often  there  is  a  tendency  to  nose-bleed. 
Many  patients  complain  also  of  headache. 

The  frequent  involvement  of  neighboring  organs  is  important.  This  applies 
particularly  to  the  ear.  Deafness  is  caused  both  by  the  obstruction  of  the  open- 
ings of  the  Eustachian  tubes,  and  not  infrequently  also  by  extension  of  the  catarrh 
to  the  lining  membrane  of  the  tubes  and  the  middle  ear.  Very  frequently  the 
disease  is  associated  with  chronic  naso-pharyngitis  or  pharyngitis.  The  visible 
portion  of  the  nose  is  not  infrequently  affected,  as  shown  by  redness  and  swelling 
of  its  tip. 

A  fact  of  especial  interest  is  that  such  a  diseased  state  of  the  nasal  mucous 
membrane  may  give  rise  to  reilex  neuroses  (Voltolini,  Hack,  and  others).  Al- 
though, in  our  opinion,  many  of  the  specialists  on  the  nose  go  too  far  in  this 
direction,  there  is  no  room  for  doubt  that  attacks  of  migraine,  vertigo,  certain 
varieties  of  headache,  and,  above  all,  many  forms  of  bronchial  asthma,  may  bear 
a  close  relation  to  diseases  of  the  nose.  We  shall  revert  to  this  point  later  on.  (See 
especially  the  chapter  on  bronchial  asthma.) 

The  treatment  of  chronic  hypertrophic  rhinitis,  in  order  to  be  successful,  de- 
mands complete  destruction  and  removal  of  the  hypertrophic  portions  by  means 
of  the  galvano-cautery.  Eor  particulars,  we  must  refer  to  the  directions  of  spe- 
cialists. In  milder  cases,  however,  benefit  may  follow  the  insufflation  of  a  powder 
composed  of  one  part  of  nitrate  of  silver  to  ten  or  twenty  of  common  starch,  or 
applications  of  lunar  caustic  may  be  made. 

2.  Simple  Chronic  Atrophic  and  Fetid  Atrophic  Rhinitis.  Ozaena  Simplex. — 
The  disease  consists  in  a  slow,  progressive  atrophy  not  only  of  the  mucous  mem- 
brane with  its  vessels  and  glands,  but  finally  also  of  the  bones,  and  this  atrophy 
is  not  preceded  by  hypertrophy.  Thus  the  nasal  cavities  become  abnormally 
large.  The  turbinated  bones  grow  smaller  and  smaller,  so  that  finally  they  are 
represented  merely  by  narrow  ridges.  Furthermore,  the  scanty  purulent  secretion 
has  a  tendency  to  diy  up  and  form  adherent  greenish-yellow  scabs  and  crusts, 
which  undergo  a  peculiar  putrefactive  decomposition  and  give  rise  to  an  unbear- 


138  DISEASES    OF    THE   EESPIRATOEY   OEGAXS 

able  stench.  We  do  not  yet  know  what  special  form  of  bacterium  causes  this 
putrefactive  decomposition  of  the  secretion.  When  this  very  characteristic  and 
extremely  repulsive  stench  occurs  in  the  nose,  we  usually  give  the  affection  the 
brief  name  of  ozaena  (o^ecv,  to  stink),  but  in  the  other  and  practically  less 
important  cases  we  speak  of  a  simple  atrophic  rhinitis.  The  latter  may  sometimes 
become  ozsena. 

Ozgena  generally  develops  in  childhood.  It  usually  begins  insidiously,  but 
in  other  cases  apparently  is  a  sequel  of  some  acute  disease,  such  as  measles,  etc. 
Ansemia  and  scrofula  deservedly  rank  as  important  predisposing  causes.  Stork 
thinks  that  ozsena  is  usually  connected  with  syphilis  in  the  parents.  It  is  also 
worthy  of  note  that  patients  with  ozeena  often  have  from  birth  a  nose  with  a  fiat, 
broad  bridge,  which  is  perhaps  a  family  trait,  favoring  the  development  of  the 
disease. 

The  subjective  symptoms  are  often  not  marked.  This  is  partly  explained  by 
the  fact  that  the  patient  has  usually  completely  lost  his  sense  of  smell,  but  for 
that  very  reason  the  discomfort  of  his  friends  may  be  the  greater.  The  feeling 
of  dryness  in  the  nose  may  prove  annoying,  and  there  are  often  complaints  of 
headache  and  of  pressure  in  the  eyes.  Inasmuch  as  the  naso-pharynx  and  the 
posterior  pharyngeal  wall  are  almost  always  implicated  in  the  process,  the  patient 
often  suffers  from  hacking  and  a  tendency  to  cough  and  vomit.  Such  portions 
of  the  secretion  as  are  swallowed  sometimes  give  rise  to  a  considerable  chronic 
disturbance  of  the  stomach.  Upon  physical  examination  we  are  first  struck  by 
the  unusual  breadth  of  the  nostrils.  With  the  rhinoscope  the  extent  of  the 
atrophy  is  still  better  seen.  The  mucous  membrane  is  pale  or  slightly  red,  and 
covered  with  dry  scabs.  Sometimes  superficial  ulcers  are  formed.  Usually,  as  we 
have  said,  the  superior  portion  of  the  pharyngeal  mucous  membrane  shai'es  in  the 
disease.  The  posterior  wall  of  the  pharynx  is  seen  to  be  atrophied,  smooth  as  if  it 
were  varnished,  and  often  covered  with  crusts.  The  process  may  involve  the  soft 
palate,  and  even  the  larynx,  and  not  infrequently  the  disease  is  associated  with 
infiammation  of  the  middle  ear. 

It  should  be  added  that  the  true  ozsena  must  not  be  confounded  with  other 
processes  which  likewise  give  rise  to  a  foul  smell  from  the  nose.  Tuberculous 
disease  of  the  nasal  mucous  membrane  and  nasal  bones  is  not  rare,  particularly  in 
"  scrofulous  "  children  (Demme) ;  nor  should  we  forget  the  syphilitic  affections  of 
the  nose,  tertiary  and  hereditaiy  sjTphilis. 

Treatment. — An  alleviation  of  ozsena  can  be  accomplished  only  by  the  aid  of 
local  applications  as  prescribed  by  specialists.  Even  then  the  treatment  is  a 
prolonged  one,  and  demands  much  patience  on  the  part  of  both  patient  and 
physician.  A  complete  cure  of  atrophic  rhinitis  is  impossible.  Besides  local 
applications,  we  must  also  bear  in  mind  the  necessity  of  constitutional  treatment. 

The  object  of  local  treatment  is  to  remove  the  secretion  in  order  to  get  rid  of 
the  bad  odor.  Nasal  douches,  with  disinfectant  solutions  such  as  permanganate  of 
potassium  (1-3,000)  or  carbolic  or  corrosive  sublimate,  are  here  most  useful.  The 
solution  is  carefully  injected  into  the  nose,  or  the  fluid  is  allowed  to  run  gently 
into  one  nostril  from  an  irrigator  while  the  patient  keeps  his  head  bent  forward; 
it  then  runs  through  the  naso-pharynx  and  out  through  the  other  nostril.  The 
patient  soon  learns  to  retain  the  fluid  in  the  pharynx  and  eject  it  from  the  mouth. 
All  nasal  douches  must  at  first  be  used  with  care  and  under  the  eye  of  the  physi- 
cian. The  fluid  should  be  injected  at  the  lowest  pressure  possible,  so  that  none  of 
it  may  enter  the  adjacent  cavities  or  the  Eustachian  tube.  Furthermore,  all  solu- 
tions used  as  a  douche  must  be  lukewarm — 90°  to  95°  (25°-28°  E.).  Besides 
the  regular  use  of  douches,  painting  and  the  insufilation  of  powders,  such  as 
boracic  acid,  aceto-tartrate  of  aluminum,  etc.,  are  sometimes  employed.  The  in- 
sertion of  tampons  of  dry  absorbent  cotton  is  to  be  recommended ;  under  their  use 


NOSE-BLEED  139 

the  secretion  dries  less  easily  and  the  odor  is  diminished.  These  tampons  should  be 
changed  daily.  It  is  advantageous  to  medicate  the  tampons  with  a  one-per-cent. 
solution  of  ereoline  or  with  Peruvian  balsam  or  some  similar  drug.  Tincture  of 
iodine  is  also  recommended.  Of  late  many  attempts  have  been  made  to  treat 
■chronic  nasal  catarrh  by  the  galvano-eautery.  With  regard  to  the  details  of  this 
-as  well  as  of  other  methods,  we  must  refer  to  special  treatises  on  the  subject. 


CHAPTEE  III 

NOSE-BLEED 

(Einstaxis) 

Although  in  many  cases  nose-bleed  is  only  a  symptom,  still  we  are  justified 
in  a  short  description  of  it,  partly  because  frequently  repeated  nose-bleeds  often 
first  call  our  attention  to  some  other  existing  disease,  and  partly  because  the 
treatment  is  of  practical  importance. 

Many  persons  are  subject  to  habitual  nose-bleed,  which  comes  on  either  from 
slight  causes,  from  violently  blowing  the  nose,  from  physical  exertion,  from  over- 
heating, or  even  without  any  special  cause.  This  habitual  nose-bleed  is  sometimes, 
but  by  no  means  always,  the  sign  of  a  general  hsemorrhagic  diathesis,  which  is 
hereditary  in  many  families.  (See  the  chapter  on  haemophilia.)  In  other  cases 
the  nose-bleed  is  the  result  of  some  chronic  disease.  It  occurs  especially  in  leu- 
kaemia, in  disease  of  the  heart,  in  contracted  kidney,  and  as  a  symptom  of  the 
so-called  hsemorrhagic  diseases,  such  as  scurvy,  purpura  htemorrhagica,  etc.  Final- 
ly, diseases  of  the  nose  itself  may  give  rise  to  haemorrhage.  The  periodic  occur- 
rence of  nose-bleed  in  young  girls  as  a  form  of  so-called  "  vicarious  menstrua- 
tion "  has  often  been  described,  but  we  must  always  be  very  guarded  in  admit- 
ting it  as  a  fact.  ISTose-bleed  sometimes  occurs  at  the  beginning  of  many  infec- 
tious diseases,  especially  typhoid  and  scarlet  fevers,  etc.  We  may  add  that  the 
point  of  haemorrhage  is  very  frequently  at  the  anterior  lower  end  of  the  cartilag- 
inous septum  (Kiesselbach), 

In  many  cases  nose-bleed  is  a  very  transitory  symptom,  wholly  without  danger, 
and  in  one  sense  it  may  even  be  advantageous.  When  there  is  headache,  or  a 
feeling  of  fullness  in  the  head,  there  is  often  relief  after  an  epistaxis.  JSTose- 
bleed  is  dangerous,  however,  when  it  takes  place  in  those  who  are  already  weak 
and  anaemic,  or  when  it  is  so  persistent  and  abundant  as  to  cause  a  marked  gen- 
eral anaemia.  The  latter  is  recognized  by  the  pallor  of  the  face,  by  the  appearance 
of  general  weakness,  by  vertigo,  tinnitus,  and  a  weakened  pulse.  In  such  cases  the 
physician's  interference  is  always  necessary.  In  every  case  of  nose-bleed  it  is 
important  to  examine  the  posterior  wall  of  the  pharynx  in  order  to  see  whether 
the  blood  is  not  flowing  backward  from  the  posterior  nares.  The  haemorrhage  is 
often  thought  to  stop  when  no  more  blood  comes  from  the  nostrils,  and  yet  the 
blood  keeps  flowing  posteriorly. 

In  every  severe  nose-bleed  rest  is  the  chief  thing  to  be  enjoined,  and  the  patient 
must  be  told  to  avoid  unnecessarily  blowing,  wiping,  or  drying  the  nose.  By 
quietly  and  persistently  closing  the  nostrils  with  a  handkerchief  a  thrombus  is 
often  formed  Avithout  any  further  medication,  and  the  bleeding  stops.  The  appli- 
cation of  cold  water  (iced  water),  in  which  a  little  vinegar  may  be  put,  is  a  good 
thing.  If  the  bleeding  does  not  stop,  we  may  next  tiy  a  tampon  of  common 
absorbent  cotton  or  styptic  cotton  in  the  nostril  from  which  the  blood  comes.  If 
this  does  not  succeed,  the  posterior  nares  must  be  plugged  by  means  of  a  "  Bel- 


140  DISEASES    OF   THE   EESPIRATOEY   OEGAISTS 

locq's  canula."  In  case  of  emergency  we  may  use  an  elastic  catheter,  which  is. 
passed  through  the  inferior  meatus  into  the  pharynx  and  out  by  the  mouth.  The 
tampon  is  fastened  to  the  catheter  and  brought  up  into  the  posterior  nares  by 
drawing  the  catheter  back  through  the  nose.  Internal  remedies  to  check  the 
flow  of  blood  are  very  uncertain  in  their  action. 


SECTION  II 

Diseases  of  the  Larynx 

CHAPTER  I 

ACUTE  LARYNGEAL  CATARRH 

{Acute  Laryngitis) 

.3jtiology. — Taking  cold  plays  a  prominent  part  in  the  popular  aetiology  of 
acute  laryngeal  catarrh.  Its  influence  can  not  be  wholly  denied,  although  the 
more  intimate  relation  between  taking  cold  and  the  origin  of  a  catarrh  is  still 
unknown.  The  disposition  to  laryngitis  differs  very  much  in  different  people, 
so  that  some  take  a  catarrh  much  more  easily  and  more  frequently  than  others. 
Besides  cold,  direct  irritants  which  attack  the  laryngeal  mucous  membrane  often 
set  up  a  laryngitis;  among  these  are  in  particular  the  inhalation  of  smoke  and 
of  noxious  gases  and  vapors.  Many  laryngeal  catarrhs,  too,  arise  from  excessive 
speaking,  shouting,  or  singing,  particularly  if  other  injurious  influences  act  on  the 
larynx  at  the  same  time.  Finally,  laryngitis  may  appear  as  a  complication  or  as 
a  secondary  affection,  in  other  diseases,  especially  in  measles,  less  frequently  in 
typhoid,  scarlet  fever,  and  erysipelas.  Catarrh  of  the  larynx  is  very  often  com- 
bined with  catarrh  of  the  nose,  the  pharynx,  and  the  larger  bronchi. 

Symptomatology. — Althoiigh  the  symptoms  of  laryngitis  usually  make  the 
diagnosis  easy  and  certain,  yet  an  accurate  understanding  of  the  extent  and 
intensity  of  the  catarrh  can  be  obtained  only  by  a  laryngoscopic  examination,* 
which  therefore  should  be  employed  in  every  severe  case.  The  laryngeal  mirror 
shows  a  decided  reddening  and  swelling  of  the  mucous  membrane,  varying  with 
the  intensity  of  the  catarrh,  and  most  marked  on  the  true  and  false  vocal  cords 
and  between  the  arytenoid  cartilages.  We  often  see  small  collections  of  mucus 
here  and  there  on  the  membrane.  In  individual  cases  different  parts  of  the 
larynx  are  especially  affected.  In  intense  inflammations  superficial  erosions  are 
often  met  with,  especially  on  the  vocal  cords.  In  other  cases  the  mucous  mem- 
brane shows  a  grayish-white  coloring  in  some  places,  due  to  a  thickening  of  the 
epithelium.  Small  haemorrhages  in  the  mucous  membrane  are  also  occasionally 
seen.     Veiy  often  we  see  on  phonation  an  incomplete  closure  of  the  glottis,  so 

*  More  extensive  observations  on  laryngoscopy  and  on  many  details  of  the  pathology  of  laryngeal 
diseases,  which  have  been  carefully  investigated  by  specialists  and  which  can  not  be  mentioned  here, 
are  to  be  found  in  the  following  works :  Turck,  "  Klinik  der  Krankheiten  des  Kehlkopfes,"  1866. 
Semeleder,  " Laryngoskopie,"  1863.  Tobold,  " Laryngoskopie,"  1874.  Stork,  "Klinik  der  Krank- 
heiten des  Kehlkopfes,  der  Nase,  u.  des  Rachens,"  1880.  Mackenzie,  "  Diseases  of  the  Throat  and 
Nose,"  1880.  B.  Fraenkel  and  v.  Ziemsseu,  "  Diseases  of  the  Larynx,"  in  Zierassen's  "  Cyclopeedia." 
G-ottstein,  "Krankheiten  des  Kehlkopfes,"  third  edition,  1890.  Schrotter,  "  Vorlesungen  tiber  die 
Krankheiten  des  Kehlkopfes."  [See  also  the  treatises  of  Bosworth,  Burnett,  and  Ingals  referred  to 
on  page  131.] 


ACUTE  LAEYFGEAL  CATAREH  141 

tHat  a  little  oval  space  is  left  between  the  vocal  cords.  This  slight  "  catarrhal 
paresis  of  the  vocal  cords"  is  probably  of  muscular  origin,  and  depends  chiefly 
upon  an  affection  of  the  thyro-aryta?noid  muscles. 

Of  the  other  symptoms  of  laryngeal  catarrh,  hoarseness  is  pai*ticularly  to  be 
mentioned,  for  in  many  cases  the  diagnosis  of  laryngitis  may  be  made  from  this 
alone.  It  is  either  due  directly  to  the  anatomical  changes  of  the  cords,  or  to  the 
paresis  just  mentioned.  The  degree  of  hoarseness  is  of  course  very  different  ii. 
different  cases,  and  varies  from  a  simple  "  roughening  "  or  "  deadening  "  of  the 
voice  to  a  complete  loss  of  voice  (aphonia). 

The  cough  in  laryngitis  may  be  very  severe,  and  is  often  recognizable  by  its 
hai-sh,  hoarse  ring  as  a  "  laryngeal  cough."  It  is  usually  dry  at  first,  and  later  on 
it  is  associated  with  a  scanty  muco-purulent  expectoration,  which  is  sometimes 
tinged  with  blood. 

Pain  in  the  larj-nx  is  generally  only  moderate.  The  subjective  symptoms  con- 
sist chiefly  of  a  disagreeable  feeling  of  itching,  burning,  and  dryness  in  the  throat. 
After  prolonged  speaking,  however,  the  pain  in  the  larynx  may  sometimes  be  quite 
severe.  External  pressure  on  the  larynx  is  often  somewhat  painful.  Difficulty 
in  swallowing,  when  it  occurs,  is  due  usually  to  an  accompanying  pharyngitis, 
hut  it  may  also  be  dependent  upon  an  affection  of  the  epiglottis  and  the  aryttenoid 
cartilages. 

The  general  health  is  affected  in  very  different  degrees.  Many  patients  feel 
quite  well  except  for  the  hoarseness,  while  others  are  affected  with  considerable 
■debility,  mild  headache,  and  even  at  times  slight  febrile  disturbances.  Of  late 
years  we  have  frequently  seen  cases  of  primary  acute  laryngitis,  with  great 
hoarseness  and  marked  catarrhal  inflammation  of  the  upper  part  of  the  larynx, 
especially  of  the  vocal  cords.  These  cases  begin  with  high  fever  (over  104° 
[40°  C.])  and  quite  severe  general  symptoms,  and  make  a  complete  recovery  in 
a  week  or  two.  They  apparently  have  an  infectious  origin,  and  are  perhaps  con- 
nected with  influenza. 

Dyspnoea  is  not  present  in  the  common  laryngitis  of  adults,  even  if  there  is 
decided  swelling  of  the  false  vocal  cords  or  of  the  ary-epiglottic  folds.  There 
is,  however,  a  severe  form  of  acute  laryngitis,  the  so-called  laryngitis  hypoglot- 
tica  acuta  gravis  (cJiorditis  vocalis  inferior),  affecting  not  only  children,  but 
adults,  in  which  well-marked  symptoms  of  suffocation  may  be  present.  In  this 
form  there  is  an  acute,  very  well-marked  swelling  of  the  mucous  membrane  in  the 
inferior,  sub-chordal,  laryngeal  space,  which  leads  to  a  stenosis.  The  rare 
cases  of  phlegmonous  inflammation  of  the  larynx  may  also  cause  considerable 
stenosis  and  dyspnoea. 

In  children,  however,  on  account  of  the  greater  narrowness  of  the  child's 
larjTix,  symptoms  of  stenosis  are  not  rare  even  in  the  milder  forms  of  laryngitis, 
and  therefore  they  have  led  to  the  establishment  of  a  special  disease,  the  so-called 
false  croup. 

The  false  croup  (laryngitis  stridula)  of  children  usually  follows  a  slight 
coryza.  A  harsh,  hollow,  ringing  cough  comes  on,  almost  always  suddenly  and 
usually  at  night,  by  which  the  child  is  awakened  out  of  sleep.  The  paroxysms  of 
•coughing  are  broken  by  long-drawn,  noisy  inspirations.  The  child  is  anxious  and 
restless,  the  respiration  is  labored.  The  accessory  muscles  of  respiration  are 
brought  into  action,  but  the  deep  inspirator?'  retraction  of  the  lower  intercostal 
spaces  and  the  epigastrium  shows  how  imperfectly  the  air  enters  the  lungs.  The 
pulse  is  small  and  rapid.  The  attack  lasts  several  hours,  when  the  cough  gradually 
hecomes  looser  and  the  breathing  easier.  Finally  the  child  falls  asleep  and  usually 
wakes  the  next  morning  quite  lively  and  playful,  a  slight  cough  being  the  only 
Telic  of  the  terrifying  events  of  the  night  before.  The  next  night  the  same  severe 
.attack  may  be  repeated,  and  perhaps  for  two  or  three  nights  more.     After  that 


142  DISEASES    OF   THE   EESPIRATOKY   OEGANS 

there  remains,  as  a  rule,  nothing  but  a  slight  catarrh,  which  completely  disappears 
in  a  week  or  two.  The  anatomical  cause  of  false  croup  is  acute  laryngitis  with 
marked,  swelling  of  the  mucous  membrane  on  and  below  the  vocal  cords.  In  the 
narrow  space  of  the  child's  larynx  this  speedily  causes  marked  stenosis,  and  the 
individual  attacks  are  probably  excited  by  the  accumulation  and  drying  of  the 
secretion  during  the  night.  There  is  never  any  true  croupous-diphthei'itic  change 
to  be  seen  either  in  the  pharynx  or  the  larynx.  It  is  remarkable  that  many  chil- 
dren, and  sometimes  several  children  of  the  same  family,  have  a  specially  marked 
predisposition  to  false  croup.  The  statement,  therefore,  that  a  child  has  had  the 
croup  several  times  almost  always  means  that  it  has  had  this  form  of  false  croup 
just  described. 

Acute  laryngitis  lasts  only  a  few  days  in  mild  cases,  and  a  week  or  more  in 
severe  cases.  With  improper  care  and  unreasonable  conduct  on  the  patient's  part 
an  acute  catarrh  may  run  into  the  chronic  form.  We  hardly  ever  see  a  fatal  re- 
sult in  adults,  even  in  the  severe  form,  and  in  children  false  croup  very  rarely  has 
an  unfavorable  termination  unless  the  child  is  extremely  weak  or  rachitic. 

The  treatment  of  acute  laryngitis  requires  that  especial  attention  be  paid  to 
the  removal  of  all  injurious  influences.  In  every  severe  laryngitis  the  patient 
should  stay  in  his  room,  and  children  are  better  off  in  bed.  The  patient  should 
talk  as  little  as  possible.  In  all  severe  cases  smoking,  too,  is  to  be  forbidden.  It 
is  a  good  plan  to  furnish  plenty  of  warm  drink.  Hot  milk,  mixed  with  Seltzer 
or  Ems  water,  is  readily  taken  by  most  patients.  If  there  is  a  steam  atomizer  at 
our  disposal,  we  may  let  the  patient  inhale  simple  steam,  or  a  one-  or  two-per-cent.. 
solution  of  common  salt.  Inhalations  of  astringents  are  usually  unnecessary. 
The  patient  may  also  breathe  steam  without  any  special  apparatus.  When  there 
is  marked  irritation  from  coughing  we  may  give  a  little  morphine.  With  more 
marked  local  symptoms,  especially  if  there  is  much  pain  on  swallowing,  from 
swelling  of  the  epiglottis  and  the  mucous  membrane  over  the  arytsenoid  cartilages, 
the  patient  may  suck  j)ieces  of  ice  slowly.  In  severe  cases  of  acute  laryngitis,  with 
evident  symptoms  of  stenosis,  ice  must  be  energetically  used  as  an  internal  and  an 
external  application.  Sometimes,  too,  a  few  leeches  applied  in  the  region  of  the 
larynx  afford  distinct  relief.  Among  external  applications  a  mustard  plaster  over 
the  front  of  the  neck  is  to  be  recommended  when  there  are  marked  local  symp- 
toms.    Cold,  wet  compresses  about  the  neck  are  also  of  advantage  in  all  cases. 

In  the  false  croup  of  children  we  should  use,  as  a  rule,  the  same  treatment  as 
has  just  been  described.  The  child  should  take  plenty  of  warm  drink,  inhale 
warm  steam  or  salt  solution,  and  a  mustard  paste  or  hot  poultices  should  be  applied 
to  the  neck.  An  ice-bag  on  the  neck  is  sometimes  useful.  We  should  be  rather 
cautious  with  regard  to  the  favorite  treatment  with  emetics,  such  as  ipecac  and 
sulphate  of  copper,  although  it  can  not  be  denied  that  they  sometimes  work  very 
well  in  severe  dysiDnoea. 

These  means  are  entirely  sufficient  for  the  treatment  of  acute  laryngitis.  It  is 
only  exceptionally  that  we  find  ourselves  led  to  employ  in  acute  laryngeal  catarrh 
an  energetic  loc^l  treatment  of  the  laryngeal  mucous  membrane,  like  painting 
with  a  1-15  solution  of  nitrate  of  silver. 

We  must  bear  in  mind  that  a  rational  hardening  process  is  of  distinct  prophy- 
lactic value  in  persons,  especially  in  children,  with  a  recognized  tendency  to 
laryngitis,  sore  throat,  etc.  The  best  method  is  to  bathe  the  neck  and  chest  with 
cold  water  regularly  morning  and  night. 

[A  mild  emetic  can  do  no  possible  harm  in  false  croup,  and  very  often  cuts  the 
attack  short.  The  application  of  a  sponge,  moistened  with  water  as  hot  as  the 
child  will  bear,  to  the  region  of  the  larynx  deserves  mention.] 


CHKONIC   LAEY]^GITIS  143 

CHAPTER   II 

CHRONIC    LARYNGITIS 

{Chronic  Laryngeal  Catarrh) 

etiology. — Chronic  laryngitis  develops  from  an  acute  catarrh,  or  comes  on 
gradually  from  the  action  of  injurious  influences  on  the  larynx  (see  the  preceding 
chapter).  Chronic  laryngitis,  therefore,  is  in  many  cases  due  to  the  occupation, 
and  is  seen  especially  in  singers,  public  speakers,  criers,  inn-keepers,  workmen  ex- 
posed to  dust,  etc.  It  is  very  frequent  in  drunkards,  and  in  such  cases  it  is 
almost  always  associated  with  a  chronic  pharyngitis.  It  is  not  probably  true 
that,  as  frequently  stated,  too  long  a  uvula  may  set  up  laryngitis  by  irritation  of 
the  entrance  to  the  larjaix. 

Symptomatology. — A  laryngoscopic  examination  is  very  desirable  in  acute 
laryngeal  catarrh,  but  it  is  the  physician's  absolute  duty  to  make  one  in 
chronic  laryngitis,  for  only  too  frequently  a  persistent  hoarseness  is  referred 
to  a  "  simple  "  catarrh  when  the  laryngoscope  gives  quite  another  cause  for  it, 
such  as  paralysis  of  the  vocal  cords  or  new  growths.  Furthermore,  we  must  al- 
ways remember  that  a  chronic  laryngitis  may  be'  a  complication  of  tuberculosis, 
syphilis,  or  chronic  nephritis.  We  shovild  never  omit  a  careful  examination  of 
the  rest  of  the  body  as  well  as  the  larynx. 

The  laryngoscopic  appearance  in  chronic  catarrh  may  be  so  like  that  in  an 
acute  catarrh  that  we  can  not  distinguish  between  them  without  the  history 
obtained  from  the  patient.  The  redness  of  the  mucous  membrane,  however,  is 
usually  less  intense,  and  the  vocal  cords  have  more  of  a  dirty  grayish-red  appear- 
ance. In  most  cases  there  is  also  considerable  swelling  of  the  mucous  membrane 
as  well  as  redness.  Much  more  rarely  we  find  atrophic  conditions,  resembling 
those  of  oz£ena  and  sometimes  associated  with  it.  Quite  frequently  in  persistent 
catarrhs  a  thickening  of  particular  parts  of  the  mucous  membrane  is  developed, 
especially  of  the  folds  between  the  arytsenoid  cartilages.  This  swelling  is  of 
practical  importance,  because  it  furnishes  a  mechanical  hindrance  to  the  closure 
of  the  arytsenoid  cartilages,  and  in  that  way  contributes  to  the  development  of  the 
hoarseness.  We  also  find  marked  thickening  of  the  false  vocal  cords  (especially  in 
public  speakers  and  preachers)  and  of  the  true  vocal  cords.  Yirchow  described, 
under  the  name  of  pachydermia  laryngis,  a  condition  of  the  larynx  seen  espe- 
cially in  drinkers  and  characterized  by  a  thickening  of  the  epithelium  over  the 
whole  laryngeal  mucous  membrane.  Tiirck  has  described  a  peculiar  form  of 
chronic  laryngitis,  in  which  rough  prominences  are  formed  in  the  middle  of  the 
true  vocal  cords,  under  the  name  of  chorditis  tuherosa.  We  not  infrequently  find 
in  chronic  catarrh  superficial  erosions,  especially  on  the  vocal  cords.  We  never 
see  actual  ulceration  in  simple  laryngitis.  We  also  very  often  see  a  disturbance 
of  motion  of  one  or  both  vocal  cords,  especially  incomplete  closure,  due  some- 
times to  muscular  paresis  and  sometimes  to  mechanical  conditions. 

The  other  symptoms  of  chronic  laryngitis  are  hoarseness,  cough,  and  abnormal 
sensations  in  the  larynx.  The  hoarseness  is  of  every  degree,  from  mere  rough- 
ness, frequent  "  cracking  "  of  the  voice,  to  almost  complete  aphonia.  The  cough 
is  ringing,  hoarse,  deep,  and  rough.  The  expectoration  is  scanty,  usually  simply 
mucous,  but  sometimes  a  little  bloody.  The  subjective  sensations  in  the  larynx 
are  a  feeling  of  burning  and  itching,  and  of  dryness  and  tickling.  They  usually 
increase  after  any  jirotracted  use  of  the  voice. 

We  must  also  mention  as  a  peculiar  and  very  rare  but  practically  important 
form  of  chronic  laryngitis  the  chorditis  vocalis  inferior  hypertrophica  (Ger- 
hardt),  or  laryngitis  hypoglottica  chronica  hypertrophica  (Ziemssen).  In  this 
form  there  is  a  very  gradual  hypertrophy,  and  finally  a  contraction  of  the  mucous 


144  DISEASES    OF   THE   EESPIEATOET   OEGANS 

and  especially  the  submucous  connective  tissue  in  the  inferior  laryngeal  space. 
More  rarely  the  same  changes  are  seen  in  the  upper  part  of  the  larynx.  The  spe- 
cial symptom  of  the  disease,  besides  a  chronic  hoarseness,  is  the  appearance  of  a 
gradually  increasing  stenosis  of  the  larynx.  The  respiration  is  always  labored, 
the  inspiration  noisy  and  protracted.  In  many  cases  there  are  at  times  such 
attacks  of  suffocation  that  life  can  be  prolonged  only  by  tracheotomy.  The  diag- 
nosis can  be  made  only'  by  the  aid  of  the  laryngoscope.  We  see  beneath  the 
glottis  a  little  fissure  surrounded  by  the  thick  and  swollen  mucous  membrane  of 
the  laryngeal  walls. 

The  nature  of  this  affection  is  not  yet  fully  explained.  It  often  seems  to  be 
a  simple  chronic  hypertrophic  inflammation,  but  in  other  case  Schrotter  considers 
it  the  same  bacillary  disease  of  the  mucous  membranes  which  is  known  as  rhino- 
scleroma  when  it  occurs  in  the  nose. 

The  treatment  of  chronic  laryngeal  catarrh  is  always  a  tedious  and  laborious 
task,  the  success  of  which  depends  in  great  measure  upon  the  good  will  and 
energy  of  the  patient.  In  the  first  place,  then,  we  should  endeavor  to  remove  as 
far  as  possible  those  injurious  influences  which  have  excited  and  kept  up  the 
catarrh.  It  is  often  easier  to  give  good  advice  here  than  to  follow  it.  Neverthe- 
less, it  is  the  duty  of  the  physician  to  impress  upon  the  patient  the  urgent  neces- 
sity of  taking  care  of  the  larynx,  and  to  forbid  as  far  as  possible  all  protracted 
speaking,  singing,  staying  in  smoke  or  dust,  smoking,  and  the  use  of  alcohol. 

Local  treatment  takes  the  second  place.  Among  the  most  useful  means  to 
employ  are  sprays  of  astringent  solutions,  such  as  a  one-per-cent.  solution  of 
either  tannin  or  alum.  If  there  is  much  secretion  of  mucus,  turpentine  inhala- 
tions are  advisable.  When  there  is  great  irritability  of  the  larynx,  the  patient 
may  also  inhale  vaporized  narcotics,  a  mixture  of  fifty  parts  of  cherry-laurel  water 
with  a  thousand  parts  of  water,  or  a  four-per-cent.  solution  of  bromide  of  potas- 
sium. The  inhalations  should  be  used  two  or  three  times  a  day,  and  last  about  five 
minutes  each  time.  Direct  applications  to  the  larynx  are  much  more  effective  than 
inhalations,  but  these  can  be  employed  only  by  the  aid  of  a  laryngeal  mirror. 
Of  these  we  use,  first  of  all,  nitrate  of  silver,  at  first  in  a  weak  solution  (one  to 
fifty)  ;  later  in  a  more  concentrated  form  (one  to  ten,  or  even  one  to  five).  These 
applications  are  made  every  two  or  three  days.  Besides  nitrate  of  silver,  the 
larynx  may  also  be  painted  with  pure  tincture  of  iodine,  or  with  iodine  and 
glycerine  (iodine,  4  parts,  iodide  of  potassium,  6  parts,  and  glycerine,  500  parts), 
or  with  concentrated  solutions  of  alum  or  tannin. 

Water-cures  are  also  often  prescribed  in  chronic  catarrh  of  the  larynx.  These 
are  of  advantage  from  the  greater  care  which  the  patient  takes,  and  from  the 
good  air,  the  catarrh  improves.  Empirically,  we  prescribe,  especially  for  "  full- 
blooded  "  patients,  the  cold  sulphur  springs,  such  as  ISTenndorf,  Eilsen,  or  Weil- 
bach,  or  the  sulphate  of  sodium  waters,  such  as  Carlsbad  and  Marienbad,  while 
we  send  those  of  delicate  constitutions  to  Ems,  Salzbrunn,  Salzungen,  Eeichen- 
hall,  etc. 

The  treatment  of  laryngitis  hypertrophica,  when  it  leads  to  stenosis,  must  be 
mechanical.  Schrotter,  in  particular,  has  devised  several  methods  of  dilating 
the  stenosis  gradually  by  the  introduction  of  bougies  and  harder  dilators.  The 
details  of  this  treatment  are  to  be  found  in  the  later  special  works  referred  to 
above. 


LAEYNGEAL   PEEICHONDEITIS  145 

CHAPTEE   III 
LARYNGEAL    PERICHONDRITIS 

etiology  and  Pathological  Anatomy. — The  inflammation  of  the  perichon- 
drium of  the  laryngeal  cartilages  is  in  very  rare  cases  apparently  a  primary 
disease.  It  is  much  more  frequently  secondary  to  other  laryngeal  affections, 
especially  tuberculosis  and  syphilis  of  the  larynx.  Furthermore,  it  develops 
secondarily  in  severe  acute  diseases,  most  frequently  in  typhoid  fever,  more 
rarely  in  small-pox,  diphtheria,  etc.  Superficial  ulcerative  processes  in  the  mu- 
cous membrane  often  precede  the  perichondritis  in  these  cases,  and  the  participa- 
tion of  the  perichondrium  in  the  inflammation  arises  from  their  gradual  deep- 
ening. Anatomically,  we  have  to  do  as  a  rule  with  a  purulent  inflammation, 
which  usually  leads  to  the  formation  of  circumscribed  abscesses.  Most  laryn- 
geal abscesses  have  their  origin  in  the  perichondrium.^  The  perichondrium  is 
in  part  destroyed  by  the  abscess  and  in  part  elevated  from  the  cartilage.  The 
cartilage  then  becomes  necrotic,  breaks  in  pieces,  and  is  expelled  in  small  particles 
or  in  masses. 

Perichondritis  occurs  most  frequently  in  the  cricoid  and  arytasnoid  cartilages, 
much  more  rarely  on  the  internal  or  external  surface  of  the  thyroid  cartilage. 
Hence  we  distinguish  an  iiaternal  and  an  external  perichondritis.  A  perichon- 
dritis of  the  epiglottis  has  also  been  repeatedly  observed. 

Symptomatology. — In  the  rare  cases  of  primary  perichondritis,  marked  laryn- 
geal symptoms  are  speedily  developed  in  a  person  previously  healthy.  These 
symptoms  are  pain  and  tenderness  on  pressure  over  the  larynx,  hoarseness,  and 
cough;  and  to  them  are  usually  soon  added  the  signs  of  a  dangerous  stenosis  of 
the  larynx.  In  secondary  cases,  which  occur  almost  always  in  patients  who  are 
already  seriously  ill,  the  symptoms  of  stenosis  are  often  the  first  to  point  to  a 
severe  disease  of  the  larynx.  On  laryngoscopic  examination,  besides  the  general 
redness  and  swelling  in  particular  places,  we  can  sometimes  recognize  a  circum- 
scribed prominence  of  the  mucous  membrane  caused  by  the  abscess.  If  the  abscess 
be  already  broken  we  can  see  the  abscess  cavity  and  sometimes  the  cartilage  lying 
free  within  it.  In  most  cases  we  find  a  considerable  collateral  cedema  of  the  sur- 
rounding mvicous  membrane,  which  a?dema  frequently  has  a  greater  share  in  the 
production  of  stenosis  than  has  the  primary  affection  itself.  The  dreaded  oedema 
of  the  glottis  (oedema  of  the  ary-epiglottic  ligament)  in  typhoid,  tuberculosis  of 
the  larynx,  etc.,  is  usually  due  to  perichondritis  of  the  cricoid  or  arytsenoid  car- 
tilages. Finally,  we  can  see  with  the  laryngoscope,  especially  in  perichondritis 
arytsenoidea,  a  considerable  disturbance  of  motion  of  the  affected  arytenoid 
cartilage,  and  also  of  the  vocal  cords. 

Laryngeal  perichondritis  terminates  fatally  in  a  great  number  of  cases  from 
the  development  of  stenosis.  In  thyroid  perichondritis  the  pus  may  sometimes 
gravitate,  causing  a  severe  purulent  inflammation  of  the  mediastinum.  In  other 
cases  the  most  threatening  symptoms  may  be  averted  for  a  time,  but  the  primary 
disease,  such  as  tuberculosis,  finally  comes  to  an  unfavorable  termination.  In  the 
rare  cases  in  which  recovery  occurs  after  primary  perichondritis  or  after  the 
termination  of  the  primary  disease,  such  as  typhoid,  this  recovery  is  often  incom- 
plete, since  a  chronic  stenosis  of  the  larynx  remains  from  the  ensuing  cicatricial 
contractions. 

The  diagnosis  is  visually  obscure  during  the  first  period  of  severe  symptoms  of 
stenosis,  since  it  is  difficult  to  make  a  laryngoscopic  examination,  and  it  is  also 
not  always  easy  to  determine  the  condition.     We  are  usually  justified,  however, 

*  True  submucous  abscesses,  tlie  sri-ealled  [ilileii-nioiious  laryngitis,  occur  only  in  very  rare  cases. 
10 


146  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

in  making  the  diagnosis,  if  in  those  diseases  which  we  have  mentioned,  in  which 
we  know  by  experience  that  a  perichondritis  quite  frequently  occurs,  the  danger 
of  suffocation  arises  in  addition  to  the  other  laryngeal  symptoms.  It  is  of  prac- 
tical importance  to  recognize  stenosis  of  the  larynx  with  certainty,  for  it  demands 
speedy  therapeutic  interference. 

Treatment. — In  the  beginning  of  the  affection  we  may  try  to  reduce  the  in- 
flammation by  the  internal  and  external  application  of  ice  or  by  leeches.  The 
pain  may  be  alleviated  by  injections  of  morphine  or  painting  with  cocaine.  If 
stenosis  of  the  larynx  occurs,  surgical  interference  is  usually  necessary,  for  only  in 
very  rare  cases  do  we  see  the  abscess  open  of  itself  with  a  subsidence  of  the  dan- 
gerous symptoms.  In  the  majority  of  cases  the  patient  can  be  saved  from 
suffocation  only  by  the  timely  performance  of  tracheotomy  or  laryngotomy.  The 
laryngeal  abscess  has  been  repeatedly  opened  internally  by  laryngologists  with 
favorable  results.  If  a  chronic  stenosis  of  the  larynx  remains  after  a  favorable 
termination  of  the  disease,  either  the  patient  must  wear  a  tracheal  canula  all  his 
life,  or  the  attempt  may  be  made  to  dilate  the  stenosis  gradually  by  the  methods 
referred  to  in  the  preceding  chapter. 


CHAPTEE   IV 
CEDEMA    OF    THE    GLOTTIS 

The  practical  importance  of  the  subject  demands  a  brief  special  description  of 
loedema  of  the  glottis,  by  which  we  mean  oedema  of  the  entrance  of  the  lar- 
ynx, esi^ecially  of  the  ary-epiglottic  ligaments.  We  have  already  learned  to 
recognize  laryngeal  perichondritis  as  one  of  its  most  frequent  causes.  In  less 
deeply  seated  inflammations  in  the  larynx  and  its  neighborhood,  however,  oedema 
of  the  glottis  may  sometimes  develop  as  a  dangerous  complication,  especially  in 
cases  of  laryngitis  occurring  in  the  course  of  severe  acute  diseases,  such  as  typhoid, 
small-pox,  or  erysipelas,  or  in  inflammations  of  the  larynx  arising  from  severe 
mechanical  or  chemical  irritation,  as  from  hot  steam  or  corrosive  substances,  or 
from  wounds  of  the  larynx,  or,  finally,  from  foreign  bodies  in  the  larynx.  The  col- 
lateral oedema  in  angina  Ludovici,  in  intense  inflammations  of  the  parotid  gland, 
or  the  tonsils,  etc.,  may  in  rare  cases  extend  to  the  ary-epiglottic  ligaments. 
Finally,  oedema  of  the  glottis  occurs  in  rare  cases  as  a  complication  of  general 
oedema  of  the  body,  as  a  result  of  Bright's  disease,  disease  of  the  heart,  emphysema 
of  the  kuigs,  etc.  (Edema  of  the  glottis,  without  extensive  oedema  elsewhere, 
has  been  repeatedly  observed  to  come  on  quite  suddenly,  especially  in  acute  and 
chronic  nephritis. 

The  chief  symptom  of  oedema  of  the  glottis  is  dyspnoea,  which  comes  on  as 
a  result  of  the  stenosis  of  the  entrance  of  the  larynx,  and  is  sometimes  extreme. 
At  first  this  is  chiefly  on  inspiration,  but  it  soon  comes  on  with  expiration  also. 
Eespiration,  especially  inspiration,  is  accompanied  by  a  loud  laryngeal  stridor. 
As  a  result  of  the  incomplete  entrance  of  the  air,  the  efforts  at  inspiration  cause 
depression  of  the  root  of  the  neck,  the  epigastrium,  and  the  sides  of  the  thorax. 
We  see  with  the  laryngoscope,  if  the  examination  be  successful,  an  oedematous 
swelling  of  the  ary-epiglottic  ligaments,  and  often  a  swelling  of  the  epiglottis  and 
the  false  vocal  cords.  Sometimes  we  succeed  in  feeling  the  swollen  parts  with  the 
finger. 

If  the  dyspnoea  reaches  a  degree  which  threatens  life,  an  operation  is  the  only 
thing  which  can  afford  relief.     Laryngologists  attempt  to  reduce  the  swelling 


TUBEECULOSIS    OF    THE   LARYITX  147 

by  long  incisions  in  the  oedematovxs  parts.  If  this  does  not  succeed,  tracheotomy 
must  be  performed.  If  the  immediate  danger  to  life  is  thus  averted,  further 
treatment  should  be  directed  to  the  disease  which  has  given  rise  to  the  cedema. 


CHAPTER   V 


TUBERCULOSIS    OF    THE    LARYNX 

{Laryngeal  Phthisis.      Consximption  of  the  Larynx) 

iEtiology. — Since  tuberculosis  of  the  larynx  is  in  most  cases  combined  with 
tuberculosis  of  other  organs,  especially  of  the  lungs,  we  must  refer  to  the  descrip- 
tion of  tuberculosis  of  the  lungs  for  the  general  setiology  and  pathology  of  the 
disease.  A  particular  description  of  the  special  appearances  in  laryngeal  tuber- 
culosis is,  however,  justifiable,  because  tuberculosis  may  at  times  begin  in  the 
larynx  and  may  remain  isolated  there,  at  least  for  a  time ;  and,  furthermore,  in 
many  cases  of  laryngeal  tuberculosis,  which  are  evidently  combined  with  pulmo- 
nary tuberculosis,  the  laryngeal  symptoms  are  predominant  in  the  clinical  picture 
of  the  disease.  Many  physicians  have,  wrongly  as  we  think,  disputed  the  fact 
that  tuberculosis  can  begin  in  the  larynx.  Clinical  experience  not  infrequently 
teaches  us  that  men,  who  have  been  apparently  in  good  health,  are  attacked 
with  hoarseness,  the  disease  being  at  first  thought  to  be  a  common  laryngitis, 
but  at  last,  by  its  course,  proving  to  be  tuberculosis.  In  spite  of  the  most 
careful  examination,  there  are  not  to  be  found  at  first  the  slightest  physical 
signs  of  disease  in  the  lungs,  and  not  till  later  do  the  manifest  signs  of  a  pul- 
monary tuberculosis  succeed  the  symptoms  of  a  laryngeal  affection.  In  such  cases 
it  seems  to  us  an  affectation  to  claim  that  there  is  a  primary  pulmonary  tubercu- 
losis which  could  not  be  made  out  at  first.  Everything  is  much  more  in  favor  of 
the  opinion  that  the  tubercular  poison,  the  tubercle  bacilli,  may  sometimes,  if  not 
frequently,  first  fix  ixpon  the  larynx,  excite  the  first  symptoms  of  tuberculosis 
there,  and  then  attack  the  lungs. 

In  the  great  majority  of  cases  of  laryngeal  tuberculosis  the  symptoms  are  de- 
veloped, of  course,  secondarily  in  the  course  of  chronic  pulmonary  phthisis.  We 
shall  see  that  in  most  cases  the  disease  of  the  larynx  is  to  be  considered  as  the 
result  of  an  infection  of  the  mucous  membrane  of  the  larynx  by  the  tuberculous 
sputum  which  passes  over  it.  More  rarely  the  infectious  material  seems  to  reach 
the  larynx  by  way  of  the  lymph-  or  blood-vessels.  In  favor  of  this  theory  we  may 
mention  that  men  of  great  experience  (Schrotter  and  others)  have  stated  that, 
where  the  laryngeal  trouble  was  particularly  marked  on  one  side,  that  side  was 
very  often  affected  which  corresponded  to  the  affected  lung.  In  about  one  fourth 
of  all  cases  of  pulmonary  tuberculosis  this  complication  occurs,  if  we  include  all 
the  mild  laryngeal  cases.  Marked  and  extensive  tuberculosis  of  the  larynx  is 
much  rarer,  however. 

Pathological  Anatomy. — Tuberculosis  of  the  laryngeal  mucous  membrane  be- 
gins, like  tuberculosis  of  other  mucous  membranes,  with  the  formation  of  small 
subepithelial  nodules,  which  soon  become  cheesy,  break  down,  and  form  small 
ulcers.  In  the  further  course  of  the  disease  there  is  very  often  a  more  extensive 
tubercular  infiltration,  which  gives  rise  on  the  one  hand  to  irregular  thickening 
of  the  mucous  membrane,  and  on  the  other  to  deep  ulceration.  The  tubercular 
infiltration  is  most  frequently  situated  in  the  interaryttenoid  space,  on  the  false  or 
true  cords  (at  first  on  one  side),  and  on  the  epiglottis.  The  tuberculous  ulceration 
usually  develops  later  in  one  of  these  places.     The  iilceration  may  extend  from 


148  DISEASES    OF   THE   EESPIEATOEY   OKGANS 

the  epiglottis  to  the  neighboring  parts  of  the  tongue.  In  severe  cases  we  often 
find  a  marked  collateral  oedema  in  the  surrounding  parts  accompanying  the  in- 
flammation, and  sometimes  the  tubercular  perichondritis  which  has  already  been 
described. 

The  rest  of  the  laryngeal  mucous  membrane  (especially  the  vocal  cords)  not 
involved  in  the  specific  tubercular  process  is  usually  the  seat  of  a  simple  catarrh. 

Clinical  Symptoms. — In  the  beginning  of  tuberculosis  of  the  larynx  the  laryn- 
goscope usually  shows  nothing  but  the  appearances  of  a  simple  catarrh,  since  the 
primary  miliary  nodules  of  tuberculosis  are  usually  hard  to  make  out.  If  the 
catarrhal  symptoms  be  only  on  one  side,  we  should  always  suspect  tuberculosis. 
In  the  later  stages,  however,  most  of  the  special  details  of  the  destructive  tuber- 
cular process,  described  above  (ulcers,  infiltration,  etc.),  can  be  very  satisfacto- 
rily made  out  with  the  laryngoscope.  The  infiltration  and  ulcers  are  either  chiefly 
on  one  or  on  both  vocal  cords  or  on  the  posterior  wall  of  the  larynx,  or  mainly  in 
the  neighborhood  of  one  arytsenoid  cartilage,  or  the  whole  epiglottis  is  irregularly 
ulcerated  on  its  edge.  Single  tubercular  nodules  are  often  plainly  to  be  seen. 
In  severe  cases  almost  the  whole  upper  portion  of  the  larynx  appears  like  an  ulcer- 
ated surface  covered  with  mucus.  In  laryngeal  tuberculosis,  however,  the  soft 
palate  usually  looks  very  pale  and  antemic.  The  redness  and  swelling  of  the 
affected  parts  are  more  distinct  in  the  living  subject  than  in  the  cadaver;  but 
the  autopsy  often  shows  a  far  greater  extension  of  the  tubercular  disease  than  we 
can  determine  by  the  laryngoscope. 

The  other  clinical  symptoms  of  tuberculosis  of  the  larynx  vary  very  much  with 
the  extent  and  intensity  of  the  process.  Sometimes  they  consist  merely  in  mod- 
erate roughness  and  hoarseness  of  the  voice,  but  in  other  cases  they  increase  to  the 
most  painful  condition  which  is  ever  seen  in  any  variety  of  tuberculosis.  This 
is  especially  apt  to  be  the  case  if  the  ulceration  involves  the  epiglottis  and  the 
arytsenoid  cartilages.  Swallowing  is  then  extremely  painful,  so  that  the  nutri- 
tion is  very  often  impaired,  and  painful  attacks  of  coughing  frequently  occur.  A 
practiced  ear  can  often  distinguish  at  once  the  hoarse  sound  of  a  "  laryngeal 
cough "  from  the  ordinary  pulmonary  cough.  If  severe  ulcerations  attack  the 
vocal  cords,  and  their  free  mobility  is  affected  to  a  marked  degree,  the  hoarseness 
increases,  and  flnally  reaches  a  complete  aphonia.  Death  finally  occurs  from 
general  inanition,  or,  exceptionally,  from  oedema  of  the  glottis. 

The  diagnosis  of  tuberculosis  of  the  larynx  is  not  difiicult  if  pulmonary 
phthisis  is  already  known  to  be  present.  When  attention  has  been  called  to  it 
from  the  onset  of  hoarseness  or  from  some  disturbance  in  swallowing,  we  recog- 
nize the  character  and  seat  of  the  changes  by  the  aid  of  the  laryngoscope.  The 
diagnosis,  however,  may  present  much  difiiculty  in  cases  where  we  are  not  sure 
that  an  affection  of  the  lungs  co-exists.  As  has  been  said,  the  symptoms  at  first 
are  not  unlike  those  of  a  simple  catarrh,  and  the  suspicion  of  the  existence  of 
tuberculosis  is  first  aroused  from  the  stubbornness  of  the  disease,  the  condition 
of  the  patient,  the  knowledge  of  some  inherited  taint,  the  onset  of  fever,  and  the 
remarkable  anaemia  and  emaciation.  With  the  changes  in  the  larynx  Avhich  have 
been  described,  without  evidence  of  pulmonary  tuberculosis,  the  distinction  be- 
tween tuberculosis  and  syphilis  may  be  very  difiicult.  In  syphilis  of  the  larynx, 
however,  we  find  that  co-existing  changes  in  the  pharynx  are  much  commoner 
than  in  tuberculosis,  and  the  cicatricial  formation  which  is  usually  visible  fur- 
nishes, besides,  a  very  characteristic  evidence  of  syphilis.  The  diagnosis  of  tuber- 
culosis of  the  larynx,  however,  is  made  perfectly  certain  in  all  doubtful  cases  by 
the  discovery  of  tubercle  bacilli  in  the  patient's  expectoration  or  in  the  secretion 
from  the  ulcer,  which  often  can  be  easily  obtained  by  the  aid  of  a  fine  laryngeal 
brush.  In  regard  to  the  laryngoscopic  appearances,  we  may  also  saj  that  a  thick- 
ening and  infiltration  of  the  epiglottis  Avith  a  partial  ulceration  of  the  same  is  an 


TUBEECULOSIS    OF   THE   LARYNX  149 

appearance  which  is  ahnost  exchisively  coniinecl  to  tuberculosis.  The  same  is  true 
with  regard  to  a  marked  projecting  infiltration  of  the  inter-aryttenoid  region. 
In  doubtful  cases  it  may  aid  the  diagnosis  to  inject  tuberculine  (see  the  chapter 
on  iDulmonary  tuberculosis). 

Treatment. — For  the  constitutional  treatment  of  tuberculosis  of  the  larynx  the 
reader  is  referred  to  the  description  of  pulmonary  tuberculosis.  We  shall  here 
discuss  merely  the  local  treatment.  This  is  in  the  milder  forms  the  same  as  for 
simple  laryngeal  catarrh.  There  is  no  doubt  that  even  genuine  tiiberculous  ulcer- 
ation of  the  larynx  may  be  healed.  ISTevertheless  permanent  cures  of  this  sort 
are  exceptional.  Of  course  very  much  depends  upon  the  co-existing  state  of  the 
limgs.  For  local  treatment  insufflations  of  iodoform  and  iodol  were  for  a  time 
strongly  recommended,  but  they  are  now  for  the  most  part  abandoned.  Cauter- 
izing the  tuberculous  ulcers  with  nitrate  of  silver  does  more  harm  than  good. 
We  sometimes  see  better  results  from  blowing  powdered  boracic  acid  on  the  ulcers 
or  from  a  twenty-per-cent.  solution  of  menthol  in  oil.  At  present  lactic  acid 
is  most  recommended — cauterizing  the  ulcers  with  a  solution  of  increasing 
strength  (twenty  to  eighty  per  cent.),  at  first  daily,  and  later,  after  the  ulcers 
have  been  cleaned  off,  less  frequently. 

If  we  were  to  give  a  general  estimate  of  the  local  treatment  of  laryngeal  tuber- 
culosis we  should  have  to  admit  that  its  success  has  not  been  great.  We  do  not 
deny  that  skill  and  perseverance  may  be  of  much  service,  but  only  too  often 
do  we  become  discouraged  by  the  failure  of  the  most  careful  local  treatment, 
and  in  many  cases  cauterization  of  the  larynx  is  only  a  useless  distress  to  the 
patient. 

With  incipient  disease  there  may  be  considerable  improvement  and  even 
recovery  without  any  local  treatment  if  the  larynx  be  spared  any  exertion  and 
given  complete  rest  and  if,  at  the  same  time,  careful  general  treatment  be  insti- 
tuted. The  most  we  need  to  use  is  the  atomizer  or  nebvilizer  with  simple  salt  solu- 
tion, alkaline  waters,  etc.  We  have  also  found  inhalations  of  a  weak  carbolic  solu- 
tion, and  especially  of  vapor  of  Peruvian  balsam,  of  service.  In  advanced  cases, 
where  pronounced  pulmonary  tuberculosis  co-exists,  we  must  content  ourselves 
with  a  purely  palliative  treatment.  The  constant  use  of  cracked  ice,  and  especially 
a  lavish  employment  of  narcotics,  are  of  most  service  in  relieving  the  pain  and  the 
difficulty  in  swallowing.  Subcutaneous  injections  of  morphine  a  quarter  of  an 
hour  before  a  meal  often  afford  great  relief.  We  have  seen  very  good  results 
from  cocaine.  If  we  paint  the  ulcerated  mucous  membrane  at  the  entrance  of 
the  larynx  with  a  ten-  or  twenty-per-cent.  solution  of  cocaine,  in  a  few  minutes 
such  an  anaesthesia  of  the  affected  parts  ensues  that  swallowing  may  take  place 
without  any  pain.     The  following  formula  may  be  used : 

I^   Cocainse  muriatis   gr.  xv-xxx,  gramme  1.0-2.0 ; 

Alcohol  OSS  "         2.0; 

Aqua3  destillatEe  5ij  "  8.0.       M. 

Unfortunately  the  action  of  cocaine  is  very  transitory,  so  that  the  painting 
must  be  frequently  repeated.  With  a  severe  laryngeal  cough  and  irritation  relief 
may  also  be  obtained  by  inhalations  of  a  two-  to  three-per-cent.  solution  of 
bromide  of  potassium  or  a  three-  to  ten-per-cent.  solution  of  bitter-almond  water. 

If  a  pronounced  stenosis  of  the  larynx  develop,  tracheotomy  is  indicated. 
Many  recent  observations  seem  to  show  that  tracheotomy  may  also  be  of  service 
in  marked  laryngeal  tuberculosis.  When  the  laryngeal  respiration  is  shut  off 
the  tubercular  lesions  seem  to  improve  faster. 

In  cases  of  pronounced  but  comparatively  limited  laryngeal  tuberculosis,  with- 
out much  implication  of  the  lungs,  the  attempt  has  been  made,  after  a  preliminary 
laryngotomy,  to  remove  the  diseased  parts  as  completely  as  possible  by  surgical 


150  DISEASES    OF   THE   EESPIRATORY   ORGANS 

means.     We  still  lack  extended  practical  experience  in  this  matter,  but  further 
trials  of  the  operation  seem  very  desirable. 


CHAPTER    VI 
PARALYSES    OF    THE    LARYNGEAL    MUSCLES 

1.  Paralyses  in  the  Distribution  of  the  Superior  Laryngeal  Nerve.— The  su- 
perior laryngeal  nerve,  arising  from  the  vagus,  is  the  sensory  nerve  for  the  mucous 
membrane  of  the  upper  portion  of  the  larynx  down  to  the  glottis,  and  also  for 
the  mucous  membrane  of  the  epiglottis  and  its  neighborhood.  Besides  this,  it 
also  supplies  motor  fibers  to  the  erico-thyroid  muscle,  probably  from  the  accessory 
nerve.  Clinical  experience  renders  it  probable  that  the  superior  laryngeal  nerve 
also  supplies  the  depressors  of  the  epiglottis,  the  thyro-epiglottideus,  and  the 
aryta3no-epiglottidei  muscles,  and  perhaps  also  the  arytsenoideus  muscle.  The 
last  three  muscles  mentioned,  hoAvever,  perhaps  derive  some  motor  fibers  from  the 
recurrent  nerve  also   (the  inferior  laryngeal  nerve). 

Paralysis  of  the  crico-thyroid  muscles  and  of  the  depressors  of  the  epiglottis  is 
seen  most  frequently  after  recovery  from  diphtheria.  It  is  usually  a  part  of  a 
more  extensive  paralysis,  and,  in  addition,  is  sometimes  associated  with  anaesthe- 
sia of  those  portions  of  the  mucous  membrane  which,  as  we  have  seen,  derive  their 
sensory  fibers  from  the  superior  laryngeal  nerve  (von  Ziemssen).  Choking  is 
therefore  easy  and  there  is  danger  of  inhalation  pneumonia. 

Paralysis  of  the  thyro-epiglottideus  and  the  arytseno-epiglottidei  muscles  is 
recognized  by  the  immobility  and  the  erect  position  of  the  epiglottis,  which  is 
directed  toward  the  back  of  the  tongue. 

Paralysis  of  the  crico-thyroid  muscles  makes  the  voice  rough,  and  especially 
renders  the  production  of  high  tones  impossible,  since  for  this  purpose  we  need 
the  action  of  this  muscle  as  a  tensor  of  the  vocal  cords  by  approximating  the 
cricoid  and  thyroid  cartilages.  The  detection  of  this  paralysis  by  the  laryngo- 
scope is  extremely  ditficult.  Its  chief  signs  are  a  concavity  of  the  edges  of  the 
vocal  cords,  a  lack  of  visible  vibration  in  them,  and  perhaps,  in  unilateral  paraly- 
sis, a  higher  jjosition  of  the  vocal  cord  on  the  sound  side. 

For  paralysis  of  the  arytasnoideus  muscle,  vide  infra. 

2.  Paralyses  in  the  Distribution  of  the  Inferior  Laryngeal  or  Eecurrent 
Nerve. — The  recurrent  nerve  supplies  with  sensory  fibers  the  mucous  membrane 
of  the  inferior  cavity  of  the  larynx  below  the  glottis,  and  it  is  the  motor  nerve  for 
all  the  laryngeal  muscles  except  the  crico-thyroid,  and  except  possibly  the  de- 
pressors of  the  epiglottis  (vide  supra).  The  muscles  innervated  by  it  are  ar- 
ranged according  to  their  function  in  the  three  following  groups : 

a.  The  openers  of  the  glottis — the  posterior  crico-arytfenoid  muscles. 

h.  The  closers  of  the  glottis — the  lateral  crico-arytasnoids  and  the  arytfenoi- 
deus  (transverse  and  oblique). 

c.  The  tensors  of  the  vocal  cords — the  thyro-arytsenoids,  which  act  usually 
as  closers  of  the  glottis,  but  which  very  often  produce  the  fine  differences  in  ten- 
sion in  the  vocal  cords  which  are  necessary  in  singing  and  in  modulations  of 
speech.  They  accordingly  have  the  same  task  as  the  coarser-working  crico-thy- 
roid muscles,  which  are  innervated  by  the  superior  laryngeal  nerve. 

The  motor  fibers  for  all  these  muscles  have  their  special  origin  in  the  accessory 
nerve,  from  which  they  pass  into  the  trunk  of  the  vagus,  and  from  this  into  the 
laryngeal  nerves. 


PAEALYSIS    OF   THE   LAEYNGEAL   MUSCLES  151 

Most  of  the  paralyses  of  the  recurrent  nerve  are  of  peripheral  origin.  Except 
in  the  pure  muscular  pareses  (vide  supra),  which  arise  not  infrequently  in  the 
course  of  other  laryngeal  affections,  peripheral  paralyses  of  the  vocal  cords  occur 
with  the  greatest  relative  frequency  from  an  abnormal  pressure  on  the  trunk  of 
the  recurrent  nerve,  especially  in  aneurism  of  the  arch  of  the  aorta,  which  may 
cause  a  left-sided  paralysis.  Tumors  of  the  bronchial  glands,  cancer  of  the 
cesophagus,  thj^roid  or  mediastinal  tumors,  and,  in  rare  cases,  even  large  pericar- 
dial effusions,  may  also  cause  a  paralysis  of  the  recurrent  on  one  side.  Paralyses 
on  the  right  side  are  seen  quite  frequently  in  contractions  at  the  apex  of  the  right 
lung  and  in  the  rare  cases  of  aneurism  of  the  subclavian  artery.  The  paralyses 
of  the  laryngeal  muscles,  which  are  sometimes  met  with  after  recovery  from  diph- 
theria {q.v.),  also  belong  to  the  peripheral  paralyses  of  the  recurrent  nerve, 
and  their  cause  is  to  be  found  in  a  degeneration  of  the  branches  of  the  affected 
nerves.  In  other  cases  the  paralysis  of  the  recurrent  nerve  is  due  to  an  affection 
•of  its  fibers  in  the  vagus  or  even  in  the  accessorius.  Excluding  certain  injuries 
from  operations,  these  affections  are  usually  due  to  new  growths  which  cause  a 
paralysis  of  conduction.  Paralyses  of  the  recurrent  nerve  also  arise  from  affec- 
tions of  the  nucleus  of  the  accessory  nerve  in  diseases  of  the  medulla,  in  the 
different  forms  of  acute  bulbar  paralysis,  in  chronic  bulbar  paralysis,  in  multiple 
sclerosis,  etc.  The  frequent  hysterical  paralyses  affecting  the  closers  of  the  glottis 
and  the  tensors  of  the  vocal  cords  are  to  be  regarded  as  central  disturbances  of 
innervation  (see  the  chapter  on  hysteria). 

1.  Complete  Paralysis  of  the  Recurrent  Nerve. — Paralysis  of  all  the  laryngeal 
muscles  supplied  by  the  recurrent  nerve  occurs  quite  frequently  in  the  pressure 

paralysis  of  the  trunk  of  the  recurrent,  or  of  its  

fibers  in  the  vagus.  With  the  laryngoscope  (see 
Eig.  16)  we  find  the  vocal  cord  on  the  paralyzed 
side  in  a  middle  position,  often  falsely  called  a 
"  cadaveric  position,"  and  completely  motionless 
on  respiration,  and  also  on  phonation.  The 
arytsenoid  cartilage  on  the  paralyzed  side  is  often 
turned  inward.     On  phonating  as  strongly  as  pos-  ^  ,- 

sible,  the  vocal  cord  on  the  sound  side  passes  beyond  ^j^  ]6.-(rrom  Ziemssen.)  Position 
the  median  line,  the  arytsenoid  cartilage  also  crosses         pn  inspiration  in  paralysis  of  the 

nil**  I*  i0rt    voc9j1    corQ,    or    ps-rsiiA  sis    or 

the    line,    and   consequently    the    glottis    is    put    m  conduction  in  thie  recurrent  nerve. 

an    oblique    position.     The    other    symptoms    are 

sometimes  so  slight  that  without  a  laryngoscopic  examination  we  do  not  even 
think  of  a  paralysis.  The  voice,  however,  is  usually  not  pure;  it  often  breaks 
into  a  falsetto,  and  the  patient  is  easily  tired  by  speaking.  With  complete 
hilateral  paralysis  of  the  recurrent  nerve,  which  is  very  rare,  we  find  both  vocal 
cords  motionless  in  a  middle  position.  Complete  aphonia  exists,  and  it  is  impos- 
sible to  cough,  since  in  coughing  Ave  have  to  make  at  first  a  complete  closure 
of  the  glottis.     There  is  no  dyspnosa,  however,  if  the  patient  keeps  quiet. 

It  is  an  interesting  fact,  first  reported  by  Eosenbach,  that  in  incomplete  re- 
current paralysis  almost  invariably  the  abductors  of  the  vocal  cords  (the 
openers  of  the  glottis)  are  alone  paralyzed,  whence  the  cords  remain  in  ad- 
duction. Only  with  the  further  advance  of  the  disease  does  complete  recurrent 
paralysis  occur;  then  the  adductors  also  become  paralyzed,  and  the  vocal  cords 
hecome  completely  motionless,  and  assume  the  middle,  so-called  cadaveric 
position. 

2.  Paralysis  of  the  Dilators  of  the  Glottis,  the  Posterior  Crico-arytaeiioid 
Muscles. — Bilateral  paralysis  of  these  muscles  is  quite  a  rare  phenomenon,  but 
-clinically  it  is  of  the  utmost  importance,  since  it  results  in  a  condition  of  most 
marked  inspiratory  dyspnoea.     ]SJ"euritic  changes,  central  diseases  (tabes,  multi- 


152 


DISEASES    OE    THE   EESPIRATOEY    OEGAXS 


Fig.  17. — (From  Ziemssex.  i  Complete 
bilateral  paralysis  of  the  posticus 
at  the  moment  of  inspiration. 


pie  sclerosis,  etc.),  cancer  of  the  cesopliagus,  etc.,  may  lead  to  paralysis  of  the 
posterior  muscles.  In  many  cases  the  cause  is  obscure.  The  sequelae  of  the 
paralysis  usually  develop  slo^vly  and  gradually.  The  affection  may  last  for  years. 
The  greatest  impairment  of  breathing  probably  occurs  ^vhen  the  vocal  cords  are 
fixed  in  adduction  by  the  contracture  of  the  antagonistic  closers  of  the  glottis. 
The  dyspnoea  may  increase,  especially  from  external  causes,  to  severe  attacks  of 
sufPocation,  and  tracheotomy  is  frequently  necessaiy.  The  respiration  is  affected 
in  such  a  ^ay  that  inspiration  only  is  difficult,  protracted,  and  noisy,  while  expira- 
tion is  free  and  uiihindered.  This  depends  on  a  valve-like  action  of  the  vocal  cords. 
They  are  dravm  together  by  the  dilatation  of  the  thorax  on  inspiration,  vhile  the 
current  of  air  in  expiration  easily  pushes  them  aside.  Phonation  is  usually 
entirely  undisturbed.     "With  the  laryngoscope  (see  Eig.  17)  we  find  the  glottis 

changed  to  a  small  slit,  which  gTows  narrower  in- 
stead of  wider  on  inspiration.  The  prognosis  is 
usually  unfavorable.  Only  in  the  hysterical  can 
these  apparently  severe  conditions  appear  and  dis- 
appear again  in  a  short  time. 

In  unilateral  paralysis  of  the  posterior  crico- 
arytsenoid  muscle  there  is,  as  a  rule,  no  marked 
dyspnoea.  The  voice  is  somewhat  hoarse,  and  with 
the  larj-ngoscope  we  can  see  that  the  paralyzed 
vocal  cord  does  not  deviate  outward  on  inspi- 
ration. 

.3.  Paralysis  of  the  Thyro-arytsenoid  Muscles. 
— The  paralysis  or  paresis  of  these  muscles,  which  run  into  the  vocal  cords,  and 
which  are  their  chief  tensors,  is  one  of  the  most  frequent  of  the  paralyses  of  the 
laryngeal  muscles.  It  occurs  especially  in  acute  and  chronic  catarrh  of  the 
laryngeal  mucous  membrane,  and  is  often  the  chief  cause  of  the  accompanying 
hoarseness.  It  also  frequently  develops  as  the  result  of  an  habitual  strain  of  the 
voice  in  singers  and  public  speakers,  and  it  is  one  of  the  commonest  causes  of 
hysterical  aphonia. 

Paralysis  of  the  thyro-arytsenoid  muscles  may  be  bilateral  or  unilateral.     It  is 
frequently  associated  with  a  paresis  of  the  other  closers  of  the  glottis,  the  arytffi- 
noidei  and  the  crico-thyi'oid  muscles.     With  the  laryngoscope  (see  Eig.  18),  in  the 
ordinary  bilateral  paresis  of  the  thyro-arytaenoid  mus- 
cles, we  see  that  on  phonation  the  glottis  doe?  not  close 
completely,  but  that  an  oval  space  is  left  between  the 
vocal  cords. 

In  unilateral  paralysis  the  affected  cord  shows  a 
concavity  of  its  edge.  The  voice  is  always  more  or 
less  hoarse  and  low  and  the  speech  is  strained. 

In  many  cases,  after  a  cure  of  the  original  catarrh, 
a  complete  recovery  from  the  paralysis  may  follow  by 
taking  good  care  of  the  voice.  Hysterical  paralyses  are 
diagnosticated  by  their  sudden  disappearance  and  reap- 
pearance, usually  after  some  psychical  disturbance.  They  are  quite  common  in 
children  of  the  age  of  ten  to  fourteen  years,  especially  in  girls.  (See  chapter  on 
hysteria.) 

4.  Paralysis  of  the  arytseiioideus  muscle  is  rarely  an  isolated  phenomenon.  It 
is  sometimes  seen  in  laryngeal  catarrh  or  in  hysterical  aphonia.  The  voice  is 
quite  hoarse,  and  with  the  laryngoscope  (see  Eig.  19)  we  find  on  phonation  that 
the  whole  anterior  part  of  the  vocal  cords  closes  well,  but  that  the  cartilaginous 
glottis  remains  open  as  a  triangular  gap  on  account  of  the  imperfect  motion  of  the 
arytsenoid  cartilages  toward  each  other.     When  the  thyro-arytsenoids  are  para- 


FiG.  18.— (From  Ziemssex.)  Pa- 
ralysis of  both  internal  thy- 
ro-arytaenoid  muscles  in  the 
course  of  an  acute  laryngitis. 


SPASM   OF   THE    GLOTTIS 


153 


lyzed  with  the  arytsenoideus,  the  glottis  shows  on  phonation  a  narrow  hour-giass 
opening  (see  Fig.  20).  Both  the  anterior  and  the  posterior  portions  of  the  glottis 
fail  to  close,  while  the  vocal  processes  take  their  usual  median  position  on  phona- 
tion from  the  normal  turning  of  the  arytsenoid  cartilages  inward  by  the  action 
of  the  lateral  crico-aryt^enoid  muscles. 

5.  Paralysis  of  the  lateral  crico-arytaenoid  muscles,  as  an  uncomplicated  con- 
dition, has  never  been  observed  with  certaintj'.  Some  cases  of  a  complete  and 
simultaneous  paralysis  of  all  the  closers  of  the  glottis  have  been  described,  how- 
ever, in  which  the  vocal  cords  are  immovable  laterally  and  the  glottis  remains 
abnormally  wide  open. 

We  may  expect  success  from  the  treatment  of  paralysis  of  the  vocal  cords  only 
when  the  primary  disease  is  capable  of  cure.  If  catarrhal  or  other  diseases  of  the 
larynx  co-exist,  we  must  first  treat  these  by  the  methods   already  mentioned. 


Fig.  19.— (From  Ziemssen.)  Paral- 
ysis of  the  aryteenoideus  in 
acute  laryngitis. 


Fig.  20. — (From  Ziemssen.)  Bilateral 
paralysis  of  the  thyro-arytsenoids 
combined  with  paresis  of  the  ary- 
tasnoideus. 


Paralysis  from  the  compression  of  tvimors,  etc.,  may  be  relieved  in  rare  eases  by 
extirpation,  or  by  partial  resolution  of  the  tumors  when  of  strumous  origin.  In 
catarrhal,  diphtheritic,  and  the  so-called  "  rheumatic  "  pareses — that  is,  those 
which  occur  without  any  assignable  cause — and  also  in  all  hysterical  aphonias, 
electricity  often  works  very  well.  Von  Ziemssen  has  made  electrodes  for  the 
endolaryngeal  stimulation  of  single  muscles,  but  external  galvanization  is  usually 
sufiicient  in  practice.  In  hysterical  aphonia  the  chief  task  is  to  accustom  the 
patient  again  to  the  necessary  and  proper  voluntary  innervation.  We  usually 
accomplish  our  purpose  most  rapidly  by  commanding  the  patient  to  cough  and 
then  say  "  Ah,"  while  we  faradize  or  galvanize  the  neck.  It  is  often  of  advantage 
to  reverse  the  current.  If  the  patient  succeeds  in  saying  "  Ah  "  once,  the  voice 
usually  returns  very  quickly.  Internally  we  may  try  subcutaneous  injections  of 
strychnine  in  doses  of  gr.  g^  to  gr.  ^  daily  (grm.  0.003  to  0.01). 


CHAPTEE   VII 


SPASM    OF    THE    GLOTTIS 

{Laryngis7nns  Stridulus.     MllUw^s  Astlinut.     Thijinic  Asthma) 

.Sltiology. — Spasm  of  the  glottis  is  a  disease  which  occurs  almost  exclusively 
in  children  under  three  years  of  age,  and  consists  of  attacks  of  spasmodic  clos- 
ure of  the  glottis,  and  consequently  of  most  severe  dyspnoea.  Boys  are  more 
frequently  attacked  by  this  disease  than  girls,  but  the  cause  of  this  is  wholly 
unknown.  The  old  name  of  thymic  asthma  arose  from  the  idea  that  the  at- 
tacks were  due  to  an  increase  in  the  size  of  the  thymus  gland,  but  this  opinion 
is  wholly  unfounded.     The  relation  betAveen  spasm  of  the  glottis  and  rachitis  is 


loi  DISEASES    OE    THE   EESPIEATOEY   OEGAISts 

remarkable,  but  it  is  unexplained.  ]Srearly  two  thirds  of  all  the  children  who 
suffer  from  spasm  of  the  glottis  are  rachitic,  but  the  opinion  which  was  once  held 
that  spasm  of  the  glottis  has  a  special  relation  to  the  rachitic  craniotabes  is  not 
clearly  proved.  The  fact  that  it  is  often  combined  with  eclampsia,  in  that  the 
attacks  of  spasm  of  the  glottis  are  aggravated  by  eclamptic  attacks,  and  that  the 
two  alternate  with  each  other,  is  an  argument  in  favor  of  a  central  origin  for 
the  disease.  In  the  cases  which  come  on,  as  they  often  do,  at  the  time  of  denti- 
tion, we  think  it  possible  to  assume  a  reflex  origin  for  the  spasm,  just  as  we  may 
in  those  cases  which  seem  to  follow  a  laryngitis  due  to  taking  cold. 

Symptomatology. — The  single  attacks  usually  come  on  suddenly  by  day  or  by 
night,  either  without  any  cause  or  from  some  external  influence,  such  as  crying, 
SAvallowing  fluid,  or  some  psychical  disturbance.  They  usually  begin  with  a  deep 
inspiration,  followed  by  complete  cessation  of  respiration.  The  child  becomes 
pale,  cyanotic,  looks  anxiously  about,  rolls  his  eyes,  and  makes  strained  and 
labored  efforts  at  respiration.  In  severe  cases  there  is  a  temporary  loss  of  con- 
sciousness, and  tonic  and  clonic  spasms  in  the  muscles  of  the  extremities  and 
the  trunk,  as  has  been  mentioned.  The  attack  lasts  from  some  seconds  up  to  two 
minutes.  In  very  severe  cases  the  attack  may  be  immediately  fatal.  As  a  rule, 
however,  the  spasm  passes  off,  deep,  noisy  inspirations  follow,  and  in  a  short  time 
the  child  is  completely  well.  The  severity  of  the  attacks  varies,  moreover,  in 
different  cases,  and  it  varies  very  markedly,  too,  in  the  same  child.  Sometimes 
we  have  only  one  attack  or  a  small  nimiber  of  them,  while  in  other  children  they 
may  come  on  ten  or  twenty  times  a  day,  and  even  oftener,  and  may  last  with 
varying  intensity  for  months.  If  the  child  reaches  his  third  year  the  disease 
almost  always  disappears,  but  quite  a  large  number  of  the  children  who  suffer 
from  spasm  of  the  glottis  die  before  that  age,  either  in  the  attack  itself  or  from 
other  affections. 

Genuine  spasm  of  the  glottis  hardly  ever  occurs  in  adults,  but  similar  attacks, 
which,  of  course,  have  quite  a  different  significance,  are  sometimes  observed  in 
hysteria. 

The  treatment  must  be  especially  directed  to  the  child's  general  condition. 
The  child  is  usually  pale  and  emaciated,  and  if  we  succeed  in  improving  its  nutri- 
tion with  iron  and  cod-liver  oil,  the  attacks  become  less  frequent,  and  milder,  and 
finally  may  wholly  disappear.  If  rachitis  exists,  we  should  first  of  all  try  phos- 
phorus (1  part  in  10,000  of  cod-liver  oil).  The  child  should  also  be  kept  in  mod- 
erately warm  air  and  guarded  from  any  exposure  to  cold.  Internal  remedies  to 
prevent  the  recurrence  of  the  attacks  are  very  uncertain  in  their  action.  We  may 
employ  one  or  two  grains  (gramme  0.05-0.10)  of  chloral  hydrate  in  solution  every 
hour  or  two;  bromide  of  potassium,  ten  to  thirty  grains  daily  (grammes  0.5-2.0)  ; 
extract  of  belladonna,  etc.   - 

In  the  attack  itself  the  child  must  be  raised  up.  The  face  should  be  sprinkled 
with  water,  or,  if  the  attack  be  of  long  duration,  a  cool  shower-bath  should  be 
given.  Eriction  should  be  applied  to  the  skin,  aided  by  mustard,  or  a  mustard 
plaster  applied  to  the  chest  and  calves.  If  the  attacks  are  very  frequent  and  in- 
tense, we  must  use  narcotics,  either  inhalations  of  chloroform  or  subcutaneous  in- 
jections of  morphine,  Avith  care,  in  doses  for  a  child  of  ^V  to  yV  of  a  grain  (gramme 
0.001  to  0.005). 


NEW   GEOWTHS   IX   THE   LAEYXX 


155 


CHAPTER   VIII 
NEW    GROWTHS    IN    THE    LARYNX 

SixCE  new  growths  in  the  larynx  are  of  interest  mainly  to  specialists  and  sur- 
geons, we  will  here  only  glance  briefly  at  them.  We  must  remember  especially, 
however,  that  they  can  be  recognized  only  by  the  aid  of  the  laryngoscope.  It 
unfortunately  often  happens  that  a  patient  is  treated  for  a  long  time  without 
success  for  a  "  chronic  laryngeal  catarrh,"  when  the  laryngoscope  finally  shows 
that  a  new  growth  is  the  cause  of  the  hoarseness.  It  is  of  especial  importance, 
however,  to  make  a  diagnosis  as  early  as  possible,  particularly  in  carcinoma, 
since  the  earlier  the  operation  is  done  the  better  is  the  chance  for  success  (vide 
infra). 

A.  Benigxant  Growths  ix  the  Larynx 

1.  Papilloma  is  one  of  the  commonest  new  growths  in  the  larynx.  It  forms 
glandular,  cauliflower-like  excrescences,  which  are  usually  situated  on  the  ante- 
rior part  of  the  vocal  cords,  rarely  on  the  false  cords.  The  base  of  the  swelling  is 
broad  or  pediculated.  The  growths  are  often  multiple.  We  do  not  know  the  spe- 
cial cause  of  their  origin.  It  is  Avorthy  of  note  that  papilloma,  like  other  benignant 
growths  in  the  larynx,  is  seen  much  more  frequently  in  men  than  in  women. 

2.  Fibroma  in  the  larynx  is  comparatively  common.  The  pediculated  tumors 
known  as  "  laryngeal  polypi  "  are  usually  fibromata.  They  are  generally  situated 
on  the  vocal  cords  and  form  whitish  or  reddish-brown  swellings,  from  the  size  of 
a  -pea  to  that  of  a  cherry,  vascular  and  dense  or  soft  (see  Eigs.  21  and  22).     There 


Figs.  21  and  22.— iTrom  Ziemssen.)    Pediculated  fibromata. 

is  no  evidence  that  persons  who  use  their  voices  very  much  are  especially  liable  to 
the  formation  of  fibromata. 

3.  Cysts  and  "  mucous  polypi  "  rarely  occur.  They  are  probably  due  to  the 
retention  of  the  secretion  in  a  mucous  gland  from  the  stoppage  of  its  orifice. 
We  find  them  in  the  ventricles  of  Morgagni,  on  the  epiglottis,  etc.  In  a  very  few 
cases  we  also  see  in  the  larynx  lipomata,  myxomata,  separated  portions  of  thyroid 
gland  tissue  which  have  begun  to  grow,  enchondromata,  etc. 

The  symptoms  which  are  excited  by  benignant  tumors  in  the  larynx  depend 
partly  upon  the  situation  and  partly  upon  the  size  of  the  new  groAvth.  Small 
polypi  may  exist  wholly  without  symptoms,  and  they  are  found  only  by  chance  on 
laryngoscopic  investigation.  Usually,  howcA'er,  the  presence  of  disturbances  of 
phonation  (hoarseness,  a  marked  change  in  pitch,  secondary  tones),  persistent 
cough,  or  respiratory  disturbances  when  the  tumor  is  a  large  one,  are  the  symp- 
toms which  give  occasion  for  an  examination.  Abnormal  sensations  in  the  larynx 
are  by  no  means  the  rule,  and  pain  is  wholly  absent. 

B.  Maligxaxt  Growths.     Carcixoma  of  the  Laryxx 
Sarcomata,  arising  from  the  true  or  false  vocal  cords,  are  very  rare.    The  only 
malignant  new  growth  of  the  larynx  of  great  practical  importance  is  carcinoma. 


156  DISEASES    OF    THE   EESPIEATOEY   OEGANS 

Carcinomata  develop  usually  in  old  people,  either  primarily  in  the  larynx  or 
secondarily  from  affection  of  the  neighboring  organs.  In  the  first  case  the  vocal 
cords  or  the  ventricles  of  Morgagni  are  the  points  most  frequently  attacked.  An 
extension  of  the  disease  to  the  larynx  is  seen  especially  in  cancer  of  the  tongue  or 
pharynx,  rarely  in  cancer  of  the  oesophagus. 

The  symptoms  of  cancer  of  the  larynx  develop  slowly.  Hoarseness,  dysphagia, 
pains  in  the  larynx  often  shooting  up  into  one  ear  or  the  temporal  region,  the 
appearance  of  respiratory  symptoms,  and  finally,  but  only  in  the  later  stages  as  a 
rule,  the  signs  of  general  weakness  and  emaciation  which  are  seen  in  almost  all 
forms  of  carcinoma,  form  the  picture  of  the  disease.  Enlargement  of  the  cer- 
vical lymph-glands  is  sometimes  an  early  symptom,  but  it  may  be  wholly  lack- 
ing. The  diagnosis  is  possible  only  by  the  aid  of  the  laryngoscope.  Besides 
this,  a  digital  examination  may  at  times  be  of  diagnostic  value  by  the  detection 
of  the  characteristic  hardness  about  the  entrance  or  in  the  neighborhood  of 
the  larynx.  A  general  description  of  the  laryngoscopic  appearances  can  not 
be  given  on  account  of  the  diverse  character  of  the  cases.  We  see  the  uneven, 
injected  new  growth,  covered  with  mucus  and  often  ulcerated,  and  besides  this 
at  times  the  secondary  appearances  of  catarrh,  a  developing  perichondritis,  etc. 
In  many  instances  the  diagnosis  is  quite  easy,  but  in  other  cases  protracted  ob- 
servation is  required.  It  may  be  difficult,  however,  at  times,  to  distinguish  it  from 
tuberculosis  or  from  syphilis.  We  may  be  aided  in  such  cases  by  a  search  for 
tvibercle  bacilli,  by  tuberculine  injections,  or  by  the  results  of  anti-syphilitic  treat- 
ment. All  the  other  organs  of  the  patient  therefore  must  always  be  carefully 
examined.  In  doubful  cases  it  is  proper  to  remove  a  bit  of  the  endolaryngeal 
growth  and  examine  it  histologically. 

Surgical  treatment  is  the  only  one  for  all  laryngeal  new  growths.  We  must 
refer  to  the  special  works  for  the  details.  Laryngologists  have  devised  numer- 
ous instruments  for  the  removal  of  benignant  polypi,  by  which,  under  the  guid- 
ance of  the  laryngoscope,  the  new  growth  is  cut,  snared,  crushed,  or  torn  off. 
The  performance  of  the  operation  is  made  much  easier  by  inducing  local  anaes- 
thesia of  the  laryngeal  mucous  membrane  by  painting  with  cocaine.  ISTever- 
theless  we  firmly  believe  that  in  all  severe  cases  the  "  endolaryngeal "  operations 
should  be  superseded  by  laryngotomy. — Carcinoma  of  the  larynx  can  be  cured  only 
through  removal  of  the  tumor  by  laryngotomy  (splitting  of  the  larynx)  or  by 
total  extirpation  of  the  larynx.  Laryngotomy  is  comparatively  free  from  danger, 
while  total  extirpation  has  met  with  permanent  success  as  yet  in  but  few  instances. 
If  surgical  interference  is  no  longer  practicable,  we  can  endeavor  merely  to  miti- 
gate the  suffering  of  the  patient  by  means  of  morphine,  cocaine,  and  other  nar- 
cotics. 


SECTION  III 

Diseases  of  the  Trachea  and  the  Bronchi 
CHAPTEE  I 

ACUTE    CATARIIH   OF   THE   TRACHEA  AND    THE   BRONCHI 

( Tracheitis  and  Actite  Catarrhal  Bronchitis) 

.ffitiology. — Acute  catarrh  of  the  larger  air-passages,  of  the  trachea,  and 
larger  bronchi,  is  a  frequent  disease,  and  it  may  often  arise  from  taking  cold.  It 
is  conceivable  that  the  inhalation  of  cold,  damp  air  sometimes  directly  affects  the 
mucous  membrane  of  the  upper  air-passages.    Bronchial  catarrh  is  very  often  asso- 


ACUTE  CATAEEH  OF  THE  TEACHEA  AXD  THE  BEOXCHI  157 

ciated  with  a  coincident  catarrh  of  the  larynx,  and  more  rarely  of  the  pharynx. 
In  the  ordinary  mild  forms  the  catarrh  is  usually  conj&ned  to  the  trachea  and  the 
first  large  branches  of  the  bronchi,  while  the  finer  bronchi  remain  healthy. 

More  intense  inflammation  of  the  bronchial  mucous  membrane  is  the  result  of 
active  mechanical  or  chemical  irritation.  A  severe  bronchitis  develops  after 
the  inhalation  of  noxious  gases,  nitrous  and  sulphurous  oxides,  chlorine,  bromine, 
etc.,  as  is  often  observed  in  operatives.  The  inhalation  of  smoke  and  dust,  espe- 
cially vegetable  dust,  works  in  the  same  injurious  fashion,  and  the  followers  of 
many  trades  and  employments,  such  as  millers,  wool-workers,  colliers,  etc.,  are 
especially  subject  to  disease  from  this  cause.  In  this  form  of  bronchitis  the 
catarrh  often  extends  to  the  finer  bronchi. 

The  bronchitis  which  develops  in  the  course  of  other  acute  and  chronic  dis- 
eases is  still  commoner  than  the  primaiy  forms  already  mentioned.  It  is  often 
due  to  infectious  causes,  such  as  certain  infectious  diseases,  especially  measles, 
whooping-cough,  and  influenza.  In  these  diseases  bronchitis  is  one  of  the  most 
constant  local  affections,  and  is  probably  dependent  immediately  upon  the  primary 
infection.  Bronchitis,  however,  develops  secondarily  in  most  of  the  other  acute 
infectious  diseases,  and  is  due  largely  to  the  inhalation  of  noxious  substances  from 
the  upper  part  of  the  air-passages.  This  is  the  explanation  of  the  bronchitis  in 
diphtheritic  processes  in  the  pharynx  and  larynx,  in  so  far  as  it  does  not  depend 
upon  a  direct  extension  of  the  disease,  and  also  of  the  bronchitis  in  small-pox, 
etc.  Bronchitis  may  also  be  met  with  in  all  other  forms  of  severe  disease,  because 
retention  of  secretion,  putrefactive  processes,  inflammation,  thrush,  etc.,  occur 
in  the  cavity  of  the  mouth  and  pharynx,  and  from  them  chemical  or  organic  irri- 
tants may  easily  be  inhaled  into  the  bronchi.  The  imperfect  expectoration  in  all 
severe  diseases  is  a  still  more  harmful  factor  than  this  inhalation.  The  secre- 
tion remains  in  the  bronchi,  processes  of  decomposition  arise  in  the  stagnating 
mucus,  bacteria  collect  and  lead  to  a  bronchitis,  and  finally  to  the  lobular  jjneu- 
monia  which  is  so  often  found  (vide  infra).  The  lessened  power  of  resisting 
injurious  influences,  produced  in  the  mucous  membrane  by  severe  bodily  disease, 
also  facilitates  the  development  of  catarrhal  inflammation.  In  all  diseases  in  which 
deglutition  is  affected  (as  in  paralysis  of  the  epiglottis  or  of  the  pharyngeal 
muscles),  and  in  all  diseases  attended  by  frequent  vomiting  or  choking  (cancer  of 
the  oesophagus,  etc.),  secondary  bronchitis  with  its  sequelae  may  ensue  from  the 
inhalation  of  small  particles  of  easily  decomposable  food. 

We  do  not  know  how  far  we  may  claim  that  infectious  agents  act  as  a  cause  of 
primary  bronchitis,  yet  it  is  not  improbable  that  many  cases  have  such  an  aeti- 
ology. It  is  especially  likely  that  many  cases  of  bronchitis  due  to  "  catching  cold  " 
really  have  something  infectious  about  them,  and  that  the  preceding  exposure  to 
cold  has  merely  lowered  the  natural  powers  of  resistance,  and  thus  permitted,  or 
at  any  rate  promoted,  infection.  This  infection  is  probably  not  due  to  any  special 
speciflc  bacteria  but  to  the  ordinary  germs  of  inflammation  (staphylococci,  etc.). 

Finally,  we  must  mention  that  acute  bronchitis  is  sometimes  merely  an  ex- 
acerbation of  a  previous  chronic  bronchitis.  We  will  return  later  to  this  impor- 
tant and  not  uncommon  process. 

The  predisposition  to  acute  bronchitis  varies  in  different  persons.  We  do  not 
know  deflnitely  on  what  ground  such  an  increased  predisposition  to  bronchial  dis- 
ease rests,  nor  why  we  meet  with  it  sometimes  in  the  weak  and  anaemic,  and  at 
other  times  in  so-called  "  full-blooded "  persons.  Bronchitis  is  more  frequent 
in  children  and  old  people  than  in  those  in  middle  life.  Most  of  the  cases  occur 
in  the  spring  and  autumn. 

Symptoms. — Pain  in  the  chest  may  be  present  in  some  cases  of  simple  catarrhal 
bronchitis,  but  usually  only  in  a  modei-ate  degree.  In  severe  tracheitis  patients 
often  have  a  painful  feeling  of  soreness  in  the  neck  and  behind  the  upper  part  of 


158  DISEASES    OF   THE   EESPIEATORY   OEGANS 

the  sternum,  and  this  is  increased  on  coughing.  The  mucous  membrane  of  the 
bronchi,  apparently,  has  no  nerve-fibers  which  are  sensitive  to  pain,  and  the  pains 
in  the  chest  which  are  often  present  in  bronchitis  are,  as  a  rule,  muscular  pains 
in  the  intei'costal  muscles,  or  the  insertion  of  the  diaphragm,  due  to  the  severe 
paroxysms  of  coughing. 

Cough  is  one  of  the  most  constant  symptoms  of  bronchitis,  and  by  it  usually 
the  attention  of  the  patient  or  of  the  physician  is  first  called  to  the  existing 
thoracic  affection.  The  cough  may  of  course  be  due  to  a  laryngitis,  if  that  is  also 
present.  There  is  no  doubt,  however,  that  a  cough  may  be  excited  in  a  reflex 
manner  from  the  mucous  membrane  of  the  trachea  and  of  the  larger  as  well  as  of 
the  finer  bronchi.  Experiments  have  shown  that  the  point  of  bifurcation  of  the 
trachea  is  especially  irritable,  and  many  severe  paroxysms  of  coughing  may  be 
due  to  an  irritation  of  this  very  spot  from  the  accumulation  of  secretion.  The 
intensity  of  the  cough,  moreover,  is  very  different  in  individual  cases,  which  is 
due  in  part  to  the  degree  and  extent  of  the  bronchitis  and  in  part  to  the  individual 
irritability  of  the  person  affected. 

The  expectoration  consists  of  the  secretion  and  exudation  from  the  inflamed 
mucous  membrane.  Its  abundance  and  consistency  vary  considerably  in  the  dif- 
ferent cases.  We  distinguish  a  catarrh  with  an  abundant  secretion  from  the  so- 
called  "  dry  catarrh."  In  the  latter  only  a  little  viscid  sputum  is  expectorated,  but 
in  the  former  the  expectoration  is  more  abundant  and  muco-purulent,  or  sero- 
mucous,  a  thin  fluid  separating  into  layers  on  standing  (vide  infra).  Very  often  in 
the  beginning  of  the  disease  the  expectoration  is  scanty  and  viscid — the  sputum 
cruclum  of  the  old  physicians;  and  later  it  becomes  more  abinidant,  more  fluid, 
and  more  purulent — the  sputum  coctum.  In  catarrh  of  the  finer  bronchi  the  ex- 
pectoration may  contain  little  tough  miicous  or  muco-purulent  casts  of  the 
bronchi.  It  may  be  stated  in  general  that  the  characteristic  of  simple  bronchitic 
sputum  is  the  mucous  admixture  in  contrast  to  the  purulent  or  sero-purulent 
sputum  from  phthisical  cavities,  etc.  We  may  readily  recognize  the  mucous  con- 
tents of  the  sputum  by  the  tenacity  with  which  it  clings  to  the  bottom  of  the 
sputum-cup  when  the  cup  is  tijiped.  A  simple  catarrhal  expectoration  shows  noth- 
ing peculiar  under  the  microscope.  The  pus-corpuscles  are  often  swollen,  and 
show  more  or  less  marked  fatty  degeneration.  A  slight  admixture  of  blood  may 
occasionally  be  present  in  severe  bronchitis,  but  it  usually  has  no  special  signifi- 
cance, being  at  times  merely  the  result  of  severe  fits  of  coughing.  A  more 
marked  and  persistent  admixtiire  of  blood  is  seen  in  the  catarrhal  sputum  of  some 
cases  of  intense  bronchitis  in  drunkards,  so  that  we  may  even  speak  of  a  "  hsemor- 
rhagic  bronchitis." 

Dyspnoea  is  ustially  entirely  absent  in  simple  mild  bronchitis,  but  marked  short- 
ness of  breath  may  be  noticed  in  extensive  catarrh  of  the  finer  bronchi. 

Physical  Examination. — We  may  obtain  direct  evidence  of  the  condition  of 
the  tracheal  mucous  membrane,  with  due  practice,  by  the  laryngoscope.  We 
see  a  reddening  of  the  membrane,  and  sometimes  an  abnormal  abundance  of 
secretion  on  it,  if  there  is  a  tracheitis.  Other  methods  of  physical  examination 
are  at  our  service  for  jvidging  of  the  changes  in  the  bronchi. 

Inspection  of  the  thorax  shows  nothing  abnoiinal  in  the  milder  forms  of  bron- 
chitis. The  respiration  is  somewhat  accelerated  and  the  expiration  prolonged  in 
severe  bronchitis,  especially  if  the  finer  bronchi  are  affected.  Percussion  in 
uncomplicated  bronchitis  shows  nothing  abnormal  in  the  pulmonary  resonance. 
In  extepsive  catarrh  of  the  finer  bronchi  an  acute  dilatation  of  the  lung  is  apt  to 
occur,  with  a  descent  of  the  lower  margin  of  the  lung.  Auscultation,  too,  shows 
nothing  unusual  in  many  cases  of  mild  catarrh  limited  to  the  trachea  and 
large  bronchi,  but  in  the  cases  in  which  the  smaller  bronchi  are  the  seat  of  the 
catarrh  and  there  is  a  marked  accumulation  of  secretion  in  them,  we  hear,  besides 


ACUTE  CATAERH  OF  THE  TRACHEA  AND  THE  BEON'CHI  159 

the  vesicular  respiration,  the  so-called  rhonchi  which  almost  wholly  hide  it.  In 
dry  bronchitis  Ave  speak  of  humming  or  buzzing  sounds  (sonorous  rhonchi)  or 
shrill,  whistling  sounds  (sibilant  rhonchi)  according  to  their  pitch.  These  sounds 
are  probably  due  to  stenosis,  and  are  caused  by  the  passage  of  the  air  through 
narrow  portions  of  the  bronchi.  The  narrowing  occurs  in  part  from  the  swelling 
of  the  mucous  membrane,  in  part  from  the  accumulation  of  secretion.  The  masses 
of  secretion  themselves,  if  they  are  set  in  vibration  at  the  same  time,  may  pos- 
sibly take  part  in  the  production  of  the  humming  noises.  If  the  amount  of  secre- 
tion collected  in  the  bronchi  is  more  abundant  and  of  a  more  fluid  consistency, 
it  gives  rise  to  "  moist  rales  "  on  the  passage  of  the  air.  These  are  distinguished 
as  "  coarse,"  "  medium,"  or  "  fine  moist  rales,"  according  as  they  occur  in  the 
larger  or  smaller  bronchi. 

Other  symptoms  of  disease  are  often  present  besides  those  already  mentioned 
as  being  due  directly  to  the  bronchitis.  The  general  health  is  usually  disturbed 
in  a  severe  bronchial  catarrh.  The  patient  does  not  feel  well,  and  has  less  appe- 
tite than  usual.  A  moderate  amount  of  fever  is  often  present,  especially  toward 
evening.  An  increase  of  temperature  above  102°  or  103°  (39°  C.)  is  rarely  seen 
except  in  children.  The  patient  sometimes  complains  of  headache,  which  is  in- 
creased by  severe  coughing.  There  can  be  a  question  of  complications  only  when 
the  inflammation  extends  to  other  parts  of  the  res^Diratory  mucous  membrane. 
Mild  bronchitis  is  often  associated  with  coryza  and  laryngitis,  while  severe  bron- 
chitis may  lead  to  catarrhal  pneumonia  {vide  infra). 

The  separate  forms  of  bronchitis  are  distinguished  chiefly  by  the  degree  of 
extension  of  the  catarrh. 

1.  The  Milder  Forms  of  Acute  Bronchitis. — In  most  cases  of  simple  primary 
bronchitis,  as  well  as  in  many  milder  attacks  of  secondary  bronchitis,  the  catarrh 
is  limited  to  the  mucous  membrane  of  the  larger  bronchi.  Exposure  to  cold  and 
other  injurious  influences  are  frequent  causes  of  the  primary  form.  The  symp- 
toms are  moderate.  The  cough,  however,  may  be  quite  troublesome.  Often  fever 
is  absent  or  but  slight.  Upon  auscultation,  particularly  over  the  lower  lobes,  but 
sometimes  over  the  entire  lungs,  are  heard  numerous  rather  coarse  wheezing  or 
rattling  sounds,  usually  with  some  symmetry  of  distribution;  but  in  many  cases, 
as  we  have  said,  there  may  be  nothing  abnormal  heard,  so  that  the  diagnosis  will 
have  to  rest  merely  upon  the  subjective  discomfort  in  the  chest,  the  cough,  and 
the  expectoration.  With  proper  care,  simple  primary  bronchitis  runs  its  course  in 
a  few  days,  or  at  the  most  in  a  few  weeks,  and  ends  in  complete  recovery.  If  the 
patient  exposes  himself  recklessly,  or  the  ^etiological  factors  continue  to  be  active, 
the  disease  may,  however,  grow  worse,  prove  to  be  veiy  tedious,  and  finally  develop 
into  chronic  bronchitis. 

2.  The  Severer  Febrile  Forms  of  Acute  Bronchitis. — Sometimes  acute  bron- 
chitis assumes  a  severer  form,  whether  because  the  influences  which  give  rise  to 
it  are  unusually  violent,  or  because  it  is  due  to  some  special  and  perhaps  infectious 
cause.  In  such  cases  the  symptoms  are  more  marked,  the  bronchial  rales  more 
abundant,  the  general  condition  of  the  patient  worse.  Not  infrequently  there  is 
fever  for  several  days,  or  even  for  one  or  two  weeks,  the  type  being  irregularly 
remittent,  but  the  temperature  is  usually  102°  or  103°  (39°  to  39.5°  C),  although 
it  may  go  higher.  The  expectoration  is  usually  muco-purulent,  but  it  often  con- 
tains much  pus;  in  other  cases  it  may  be  sero-muco-purulent.  The  amount  is 
then  greater,  and  it  forms  distinct  layers  on  standing  in  a  beaker  glass.  The 
author  has  not  infrequently  noticed  that  there  is  more  liability  in  the  severer 
forms  of  acute  bronchitis  to  have  the  disease  mainly  limited  to  one  lobe,  or  at 
least  to  one  lung,  but  we  may  have  a  severe  acute  diffuse  bronchitis  on  both  sides. 

The  aetiology  of  acute  febrile  bronchitis  has  been  but  little  studied.  Bacterio- 
logical examination  of  the  sputum  usually  gives  no  definite  results,  since  we  always 


160  DISEASES    OF   THE   EESPIRATOEY   ORGA^Tg 

find  many  micro-organisms.  Many  acute  cases  may  be  caused  by  the  ordinary  pus 
cocci.  At  the  time  of  a  pneumonia  epidemic  we  have  repeatedly  seen  cases  of 
acute  bronchitis  with  high  fever  and  herpes,  but  without  any  signs  of  pneumonic 
infiltration.  These  were  probably  due  to  pneumococcus  infection.  In  other  cases 
there  is  perhaps  an  influenza  infection. 

We  would  add  in  particular  that  many  acute  febrile  cases  of  bronchitis  prove 
on  closer  investigation  (more  careful  questioning)  to  be  acute  exacerbations  of  a 
mild  chronic  bronchitis — "  acute  recurrent  bronchitis."  The  chronic  disease  of 
the  bronchial  mucous  membrane  apparently  affords  a  favorable  opportunity  for 
new  infection.  In  other  instances  it  is  merely  an  acute  exacerbation  of  the  same 
chronic  process.  Such  an  acute  bronchitis  may  of  course  occur  repeatedly  in  the 
same  patient. 

3.  Catarrh  of  the  Finer  Bronchi— Capillary  Bronchitis.— A  simple  primary 
bronchial  catarrh  rarely  extends  to  the  finest  bronchi  in  adults.  The  secondary 
bronchitis,  however,  which  develops  in  other  severe  diseases  (vide  supra)  often 
extends  into  the  ultimate  divisions  of  the  bronchi,  and  finally  leads  to  the  forma- 
tion of  nodules  of  lobular  pneumonia — "  catarrhal  pneumonia  "  (vide  infra).  We 
recognize  the  implication  of  the  finer  bronchi  by  hearing  the  high,  shrill,  whis- 
tling rhonchi  (sibilant  rhonchi),  or  the  abundant  fine,  moist  rales.  Respiratory 
symptoms  may  be  quite  marked  in  extensive  catarrh  of  the  finer  bronchi.  Res- 
piration is  evidently  accelerated,  the  inspiration  is  of  the  costal  type  and  re- 
quires the  aid  of  the  accessory  respiratory  muscles  of  the  neck  (the  sterno- 
mastoids  and  scaleni),  and  expiration  is  usually  prolonged.  There  is  often  quite 
a  severe  cough.  The  expectoration  is  muco-purulent  and  usually  not  very 
abundant. 

Capillary  bronchitis  in  children  is  of  great  practical  importance.  Bronchitis 
in  young  children  always  has,  as  experience  tells  us,  a  tendency  to  attack  the 
smaller  bronchi.  Extensive  bronchitis  is  seen  especially  in  weak  children  who 
are  rachitic  or  predisposed  to  tuberculosis.  Children  have  a  great  tendency  to 
be  attacked  with  bronchitis  at  the  time  of  the  first  dentition. 

The  parents'  attention  is  usually  called  to  the  disease  by  the  appearance  of  a 
cough,  which  is  excited  especially  by  the  child's  crying.  Small  children  never 
expectorate,  for  they  swallow  the  secretion  which  is  coughed  up  into  the  pharynx. 
The  rapidity  of  respiration  is  verj^  striking,  it  being  increased  to  sixty  or  eighty, 
or  even  more,  in  a  minute.  The  respiration  is  also  labored,  but  it  is  usually  super- 
ficial, and  in  severe  cases  irregular.  There  is  generally  a  distinct  respiratory  play 
of  the  alse  nasi.  We  often  see  a  retraction  of  the  lower  lateral  portions  of  the 
thorax  on  inspiration  as  a  result  of  the  imperfect  entrance  of  air  into  the 
smaller  bronchi.  The  expiration  is  frequently  noisy  and  groaning  in  children. 
We  hear  extensive  fine,  moist  rales  over  the  lungs.  In  severe  cases  the  child 
becomes  restless,  anxious,  perhaps  markedly  pale  and  cyanotic,  and  finally  apa- 
thetic and  stupid.  In  such  cases,  however,  we  have  no  longer  to  deal  with  simple 
bronchitis,  but  catarrhal  pneumonia  has  already  developed.  The  disease  almost 
always  runs  its  course  with  fever,  the  temperature  rising  to  104°  (40°  C.)  and 
over.  The  pulse  is  increased  to  120  or  140  or  more  per  minute.  The  duration  of 
the  disease  is  seldom  less  than  two  or  three  weeks,  and  it  may  last  much  longer. 
Death  may  ensue,  especially  in  ill-nourished  children,  partly  as  a  result  of  general 
weakness,  and  also  directly  from  the  imperfect  respiration.  In  such  cases  we  find 
at  the  autopsy  not  only  diffuse  bronchitis,  but  also  almost  always  lobular  pneu- 
monia. In  many  cases  a  gradual  recovery  finally  takes  place  in  spite  of  the  most 
severe  symptoms. 

The  secondary  bronchitis  in  children  complicating  measles,  whooping-cough, 
diphtheria,  etc.,  has  the  same  tendency  to  involve  the  finer  bronchi  and  to  lead  to 
lobular  pneumonia. 


ACUTE  CATAERH  OF  THE  TRACHEA  AND  THE  BRONCHI  161 

In  conclusion,  we  must  mention  that  acute  bronchitis  in  old  persons  is  also  apt 
to  attack  the  finer  bronchi,  and  it  may  be  dangerous  partly  from  the  general  ex- 
haustion, partly  from  the  occurrence  of  respiratory  symptoms  and  cardiac  weak- 
ness, as  in  lobular  pneumonia. 

Diagnosis. — The  diagnosis  of  bronchitis  presents  no  special  difficulty.  It  is 
obtained  directly  by  the  discovery  of  rhonchi  on  auscultation.  If  these  fail,  we 
conclude  that  there  is  a  mild  catarrh  of  the  larger  bronchi  from  the  presence  of 
cough  and  expectoration,  if  no  cause  for  the  cough  is  to  be  found  in  an  alfection 
of  the  larynx.  The  question  is  more  difficult,  but  it  must  always  be  considered, 
whether  a  given  bronchitis  is  a  common  primary  catarrh  or  secondary  to  some 
other  affection.  This  question  naturally  can  be  decided  only  by  a  very  careful 
examination  of  the  body.  We  must  always  remember,  furthermore,  that  severe 
pulmonary  affections  may  be  at  first  quite  latent  and  show  objectively  merely  the 
signs  of  simple  bronchitis,  while  later  pneumonia,  a  tubercular  affection,  or  some- 
thing similar,  develops.  A  bronchitis  which  is  unilateral,  or  in  which  the  signs 
are  to  be  found  in  circumscribed  localities,  must  therefore  be  regarded  as  sus- 
picious. It  has  long  been  known  that  bronchitis  in  the  apices  of  the  lungs,  the 
"  apex-catarrh,"  is  often  the  first  objective  change  to  be  met  with  in  pulmonary 
phthisis.  We  can  only  conjecture,  and  not  pronounce  with  certainty  on  objective 
evidence,  whether  nodules  of  lobular  pneiunonia  are  present  or  not  in  diffuse 
bronchitis  affecting  the  finer  bronchi. 

From  what  has  been  said,  it  is  clear  that  we  should  be  cautious  in  our  prog- 
nosis regarding  cases  of  severe  bronchitis,  especially  in  children  and  old  people. 
The  prognosis  in  the  milder  forms  of  bronchitis  is  of  course  always  very  favor- 
able. 

Treatment. — The  prophylaxis  of  primary  bronchial  catarrh  consists  in  the 
removal  of  all  the  injurious  influences  mentioned  which,  as  experience  shows, 
may  give  rise  to  bronchitis.  Careful  hardening  of  the  skin  to  the  effects  of  a 
change  in  temperature  is  of  service  in  persons,  particularly  children,  who  have  a 
special  tendency  to  bronchitis,  as  we  have  already  said  in  regard  to  the  prophy- 
laxis of  laryngitis.  It  is  very  important  to  remember,  in  this  connection,  that  we 
can  also  be  successful  in  our  prophylactic  measures  against  secondary  bronchitis. 
Keeping  the  mouth  and  pharynx  clean,  urging  deep  inspirations,  and  aiding 
expectoration  by  the  timely  use  of  tepid  baths  and  shower-baths,  may  often  pre- 
vent bronchitis  or  keep  it  within  bounds,  when  it  would  surely  develop  if  the 
patient  were  neglected. 

Simple  hygienic  measures  suffice  in  the  treatment  of  mild  cases  of  acute  bron- 
chitis. The  patient  should  be  kept  warm,  should  remain  in  his  room,  or,  if  there 
be  any  fever,  in  bed.  Diaphoretic  remedies  have  long  been  praised  as  especially 
potent  in  the  treatment  of  acute  bronchial  catarrh.  The  patient,  therefore,  should 
drink  hot  tea,  pectoral  tea  *  (Brustthee),  or  elder  tea,  etc.,  or  hot  milk  mixed 
with  Seltzer,  a  remedy  whose  efficacy  is  frequently  praised  by  the  patient.  The 
tougher  the  sputum  and  the  more  difficult  expectoration,  the  more  abundantly 
should  we  give  warm  drinks  (Ems  water,  pectoral  tea,  etc.).  Local  treatment  of 
the  mucous  membrane  by  inhalations  is  usually  illusory,  for  only  the  smallest  part 
of  the  inhaled  fluid  reaches  the  bronchi.  We  may,  however,  prescribe  inhala- 
tions of  warm  steam,  or  a  one-  or  two-per-cent.  solution  of  common  salt,  especially 
with  a  dry  cough  and  a  secretion  which  is  hard  to  loosen. 

Otherwise  we  must  employ  symptomatic  treatment.  A  mustard  plaster  or  a 
cold,  wet  compress  about  the  chest  does  good  service  with  severe  subjective  tho- 

*  A  favorite  German  houseliold  remedy,  consisting  of  an  infusion  of  eiglit  parts  of  altli«>a,  tlirce 
parts  of  licorice,  one  part  of  orris-root,  four  parts  of  colt's-foot,  and  two  parts  each  of  mullein  and  anise- 
seed. — Traxs. 

11 


162  DISEASES    OF   THE   EESPIRATOEY   OEGANS 

racic  symptoms.  In  severe  cases  a  few  dry  cups  may  be  very  useful  in  adults,  but 
local  abstractions  of  blood  are  never  necessary  in  simple  bronchitis.  If  there  is 
troublesome  irritation  on  coughing,  so  as  to  disturb  the  rest  at  night,  we  may  pre- 
scribe small  doses  of  morphine,  five  to  ten  grains  of  Dover's  powder  (gramme 
0.3-0.5),  fifteen  to  twenty  drops  of  cherry-laurel  water,  codeine,  etc.  When  ex- 
pectoration is  difiicult,  we  may  use  the  so-called  expectorants — ipecac,  chloride  of 
ammonium,  apomorphine,  senega,  etc. 

We  have  already  repeatedly  mentioned  the  use  of  tepid  baths  and  shower- 
baths,  indicated  in  severe  diffuse  bronchitis  developing  secondarily  in  the  course 
of  other  acute  diseases. 

Tepid  baths  with  shower-baths,  two  or  three  times  a  day,  are  also  to  be  used  as 
a  most  powerful  remedy  in  severe  cases  of  capillary  bronchitis  in  children.  The 
baths  assist  expectoration  and  guard  against  the  possibility  of  the  development  of 
lobular  pneumonia.  Wet  packs  applied  to  the  thorax  or  over  the  whole  body  are 
serviceable.  The  child  should  be  wrapped  to  the  neck  in  a  sheet  which  has  been  pre- 
viously dipped  in  water  at  a  temperature  varying  with  the  degree  of  the  fever 
from  68°  to  77°  (16°  to  20°  E.)  and  well  wrung  out.  It  is  best  to  leave  the  arms 
free.  A  dry  woolen  blanket  may  be  wrapped  around  the  moist  sheet.  This  pro- 
cedure must  be  repeated  three  or  four  times  a  day.  As  to  other  remedies,  we  use 
the  same  as  in  adults.  With  weak  children  our  care  must  be  to  keep  up  the 
strength  by  giving  the  most  nourishing  food  possible  and  small  amounts  of  wine. 
An  emetic  is  sometimes  indicated  in  cases  with  an  abundant  accumulation  of 
mucus  in  the  bronchi,  and  is  of  good  service.  As  experience  has  shown,  we  should 
use  opiates  for  small  children  only  with  the  greatest  caution.  Senega  and  ben- 
zoin may  be  employed  as  expectorants. 

In  the  bronchitis  of  old  people  our  chief  aim  should  be  to  keep  up  and  improve 
the  patient's  strength.  We  prescribe  liquor  ammonii  anisatus,  infusion  of  senega, 
etc.,  to  aid  expectoration,  which  is  usually  difficult,  since  the  cough  is  feeble.  We 
must  keep  close  watch  on  the  condition  of  the  heart  (digitalis).  Tepid  baths 
may  be  of  advantage,  but  they  must  be  used  with  care. 


CHAPTEE   II 

CHRONIC    BRONCHITIS 

{Chronic  Bronchial  Catarrh) 

.ffitiology. — Chronic  bronchial  catarrh  may  develop  gradually  from  external 
causes,  or  in  rare  cases  it  may  follow  acute  bronchitis.  The  same  noxious  influ- 
ences which  excite  acute  bronchitis  may,  by  the  frequent  repetition  of  their 
action,  result  in  chronic  bronchitis.  The  constant  inhalation  of  dust  is  one  of 
the  commonest  causes  of  primary  chronic  bronchitis  (see  the  chapter  on  diseasec 
from  the  inhalation  of  dust).  In  maay  cases  it  is  therefore  a  definite  occupation 
disease,  and  is  seen  in  millers,  bakers,  wool-workers,  stone-cutters,  colliers,  etc. 

In  a  large  number  of  cases  severe  chronic  bronchial  catarrh  is  not  an  inde- 
pendent disease,  but  occurs  as  a  complication  or  a  result  of  other  diseased  condi- 
tions. The  combination  of  chronic  bronchitis  with  emphysema  of  the  lungs  {v'lde 
infra)  is  the  most  common.  A  large  number  of  cases  also  are  the  result  of  some 
form  of  heart  disease,  such  as  valvular  disease  or  myocarditis,  or  of  disease  of  the 
vessels,  leading  to  stasis  in  the  pulmonary  circulation,  and  finally  to  a  chronic 
catarrh  of  the  bronchi.  Chronic  bronchial  catarrh  in  renal  diseases  also  depends 
in  part  upon  circulatory  disturbances,  and  in  part  on  the  toxic  action  of  urinary 


CHKONIC   BEONCHITIS  163 

constituents  wHich  have  not  been  normally  excreted.  Finally,  we  find  a  more  or 
less  extensive  chronic  catarrh  of  the  bronchi  in  other  chronic  affections  of  the 
lungs  and  pleura,  as  in  tuberculosis  or  pleurisy. 

Chronic  bronchitis  is  seen  especially  in  adults  and  old  people,  and  more  fre- 
quently in  men,  on  account  of  their  exposure  in  the  various  trades,  than  in  women,, 
but  children  may  also  have  pronounced  cases  of  chronic  diffuse  bronchitis.  Such 
cases  may  often  be  referred  to  a  previous  acute  disease  of  the  respiratory  organs, 
especially  whooping-cough,  less  often  measles,  etc.  Such  cases  in  childhood  often 
continue  into  later  life,  and  on  careful  inquiry  we  may  trace  many  of  the  severe^ 
cases  of  chronic  bronchitis  in  adults  back  to  childhood. 

Pathological  Anatomy. — Chronic  bronchitis  is  characterized  anatomically  by 
a  persistent  and  chiefly  venous  hyper^emia  and  swelling  of  the  bronchial  mucous, 
membrane  with  increased  secretion  of  mucus  and  morbid  exudation  of  serum  and 
pus-corpuscles.  There  is  often  a  hyperplasia  of  the  mucous  membrane  with  puffi- 
ness  of  the  surface.  In  old  cases,  however,  we  finally  meet  with  an  atrophy  of 
all  the  layers  of  the  mucous  membrane.  One  of  the  most  frequent  results  of 
chronic  bronchitis  is  a  cylindrical  dilatation  of  the  middle  and  lesser  bronchi — 
bronchiectasis — especially  in  the  lower  lobes.  This  arises  gradually  from  the  loss 
of  elasticity  of  the  diseased  bronchial  walls,  and  their  diminished  resistant  pow- 
ers, as  well  as  from  the  pressure  of  the  stagnating  secretions. 

Symptoms  and  Course  of  the  Disease. — The  symptoms  which  are  due  to 
chronic  bronchitis  are  dyspnoea,  cough,  and  expectoration.  To  these  should  be 
added  the  results  of  a  physical  examination,  in  making  a  diagnosis. 

The  cough  is  of  very  different  severity  in  different  cases.  Usually  it  is  worse 
early  in  the  morning,  in  the  evening,  and  at  night,  than  in  the  daytime.  The 
amount  of  expectoration  is  also  subject  to  great  variations.  In  many  cases  there 
is  a  dry  cough  (catarrhe  sec,  vide  infra),  in  which  only  small  amounts  of  tough, 
viscid  sputum  are  expectorated.  In  other  cases  the  expectoration  is  more  abun- 
dant and  muco-purulent,  sometimes  rather  sero-purulent,  and  occasionally  thin 
and  separating  into  layers  on  standing.  In  catarrh  of  the  finer  bronchi  the  muco- 
purulent sputum  at  times  indicates  its  origin  by  partly  formed  casts.  We  may 
also  note  the  formation  of  so-called  spirals  (vide  infra,  bronchial  asthma).  Mi- 
croscopically, the  expectoration  has  no  special  characteristic  appearances,  but 
contains  only  the  usual  elements  of  sputum — pus-corpuscles  mixed  with  pavement 
epithelium,  ciliated  epithelium,  often  many  bacteria,  sometimes  needles  of  fat 
acids,  and  rarely  a  few  pointed  octahedral  crystals,  the  so-called  asthma  crystals 
(vide  infra).  Small  amounts  of  blood  may  be  seen  in  severe  chronic  bronchitis, 
especially  in  the  catarrh  of  passive  congestion,  bronchitis  with  very  severe  at- 
tacks of  coughing,  etc.,  but  they  do  not  have  any  bad  significance. 

Dyspnoea  of  moderate  or  even  severe  degree  may  be  due  solely  to  an  extensive 
catarrh  of  the  finer  bronchi  with  narrowing  of  their  lumen.  In  many  cases  in 
which  there  is  bronchitis  the  dyspnoea  is  due  chiefly  to  some  co-existing  abnormal 
condition  of  the  heart  or  lungs. 

Physical  Examination. — The  percussion  in  bronchitis  shows  no  special 
change.  At  most  the  resonance  may  be  somewhat  tympanitic  from  the  relaxa- 
tion of  the  lung-tissue,  especially  in  the  lower  and  posterior  portions  of  the  lungs, 
or,  with  an  abundant  retention  of  secretion  in  the  bronchi,  it  may  be  a  little 
diminished.  The  inspiratory  descent  of  the  lower  edge  of  the  lung  is  lessened 
when  the  entrance  of  air  is  much  impeded  by  the  contracted  or  plugged  bronchi. 
Auscultation  may  give  either  rhonchi,  whistling,  hissing,  humming,  etc.,  or  moist 
rales,  according  to  the  extent  of  the  catarrh  and  the  amount  and  consistency  of 
the  secretion.  The  sounds  are  usually  to  be  heard  over  the  whole  lung,  or  espe- 
cially over  the  lower  lobes,  because  here  the  catarrh  is  usually  most  marked,  and 
retention  of  secretion  is  most  apt  to  occur.     The  respiratory  murmur  in  some 


164  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

places  may  be  quite  obscured  by  the  rales.  Otherwise  it  is  vesicular,  sometimes 
exaggerated,  sometimes  rough  and  indefinite.  Expiration  is  usually  prolonged, 
because  the  exit  of  air  from  the  alveoli  is  much  hindered  by  the  narrowed  bron- 
chioles. The  respiratory  murmur  may  be  much  diminished,  or  even  entirely  sup- 
pressed in  places  where  the  bronchi  are  stopped  by  secretion,  which  happens  most 
frequently  in  the  lower  lobes. 

Except  in  mild  eases,  we  usually  distinguish  several  different  forms  of  chronic 
bronchial  catarrh,  which  may  run  into  one  another. 

1.  The  dry  chronic  catarrh  (catarrhe  sec  of  Laennec)  is  the  form  in  which  the 
mucous  membrane  has  only  a  slight  secretion.  The  cough  is  usually  very  trou- 
blesome and  labored,  but  the  patient  raises  merely  a  little  tough  sputum,  or  none 
at  all.  On  auscultation  we  hear  sibilant  rhonchi,  but  no  moist  rales.  This  form 
of  catarrh  is  usually  associated  with  pulmonary  emphysema,  and  asthmatic  at- 
tacks are  also  frequent.     The  disease  is  stubborn,  and  usually  lasts  for  years. 

2.  The  so-called  bronchial  blennorrhcea  is  that  form  of  chronic  bronchitis  in 
which  we  find  a  very  copious  sero-purulent  exudation  on  the  surface  of  the  mucous 
membrane.  The  cough  is  therefore  associated  with  a  very  abundant  and  quite 
thin  expectoration,  the  amount  of  which  in  the  twenty-four  hours  may  exceed  a 
pint  (half  a  litre).  The  expectoration  runs  together  in  the  sputa-cup  and  usually 
separates  on  standing,  the  more  purulent  portion  sinking  to  the  bottom,  and  the 
sero-mucous  portion,  which  is  usually  frothy  on  the  surface,  remaining  at  the  top. 
ISTumerous  moist  rales  are  heard  in  the  lungs,  especially  in  the  lower  portions. 
These  diminish  if  large  amounts  of  sputum  are  coughed  up.  Anatomically,  the 
bronchi  are  almost  always  found  dilated  in  this  form  of  chronic  bronchitis. 

3.  The  so-called  serous  bronchorrhcea  ("  catarrhe  pituiteux  "  of  Laennec)  is 
quite  rare  but  very  interesting.  It  is  characterized  by  the  expectoration  of  a  very 
large  amount  of  frothy,  almost  purely  serous,  or  sero-mucous,  thin  sputum  con- 
taining only  a  slight  admixture  of  pus.  The  cough  usually  comes  on  in  very  vio- 
lent paroxysms  which  last  from  half  an  hour  to  an  hour  or  more.  The  respiratory 
symptoms  are  quite  severe,  especially  during  these  attacks,  and  have  given  rise 
to  the  old  and  useful  term  "  asthma  humidum."  The  expectoration  collected  in 
twenty-foiir  hours  may  amount  to  one  or  two  quarts  (litres).  Examination  of 
the  lungs  usually  reveals  very  abundant  and  extensive  moist  rales.  The  reso- 
nance on  percussion  is  normal  or  a  little  diminished,  from  the  accumulation  of 
secretion. 

The  special  cause  of  this  peculiar  disease  is  quite  obscure.  There  are  mild 
afebrile  and  also  very  severe  forms  of  this  type  of  chronic  bronchitis.  We  have 
seen  several  chronic  cases,  which  were  attended  with  persistent  fever,  and  which 
led  to  great  emaciation  and  weakness.  In  one  case  which  came  to  autopsy  there 
was  found  a  marked  tuberculosis  of  the  retro-bronchial  lymph-glands,  while  the 
lungs  themselves  showed  hardly  any  striking  changes.  One  vagus  nerve  was 
wholly  imbedded  in  the  tubercular  mass  of  the  glands,  and  it  is  not  impossible  that 
the  peculiar  attacks  of  serous  expectoration  were  due  to  irritation  of  this  nerve. 
At  any  rate,  we  should  consider  the  possibility  of  such  conditions  in  the  future. 
It  is  worthy  of  note  that  attacks  of  "  humid  asthma,"  with  expectoration  of  large 
amounts  of  serous  sputum,  have  also  been  observed  in  chronic  nephritis,  espe- 
cially in  contracted  kidney  (q.  v.). 

Course  of  the  Disease. — The  course  of  most  chronic  bronchial  catarrhs  is  very 
protracted.  The  disease  usually  has  frequent  remissions  and  fresh  exacerbations. 
The  patient  is  tolerably  well  in  the  pleasanter  time  of  the  year  if  he  takes  good 
care  of  himself,  but  in  autumn  and  winter,  or  after  exposure  to  various  noxious 
influences,  the  catarrh  grows  worse  and  the  patient's  symptoms  increase.  If  the 
disease  has  lasted  for  years,  we  usually  find  symptoms  in  the  lungs,  such  as  emphy- 
sema or  chronic  tuberculosis,  or  in  the  heart,  such  as  secondaiy  dilatation  and 


CHKONIC   BEONCHITIS  105 

hypertrophy  of  the  right  ventricle,  which  symptoms  gradually  become  more  se- 
vere.    The  details  of  these  conditions  are  to  be  found  in  the  appropriate  sections. 

Diagnosis. — The  diagnosis  of  chronic  bronchitis  is  not  difficult  in  itself,  and 
may  easily  be  made  by  considering  the  patient's  symptoms  and  by  judging  of  the 
result  of  the  physical  examination.  We  must  always  consider,  however,  whether 
the  bronchitis  is  actually  a  primary  disease  or  a  result  or  a  complication  of  some 
other  chronic  disease.  Therefore,  in  every  case  of  chronic  bronchitis,  the  heart 
and  the  kidneys  (urine)  must  be  carefully  examined,  as  well  as  the  lungs. 

Prognosis. — Chronic  bronchitis  is  in  most  cases  a  very  stubborn  affection, 
which  frequently,  as  we  have  said,  shows  improvement,  but  from  which  complete 
recovery  is  rare.  The  prognosis  also  depends  greatly  upon  the  patient's  circum- 
stances, and  upon  the  possibility  of  his  taking  care  of  himself  and  avoiding  all 
harmful  exposure.  In  secondary  bronchitis  the  question  whether  the  bronchitis 
is  capable  of  material  improvement  or  not  of  course  depends  mainly  upon  the 
prognosis  of  the  primary  disease. 

The  danger  in  primary  chronic  bronchitis  comes  from  the  final  development 
of  its  sequelse,  especially  from  the  gradual  appearance  of  pulmonary  emphysema, 
dilatation  of  the  heart,  secondary  tuberculosis,  etc. 

Treatment. — The  only  hope  of  success  in  severe  cases  in  any  method  of  treat- 
ing chronic  bronchitis  lies  in  removing  the  patient  completely,  at  least  for  a  time, 
from  the  action  of  injurious  influences.  The  favorable  result  of  the  baths  and 
health  resorts  that  are  employed  depends  largely  upon  this,  that  patients  enjoy  in 
them  complete  bodily  rest,  and  are  far  better  protected  from  dust  and  the  changes 
in  the  weather  than  at  home.  We  must  make  the  patient  comprehend  the  neces- 
sity of  this  condition  as  the  basis  of  any  treatment.  If  he  can  not  go  to  a  suit- 
able climate  during  the  cold  season,  he  must  keep  his  room  in  all  unpleasant 
weather,  but  at  other  times  he  may  be  permitted  to  stay  in  the  open  air.  Further- 
more, the  patient  must  be  warned  to  avoid  as  completely  as  possible  those  harm- 
ful influences  which  his  calling  and  manner  of  life  entail,  and  among  which 
especially  to  be  mentioned  is  the  bad  air  in  our  inns  and  restaurants.  Food  should 
be  easily  digestible,  and,  in  persons  inclined  to  corpulence,  sparingly  taken.  Alco- 
hol is  to  be  permitted  only  in  a  moderate  degree.  We  combat  the  tendency  to  con- 
stipation, which  is  often  present,  by  dietetic  remedies,  by  taking  fruit,  especially 
grapes,  prunes,  etc.,  honey,  Graham  bread,  or  by  mild  laxatives,  such  as  the  bitter 
waters,  Friedrichshall,  Ofner,  etc.,  since  any  persistent  constipation  aggravates  the 
patient's  symptoms. 

If  the  circumstances  of  the  patient  permit  and  his  condition  requires  it,  we 
should  send  him  south  in  the  autumn  in  order  to  avoid  the  evils  of  a  northern 
winter,  but  we  must  always  consider  whether  the  patient  has  the  strength  to  bear 
the  burden  and  unavoidable  discomfort  of  such  a  journey  without  permanent 
harm.  The  rule  is  to  send  patients  with  a  bronchial  catarrh  when  there  is  much 
secretion  to  health-resorts  with  a  dry  climate — for  example,  to  the  western  Ri- 
viera, San  Remo,  Bordighera,  Mentone,  etc.  The  somewhat  dry  yet  cooler  cli- 
mate of  Meran,  Gries,  or  Arco  is  suitable  for  patients  with  a  stronger  constitu- 
tion. Patients  with  dry  bronchitis  usually  find  themselves  at  their  best  in  a 
warm  but  not  too  dry  climate.  If  we  wish  to  be  sure  of  avoiding  the  winter's 
cold,  we  must  choose  Sicily,  Egypt,  or  Madeira  for  a  residence.  Of  the  more 
northern  winter  resorts  we  may  mention  places  on  the  eastern  Riviera,  especially 
Nervi. 

We  must  recommend,  in  bronchitis,  a  suitable  summer  residence,  particularly 
for  those  who  dwell  in  large  and  dusty  cities.  Any  private  country  house  in  a 
well-wooded  and  protected  place  is  suitable.  If  we  wish  to  send  patients  to  a  bath, 
Marienbad,  Kissingen,  or  Homburg  are  proper  places  for  corpulent  people  Avho 
also  suffer  from  digestive  disturbances,  while  we  may  send  weaker  patients  to 


166 


DISEASES    OF   THE   EESPIRATOET   OEGANS 


Ems,  Soden,  Badenweiler,  Ischl,  Eeiclienhall,  etc.     A  summer  residence  on  the 
sea,  best  on  the  Baltic,  is  very  serviceable  for  many  patients. 

The  inhalation  treatment  is  much  employed  in  chronic  bronchitis,  but  we 
should  not  cherish  too  high  hopes  about  its  use.  The  best  inhalations  in  dry 
catarrhs  are  simple  steam,  a  one-  or  two-per-cent.  solution  of  common  salt  or 
bicarbonate  of  sodium.  Ems  water,  etc.  In  cases  with  marked  secretion,  inhala- 
tions of  oil  of  turpentine  are  most  to  be  praised.  The  simplest  way  is  to  pour  a 
teaspoonful  of  oil  of  turpentine  into  hot  water  and  inhale  the  vapor  as  it  arises. 
The  so-called  turpentine-pipe,  however,  is  more  convenient  and  more  efficacious 
(Fig.  23).     This  consists  of  a  flask,  which  is  filled  to  the  height  of  several  inches 

with  water  and  then  with  a  layer  of  oil  of  tur- 
pentine or  of  oleum  pini  pumilionis  (P.  G.), 
some  two  centimetres  thick.  Two  glass  tubes, 
open  at  both  ends,  are  passed  through  the  cork. 
One,  straight,  tube  extends  down  into  the  layer 
of  water  :  the  lower  end  of  the  other  is  free  in 
the  upper  part  of  the  flask.  The  outer  portion 
of  this  last  tube  is  bent  at  an  angle  and  is  con- 
nected with  the  mouthpiece  through  which  the 
patient  inhales.  The  formation  of  turpentine 
vapor  is  aided  by  putting  the  flask  in  hot 
water.  We  have  treated  many  patients  in  this 
way,  who,  for  a  number  of  hours  a  day, 
"  smoked  "  their  turpentine-pipes. 

In   treating   chronic   bronchitis    the   pneu- 
matic method  was  considerably  employed  for  a 
time;  that  is,  the  patient  was  made  to  breathe 
artificially  compressed  air,  or  to  expire  into  air 
of  less  than  the  atmospheric  pressure,  by  means 
of    a   movable    pneumatic    apparatus,    as   pro- 
posed   by   Waldenburg   and   others.     Of   late, 
however,    this    method    of    treatment    has    re- 
ceived less  favor,  inasmuch  as   actual  results 
have  fallen  decidedly  short  of  the  benefit  promised.     In  Eras,  Eeichenhall,  and 
other  places  special  pneumatic  cabinets  have  been  arranged,  filled  with  compressed 
air,  in  which  patients  remain  for  varying  lengths  of  time. 

One  of  the  most  serviceable  remedies  in  dry  chronic  bronchitis  is  a  large 
amount  of  warm  drink  (pectoral  tea.  Ems  water,  Seltzer,  etc.).  Iodide  of  potas- 
sium in  small  doses  (gr.  iij-v,  grm.  0.2-0.3,  thrice  daily)  often  acts  favorably  in 
making  a  tough  secretion  fluid.  Of  expectorants,  ipecac  and  apomorphine  are 
most  recommended  in  this  form  of  bronchitis.  For  distressing  cough  we  may 
give  Dover's  powder,  morphine,  or  codeine.  In  bronchial  blennorrhoea  we  know 
empirically  that  the  internal  use  of  balsams  causes  a  distinct  diminution  of  the 
secretion.  Oil  of  turpentine  is  the  most  active,  and  may  be  given  internally  in 
gelatine  capsules,  or  mixed  with  milk,  in  doses  of  ten  or  fifteen  drops  three  or 
four  times  a  day.  After  each  dose  of  turpentine  we  should  give  a  glass  of 
milk.  Lepine,  G.  Seej  and  other  French  physicians  recommend  terpine  as  still 
more  effectual.  This  is  a  derivative  of  turpentine,  and  is  best  employed  in  pills 
containing  a  grain  and  a  half  (gramme  0.1),  of  which  two  or  even  more  are  to 
be  taken  three  times  a  day.  It  may  also  be  given  in  solution  as  follows :  Terpine, 
2^  drachms  (grm.  10)  ;  alcohol,  q.  s.  ad  sol.  f aciendam ;  aq.  dest.,  6  ounces,  6 
drachms  (200  grm).  Misce.  Sig:  Two  or  three  tablespoonfuls  daily.  Myrtol, 
balsam  of  copaiba,  and  balsam  of  Peru  are  also  used  internally.  The  chief  ex- 
pectorants are  infusion  of  senega  root,  liquor  ammonii  anisatus,  etc.     We  should 


Turpentine-pipe. 


FCETID   BEO:NrCHITIS  167 

be  very  sparing  of  narcotics  at  first,  but  in  severe  cases  "we  can  not  wholly  dis- 
pense "with  them. 

[The  iodide  of  potassium  in  doses  of  five  to  ten  grains  thrice  daily  is  sometimes 
distinctly  curative.  An  out-door  life,  free  diet,  moderate  alcoholic  stimulus, 
tonics,  and  woolen  clothing  do  much  to  promote  recovery.] 

Local  applications  to  the  chest  in  the  form  of  embrocations,  mustard  plasters, 
dry  cups,  or  cool  or  warm  wet  compresses  are  to  be  used,  especially  with  severe 
dj^spnoea,  or  with  pain  and  a  feeling  of  oppression  in  the  chest.  Warm  baths  are 
very  well  borne  by  many  patients  with  chronic  bronchitis.  Sometimes,  too,  vapor 
baths,  if  taken  with  caution,  may  be  of  service,  especially  in  strong  and  corpu- 
lent patients.     In  dry  chronic  bronchitis  we  often  give  the  patient  a  sweat  in  bed. 

In  all  secondary  chronic  catarrhs  our  chief  attention,  beyond  the  symptomatic 
treatment  of  the  bronchitis,  must  be  directed  to  the  treatment  of  the  underlying 
disease.  If  we  succeed  in  once  more  regulating  the  heart's  action  by  digitalis 
when  there  is  uncompensated  heart  disease,  or  in  establishing  diuresis  when 
there  is  renal  disease,  or  in  improving  the  general  physical  condition  by  proper 
dietetic  measures  in  the  corpulent,  gouty,  alcoholic,  etc.,  we  may  also  in  that  way 
cause  improvement  in  the  existing  bronchial  catarrh. 


CHAPTER  ni 

rCETID    BRONCHITIS 

[Putrid  BroncJcitis) 

.31tiology. — By  putrid  or  foetid  bronchitis  we  mean  that  form  of  bronchitis  in 
which  the  secretion  of  the  mucous  membrane  undergoes  a  putrid  decomposition, 
and  in  which,  consequently,  the  expectoration  takes  on  a  peculiar  and  extremely 
foul  odor.     The  special  agents  which  cause  foetid  bronchitis  are  still  unknown. 

The  opportunity  for  the  agents  of  putrefaction  to  enter  the  bronchi  with  the 
inspired  air  is  of  course  often  given,  but  a  foetid  bronchitis  naturally  is  excited 
only  when  they  can  remain  there  and  increase.  Foetid  bronchitis  therefore  de- 
velops quite  rarely  in  a  previously  healthy  lung  (primary  foetid  bronchitis).  The 
retention  and  the  further  development  of  the  bacteria  of  putrefaction  are  chiefly 
favored,  as  we  know,  by  diseased  conditions  which  already  exist  in  the  bronchi.  A 
great  number  of  cases  of  foetid  bronchial  catarrh  therefore  develop  secondarily 
upon  other  pulmonary  affections  of  longer  standing.  Thus  the  expectoration  may 
quite  suddenly  change  and  take  on  a  foetid  character  in  the  course  of  a  chronic 
or  rarely  of  an  acute  bronchitis  or  of  phthisis.  Bronchiectasis  {vide  infra)  great- 
ly favors  the  development  of  this  putrid  change,  for  in  it  the  retention  and  stag- 
nation of  large  amounts  of  secretion  promote  and  occasion  the  putrid  decom- 
position. If  a  putrid  decomposition  of  the  secretion  begins  in  one  part  of  the 
bronchial  system,  the  further  extension  of  the  process  follows  from  direct  infection. 

In  rare  cases  putrid  bronchitis  also  develops  as  a  result  of  an  embolic  pulmo- 
nary gangrene. 

Symptoms  and  Course ;  Anatomical  Changes. — If  a  foetid  bronchitis  arises  in 
the  course  of  some  other  chronic  pulmonary  disease,  its  appearance  may  be  marked 
by  a  sudden  impairment  of  the  general  condition,  by  high  fever,  often  associated 
with  numerous  chills,  and  by  an  increase  of  the  thoracic  symptoms,  such  as  pain 
and  cough.  The  change  in  the  expectoration,  the  peculiarity  of  which  was  first 
accurately  described  by  Traube,  is  characteristic.  The  expectoration  shows  the 
same  character  in  cases  of  apparently  primary  foetid  bronchitis. 


168  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

The  sputum  has  a  very  repulsive,  sweetish,  putrid  smell.  The  expectoration  is 
usually  quite  abundant;  the  consistency  is  rather  thin.  On  standing,  the  sputum 
shows  a  very  marked  division  into  three  layers.  This  division  is  due  to  the  abun- 
dant serous  exudation  in  the  bronchial  mucous  membrane  and  to  the  thin  fluid 
character  of  the  expectoration,  Avhich  permits  an  unequal  division  and  a  settling 
of  the  solid  constituents.  The  upper  layer  consists  of  a  very  frothy,  muco-puru- 
lent  stratum,  consisting  in  part  of  individual  masses,  from  which  a  number  of 
coarser  or  finer  fibers  float  down  into  the  middle  layer.  This  middle  layer  con- 
sists of  a  dirty-green  muco-serous  fluid.  At  the  bottom  of  the  vessel  is  found  the 
third  layer,  which  is  often  the  thickest,  and  is  composed  entirely  of  pus.  It  con- 
sists of  pus-corpuscles  which  have  sunk  to  the  bottom,  and  is  of  a  rather  thin, 
greasy  consistency.  With  the  naked  eye  we  generally  recognize  a  number  of 
little  whitish-gray  plugs  and  particles  in  it.  These  so-called  "  Dittrich's  plugs," 
which  are  easily  crushed  under  a  cover-glass,  are  quite  characteristic.  Microscop- 
ically, they  consist  of  decomposed  pus-corpuscles,  detritus,  and  bacteria,  and 
usually  contain  very  many  needles  of  fat  acids  arranged  in  bundles  (see  Fig.  24). 

We  often  find  also  in  the  sputum  large  masses  of 
fungi,  especially  great  bunches  of  twisted  lepto- 
thrix  fibers,  which,  by  an  unpracticed  eye,  may 
readily  be  mistaken  for  elastic  fibers.  The  latter 
are,  of  course,  never  found  in  the  expectoration 
of  a  simple  foetid  bronchitis,  but  only  in  the 
deep-seated,  destructive  processes  in  the  lung, 
like  gangrene.  On  chemical  examination  of  the 
sputum,  the  ordinary  products  of  putrefaction 
may  be  found — volatile  fat  acids,  especially 
butyric  and  valerianic  acids,  also  sulphuretted 
hydrogen,  leucine,  tyrosine,  etc. 
Fig.  24.— Crystals  of  fat  acids.  j^   jg   ^.^^.j   characteristic    of   many   cases    of 

foetid  bronchitis  that  the  sputum  does  not  have  a 
putrid  character  at  all  times.  Sometimes  for  days  the  patient  coughs  up  a  simple 
catarrhal  secretion,  and  then  all  at  once  comes  an  outburst  of  intolerable  stinking 
expectoration.  This  is  probably  because  a  circumscribed  putrid  focus  is  fre- 
quently shut  off,  the  expectoration  coming  solely  from  the  other  bronchi,  where 
there  is  merely  a  simple  catarrh,  until  finally  the  accumulation  of  putrid  secretion 
is  all  at  once  coughed  up  again  in  large  amount  by  mouthfuls. 

When  foetid  sputum  is  coughed  up,  the  patient's  breath  also  becomes  very  foul- 
smelling,  so  that  he  often  becomes  a  burden  to  his  associates. 

The  signs  which  foetid  bronchitis  gives  on  physical  examination  are  those  of 
an  ordinary  bronchitis ;  but  it  is  characteristic  of  many  cases,  in  distinction  from 
ordinary  chronic  bronchitis,  that  the  physical  signs  (rales,  dry  rhonchi)  are 
limited  chiefly  to  a  definite  portion  of  the  lung,  usually  one  lower  lobe.  In  a 
great  number  of  cases  we  also  find  signs  of  consolidation  and  contraction  of  the 
lung,  of  pleurisy,  etc.,  which  do  not  belong  to  foetid  bronchitis  as  such,  but  are 
due  to  complications  or  sequelse. 

The  most  frequent  of  these  sequelse  is  the  development  of  a  "  reactive  "  lobular 
inflammation,  a  geniiine  pneumonia,  which  follows  a  catarrh  of  the  finer  bronchi. 
These  pneumonias  frequently  run  into  gangrene,  so  that  Ave  very  often  find  a 
number  of  larger  or  smaller  nodules  of  gangrene  besides  the  extensive  foetid  bron- 
chitis in  the  lungs.  In  many  of  these  cases  the  foetid  bronchitis  is  certainly 
the  primary  process,  and  the  development  of  the  nodules  of  gangrene  is  sec- 
ondary; yet  we  shall  see  later  that  the  reverse  may  also  be  true.  Foetid  bron- 
chitis and  gangrene  of  the  lungs  run  into  each  other  so  often,  both  clinically  and 
anatomically,  that  there  is  no  sharp  line  to  be  drawn  between  them.     If  the 


FCETID   BR0:N^CHITIS  169 

nodules  are  superficial,  and  reach  the  pleura,  the  infection  attacks  this,  and  we 
have  a  purulent  or  even  an  ichorous  pleurisy. 

The  smaller  and  medium-sized  bronchi  are  almost  always  found  in  a  condition 
of  cylindrical  dilatation  in  old  foetid  bronchitis.  Their  mucous  membrane  is  in- 
tensely inflamed,  and  often  ulcerated  superficially.  On  its  surface  we  see  in  the 
cadaver  the  greasy  purulent  masses  and  the  plugs  which  we  find  in  the  expectora- 
tion during  life. 

Whatever  may  be  the  case  with  the  general  course  of  foetid  bronchitis,  its 
beginning  is  often  quite  sudden  and  acute,  both  in  the  primary  and  in  the  second- 
ary forms,  as  we  have  said.  The  patient  is  attacked  with  fever,  which  may  often 
be  quite  high,  and  with  a  stitch  in  the  side,  cough,  and  expectoration.  Later, 
the  characteristic  peculiarities  described  above  appear.  The  further  course  of  the 
disease  is  almost  always  chronic,  lasting  for  years,  but  subject  to  many  variations. 
Very  often  manifest  improvement,  and  even  apparent  recoveiy,  takes  place,  when 
suddenly  there  is  a  new  attack  of  fever  and  thoracic  symptoms.  The  general 
condition  and  nutrition  of  the  patient  may  be  quite  good  for  a  long  time, 
except  during  the  periods  of  marked  exacerbation  of  the  disease.  Patients  with 
chronic  foetid  bronchitis  often  appear  somewhat  bloated,  but  also  pale  and  slightly 
cyanotic.  Peculiar  clubbed  thickenings  of  the  terminal  phalanges  of  the  fingers, 
or  more  rarely  of  the  toes,  gradually  develop,  as  in  many  cases  of  bronchiectasis. 
Slight  oedema  of  the  lower  extremities  is  also  sometimes  present. 

Symptoms  referable  to  other  organs  may  be  wholly  absent.  We  see  most  fre- 
quently disturbances  of  the  stomach,  loss  of  appetite,  and  nausea,  which  proba- 
bly comes  from  swallowing  the  foetid  sputum.  Patients  also  complain  of  occa- 
sional rheumatic  pains  in  the  muscles  and  joints,  which  are  probably  due  to  an 
absorption  of  septic  matter.  In  conclusion  it  must  be  mentioned  that,  in  fortu- 
nately rare  cases  of  foetid  pulmonary  disease,  pyogenic  germs  reach  the  brain  by 
metastasis,  and  give  rise  to  purulent  meningitis  or  cerebral  abscess. 

The  danger  of  the  disease,  apart  from  the  exceptional  occurrence  just  men- 
tioned, lies  in  the  possible  extension  of  the  process  to  the  lungs  and  the  develop- 
ment of  pulmonary  gangrene  and  its  sequelae.  We  hardly  ever  find  a  simple  fcetid 
bronchitis  in  the  cadaver,  but  we  almost  always  see  other  processes  besides,  which 
have  been  mentioned  above — reactive  pneumonia,  pulmonary  gangrene,  pleurisy, 
etc.  All  these  processes  develop  very  readily,  and  make  rapid  progress  in  old, 
decrepit  persons,  who  live  under  bad  hygienic  conditions,  in  whom  putrid  processes 
in  the  lungs  are  frequent. 

The  diagnosis  of  foetid  bronchitis  is  not  difficult  in  itself,  for  the  diagnosis  of 
a  putrid  process  in  the  lung  may  be  made  from  the  stinking  sputum  alone.  It  may 
be  difficult  to  decide  whether  we  have  to  do  merely  with  a  foetid  bronchitis,  or 
with  a  pulmonary  gangrene  also.  Decisive  indications  of  pulmonary  gangrene  are 
derived  from  physical  examination — dullness,  bronchial  respii'ation,  and  coarse, 
moist  rales,  signs  of  a  cavity — and  also  the  discovery  of  elastic  fibers  and  frag- 
ments of  parenchyma  in  the  expectoration. 

The  prognosis  must  be  made  with  care  in  every  case  of  foetid  bronchitis.  If 
the  external  circumstances  of  the  patient  are  favorable,  he  may  remain  in  toler- 
able health  for  years.  We  must  always  be  prepared  for  the  appearance  of  new 
exacerbations  of  the  disease  and  of  affections  of  the  lung  itself,  and  must  also 
bear  in  mind  the  rarer  scqueke  (empyema,  abscess  of  the  brain). 

Treatment. — The  chief  aini  of  treatment  must  be  to  bring  the  putrid  pro- 
cesses in  the  bronchi  to  a  stand-still  by  the  death  of  the  agents  of  putrefaction. 
The  difficulty  of  fulfilling  this  task  lies  in  the  impossibility  of  getting  the  disin- 
fecting material  to  act  on  the  bronchial  mucous  membrane  in  the  necessary 
amount  and  concentration.  Xevertheless,  we  can,  without  doubt,  at  least  relieve  a 
foetid  bronchitis  and  keep  it  in  check  by  the  judicious  use  of  inhalations.    Inhala- 


170  DISEASES    OF   THE   EESPIEATOET   OKGAIs^S 

tions  of  a  two-per-cent.  solution  of  carbolic  acid  are  most  useful,  given  for  five 
or  ten  minutes  several  times  a  day.  These,  however,  are  sometimes  not  well  borne 
if  long  continued,  and  they  may  excite  mild  symptoms  of  carbolic  poisoning — such 
as  headache,  malaise,  and  dark  carbolic  urine.  We  have  often  used  with  good  re- 
sults the  "  carbolic  mask "  recommended  by  Curschmann,  a  kind  of  respirator 
fastened  in  front  of  the  nose  and  mouth,  containing  cotton  in  a  special  receptacle 
impregnated  with  carbolic  acid,  equal  parts  of  carbolic  acid  and  alcohol,  or  other 
remedies  such  as  turpentine  or  creasote.  Many  patients  can  wear  these  masks, 
with  occasional  interruptions,  for  many  hours  a  day.  Besides  carbolic  acid  we 
may  use  inhalations  of  turpentine  (turpentine-pipe  or  vapor),  oleum  pini  pumil- 
ionis,  creasote,  etc.  The  internal  use  of  these  and  similar  remedies  also  seems  fre- 
quently to  be  of  service  in  putrid  bronchitis.  We  recommend  especially  the  in- 
ternal use  of  turpentine  (in  gelatine  capsules),  myrtol  (also  in  gelatine  capsules), 
also  terpine  hydrate  (six  to  ten  two-grain  [gramme  0.1]  pills  a  day),  creasote,  etc. 
In  other  respects  all  the  general  hygienic  and  symptomatic  methods  of  treat- 
ment recommended  for  common  chronic  bronchitis  (expectorants,  narcotics., 
climatic  health  resorts,  etc.)  are  also  useful  in  foetid  bronchitis.  The  sputum 
should  be  disinfected  by  putting  strong  carbolic  acid,  etc.,  into  the  sputum-cup  to 
lessen  the  bad  odor.  It  is  a  very  good  plan  to  keep  the  carbolic  spray  at  work  in 
the  patient's  room  as  often  and  as  long  as  possible ;  or  the  air  may  be  impregnated 
with  oleum  pini  pumilionis. 


CHAPTEE  IV 

CBOUPOTJS   BRONCHITIS 

{Fibrinous  or  Fseudo-membranous  Bronchiti&) 

Croupous  bronchitis  is  a  peculiar  form  of  disease  of  the  bronchial  mucous 
membrane,  of  very  rare  occurrence,  in  which  there  is  a  formation  of  extensive 
fibrinous  patches  in  the  bronchi.  Only  that  form  of  croupous  bronchitis  which 
occurs  primarily  in  the  bronchi  is  to  be  considered  here,  and  not  the  secondary 
form,  which  on  the  one  side  is  associated  with  diphtheria  in  the  pharynx  and 
larynx,  and  on  the  other  with  croupous  pneumonia. 

The  aetiology  of  the  disease  is  as  yet  wholly  unknown.  From  analogy  with 
other  well-known  croupous  inflammations  of  mucous  membranes,  we  must  look 
here  for  some  noxious  influence  which  destroys  the  epithelium,  but  up  to  this  time 
we  are  entirely  ignorant  of  its  character.  Individuals  in  youth  and  middle  age, 
somewhere  between  ten  and  thirty  years  old,  are  the  chief  victims.  Men  are 
attacked  somewhat  more  frequently  than  women.  The  disease  comes  on  either  in 
persons  who  were  previously  healthy — the  essential  fibrinous  or  croupous  bron- 
chitis— or  in  those  who  have  already  suffered  from  some  other  disease,  especially 
some  chronic  pulmonary  affection — the  symptomatic,  secondary  croupous  bron- 
chitis. It  is  not  certain  whether  the  last-named  cases  have  the  same  astiological 
relations  as  the  cases  of  genuine  primary  fibrinous  bronchitis.  Fibrinous  bron- 
chitis has  been  observed  in  the  course  of  typhoid  fever  and  other  acute  infectious 
diseases. 

Symptoms  and  Course. — Primary  fibrinous  bronchitis  occurs  in  two  forms, 
acute  and  chronic.  The  acute  form  begins  quite  suddenly,  with  fever,  cough,  pain 
in  the  chest,  and  as  a  rule  severe  dyspnoea.  The  fibrinous  coagula,  which  alone 
render  the  diagnosis  possible,  appear  in  the  expectoration  either  at  once,  or  after 
the  existence  for  some  days  of  what  is  apparently  simple  catarrhal  bronchitis. 

These  coagula  form  complete  casts  of  the  bronchi,  and  are  more  or  less  branch- 


CEOUPOUS   BEOXCHITIS  171 

ing.  They  are  of  a  whitish  color  and  of  quite  a  dense,  elastic  consistency.  The 
main  stem  may  be  a  centimetre  thick,  and  from  it  the  further  ramifications  extend, 
dividing  dichotomously.  The  largest  casts  are  ten  or  fifteen  centimetres  long. 
On  section,  we  usually  find  a  free  lumen  within,  and  generally  recognize  a  definite 
laminated  structure  in  the  membrane.  In  many  places  they  are  enlarged  and 
swollen.  Microscopically,  we  find  white  blood-corpuscles  in  and  upon  the  hyaline 
ground-substance  of  the  casts,  and  also  red  blood-corpuscles,  sometimes  epithelial 
cells,  and  quite  often  the  peculiar  pointed  octahedral  crystals  which  are  also  found 
in  the  expectoration  in  bronchial  asthma  {vide  infra).  The  so-called  "spirals" 
(vide  infra)  have  also  been  found  in  the  expectoration  of  fibrinous  bronchitis. 
Chemically  the  casts  apparently  consist  of  coagulated  albumen.  It  is  doubtful 
whether  they  actually  consist  of  fibrine.  Weigert's  fibrine  stain  does  not  affect 
them.  Their  solubility  in  alkalies,  especially  in  lime-water,  is  of  therapeutic 
importance. 

On  coughing,  the  patient  usually  raises  a  simple  mucous  or  muco-purulent  ex- 
pectoration besides  the  casts,  and  in  this  sputum  the  casts  are  imbedded.  They 
are  often  first  discovered  by  pouring  the  whole  amount  of  sputum  into  water, 
when  they  unfold  and  spread  out.  The  expectoration  also  contains  not  infre- 
quently a  slight  admixture  of  blood. 

The  subjective  symptoms  of  the  patient  may  be  very  violent.  The  dyspnijea 
sometimes  attains  a  high  and  alarming  degree.  It  ceases  when  a  large  cast  is  ex- 
pectorated after  a  severe  paroxysm  of  coughing.  Such  attacks  may  recur  every 
day  or  two.  In  other  cases,  however,  the  subjective  symptoms  are  comparatively 
slight. 

Physical  examination  of  the  lungs  reveals  little  that  is  characteristic.  In  un- 
complicated cases  percussion  shows  nothing  abnormal,  or  at  most  the  signs  of  an 
acute  emphysema.  Auscultation  gives  the  ordinary  signs  of  bronchitis,  not  char- 
acteristic in  themselves,  such  as  rhonchi,  or  moist  rales.  If  a  large  bronchus  is 
plugged,  the  respiratory  excursions  and  the  respiratory  murmur  are  almost  en- 
tirely absent  in  the  corresponding  portion  of  the  lung,  but  after  the  expectoration 
of  a  cast  the  murmur  becomes  once  more  audible. 

The  duration  of  acute  cases  is  sometimes  only  a  few  days,  at  most  a  few  weeks. 
In  favorable  cases  the  fever,  which  at  times  is  quite  high,  soon  disappears,  the 
respiratory  symptoms  grow  milder,  the  expectoration  of  the  casts  ceases,  and  there 
is  a  complete  and  permanent  recovery.  In  severe  cases,  however,  death  often 
ensues  with  all  the  symptoms  of  suffocation.  The  acute  form  sometimes  becomes 
chronic,  but  this  is  rare. 

The  chronic  form  of  fibrinous  bronchitis  may  last  for  years.  Usually  the  con- 
dition grows  worse  periodically,  at  varying  intervals  of  time,  and  at  each  exacer- 
bation casts  are  expectorated,  while  in  the  interval  there  is  apparently  merely  a 
simple  bronchial  catarrh.  Some  observations  are  also  recorded  in  medical  litera- 
ture of  persons  who  have  expectorated  these  casts  at  intervals  for  years  without 
any  special  disturbance  of  their  health  or  their  nutrition.  In  some  cases  other 
chronic  pulmonary  affections,  such  as  tuberculosis,  finally  develop. 

The  pathological  anatomy  of  fibrinous  bronchitis  is  not  yet  satisfactorily 
known  on  account  of  the  rarity  of  the  affection.  The  changes  in  the  lungs 
found  at  the  autopsy  of  fatal  cases  have  usually  been  complications,  such  as  pneu- 
monia, pleurisy,  or  tuberculosis,  which  stood  in  no  direct  relation  to  the  fibrinous 
bronchitis.  A  loss  of  epithelium  has  been  discovered  in  some  cases  in  the  parts 
of  the  bronchial  mucous  membrane  that  were  attacked. 

Prognosis. — In  all  acute  cases  the  prognosis  should  be  guarded,  for  we  know 
that  about  one  fourth  of  the  cases  terminate  fatally.  The  chronic  cases,  as  has 
been  said,  are  usually  very  protracted  and  are  subject  to  frequent  exacerbations, 
but  they  differ  from  the  acute  cases  in  being  much  less  dangerous. 


172  DISEASES    OF   THE   EESPIRATOEY   OEGANS 

Treatment. — We  make  special  use  for  inhalations  of  those  remedies  which,  as 
wo  have  said,  have  power  to  dissolve  the  casts.  We  usually  employ  a  two-  to  five- 
per-cent.  solution  of  carbonate  or  bicarbonate  of  sodium,  and  above  all  lime- 
water,  either  pure  or  diluted  with  an  equal  volume  of  water.  The  internal 
administration  of  iodide  of  potassium,  in  doses  of  twenty  to  forty-five  grains 
(gramme  1.5-3.0)  a  day,  proves  of  advantage  in  many  cases.  Energetic  inimction 
with  merctirial  ointment  is  sometimes  of  service.  Expectoration  of  the  casts  may 
be  aided  in  many  cases  by  such  expectorants  as  senega  and  benzoic  acid,  or  by 
the  timely  use  of  emetics.  We  do  not  know  any  remedies  which  can  prevent  a 
return  of  the  attacks  in  the  chronic  form.  The  treatment,  except  at  the  time  of 
the  attacks,  is  the  same  as  in  ordinary  chronic  bronchial  catarrh.     - 


CHAPTEE  V 

WHOOPING-COUGH 

{Pertussis.     Tussis  convulsiva) 

.Sltiology. — By  the  name  "whooping-cough"  we  mean  a  specific  disease  of  the 
mucous  membrane  of  the  air-passages,  which  is  seen  chiefly  in  children,  and  is 
characterized  by  a  peculiar  violent  and  paroxysmal  cough.  Sporadic  cases  are  of 
almost  constant  occurrence  in  large  cities,  but  the  disease  often  appears  in  epi- 
demic outbreaks.  Epidemics  of  whooping-cough  follow  epidemics  of  measles 
with  remarkable  frequency. 

Whooping-cough  is  without  doubt  contagious,  and  therefore  often  attacks  one 
child  after  another  in  the  same  family.  Kindergartens,  orphan  asylums,  and  day- 
nurseries  aid  very  much  in  extending  the  disease.  The  contagious  element  seems 
to  be  connected  with  the  air  expired  by  the  patient,  particularly  with  the  secretion 
from  the  mucous  membrane  expectorated  after  coughing.  Children  are  most  sub- 
ject to  an  attack  up  to  the  age  of  six  years;  from  that  age  the  liability  to  the 
disease  decreases  rapidly  with  increasing  years.  Whooping-cough  is  seen,  indeed, 
in  adults,  but  it  is  quite  rare,  and  almost  always  without  the  pronounced  features 
of  tussis  convulsiva. 

The  epidemic  onset,  the  contagiousness,  and  the  whole  course  of  the  disease 
favor  the  theory  of  its  infectious  nature.  The  presence  of  the  organisms  which 
are  supposed  to  be  the  poison  of  the  disease  has  not  yet  been  certainly  demon- 
strated, although  many  have  claimed  to  discover  characteristic  bacteria  in  the 
sputa  of  patients.  These  assertions,  however,  do  not  harmonize  with  one  another, 
and  lack  well-attested  and  methodical  proof.  If  a  patient  has  once  had  the  disease, 
he  is  almost  invariably  safe  from  a  second  attack. 

Symptoms  and  Course  of  the  Disease. — Whooping-cough  begins  with  the 
symptoms  of  a  catarrh  of  the  trachea  and  bronchi,  which  develops  more  or  less 
rapidly,  and  which  at  first  often  shows  nothing  characteristic.  We  can  at  this 
period  make  a  tolerably  probable  diagnosis  only  at  a  time  when  an  epidemic  is 
prevailing,  or  in  case  the  child's  associates  have  already  been  attacked  with  the 
disease.  The  cough  is  often  very  persistent,  obstinate,  and  severe  at  the  begin- 
ning, but  it  does  not  yet  come  on  in  distinct  paroxysms.  Examination  of  the 
chest  shows  nothing  peculiar  except  a  few  rhonchi.  There  is  often  a  coryza,  with 
frequent  sneezing,  and  there  is  sometimes  a  mild  conjunctivitis.  The  child  is 
restless  and  feverish,  especially  toward  night.  Tlie  temperature  may  repeatedly 
reach  103°  or  104°  (39°-40°  C.)  in  this  initial  fever.  The  duration  of  this  first 
so-called  catarrhal  stage  varies,  but  it  usually  lasts  a  week  or  ten  days. 


WHOOPIXG-COUGH  173 

The  catarrhal  stage  gradually  passes  into  the  second,  convulsive  stage,  without 
any  sharp  boundary.  The  cough  becomes  more  violent,  and  comes  on  in  the 
separate  paroxysms  of  whooping-cough  which  are  characteristic  of  the  disease. 
We  do  not  know  the  particular  reason  why  the  cough  has  this  paroxysmal  char- 
acter, but  a  nei-vous  factor  probably  plays  the  chief  part  in  it. 

The  peculiarity  of  the  attack  consists  in  the  violent,  paroxysmal  fits  of  cough- 
ing, which  are  from  time  to  time  interrupted  by  deep,  long-drawn,  loud,  and 
shrill  inspirations,  due  to  the  occurrence  of  a  spasmodic  contraction  of  the  glottis. 
Exceptionally  there  are  cases  without  this  loud  whistling  inspiration.  The  child 
becomes  markedly  cyanotic  during  the  attack,  the  veins  in  the  neck  swell,  and 
tears  come  into  the  eyes.  HaBmorrhage  into  the  conjunctiva,  nose-bleed,  and  in 
some  cases  haemorrhages  into  other  organs,  as  the  ear  and  the  skin,  often  come 
on  as  a  result  of  this  stasis.  Vomiting  very  often  occurs  either  during  a 
paroxysm  or  at  its  close.  Involuntary  evacuations  of  urine  and  fseces  may  also 
follow  from  the  violent  contraction  of  the  abdominal  muscles.  Exceptionally  we 
observe  still  more  severe  symptoms  with  a  paroxysm :  a  complete  spasmodic  cessa- 
tion of  respiration  with  imminent  danger  of  suffocation,  or  sometimes  general 
convulsions.  In  two  cases  we  have  seen  hemiplegia  in  children  which,  accord- 
ing to  the  positive  statements  of  their  parents,  came  on  suddenly  during  a  severe 
attack  of  whooping-cough.  It  is  still  undetermined  whether  these  "whooping- 
cough  hemiplegias  "  are  due  to  an  actual  cerebral  hasmorrhage  or  whether  they 
come  from  the  enormous  venous  stasis  in  the  brain. 

The  paroxysms  vary  with  the  severity  of  the  disease,  frequently  appearing 
ten  or  fifteen  times  in  twenty-four  hours;  sometimes  with  greater  frequency — 
fifty  times  or  more.  They  also  occur  at  night  as  often  or  even  oftener  than  in 
the  daytime.  They  come  on  either  spontaneously  or  from  some  special  predis- 
posing cause.  The  attacks  which  come  on  during  eating  cause  the  most  dis- 
turbance, because  the  food  taken  is  almost  always  vomited  again.  In  chil- 
dren with  whooping-cough  we  can  often  excite  a  spasm  at  any  time,  and  this 
is  important  in  diagnosis — by  putting  a  spatula  in  the  mouth,  by  pressing  on 
the  larynx,  or  by  making  the  child  cry.  If  there  are  several  children  with 
whooping-cough  in  the  same  room  and  a  paroxysm  attacks  one  of  them,  the 
others,  as  a  rule,  soon  begin  to  cough  too.  Some  prodromal  symptoms  often  pre- 
cede the  peculiar  paroxysm,  such  as  general  uneasiness,  rapid  respiration,  or 
vomiting.  At  the  end  of  a  paroxysm  many  children  are  very  feeble  and  exhausted, 
but  others  recover  rapidly,  and  are  playing  again  quite  briskly  a  few  minutes  after. 

In  general  the  child  feels  quite  well  in  the  interval  between  the  paroxysms, 
but  the  effects  of  the  violent  attacks  of  coughing  may  of  course  often  be  seen. 
Besides  the  occasional  hemorrhages  into  the  conjunctiva,  we  find  the  eyelids 
somewhat  swollen,  their  veins  dilated  and  blue,  and  showing  through  the  skin. 
Many  children  grow  very  thin  from  the  repeated  vomiting.  A  small  ulcer  is 
quite  frequently  formed  on  the  fraenum  of  the  tongue,  the  origin  of  which  is 
to  be  referred  to  mechanical  causes.  The  tongue  is  violently  protruded  in  the 
severe  paroxysms  of  coughing,  and  the  froenum  is  thus  torn,  or  injured  by  the 
sharp  lower  incisors. 

Physical  examination  of  the  lungs  shows  nothing  abnormal  in  uncomplicated 
cases  except  a  few  moist  rales  or  rhonchi.  Sometimes  the  rhonchi  are  wanting, 
or  are  present  in  small  numbers  only  a  short  time  before  a  paroxysm,  but  in  other 
cases  an  intense  diffuse  bronchitis  is  developed,  which  often  leads  to  the  develop- 
ment of  a  lobular  pneumonia  (vide  infra).  Sometimes,  but  not  always,  there  is 
an  acute  catarrhal  inflammation  of  the  bronchi,  and  especially  of  the  posterior 
wall  of  the  larynx. 

The  fever,  which  is  usually  present  in  the  first  or  catarrhal  stage,  is  absent  in 
the  convulsive  stage.     The  child  is  free  from  fever  for  the  most  part.  "  We  often 


174  DISEASES    OE   THE   EESPIRATOEY   ORGANS 

find  a  slight  rise  of  temperature  up  to  100°  or  101°  (38°-38.5°  C),  but  only 
toward  night.  Higher  and  more  persistent  fever  points  to  the  development  of 
complications,  especially  on  the  part  of  the  lungs. 

The  convulsive  stage  seldom  lasts  less  than  three  or  four  weeks,  and  often 
much  longer,  up  to  three  or  four  months.  The  paroxysms  gradually  become  less 
frequent  and  less  violent  (stadium  decrementi),  until  they  finally  disappear 
entirely;  but  relapses  and  fresh  exacerbations  also  occur  in  this  stage.  A  cer- 
tain "  irritability  "  of  the  bronchial  mucous  membrane  remains  for  a  long  time 
after  whooping-cough.  Einally,  however,  the  disease,  in  uncomplicated  cases, 
goes  on  to  a  permanent  and  complete  recovery. 

Complications  and  Sequelae. — The  severe  results  which  sometimes  follow 
whooping-cough  are  probably  due  in  part  to  the  direct  action  of  the  specific  causes 
of  the  disease,  and  in  part  to  complications  of  a  secondary  nature  whose  develop- 
ment is  merely  favoi'ed  by  the  whooping-cough.  The  most  important  are  complica- 
tions in  the  lungs.  A  lobular  catarrhal  pneumonia  often  develops  after  a  severe 
bronchitis  which  involves  the  finer  bronchi.  In  such  cases  the  respiration  be- 
comes hurried  and  superficial,  the  fever  higher,  and  the  general  condition  bad 
even  in  the  times  between  the  paroxysms.  On  examination  of  the  lungs,  we  hear 
numerous  moist  rales,  especially  over  the  lower  lobes;  and  we  can  sometimes 
make  out  dullness  on  one  or  both  sides,  if  there  is  extensive  pneumonic  infiltra- 
tion. Such  cases  are  always  very  larotracted,  and  many  children  succumb,  partly 
from  the  disturbance  of  respiration  and  partly  from  general  weakness  and  in- 
anition. 

Complications  in  other  organs  are  much  rarer.  Among  the  most  frequent  are 
attacks  of  diarrhoea  which  impair  the  child's  nutrition.  Many  observers  have 
also  mentioned  the  quite  frequent  occurrence  of  a  croupous  or  diphtheritic  in- 
flammation in  the  pharynx  and  larynx  in  the  course  of  whooping-cough.  Finally, 
a  case  under  our  own  observation  may  here  be  mentioned,  in  which  death  oc- 
curred with  severe  nervous  symptoms,  convulsions,  and  coma.  At  the  autopsy 
very  numerous  capillary  haemorrhages  were  found  in  the  brain. 

Pulmonary  emphysema  is  the  first  thing  to  be  mentioned  among  the  sequelae 
of  whooping-cough.  Erom  the  marked  pressure  which  the  severe  and  frequent 
outbursts  of  coughing  exert  from  within  upon  the  alveoli  of  the  lungs,  they  gradu- 
ally become  dilated.  An  acute  lobular  emphysema  ("  acute  pulmonary  infla- 
tion ")  is  set  up,  which  sometimes  passes  into  a  typical  chronic  pulmonary  emphy- 
sema (vide  infra).  Chronic  bronchial  catarrh  may  also  remain  for  a  long  time 
after  an  attack  of  whooping-cough.  We  have  already  stated  (see  page  163) 
that  many  incurable  cases  of  chronic  bronchitis  in  adults  are  to  be  referred  to 
an  attack  of  whooping-cough  in  childhood. 

A  third  important  sequel  of  whooping-cough  is  pulmonary  tuberculosis.  The 
bronchitis  and  lobular  pneumonia  which  occur  during  whooping-cough  some- 
times do  not  improve,  especially  in  weak  children  with  a  tubercular  tendency. 
The  fever  continues  high,  the  child  grows  thin,  and  constantly  becomes  more  and 
more  miserable.  At  the  autopsy  we  find  cheesy  nodules  in  the  lungs,  cheesy  bron- 
chial glands,  and  at  times  tuberculosis  of  other  organs.  These  cases  signify  that 
when  a  tubercular  infection  is  present,  but  is  still  latent,  the  whooping-cough  acts 
as  an  exciting  cause  for  the  outbreak  of  the  disease,  or  that  a  greater  receptivity 
to  infection  with  tubercular  poison  is  created  by  the  whooping-cough.  Mobius 
has  lately  reported  the  occurrence,  in  a  few  cases,  of  paralysis  as  a  sequel  of 
whooping-cough.  This  usually  begins  in  the  lower  and  extends  to  the  upper 
extremities,  and  is  due  apparently  to  neuritis. 

The  diagnosis  of  whooping-cough  can  not  be  made  with  certainty,  as  we  have 
said,  until  the  second  or  convulsive  stage.  It  is  easy  then,  however,  since  the 
characteristic  attacks  occur  in  no  other  affection  of  the  lungs  in  like  manner 


WHOOPING-COrGH  175 

and  with  like  frequency  and  duration.  If  we  have  no  opportunity  to  observe  the 
attack  itself,  and  have  to  depend  upon  the  description  of  the  friends,  the  diagno- 
sis is  sometimes  more  uncertain;  but  the  accounts  of  the  occurrence  of  cough, 
in  individvxal  paroxysms  associated  with  vomiting,  are  usually  so  characteristic 
that  errors  are,  on  the  whole,  rare.  Furthermore,  the  child  between  the  parox- 
ysms usually  presents  certain  signs:  he  has  a  bloated  aspect,  or  we  may  find 
slight  haemorrhages  into  the  conjunctiva,  or  ulcers  on  the  frsenum  of  the  tongue, 
which  make  the  diagnosis  highly  probable.  Under  some  circumstances  we  may 
also  make  the  attempt  to  bring  on  the  paroxysm  artificially  (vide  supra).  In 
adults,  as  we  have  said,  the  attacks  are  rarely  as  characteristic  as  in  children. 
There  are  usually  the  symptoms  of  a  more  or  less  severe  bronchitis  with  obsti- 
nate paroxysmal  covigh,  but  without  the  characteristic  attacks  and  usually  with- 
out vomiting.  The  diagnosis  of  whooping-cough  therefore  rests  mainly  upon  the 
existence  of  special  setiological  conditions  (the  co-existence  of  the  disease  in 
children,  etc.). 

The  prognosis  is  favorable  with  the  majority  of  children  if  they  are  previously 
strong  and  healthy.  Very  young  children  are  in  more  danger  than  older  ones. 
[Under  two  years  there  is  great  danger,  and  over  five  scarcely  any.  It  has  been 
said  that  whooping-cough  causes  one  fourth  the  total  mortality  of  children  in 
London. — V.]  There  is  danger  if  secondary  pneumonia  develops,  and  if  the  gen- 
eral nutrition  and  strength  of  the  child  suffer.  As  soon  as  the  diagnosis  is  certain 
we  must  call  thte  attention  of  the  parents  to  the  probable  long  duration  of  the  dis- 
ease. Regard  must  also  be  paid  to  the  possibility  of  the  development  of  sequelae, 
especially  in  weak  children  suspected  of  tuberculosis. 

Treatment. — Since  the  disease  is  protracted  and  is  not  devoid  of  danger,  it  is 
our  duty,  when  an  epidemic  of  whooping-cough  prevails,  to  guard  children  from  it 
as  far  as  possible.  If  one  child  in  a  family  is  taken  ill,  the  other  children  must 
be  rigorously  kept  away  from  him.  If  circumstances  permit,  we  should  prefer 
to  send  them  away  to  another  place  free  from  whooping-cough. 

With  regard  to  the  treatment  of  the  disease,  we  must  first  endeavor  to  fulfill 
general  dietetic  and  hygienic  indications.  The  child  should  breathe  good,  pure 
air,  and  for  this  reason  it  is  often  advisable  to  transfer  the  patient  to  a  larger 
room,  with  as  much  air  and  sunlight  as  possible.  The  atmosphere  should  not  be 
too  dry,  and  it  is  advisable  to  employ  a  spray  of  water  (carbolic  solution)  fre- 
quently, or  to  hang  up  moist  sheets  in  the  room.  In  good  weather  the  child 
should  be  out  of  doors  a  large  part  of  the  time,  provided  fever  has  ceased.  City 
children  are  to  be  sent,  if  possible,  into  the  country.  The  food  should  be  good  and 
nourishing,  but  dry  and  crumbly  articles  should  be  avoided,  being  apt  to  excite 
cough.  W.arm  or  lukewarm  baths  frequently  prove  very  beneficial,  particularly 
when  there  is  considerable  bronchitis,  as  they  lessen  the  danger  of  a  lobular 
pneumonia. 

The  medicinal  treatment  of  whooping-cough  has  not  yet  shown  brilliant 
results  despite  the  large  number  of  remedies  recommended.  During  the  ca- 
tarrhal stage  it  is  usually  sufficient  to  give  a  simple  expectorant  (ipecac,  etc.) 
and  plenty  of  warm  drink.  In  the  convulsive  stage  the  best  remedies  to  try  are 
quinine,  antipyrine,  belladonna,  bromide  of  potassium,  and  bromoform.  The 
latter  has  been  much  recommended  of  late.  Quinine  is  given  in  powders  of  one 
and  a  half  to  eight  grains  (grm.  0.1  to  0.5)several  times  a  day,  either  in  capsules  or, 
in  the  case  of  smaller  children,  with  chocolate.  The  earlier  this  remedy  is  em- 
ployed the  more  prompt  is  said  to  be  its  beneficial  influence.  Antipyrine  is  at 
present  used  more  frequently  than  quinine,  and  in  doses  of  four  to  eight  grains 
(grm.  0.25-0.6)  several  times  a  day  it  often  produces  distinct  improvement.  Bella- 
donna is  prescribed  in  powders  containing  one  twelfth  to  one  sixth  grain  (grm. 
0.005  to  0.01)  of  the  extract  of  belladonna,  giving  three  to  five  such  powders  a 


176  DISEASES    OE   THE   EESPIRATOEY   ORGAISTS 

day.  This  remedy  has  often  seemed  to  the  author  to  diminish  the  number  and 
violence  of  the  paroxysms.  Bromide  of  potassium  is  employed  in  an  aqueous  solu- 
tion in  the  dose  of  fifteen  to  forty-five  grains  per  diem  (grm.  1  to  3).  Its 
efficacy  is  probably  due  to  its  power  to  diminish  reflex  excitability.  The  same 
drug'  employed  in  an  atomizer  often  has  a  palliative  effect.  Bromoform  is  the 
remedy  most  used  of  late;  two  to  five  drops  or  more  are  given  several  times  a 
day  in  sweetened  water  or  fruit  juice.  It  is  readily  taken,  and  it  seems  to  act 
favorably  both  on  the  severity  of  the  individual  attacks  and  on  the  whole  course 
of  the  disease. 

If  the  paroxysms  are  very  violent  we  may  cautiously  administer  small  doses 
of  morphine  or  codeia.  Inhalations  of  chloroform  and  ether  have  also  been 
recommended.     The  following  mixture  is  a  suitable  one : 

]^   Chloroformi §3         (grm.  30)  ; 

iEtheris §ij        (grm.  60)  ; 

01.  terebinthinse  ........................   Sijss.    (grm.  10).     M. 

Sig.  One  or  two  teaspoonfuls  to  be  poured  upon  a  pocket-handkerchief  for  in- 
halation. 

Finally,  efforts  have  been  repeatedly  made  to  lessen  the  frequency  and  the 
severity  of  the  attacks  by  anaBsthetizing  the  pharynx  and  larynx  by  painting  with 
a  ten-  to  fifteen-per-cent.  solution  of  cocaine.  Michael  advocates  the  daily  in- 
sufflation into  the  nostrils  of  powdered  benzoin.  Neither  method  of  treatment 
has  succeeded  in  establishing  itself  in  practice. 

Sprays  of  various  antiseptic  remedies  have  been  frequently  employed  be- 
cause of  the  infectious  nature  of  the  disease.  The  practitioner  must  not  expect 
too  much  from  them,  however,  although  they  sometimes  act  well.  A  one-per- 
cent, or  two-per-cent.  solution  of  carbolic  acid  is  most  frequently  employed  for 
inhalation.  It  may  be  given  several  times  a  day  for  periods  of  two  or  three 
minutes  at  a  time,  Next  to  this,  turpentine  and  benzine  are  most  to  be  recom- 
mended; of  these,  twenty  or  thirty  drops  are  poured  upon  a  sponge  previously 
moistened  with  hot  water.  Turpentine  and  especially  terpine  hydrate  (grains 
vij,  gramme  0.5,  thrice  daily)  are  also  given  internally.  [Earlow  and  others 
report  marked  success  from  spraying  the  upper  air-passages  with  a  two-per-cent. 
solution  of  resorcine.] 

In  very  many  cases  we  finally  content  ourselves  with  taking  good  general 
care  of  the  child,  and,  if  the  weather  permit,  with  keeping  him  as  much  as 
possible  in  the  open  air.  For  the  treatment  of  the  complications  and  sequelse 
of  whooping-cough  the  reader  is  referred  to  the  appropriate  chapters  of  this  book. 


CHAPTER   VI 

BRONCHIECTASIS 

{BroncJiial  Dilatation) 

Dilatation  of  the  bronchi  is  not  a  separate  disease,  but  it  is  a  result  of  various 
affections  of  the  lungs  and  bronchi.  Nevertheless,  we  will  speak  of  it  briefly  in 
this  connection  since  many  cases  actually  present  the  appearance  of  a  very  char- 
acteristic disease. 

We  distinguish  anatomically  the  cylindrical  and  saccular  bronchiectases. 

Cylindrical  bronchiectasis  consists  of  a  uniform  dilatation  of  a  bronchial 
tube,  and  occurs  most  frequently  in  the  medium-sized,  or  rarely  in  the  finer 


BKONCHIECTASIS  177 

bronchi  of  one  or  more  lobes  of  tbe  lung.  We  usually  find  at  tlie  autopsy  tliat,  on 
slitting  up  the  bronchi,  the  point  of  the  scissors  can  easily  be  pushed  through  the 
dilated  bronchial  tube  close  up  to  the  pleura.  Cylindrical  bronchiectasis  is  usu- 
ally due  to  a  long-continued  bronchitis,  and  develops  most  frequently  in  cases  of 
emphysema,  and  also  in  whooping-cough,  measles,  and  sometimes  in  phthisis,  etc. 
The  primary  process  is  probably  always  the  atrophy  which  follows  the  catarrh, 
and  the  diminished  resistance  of  the  bronchial  walls  thus  occasioned.  The  dila- 
tation of  the  lumen  of  the  bronchus  is  produced  gradually,  partly  by  the  trac- 
tion of  the  thorax  during  inspiration,  and  still  more  by  the  increased  pressure  in 
the  bronchi  due  to  the  frequent  and  violent  fits  of  coughing,  and  finally,  perhaps, 
by  the  constant  pressure  of  the  stagnating  secretion. 

The  diagnosis  of  cylindrical  dilatation  of  the  bronchi  is  only  a  probable  one. 
We  suspect  that  a  bronchiectasis  has  formed  if  the  conditions  are  fulfilled 
which  we  know  lead  to  it.  In  the  chronic  bronchial  catarrh  of  emphysema  we 
judge  that  there  is  cylindrical  dilatation  of  the  bronchi  if  the  secretion  is  very 
abundant  and  comparatively  thin,  and  separates  into  layers  on  standing  in  a 
sputum-cup.  The  dilatation  is  usually  emptied  by  a  severe  paroxysm  of  coughing, 
such  as  is  apt  to  occur  in  the  morning  if  the  secretion  collects  in  great  quantity 
during  the  night.  Physical  examination  usually  gives  numerous,  low,  fine,  and 
medium  moist  rales,  especially  in  the  lower  lobes.  The  respiratory  murmur  some- 
times loses  its  vesicular  character  in  marked  cylindrical  bronchiectasis,  and  has  a 
more  indefinite  and  tubular  quality.  Sometimes  it  is  quite  obscured  in  the  lower 
part  of  the  lung  by  the  abundant  rales. 

Saccular  bronchiectases  are  spherical  or  oval  dilatations  which  are  confined  to 
a  definite  portion  of  the  bronchial  tube.  They  may  attain  a  diameter  of  several 
centimetres.  The  bronchus  passes  suddenly  or  gradually  into  the  dilatation,  and 
it  is  often  obliterated  so  that  the  bronchiectasis  forms  a  completely  closed  cavity. 
The  wall  of  a  saccular  bronchiectasis  loses  in  great  measure  the  character  of  a 
normal  bronchial  wall.  As  a  rule  it  is  atrophied  to  a  high  degree,  the  atrophy 
involving  not  only  the  mucous  glands,  but  also  the  muscular  fibers,  the  elastic 
elements,  and  even  the  cartilages,  so  that  the  bronchiectatic  cavities  seem  lined 
with  nothing  but  a  thin  membrane.  The  occurrence  of  many  dilated  vessels  in 
the  walls  of  a  bronchiectasis  is  due  perhaps  to  an  atrophy  of  the  vessel  walls  and 
is  a  symptom  of  great  clinical  importance  (vide  infra).  In  other  cases,  however, 
we  find  hypertrophic  processes,  which  involve  the  connective  tissue  of  the  mucous 
membrane,  and  lead  to  band-like  projections  and  swellings.  Finally,  ulcerative 
processes  may  develop  on  the  inner  surface  of  a  bronchiectasis  and  attack  the 
surrounding  lung-tissue,  and  change  the  bronchiectatic  cavity  into  a  typical  ulcer- 
ating cavity. 

Only  rarely,  for  example  in  emphysema,  do  we  find  a  single  saccular  bron- 
chiectasis surrounded  by  tolerably  normal  lung-tissue.  Its  origin,  then,  is  to  be 
referred  tp  causes  like  those  which  have  been  given  above  for  the  much  com- 
moner cylindrical  bronchiectases.  In  the  great  majority  of  cases  we  find  saccular 
bronchiectases,  singly  or  in  large  numbers,  surrounded  by  indurated  and  con- 
tracted lung-tissue.  They  form  one  of  the  complications  of  "  pulmonary  con- 
traction"  [fibroid  phthisis],  which  is  almost  always  associated  with  contraction 
of  the  pleura.  Since  Corrigan's  day  we  have  with  good  reason  looked  upon  this 
contraction  as  the  chief  cause  for  their  origin.  By  the  gradual  shrinking  and 
retraction  of  the  lung,  which  as  a  rule  has  become  adherent  to  the  costal  pleura, 
a  traction  is  exerted  upon  the  bronchial  walls  from  without  to  which  they  grad- 
ually yield.  Stagnation  and  pressure  of  the  secretion  work  at  the  same  time  in 
like  manner  to  dilate  the  bronchial  tube.  Thus  arises  the  frequent  combination 
of  pulmonary  contraction  with  the  formation  of  bronchiectases.  This  combina- 
tion is  usually  unilateral,  and  involves  the  whole  lung  or  only  one  of  the  upper 
12 


178  DISEASES    OF   THE   EESPIEATOEY   OEGAXS 

or  lower  lobes.  Our  knowledge  is  still  very  defective  as  to  the  cause  of  this 
"  chronic  interstitial  pneumonia  "  leading  to  contraction.  It  often  seems  to  be 
a  quite  insidious  and  gradual  circumscribed  chronic  inflammatory  process;  in 
other  cases  by  careful  inquiry  we  can  discover  a  previous  acute  process  (pneu- 
monia, severe  acute  bronchitis,  etc.)  as  a  starting-point  for  the  disease.  Inha- 
lation of  dust  often  plays  a  part  in  the  causation. 

We  sometimes  see  the  form  of  pulmonary  contraction  in  question  developing 
as  a  result  of  pleurisy.  Laennec  first  advanced  the  opinion  that  in  such  cases  the 
pleurisy  was  the  primary  trouble,  and  that  from  it  an  interstitial  inflammatory 
process  attacked  the  connective  tissue  of  the  underlying  lung  and  led  to  contrac- 
tion and  then  to  the  formation  of  bronchiectases.  Unfortunately  we  lack  further 
confirmatory  evidence  in  this  regard. 

Most  saccular  bronchiectases  are  situated  in  the  lower  lobes,  but  genuine 
bronchiectasis  is  not  very  rare  in  the  upper  lobes.  As  a  rule,  the  trouble  is  uni- 
lateral, or  at  least  afl'ects  one  side  the  most.  Sometimes  large  portions  of  a 
lung  may  be  completely  transformed  into  a  cicatricial  tissue  studded  with  many 
bronchiectatic  cavities. 

"  Pure  cases  "  of  bronchiectasis  have  nothing  to  do  with  tuberculosis.  Before 
the  discovery  of  the  tubercle  bacillus  there  was,  of  course,  confusion  between 
bronchiectatic  and  chronic  tubercular  contraction  of  the  lungs;  but  we  must 
remember  that,  under  some  circumstances,  chronic  tuberculosis  may  lead  to  the 
formation  of  bronchiectasis,  and  that,  on  the  other  hand,  in  bronchiectatic  pro- 
cesses there  is  not  infrequently  a  secondary  development  of  tuberculosis.  There 
are  cases  in  which  it  is  hard  to  decide,  even  at  the  autopsy,  whether  an  exist- 
ing chronic  contraction  in  a  portion  of  the  lung,  with  induration  of  tissue  and 
the  formation  of  bronchiectasis,  was  originally  tubercular  or  of  some  other 
nature. 

The  symptoms  caused  by  saccular  bronchiectasis  are  derived  in  part  from  phys- 
ical examination  and  in  part  from  observation  of  the  sputum  and  of  the  gen- 
eral course  of  the  disease.  If  great  bronchiectatic  cavities  lie  near  the  chest- 
wall,  they  may  give  the  same  physical  signs  that  we  shall  learn  to  recognize 
later  in  the  description  of  tubercular  cavities.  Bronchiectases  lying  within 
the  lung,  however,  are  often  devoid  of  definite  physical  signs,  so  that  at  most 
we  may  suspect  them  from  other  symptoms,  such  as  the  peculiarities  of  the 
sputum.  The  more  abundant  the  formation  of  bronchiectases  the  more  does 
the  respiration  lose  its  vesicular  character  and  become  harsh  and  finally  bron- 
chial. Inasmuch  as  there  is  usually  a  very  considerable  secretion  of  mucus,  we 
generally  find,  upon  auscultation,  abundant  medium  and  even  coarse  moist 
rales.  The  percussion  note  over  the  bronchiectatic  portion  of  the  lung  is  usually 
dull  or  dull-tympanitic,  a  result  of  the  chronic  interstitial  pneumonia  about  the 
bronchiectasis.  The  whole  thorax  near  an  extensive  bronchiectasis  is  often  much 
retracted  and  distorted. 

The  expectoration  is,  as  a  rule,  very  abundant,  and  it  is  often  raised  by  large 
mouthfuls.  On  standing,  as  a  result  of  its  thin  fluid  character,  it  exhibits  a  dis- 
tinct division  into  an  upper  frothy,  muco-purulent  layer,  a  middle  muco-serous 
layer,  and  a  lower  purulent  layer.  It  usually  has  ■  a  peculiar  stale,  sweet- 
ish odor,  but  it  may  be  foetid.  The  latter  is  almost  always  associated  with 
stagnation  of  the  secretion.  So  long  as  the  expectoration  is  loose  and  easily 
evacuated,  it  is  not  foetid  and  the  patient  feels  well.  Then  a  cessation  of  the 
expectoration  may  ensue.  The  patient  feels  poorly,  there  may  be  a  slight  rise 
of  temperature,  and  the  expectoration  becomes  scanty  and  has  a  stinking  foetid 
character.  Periods  of  improvement  may  thus  alternate  with  exacerbations.  It 
is  a  favorable  sign  when  the  amount  of  the  expectoration  decreases,  provided  that 
it  does  not  become  foetid  and  that  the  patient  does  not  feel  worse.    Since  bronchi- 


BEONCHIECTASIS  179 

ectasis  may  give  rise  to  a  permanent  foetid  bronchitis,  and  since,  on  the  other 
hand,  as  we  have  said,  foetid  bronchitis  itself  often  leads  to  the  formation  of  bron- 
chiectasis, we  can  understand  the  manifold  inter-relations  and  transitions  which 
the  two  forms  of  disease  present. 

The  not  infrequent  pulmonary  hsemorrhages  in  bronchiectasis  are  of  great 
clinical  importance.  They  are  due  to  rupture  of  the  dilated  vessels  (vide  supra) 
in  the  walls  of  the  bronchiectasis.  They  may  also  be  due  to  ulcerative  processes. 
Slight  precursors  may  precede  a  severe  haemoptysis.  The  haemorrhage  may  be" 
very  abundant,  and  it  may  be  repeated  during  a  long  period — several  weeks — so 
that  the  patient  becomes  extremely  anaemic.  Finally  the  haemorrhages  cease  and 
the  patient  improves  quite  rapidly.  Such  attacks  of  haemoptysis  may  be  repeated 
very  often  in  the  course  of  the  year.  When  we  hear  comparatively  well-nourished 
patients  with  lung  disease  say  that  they  have  suffered  for  years  from  frequent 
and  severe  haemoptyses,  we  can  usually  infer,  from  such  statements,  that  there 
is  a  saccular  bronchiectasis. 

The  whole  course  of  the  disease  is  very  variable,  but  it  usually  lasts  for  many 
years.  It  is  doubtful  whether  a  saccular  bronchiectasis  can  actually  be  cured; 
but  if  no  more  serious  sequelae  occur,  many  patients  may  live  for  years  in  a 
tolerable  condition,  and  may  even  reach  an  advanced  age.  The  general  nutrition 
often  remains  very  good,  although  a  certain  very  characteristic,  anaemic,  cyanotic 
tinge  of  the  skin  gives  even  to  corpulent  patients  an  unmistakable  morbid  ap- 
pearance. A  very  characteristic  sign  is  that  the  terminal  phalanges  of  the  fingers 
gradually  become  clubbed  and  thickened,  and  the  nails  are  much  bent.  This 
peculiar  trophic  change,  the  cause  of  which  is  still  unexplained,  is  much  rarer  in 
chronic  tubercular  processes  (vide  infra). 

The  diagnosis  of  extensive  formation  of  bronchiectasis  in  the  lungs  is  in 
many  cases  easy,  but  in  other  cases  it  may  present  great  difficulties.  In  order 
to  avoid  confounding  it  with  chronic  tuberculosis  the  following  should  be  espe- 
cially considered :  In  bronchiectasis  the  patient  does  not  present  a  true  cachexia ; 
he  is  usually  somewhat  cyanotic  and  pale  at  the  same  time.  The  layer  of 
subcutaneous  fat  often  remains  well  marked  for  a  long  time.  The  terminal 
phalanges  of  the  fingers  are  often  clubbed,  as  in  foetid  bronchitis.  Fever  is  usually 
absent,  unless  there  are  some  special  complications.  The  expectoration  is  more 
abundant  and  more  distinctly  stratified  than  is  often  seen  in  tuberculosis;  and, 
most  important  of  all,  it  contains,  of  course,  no  tubercle  bacilli.  Finally,  bron- 
chiectatic  conditions  ordinarily  (though,  of  course,  not  always)  develop  in  a  lower 
lobe,  while  tuberculosis  is  apt  to  affect  an  upper  lobe  first. 

We  will  refer  to  the  appropriate  chapters  for  the  relations  of  bronchiectasis 
to  foetid  bronchitis,  pulmonary  gangrene,  etc. 

The  treatment  is  never  directed  against  the  bronchial  dilatation  as  such,  but 
toward  its  causes  or  sequelae.  The  treatment  of  bronchiectasis,  therefore,  coin- 
cides with  the  treatment  of  chronic  bronchitis,  foetid  bronchitis,  etc.  Besides 
general  hygienic  measures  (climatic  resorts),  balsamic  remedies  (turpentine,  etc.) 
are  chiefly  used.  Any  pulmonary  ha3morrhage  is  to  be  treated  symptomatically  in 
the  same  way  as  haemoptysis  in  pulmonary  tuberculosis  (q.v.). 


180  DISEASES    OF   THE   EESPIEATOET   OEGAXS 

CHAPTEE  YII 
STENOSIS  OF  THE  TRACHEA  AND  BRONCHI 

1.  Tracheal  Stenosis 

Etiology. — Stenosis  of  the  trachea  may  be  caused  either  by  diseases  in  the 
vicinity  of  the  trachea,  or  by  diseases  of  the  trachea  itself.  The  first-named 
mode  of  origin  is  the  m^ore  frequent.  To  this  are  due  all  the  stenoses  of  the 
trachea  from  compression.  Enlargements  of  the  thyroid  gland  from  simple 
struma  and  new  growths,  aneurisms  of  the  arch  of  the  aorta  and  of  the  in- 
nominate artery,  tumors  and  abscesses  in  the  anterior  mediastinum,  swelling  of 
the  lymph-glands  at  the  bifurcation  of  the  trachea,  abscess  on  the  anterior  sur- 
face of  the  cervical  vertebrte,  etc.,  may  exert  so  great  a  pressure  on  the  trachea 
from  without  that  its  lumen  is  made  narrower.  Besides  the  direct  action  of  pres- 
sure, iu  most  cases,  a  gradual  atrophy  and  a  softening  of  the  rings  of  cartilage, 
due  to  pressure,  sometimes  play  an  important  part,  according  to  Eose,  in  the 
occurrence  of  stenosis.  A  collapse  of  the  trachea  may  arise  from  this  "  flaccid 
softening,"  which  may  come  on  quite  suddenly,  and  may  cause  many  of  the  cases 
of  sudden  "  death  due  to  goitre." 

Changes  in  the  trachea  itself  leading  to  stenosis  are  quite  rare.  Cicatricial 
stenosis  as  a  result  of  syphilitic  ulcerations  is  relatively  the  most  frequent.  New 
growths  in  the  trachea  are  also  to  be  mentioned,  such  as  polypi  and  cancer, 
the  latter  almost  always  having  invaded  the  trachea  from  the  adjacent  parts. 
Very  rarely  acute  and  chronic  inflammatory  processes  such  as  perichondritis  lead 
to  a  swelling  of  the  mucous  membrane  sufficient  to  cause  stenosis.  In  conclusion, 
we  may  mention  that  stenosis  of  the  trachea  may  be  due  to  the  presence  of  foreign 
bodies. 

Symptcms. — If  the  stenosis  is  so  extreme  that  there  is  a  real  hindrance  to 
respiration,  a  very  striking  modification  of  the  breathing  occurs.  It  is  difficult 
and  labored,  and  is  performed  only  by  the  help  of  the  accessory  muscles.  Both 
expiration  and  inspiration  are  protracted,  long  drawn,  and  accompanied  by  a  loud 
stridor.  In  many  cases  inspiration  is  more  difficult  than  expiration,  so  that  there 
is  accordingly  a  preponderating  inspiratory  dyspno3a,  and  the  number  of  respira- 
tions a  minute  is  diminished.  If  the  entrance  of  air  into  the  lungs  is  incomplete 
in  spite  of  the  lengthening  of  the  respirations,  we  see  an  inspiratory  retraction  of 
the  lower  part  of  the  thorax,  and  sometimes  of  the  throat  and  the  supra-clavicular 
fossse.  In  tracheal  stenosis  the  larynx,  however,  shows  little  or  no  to-and-fro 
movement  on  respiration.  This  fact  is  of  value  in  diagnosis  in  distinguishing 
tracheal  from  laryngeal  stenosis,  for  in  the  latter  the  respiratory  movements  of 
the  larynx  are  quite  well  marked. 

We  sometimes  notice  in  the  pulse  during  inspiration  a  marked  fall  in  tension 
and  in  the  height  of  the  pulse-wave,  the  pulsus  paradoxus.  With  the  sphygmo- 
graph  we  can  show  still  more  plainly  the  changes  in  blood-pressure,  which  vary 
quite  markedly  with  the  respiration.  The  frequency  of  the  pulse  is  usually  a 
little  increased,  but  sometimes  it  is  diminished. 

The  symptoms  of  the  disease  just  described  may  form  so  characteristic  a 
picture  that  we  can  recognize  it  at  the  first  glance.  More  precise  information 
as  to  the  seat  of  the  stenosis,  or  the  accurate  differentiation  of  tracheal  stenosis 
from  the  very  similar  picture  presented  by  larjmgeal  stenosis,  demands  a  direct 
laryngoscopic  examination  of  the  larynx  and  trachea,  which,  of  course,  is  hardly 
practicable  in  a  patient  with  a  high  degree  of  dyspna3a. 


BEONCHIAL   ASTHMA  181 


2.  Bronchial  Stenosis 


ISTarrowing  of  a  primary  bronchus,  which  is  the  only  form  to  be  mentioned 
here,  arises  most  frequently  as  a  result  of  the  presence  of  foreign  bodies — e.  g., 
bits  of  bone,  plum-stones,  buttons,  etc.  These  may  enter  the  air-passages  by 
means  of  a  deep  inspiration,  especially  while  eating,  or  during  sleep.  We  know 
that  foreign  bodies  get  into  the  right  bronchus,  which  is  wider,  somewhat  more 
frequently  than  they  do  into  the  left.  Stenosis  of  the  main  bronchi  from  pres- 
sure also  arises  from  aneurisms  of  the  aorta,  mediastinal  tumors,  enlarged  bron- 
chial lymph-glands,  etc.  Stenosis  of  the  left  bronchus  from  the  pressure  of  the 
greatly  dilated  left  auricle  has  been  observed  in  mitral  stenosis. 

The  symptoms  are  not  equally  distinct  in  all  cases,  and  they  depend  upon  the 
shutting  off  of  the  corresponding  part  of  the  lung.  The  dyspnoea  is  usually  very 
evident,  especially  in  acute  cases.  The  respiratory  excursions  are  much  less  on 
the  affected  side  than  on  the  sound  side.  The  percussion-note  remains  clear; 
sometimes  it  is  very  deep,  because  the  lung  beyond  the  narrowed  bronchus  is  con- 
stantly inflated.  Auscultation  shows  complete  absence  of  the  vesicular  respiratory 
murmur.  We  either  hear  nothing  or  we  sometimes  hear  over  the  whole  side  a 
loud  whistling  or  humming  sound,  the  vibration  of  which  can  in  some  cases  be 
felt  by  the  hand  applied  to  the  chest-wall.  The  vocal  fremitus  is  diminished  on 
the  affected  side.    A  vicarious  emphysema  soon  develops  in  the  other  lung. 

Lobular  pneumonia  frequently  develops  as  a  result  of  the  entrance  of  foreign 
bodies  into  a  bronchus,  because  the  agents  of  inflammation  have  entered  at  the 
same  time  with  these  bodies,  and,  as  the  expectoration  can  be  evacuated  only  with 
difficulty,  and  hence  is  more  or  less  stagnant,  these  irritants  can  readily  establish 
themselves  in  it.  In  stenosis  from  pressure  the  condition  may  of  course  be  modi- 
fied in  many  ways  by  the  primary  disease. 

The  prognosis  and  treatment  of  tracheal  and  bronchial  stenosis  depend  en- 
tirely upon  the  nature  of  the  primary  disease.  General  statements  as  to  treat- 
ment, therefore,  need  not  be  given  here.  A  direct  mechanical  treatment  of  tracheal 
stenosis  in  appropriate  cases,  such  as  cicatricial  stenosis,  may  be  undertaken  ac- 
cording to  the  different  modes  of  dilatation  above  enumerated.  The  methods 
for  removing  foreign  bodies  from  the  larger  air-passages  belong  to  the  domain  of 
surgery.  The  employment  of  an  emetic  has  met  with  distinct  success  in  such 
cases,  but  it  is  not  without  danger,  for  the  foreign  body  may  wedge  itself  into  the 
glottis  during  the  act  of  vomiting  and  occasion  danger  of  instant  suffocation. 


CHAPTER  VIII 

BRONCHIAL   ASTHMA 

(Exudative  Bvoncliiolitis.     Asthmatic  Bronchiolitis) 

Definition  and  Causes  of  the  Disease. — Bronchial  asthma  is  the  name  we 
give  to  a  morbid  condition  whose  chief  symptom  is  a  special  form  of  severe 
dyspnoea.  The  characteristic  features  of  the  dyspnoea  of  bronchial  asthma  are, 
first,  that  it  occurs  in  paroxysms,  or  at  least  that  it  grows  worse  paroxysmally, 
and,  second,  its  peculiar  manner  of  onset.  The  special  character  of  the  dyspnoea 
of  bronchial  asthma  is  explained  by  the  fact  that  every  true  bronchial  astlnna  is 
due  to  an  extensive  and  quite  rapid  contraction  of  the  smaller  and  smallest  bron- 
chial branches.  This  always  gives  rise  to  a  form  of  distress  for  breath  which  differs 
materially  from  every  other  form  of  dyspnoea. 


182  DISEASES    OE   THE   EESPIRATORY   OEGA:NtS 

The  question  as  to  the  origin  of  bronchial  asthma  coincides,  then,  with  the 
question  as  to  the  origin  of  that  extensive  contraction  of  the  bronchioles  which 
is  the  root  of  the  disturbance.  There  seems  to  us  no  doubt  that  the  latter 
should  not  always  be  referred  to  the  same  cause.  We  must  therefore  distinguish 
several  forms  of  bronchial  asthma,  which,  as  a  result  of  the  similar  conditions 
of  dyspnoea,  have  many  points  of  clinical  similarity. 

Eormerly  the  so-called  nervous  bronchial  astlnna  was  considered  to  be  the 
commonest  form.  Asthma  in  many  cases  was  regarded  as  a  pure  "  neurosis,"  due 
to  paroxysms  of  tonic  spasm  of  the  circular  muscles  in  the  small  bronchi  (Trous- 
seau, Biermer).  The  sudden  contraction  of  the  bronchi  and  the  consequent 
dyspncea  could,  in  fact,  be  very  well  explained  in  this  way.  The  only  thing  left 
unexplained  is  the  conditions  causing  the  sudden  onset  of  such  a  spasm. 

Many  recent  observations  (Voltolini,  B.  Eriinkel,  Hack,  etc.)  have  rendered  it 
extremely  probable  that,  in  at  least  a  part  of  the  cases,  reflex  processes  play  a 
great  part,  and  especially  reflex  processes  from  the  nasal  mucous  membrane. 
Many  patients  with  asthma  have  been  found  to  have  marked  changes  in  the  nose, 
most  frequently  enlargement  of  the  so-called  erectile  bodies  on  one  or  more  tur- 
binated bones,  also  nasal  polypi,  chronic  catarrh  of  the  mucous  membrane,  etc. 
The  evidence  of  the  close  connection  between  the  attacks  of  bronchial  asthma 
and  those  morbid  processes  rest,  in  the  first  place,  upon  the  clinical  fact  that  the 
asthmatic  attack  usually  begins  with  a  marked  increase  of  the  nasal  symptoms  (a 
stuffed  nose,  greater  secretion,  etc.) ;  and,  in  the  second  place,  especially  upon  the 
important  therapeutic  observation  that  in  such  cases  the  asthma  may  be  made 
permanently  to  disappear  by  removing  the  nasal  trouble. 

Accordingly  there  can  hardly  remain  a  doubt  that  in  such  instances  it  is  proper 
to  speak  of  a  reflex  bronchial  asthma.  Certain  observations  which  have  long  been 
familiar  are  probably  connected  with  these  facts  we  have  mentioned — namely, 
the  cases  in  which  persons  are  said  to  have  genuine  asthmatic  attacks  from 
particular  odors  (ipecac,  burnt  coffee,  violets,  etc.).  This  is  probably  a  reflex 
process  coming  from  the  nose.  Similar  relations  doubtless  exist  in  the  so-called 
hay  asthma  (see  page  135). 

Although  we  may  not  question  the  occurrence  of  a  reflex  bronchial  asthma, 
yet  we  can  not  regard  the  theory  that  it  is  caused  by  a  tonic  spasm  of  the  bron- 
chial muscles  as  absolutely  proved.  So  far  as  our  own  experience  goes,  even  in 
"  reflex  asthma  "  there  are  usually  during  the  attack  plain  signs  of  an  abnormal 
secretion  or  exudation  in  the  smaller  bronchi  (expectoration,  bronchitic  rales, 
etc.)  ;  but  this  condition  requires  further  explanation  than  by  the  assumption  of 
a  muscular  spasm.  We  are  therefore  of  the  opinion  that  we  should  not  wholly 
reject  the  hypothesis  advanced  by  many  authors  (Weber,  Stork,  Erantzel).  Ac- 
cording to  this  hypothesis,  acute  stenosis  of  the  bronchioles  is  caused  much  less 
by  a  muscular  spasm  than  by  an  acute  dilatation  of  the  blood-vessels  and  acute 
swelling  of  the  mucous  membrane.  Such  a  "  vaso-motor  "  change  may  very  well 
be  excited  by  reflex  causes,  and  it  would  much  better  explain  the  conditions  in 
an  asthmatic  attack  than  would  the  assumption  of  a  purely  muscular  spasm. 

It  is  doubtful  whether  genuine  bronchial  asthma  may  be  due  to  a  reflex  from 
any  other  organ  than  the  nose.  The  most  credible  statements  are  those  in  regard 
to  the  connection  between  bronchial  asthma  and  disease  of  the  pharynx  (hyper- 
trophy of  the  tonsils),  but  the  statements  in  regard  to  the  occurrence  of  asthmatic 
attacks  in  diseases  of  the  ear,  stomach  ("dyspeptic  asthma"),  intestines,  female 
sexual  organs,  etc.,  are  to  be  regarded  with  the  greatest  skepticism.  In  these  cases 
there  is  usually  confusion  between  true  asthma  and  other  conditions  of  dyspnoea 
(hysterical  asthma,  conditions  of  cardiac  weakness,  etc.). 

Although,  from  what  has  been  said,  it  follows  that  the  occurrence  of  a  nervous 
reflex  asthma  can  not  be  questioned,  our  knowledge  as  to  the  onset  of  nervous 


BKOXCHIAL  ASTHMA  183 

asthma  as  a  primary  affection  is  still  very  vague.  At  any  rate  the  cases  which, 
after  careful  investigation,  allow  no  other  explanation  are  very  rare.  It  is  also 
doubtful  whether  we  have  to  do  with  a  primary  bronchial  spasm  or  with  vaso- 
motor conditions.  The  theory  formerly  maintained  by  many  writers,  that  a  tonic 
spasm  of  the  diaphragm  could  be  the  cause  of  a  true  asthmatic  attack,  is  at  present 
almost  universally  abandoned.  This  theory  is  contradicted  by  the  occurrence  of 
manifest  respiratory  movements  of  the  diaphragm  during  the  asthmatic  attack. 
These  movements  have  also  been  demonstrated  of  late  by  the  Rontgen  rays. 

Apart  from  the  reflex  asthmatic  conditions,  most  cases  of  so-called  "  bronchial 
asthma  "  are  undoubtedly  due  to  a  primary  catarrhal  inflammation  of  the  smallest 
bronchi  and  bronchioles;  but  since  not  even  catarrh  of  the  finer  bronchi  causes 
typical  asthmatic  attacks,  we  must  assume  that  in  asthma  we  have  to  do  with  a 
special  form  of  bronchiolitis  or  at  least  with  special  attendant  conditions  which 
cause  the  asthma.  Curschmann,  to  whom  we  owe  the  first  accurate  clinical  investi- 
gation of  this  most  common  form  of  bronchial  asthma,  termed  the  bronchial 
affection,  which  forms  the  basis  of  it,  "  exudative  bronchiolitis,"  but  we  have 
ourselves  for  a  good  while  usually  employed  the  name  of  "  asthmatic  bronchio- 
litis." We  would  indicate  by  this  term  a  peculiar  disease  of  the  smaller  bronchi 
and  bronchioles  whose  characteristic  features  are  a  peculiar  sort  of  expectoration 
(vide  infra)  and  characteristic  "  asthmatic "  {vide  infra)  attacks  of  dyspnoea 
which  grow  worse  paroxysmally.  It  is  indeed  possible,  but  not  certain,  that  in 
the  latter  regard  nervous  reflex  processes  in  the  bronchioles  also  play  a  part, 
somewhat  like  the  spasm  of  the  glottis  in  whooping-cough.  The  causes  of  this 
asthmatic  exudative  bronchiolitis  are  not  always  evident.  Sometimes,  however, 
circumstances  apparently  play  a  part  similar  to  those  producing  ordinary  bron- 
chitis, especially  the  continuous  inhalation  of  vegetable  dust  (wool,  meal,  etc.). 
Many  cases  of  bronchial  asthma  may  also  with  great  probability  be  referred  to 
some  severe  bronchial  disease  in  childhood  (whooping-cough,  severe  bronchitis  of 
measles,  etc.). 

Symptoms  and  Course  of  the  Disease. — We  will  begin  the  account  of  the 
symptomatology  by  a  description  of  the  asthmatic  "  attack."  In  its  purest  form 
"  nervous  "  bronchial  asthma  consists,  in  fact,  of  single  attacks  of  dyspnoea,  dif- 
fering in  frequency  and  duration,  which  occur  at  least  without  special  cause  or 
without  any  discoverable  reason  in  persons  otherwise  apparently  healthy.  In  the 
intervals  between  the  attacks  the  patient  is  perfectly  well,  and,  in  partictilar, 
shows  no  signs  of  disease  of  the  respiratory  organs.  In  most  cases  of  "  bronchial 
asthma,"  however,  the  attacks,  as  we  have  said,  are  only  more  or  less  sudden  ex- 
acerbations of  a  condition  which  in  the  intervals  is  not  perfectly  normal.  While 
ordinarily  only  the  signs  of  a  chronic  bronchitis  are  present,  often  associated 
with  pulmonary  emphysema,  from  time  to  time  exacetbations  occur,  usually  in 
the  form  of  long-continued  asthmatic  dyspnoea,  lasting  for  days  or  weeks.  It  is 
this  latter  form  especially  which  can  be  explained  only  by  the  assumption  of  a 
true  bronchiolitis. 

The  asthmatic  attack  either  begins  quite  suddenly,  or,  is  preceded  for  a 
shorter  or  longer  period  by  prodromata.  These  consist  in  a  general  feeling  of  dis- 
comfort, in  abnormal  sensations  in  the  larynx  or  epigastrium,  sometimes  in  re- 
markably frequent  gaping,  and  often  in  a  marked  coryza  associated  with  a  good 
deal  of  secretion  and  frequent  sneezing  (compare  the  relation  between  many  at- 
tacks of  asthma  and  diseases  of  the  nose,  given  above).  The  attack  begins  in 
most  cases  at  night  (before  midnight).  The  patient  wakes  up  with  an  intense 
feeling  of  pressure  and  anxiety.  Sometimes  he  complains  of  a  feeling  of  pain 
in  the  chest.  He  has  to  sit  up  straight,  and  in  severe  cases  even  to  get  out 
of  bed.  He  often  hurries  to  an  open  window  in  order  to  "  get  air."  His  ex- 
pression is  anxious;    his  skin  becomes  pale  and  cyanotic,  and  sometimes  is  cov- 


184  DISEASES    OF   THE   EESPIEATORY   OEGANS 

ered  with  a  cold  sweat.  On  objective  examination  we  are  at  once  struck  by  the 
characteristic  change  in  the  respiration.  Both  inspiration  and,  especially,  expira- 
tion are  almost  always  accompanied  by  a  high-pitched  whistling  sound,  audible 
at  a  distance.  Both  respiratory  acts  are  labored,  requiring  the  aid  of  the  acces- 
sory muscles.  On  inspiration,  only  the  upper  part  of  the  thorax  is  elevated  to 
any  extent.  We  see  in  the  neck  the  inspiratory  contraction  of  the  sterno-cleido- 
mastoids,  the  scaleni,  etc.  Still  more  striking,  however,  is  the  labored,  panting, 
long-protracted  expiration,  during  which  the  abdominal  muscles  are  contracted 
to  a  board-like  hardness.  We  therefore  recognize  the  disturbance  of  respiration 
in  asthma  as  essentially  an  expiratory  dyspnoea.  The  frequency  of  respiration  is 
in  many  cases  normal,  oj  even  somewhat  diminished,  yet  we  have  repeatedly 
counted  thirty  or  forty  respirations  a  minute. 

On  physical  examination  of  the  lur^s  during  the  paroxysm,  we  find  the  per- 
cussion-note over  them  normal  or  even  strikingly  loud  and  deep — the  "  box-tone." 
The  lower  boundary  of  the  lung  is  usually  found  one  or  two  intercostal  spaces 
lower  than  normal,  l^ot  only  is  this  condition  shown  in  the  cases  with  a  perma- 
nent pulmonary  emphysema,  but  during  the  asthmatic  attack  itself  there  occurs 
an  acute  inflation  of  the  lung.  The  latter  is  probably  explained  by  the  fact  that 
the  lung  is  much  stretched  by  the  strenuous  inspirations  which  are  made  by  aid 
of  the  accessory  muscles,  while  the  weaker  expiratory  force  is  not  enough  wholly 
to  drive  out  the  air  again  through  the  contracted  bronchioles.  Therefore  it  hap- 
pens in  bronchial  asthma,  as  in  every  other  bronchial  disease,  that  the  expiration 
is  usually  more  labored  and  protracted  than  the  inspiration.  On  auscultation, 
high-pitched  whistling  and  creaking  sounds,  which  quite  obscure  the  vesicular 
murmur,  are  heard  over  most  of  the  lung,  especially  during  the  long  expiration^. 
In  many  places,  indeed,  where  the  bronchioles  are  almost  completely  closed,  the 
respiratory  murmur  is  entirely  absent,  or  we  hear  only  a  low  whistle  on  expira- 
tion. Toward  the  end  of  the  paroxysm  the  noises  become  deeper  and  more  boom- 
ing, and  sometimes  we  hear  a  few  moist  rales. 

In  brief  paroxysms  there  may  be  scarcely  any  cough  or  expectoration.  In 
most,  particularly  in  the  tedious  cases  of  true  asthmatic  bronchiolitis,  there  is, 
however,  a  scanty  tough  mucous  expectoration.  In  this  are  found,  beside  the 
ordinary  constituents  of  simple  bronchitic  sputum,  larger  or  smaller  numbers  of 
very  characteristic  clumps.  These  may  be  yellow  or  greenish-yellow,  or,  on  the 
other  hand,  gray.  The  yellowish  masses,  which  are  usually  very  tough,  and  often 
consist  of  a  bunch  of  thready  matter,  represent  swollen  and  fatty-degenerated  pus 
corpuscles,  between  which  are  very  frequently  interspersed  a  considerable  number 
of  pointed  octahedral  crystals.  These  crystals  were  first  described  by  Leyden  in 
the  sputum  of  asthmatic  patients,  and  are  usually  termed  asthma  crystals  (see  Fig. 
25).  Chemically  they  are  identical  with  "Charcot's  crystals,"  which  are  found 
in  the  leukemic  spleen,  the  bone  marrow,  etc.,  and  they  probably  represent  the 
phosphoric-acid  salt  of  an  organic  base  (Schreiner's  base,  C^H^jST),  although  this 
has  lately  been  questioned.  As  soon  as  the  paroxysms  cease  the  number  of  crystals 
in  the  sputum  usually  begins  to  diminish  rapidly,  and  it  is  often  possible  to 
observe  in  them  evident  signs  of  disintegration.  Nothing^is  known,  as  to  the 
origin  of  these  crystals.  Often,  also,  numerous  ciliated  epithelial  cells  are  found, 
in  addition  to  the  crystals,  in  the  yellow  masses.  The  gray  plugs  in  the  sputum 
of  asthmatic  patients  consist  mainly  of  clumps  of  thready  mucus,  and  contain 
the  peculiar  "spirals"  which  were  first  described  by  Ungar  and  by  Cursch- 
mann.  Many  of  these  spiral  threads  are  visible  to  the  naked  eye,  but  others 
demand  the  microscope  for  their  recognition,  through  which  they  are  seen  as 
brilliant  forms  composed  entirely  of  various  sized  bands  and  threads  collected 
in  spirals  (see  Fig.  25).  Sometimes  a  brilliant  central  thread  of  small  diameter 
is  seen  in  the  midst  of  the  spiral.    Around  the  spirals  are  found  round  cells,  drops 


BEONCHIAL  ASTHMA 


185 


of  fat  and  myeline,  and  sometimes  ciliated  epithelium,  and  epithelial  cells  from 
the  pulmonary  alveoli.  As  to  the  precise  way  in  which  the  spirals  and  their 
central  thread  develop,  the  question  is  not  yet  settled,  but  it  is  certain  that  the 
spirals  represent  casts  of  the  minutest  spirally  twisted  branches  of  the  bronchi, 


R^^%>^ 


Fig.  25.— Asthma  crystals  and  Curschmann's  spirals  (a,  central  fiber). 

and  therefore  clearly  indicate  the  existence  of  a  peculiar  disease  of  the  finest 
terminal  bronchial  twigs. 

Of  the  other  peculiarities  of  the  sputum  in  bronchial  asthma  we  may  mention, 
first  of  all,  the  almost  invariable  occurrence  of  very  many  eosinophilous  cells 
in  the  sputum,  and  also,  apparently,  in  the  blood.  The  significance  of  this  fact  is 
still  unknown.  We  occasionally  find  in  the  sputum  of  astlimatics  crystals  of  calcic 
oxalate  and  calcic  phosphate. 

The  pulse  is  usually  accelerated  during  the  asthmatic  paroxysm,  the  arteries 
contracted;  the  bodily  temperature  is  normal,  or  sometimes  even  subnormal.  In 
protracted  attacks  we  have  repeatedly  seen  a  slight  febrile  movement  up  to  about 
102°  (39°  C). 

The  duration  of  the  asthmatic  paroxysm  is  very  different  in  individual  cases, 
as  has  already  been  said.  Sometimes  it  lasts  only  a  few  hours,  but  sometimes 
it  lasts  several  days,  and  even  weeks.  Marked  exacerbations  and  remissions  of 
the  disease  usually  alternate.  The  frequency  of  the  paroxysms  in  ordinary 
astlmia  also  varies  exceedingly.  Sometimes  they  come  on  almost  every  night,  and 
then  there  are  long  pauses  of  months  and  years,  so  that  we  can  not  make  any 
general  statements  as  to  the  course  of  the  disease.  Many  asthmatic  patients  make 
very  remarkable  statements  as  to  the  individual  exciting  causes  of  their  attacks. 
Many  patients  claim,  for  example,  that  the  attacks  occur  only  in  certain  places, 
while  in  other  places  they  are  wholly  free  from  the  trouble,  that  they  can  live 
only  in  the  upper  storeys  of  the  house,  etc.  Such  statements  should  not  remain 
unheeded,  although  it  is  certain  that  they  are  often  due  to  imagination.  Definite 
recoveries  are  quite  rare,  since  long-continued  asthma  almost  always  leads  to 
chronic  pulmonary  emphysema  with  all  its  consequences. 

Diagnosis. — The  diagnosis  of  the  bronchial  asthmatic  condition  as  such  is 
not  difficult  if  we  limit  ourselves  strictly  to  the  characteristic  type  of  the  disease : 
the  strenuous  respiration  with  wheezing  that  can  be  heard  at  a  distance,  the 
labored,  prolonged  expiration,  the  characteristic  physical  signs  in  the  lungs,  and 
the  peculiar  sputum.  Usually  we  can  easily  distinguish  bronchial  asthmatic 
dyspnoea  from  cardiac  asthma  (q.v.),  spasm  of  the  glottis  (q.v.),  and  also 
from  hysterical  dyspnoea  with  its  superficial  and  very  rapid  respiration  and 
normal  conditions  in  the  lungs.  This  latter  distinction  of  true  bronchial  asthma 
f  i-om  "  hysterical  asthma  "  is  very  important  both  in  prognosis  and  treatment, 
since  the  two  are  frequently  confounded.     If  we  are  sure  that  we  are  dealing 


186  DISEASES    OF   THE   EESPIEATOKT   OEGAlv^S 

with  true  asthmatic  attacks,  the  next  question  is  whether  it  is  a  "  pxirely  nervous  " 
reflex  asthma  qr  an  asthmatic  exudative  bronchiolitis.  Here,  of  course,  we  can 
decide  only  after  a  careful  and  thorough  examination  of  the  patient  (especially  of 
the  nasal  cavities)  and  after  observing  the  course  of  the  disease.  Finally,  we  must 
also  consider  the  possibility  of  a  purely  symptomatic  asthma  in  chronic  pulmonary 
emphysema,  in  the  chronic  bronchitis  of  renal  disease  or  arthritis,  etc.  We  must, 
however,  confine  our  iise  of  the  term  "  symptomatic  bronchial  asthma  "  to  those 
cases  in  which  we  actually  have  a  dyspnoea  with  all  the  characteristic  peculiari- 
ties of  true  bronchial  asthma. 

Treatment. — In  every  case  of  asthma  the  first  thing  to  be  thought  of  is 
whether  there  is  not  a  definite  cause  whose  removal  may  cure  the  disease.  In  this 
connection  we  should  examine  the  nose  carefully,  since  numerous  recent  ob- 
servations have  shown  that  a  previously  existing  asthma  may  wholly  disappear 
or  at  least  be  materially  relieved  after  the  treatment  of  some  nasal  disease  which 
may  be  present,  such  as  the  removal  of  polypi,  the  destruction  of  the  erectile  bodies 
by  the  galvano-cautery,  etc.  Of  course  these  results  should  not  be  over-estimated. 
It  has  repeatedly  been  claimed  by  nasal  specialists  that  in  many  asthmatic  patients 
we  can  find  a  definite  spot  in  the  nose  and  excite  an  asthmatic  attack  by  touching 
it  with  a  probe.  This  spot  must  then  be  treated  first  of  all.  "We  will  not  wholly 
reject  these  statements,  but  we  are  somewhat  skeptical  in  regard  to  them.  At  any 
rate,  the  nose  should  be  treated,  in  our  opinion,  only  when  it  presents  actual 
morbid  changes. 

If  we  can  not  satisfy  the  causal  indication  in  this  way,  we  should  always  try 
next  a  remedy  which  must  pass  for  a  direct  specific  against  certain  forms  of 
asthma — iodide  of  potassium.  In  doses  of  twenty  to  forty-five  grains  a  day  (grm. 
1.5-3.0),  or  even  more  if  necessary,  this  usually  causes  a  rapid  improvement, 
which  of  course  is  not  always,  although  it  is  frequently,  permanent.  In  asthmatic 
bronchiolitis,  especially,  iodide  of  potassium  in  large  doses  often  acts  excellently. 
It  seems  to  make  the  tough  secretion  more  fluid,  to  ease  the  expectoration,  and 
in  this  way  to  lessen  the  stenosis  of  the  bronchioles.  Of  course  a  permanent  and 
^-complete  cure  is  only  rarely  obtained  from  iodide  of  potassium.  If  iodide  of  potas- 
sium has  been  used  in  vain,  we  must  turn  to  the  other  remedies  which  have  been 
employed  against  asthma,  although  their  action  is  often  quite  uncertain.  We  may 
mention  here  the  nitrite  of  sodium  (two  parts  in  one  hundred  and  twenty  of  water, 
two  to  three  teaspoonfuls  a  day),  and  nitro-glycerine,  which  has  an  analogous 
action  (twenty  drops  of  a  one-per-cent.  alcoholic  solution  in  six  and  a  half  ounces 
[grm.  200]  of  water,  a  tablespoonful  two  or  three  times  a  day) ;  also  bromide  of 
potassium,  belladonna,  atropine,  etc.  In  some  cases  pneumatic  treatment,  such 
as  the  inhalation  of  compressed  air,  has  been  successful,  and  sometimes,  too,  elec- 
tricity (galvanization  and  faradization  of  the  neck),  or  hydrotherapy,  has  been 
claimed  to  give  relief.  Change  of  climate  may  sometimes  be  of  distinct  service. 
Many  patients  bear  the  sea-air  well,  while  with  others  a  mountain  residence 
exerts  a  favorable  influence.  Special  resorts  (Marienbad,  Kissingen,  ferruginous 
baths,  etc.)  may  often  be  recommended  with  advantage  if  appropriate  to  the 
patient's  general  constitution. 

In  severe  cases  a  special  symptomatic  treatment  of  the  attack  itself  is  often 
necessary.  Narcotics  are  without  doubt  the  most  effective,  especially  chloral  and 
morphine.  In  severe  attacks  we  can  not  avoid  injections  of  morphine,  but  we 
must  always  be  cautious  in  order  that  the  patient  may  not  form  the  habit  of 
using  this  to  excess.  Chloral  hydrate  (gr.  xv-xxx,  grm.  1.0-2.0)  often  relieves  the 
individual  attack.  Among  other  symptomatic  remedies  we  may  mention  mus- 
tard-plasters to  the  chest  and  calves,  putting  the  hands  and  feet  into  hot 
water,  inhalations  of  nitrite  of  amyl,  turpentine,  chloroform,  pyridine,  etc. 
Fumigation  with  saltpeter  paper — unsized  paper  dipped  in  a  concentrated  solu- 


PULMOK"ARY   EMPHYSEMA  187 

tion  of  nitrate  of  potassium  and  dried — and  the  stramonium  cigarettes  to  be 
had  in  most  drug-stores,  are  much  praised.  The  patient  may  also  smoke  with 
benefit  stramonium  or  belladonna  leaves  which  have  previously  been  dipped  in  a 
solution  of  saltpeter  and  then  dried.  Many  patients  praise  highly  the  different 
asthma  cigarettes  and  smoke-producing  powders  or  pastilles,  which  are  sold  as 
secret  remedies,  especially  in  America.  Such  apparent  success  is  certainly  due  in 
great  measure  to  the  psychical  suggestion  wrought  by  these  remedies. 

[Potassic  iodide  is  more  likely  to  prevent  recurrence  if  it  is  given  continu- 
ously, for  several  months  at  least,  and  it  should  not  be  thrown  aside  as  useless 
until  it  has  been  pushed  to  the  limit  of  toleration  without  avail.  A  convenient 
form  of  administration  is  in  saturated  aqueous  solution,  a  minim  of  which  repre- 
sents about  a  grain  of  the  drug. 

The  syrup  of  hydriodic  acid  may  be  substituted  for  potassic  iodide  in  cases 
of  intolerance  of  the  latter.  Grindelia  robusta,  a  drachm  of  the  fluid  extract 
three  or  four  times  a  day,  serves  sometimes  to  prevent  recurrence  of  attacks. 
Marked  alleviation  of  the  paroxysms  is  often  obtained  from  the  inhalation  of 
fifteen  to  thirty  drops  of  the  iodide  of  ethyl.] 


SECTIOISr  IV 

Diseases  of  the  Lungs 

CHAPTER  I 

PULMONARY  EMPHYSEMA 

{Alveolar  Ectasia.     Pneumatosis  pidmonum) 

Nature  and  .^Etiology  of  the  Disease. — Pulmonary  emphysema,  the  abnormal 
inflation  and  dilatation  of  the  lungs,  is  one  of  the  commonest  pulmonary  affec- 
tions. It  either  develops  in  separate  parts  of  the  lung,  in  which  case  it  is  subordi- 
nate to  other  pathological  changes  which  co-exist  in  the  lungs,  or  it  involves 
almost  the  whole  extent  of  both  lungs,  and  then  presents  the  symptoms  of  a  char- 
acteristic affection,  which  it  is  usually  easy  to  recognize. 

The  essence  of  pulmonary  emphysema,  the  condition  from  which  most  symp- 
toms are  immediately  derived,  is  the  loss  of  elasticity  in  the  lungs.  If  we  com- 
pare the  sound  lung,  with  its  normal  elastic  force,  to  a  new  and  very  tense  rub- 
ber band,  the  emphysematous  lung  must  be  compared  to  an  old  and  lax  band  that 
is  stretched  and  pulled  out.  We  therefore  see  why  the  emphysematous  lung  takes 
up  a  greater  space  than  the  sound  one,  for,  on  account  of  its  lack  of  elasticity,  it 
can  no  longer  contract  to  its  former  volume.  We  may  therefore  call  emphysema  a 
permanent  inspiratory  distention  of  the  lung  from  which  it  can  no  longer  return 
to  its  expiratory  condition.  If  we  open  the  thorax  of  a  subject  with  nonnal 
lungs,  they  contract,  as  is  well  known,  but  the  emphysematous  lungs  remain  in 
their  inflated  condition  after  the  thorax  has  been  opened. 

If  we  inquire  into  the  factors  which  cause  this  loss  of  elasticity  in  the  lung. 
we  find  that  they  are  the  same  kind  of  influences  which  tend  to  diminish  the  elas- 
ticity of  any  other  elastic  body.  As  a  rubber  band,  by  much  pulling  and  stretch- 
ing, gradually  gets  longer  and  less  elastic,  so  the  lungs,  as  a  result  of  their  abnor- 
mally frequent  and  severe  distention,  gradually  become  inelastic  and  emphy- 
sematous. Emphysema  in  many  cases  is  a  true  wearing  out  of  the  lung.  The 
normal  traction  of  inspiration,  which  is  continually  making  new  demands   on 


188  DISEASES    OF   THE   EESPIEATOEY   OEGA^tS 

the  elastic  powers  of  the  lungs,  finally  leads  to  a  loss  of  elasticity  in  them.  In 
advanced  age  most  lungs  become  more  or  less  inelastic.  The  lungs  of  an  old 
man  are  like  an  elastic  band  which  has  done  its  work  for  years  but  which  has 
finally  given  out.  We  therefore  class  emphysema  of  the  lungs  in  old  age 
rather  among  the  states  of  involution,  such  as  develop  in  almost  all  organs  in 
advanced  life,  than  among  special  pathological  changes.  We  distinguish,  more- 
over, most  lungs  with  senile  emphysema  from  other  emphysematous  lungs  by 
the  fact  that  their  volume  as  a  whole  is  not  increased,  but  is  rather  diminished 
below  that  of  the  healthy  lung,  since  we  find  in  them  the  extensive  atrophic 
processes  of  old  age. 

The  condition  becomes  pathological,  however,  if  the  elasticity  of  the  lung  is 
deficient  in  earlier  years  and  independently  of  the  action  of  the  special  in- 
jurious influences  which  will  soon  be  mentioned.  In  such  cases  of  emphysema, 
developing  in  middle  life  or  even  in  youth,  the  idea  of  a  congenital  weakness  of 
the  elastic  elements  in  the  lungs  can  not  be  set  aside.  It  probably  consists  in  a 
quantitative  or  a  qualitative  defect  of  the  elastic  tissue.  Some  observations  seena 
to  corroborate  the  statement  that  a  disposition  to  emphysema  may  be  present  in 
several  members  of  the  same  family. 

If  a  lung  whose  elasticity  is  previously  subnormal  can  not  persistently  satisfy 
the  ordinary  demands  upon  it,  a  normal  lung,  on  the  other  hand,  also  loses  its 
elasticity  if  the  demands  made  upon  it  are  greater  than  it  can  perform.  This  is 
the  reason  why  pulmonary  emphysema  is  in  some  instances  to  be  regarded  as  a  dis- 
ease arising  from  the  occupation.  We  mean  here  not  only  those  influences  which 
lead  to  chronic  bronchitis  and  thus  later  to  emphysema  (vide  infra),  but  more  espe- 
cially the  abnormal  demands  upon  the  lungs  in  all  those  callings  which  necessitate 
severe  physical  labor.  We  must  not  only  regard  the  deeper  and  more  rapid  res- 
pirations, but  also  the  increased  pressure  during  expiration  to  wliich  the  lungs  are 
often  exposed  in  the  raising  of  heavy  weights,  etc.  This  explains  the  common  oc- 
currence of  emphysema  in  the  laboring  classes,  and  also  its  greater  frequency  in 
men  than  in  women.  Besides  this,  we  must  add  that  in  certain  callings,  such  as 
glass-blowing  and  horn-blowing,  the  over-straining  of  the  lungs  is  much  more 
direct.  In  all  such  cases  emphysema  may  be  termed  simply  a  premature  exhaustion 
of  the  lungs. 

In  very  many  cases  emphysema  develops  as  a  result  of  other  diseases  of  the 
lung,  and  especially  as  a  result  of  chronic  bronchitis.  Dry  catarrh  of  the  medium- 
sized  and  finer  bronchi  when  of  long  duration  leads,  as  a  rule,  to  pulmonary  emphy- 
sema. The  abnormal  mechanical  influences  to  which  the  lungs  are  thus  exposed 
act  both  in  inspiration  and  in  expiration.  Since  the  entrance  of  air  to  the  alveoli 
is  rendered  more  diflicult  by  the  swelling  of  the  mucous  membrane  in  the  smaller 
bronchi,  abnormally  deep  and  strong  inspirations  are  necessary,  with  a  marked 
expansion  of  the  alveoli,  in  order  to  draw  a  sufficient  quantity  of  air  into  the 
alveoli.  The  alveolar  walls  are  therefore  exposed  to  an  abnormal  traction  at  each 
inspiration.  On  expiration,  a  pressure  from  within,  which  is  perhaps  even  more 
injurious,  acts  on  the  alveoli.  The  ordinary  expiration,  which  usually  needs  only 
the  elastic  power  of  the  lungs,  is  not  sufficient  in  chronic  bronchitis  to  drive  the 
air  out  of  the  alveoli  through  the  narrowed  bronchi.  Thus  arise  the  difficulty 
and  delay  in  expiration  which  are  present  in  chronic  bronchitis,  and  which  lead 
to  the  active  participation  of  the  muscles  of  expiration,  the  abdominal  group  of 
muscles.  On  forced  expiration,  however,  the  pressure  does  not  act  simply  upon 
the  contents  of  the  alveoli,  but  much  more  upon  the  smaller  bronchi  themselves. 
The  channel  of  exit  for  the  air  from  the  alveoli,  therefore,  becomes  still  narrower. 
Since  the  air  can  not  at  once  escape,  the  pressure  within  the  alveoli  is  raised  by 
the  efforts  at  expiration,  and  the  alveolar  wall  is  thus  again  abnormally  expanded. 
The  cough,  which  is  often  present  in  chronic  bronchitis,  is  a  further  factor,  which 


PULMONAKY  EMPHYSEMA  189 

acts  in  a  precisely  similar  injurious  fashion.  The  attacks  of  coughing  begin  with 
a  forced  contraction  of  the  muscles  of  expiration,  which  follows  the  closure  of  the 
glottis.  Until  the  glottis  opens,  therefore,  the  lower  parts  of  the  lung  especially 
are  put  under  strong  pressure.  The  air  in  them,  which  can  not  escape  outward, 
is  driven  into  the  upper  parts  of  the  lung,  and  there  leads  to  expansion  of  the 
alveoli,  and  finally  to  emphysema. 

We  accordingly  see  that  a  number  of  injurious  influences  co-operate  in  the 
gradual  development  of  emphysema  from  chronic  bronchitis,  and  that,  sooner  or 
later,  these  influences  have  as  their  result  the  gradual  dilatation  of  the  lungs. 
Here,  too,  we  must  bear  in  mind  the  individual  differences  in  the  resisting  power 
of  the  lungs. 

Conditions  precisely  similar  to  those  in  chronic  bronchitis  occur  in  other  dis- 
eases, and  lead  in  like  manner  to  pulmonary  emphysema.  We  very  often  see  the 
development  of  emphysema  in  severe  and  persistent  whooping-cough.  The  worst 
factor  here,  besides  the  existing  bronchitis,  is  the  f reqvient  paroxysms  of  coughing. 
Many  cases  of  pulmonary  emphysema  and  chronic  bronchitis  may  be  ultimately 
referred  to  such  a  severe  bronchial  disease  occurring  in  childhood.  We  have 
already  mentioned,  in  the  description  of  bronchial  asthma,  both  the  acute  emphy- 
sema, which  occurs  during  the  attacks,  and  the  final  development  of  a  permanent 
emphysema. 

In  conclusion,  we  must  here  consider  a  theory  advanced  by  Freund,  which 
would  make  the  development  of  an  emphysema  dependent  upon  a  "  primary  rigid 
dilatation  of  the  thorax."  It  is  indeed  conceivable  that  from  certain  pathological 
changes  in  the  costal  cartilages,  as  Freund  claims,  a  thorax,  which  had  become 
fixed  in  the  position  of  inspiration,  might  exert  a  constant  abnormal  traction  on 
the  lungs  and  so  give  rise  to  an  emphysema.  The  occurrence  of  this  hypothetical 
•  primary  disease  of  the  cartilages,  however,  has  up  to  the  present  time  not  been 
established.  It  is  rather  considered  by  the  majority  of  authors  as  a  secondary 
change,  developing  as  a  result  of  emphysema  or  else  simultaneously  with  it.  On 
the  other  hand,  it  is  certainly  remarkable  that  we  sometimes  observe  in  children 
the  "  emphysematous  habit "  of  the  thorax  and  neck,  which  will  be  more  fully  de- 
scribed further  on,  and  that  in  fact  we  can  often  discover  in  such  children  a 
beginning  emphysema  early  in  life.  We  might  perhaps  imagine  a  congenital, 
failure  of  harmony  between  the  size  of  the  thorax  and  the  size  of  the  lungs, 
whereby  the  latter  are  from  the  start  in  constant  overtension. 

Besides  the  already  described  essential  or  substantial  emphysema,  which  is  a 
special  disease  attacking  both  lungs  uniformly,  we  distinguish  a  so-called  vicarious 
or  complementary  emphysema.  If,  by  any  disease,  certain  portions  of  the  lungs 
are  incapacitated  in  their  functions,  the  parts  which  remain  healthy  must  then 
assume  the  whole  business  of  respiration.  They  become  excessively  expanded  on 
inspiration,  and  as  a  result  they  become  emphysematous.  Thus  we  see  emphysema 
of  the  upper  lobes  in  affections  of  the  lower  lobes.  Emphysema  of  one  lung  is 
most  frequently  observed  clinically  when  the  other  lung  is  extensively  diseased, 
especially  in  unilateral  chronic  contractions  of  the  lungs  and  pleurae,  usually  seen 
in  tuberculosis.  Vicarious  emphysema  may  also  be  confined  to  quite  small  por- 
tions of  the  lung,  but  then  it  is  merely  of  pathological  and  not  of  clinical  interest. 

Pathological  Anatomy. — As  we  have  seen,  the  actual  abnormality  of  the  lung 
in  emphysema  is  not  due  to  a  pathological  change,  but  to  a  change  in  its  physical 
conditions.  The  loss  of  elasticity  of  the  lung  is  shown  in  its  greater  volume,  in 
its  lack  of  contractility,  and  in  its  persistence  in  a  position  of  inspiration. 

The  single  alveoli  are  of  course  just  as  much  expanded  as  the  whole  lung,  but 
their  walls  sljow  at  first  no  histological  changes.  We  have  here,  then,  a  condi- 
tion which  Traube  has  called  "  increased  volume  of  the  lungs,"  and  has  distin- 
guished from  the  "  pulmonary  emphysema  "  proper.     This  distinction  is  without 


190  DISEASES    OF   THE   EESPIRATORY   OEGANS 

doubt  justified  anatomically,  but  clinically  it  can  not  well  be  maintained.  As  the 
distention  is  constant,  the  alveolar  walls  can  not  withstand  the  constant  traction 
and  pressure.  This  leads  to  progressive  atrophy  of  their  tissue  from  pressure — 
that  is,  it  leads  to  a  real  disappearance  of  the  elastic  elements  of  the  lung.  The 
atrophy  begins  quite  gradually.  The  partition-walls  of  the  alveoli  are  first  per- 
forated, and  then  they  partly  or  wholly  break  down.  The  neighboring  alveoli  run 
more  and  more  into  one  another,  and  thus  finally  arise  alveolar  ectasis  and  in- 
fundibular ectasis,  which  can  be  made  out  with  the  naked  eye,  and  which  may 
attain  a  diameter  of  five  or  ten  millimetres  or  more.  If  single  air-bubbles  enter 
the  interlobular,  interstitial,  or  subpleural  connective  tissue,  which  may  happen 
perhaps  in  severe  fits  of  coughing,  we  speak  of  an  interstitial  or  interlobular  em- 
physema, in  distinction  from  the  ordinary  vesicular  or  alveolar  emphysema. 

The  tissue  atrophy  in  the  septa  of  the  alveoli  affects  not  only  the  elastic  tissue, 
however,  but  also  the  branches  of  the  pulmonary  capillaries  in  the  alveo- 
lar walls.  The  affection  of  the  elastic  tissue  adds  no  new  conditions  to  the  dis- 
turbed functions  of  the  emphysematous  lung,  which  we  have  just  described.  The 
destruction  and  final  atrophy  of  the  pulmonary  capillaries,  however,  is  the  second 
important  factor  in  the  pathology  of  pulmonary  emphysema,  for,  with  the  destruc- 
tion of  so  great  a  part  of  the  vascular  area  in  the  lungs,  the  outflow  from  the 
right  side  of  the  heart  is  considerably  impeded.  There  must  therefore  necessarily 
be  a  stasis  in  the  pulmonary  arteries  and  the  right  side  of  the  heart,  and  the  right 
side  of  the  heart  can  overcome  the  increased  resistance  only  by  increased  work, 
and  thus  in  every  chronic  pulmonary  emphysema  there  finally  arise  a  dilatation 
and  consecutive  hypertrophy  of  the  right  ventricle  with  their  further  conse- 
quences, n,  ^  ^ 

Symptoms  and  Course  of  the  Disease 

General  Course  of  the  Disease. — Although  a  pulmonary  emphysema  may  . 
sometimes,  as  in  whooping-cough,  develop  in  a  comparatively  short  time,  still  its 
course  is  always  very  chronic.  In  most  cases  the  origin  of  the  disease  is  quite 
gradual,  as  in  all  those  instances  in  which  emphysema  develops  from  chronic 
bronchitis  or  asthma,  or  as  a  result  of  some  injurious  occupation.  The  symp- 
toms gradually  and  insidiously  associate  themselves  with  those  of  the  chronic 
bronchitis. 

The  symptoms  of  emphysema  usually  begin  in  middle  or  advanced  life,  but 
marked  emphysema  may  occur  in  youth  and  childhood.  The  disease  always  lasts 
for  years,  unless  some  fatal  intercurrent  disease  arises. 

The  objective  and  subjective  symptoms  are  due  either  to  the  chronic  bron- 
chitis, which  very  often  co-exists,  or  to  the  emphysema  itself.  Not  only  is  the 
bronchitis,  as  we  have  seen  above,  very  often  the  cause  of  emphysema,  but,  on 
the  other  hand,  the  development  of  chronic  bronchitis  is  greatly  favored  by  the 
circulatory  disturbances  in  the  lung  associated  with  emphysema.  Thus  the  two 
diseases,  emphysema  and  chronic  bronchitis,  are  closely  connected  clinically. 

Bronchitis  causes  its  well-known  symptoms — cough,  expectoration,  moderate 
dyspnoea,  and  a  feeling  of  pressure  in  the  chest.  The  bronchiectases,  which  are 
often  gradually  formed,  especially  in  the  lower  lobes,  may  lend  a  peculiar  stamp 
to  the  cough  and  expectoration  (see  page  178).  Emphysema  increases  the  pa- 
tient's dyspnoea  to  a  degree  which  can  never  be  caused  by  chronic  bronchitis  alone. 
The  emphysematous  lungs  soon  become  incapable  of  satisfying  any  extraordinary 
demands  of  respiration.  Many  patients  are  only  slightly  conscious  of  the  diifi- 
eulty  in  breathing  so  long  as  they  keep  quiet,  but  whenever  they  make  a  trifling 
physical  exertion,  go  up-stairs,  or  take  a  little  longer  walk  than  usual,  the  dyspnoea 
comes  on. 

The  variations  in  the  intensity  and  extent  of  the  bronchitis  correspond  to  the 
frequent  and  quite  marked  variations  in  the  patient's  feelings.    These  variations 


PULMO]STAEY  EMPHYSEMA  191 

depend  -upon  the  condition  of  the  patient,  his  circumstances,  and  the  possibility 
of  his  taking-  care  of  himself  ;  the  change  of  seasons,  too,  has  an  influence  on 
him.  In  pleasant  weather  many  patients  live  in  tolerable  comfort,  but  autumn 
and  winter  bring  an  aggravation  of  all  their  symptoms  with  the  increase  in 
their  bronchitis. 

The  last  stage  of  the  disease  is  characterized  by  the  appearance  of  disturb- 
ance of  compensation  in  the  heart.  We  have  seen  above  that  the  cause  of  the 
impairment  of  the  pulmonary  circulation,  and  of  the  resulting  hypertrophy  of 
the  right  ventricle,  is  the  closure  of  numerous  pulmonary  capillaries.  A  further 
reason  for  the  impairment  of  the  circulation  comes  from  the  disturbance  of  res- 
piration itself,  since  the  influence  of  the  respiratoiy  movements  on  the  circulation 
is  well  known.  The  appearance  of  a  marked  disturbance  of  the  circulation  may 
be  deferred  for  some  time  by  the  increased  efforts  of  the  right  ventricle.  The 
cyanosis  of  most  patients,  however,  is  due  not  only  to  incomplete  oxidation  but  to 
the  blood-stasis  which  extends  backward  from  the  right  side  of  the  heart  into 
the  veins  of  the  body.  Finally,  the  right  ventricle  becomes  more  and  more 
feeble,  the  stasis  in  the  veins  increases,  oedema  of  the  extremities  and  transudation 
into  the  various  cavities  of  the  body  ensue,  and  after  long  suffering  the  patient 
succumbs  to  dropsy. 

Emphysema  is  frequently  combined  in  its  later  stages  with  other  chronic  dis- 
eases. Pulmonary  emphysema  with  its  sequela3  is  seldom  found  at  the  autopsy 
as  a  single  lesion,  but  we  discover  in  the  cadaver  co-existing  disease  of  the  heart, 
the  blood-vessels,  or  the  kidneys,  all  a  genuine  wearing  out  of  the  aging  body. 
Pulmonary,  tuberculosis  is  often  a  final  development  in  emphysema,  but  it  is 
usually  of  the  chronic  indurated  form,  and  is  not  very  extensive. 

Physical  Examination.  1.  Inspection. — ^In  many  patients  we  can  detect  the 
disease  with  considerable  confidence  at  the  first  glance ;  we  are  therefore  justified 
in  speaking  of  an  emphysematous  habit.  The  patients  are  usually  quite  well 
nourished,  at  least  in  the  early  stages  of  the  disease,  and  are  often  rather  cor- 
pulent. They  appear  plump  or  even  somewhat  bloated,  and  their  faces  are  more 
or  less  markedly  cyanotic.  The  configuration  of  the  neck  and  thorax  is  especially 
characteristic.  The  neck  is  usually  short  and  thick;  the  sterno-eleido-mas- 
toid  muscles,  which  have  to  act  as  auxiliaries  in  inspiration,  are  tense  and 
hypertrophied.  The  inspiratory  contraction  of  the  scaleni  may  also  be  seen  and 
felt.  The  veins  in  the  neck  are  visibly  dilated,  and  in  severe  cases  are  swollen 
to  thick  blue  cords,  and  we  sometimes  see  in  them  evident  undulating  or  pulsating 
movements.  The  thorax  is  rather  short,  but  broad  and  strikingly  deep — the  "  bar- 
rel-shaped thorax."  The  intercostal  spaces  are  narrow,  and  the  lower  ribs  incline 
only  a  little  downward.  The  epigastric  angle  is  therefore  obtuse,  and  sometimes 
becomes  almost  a  straight  line.  The  respiratory  movements  are  almost  always 
accelerated  in  severe  cases.  Inspiration  becomes  short  and  labored.  The  excur- 
sions of  single  ribs  are  therefore  slight,  and  the  thorax  is  raised  rigidly  and  more 
as  a  whole.  Expiration  is  visibly  prolonged.  There  may  be  a  noticeable  retrac- 
tion of  the  intercostal  spaces  on  inspiration,  in  the  lower  and  lateral  portions  of 
the  thorax. 

This  characteristic  form  of  the  thorax  in  emphysema  is  regarded  as  a  constant 
inspiratory  position  of  the  ribs,  and  corresponds  to  the  permanent  inspiratory 
dilatation  of  the  lungs.  The  peculiar  rigidity  of  the  thorax  is  probably  due  to 
the  changes  in  the  costal  cartilages  already  described,  which,  according  to 
Ereund,  are  primary.  In  many  cases  the  emphysematous  form  of  the  thorax 
gradually  develops  in  the  course  of  the  disease,  but  in  other  cases  it  seems  to 
depend  on  some  original  predisposition  to  the  disease  (vide  supra). 

In  conclusion,  we  must  state  that  the  above  description  corresponds  to  the  typi- 
cal form  of  emphysema,  from  which  we  may  have  many  deviations.    In  the  para- 


192  DISEASES    OE   THE   EESPIEATOEY   OEGANS 

lyzed  thorax,  for  instance,  we  may  meet  with,  a  high  degree  of  essential  emphyseriia 
of  the  lungs,  which  has  often  given  rise  to  errors  in  diagnosis. 

2.  Percussion. — Percussion  gives  very  decided  results  in  the  diagnosis  of  pul- 
monary emphysema.  We  find  the  inferior  border  of  the  lungs  one  or  two  inter- 
costal spaces  lower  than  under  normal  conditions,  corresponding  to  their  perma- 
nent inspiratory  inflation.  Clear  pulmonary  resonance  on  the  right  front  in  the 
line  of  the  nipple  extends  to  the  lower  border  of  the  seventh,  and  sometimes  of  the 
eighth  rib.  On  the  left  front  it  extends  to  the  fifth  or  sixth  rib,  so  that  the  cardiac 
dullness  is  lessened.  The  area  of  cardiac  dullness  can  often  not  be  made  out  at 
all;  or  at  most,  on  strong  percussion,  it  is  made  out  in  a  limited  extent  as  rela- 
tive dullness.  The  pulmonary  resonance  extends  on  both  sides  in  the  back  to  the 
first  or  second  lumbar  vertebra.  These  results  of  percussion  in  emphysema,  how- 
ever, are  frequently  altered,  because  other  conditions,  such  as  passive  congestion 
of  the  liver,  meteorism,  and  ascites,  may  be  present  at  the  same  time,  and  push 
up  the  diaphragm.  Thus  the  detection  of  emphysema  by  percussion  is  made  decid- 
edly difiicult. 

Qualitative  changes  in  the  percussion-note  may  be  entirely  wanting  in  emphy- 
sema. The  pitch  is  sometimes  remarkably  loud  and  deep — the  "  box-tone  "  [tym- 
panitic resonance]  ;  but  in  other  cases,  especially  in  the  back,  we  find  it  somewhat 
raised.  This  may  depend  in  part  upon  the  poor  vibratory  conditions  in  the  rigid 
chest-walls,  but  in  other  cases  it  is  caused  by  the  retention  of  an  abundant  secre- 
tion in  the  lower  lobes. 

On  inspiration,  the  lower  edge  of  the  lung  moves  downward  very  little  or 
not  at  all.  This  is  an  important  sign  in  diagnosis.  Since  the  lung  is  always  in  a 
state  of  abnormal  inspiratory  distention,  and  since  the  entrance  of  air  is  impeded 
by  the  accompanying  catarrh  of  the  bronchi,  the  difference  between  the  inspiratory 
and  expiratory  expansion  of  the  lung  is  much  diminished.  The  difference  caused 
by  respiration  in  the  lower  limit  of  the  lung  affords  a  good  measure  of  the 
respiratory  disturbance  in  the  lower  lobes. 

The  detection  of  dilatation  and  hypertrophy  of  the  right  ventricle  by  percus- 
sion is  in  many  cases  difficult,  because  the  lungs  cover  the  heart.  A  positive 
result  can  be  obtained  only  by  carefully  defining  the  relative  cardiac  dullness  [by 
very  light  percussion].  The  epigastric  pulsations  frequently  seen  in  emphysema, 
and  also  the  marked  undulating  and  pulsating  movements  in  the  jugular  veins,  are 
to  be  regarded  as  quite  certain  signs  of  dilatation  of  the  right  side  of  the  heart. 

3.  Auscultation. — The  characteristic  auscultatory  sign  of  emphysema  is  the 
prolonged  expiration.  As  a  flabby  rubber  band,  when  it  is  stretched  and  then  let 
loose,  no  longer  snaps  back  quickly  and  strongly,  so  the  emphysematous  lung, 
when  it  has  been  stretched  in  inspiration,  comes  back  again  only  slowly.  We  hear 
with  it  a  somewhat  aspirated,  sonorous  sound,  which  plainly  exceeds  the  vesicular 
inspiratory  sound  in  duration.  The  vesicular  murmur  itself  often  undergoes  a 
modification  in  pulmonary  emphysema.  It  sounds  exaggerated,  and  shuffling, 
or  in  other  cases  it  is  rougher  and  more  indefinite.  In  a  high  degree  of  em- 
physema the  vesicular  respiration  is  sometimes  very  faint  and  obscure,  because 
the  inspiratory  current  of  air  is  reduced  to  a  small  amount  in  the  lungs,  which 
are  already  excessively  dilated.  In  many  cases  we  hear  rhonchi  beside  the  respir- 
atory murmur,  dry  whistling,  buzzing,  and  creaking  sounds  on  inspiration  and 
expiration.  If  cylindrical  bronchiectases  have  already  formed,  we  hear,  especially 
over  the  lower  lobes,  numerous  fine  and  medium  moist  rales,  but  no  sonorous 
rhonchi.  The  adventitious  sounds  may  wholly  conceal  the  respiratory  murmur. 
With  a  marked  retention  of  secretion  we  sometimes  hear  nothing  but  a  low,  sup- 
pressed rattling. 

In  the  heart  the  sounds  are  usually  rather  feeble,  because  it  is  covered  by  the 
lung.    The  "  functional  systolic  murmur  of  emphysema  "  at  the  apex,  described  by 


PULMOl^AKY   EMPHYSEMA  193 

some  writers,  we  have  heard  much  less  frequently  than  we  should  expect  after  the 
statements  relating  to  it.  If  present,  it  is  probably  due  to  co-existing  valvular 
changes.  The  pulmonic  second  sound  in  emphysema  is,  as  a  rule,  markedly  accen- 
tuated, as  a  result  of  the  stasis  in  the  pulmonary  circulation. 

The  diminution  of  the  expiratory  pressure  in  emphysema  may  be  measured 
with  the  manometer,  or  with  Waldenburg's  "  pneumatometer."  The  normal  ex- 
piratory pressure  of  110  to  130  raillimetres  sinks  in  emphysema  to  100  or  80  milli- 
metres. As  we  should  expect,  the  spirometer  shows  a  diminution  of  the  vital  lung 
capacity,  which  can  be  readily  explained.  The  normal  lung  capacity  of  about 
3,500  cubic  centimetres  falls  to  2,000  or  1,000  cubic  centimetres. 

Other  Symptoms  in  the  Lungs  and  in  Other  Organs 

In  regard  to  the  other  symptoms  in  the  lungs  we  have  only  a  little  to  add  to 
what  has  already  been  said.  The  intensity  of  the  cough  naturally  varies  in 
individual  cases  according  to  the  degree  of  the  existing  bronchial  catarrh.  Many 
patients  are  troubled  by  a  dry  cough,  while  others  have  abundant  expectoration. 
There  is  nothing  characteristic  of  emphysema  in  the  composition  of  the  latter. 
All  the  kinds  of  sputa  which  are  found  in  the  different  forms  of  chronic  bronchitis 
are  also  found  in  pulmonary  emphysema.  The  dyspnoea,  whose  predominant  ex- 
piratory character  we  have  already  mentioned,  increases  in  advanced  cases  to  a 
most  marked  degree.  Sometimes  the  increase  shows  itself  by  the  appearance  of 
distinctly  paroxysmal  dyspnoea.  This  is  often  really  to  be  regarded  as  a  symptom- 
atic bronchial  asthma,  but,  on  the  other  hand,  we  must  not  overlook  the  fact  that 
a  temporaiy  increase  of  the  bronchitis,  retention  of  secretion,  and  cardiac  failure, 
may  also  excite  attacks  of  dyspnoea,  which  can  not  properly  be  termed  asthma. 

The  important  changes  in  the  heart  resulting  from  emphysema  have  already 
been  described.  The  exhausted  right  ventricle  can  no  longer  overcome  the  in- 
creased resistance  in  the  pulmonary  circulation.  The  difficulty  of  respiration  is 
still  greater,  from  the  passive  congestion  of  the  pulmonary  vessels.  The  skin  be- 
comes still  more  cyanotic,  and  finally  oedema  and  general  dropsy  develop.  The 
failure  of  compensation  is  indicated  by  the  smallness  of  the  pulse,  its  increased  fre- 
•quency,  and  sometimes  by  its  irregularity.  The  difficulty  of  an  objective  exam- 
ination of  the  heart  in  emphysema  has  been  spoken  of  above. 

The  appearances  of  blood-stasis  in  the  internal  organs  are  shown  especially  in 
the  liver  and  kidneys.  The  liver  is  swollen,  and  its  increase  in  size  (the  liver 
of  passive  congestion)  can  frequently  be  made  out  by  percussion  or  palpation. 
The  pains  in  the  hepatic  region,  of  which  many  patients  complain,  are  per- 
haps due  sometimes  to  the  stretching  of  the  capsule  of  the  liver,  but  they  are  prob- 
ably more  often  muscular  pains  excited  by  the  frequent  coughing. 

In  the  kidneys  the  effect  of  stasis  is  first  shown  by  a  diminished  excretion  of 
urine.  The  urine  is  more  scanty  in  amount,  more  concentrated,  of  a  higher  spe- 
cific gravity,  and  of  a  darker  color.  It  generally  gives  an  abundant  sediment  of 
urates,  and  it  may  contain  a  small  amount  of  albumen.  Microscopically  we  may 
'&nd  a  few  hyaline  casts,  and  a  few  red  and  white  blood-corpuscles.  It  is  evident 
that  this  diminished  activity  of  the  kidneys  favors  the  development  of  dropsy. 

The  spleen  is  not  infrequently  found  congested  at  the  autopsy.  The  evidence 
of  this,  however,  is  often  uncertain  during,  life,  for  percussion  of  the  spleen  is 
•difficult  on  account  of  the  emphysema,  and  palpation  is  difficult  from  the  anasarca. 

Gastro-intestinal  symptoms  may  be  present  in  emphysema.  The  appetite 
seldom  remains  good  throughout  the  disease.  Many  patients  suffer  from  chronic 
constipation;  and  more  rarely  there  is  a  tendency  to  diarrhoea. 

Fever  is  not  present  in  simple  pulmonary  emphysema.    Whenever  fever  exists 
for  a  long  time  it  depends  on  other  complications,  such  as  severe  bronchitis,  pneu- 
monia, or  tTiberculosis. 
13 


194  DISEASES    OF   THE   EESPIEATORY   OEGANS 

Complications  of  emphysema  with  other  chronic  diseases  are  frequent.  The 
old  opinion  that  emphysema  and  tuberculosis,  and  emphysema  and  chronic  heart 
disease,  were  antagonistic  to  each  other  is  entirely  false.  These  complications  are 
not  very  rare.  We  may  also  mention  the  complication  with  general  arterio- 
sclerosis and  with  chronic  nephritis,  especially  the  contracted  kidney.  Among 
acute  diseases  we  must  mention  particularly  the  acute  accidental  pulmonary 
complications,  to  which  emphysematous  patients,  particularly  of  the  lower  classes, 
are  much  exposed  as  a  result  of  over-exertion,  exposure  to  cold,  etc.  Acute  febrile 
bronchitis  and  lobular  pneumonia  cause  marked  exacerbations,  and  attacks  of 
true  influenza  and  croupous  pneumonia  in  aged  patients  are  not  infrequently 
dangerous  to  life. 

The  diagnosis  of  emphysema  can  be  made  directly  from  the  results  of  the 
physical  examination,  and  usually  presents  no  difficulties.  We  think  it  important 
merely  to  say  that  too  much  stress  should  not  be  laid  upon  a  low  position  of  the 
lower  edge  of  the  lung  alone.  Many  men  apparently  have  dilated  lungs  but  no 
symptoms  at  all.  The  chief  thing,  therefore  (besides  the  dilatation  of  the  lungs), 
is  the  presence  of  delayed  and  difficult  expiration  and  lessened  power  of  inspira- 
tion. The  diagnosis  is  difficult  when  a  patient  with  emphysema  is  not  examined 
until  the  final,  dropsical  stage.  In  such  cases  it  is  often  very  difficult  to  avoid 
confusion  with  heart  disease  (primary  hypertrophy,  myocarditis,  mitral  stenosis), 
contracted  kidney,  etc.  It  is  often  difficult,  also,  to  come  to  a  decision  in  those 
cases  in  which  there  are  evident  signs  of  co-existing  cardiac  or  renal  disease  besides 
the  emphysema.  In  such  cases  it  is  often  hardly  possible  to  decide  upon  which 
of  the  different  organic  changes  the  chief  stress  is  to  be  laid.  In  all  such  cases 
we  must  place  especial  confidence  in  an  accurate  history  as  well  as  a  careful 
physical  examination.  The  special  nature  and  the  sequence  in  development  of 
the  individual  symptoms  often  afford  valuable  data  for  a  correct  appreciation 
of  the  whole  clinicial  picture. 

Prognosis. — Pulmonary  emphysema  of  acute  origin — that  is,  acute  infla- 
tion of  the  lung — like  that  resulting  from  whooping-cough  and  analogous  affec- 
tions, may  be  recovered  from  in  many  cases.  Otherwise,  as  regards  the  final 
curability  of  the  disease,  the  prognosis  is  wholly  bad.  The  duration  of  the  dis- 
ease and  the  intensity  of  the  symptoms  are  of  course  very  different  in  individ- 
ual cases.  Here  almost  everything  depends  upon  the  circumstances  in  which  the 
patient  is  placed.  With  sufficient  care  the  disease  may  be  tolerably  well  borne 
for  many  years,  but  without  it  the  first  symptoms  of  respiratory  and  cardiac 
insufficiency  appear  much  earlier.  The  final  termination  is  usually  due  to  com- 
plications (vide  supra). 

Treatment. — Since  emphysema  itself  is  only  slightly  amenable  to  treatment,, 
most  of  our  therapeutic  remedies  are  directed  to  that  accompanying  condition 
upon  which  the  greater  part  of  the  symptoms  depend — the  chronic  bronchitis.. 
If  we  succeed  in  improving  this,  or  even  in  wholly  removing  it,  we  always  obtain 
a  decided  improvement  in  all  the  patient's  symptoms.  The  therapeutic  agents 
mentioned  in  the  description  of  chronic  bronchitis  are  therefore  of  frequent  use 
in  emphysema. 

In  the  first  place,  we  must  seek  the  best  hygienic  conditions  for  the  patient, 
and  remove  him  from  all  injurious  influences,  such  as  dust,  bad  air,  and  great 
physical  exertion.  In  drj-  catarrh  we  should  use  the  alkaline  mineral  waters, 
and  when  there  is  abundant  mucous  secretion  the  balsams,  such  as  turpentine 
internally  and  by  inhalation.  The  most  valuable  expectorants  are  iodide  of 
potassium,  apomorphine,  and  ipecac  when  the  expectoration  is  tough,  and  liquor 
ammonii  anisatus  and  senega  when  it  is  abundant.  Their  action,  of  course, 
too  often  fails  of  the  desired  result,  so  that  we  frequently  have  to  change 
our  remedies.     When   there  is   a  troublesome  cough,   disturbing  the   sleep,   we 


PULMOlSrAKY   ATELECTASIS  195 

can  not  dispense  with  narcotics,  such  as  morphine,  codeine,  or  Dover's  powder.  If 
severe  dyspnoea  comes  on,  we  may  try  to  obtain  relief  by  mustard  plasters  to  the 
chest,  or  by  immersing  the  hands  and  feet  in  hot  water.  With  asthmatic  attacks 
we  may  try  iodide  of  potassium,  besides  the  other  remedies  mentioned  for  asthma. 
Here,  too,  we  must  finally  resort  to  narcotics. 

We  must  carefully  watch  the  condition  of  the  heart,  and  use  digitalis  when 
there  are  signs  of  beginning  disturbance  of  compensation  and  the  pulse  grows 
small  and  irregular,  and  this  drug  may  prove  very  useful.  If  symptoms  of  dropsy 
set  in,  we  may  sometimes  prescribe  diuretic  remedies,  such  juniper-tea,  acetate 
of  potassium,  diuretine,  calomel,  etc.,  besides  digitalis.  When  there  is  persistent 
weakness  of  the  heart  we  should  also  use  digitalis  and  other  stimulants  (stro- 
phanthus,  camphor,  wine,  etc.). 

Besides  the  purely  symptomatic  treatment  thus  described,  the  attempt  has 
been  made  to  meet  the  causal  indications  in  emphysema,  and  especially  to  aid 
the  patient  in  expiration,  and  thus  to  improve  the  power  of  the  lung  to  contract, 
where  it  is  possible.  To  this  end  Gerhardt  has  recommended  assisting  expiration 
mechanically  by  compression  of  the  thorax.  This  compression  must  be  done 
methodically  by  another  person,*  about  five  or  ten  minutes  every  day,  by  the  aid 
of  both  hands  laid  flat  on  the  lower  lateral  portions  of  the  thorax.  The  effect  of 
this  manipulation  in  diminishing  the  dyspnoea  and  making  expectoration  easier 
is  in  many  cases  very  satisfactory.  The  "  breathing  chair  "  made  by  Eossbach 
has  a  similar  mechanical  action. 

The  employment  of  the  pneumatic  treatment  has  also  become  quite  general, 
especially  since  the  introduction  of  Waldenburg's  portable  apparatus.  The  expi- 
ration into  rarefied  air,  which  meets  the  causal  indication,  may  procure  great 
relief  for  the  patient  in  many  cases,  and  sometimes,  too,  may  result  in  an  improve- 
ment of  the  emphysema  which  can  be  demonstrated  on  physical  examination.  In- 
halations of  compressed  air  are  also  employed  when  there  is  severe  bronchial 
catarrh.     Still,  too  much  must  not  be  anticipated  from  pneumatic  treatment. 


CHAPTEE   II 


PULMONARY    ATELECTASIS 

{Compression  of  the  Lungs.     Aplasia  of  the  Lungs  in  Cases  of  IZyphoscoliosis) 

^tiolog'y. — Atelectasis  of  the  lungs  is  a  condition  the  direct  opposite  of  em- 
physema. While  in  the  latter  the  lungs  are  abnormally  inflated,  in  the  former 
they  are  abnormally  collapsed.  The  air  has  disappeared  from  the  alveoli  and 
lesser  bronchi,  and  in  the  most  advanced  cases  even  from  the  larger  bronchi.  The 
atelectatic  portions  of  the  lung  are  not  altered  histologically,  but  are  changed  to 
a  firm  tissue,  deprived  of  air — so-called  splenization  or  carnification. 

The  atelectasis  of  the  new-born  is  due  simply  to  deficient  respiration  and  to 
the  consequent  imperfect  entrance  of  air  into  the  lungs.  In  weak  children,  who 
die  soon  after  birth,  we  often  find  the  lower  lobes  wholly  or  in  part  in  a  foetal, 
uninflated  condition — that  is,  atelectatic.     By  artificial  inflation  we  can  readily 


*  One  of  the  author's  patients  at  the  policlinique  in  Leipsic  made  himself  a  very  simple  but  very 
effective  apparatus  for  producing  this  compression  of  the  thorax  on  Jiimself  by  the  aid  of  two  nar- 
row boards,  which  are  fastened  together  at  one  end  by  a  cord  of  suitable  length.  These  boards 
which  are  furnished  with  a  pad  at  this  end  fitted  to  the  wall  of  the  chest,  are  laid  fiat  on  the  two 
sides  of  the  thorax  so  that  their  free  ends  project  forward  some  six  inches  or  a  foot,  and  serve  as  a  one- 
armed  lever.  By  pressing  them  together  the  patient  himself  can  thus,  without  any  strain,  exert  a  con- 
siderable pressure  on  his  thorax  with  each  expiration. 


196  DISEASES    OF   THE   EESPIRATORY   ORGANS 

expand  the  lungs  to  their  normal  extent.  In  many  cases  of  weak,  newly-born 
infants  there  is  at  first  an  atelectasis  of  parts  of  the  lung,  which  gradually  dis- 
appears entirely  and  is  replaced  by  normal  conditions. 

Acquired  atelectasis  occurs  in  two  ways.  We  may  mention,  as  the  first  and 
most  frequent  setiological  factor,  the  plugging  of  the  smaller  bronchi.  If  a  com- 
plete closure  of  a  bronchus  arises  from  the  accumulation  of  secretion,  as  may 
easily  happen  in  the  narrow  bronchi  of  children,  the  air  can  no  longer  enter,  on 
inspiration,  into  that  portion  of  lung  supplied  by  the  plugged  bronchus.  The  air 
which  is  shut  up  in  it  is  gradually  absorbed  by  the  blood.  The  adjacent  parts  of 
the  lung  expand,  and  the  portion  that  is  excluded  from  respiration  collapses, 
leaving  a  circumscribed  pulmonary  atelectasis,  usually  rich  in  blood  but  devoid 
of  air.  Such  atelectases,  in  greater  or  less  number  and  extent,  are  very  often 
found  in  the  bodies  of  children  who  have  suffered  from  severe  bronchitis,  espe- 
cially after  measles,  whooping-cough,  or  diphtheria.  Besides  the  direct  action  of 
the  plugging  of  the  bronchus,  the  weakness  of  the  respiratory  movements  and  the 
cough,  conditional  upon  the  general  state  of  the  disease,  play  a  significant  part. 

The  second  very  frequent  and  important  cause  of  pulmonary  atelectasis  is 
compression  of  the  lung.  In  all  the  diseases  which  diminish  the  space  for  the 
expansion  of  the  lungs,  the  lungs  are  compressed  to  a  greater  or  less  extent, 
whereby  the  air  is  squeezed  out  of  them.  Thus  arise  the  atelectases  from  pressure 
in  pleuritic  effusion,  hydrothorax,  pneumothorax,  in  marked  cardiac  hypertrophy, 
pericardial  effusion,  and  aneurism  of  the  aorta.  Atelectasis  of  the  lower  lobes 
also  arises  in  the  same  way  from  great  upward  pressure  on  the  diaphragm  by 
ascites,  meteorism,  abdominal  tumors,  etc. 

That  form  of  pulmonary  atelectasis  which  arises  from  deformities  of  the  thorax 
is  of  great  practical  importance.  In  severe  kyphoscoliosis,  the  half  of  the  thorax 
corresponding  to  the  convexity  of  the  vertebral  column  is  much  narrowed.  The 
lungs  are  materially  hindered  in  their  expansion,  and  even  in  their  growth,  if  the 
deformity  occurs  in  youth.  This  is  called  "  aplasia  of  the  lungs,"  a  condition 
which  may  give  rise  to  grave  results  (vide  infra). 

Symptoms. — In  the  majority  of  eases  the  symptoms  of  atelectasis  are  subordi- 
nate to  the  disturbance  caused  by  the  primary  disease.  This  is  especially  the 
case  in  most  of  the  atelectases  from  pressure,  although  the  most  dangerous  factor 
lies  in  the  compression  of  the  lung. 

The  atelectasis  of  the  lungs  developing  as  a  result  of  diffuse  capillary  bron- 
chitis, especially  in  children,  can  of  course  not  be  detected  by  physical  examina- 
tion until  it  is  of  great  extent.  The  respiration,  in  extensive  formation  of  atel- 
ectasis, often  shows  a  very  striking  and  characterstic  deviation  from  the  ordinary 
type,  especially  when  the  atelectasis  develops  in  the  lower  lobes.  It  is  accelerated 
and  labored,  and  is  performed  chiefly  by  the  upper  and  anterior  portions  of  the 
thorax.  In  the  lower  portions  we  see  marked  inspiratory  retractions,  which  are 
caused  in  part  by  the  external  pressure  of  the  air,  and  in  part  by  the  exaggerated 
contraction  of  the  diaphragm. 

Physical  examination  can,  of  course,  reveal  abnormal  conditions,  especially 
dullness  on  percussion,  only  when  the  atelectasis  is  extensive.  Dullness,  however, 
is  usually  hard  to  make  out  in  children.  Auscultation  gives  signs  of  existing 
bronchitis ;  and  sometimes,  too,  with  more  extensive  consolidation,  there  is  bron- 
chial respiration.  In  other  cases,  as  may  be  easily  seen,  the  respiratory  murmur 
is  much  diminished  or  wholly  absent.  Thus,  the  physical  signs  of  atelectases  are 
not  easily  distinguishable  from  those  of  pneumonia,  especially  of  lobular  pneu- 
monia. In  fact,  a  sharp  distinction  between  atelectatic  nodules  and  nodules  of 
lobular  pneumonia  in  the  lung  can  not  be  drawn  clinically. 

Aplasia  of  the  lungs  in  kyphoscoliosis  demands  a  special  description,  because  it 
is  of  great  practical  significance.     Many  patients  with  kyphoscoliosis  may  live  for 


PULMONARY   (EDEMA  197 

years  without  special  respiratory  disturbance.  Careful  observation,  of  course, 
usually  shows  a  somewhat  labored  and  hurried  respiration,  but  the  patients 
have  not  paid  much  attention  to  it.  In  other  cases  the  difficulty  in  breathing  is 
more  noticeable.  The  person  affected  is  incapable  of  any  severe  physical  ex- 
ertion; he  always  feels  short  of  breath,  and  often  suffers  from  cough  and  expec- 
toration. In  the  cases  first  mentioned,  however,  which  for  years  have  had  little 
or  no  trouble,  disturbances  in  respiration  sometimes  come  on  quite  suddenly. 
They  may  also  frequently  arise  without  any  special  cause,  and  may  attain  a  very 
threatening  degree.  The  condition  may  improve,  or  it  may  lead  to  comparatively 
or  even  absolutely  sudden  death.  Examination  of  the  lungs  during  life  usually 
shows  nothing  but  the  signs  of  an  extensive  bronchitis.  By  careful  percussion  we 
may  quite  frequently  detect  an  increase  of  cardiac  dullness  to  the  right.  Some- 
times a  moderate  oedema  develops.  In  such  cases  the  autopsy  shows  nothing  as  the 
cause  of  death  but  the  changes  in  the  chest.  The  lungs  are  deficient  in  air, 
small,  and  compressed,  but  in  circumscribed  portions,  on  the  contrary,  emphy- 
sematous and  expanded.  The  right  side  of  the  heart  in  the  great  majority  of 
cases  is  dilated  and  hypertrophied.  There  can  scarcely  be  a  doubt,  therefore, 
that  the  cause  of  the  onset  of  severe  symptoms  and  the  final  cause  of  death  is  to 
be  sought  in  the  cardiac  failure. 

Finally,  it  is  worthy  of  mention  that  there  is  a  frequent  form  of  mild  atelec- 
tasis in  the  lower  lobes,  which  occurs  in  very  sick  and  bed-ridden  patients  who 
usually  keep  in  one  position — on  the  back — as  in  typhoid  fever.  On  making  such 
patients  sit  up  we  hear  during  the  first  inspirations  exquisite  crepitant  rales  over 
the  lower  lobes,  which  sometimes  disappear  after  a  few  deep  inspirations.  Here 
we  have  to  do  with  a  mild  atelectatic  condition,  with  a  temporary  collapse  of 
the  alveoli  and  smallest  bronchi. 

The  treatment  of  atelectasis  coincides  in  great  measure  with  the  treatment  of 
the  primary  disease,  and  is  therefore  to  be  looked  for  in  the  corresponding  chap- 
ters. The  prophylaxis  of  atelectasis,  by  constant  attention  to  the  respiration,  is  of 
great  practical  importance.  We  should  try  to  keep  the  patient  from  lying  con- 
tinually on  his  back,  and  we  should  make  him  take  deep  inspirations.  The  timely 
use  of  tepid  baths,  with  shower-baths,  is  a  special  preventive  of  the  development 
of  atelectasis,  and  it  may  bring  about  a  recovery  when  atelectasis  is  already 
present. 

Tepid  baths  may  also  be  used  with  care  in  the  treatment  of  dyspnoea  caused  by 
kyphoscoliosis.  The  condition  of  the  heart,  however,  deserves  especial  attention 
(stimulants  and  digitalis).  The  reader  is  referred  to  the  consideration  of  the 
general  treatment  of  circulatory  disturbances  in  the  chapters  on  diseases  of  the 
heart.  In  other  respects  the  symptomatic  treatment  by  expectorants,  etc.,  is  the 
same  as  in  other  chronic  pulmonary  affections. 


CHAPTER   III 

PULMONARY    (EDEMA 

Etiology  and  General  Pathology. — We  have  in  pulmonary  oedema  the  exuda- 
tion of  a  highly  albuminous  fluid,  usually  somewhat  hfemorrhngic,  not  only  into 
the  interstitial  tissue,  but  also  into  the  alveoli  themselves.  The  danger  of  the 
condition  is  easily  understood  from  the  high  degree  of  dyspnoea. which  immedi- 
ately ensues  from  it.  In  fact,  pulmonary  oedema  is  in  many  cases  a  terminal 
symptom,  which  comes  on  in  all  forms  of  acute  and  chronic  disease.     Many  pa- 


198  DISEASES    OF   THE   EESPIRATOET   ORGA^tS 

tients  are  said  to  die  with  the  signs  of  pulmonary  oedema,  especially  patients  with 
heart  disease,  pulmonary  and  renal  disease,  and  also  with  other  affections  of  the 
most  different  kinds. 

In  rare  cases  pulmonary  oedema  is  a  transitory  symptom.  Repeated  attacks 
of  it  may  occur,  especially  in  heart  disease  and  chronic  renal  disease,  and,  for  a 
time  at  least,  the  patient  recover  from  them. 

In  spite  of  much  clinical  and  experimental  work,  the  special  causes  of  pulmo- 
nary cedema  are  still  quite  obscure.  For  one  class  of  cases  the  work  of  Cohn- 
heim  and  Welch  shows  that  pulmonary  oedema  is  to  be  considered  as  purely  the 
result  of  stasis.  Pulmonary  oedema  takes  place  when  the  outflow  of  venous  blood 
in  the  lung  meets  an  obstacle  which  can  no  longer  be  overcome  by  the  mechanical 
force  of  the  right  ventricle.  The  obstacle  which  plays  the  most  significant  part 
here,  and  which  may  occur  in  all  possible  forms  of  disease — of  course  more  read- 
ily in  those  mentioned  above  than  in  others — is  paralysis  of  the  left  ventricle. 
If  the  further  progress  of  the  blood  is  much  hindered  by  this,  the  overfilling  of 
the  pulmonary  circulation  and  a  consequent  pulmonary  oedema  will  necessarily 
follow,  in  spite  of  the  most  vigorous  action  of  the  right  ventricle.  Many  cases 
of  terminal  pulmonary  cedema  seem  to  depend  upon  this  fact,  that  the  left  ven- 
tricle is  paralyzed  in  its  action  sooner  than  the  right. 

The  paralysis  of  the  left  ventricle,  however,  is  certainly  not  the  only  factor 
to  be  considered  in  the  origin  of  pulmonary  oedema.  We  must  also  consider 
the  condition  of  the  walls  of  the  blood-vessels  in  the  lungs.  In  many  cases, 
especially  in  renal  disease,  pulmonary  oedema  seems  to  depend  upon  local  changes 
in  the  vessel  walls  (Sahli).  This  form  of  pulmonary  oedema  is  somewhat  akin 
to  true  inflammatoiy  oedema.  The  latter  is  found  chiefly  in  the  vicinity  of  por- 
tions of  lung  infiltrated  with  pneumonia;  it  is  usually  of  limited  extent,  and 
therefore  it  is  of  subordinate  importance  as  a  cause  of  disturbances  in  respiration 
compared  with  the  diffuse  oedema  of  stasis. 

In  very  rare  cases,  as  we  have  ourselves  seen,  an  apparently  primary  acute  pul- 
monaiy  oedema,  with  a  speedily  fatal  termination,  develops  in  men  who  are 
apparently  perfectly  healthy,  and  the  autopsy  gives  no  explanation  of  its  origin. 
We  perhaps  have  to  do  in  these  cases  with  the  sudden  failure  of  the  left  ven- 
tricle, but  probably  with  acute  vascular  changes  as  well. 

Symptoms. — Marked  dyspnoea  is  the  most  striking  symptom  in  pulmonary 
oedema.  It  is  subordinate  only  when  the  patient  is  found  in  the  death  agony 
and  is  no  longer  fully  conscious. 

In  pulmonary  oedema  the  respiration  is  hurried,  labored,  and  rattling.  All 
the  accessory  muscles  of  respiration  are  called  into  play.  The  patient  usually  sits 
upright  in  bed.  We  see  on  his  lips  and  cheeks  a  gradually  and  constantly  in- 
creasing cyanosis,  and  we  often  hear  at  a  distance  the  moist  rales  originating  in 
the  larger  bronchi. 

On  examination  of  the  lungs,  the  percussion  is  essentially  normal,  if  there  is 
no  other  disease  of  the  lungs.  Sometimes  the  percussion-note  is  a  little  higher  in 
pitch,  and  often  it  is  slightly  tympanitic.  On'  auscultation,  we  hear  everywhere 
many  fine  and  medium  moist  rales.  If  the  patient  can  still  expectorate,  he 
raises  a  large  amount  of  frothy,  sero-sanguineous  sputum.  The  whole  picture 
of  the  disease  is  so  characteristic  that  the  condition  can  scarcely  be  mistaken. 

Treatment. — Since  in  most  cases  pulmonary  oedema  is  not  so  much  the  cause 
as  a  symptom  of  approaching  death,  our  remedies  against  it  are  apt  to  prove  pow- 
erless, but  it  must  always  be  our  duty,  at  least  in  all  cases  that  are  not  absolutely 
hopeless,  to  try  to  relieve  the  pulmonary  circulation.  From  the  pathogenesis 
of  pulmonary  oedema  it  follows  that  we  must  pay  particular  attention  to  the 
condition  of  the  heart,  especially  of  the  left  ventricle.  Hence  we  should  use 
energetic  stimulants,  especially  subcutaneous  injections   of  camphor   or   ether. 


CATAREHAL  PNEUMONIA  199 

■every  half  hour  or  hour.  Internally  we  give  first  strophanthus  (ten  drops  of  the 
tincture  every  hour)  and  also  camphor,  wine,  and  very  strong  cafe  noir.  Besides 
that,  we  apply  strong  irritants  to  the  chest,  such  as  large  mustard  plasters  or 
hot  sponges.  Sometimes  an  actual  improvement  of  the  respiration,  when  it  has 
nearly  stopped,  may  be  obtained  by  a  bath  with  cold  douching.  When  there  is 
marked  general  cyanosis,  if  the  patient  is  on  the  whole  strong  and  well  nour- 
ished, venesection  is  sometimes  of  manifest  benefit.  Emetics,  however,  accom- 
plish little,  and  are  even  dangerous  on  account  of  the  collapse  which  is  apt  to 
come  on  after  them.  Expectorants  (benzoin,  liquor  ammonii  anisatus)  are  more 
frequently  prescribed,  and  an  energetic  "  derivation  to  the  intestines,"  by  senna, 
calomel,  or  enemata  of  vinegar,  seems  sometimes  to  be  really  of  service.  Acetate 
of  lead  in  large  doses,  one  or  two  grains  (gramme  0.05-0.10),  in  powder,  every 
hour,  employed  empirically  by  Traube,  is  deserving  of  trial. 

In  this  way,  especially  in  acute  diseases  like  typhoid  and  pneumonia,  we  in 
fact  sometimes  succeed  in  averting  the  danger  of  pulmonary  oadema  by  rapid  and 
energetic  action.  In  the  cases  of  oedema  occurring  in  incurable  chronic  diseases 
of  the  heart  and  kidneys,  the  remedies  employed  are  of  course  unfortunately 
incapable  of  preventing  death. 


CHAPTER   IV 

CATARRHAL    PNEUMONIA 

(Bro7icho-p>ieumonia.     Lobular  Pneumonia) 

.ffitiology. — Catarrhal  pneumonia  is  neither  setiologically  nor  anatomically 
one  single,  absolutely  independent  disease,  but  from  a  clinical  standpoint  we  are 
perfectly  justified  in  grouping  together  the  catarrhal,  lobular  pneumonias,  which 
are  usually  secondary  to  other  diseases,  and  especially  to  a  previous  bronchitis,  and 
in  contrasting  them  with  croupous,  lobar,  "  genuine  "  pneumonia.  In  the  great 
majority  of  catarrhal  pneumonias  the  belief  is  certainly  correct,  that  the  agents 
of  inflammation  do  not  enter  the  pulmonary  alveoli  directly  from  without,  but 
that  the  inflammatory  process  is  situated  originally  in  the  bronchi,  and  from 
this  point  extends  downward  to  the  special  respiratory  parenchyma  of  the 
lung.  This  extension  of  the  inflammation  may  take  place  entirely  by  conti- 
nuity, or  it  may  skip  some  part,  as  the  germs  are  often  inhaled  from  the  bronchi 
directly  into  the  infundibula  and  alveoli.  The  last-mentioned  parts  must,  how- 
ever, possess  considerable  power  of  resisting  germs,  since  the  danger  of  an  exten- 
sion of  bronchitis  to  the  alveoli  generally  exists  only  in  the  severer  and  more 
extensive  cases  of  bronchitis  or  under  other  peculiar  conditions.  This  exten- 
sion of  the  process  is  not  uniform  in  all  parts,  but  it  occurs  first  in  the  distribu- 
tion of  some  small  branches  of  the  bronchi,  and  this  is  the  reason  why  the  pneu- 
monic infiltration  affects  first  only  a  few  bronchial  areas — that  is,  individual 
lobules. 

In  opposition  to  this  generally  accepted  theory  of  the  method  of  origin  of 
the  true  "  lobular  "  or  "  broncho-pneumonic  "  foci,  the  attempt  has  recently  been 
made  to  show  that  the  inflammatory  process  can  pass  through  the  walls  of  a 
small  bronchus  directly  into  the  neighboring  parenchyma  of  the  lung,  and  that 
it  may  then  extend  further  along  the  lymph-channels.  Clinically,  however,  we 
can  not  yet  distinguish  this  form  of  focal  pneumonia  from  the  ordinary  catarrhal 
pneumonia. 

If  we  ask  what  are  the  conditions  under  which  we  are  most  apt  to  observe  the 
development  of  lobular  pneumonia,  we  must  first  mention  a  number  of  acute 


200  DISEASES    OE    THE   RESPIEATOEY   OEGAl^S 

infectious  diseases,  in  wMch.  the  air-passages  are  primarily  affected,  or  in  wMcli 
they  may  very  readily  be  involved  sympathetically.  Chief  among  these  are 
measles  and  whooping-cough,  and  next  diphtheria,  influenza,  small-pox,  etc.  In 
all  these  diseases  there  is  either  a  bronchitis  at  the  beginning,  or  else  it  can  de- 
velop very  easily  in  them.  It  is  in  these  same  diseases,  also,  that  simple  bron- 
chitis comparatively  often  develops  into  lobular  pneumonia. 

Eurthermore,  in  almost  all  severe  acute  and  in  many  chronic  diseases  the 
conditions  favor  the  development  of  secondary  bronchitis  and  subsequently,  at 
times,  of  lobular  pneiunonia.  Everywhere  in  the  air-passages,  as  well  as  in  the 
cavities  of  the  mouth  and  pharynx,  saliva,  mucus,  etc.,  readily  collect  if  the 
patient  is  very  ill.  Expectoration  is  imperfect,  and  the  constant  dorsal  decubitus 
favors  the  accumulation  of  secretion,  especially  in  the  lower  lobes.  The  mouth 
and  pharynx  are  harder  to  keep  clean  than  under  normal  conditions.  Fungi  and 
bacteria  collect  in  the  secretion  itself,  as  well  as  in  the  epithelium  and  particles 
of  food  which  are  left  in  the  mouth,  and  these  excite  and  keep  up  processes  of 
decomposition.  The  inflammatory  agents,  which  are  carried  into  the  air-pas- 
sages with  the  inspired  air,  find  everywhere  favorable  conditions  for  settling  and 
further  development.  From  the  upper  portions  they  are  drawn  farther  downward. 
From  the  larger  bronchi  the  process  invades  the  alveoli,  and  leads  to  catarrhal 
pneumonia.  It  is  probably  of  significance,  too,  that  in  such  very  sick  persons 
the  vital  resistance  of  the  tissues  has  suffered,  and  that  the  development  of  such  sec- 
ondary inflammation  is  consequently  facilitated.  We  must  also  bear  in  mind 
that  many  patients  who  are  very  ill  have  difiiculty  in  swallowing.  They  get 
choked,  and  particles  of  food,  with  the  germs  of  inflammation  clinging  to  them, 
are  carried  into  the  air-passages.  These  particles,  which  a  healthy  person  could 
easily  cough  up  again,  remain  there,  are  decomposed,  and  give  rise  to  bronchitis 
and  lobular  pneumonia. 

This  is  the  explanation  of  the  frequent  development  of  lobular  iDneumonia  in 
the  course  of  diseases  which  are  entirely  dissimilar.  We  observe  it  especially  in 
severe  bed-ridden  cases,  in  all  patients  with  stupor,  in  severe  infectious  diseases,  in 
meningitis,  and  also  in  cases  of  nervous  disease,  in  which  coughing  and  deglutition 
are  impaired  as  a  result  of  bulbar  affections.  In  all  such  cases  lobular  pneu- 
monia is  to  be  considered  a  complication,  and  with  reference  to  its  origin  de- 
serves the  name  of  inhalation  pneumonia  or  deglutition  pneumonia.  We  shall 
soon  see  that  this  form,  under  some  circumstances,  may  pass  into  circumscribed 
gangrene. 

Although  in  the  preceding  we  have  alwaj's  spoken  of  "  agents  of  inflamma- 
tion "  in  general,  the  precise  variety  is  not  necessarily  the  same  in  all  cases.  In 
the  lobular  pneumonias  occurring  in  the  course  of  measles,  whooping-cough,  influ- 
enza, etc.,  it  is  possible  that  the  original  specific  germs  may  penetrate  as  far  as 
the  alveoli,  and  there  cause  an  inflammatory  exudation ;  but  this  is  certainly  not 
always  the  case,  and  there  are  many  reasons  why  in  these  affections,  as  well  as 
in  all  the  others  mentioned  above,  catarrhal  pneumonia  should  be  regarded  as  a 
secondary  complication,  dependent  upon  the  secondary  invasion  of  other  vari- 
eties of  agents  which  cause  inflammation.  Different  micro-organisms  may  prob- 
ably act  as  such  agents.  So  far  as  our  present  investigations  go,  streptococci 
seem  most  frequently  to  be  the  special  cause  of  broncho-pneumonia,  and  some- 
times in  other  cases  staphylococci,  diplococei,  etc.  Clinically,  we  can  not  at 
present  make  a  complete  separation  on  a  strictly  ^etiological  basis. 

The  development  of  lobular  pnev;monia  from  bronchitis  is  most  frequent,  as 
we  know,  in  children  and  old  people.  The  frequency  of  catarrhal  pneumonia  in 
childhood  is  due  in  part  to  the  limited  dimensions  of  the  bronchi.  Besides 
that,  however,  the  diseases  in  which  it  is  especially  frequent — namely,  measles 
and  whooping-cough — are  children's  diseases.     In  old  people  its  comparatively 


CATAEEHAL   PKEUMONIA  201 

easy  development  is  due  to  imperfect  expectoration,  and  perhaps  to  the  dimin- 
ished resistance  of  the  tissues. 

The  mild  cases  of  primary  bronchitis  scarcely  ever  lead  to  lobular  pneumonia, 
but  sometimes  in  children,  and  less  often  in  adults,  a  severe  febrile  bronchitis 
may  occasion  the  formation  of  pneumonic  foci.  In  Erlangen,  the  author  has 
seen  a  good  many  cases  which  can  not  be  regarded  otherwise  than  as  primary 
catarrhal  pneumonia.  We  may  also  state  that  the  inhalation  of  irritating  chem- 
icals may  occasion  lobular  pneumonia  as  well  as  bronchitis. 

Pathological  Anatomy. — It  is  characteristic  of  catarrhal  pneumonia  that  the 
inflammation  is  usually  plainly  circumscribed  (vide  supra),  being  limited  to  the 
territory  of  a  small  bronchus.  Hence  the  name  of  "  lobular "  pneumonia  or 
broncho-pneumonia,  in  distinction  from  croupous  lobar  pneumonia.  An  atelec- 
tasis (_vide  supra)  of  the  affected  lobule,  arising  from  the  plugging  of  the 
bronchus  leading  to  it,  often,  but  not  always,  precedes  the  inflammation.  The 
atelectasis  of  course  becomes  pneumonia  only  when  germs  enter  the  atelectatic 
spot.  The  inflammatory  process  itself  consists  of  the  exudation  of  a  scanty  fluid, 
which  usually  does  not  coagulate,  and  of  numerous  pus-corpuscles  (white  blood- 
corpuscles)  into  the  lumen  of  the  alveoli.  With  this  is  usually  associated  more 
or  less  marked  desquamation  of  the  alveolar  epithelium,  in  which  we  often  fljid 
necrosis  or  fatty  degeneration.  The  alveolar  cavities  are  completely  filled  with 
leucocytes  and  epithelium;  few  if  any  red  blood-corpuscles  are  to  be  seen,  al- 
though in  some  cases  they  may  be  more  abundant.  The  vessels  of  the  alveolar 
walls  are  hypersemic,  and  the  connective  tissue  also  contains  a  few  wandering- 
leucocytes. 

The  inflamed  lobules  are  readily  apparent  to  the  eye  and  the  touch  by  their 
firm  consistence,  being  devoid  of  air.  Their  color  at  first,  from  the  blood  con- 
tained in  the  inflamed  part,  is  a  dark  red  ("  splenization  ")»  but  later  it  becomes 
m.ore  grayish.  A  bit  of  such  an  inflamed  spot,  cut  out  with  the  scissors,  does 
not  float  in  water  but  sinks,  because  it  contains  no  air.  The  lobular  boundary 
of  the  individual  nodules  is  usually  easily  distinguished  from  the  neighboring 
healthy  tissue,  but,  by  confluence  of  adjacent  nodules,  large  portions  of  the  lung, 
and  even  whole  lobes,  may  become  infiltrated  throughout — generalized  lobular 
pneumonia. 

Symptoms. — 1.  Primary  Catarrhal  Pneumonia  of  Adults. — The  primary  ca- 
tarrhal pneumonia  which  infrequently  occurs  in  adults  usually  begins  with  the 
same  phenomena  as  a  severe  attack  of  acute  bronchitis.  The  patient  feels  pros- 
trated, and  has  cough,  dyspnoea,  and  pain  upon  the  side  which  is  chiefly  affected. 
There  is  almost  never  a  pronounced  initial  chill,  as  in  croupous  pneumonia.  The 
fever  is  usually  not  very  high,  from  101°  to  103°  (38.5°  to  39.5°  C),  but  higher 
temperatures  sometimes  occur,  especially  at  the  beginning  of  the  disease.  The 
expectoration  is  simply  catarrhal  or  muco-purulent,  never  muco-sanguineous,  as 
in  croupous  pneumonia.  The  physical  examination  gives  almost  invariably  in 
one  lower  lobe  many  moist  rales  and  a  slight  tympanitic  or  dull  tympanitic  per- 
cussion-note. Marked  dullness  and  definite  bronchial  breathing  are  rare.  In 
the  lower  lobe  on  the  other,  unaffected  side,  we  often  find  signs  of  a  slight  bron- 
chitis; but  in  general  the  unilateral  character  of  the  symptoms  is  characteristic 
of  primary  catarrhal  pneumonia,  in  distinction  from  ordinary  bronchitis  and 
secondary  broncho-pneumonia.  In  mild  cases  the  fever  lasts  from  four  to  eight 
days,  but  the  disease  may  last  two  or  three  weeks  or  more.  There  is  never  a 
crisis;  the  fever  ends  gradually  by  lysis. 

The  getiology  of  primary  catarrhal  pneumonia  has  been  little  studied.  Many 
cases  may  be  streptococcus  pneumonia ;  we  must  also  consider  the  influenza 
bacilli,  since  catarrhal  pneumonia  is  especially  common  at  the  time  of  an  influ- 
enza epidemic. 


202  DISEASES    OE    THE    EESPIEATORY    OEGA^^S 

2.  Secondary  Catarrhal  Pneumonia. — Most  of  tlie  cases  of  catarrhal  pneu- 
monia develop,  as  we  have  already  said,  secondarily  in  the  course  of  other  affec- 
tions, hence  the  symptoms  are  frequently  overshadowed  by  those  of  the  other 
diseases.  There  are  often  found  at  autopsy  a  few  foci  of  lobular  pneumonia  in 
the  lower  lobes  which  gave  rise  to  no  clinical  symptoms  whatever. 

In  other  cases,  however,  the  development  of  extensive  lobular  pneumonia  is 
of  the  greatest  clinical  significance.  In  many  cases  of  chronic  bronchitis,  pul- 
monary emphysema,  pulmonary  tuberculosis,  etc.,  in  which  the  patient  suddenly 
grows  worse  with  a  rise  of  temperature,  the  cause  is  certainly  the  development 
of  foci  of  lobular  pneumonia.  Such  complications  may  after  a  time  completely 
disappear,  or  may  cause  a  permanent  aggravation  of  the  original  condition  (e.  g., 
tuberculosis).  The  onset  of  lobular  pneumonia  in  other  acute  diseases  is  very 
important.  The  disturbance  of  respiration,  during  the  patient's  life,  forms  the 
most  striking  symptom  of  the  disease,  and  lobular  pneumonia  is  shown  at  the 
autopsy  to  be  the  immediate  cause  of  death.  The  largest  part  of  the  fatal  cases 
of  measles  and  whooping-cough,  and  no  very  small  part  of  those  of  diphtheria, 
scarlet  fever,  typhoid,  small-pox,  influenza,  etc.,  are  due,  in  the  last  instance,  to 
the  disturbance  of  respiration  dependent  upon  lobular  pneumonia. 

Since  a  diffuse  bronchitis,  extending  into  the  finer  bronchi,  almost  always  pre- 
cedes the  development  of  lobular  pneumonia,  and  since  it  may  also  give  rise  in 
itself  to  marked  disturbance  in  respiration,  there  is  no  sharp  boundary  to  be 
drawn  clinically  between  diffuse  capillary  bronchitis  and  lobular  pneumonia. 
Only  the  experience,  a  hundred  times  repeated,  that  extensive  capillary  bronchitis 
is  apt  to  lead  to  lobular  pneumonia,  permits  us  to  suspect  the  latter,  with  con- 
siderable certainty,  even  if  there  is  no  direct  clinical  evidence  of  it.  The  most 
important  objective  physical  sign  of  broncho-pneumonia  is  the  not  very  loud, 
medium  moist  rales,  almost  always  to  be  heard  in  the  lower  lobes.  These  rales 
are  often  high-pitched.  Dullness  of  the  percussion-note  develops  only  when  many 
lobular  nodules  coalesce  and  form  a  more  extensive  infiltration  of  the  lung. 
Then  we  also  find  bronchial  respiration. 

Catarrhal  pneumonia  is  almost  always  associated  with  fever,  which  is  mod- 
erately high  and  generally  has  a  remitting  character.  We  must,  of  course,  judge 
of  the  fever  in  connection  with  the  primary  disease  and  any  other  complications. 

1^0  general  statements  can  be  made  as  to  the  duration  of  secondary  catarrhal 
pneumonia.  Sometimes  the  acute  symptoms  last  only  a  few  days,  in  other  cases 
they  continue  for  weeks.  Catarrhal  pneumonia  is  not  infrequently  followed  by 
pleuritic  effusion,  when  the  lobular  infiltration  reaches  the  pleura.  Foci  of  lobu- 
lar pneumonia  may  develop  into  abscess  or  gangrene,  but  this  is  rare. 

3.  Catarrhal  Pneumonia  in  Childhood. — The  catarrhal  pneumonia  of  child- 
hood is  very  characteristic  and  clinically  important.  It  is  observed  most  fre- 
quently in  measles  and  whooping-cough,  and  also  in  weak,  atrophic,  and  rachitic 
children.  The  increased  frequency  of  respiration  is  most  striking.  The  breath- 
ing is  superficial,  but  labored,  as  is  shown  by  the  contraction  of  the  auxiliary 
muscles  of  inspiration  and  the  play  of  the  nostrils.  We  also  notice  inspiratory 
retraction  of  the  lower  lateral  portions  of  the  thorax  as  a  result  of  the  incom- 
plete entrance  of  air.  The  number  of  respirations  in  a  minute  increases  in  chil- 
dren to  sixty  or  eighty,  or  even  more.  In  most  cases  the  child  has  a  frequent 
and  apparently  painful  cough.  Expectoration  is  entirely  absent  in  small  chil- 
dren. When  it  is  present  it  shows  no  characteristic  peculiarities  different  from 
ordinary  catarrhal  sputiam.  The  general  condition  is  always  bad.  The  child 
is  restless,  apathetic,  and  more  or  less  stvipid.  Its  face  is  usually  pale,  but  often 
quite  cyanotic.  The  pulse  is  very  rapid,  and  in  small  children  may  attain  a 
frequency  of  140  to  180  a  minute.  Fever  is  almost  always  present.  It  shows 
no  typical  course,  it  is  now  remitting  and  now  intermitting,  and  toward  evening 


CATARRHAL   PI^EUMONIA  203 

it  perhaps  rises  to  104°  or  105°  (39.5°-40.5°  C).  The  occurrence  of  such  a 
rise  in  temperature  is  not  without  value  in  the  diagnosis  of  catarrhal  pneu- 
monia. If  in  diffuse  capillary  bronchitis  a  high  fever  is  present  for  some  time, 
we  may  assume  with  considerable  certainty  that  the  lobular  infiltration  has  already 
begun. 

Physical  examination  furnishes  direct  evidence  of  the  affection  of  the  lungs, 
but  its  results  are  for  the  most  part  to  be  referred  to  the  diffuse  bronchitis  and 
not  to  the  lobular  infiltration.  Auscultation  gives  the  most  valuable  signs.  We 
hear  over  the  lungs,  in  a  greater  or  less  extent,  numerous  fine  and  medium  moist 
rales,  often  quite  high-pitched.  From  these  signs,  strictly  interpreted,  we  can 
diagnosticate  merely  bronchitis,  but  we  may  suspect  pneumonia  with  the  greatest 
probability.  With  very  confluent  broncho-pneumonia,  auscultation  sometimes 
gives  bronchial  breathing  and  bronchophony,  besides  the  rales. 

It  goes  without  saying  that  little  lobular  foci,  surrounded  by  normal  lung- 
tissue  containing  air,  give  no  special  signs  on  percussion.  With  numerous  nodules 
running  into  one  another,  the  percussion-note  is  duller,  and  there  is  sometimes 
tympanitic  resonance.  The  dullness  is  often  first  to  be  made  out  over  a  stripe 
extending  along  the  vertebral  column — so-called  "  stripe-pneumonia." 

An  attack  of  extensive  lobular  pneumonia  is  usually  quite  protracted.  Even 
in  favorable  cases  the  disease  rarely  lasts  less  than  two  or  three  weeks,  and  it 
may  persist  much  longer.  The  course  of  the  disease  is  apt  to  be  irregular,  re- 
lapses succeeding  improvement.  The  chief  danger  of  the  disease  lies  in  this 
tendency  to  a  protracted  course,  extending  over  weeks  and  months.  Many  chil- 
dren finally  die,  not  of  the  lobular  pneumonia  itself,  but  from  the  general  weak- 
ness and  emaciation  following  the  tedious  febrile  disease.  We  must  remember, 
however,  that  complete  recovery  may  sometimes  take  place  quite  late  in  the 
disease. 

The  "  transition  of  catarrhal  pneumonia  to  caseation  and  tuberculosis  "  is  a 
clinical  fact  with  which  physicians  have  long  been  conversant.  In  fact,  we  often 
find  true  tubercular  changes  in  the  lungs  of  children  who  have  died  after  a 
tedious  illness,  as  a  result  of  measles,  whooping-cough,  etc.  There  can,  of  course, 
be  no  real  question,  however,  of  an  actual  transition  from  one  disease  to  the  other. 
In  such  cases  either  we  have  to  do  with  an  acquired  tubercular  infection,  which 
has  found  a  favorable  soil  in  an  already  diseased  lung,  or  (what  is  probably  more 
frequently  the  case)  the  disease  of  the  lung  has  promoted  the  development  of  a 
previously  existing  tuberculosis.  It  is  usually  weak  children,  with  a  hereditary 
predisposition  to  tubercle,  who  succumb  to  tuberculosis  as  a  result  of  the  above- 
named  diseases.  The  diagnosis  of  a  developing  tuberculosis  is  not  always  easy, 
since  it  is  only  rarely  that  marked  phthisical  changes — like  dullness  at  the  apex, 
cavities,  etc.,  which  can  be  made  out  by  a  physical  examination — are  found  in 
the  lungs.  We  can  usually  suspect  tuberculosis  only  from  the  general  conditions 
(emaciation,  persistent  hectic  fever,  hereditary  predisposition,  or  some  secondary 
tubercular  disease  such  as  meningitis,  etc.),  especially  as  absolute  proof,  from  the 
detection  of  tubercle  bacilli  in  the  sputum,  is  only  rarely  possible  in  children. 

Treatment. — Since  we  have  already  mentioned  the  proper  treatment,  in  our 
description  of  the  various  diseases  in  which  secondary  pneumonia  is  especially 
prone  to  develop,  we  can  now  be  brief.  We  have  also  laid  repeated  stress  upon 
the  possibility  and  the  great  practical  importance  of  prophylaxis,  which  is  self- 
evident  from  a  just  comprehension  of  the  origin  of  lobular  pneumonia.  Besides 
keeping  the  nose,  the  mouth,  and  the  pharynx  as  clean  as  possible,  tepid 
baths,  perhaps  with  cool  douching,  are  the  best  means  of  preventing  the  de- 
velopment of  lobular  pneumonia,  or  of  checking  its  further  extension.  Wet 
cold  packs  are  often  used  with  advantage  (vide  infra).  It  is  an  advantage,  which 
is  indeed  to  be  considered  in  the  second  rank  in  comparison  with  the  improvement 


204  DISEASES    OF   THE   RESPIEATOEY   ORGANS 

in  respiration,  that  by  both  the  bath  and  the  pack  the  febrile  temperature  is  at 
the  same  time  reduced. 

In  the  treatment  of  the  lobular  pneumonia  of  children  a  wet  pack  including 
the  whole  body  is  the  best  remedy.  A  sheet  is  dipped  in  water,  wrung  out,  and 
wrapped  around  the  whole  of  the  patient  except  his  head  and  arms.  Outside  of 
this  is  to  be  placed  a  dry  woolen  blanket  or  a  layer  of  oiled  muslin.  The  temper- 
ature of  the  water  employed  should  be  68°  to  77°  (16°  to  20°  R.).  The  higher 
the  fever  the  colder  should  the  water  be,  and  the  oftener,  say  every  hour  or  two, 
must  the  pack  be  renewed.  In  milder  cases  and  at  night  it  may  be  allowed  to 
remain  for  three  or  four  hours.  The  beneficial  influence  of  the  pack  is  shown 
not  only  by  the  temperature,  but  still  more  by  the  respiration.  It  is  often  strik- 
ing to  see  how  much  quieter  the  child  becomes  in  the  pack.  •  If  the  breathing, 
despite  this  remedy,  remains  unsatisfactory,  and  the  patient  becomes  more  and 
more  stuporous,  the  treatment  must  be  changed  to  lukewarm  baths  of  a  tem- 
perature of  77°  to  86°  (20°  to  24°  R.),  with  douchings  of  colder  water.  It  is 
sometimes  advisable  in  severe  cases  to  add  to  the  water  employed  for  bathing  or 
for  the  wet  pack  a  few  handfuls  of  mustard.  The  stimulation  thus  exerted  upon 
the  skin  is  quite  marked. 

Among  external  applications  to  the  chest,  besides  mustard  plasters  and  poul- 
tices, dry  cups  are  to  be  mentioned,  which  often  do  very  good  service  in  strong, 
older  children,  and  especially  in  adults.  We  never  need  to  use  local  blood-let- 
tings, however,  in  catarrhal  pneumonia. 

Of  internal  remedies,  expectorants  are  most  used.  Chief  among  these  are 
ipecac,  apomorphine,  senega,  and  benzoic  acid.  This  last  is  particularly  useful 
in  the  lobular  pneumonia  of  children.  In  strong  children  the  abundant  collec- 
tion of  mucus  in  the  bronchi  may  sometimes  be  relieved  by  the  administration 
of  an  emetic,  but  we  seldom  need  to  resort  to  this.  We  should  also  be  cautious 
in  the  use  of  narcotics.  Stimulants  (camphor,  wine)  must  be  used  in  severe 
cases.  Antipyretics  may  be  given  to  reduce  the  temperature,  but  if  cool  packs 
be  used  antipyretics  can  be  wholly  dispensed  with.  Inhalations  or  sprays  are  quite 
valueless  in  lobular  pneumonia,  yet  it  is  recommended  to  keep  the  air  in  the  sick- 
chamber  constantly  moist  by  hanging  up  wet  towels,  or  by  sprinkling  with  water. 
The  room  should  also  be  as  large  and  as  well  ventilated  as  possible.  The  general 
hygienic  treatment  is  of  the  greatest  importance.  One  of  the  most  important 
duties,  of  which  the  physician  must  always  be  mindful,  is  to  keep  up  the  patient's 
strength  by  sufficient  and  proper  food.  When  convalescence  sets  in,  complete 
restoration  to  health  may  be  materially  furthered  by  going  to  a  suitable  place  in 
the  country. 


CHAPTER  V 


CROUPOTJS  PNEUMONIA 

{Lung  Fever.     Lobar  Pneumonia.     Fibrinous  Pneumonia.     Pleuro-pnevmonia) 

Croupous  pneumonia  is  a  sharply  defined  febrile  disease  of  the  lungs,  which, 
in  the  great  majority  of  cases,  displays  a  distinct  individuality  in  its  clinical, 
anatomical,  and  usually,  also,  its  setiological  relations.  Among  the  severe  acute 
diseases  it  is  decidedly  one  of  the  most  important  and  frequent,  and  it  is  univer- 
sally familiar  even  to  the  laity  under  the  names  of  pneumonia  or  inflammation  of 
the  lungs.  In  most  cases  this  disease  appears  quite  suddenly,  and  often,  appar- 
ently without  any  special  cause,  in  persons  up  to  that  time  in  perfect  health. 
Such  cases  are  described  as  primary,  genuine,  or  frank  pneumonia.     On  the  other 


CEOUPOUS   PNEUMONIA  205 

hand,  a  case  of  croupous  pneumonia  will  soinetimes  occur  as  a  complication  of  all 
sorts  of  other  diseased  conditions  (secondary  pneumonia).  The  clinical  picture 
of  pneumonia  in  these  latter  cases,  however,  is  usually  obscure  and  not  well 
characterized,  and  consequently  the  following  description  is  especially  applicable 
to  the  primary  form  of  the  disease : 

.Sitiology. — The  thought  that  croupous  pneumonia  might  be  an  acute  in- 
fectious disease  had  impressed  the  majority  of  physicians  for  a  considerable  length 
of  time,  but  this  suspicion  did  not  receive  satisfactory  substantiation  until 
the  more  recent  investigations  in  bacteriology  had  been  made.  For  instance, 
Friedlander  demonstrated  a  special  form  of  bacillus  in  lungs  affected  with 
pneumonia.  Then,  later,  A.  Frankel,  and,  soon  after  him,  Weichselbaum,  proved 
that  while  this  "  pneumonia  bacillus  of  Friedlander  "  is  perhaps  to  be  regarded 
as  the  cause  of  croupous  inflammation  of  the  lungs  in  a  few  cases,  yet  in  the 
overwhelming  majority  of  instances  the  particular  setiological  factor  is  the  so- 
called  diplococcus  pneumoniae  (diplococcus  lanceolatus  capsulatus). 

The  pneumonia  diplococcus  is  characterized  by  its  lancet-shaped  outline  ("  like 
the  flame  of  a  candle  "),  and  its  frequent  arrangement  in  pairs,  the  individuals 
of  each  pair  having  usually  their  broad  ends  apposed.  Very  often  there  are 
short  chain-forms.  The  pairs  of  diplococci  are  usually  surrounded  by  a  delicate 
capsule.  This  is  particularly  common  in  preparations  of  the  sputum.  We  have 
not  space  to  describe  particulars  as  to  the  pure  cultures  of  the  pneumococci  upon 
agar  and  similar  media. 

Pneumonia  diplococci  are  among  the  most  widely  distributed  of  pathogenic 
organisms.  They  produce  severe  disease  not  only  in  the  lungs,  but  in  many  other 
organs.  With  regard  to  the  development  of  the  pneumonic  infection,  it  is  a  par- 
ticularly interesting  fact  that  these  diplococci  have  been  not  infrequently  found 
in  the  mouths  of  healthy  persons.  This  suggests  the  thought  that  the  germs 
are  drawn  into  the  lungs  with  the  inspired  air,  and  there  settle  and  proliferate 
when  the  conditions  are  especially  favorable — for  instance,  if  the  resisting  powers 
of  the  organism  have  been  impaired,  or  perhaps  if  the  diplococci  are  especially 
virulent.  In  animals  the  injection  of  diplococci  into  the  lungs  almost  always 
excites  pneumonia,  but  yet  it  is  doubtful  whether  the  incidence  of  the  disease  in 
man  always  bears  out  the  surmise  above  mentioned.  The  severity  of  the  con- 
stitutional disturbance  at  the  very  onset  of  many  cases  certainly  justifies  the 
supposition  that  at  least  often  the  infection  takes  place  through  the  blood,  and 
that  the  pathogenic  organisms  are  carried  to  the  lungs  by  way  of  the  blood- 
vessels. Diplococci  have  been  repeatedly  found  in  the  blood  of  pneumonia  pa- 
tients, and  the  injection  of  diplococci  into  the  subcutaneous  cellular  tissue  of 
animals,  particularly  rabbits  and  mice,  invariably  excites  a  violent  and  fatal  con- 
stitutional infection  (so-called  sputum-septicsemia).  Certain  clinical  facts 
suggest  that  perhaps  in  individual  cases  there  may  be  other  modes  of  infection; 
for  instance,  by  way  of  the  intestine  in  cases  with  well-marked  intestinal  symp- 
toms. Starting  from  the  lungs,  the  diplococci  may  invade  the  pleura,  less  often 
the  pericardium,  the  meninges,  and  other  organs,  so  that  they  are  invariably 
deraonstrable  in  the  pus  of  cases  of  meta-pneumonic  empyema,  pericarditis,  and 
meningitis.  From  a  clinical  point  of  view  their  almost  invariable  presence  in 
pneumonic  expectoration  (Fig.  26)  is  of  the  greatest  importance.  They  can  be 
easily  demonstrated  by  the  staining  of  a  dried  preparation  with  gentian-violet, 
although  for  absolute  certainty  of  diagnosis  further  investigation  is  required. 
Supposing  the  infectious  nature  of  pneumonia  to  be  certain,  all  the  other  .alleged 
causes  may  of  course  be  regarded  as  at  most  "  predisposing  causes."  The  old 
opinion,  which  is  yet  current,  that  pneumonia  is  due  to  catching  cold,  is  to  be 
received  with  great  limitations,  for  croupous  pneumonia  is  very  frequently 
seen  independently  of  any  such  influence.     In  many  cases  it  will  be  found  that 


206  DISEASES    OF    THE    EESPIEATOEY    OEGANS 

an  exposure  to  cold  immediately  preceded  the  commencement  of  the  disease; 
but  in  these  instances  the  cold  is  probably  to  be  regarded  merely  as  that  circum- 
stance which  promoted  the  occurrence  of  the  infection,  possibly  because  of  the 

resultant  injury  to  the  bronchial  and  pul- 
monary epithelium.  This  explains  the  fact 
that  pneumonia  is  especially  frequent  in 
certain  classes,  for  instance,  among  day- 
laborers  and  soldiers.  With  regard  to  the 
so-called  "  traumatic  pneumonia,"  the  state 
of  the  case  is  similar  to  that  of  pneumonia 
due  to  cold.  Patients  from  the  laboring 
classes  sometimes  assert  that  they  were  taken 
ill  as  a  result  of  heavy  lifting  or  of  a  blow  on 
the  chest,  but  in  such  cases  the  subsequent 
FIG.  se.-Pneumonia  dipiococci.  (After  ^titch  in  the  side  was  probably  not  the  re- 
vierordt.)  sult  of  the  injury,  but  a  symptom  of  the 

disease  which  had  previously  begun  to  de- 
velop. But  still,  in  some  few  cases  it  may  be  that  a  preceding  trauma  injures  the 
pulmonary  tissue  in  such  a  way  as  to  promote  the  occurrence  of  the  infection. 

It  is  a  strong  argument  in  favor  of  our  conception  of  pneumonia  as  an  acute 
infectious  disease  that  it  may  rarely  be  endemic.  Extensive  endemics  of  pneu- 
monia, usually  of  quite  a  malignant  character,  have  been  repeatedly  observed  in 
single  buildings,  especially  in  barracks  or  prisons,  as  well  as  in  tenement  houses  and 
other  localities.  It  is  possible  that  precisely  these  severe  cases  of  endemic  pneu- 
monia are  setiologically  different  from  the  ordinary  croupous  form  and  occasioned 
by  some  other  pathogenic  organism;  but  it  is  also  true  that  the  diplococcus  of 
pneumonia  itself  appears  to  vary  greatly  in  its  virulence. 

Pneumonia  does  not,  as  a  rule,  show  a  decided  epidemic  character.  In  a 
large  population  sporadic  cases  occur  at  any  season.  It  has  been  observed,  how- 
ever, that  the  disease  may  become  very  frequent  or  almost  completely  disappear, 
and  then  again  for  a  time  be  decidedly  prevalent.  In  a  limited  way,  therefore, 
it  is  quite  proper  to  say  that  there  are  actual  epidemics  of  pneumonia,  and  these, 
again,  differ  from  one  another  in  special  peculiarities,  particularly  in  their  com- 
paratively benign  or  malignant  character.  Here  again,  no  doubt,  an  important 
part  is  played  by  the  varying  virulence  of  the  dipiococci  which  we  have  already 
referred  to,  which  is  also  very  evident  under  the  influence  of  different  modes 
of  artificial  cultivation  of  the  organism.  Most  attacks  occur  in  the  winter 
or  spring  months,  without  any  necessary  relation,  however,~between  the  frequency 
of  pneumonia  and  the  occurrence  of  especially  bad,  wet,  or  cold  weather. 

Individual  predisposition  plays  an  unmistakable  part  in  the  disease,  as  we 
must  suppose  that  it  does  in  all  infectious  diseases.  Like  facial  erysipelas  and 
acute  articular  rheumatism,  pneumonia  is  one  of  those  diseases  which  is  prone  to 
attack  the  same  individual  several  times.  There  are  persons  who  have  had  acute 
pneumonia  four  or  five  or  even  more  times  in  their  lives. 

We  can  not  affirm  with  certainty  that  the  liability  to  pneumonia  is  due  to  a 
special  bodily  constitution.  The  strongest  and  most  robust  often  fall  ill  with  it, 
and,  on  the  other  hand,  weak  and  delicate  people,  with  a  tendency  to  phthisis,  are 
frequently  attacked.  Drunkards  seem  to  have  a  special  predisposition  to  the  dis- 
ease, but  of  course  it  is  exceedingly  hard  to  give  any  definite  statistics  upon  this 
point.    . 

Pneumonia  occurs  at  any  time  of  life,  most  frequently  in  youth  or  middle  age ; 
but  it  is  by  no  means  rare  in  early  childhood,  and  also  in  more  advanced  years  up 
to  sixty  or  seventy.  In  general  it  is  observed  rather  more  often  in  men  than  in 
women. 


CEOUPOUS    PNEUMONIA  207 

[Defective  house  drainage  seems  to  be  a  predisposing  cause  of  pneumonia  in 
some  cases.  A  careful  inspection  of  the  local  sanitary  conditions  is  desirable, 
especially  where  more  than  one  case  occurs  in  a  house.] 

Pathological  Anatomy. — The  anatomical  process  in  croupous  pneumonia  con- 
sists in  the  formation  of  a  hsemorrhagic,  coagulable  "  fibrinous  "  or  "  croupous  " 
exudation  into  the  pulmonary  alveoli  and  the  smallest  bronchi.  The  develop- 
ment of  the  exudation  usually  extends  over  one  or  more  lobes  to  their  whole 
extent,  and,  as  the  alveoli  and  finer  bronchi  are  completely  filled  by  the  tough 
exudation,  the  spongy  lung,  filled  with  air,  is  changed  to  a  firm  tissue,  devoid  of 
air,  except  as  it  is  penetrated  by  the  large  bronchi. 

Since  Laennec's  day  we  distinguish  three  stages  in  the  development  of  the  pro- 
cess. In  the  first  stage  (stage  of  inflammatory  engorgement,  engouement)  the 
lung  is  very  hypersemic,  dark  red,  and  the  air  contained  in  it  is  even  now  much 
diminished,  but  not  entirely  absent.  The  alveoli  are  filled  with  an  abundant 
exudation,  already  hemorrhagic,  but  still  fluid  and  not  coagulated. 

In  the  second  stage  (stage  of  red  hepatization)  the  coagulation  of  the  exuda- 
tion is  complete,  and  the  lung  has  become  throughout  of  the  consistence  of  liver. 
The  hepatized  lung  shows  a  somewhat  increased  volume,  and  is  strikingly  hard. 
The  surface  of  the  section  has  a  red  and  manifestly  granular  appearance,  which 
is  due  to  the  projection  of  the  numerous  little  fibrinous  plugs  situated  in  the 
alveoli.  With  the  knife  we  can  scrape  ofl^  a  tenacious,  creamy,  grayish-red  fluid 
from  the  surface  of  the  section.  In  the  small  bronchi,  divided  by  the  knife,  we 
find  characteristic  tubular  bronchial  casts. 

In  the  third  stage  (stage  of  yellow  or  gray  hepatization),  which  gradually 
develops  from  the  second,  the  red  surface  of  the  section  changes  to  a  yellowish- 
gray  color,  often  mottled,  while  the  lung  grows  anaamic  and  the  exudation  poor 
in  red  but  rich  in  white  blood-corpuscles.  The  consistency  of  the  lung  is  still 
dense  but  more  friable.  The  fluid  scraped  from  the  surface  of  the  section  is 
more  abundant,  milky,  and  puriform. 

The  recovery  from  the  process  begins  as  the  exudation  becomes  fluid.  The 
fluid  is  in  part  absorbed  and  in  part  coughed  up. 

It  is  not  necessary  for  every  pneumonia  to  go  through  all  three  stages  com- 
pletely.    In  mild  cases  the  process  may  stop  sooner  and  recovery  begin. 

Concerning  the  finer  histological  processes  in  croupous  pneumonia,  the  pri- 
mary change  is  probably  to  be  found  in  the  injury  and  partial  destruction  of  the 
epithelium  in  the  alveoli  and  smallest  bronchi,  produced  by  inflammation  due  to 
the  specific  causes  of  the  disease.  As  in  every  croupous  inflanunation  of  a  mucous 
membrane  (see  the  chapter  on  diphtheria),  a  coagulable  exudation  is  formed  on 
the  surface  of  the  alveoli  and  smaller  bronchi  after  the  destruction  of  the  epithe- 
lium. With  the  microscope  we  see  the  fibrinous  net-work  of  the  exudation  filling 
the  alveoli.  Between  its  meshes  lie  numerous  red  blood-corpuscles — red  hepatiza- 
tion. Where  there  is  any  of  the  alveolar  epithelium  left,  we  often  notice  active 
proliferation — increase  and  growth  of  cells.  Later  on  the  white  blood-corpuscles 
increase,  migrating  from  the  vessels  into  the  exudation — yellow  hepatization. 
The  red  blood-corpuscles  are  dissolved  unless  they  are  removed  by  expectoration. 
The  fibrinous  exudation  is  also  gradually  dissolved  as  the  result  of  chemical 
changes  not  yet  clearly  understood  (peptonization  of  the  albuminous  sub- 
stances?), and  is  absorbed  like  the  cells.  The  regeneration  of  the  missing  epi- 
thelium comes  from  the  epithelium  that  has  remained  intact,  and  with  that 
follows  a  gradual  and  complete  restitutio  ad  integrum. 

The  whole  process  is  comparatively  brief,  usually  running  its  course  in  a  week 
or  ten  days.  The  most  frequent  termination  is  in  complete  recovery.  The  other 
methods  of  termination,  as  well  as  the  complications  in  other  organs,  will  be 
spoken  of  in  connection  with  the  clinical  symptoms.     We   may  here  mention 


208  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

simply  that  the  pleura  over  the  affected  portion  of  the  lung  takes  part  in  the 
inflammation,  without  exception,  as  soon  as  the  disease  reaches  the  periphery, 
and  a  fibrinous  pleurisy,  which  is  not  very  intense,  may  then  be  recognized; 
hence  the  former  use  of  the  terms  "  pleuro-pneumonia  "  and  "  peripneumonia." 

Croupous  pneumonia  usually  spreads  rapidly  over  a  great  part  of  the  lung.  It 
is  very  often  quite  sharply  limited  to  a  single  lobe — "  lobar  pneumonia  " — so  that 
the  septum  of  connective  tissue  between  two  lobes  also  forms  a  strict  boundary 
between  pneumonic  infiltration  and  healthy  lung  tissue ;  but  this  boundary  is  by 
no  means  insurmountable,  and  quite  frequently  several  lobes  are  wholly  or  in 
part  attacked  by  pneumonia.  According  to  all  statistics,  the  lower  lobes  are  more 
frequently  affected  than  the  upper.  Isolated  disease  of  the  right  middle  lobe  may 
occur,  but  it  is  much  rarer  than  pneumonia  of  the  upper  lobes.  Of  the  two  lungs, 
the  right  is  attacked  with  decidedly  greater  frequency  than  the  left.  We  have 
ourselves  seen,  in  244  cases,  137  on  the  right,  86  on  the  left,  and  21  in  which  both 
lungs  were  attacked  to  a  great  extent.  Simultaneous  affection  of  the  lower  lobe 
on  one  side  and  the  upper  lobe  on  the  other — quite  a  rare  occurrence — is  termed 
"  crossed  pneumonia." 

General  Course  of  the  Disease. — In  spite  of  the  numerous  modifications  which 
the  course  of  pneumonia  may  undergo  in  individual  instances,  we  can  still  call 
pneumonia  a  typical  disease,  considering  the  great  majority  of  cases.  The  sub- 
jective and  objective  symptoms  dependent  upon  the  local  affection  of  the  lung 
usually,  but  not  always,  take  the  chief  place  among  the  clinical  phenomena. 
In  this,  pneumonia  differs  from  many  other  infectious  diseases,  such  as  typhoid,  in 
which  the  local  organic  disease  is  subordinated  to  the  general  infection. 

Pneumonia  usually  begins  quite  suddenly.  In  the  majority  of  cases  it  starts 
with  a  pronounced  chill  of  half  an  hour  to  an  hour's  duration,  or  at  least  with  a 
marked  and  prolonged  chilliness.  The  initial  chill  may  attack  the  patient  while 
in  the  best  of  health.  Many  patients  are  able  to  tell  almost  the  very  hour  when, 
having  been  previously  in  perfect  health,  they  were  attacked  by  disease.  The  chill 
comes  on  in  the  daytime,  in  the  evening,  or  even  in  the  middle  of  the  night,  after 
a  previously  quiet  sleep.  At  the  same  time  the  patient  almost  always  feels  as  if  a 
severe  illness  were  beginning.  Almost  at  once  he  is  obliged  to  give  up  work,  has 
violent  headache,  and  loss  of  appetite.  ISTot  infrequently  there  is  a  single  initial 
act  of  vomiting.  Sometimes  there  are  at  once  pulmonary  symptoms,  such  as  a 
stitch  in  the  side  and  cough.  Usually,  however,  these  phenomena  do  not  develop 
until  later  (vide  infra). 

In  other  and  somewhat  rarer  cases  the  beginning  of  pneumonia  is  more  grad- 
ual. A  prodromal  stage  of  a  few  days,  or  even  longer,  precedes  the  severe  illness. 
The  symptoms  are  either  of  quite  a  general  and  indefinite  nature,  consisting  of 
malaise,  dullness,  loss  of  appetite,  and  headache,  or  the  prodromal  symptoms  point 
more  strongly  to  a  pulmonary  affection.  The  patient  complains  several  days,  or 
even  weeks,  before  the  onset  of  the  severe  disease,  of  cough,  thoracic  discom- 
fort, slight  dyspnoea,  and  similar  symptoms.  At  the  same  time  it  is  not  possible 
to  determine  certainly  whether  these  prodromata  are  caused  by  an  already 
existing  pneumonia  or  not.  It  is  undoubtedly  true  that  in  most  cases  we  have 
merely  a  simple  bronchitis  which  furnishes  a  favorable  soil  for  the  develop- 
ment of  pneumonia ;  but  perhaps  the  initiatory  bronchitis  may,  in  some  cases, 
itself  be  an  effect  of  the  diplococcus  infection,  already  begun,  but  not  yet  com- 
pletely developed. 

The  subjective  symptoms  in  the  chest  begin  shortly  after  the  onset  of  the 
disease,  often  on  the  very  first  day,  but  in  other  cases  later.  The  patient  has 
a  stabbing  pain  in  his  side  whenever  he  draws  a  deep  breath;  the  respiration, 
therefore,  becomes  superficial  and  accelerated,  and  often  somewhat  irregular;  his 
speech  is  interrupted  by  frequent  pauses.    In  the  further  progress  of  a  severe  case 


CEOUPOUS   PNEUMONIA  209 

the  dyspnoea  becomes  extreme  and  the  respirations  very  frequent.  With  the 
stitch  in  the  side  is  associated  a  desire  to  cough.  The  cough  is  painful,  and 
hence  short,  half  suppressed,  and  quite  frequent  and  troublesome.  From  the 
second  day  the  expectoration  may  assume  its  characteristic  viscid,  rusty,  hsemor- 
rhagic  appearance.  Physical  examination  gives  on  percussion  and  auscultation 
the  signs  to  be  described  more  fully  below.  These  are  rarely  to  be  found  on  the 
first  day,  but  more  frequently  on  the  second,  and  sometimes  not  till  later. 

In  well-marked  cases  the  severe  constitutional  symptoms  persist  or  grow  worse. 
We  observe  general  weakness,  headache,  and  complete  loss  of  appetite.  Some- 
times there  are  marked  nervous  symptoms,  such  as  restlessness,  wakefulness, 
stupor,  and  delirium;  herpes  appears  on  the  lips  or  nose;  the  bowels  are  slug- 
gish, or,  again,  they  may  be  loose;  the  urine  is  concentrated,  and  very  often  it 
contains  a  small  amount  of  albumen. 

Almost  always  the  pneumonia  is  associated  with  high  fever.  The  typical 
•character  of  the  disease  and  the  peculiarities  of  the  individual  case  are  always 
well  shown  by  the  temperature  chart.  As  the  bodily  temperature  rises  there  is  a 
corresponding  increase  in  the  frequency  of  the  pulse. 

The  course  varies  greatly  according  to  the  previous  individual  circumstances, 
the  severity  of  the  disease,  and  the  existence  of  complications.  In  the  majority 
of  cases,  after  a  comparatively  short  duration,  the  disease  takes  a  favorable  turn. 
The  beginning  of  improvement  is  often  sudden,  like  the  onset  of  the  disease. 
After  the  symptoms  have  lasted  for  some  five  to  seven  days,  or  in  rarer  cases  a 
shorter  or  a  longer  time,  at  a  constant  height  or  with  increasing  intensity,  there 
occurs  in  the  regular  course  of  the  disease  a  critical  decline  of  the  fever — fre- 
Cjuently  associated  with  quite  a  copious  perspiration — and  with  that  a  very  rapid 
improvement  of  all  the  other  symptoms.  In  a  short  time  complete  recovery 
follows. 

In  other  cases,  however,  the  course  is  not  so  favorable.  The  disease  may  have 
a  fatal  termination.  In  a  third  small  class  of  cases  the  disease  finally  takes  a 
protracted  course,  which  is  usually  due  to  the  occurrence  of  sequelae  in  the  lungs 
or  pleura. 

To  this  brief  sketch  of  the  disease  we  must  append  a  description  of  the  special 
symptoms. 

Description  of  Single  Symptoms  and  Complications 

1.  Symptoms  on  the  Part  of  the  Lungs. — First  among  the  subjective  symp- 
toms comes  the  characteristic  painful  feeling  or  "  stitch "  in  the  side.  This 
probably  always  has  its  origin  in  the  dry  pleurisy  which  accompanies  the  pneu- 
monia. It  is  therefore  absent  in  the  cases  of  central  pneumonia  (vide  infra). 
In  pneumonia  of  the  lower  and  right  middle  lobes  the  pain  is  usually  more  severe 
than  in  pneumonia  of  the  upper  lobes.  One  result  of  the  stitch  in  the  side  is  the 
difiiculty,  or  even  the  impossibility,  of  deep  inspiration.  Hence  the  patient's 
dyspnoea  is  considerably  increased,  and  this  explains  the  incongruity  between  the 
shortness  of  breath  and  the  relatively  slight  extent  of  the  pneumonia  in  many 
oases.  If  the  pneumonic  infiltration  of  the  lung  is  extensive,  of  course  the 
dyspnoea  of  the  patient  is  also  referable  in  part  to  the  diminution  of  the  respira- 
tory surface.  The  subjective  feeling  of  difficulty  of  breathing  is  prominent  in 
the  majority  of  cases,  and  it  may  become  most  distressing. 

Cough  is  one  of  the  most  constant  symptoms  in  pneumonia,  and  is  usually  very 
painful ;  hence  the  patient  often  tries  to  suppress  it.  Expectoration  is  apt  to  be 
very  difficult  at  the  onset  of  the  disease,  from  the  viscidity  and  scanty  amount  of 
the  sputum;  hence  severe  and  distressing  paroxysms  of  coughing  are  some- 
times observed.  The  cause  of  the  cough  is  probably  not  to  be  found  in  the  affec- 
tion of  the  alveoli,  but  in  the  co-existing  bronchitis.  The  irritation  of  the  pleura 
14 


210  DISEASES    OF   THE   EESPIEATOEY   ORGANS 

may  also  set  up  a  reflex  cough.  In  rare  cases  cough  is  entirely  absent  in  pneu- 
monia. Except  in  the  cases  of  limited  or  late  localization  (vide  infra),  we  ob- 
serve this  absence  of  cough  chiefly  in  the  pneumonia  of  old  or  very  v^eak  people^ 
and  also,  what  is  of  practical  importance,  in  the  drunkard's  pneumonia  associated 
with  delirium  tremens. 

The  pneumonic  expectoration  is  so  characteristic  that  we  can  often  make  the 
diagnosis  of  croupous  pneumonia  from  this  alone.  It  consists  of  a  very  tough 
viscid  mucus,  which  sticks  fast  to  the  bottom  of  the  cup  even  when  inverted,  and 
contains  an  intimate  admixture  of  blood,  which  gives  it  a  more  or  less  pronounced 
red  or  yellow  hsemorrhagic  color.  In  individual  cases  there  are  numerous  grada- 
tions. We  usually  call  the  pneumonic  sputum  "  rusty,"  or  "  brick-red,"  or  of  a 
"  prune-juice  color,"  etc.  Sometimes  it  has  only  a  slight  reddish  or  yellowish 
tint,  and  sometimes  it  consists  almost  entirely  of  blood.  Often  the  sputum  is 
very  frothy.  In  some  cases  it  assumes  a  peculiar  grass-green  ["  green-gage  "] 
color,  which  is  due  to  a  change  in  the  blood  coloring-matter,  or  to  a  mixture  with 
bile  pigment  in  "  bilious  pneumonia." 

The  red  color  of  the  sputum,  as  microscopic  examination  shows,  is  due  to 
numerous  red  blood-corpuscles,  many  of  them  still  well  preserved,  mixed  with  it. 
They  are,  however,  in  part  dissolved,  and  hence  cause  the  uniform  red  color  of  the 
sputum.  Separate  spots  containing  much  blood  are  often  seen  in  it.  Besides  the 
red  blood-corpuscles,  the  microscope  shows  numerous  partly  swollen  or  fatty-degen- 
erated pus-corpuscles.  We  also  see  long  threads  of  mucus;  sometimes  large, 
round,  pigmented  cells  (alveolar  epithelium?)  ;  and  finally,  in  rare  cases,  ciliated 
epithelium  and  crystals  of  h^matoidin. 

Frankel's  diplococci  are,  as  we  have  said,  almost  always  easily  demonstrable 
in  the  expectoration,  and  of  course  numerous  other  bacteria  besides. 

We  have  still  to  mention  the  bronchial  casts  as  important  constituents  of  pneu- 
monic sputum.  Since  they  are  usually  rolled  up  together,  we  may  not  find  them 
except  by  spreading  out  the  sputum  in  water.  They  consist  of  the  most  beautiful 
casts  of  the  small  bronchi,  with  many  dichotomous  divisions,  and  are  a  product  of 
the  croupous  inflammation  extending  into  the  bronchi.  The  casts  of  the  smallest 
bronchi  are  sometimes  found  in  the  form  of  "  spirals,"  like  those  in  asthmatic 
bronchitis  (see  page  184). 

The  amount  of  the  pneumonic  sputum  is,  as  a  rule,  not  very  considerable,  but 
it  differs  a  good  deal  in  different  cases.  The  chemical  examination  of  the  sputum 
has  so  far  given  no  remarkable  results.  The  amount  of  common  salt  contained  in 
it  is  quite  considerable. 

In  many  cases  the  pneumonic  expectoration  is  absent,  either  because  there 
is  no  cough  or  because  the  exudation  is  firmly  coagulated  and  is  absorbed  with- 
out ever  liquefying.  Sometimes  it  is  very  tough  and  slimy,  but  without  any 
admixture  of  blood;  in  other  cases  the  sputum  is  simply  catarrhal,  when  present 
at  all,  and  then,  of  course,  it  comes  not  from  the  parts  infiltrated  with  pneu- 
monia, but  from  the  catarrh  of  the  larger  bronchi.  In  many  severe  cases  the 
hsemorrhagic  expectoration  soon  assumes  more  of  a  purulent  character.  We 
often  find  simple  catarrhal  sputum,  too,  besides  the  characteristic  pneumonic 
sputum. 

The  pneumonic  sputum  is  sometimes  seen  in  the  first  or  second  day  of  pneu- 
monia, but  it  may  not  appear  until  later.  With  the  beginning  of  resolution  it 
gradually  loses  its  characteristic  appearance.  The  expectoration  then  becomes  less 
tenacious  and  simply  muco-purulent,  and  finally  disappears  entirely. 

Physical  Examination. — Inspection  shows  no  especial  anomaly  in  the  general 
contour  of  the  thorax.  A  marked  bulging  of  the  affected  side  occurs  only  when 
there  is  also  abundant  effusion  into  the  pleural  cavity.  The  action  of  the  thorax 
in  respiration  is  very  important.     With  a.  limited  pneumonia  we  often  notice 


CEOUPOUS   PNEUMONIA  211 

a  very  marked  delay  and  limitation  of  motion  of  the  affected  side  on  inspiration. 
This  is  due  in  part  to  the  pain  in  the  side,  which  comes  on  with  every  deep  inspi- 
ration, and  also,  in  extensive  pneumonia,  of  course,  to  the  physical  conditions 
resulting-  from  the  anatomical  changes.  The  unaffected  portions  of  the  lung  act 
all  the  more  forcibly. 

The  acceleration  of  respiration  is  very  striking,  its  frequency  increasing  to 
thirty  or  forty,  or  even  more,  a  minute.  We  have  repeatedly  counted  sixty  res- 
pirations in  adults,  even  in  cases  that  finally  resulted  favorably.  The  breathing 
is  shallow,  but  yet,  in  all  severe  cases,  labored,  and  often  also  irregular,  as  a 
result  of  pleuritic  pain  or  cough.  We  see  the  inspiratory  contraction  of  the 
sterno-cleido-mastoids  and  scaleni  in  the  neck,  and  often  in  the  face  a  marked 
dilatation  of  the  nostrils  on  inspiration.  If  there  is  marked  dyspnoea  the  patient 
sometimes  reclines  in  bed  with  the  upper  half  of  the  body  raised.  The  cheeks  and 
lips  are  cyanotic.  There  is  often  a  sharp  contrast  between  the  pale  portions  of 
the  face  near  the  corners  of  the  mouth  and  the  striking  feverish  and  slightly 
cyanotic  flush  of  the  cheeks. 

The  results  of  percussion  are  directly  dependent  upon  the  changed  physical 
condition  in  the  lung,  due  to  the  anatomical  processes.  In  the  beginning  of  pneu- 
monia, so  long  as  the  total  amount  of  air  in  the  lung  remains  but  little  altered, 
the  percussion-note  is  clear,  but  when  the  elasticity  and  tension  of  the  tissue  in 
the  diseased  portion  of  the  lung  diminish,  the  resonance  often  becomes  quite 
tympanitic.  With  increased  exudation  into  the  alveoli  and  smallest  bronchi  the 
amount  of  air  in  the  lung  constantly  grows  less,  and  therefore  the  percussion 
resonance  becomes  very  dull,  but  it  usually  retains  its  tympanitic  timbre.  Since 
the  pneumonic  lung  is  rarely  absolutely  deprived  of  air — for  a  certain  amount 
is  always  left  in  the  larger  bronchi — the  percussion  resonance  seldom  becomes  so 
completely  dull  or  flat,  as  it  does,  for  example,  with  a  large  pleuritic  effusion. 
The  sensation  of  resistance  upon  the  percussion  of  a  pneumonic  lung  is  likewise 
much  less  marked  than  over  a  pleuritic  exudation.  A  marked  sense  of  resistance 
implies,  therefore,  an  unusual  degree  of  involvement  of  the  pleura  in  the  inflam- 
mation. As  soon  as  the  absorption  of  the  exudation  begins,  the  volume  of  air 
in  the  lung  increases,  and  the  percussion-note  becomes  clearer,  but  remains  for 
some  time  still  markedly  tympanitic,  until  the  lung  has  regained  its  normal 
tension  and  elasticity.  We  have  also  to  note  that  the  intensity  of  the  dullness  m 
croupous  pneumonia  is  sometimes  subject  to  quite  marked  variations,  since  the 
secretion  retained  in  the  bronchi  is  at  one  time  abundant  and  at  another,  after 
expectoration,  scanty. 

The  extent  of  the  dullness  or  of  the  tympanitic  resonance  is  naturally  depend- 
ent upon  the  extent  of  the  anatomical  process.  Small  and  central  infiltrations 
may  entirely  escape  detection  by  percussion. 

Auscultation  is  of  almost  greater  importance  than  percussion  in  the  detection 
of  a  beginning  or  limited  pneumonic  infiltration.  The  auscultatory  signs  depend 
upon  the  presence  of  the  pneumonic  exvidation,  and  upon  the  consequent  trans- 
formation of  the  lung  into  a  firm  tissue  devoid  of  air  except  in  the  larger  bronchi. 
In  the  beginning  of  the  disease  we  hear  over  the  affected  portions  coarse  or  fine 
rales,  and  very  often,  too,  the  characteristic  crepitant  rale  on  inspiration  discov- 
ered by  Laennec.  This  arises  because  the  walls  of  the  alveoli  and  smallest  bron- 
chi, which  are  glued  together  by  the  viscid  exudation,  are  torn  apart  at  each 
inspiration.  The  crepitation,  however,  is  neither  pathognomonic  of  pneumonia, 
nor  heard  in  every  case  of  pneumonia.  With  increasing  infiltration,  bronchial 
breathing  replaces  the  vesicular.  The  bronchial  breathing  in  pneumonia  is  usu- 
ally very  loud,  sharp,  and  close  to  the  ear.  When  the  infiltration  is  very  com- 
plete there  is  often  to  be  heard  a  pure  and  loud  bronchial  respiration,  without  any 
adventitious  sounds;  but  of  course  there  are  often  heard,  besides  the  bronchial 


212  DISEASES    OF   THE   EESPIRATOHY   ORGAJ^S 

breathing,  high-pitched,  moist  rales  in  greater  or  less  abundance.  It  is  especially- 
true  that  with  the  eomniencement  of  "  resolution  " — that  is,  as  soon  as  the  exuda- 
tion becomes  more  fluid,  abundant  moist  rales  reappear,  enough  to  obscure  more  or 
less  the  bronchial  respiration.  These  rales  are,  for  the  most  part,  rather  coarse, 
moist,  and  have  a  musical  character.  Often  we  hear  at  this  time  the  character- 
istic crepitant  rale  again  (crepitus  redux).  The  rales  gradually  disappear,  the 
respiratory  murmur  loses  its  bronchial  character,  becomes  harsh  and  indefinite, 
and  finally  is  normally  vesicular  once  more. 

We  often  hear  a  few  rhonchi  over  the  unaffected  portions  of  the  lungs.  On 
the  diseased  side,  the  respiratory  murmur  is  often  more  or  less  diminished 
because  of  the  diminished  respiratory  movenaent.  Otherwise  respiration  in  the 
unaffected  portions  of  the  lungs  is  usually  completely  normal. 

The  auscultatory  signs  just  described  undergo  an  important  change  if  the 
larger  bronchi  leading  to  the  affected  portion  of  the  lung  are  completely  plugged 
by  the  secretion,  as  they  are  quite  liable  to  be.  The  respiratory  murmur  may 
then  almost  entirely  disappear,  and  we  hear,  perhaps,  only  here  and  there  a  few 
obscure  rales.  Since  such  a  plugging  may  be  very  transitory,  we  understand  why 
in  one  day,  over  the  same  portion  of  the  lung,  we  hear  first  loud  bronchial  breath- 
ing and  rales,  and  then  quite  obscure  and  diminished  breathing. 

Wherever  there  is  bronchial  breathing,  we  hear  marked  bronchophony.  Some- 
times one  can  discover  a  beginning  pneumonic  infiltration  by  bronchophony 
sooner  than  by  any  other  physical  sign.  The  vocal  fremitus  persists  or  is  some- 
what increased  over  a  pneumonic  lung  so  long  as  the  large  bronchi  are  open; 
but  when  they  become  plugged,  as  they  are  quite  liable  to  be,  the  vocal  fremitus 
is  weakened  or  wholly  abolished;  and  again,  the  voice  sounds  are  weakened 
whenever  there  is  a  considerable  amount  of  pleurisy  accompanying  the  pneu- 
monia. 

We  have  yet  to  ad5,  a  few  remarks  about  the  parts  of  the  lung  in  which  we 
may  expect  first  to  perceive  the  physical  signs  of  pneumonia,  especially  the  aus- 
cultatory signs. 

In  the  first  place,  we  should  never  neglect  to  examine  carefully  the  lateral  por- 
tions of  the  thorax  and  the  axillary  region  when  we  suspect  a  developing  pneu- 
monia. We  often  find  the  first  rales  here  in  pneumonia  of  the  lower  lobes.  The 
first  signs  of  infiltration  may  be  found  in  the  posterior  middle  portion  of  the 
thorax — that  is,  in  the  upper  part  of  the  lower  pulmonary  lobes — and  thence 
they  extend  downward.  Pneumonia  of  the  upper  lobes  begins  just  as  frequently 
behind  in  the  apices  as  in  front  in  the  infra-clavicular  fossae.  Isolated  jDneumonia 
of  the  right  middle  lobe  also  occurs,  to  be  made  out  in  front,  on  the  right,  between 
the  fourth  and  sixth  ribs.  This  may  remain  confined  to  the  middle  lobe,  or  extend 
to  the  neighboring  lobes. 

Few  general  statements  can  be  made  about  the  nature  or  the  rapidity  of  the 
extension  of  pneumonia,  since  in  these  respects  the  greatest  differences  are 
observed.  The  infiltration  may  remain  confined  to  a  small  portion  of  the  lung, 
or  again  it  may  spread  over  a  whole  lobe  or  more  in  a  short  time,  even  in  one 
or  two  days.  We  call  the  pneumonia,  whose  constant  extension  by  contiguity 
we  can  follow  from  day  to  day,  wandering  pneumonia  (pneumonia  migrans),  or, 
from  a  purely  superficial  resemblance,  which  has  given  rise  to  many  wrong  ideas, 
"  erysipelatous  pneumonia."  In  these  cases  all  the  signs  of  resolution  are  present 
in  the  pai-ts  first  attacked,  while  the  parts  aifected  later  are  found  still  at  the 
height  of  the  disease,  or  in  the  beginning  of  infiltration ;  but  we  may  also  find  in 
the  autopsies  of  wandering  pneumonia  the  parts  of  the  lung  affected  later  in 
a  more  advanced  stage  (gray  hepatization)  than  the  parts  first  attacked,  which 
are  still  in  the  stage  of  red  hepatization — that  is,  the  inflammatory  process  in 
such  cases  seems  to  go  through  a  more  rapid  evolution  in  the  portions  of  lung 


CEOUPOUS    PNEUMONIA  213 

later  affected.   Wandering  pneumonia   is   almost   always  severe   and   quite  pro- 
tracted. 

Pneumonia  in  rare  cases  progresses  by  leaps.  Such  cases  have  been  termed 
erratic  pneumonia.  In  severe  cases  it  is  not  unusual  for  both  lungs  to  be 
affected.  We  then  find  the  pneumonia  either  in  both  lower  lobes,  or  in  the  lower 
lobe  on  one  side  and  the  upper  lobe  on  the  other  side. 

2.  Symptoms  on  the  Part  of  the  Pleura. — As  we  have  already  mentioned, 
every  case  of  pneumonia  which  reaches  to  the  surface  of  the  lung  is  associated 
with  a  fibrinous  pleurisy,  and,  furthermore,  it  is  not  impossible  that  there  should 
be  an  infection  of  the  pleura  without  any  direct  extension  from  the  neighboring 
pulmonary  tissue.  In  many  instances,  the  mild  pleurisy  which  attends  a  pneu- 
monia causes  no  physical  signs.  On  the  other  hand,  the  pain  in  the  side  in  pneu- 
monia is  probably  always  referable  to  the  involvement  of  the  pleura.  In  other 
cases  the  dry  pleurisy  attracts  attention  by  the  clearly  audible  friction,  which  may 
often  be  very  loud,  and  is  sometimes  appreciable  to  the  touch,  if  the  hand  is 
laid  upon  the  side.  We  rarely  hear  the  pleuritic  friction  sound  in  the  begin- 
ning of  pneumonia,  but  more  frequently  in  the  later  stages,  and  perhaps  not  till 
many  days  after  the  crisis  has  taken  place. 

The  cases  in  which  pleurisy  with  effusion  complicates  pneumonia  are  more  im- 
portant. This  may  occur  quite  early.  The  abnormality  of  the  clinical  course  is 
shown  in  these  cases,  as  a  rule,  by  the  irregular  behavior  of  the  fever.  There 
will  be  no  typical  crisis,  but  instead  a  slow  lysis;  or  after  the  crisis  occurs,  the 
temperature  will  rise  again.  In  most  instances  the  exudation  is  serous,  but  it  may 
be  purulent  (metapneumonic  empyema).  Long-continued  fever  should  arouse 
suspicion  of  an  empyema.  In  the  pus  of  such  cases  of  empyema  the  pneumonic 
diplococcus  above  mentioned  (see  page  205)  has  been  repeatedly  found.  In  two 
fatal  cases  the  author  has  seen  a  hsemorrhagic  pleurisy  with  a  large  amount  of 
coagulated  blood  in  the  pleural  cavity. 

The  diagnosis  of  pleurisy  with  effusion  complicating  pneumonia  is  seldom 
difficult.  The  percussion  resonance  is  duller,  and  the  sense  of  resistance  is  more 
marked  than  in  pure  pneumonia  (vide  supra).  The  respiratory  murmur  and  the 
vocal  fremitus  are  constantly  diminished  and  finally  entirely  absent.  The  symp- 
toms of  pressure  on  the  neighboring  organs  and  cavities,  the  heart,  the  liver, 
and  the  semilunar  space  (see  page  287),  are  especially  important  because  they  are 
most  unequivocal.  An  exploratory  puncture  with  a  Pravaz's  [hypodermic] 
syringe,  that  has  been  carefully  cleansed  and  disinfected,  gives  a  certain  and 
safe  method  of  recognizing  pleurisy  in  doubtful  cases.  When  there  is  suspicion 
that  an  empyema  has  begun,  an  exploratory  puncture  is  imperative. 

A  moderate  degree  of  pleurisy  may  somewhat  delay  the  course  of  the  disease, 
but  it  has  no  special  significance.  Large  effusions,  however,  may  decidedly  in- 
crease the  difficulty  in  respiration  and  the  duration  of  the  illness.  Again,  the 
pneumonia  may  recover,  leaving  the  pleuritic  effusion  quite  undisturbed.  In 
pneumonia  of  an  upper  lobe,  too,  the  pleurisy  may  develop  below  and  lead  to 
an  effusion  there,  while  the  lower  lobe  itself  remains  quite  free  from  pneumonia. 
Metapneumonic  empyema  invariably  requires  surgical  intervention,  but  after 
operation  it  almost  always  pursues  a  rapid  course  to  recovery. 

3.  Circulatory  Apparatus.  Blood. — The  pulse  is  accelerated  from  the  begin- 
ning of  the  disease.  In  cases  of  moderate  severity  its  frequency  reaches  100  or 
120;  and,  in  very  severe  cases,  a  still  higher  rate  up  to  140  or  160  is  seen,  and  is 
always  a  dangerous  symptom.  This  high  rate  of  the  pulse  does  not  have  as  bad 
a  significance  in  children  as  it  does  in  adults.  The  consideration  of  the  quality  of 
the  pulse  is  important.  Smallness,  weakness,  and  irregularity  of  the  pulse  are 
of  bad  omen  as  symptoms  of  the  onset  of  cardiac  weakness.  The  attacks  of  col- 
lapse, which  sometimes  come  on  quite  suddenly  in  severe  cases  of  pneumonia  as 


214  DISEASES    OF   THE   EESPIRATOEY   OEGANS 

in  other  acute  diseases,  are  especially  dangerous.  They  occasion  sudden  weak- 
ness of  the  heart  with  a  very-  small  and  frequent  pulse.  The  temperature  sinks  to 
subnormal,  95°  to  93°  (35°-34°  C).  The  peripheral  parts,  the  nose  and  ex- 
tremities, become  cool,  pale,  and  somewhat  cyanotic.  The  general  weakness  and 
prostration  become  extreme.  The  collapse  may  be  recovered  from,  especially  with 
timely  assistance,  but  patients  may  die  in  it. 

Pericarditis  with  fibrinous  or  sero-fibrinous  exudation  is  one  of  the  most 
serious  cardiac  complications.  This  can  always  be  explained  by  a  direct  conduc- 
tion of  the  inflammatory  process  from  the  neighboring  pleura,  and  is  therefore 
somewhat  more  frequent  in  left-sided  pneumonia  than  in  right.  It  is  a  serious 
matter.  Its  diagnosis  is  seldom  difficult  if  we  make  a  careful  physical  examina- 
tion of  the  heart,  but  with  very  severe  and  extensive  symptoms  in  the  lungs  a 
complicating  pericarditis  may  be  overlooked. 

A  slight  fresh  endocarditis  is  sometimes  found  at  the  autopsy,  but  it  has  no 
clinical  significance.  Diseases  of  the  cardiac  muscle,  especially  fatty  and  paren- 
chymatous degeneration,  may  be  discovered  post  mortem,  but  they  are  by  no 
means  frequent.  In  very  weak  persons,  drunkards,  etc.,  who  die  of  pneumonia,  we 
sometimes,  indeed,  find  the  heart  remarkably  flabby,  with  the  right  ventricle 
dilated,  but  in  many  cases  of  pneumonia  we  find  the  muscle  of  the  heart  at  the 
autopsy  perfectly  normal.  Here  we  almost  always  have  to  do  with  conditions 
of  the  heart  which  existed  previously  to  the  pneumonia,  and  merely  became  promi- 
nent during  its  course.  When  persons  of  vigorous  and  healthy  constitution  die  of 
pneumonia,  as,  indeed,  seldom  occurs,  the  myocardium  is  found  at  the  autopsy 
essentially  healthy.  It  must  be  emphatically  stated  that  our  present  knowledge 
does  not  enable  us  to  establish  before  death  any  positive  relation  between  the  his- 
tological condition  of  the  cardiac  muscle  and  its  functional  ability.  Frequent 
experience  has  made  us  certain  of  this  fact. 

With  regard  to  the  blood,  there  is  usually  a  well-marked  leucocytosis  in 
pneumonia.  The  exact  count  shows,  not  infrequently,  twenty  to  twenty-five 
thousand  or  more  of  leucocytes  in  a  cubic  millimetre.  With  the  crisis  of  the  fever 
the  number  of  leucocytes  also  falls  abruptly,  while  in  case  of  a  pseudo-crisis  theii 
number  remains  high.  In  some  instances  the  leucocytosis  is  not  marked.  This 
is  particularly  frequent  in  severe  and  fatal  cases,  so  that  the  absence  of  leucocy- 
tosis is  regarded  with  some  justice  as  an  unfavorable  element  in  prognosis. 

4.  Digestive  Apparatus. — In  severe  cases  of  pneumonia  the  tongue  is  dry, 
coated,  and  quite  like  the  tongue  in  typhoid.  The  appetite  is  also  almost  wholly 
lost  from  the  beginning.  Vomiting  is  not  infrequent,  especially  in  the  begin- 
ning of  pneumonia,  and  it  also  occurs  later.  It  is  observed  with  especial  fre- 
quency in  the  pneumonia  of  children.  Severe  symptoms  on  the  part  of  the  intes- 
tinal canal  are  rare.  As  a  rule  the  bowels  are  constipated,  but  there  are  also  cases 
in  which  diarrhoea  is  so  troublesome  that  we  must  believe  that  the  mucous  mem- 
brane of  the  intestine  is  considerably  involved  in  the  morbid  process  (vide  infra). 

The  complication  of  pneumonia  with  jaundice  has  a  certain  significance,  but 
its  causes  are  not  always  very  clear.  It  is  apparently  sometimes  due  to  an  accom- 
panying catarrh  of  the  duodenum.  In  other  cases  the  veins  of  the  liver,  dilated 
from  stasis,  may  exert  a  pressure  on  the  bile-ducts.  Slight  jaundice  has  no  special 
significance,  and  is  frequent,  even  in  mild  cases;  a  marked  jaundice,  however,  is 
seen  only  in  severe  cases,  especially  in  drunkard's  pneumonia.  We  call  such 
cases,  associated  with  jaundice,  "bilious  pneumonia."  They  have  often  other 
severe  gastro-intestinal  symptoms,  such  as  vomiting,  diarrhoea,  and  meteorism,  and 
severe  nervous  symptoms,  such  as  stupor  and  delirium. 

The  liver  may  be  somewhat  enlarged,  usually  because  of  passive  congestion. 
The  spleen  is  often  moderately  swollen,  particularly  in  severe  cases,  just  as  in 
other  infectious  diseases  (acute  splenic  tumor). 


CROUPOUS    P]SrEUMO:N"IA  215 

5.  Kidneys  and  Urine. — The  infectious  character  of  pneumonia  is  also  shown 
hy  frequent  involvement  of  the  kidneys.  Careful  examination  of  the  urine  almost 
always  shows  a  trace,  or  even  a  considerable  amount,  of  albumen.  However,  this 
.  is  very  seldom  of  serious  import,  and  vanishes  promptly  after  the  crisis.  In  many 
instances  the  changes  in  the  urine  are  so  considerable  as  to  show  an  acute 
nephritis.  There  is  a  large  amount  of  albumen,  with  casts,  epithelium,  and  blood, 
in  the  urine.  But  even  these  cases  of  genuine  pneumonic  nephritis,  which  usually 
develop  about  the  third  to  the  sixth  day  of  the  illness,  seldom  prove  to  be  serious, 
and  scarcely  ever  result  in  oedema,  uraemia,  or  other  complications.  Usually  they 
get  well  rapidly.  In  one  single  case  the  author  has  observed  a  transition  into 
chronic  nephritis.  The  way  in  which  pneumonia  causes  albuminuria  and  ne- 
phritis— between  which  no  sharp  dividing  line  can  be  drawn — is  probably  by  the 
production  and  excretion  of  toxines. 

Great  weight  was  formerly  laid  upon  the  diminution  of  the  chlorides  in  the 
urine  in  pneumonia.  In  fact,  the  precipitate  of  chloride  of  silver,  when  we  put  a 
drop  of  solution  of  nitrate  of  silver  into  the  urine,  may  be  very  slight  or  entirely 
absent.  The  chief  cause  of  this  diminution  of  the  chlorides  is  the  small  amount 
of  nourishment  taken  by  the  patient,  but  we  must  also  bear  in  mind  the  large 
amount  of  chloride  of  sodium  contained  in  the  pneumonic  exudation,  and  the 
retention  of  the  chlorides  in  the  body. 

Great  significance  was  also  formerly  ascribed  to  the  abundant  sediment  of 
sodium  urate  (exceptionally,  uric  acid)  which  is  often  noticed  on  the  day  of 
the  crisis.  This  is  known  as  brick-dust  sediment  (sedimentum  lateritiurn),  and 
is  perhaps  due  in  part  to  a  material  increase  in  uric  acid  (query :  through  de- 
struction of  the  large  number  of  leucocytes  in  the  blood?),  but  certainly  in  greater 
part  to  the  fact  that  the  conditions  for  the  deposition  of  sediment  are  especially 
favorable  on  the  day  of  the  crisis.  The  urine  is  scanty  in  amount  because  per- 
spiration is  so  excessive,  and  hence  it  is  concentrated  and  relatively  very  acid. 
It  is,  therefore,  natural  for  the  urates  contained  in  it  to  be  deposited  in  the 
form  of  a  sediment. 

Pneumonia,  in  common  with  most  of  the  other  acute  febrile  diseases,  is  at- 
tended with  an  increased  secretion  of  urea  during  the  disease.  The  fact  is  of 
theoretic  interest  that  during  the  resolution  of  pneumonia  the  urine  often  con- 
tains a  demonstrable  quantity  of  peptone,  which  is,  in  all  probability,  due  to  the 
destruction  of  the  cells  in  the  pneumonic  exudation  and  their  absorption  into  the 
blood. 

6.  Nervous  System. — As  in  every  severe  febrile  disease,  nervous  symptoms  of  a 
mild  type  are  very  rarely  absent  in  any  case  of  pneumonia.  Among  the  nervous 
symptoms  are  general  weakness  and  dullness,  and  especially  headache,  which  is 
often  very  intense,  and  is  usually  increased  by  coughing.  The  onset  of  more 
severe  cerebral  symptoms,  particularly  delirium,  is  of  great  importance.  Delirium 
may  appear  in  any  case  of  severe  pneumonia,  but  it  is  most  marked  and  has 
peculiar  characteristics  in  alcoholic  subjects.  This  delirium  gives  the  pneumonia 
of  drunkards  {vide  infra)  its  characteristic  stamp. 

The  usual  cerebral  symptoms  in  pneumonia  do  not  correspond  with  macro- 
scopic changes  in  the  brain,  but  result  from  the  poisoning  of  the  body  with  the 
toxines  of  the  pneumonia  diplococcus;  and  yet  there  is  also  a  true  cerebral  dis- 
ease which  has  beyond  a  doubt  a  special  relation  to  pneumonia,  although  it  is  an 
infrequent  complication.  We  refer  to  purulent  cerebro-spinal  meningitis.  This 
complication  is  particularly  apt  to  appear  at  times  when  an  epidemic  of  cerebro- 
spinal meningitis  prevails,  but  it  has  been  repeatedly  observed  at  other  times.  The 
diagnosis  of  pneumonic  meningitis  may  be  obscured  by  the  severe  constitutional 
disturbances.  Factors  of  importance  are :  the  stiffness  of  the  back  and  the 
neck ;   the  pain  in  the  head  and  in  the  nape  of  the  neck ;   the  stupor,  changing  to 


216 


DISEASES    OF   THE   EESPIEATOEY   OEGANS 


10 


deep  coma;  and,  in  many  cases,  optic  neuritis,  demonstrable  by  the  opbthal- 
moscope.  The  termination  of  a  well-marked  case  of  meningitis  is  probably  in- 
variably fatal,  but  we  may  have  milder  meningeal  symptoms  in  pneumonia,  such 
as  pain  and  stiffness  in  the  neck,  followed  by  complete  recovery. — With  regard 
to  the  development  of  this  meningitis,  it  is  probably  to  be  regarded  as  a  true 
metastatic  inflammation,  inasmuch  as  the  pneumonia  diplococci  have  been  re- 
peatedly found  in  the  pus  of  the  meningitis.  As  to  the  path  which  the  pathogenic 
germs  take  to  reach  the  meninges,  we  are  not  yet  certain,  but  suppose  that  they 
travel  along  the  lymph-channels  of  the  intercostal  nerves  into  the  meninges  sur- 
rounding the  spinal  cord,  and  thence  further  to  the  membranes  of  the  brain. 

7.  Skin. — The  frequent  appearance  of  herpes  in  the  course  of  pneumonia  is 
characteristic,  and  is  of  diagnostic  importance.  It  appears  from  the  second  to  the 
fourth  day  of  the  disease,  or  sometimes  later.  Its  ordinary  seat  is  on  the  lips, 
especially  at  the  corners  of  the  mouth,  also  on  the  alse  of  the  nose,  and  more 
rarely  on  the  cheeks  or  the  ear  (herpes  lahialis,  nasalis,  etc.).  It  has  been 
seen  only  very  rarely  on  other  portions  of  the  body  besides  the  face,  for  example, 
on  the  forearm  and  the  buttock,  and  in  some  cases  on  the  cornea  and  on  the 
mucous  membrane  of  the  tongue  or  gums.  The  herpes  does  not  always  come 
out  all  at  once,  but  in  fresh  crops  on  successive  days.  We  have  several  times  seen 
two  eruptions  of  herpes  separated  by  an  interval  of  several  days.  In  repeated 
instances,  under  our  own  observation,  herpes  labialis,  with  a  fresh  rise  of  tem- 
perature, appeared  some  days  after  the  crisis  had  taken  place.  Herpes  may  be  ex- 
tensive in  the  mildest  cases,  while  it  is  particularly  apt  to  be  scanty  or  absent  in 

severe  cases.  We  are,  there- 
fore, on  the  whole,  inclined  to 
regard  a  well-marked  eruption 
of  herpes  as  of  favorable  prog- 
nosis. The  true  cause  of  the 
herpetic  eruption  is  unknown. 
One  might  think  of  referring 
it  to  the  action  of  toxines,  just 
as  in  the  herpes  of  other  infec- 
tious diseases,  such  as  inter- 
mittent and  relapsing  fevers, 
and  epidemic  meningitis. 
Other  affections  of  the  skin 
are  of  rare  occurrence.  We 
have  seen  urticaria  in  some 
cases.  The  jaundice  occurring 
in  pneumonia  has  already  been 
described. 

8.  Course  of  the  Fever  (see 
Figs.  27  and  28). — Pneumonia 
is,  almost  without  exception, 
accompanied  by  a  more  or  less 
high  fever  with  a  very  typical  course.  In  the  beginning  of  the  fever  the  tem- 
perature rises  very  rapidly  to  a  high  point.  Even  during  the  initial  chill  the 
bodily  heat  increases  from  normal  to  about  104°  (40°  C.)  and  over.  There 
are  at  present  no  observations  to  show  whether,  in  the  cases  of  pneumonia  that 
begin  gradually,  there  is  also  a  gradual  increase  of  the  fever.  During  the  course 
of  the  disease  the  fever  shows  on  the  whole  a  continuous  or  remitting  character, 
but  there  is  with  this  a  decided  tendency  to  single  deep  falls  of  temperature. 
Since  these  at  first  may  easily  be  taken  for  the  actual  occurrence  of  crises, 
although  later  they  are  proved  by  the  renewed  rise  in  temperature  to  be  a  mere 


40.0= 


39.0° 


38.0° 


87.0<^ 


36.0= 


SJ^SBJ^^SSSSBS 


sBiidsJiniHi 

■■■■■■  WflHHIIH 

■■■-=■■■■■ 

■■■■■ 


■BBBBBBB       ""  " 


Pseudo-crisis. 

Fig.  27.— Example  of  the  temperature-curve  in  croupous 
pneumonia.    (Personal  observation.) 


CEOUPOUS   PNEUMONIA 


21Y 


41.0° 


40.0' 


39.0° 


38.0° 


■■■■■HI 


rjil 


Fig.  28.- 


-Example  of  the  temperature  curve  iu  "  intermitting" 
pneumonia.     ^J:'ersonal  observation.) 


temporary  decline  in  the  bodily  heat,  they  are  termed  pseudo-crises.  Pseudo- 
crises  are  usually  seen  in  the  first  days  of  the  disease,  but  in  some  cases  they 
appear  later  and,  what  is  remarkable,  they  are  more  apt  to  appear  on  those  days, 
such  as  the  fifth  or  seventh,  on  which  the  true  crisis  is  apt  to  occur.  They  may 
be  repeated  one  or  more  times,  giving  the  fever  a  decidedly  intermitting  char- 
acter. These  intermitting 
pneumonias,  so  called  from  ^       ^ 

the  course  of  the  fever, 
have  nothing  at  all  to  do 
with  malaria,  which  fact 
must  be  especially  noted 
because  of  the  frequency 
of  erroneous  statements. 

The  fever  may  be  decid- 
edly high  in  pneumonia, 
often  reaching  104°  or 
106°  (40°^1°  C).  The 
highest  temperature  ob- 
served by  us  was  107.8° 
(42.1°  C).  This  was  tem- 
porary. There  is  a  cer- 
tain parallelism  between 
the  height  of  the  fever 
and  its  severity  to  this  ex- 
tent, that  severe  cases  are 
often  associated  with  per- 
sistent and  especially  high  fever.  But  sometimes  the  most  severe  and  even 
fatal  cases  have  a  comparatively  low  temperature — between  101°  and  103°  (38.5- 
39.5  C).  The  highest  temperatures  are  especially  common  in  the  first  days  of  the 
illness,  and  yet,  in  spite  of  very  high  fever  at  the  onset,  the  general  course  of 
the  disease  may  turn  out  to  be  favorable,  for  the  crisis  may  occur  on  the 
second  or  third  day  (inde  infra,  rudimentary  and  abortive  pneumonia).  In 
severe  cases  the  progress  of  the  disease  often  stamps  itself  plainly  on  the 
temperature.  The  pseudo-crises  correspond  to  temporary  improvements,  and 
the  fresh  exacerbations  of  temperature  to  the  invasion  of  a  fresh  lobe  of  the 
lung.  We  have  certainly  not  seen  a  special  rise  immediately  before  the  crisis — 
the  so-called  perturhatio  critica — so  often  as  many  statements  would  lead  us  to 
expect.  We  have  seen  a  gradual  decline  in  temperature  quite  frequently  in  the 
closing  days  in  fatal  cases,  but  the  opposite  condition  also  obtains.  A  marked 
rise  before  death  is  not  peculiar  to  pneumonia,  but  it  does  occur  when  there  is  a 
complicating  meningitis. 

The  decline  of  the  fever  is  the  most  characteristic  portion  of  the  pneumonia 
curve.  The  fall  in  temperature  usually  comes  on  in  the  form  of  a  decided  crisis. 
Generally  in  the  night  there  is  a  sinking  of  the  temperature  with  a  more  or 
less  abundant  perspiration,  in  which  as  a  rule  the  temperature  may  reach  a  sub- 
normal point — 96°  to  95°  (36°-35°  C).  The  critical  decline  is  often  broken  by 
new  and  slight  elevations  of  temperature,  so  that  on  the  morning  of  the  next  day 
there  may  be  a  definite  increase  of  fever,  the  so-called  protracted  crisis.  Only  in 
a  comparatively  small  number  of  cases  does  the  fever  end  by  lysis,  in  which  the 
temperature  goes  down  like  steps.  The  duration  of  lysis  is  seldom  more  than 
three  or  four  days  at  most.  A  decline  of  temperature  by  lysis  is  most  frequent  in 
severe  and  protracted  cases,  in  so-called  typhoid  pneumonia  (vide  infra),  and  also 
particularly  in  pneumonia  migrans. 

After  the  final  crisis  has  occurred,  the  active  pneumonic  process  ceases.     The 


218  DISEASES    OF    THE   EESPIRaTORY    ORGANS 

day  of  the  crisis  is  therefore  reckoned  as  the  last  day  of  actual  illness.  The 
pneumonia  makes  no  advance  after  that,  but  resolution  and  absorption  of  the 
exudation  and  the  restoration  of  the  patient's  strength  still  take  time.  Hippoc- 
rates knew  when  the  time  of  the  crisis  occurs,  and  that  the  odd  days,  especially 
the  fifth  and  the  seventh,  have  a  special  significance  in  regard  to  it.  In  an 
infectious  disease  that  has  a  typical  course  there  can  be  nothing  strange  in  the 
fact  that  the  cessation  of  fever,  to  a  certain  degree,  is  associated  with  a  definite 
period  of  time;  but  Hippocrates's  rule  has  frequent  exceptions.  The  crisis  some- 
times occurs  on  the  ninth,  the  twelfth,  or  the  thirteenth  day,  and  even  later,  and, 
on  the  other  hand,  there  are  quite  short  pneumonias  of  but  one  or  two  days'  dura- 
tion {vide  infra). 

In  the  days  following  the  crisis  the  temperature,  which,  as  we  have  said,  falls 
to  subnormal,  regains  its  normal  height.  The  pulse,  which  usually  sinks  to 
fifty  or  sixty  during  the  crisis,  when  it  often  shows  a  slight  irregularity,  reaches 
its  normal  frequency  again  in  a  few  days.  We  are  quite  apt  to  see,  in  the  days 
inxmediately  following  the  crisis,  a  slight  temporary  increase  of  temperature 
again,  100°  to  102°  at  most  (38°-39°  C),  but  this  has  no  special  significance. 

In  cases  which  run  their  course  regularly,  the  signs  in  the  lungs  upon  ausculta- 
tion and  percussion  become  normal  again  in  about  six  or  eight  days  after  the 
crisis.  Often  the  time  is  even  shorter  than  this,  or  it  may  be  longer.  Abnor- 
mally delayed  resolution  will  be  mentioned  below. 

Special  Peculiarities  and  Anomalies  in  the  Course  of  Pneumonia 

1.  Pneumonia  in  Children. — Besides  the  common  lobular  pneumonia  there  is 
also  a  genuine,  lobar,  croupous  pneumonia  in  children,  which  is  by  no  means  so  rare 
as  some  authors  formerly  supposed.  An  initial  chill  is  seen  only  in  older  chil- 
dren; initial  vomiting,  however,  is  very  common  in  children.  In  many  cases 
severe  cerebral  symptoms,  like  convulsions,  drowsiness,  or  delirium,  obscure  the 
pulmonary  symptoms  at  first.  The  further  course,  the  development  of  physical 
signs,  the  fever,  and  the  complications,  are  quite  analogous  to  the  appearances  in 
adults.  The  pneumonic  sputum  is  only  exceptionally  obtained  for  observation 
in  children  under  eight  years  of  age.  In  previously  healthy  children  the  prog- 
nosis of  croupous  pneumonia  is  almost  invariably  favorable. 

2.  Pneumonia  in  old  people  is,  on  the  other  hand,  always  dangerous.  It  may 
begin  suddenly,  as  in  people  of  middle  age,  but  often  it  begins  more  slowly  and 
insidiously.  Its  course  is  marked  by  the  speedy  onset  of  great  weakness  and 
debility.  Nervous  symptoms,  like  delirium,  are  not  infrequent.  Often  there  is 
fatal  weakness  of  the  heart. 

3.  Drunkard's  Pneumonia. — We  see  croupous  pneumonia  in  drunkards  with 
remarkable  frequency.  The  usually  severe  and  dangerous  course  of  the  disease  is 
due  to  the  feeble  resisting  powers  of  their  impaired  organs.  It  is  characterized 
by  delirium  tremens,  which  usually  develops  in  the  first  days  of  the  disease.  The 
patient's  mind  is  disturbed,  he  is  very  restless,  constantly  tries  to  get  out  of 
bed,  and  he  fumbles  night  and  day  with  his  bed-clothes  or  night-gown.  The 
alcoholic  character  of  the  delirium  is  shown  by  the  patient's  whole  manner,  the 
tremor  of  the  hands  and  tongue,  and  the  cast  of  his  thoughts,  which  are  usually 
happy  but  exceptionally  anxious  and  terrified.  His  mind  wanders  to  his  former 
occupation  or  his  usual  boon  companions,  and  the  like.  He  becomes  tearful  or 
raving  only  when  forcibly  restrained.  He  may  think  himself  involved  in  the 
tavern  brawls.  The  alcoholic  delirium  is  almost  always  associated  with  hallu- 
cinations. The  hallucinations  of  little  moving  black  figures  are  especially  char- 
acteristic. They  are  either  animals,  rats  or  beetles,  or  little  black  men  and 
similar  weird  shapes,  and  they  give  him  much  trouble.  The  subjective  symptoms 
■of  pneumonia  are  wholly  in  the  background.     No  delirious  patient  with  pneu- 


CEOUPOUS   PNEUMONIA  219 

monia  complains  of  cough,  pain  in  the  chest,  or  dyspnoea.  Careful  objective 
examination  is  the  only  thing  that  confirms  the  diagnosis.  Very  often  patients 
with  a  happy  delirium  serve  to  entertain  those  about  them,  until  suddenly  very 
severe  symptoms  arise,  and  they  become  somnolent  and  succumb,  with  the  symp- 
toms of  pulmonary  oedema.  The  prognosis  of  every  case  of  drunkard's  pneu- 
monia, therefore,  is  to  be  regarded  as  very  unfavorable. 

4.  Pneumonia  in  Pre-existing  Chronic  Diseases. — Croupous  pneumonia  is  oc- 
casionally seen  in  all  forms  of  chronic  disease.  It  is  especially  dangerous  in 
persons  who  are  already  enfeebled,  or  afflicted  with  chronic  cardiac  or  pulmonary 
disease,  such  as  phthisis  or  emphysema.  The  pneumonia  which  often  attacks  pa- 
tients with  emphysema  is  clinically  important,  since  emphysema  may  render  the 
objective  evidence  of  pneumonia  very  obscure.  The  croupous  exudation  does  not 
completely  fill  the  dilated  alveoli ;  hence  decided  dullness  and  bronchial  breathing 
are  absent. 

5.  Pneumonia  with  Late  Localization — Central  Pneumonia. — Cases  are  quite 
often  seen  whose  beginning,  course,  and  subjective  symptoms  correspond  through- 
out to  a  croupous  pneumonia,  but  in  which  the  objective  evidence  of  pneumonic 
infiltration  evades  the  most  careful  examination.  The  disease  begins  with  a 
chill,  the  fever  is  high,  the  patient  complains  of  pain  in  the  chest,  which  is  usu- 
ally slight,  there  is  perhaps  herpes,  but  not  till  the  fourth,  fifth,  or  sixth  day  can 
we  make  out  anywhere  any  bronchial  breathing  or  crepitant  rales.  In  other  cases 
even  the  crisis  may  set  in  before  we  are  able  to  localize  the  pneumonia  with  cer- 
tainty. In  most  of  these  cases  we  probably  have  to  do  less  with  an  actual  late 
localization  than  with  a  central  infiltration  which  nowhere  approaches  the  periph- 
ery, and  hence  is  made  out  objectively  only  late  or  not  at  all.  A  careful  exami- 
nation of  the  sputum  is  of  the  greatest  diagnostic  importance,  since  it  sometimes 
has  a  perfectly  characteristic  appearance  in  spite  of  the  absence  or  the  indefinite 
character  of  the  physical  signs.  If  there  is  no  sputum,  the  diagnosis  may  of 
course  remain  very  uncertain.  The  appearance  of  herpes  and  a  critical  fall  in 
the  temperature  make  the  diagnosis  of  a  pneumonic  infection  probable  even  in 
these  cases.  In  one  such  case  the  author  observed  the  development  of  a  pleuritic 
friction  rub  upon  the  first  day  after  the  crisis,  confirming  the  diagnosis  of  pneu- 
monia after  the  disease  had  run  its  course. 

6.  Rudiinentary  and  Ahortive  Forms  of  Pneumonia — Unusual  Localizations 
of  the  Pneumonic  Infection. — Particularly  at  times  of  a  pneumonia  epidemic,  but 
also  at  other  times,  the  author  has  observed  illnesses  of  short  duration  but  often 
with  high  temperature  which  did  not  seem  like  clear  cases  of  pneumonia,  although 
they  still  were,  in  all  probability,  to  be  regarded  as  pneumonic — i.  e.,  due  to  infec- 
tion with  the  specific  diplococci.  Cases  of  this  sort  usually  begin  suddenly  with  a 
chill,  headache,  and  high  temperature.  Generally  there  is  a  cough  and  pain 
in  the  chest.  Sometimes,  however,  there  are  no  thoracic  symptoms  at  all.  The 
physician  expects  pneumonia  to  develop,  but  instead,  on  the  first,  second,  or 
third  day,  the  fever  ceases  abruptly,  no  changes  in  the  lung  having  been  discov- 
ered. Very  often  there  will  be  a  herpes  facialis  in  such  cases,  and  we  doubt  not 
that  many  instances  of  so-called  herpes  fehrilis,  or  fehris  herpetica,  are  really 
cases  of  pneumonic  infection,  without  any  other  localization  than  the  herpes. 
In  other  instances,  ujDon  careful  examination  there  will  be  found,  at  some  place 
in  the  lungs,  a  slight  crepitation,  or  limited  bronchial  breathing ;  but  the  process 
does  not  extend;  and  in  a  very  brief  time,  after  a  day  or  two,  the  fever  ceases 
(rudimentary  pneumonia;  abortive  pneumonia). 

In  this  connection  we  may  remark  that  the  diplococcus  infection  may  be 
localized  in  still  other  places.  Thus,  for  example,  we  regard  it  as  very  probable 
that  many  cases  of  sore  throat  or  acute  enteritis,  associated  with  the  svidden 
onset  of  high  fever  and  with  herpes,  and  especially  when  seen  at  the  time  of  an 


220  DISEASES    OF   THE   EESPIEATOEY   OEGAITS 

epidemic  of  pneumonia,  are  due  to  diplococcus  infection.     Associated  with  these 
attacks  there  may  also  be  a  late  development  of  pulmonary  symptoms. 

7.  Typhoid  Pneumonia — Asthenic  Pneumonia.— 'Qj  typhoid  pneumonia  we 
mean  those  cases  in  which,  beside  the  local  pulmonary  symptoms,  which  may  be 
either  slight  or  well  marked,  there  are  remarkably  severe  general  symptoms. 
The  cases  do  not  often  begin  as  suddenly  as  ordinary  pneumonia,  but  more 
gradually,  like  typhoid.  Even  at  first  the  general  symptoms,  such  as  great  dull- 
ness, loss  of  appetite,  or  headache,  predominate  over  the  thoracic  symptoms.  At 
the  height  of  the  disease  there  is  a  decided  typhoidal  state,  stupor,  delirium,  a  very 
dry  tongue,  great  general  weakness,  and  also  enlargement  of  the  spleen,  and  fre- 
quently mild  jaundice,  albuminuria,  etc.  Such  cases  are  to  be  regarded  as  pneu- 
monia with  an  unusually  severe  general  infection  (or  intoxication).  They  some- 
times occur  in  epidemics.  It  is  said  that  pneumonia  of  the  upper  lobes  shows  a 
somewhat  more  frequent  tendency  to  severe  nervous  symptoms  than  pneumonia 
of  the  lower  lobes.  Eecovery  from  this  typhoid  or  asthenic  pneumonia,  which 
may  last  two  weeks  or  more,  often  follows  by  lysis.  Typhoid  pneumonia  is  by  no 
means  a  sharply  defined  disease.  The  term  serves  merely  as  a  short  name  for  the 
grave  constitutional  disturbance.  Clinically  it  is  impossible  to  distinguish  it 
sharply  from  pneumonia  migrans,  bilious  pneumonia,  and  other  forms.  We  must 
await  further  bacteriological  investigations  to  determine  whether  there  may  not 
be  some  other  special  pathogenic  organism  in  many  cases  of  severe  character. 
For  instance,  Finkler  is  inclined  to  regard  certain  cases  of  especially  severe  pneu- 
monia that  seem  to  be  endemic  or  contagious,  as  referable  to  streptococcus  infec- 
tion. In  this  connection  may  be  briefly  mentioned,  also,  the  peculiar  and  severe 
pneumonia  which  is  contracted  from  diseased  parrots.  On  the  other  hand,  it  is 
not  improbable  that  another  important  factor  may  be  a  variation  in  the  virulence 
of  the  ordinary  pneumococcus. 

Piieumo -typhoid  is  to  be  carefully  distinguished  from  typhoid  pneumonia, 
although  from  a  clinical  point  of  view  the  diagnosis  between  them  is  often  no 
easy  matter.  By  pneumo-typhoid  is  meant  typhoid  fever  with  a  localization  of 
the  typhoid  bacilli  in  the  lungs  (see  page  14),  but  it  is  also  true  that  ordinary 
croupous  pneumonia  may  occasionally  appear  as  a  complication  of  typhoid  fever. 

8.  Pneumonia  with  Delayed  Besolution. — While  the  resolution  of  pneumonia 
is  complete,  as  a  rule,  in  three  days  to  a  week  after  the  occurrence  of  the  crisis, 
there  are  cases  in  which  this  process  demands  a  much  longer  time.  Not  infre- 
quently, and  particularly  in  severe  cases  of  pneumonia,  one  sees  after  the  crisis 
a  surprisingly  rapid  disappearance  of  all  the  physical  signs,  while,  on  the  other 
hand,  recovery  is  sometimes  remarkably  slow  in  apparently  mild  cases;  but  this 
rule  is  of  course  not  without  exceptions.  The  course  of  the  disease  is  often 
enough  precisely  the  opposite.  Just  what  are  the  conditions  upon  which  the 
rapidity  or  the  slowness  of  resolution  depends  we  do  not  know.  Sometimes  unfa- 
vorable constitutional  conditions,  such  as  anaemia,  debility,  phthisical  tendencies, 
and  kyphoscoliosis,  appear  to  delay  resolution.  Sometimes,  on  the  other  hand, 
no  such  explanation  can  be  found.  It  seems  to  us  that  at  certain  times  all  the 
cases  of  pneumonia  exhibit  more  of  a  tendency  to  delayed  resolution  than  at 
others,  so  that  it  is  not  impossible  that  there  are  variations  in  the  pathological 
process  itself.  In  many  cases  of  delayed  resolution  it  is  our  opinion  that  we  have 
to  do  with  genuine  secondary  diseases,  or  a  mixed  infection  in  the  lungs  for  the 
development  of  which  the  precedent  croupous  pneumonia  had  prepared  a  favor- 
able soil. 

With  regard  to  the  symptoms  of  delayed  resolution,  there  are  various  forms. 
In  the  first  place,  we  see  cases  where  the  crisis  takes  place  in  the  usual  way,  and 
the  temperature  thereafter  remains  permanently  normal.  The  patients  perhaps 
feel  quite  well,  and  are  troubled  little  by  thoracic  symptoms;    nevertheless,  the 


CROUPOUS    PNEUMONIA  221 

dullness  upon  percussion  remains  unchanged,  or  diminishes  at  best  very  gradually, 
and  the  bronchial  breathing  and  moist  rales  can  still  be  heard.  All  the  signs 
diminish  very  slowly,  sometimes  occupying  several  weeks  in  their  disappearance, 
and  then  complete  recovery  ensues.  In  a  few  cases  it  is  striking  that,  after  the 
crisis,  bronchial  respiration  and  dullness  persist,  while  there  are  scarcely  any 
rales  and  no  expectoration.  In  these  cases  it  seems  as  if  the  pneumonic  exuda- 
tion does  not  really  liquefy  at  all,  and  is  very  slowly  absorbed.  In  other  cases 
there  is  no  distinct  crisis,  but  the  fever  continues,  although  lower  than  at  first, 
and  the  physical  signs  remain  to  a  greater  or  less  extent.  At  the  end  of  two  or 
three  weeks,  or  even  still  later,  the  fever  slowly  ceases,  and  thereupon  normal 
resonance  and  vesicular  breathing  gradually  return. 

In  still  other  cases  the  patients  remain  free  from  fever  for  the  first  few  days 
after  the  crisis  has  taken  place,  although  the  pneumonia  is  not  completely  re- 
solved. Then  there  appears  again  a  rise  of  temperature  which  is  mostly  mod- 
erate, 100.5°-103.5°  (38°-39.5°  C),  while  the  dullness  continues  and  there  are 
an  abundance  of  moist  rales  and  catarrhal  expectoration.  After  two  or  three 
weeks  the  fever  gradually  ceases  and  the  abnormal  pulmonary  signs  also  slowly 
disappear.  In  such  cases  we  may  indeed  suppose  that  some  secondary  infection, 
a  sort  of  secondary  catarrhal  pneumonia,  has  developed  upon  the  seat  of  the 
croupous  pneumonia.  The  disease  may  take  still  another  course  somewhat  dif- 
ferent from  those  thus  far  described,  and  of  this  we  have  seen  repeated  instances 
much  resembling  one  another.  After  the  occurrence  of  the  crisis  the  patient 
remains  for  about  a  week  without  fever.  During  this  time  the  dullness  and  the 
not  very  loud  bronchial  breathing  remain  unchanged.  Then  appears  a  moderate 
intermitting  fever,  with  elevations  to  about  103°  or  103°  (39.5°  C).  This  fever 
may  last  two  to  four  weeks,  or  even  longer.  Over  the  affected  portion  of  the 
lungs  are  heard  either  no  moist  rales  or  only  a  very  few.  Gradually  there  appears 
a  moderate  but  distinct  contraction  of  the  side  involved,  then  the  resonance 
gradually  grows  clear,  the  respiratory  sounds  louder  and  vesicular,  the  fever 
ceases,  and  finally  health  is  completely  restored.  In  many  other  cases  of  delayed 
resolution,  as  we  have  already  said,  we  see  this  same  striking  absence  of  moist 
rales  and  the  development  of  a  moderate  degree  of  contraction.  Under  such 
circumstances  it  is  often  very  difiicult  to  exclude  a  secondary  pleurisy,  and  we 
can  not  make  sure  except  by  repeated  exploratory  puncture.  Moreover,  it  is  not 
exceptional  to  find  delayed  resolution  and  secondary  pleurisy  both  present  in  the 
same  patient. 

9.  T ermination  of  Pneumonia  in  Phthisis,  Contraction  of  the  Lungs,  Pulmo- 
nary Gangrene,  or  Pulmonary  Abscess. — Four  terminations  of  pneumonia  are 
ordinarily  mentioned  as  unusual  and  anomalous — the  termination  in  "  chronic 
pneumonia,"  in  tuberculosis,  in  gangrene,  and  in  abscess. 

Concerning  the'  termination  in  chronic  pneumonia,  we  have  already  men- 
tioned a  process  belonging  here,  the  termination  in  contraction  with  ultimate 
recovery.  In  rare  cases  the  contraction  is  permanent.  The  anatomical  process 
consists  in  the  development  of  pulmonary  cirrhosis,  with  the  formation  of  a  large 
amount  of  connective  tissue.  This  proliferation,  it  should  be  said,  takes  place  not 
only  in  the  interstitial  tissue,  but  also  in  the  interior  of  the  alveoli  by  extension 
from  the  alveolar  walls.  Few  clinical  observations  of  the  fur.ther  course  of  these 
cases,  provided  death  does  not  shortly  ensue,  have  as  yet  been  published. 

When  croupous  pneumonia  is  said  to  terminate  in  pulmonary  tuberculosis,  of 
course  the  statement  can  be  understood  to  mean  only  that  the  symptoms  of  tuber- 
culosis follow  immediately  upon  an  attack  of  pneumonia.  When  this  is  the 
case — it  does  not  occur  often — it  is  probable  that  the  pneumonia  attacked  a  per- 
son already  suffering  from  tuberculosis,  in  whom,  however,  the  symptoms  did  not 
become  evident  until  after  the  pneumonia  had  rvm  its  course.     It  may  also  be 


222 


DISEASES    OF   THE   EESPIRATORY   ORGANS 


Fig.  29. — Cholesterine  crystals. 


that  exceptionally  tlie  pneumonia  furnishes  a  soil  for  a  secondary  infection  with 
tubercle  bacilli. 

Pneumonia  results  in  pulmonary  gangrene  in  rare  instances,  when  the  patient 
is  elderly,  delicate,  or  diabetic.  Here,  too,  in  our  opinion,  a  new  infection,  with 
a  foul  and  putrid  substance,  must  always  take  place,  and  this  excites  the  gan- 
grene. The  previous  pneumonia  furnishes  only  the  occasion  for  the  development 
of  gangrene,  and  perhaps  prepares  the  soil  for  the  agents  of  decomposition.  The 
development  of  gangrene  is  appreciated  clinically  (see  the  appropriate  chapter) 
by  the  change  in  the  sputum  and  the  persistent  fever. 

The  transition  from  pneumonia  to  pulmonary  abscess  is  very  rare.  We  can 
not  decide  whether  a  further  specific  cause  is  also  needed  for  this,  or  whether  the 

pneumonic  process  may  exceptionally  go  on 
into  the  formation  of  abscess.  We  know  that 
the  pneumococci  sometimes  excite  purulent 
inflammation  in  the  pleura  and  in  the  me- 
ninges, and  so  it  would  not  seem  impossible 
that,  under  peculiar  circumstances,  they 
should  also  cause  the  development  of  an  ab- 
scess in  the  lungs.  The  transition  to  an 
abscess  may  be  recognized  by  the  character  of 
the  sputum,  which  contains  fragments  of  pul- 
monary tissue,  such  as  elastic  fibers,  besides 
abundant  pus.  Moreover,  we  sometimes  find, 
on  microscopic  examination  of  the  sputum  in 
abscess,  scales  of  cholesterine  (Fig.  29)  and 
hsematoidine  crystals;  the  latter  may  be  so 
abundant  as  to  give  the  expectoration  a 
brownish  color.  Sometimes  we  have  seen  a  peculiar  greenish  color  of  the  sputum. 
The  signs  of  a  pulmonary  cavity  are  found  if  the  abscess  bursts. 

Diagnosis. — ISTo  special  remarks  on  diagnosis  need  to  be  added  to  the  descrip- 
tion we  have  given  of  all  the  important  symptoms  which  may  occur  in  croupous 
pneumonia.  In  the  first  place,  we  must  consider  the  sudden  onset  with  a  chill  and 
high  fever,  shortly  followed  by  subjective  thoracic  symptoms,  such  as  cough  and 
pain  in  the  side;  also  the  characteristic  sputum  and  the  objective  physical  signs,  the 
appearance  in  many  cases  of  herpes  on  the  face,  and  finally  the  general  course  of 
the  disease,  particularly  the  temperature-curve  with  its  final  sudden  drop.  We 
will  discuss  the  difi^erential  diagnosis  between  pneumonia  and  pleurisy  with 
effusion  more  fully  in  the  description  of  the  latter  affection. 

Prognosis. — Croupous  pneumonia  belongs  in  general  to  the  benignant  infec- 
tious diseases.  The  great  majority  of  cases,  in  previously  strong  and  healthy 
individuals,  run  a  favorable  course,  and  end  in  complete  recovery.  On  the  other 
hand,  pneumonia  brings  a  number  of  perils  with  it,  the  knowledge  of  which 
should  always  make  us  cautious  in  giving  a  prognosis. 

One  grave  danger  lies  in  the  extension  of  the  process.  If  the  advance  of  the 
pneumonia  can  not  be  stopped,  if  the  whole  of  one  lung  is  involved,  and,  besides 
that,  a  great  portion  of  the  other  lung,  the  diminution  of  the  respiratory  surfaces 
may  of  itself  occasion  a  fatal  termination. 

A  further  danger  lies  in  the  onset  of  certain  complications.  An  intense  pleu- 
risy, with  effusion,  especially  if  purulent,  causes  greater  difficulty  in  respiration, 
and  thus  increases  the  danger.  Still  worse  is  a  sero-fibrinous  or  purulent  peri- 
carditis, which,  in  not  very  rare  cases,  is  revealed  at  the  autopsy  as  the  special 
cause  of  death.  We  must  note,  however,  that  recovery  sometimes  finally  takes  place 
in  spite  of  an  empyema  or  of  a  purulent  pericarditis.  The  complication  with  a 
purulent  meningitis,  which  is  fortunately  very  rare,  is  probably  invariably  fatal. 


CKOUPOUS   PNEUMONIA  223 

The  dangers  of  constitutional  infection  and  constitutional  intoxication  are, 
on  the  whole,  much  smaller  in  pneumonia  than  in  other  infectious  diseases ;  e.  g., 
typhoid  fever;  but  yet,  this  possibility  deserves  some  consideration,  particularly 
in  certain  forms  of  pneumonia  already  referred  to  and  termed  "  typhoid "  or 
"  asthenic."  Such  particularly  severe  and  malignant  forms  of  pneumonia,  with 
a  high  rate  of  mortality,  sometimes  appear  as  endemics  and  epidemics;  but  it 
should  be  added  that  these  cases  are  also  often  marked  by  the  extent  of  the  local 
process  and  the  development  of  the  dangerous  complications  above  enumerated. 

The  individuality  of  the  patient  plays  the  most  important  part  in  the 
prognosis  of  pneumonia.  While  a  constitution  that  was  previously  healthy 
and  uninjured  usually  survives  the  disease,  one  that  was  previously  weak  and  dis- 
eased readily  succumbs.  In  this  fact  lies  the  danger  of  pneumonia  in  old,  weak, 
badly  nourished  persons,  and  in  persons  with  a  pre-existing  emphysema,  kypho- 
scoliosis, heart  disease,  etc.  In  this,  too,  lies  the  great  danger  of  every  pneu- 
monia in  drunkards.  Since  the  nervous  system  is  much  affected  by  chronic  alco- 
holism, we  vei-y  often  see  outbreaks  of  delirium  tremens  in  pneumonia.  In  like 
manner  the  other  nerve-centers  are  weakened  and  incapable  of  resistance,  especially 
the  regulatory  centers  for  the  heart  and  respiration.  Hence  we  can  understand 
why  even  moderate  drinkers,  though  previously  strong  and  well  to  all  appear- 
ances, succumb  to  pneTimonia  from  failure  of  the  heart  and  impairment  of  res- 
piration. 

If  we  ask  upon  what  symptoms  our  prognosis  in  any  given  case  should  depend, 
we  must  reply  that  no  single  factor  can  be  given  especial  prominence.  Chief 
stress  must  always  be  laid  upon  the  state  of  the  lungs  and  the  respiration,  but 
attention  must  also  be  given  to  the  general  condition,  the  heart's  action,  the 
height  of  the  fever,  etc.  The  worst  dangers  of  pneumonia  have  just  been  men- 
tioned. 

Of  the  abnormal  terminations  of  pneumonia,  contraction  gives  the  best  prog- 
nosis; but  recovery,  or  at  least  a  marked  subsidence  of  all  the  symptoms,  may 
sometimes  take  place  after  gangrene  and  abscess. 

Treatment. — Many  of  the  milder  cases  of  typical  pneumonia  need  no  special 
active  treatment  when  the  disease  takes  a  favorable  course.  Most  cases  get  well 
under,  or,  we  can  almost  say,  in  spite  of  any  treatment.  From  the  now  obsolete 
method  of  treatment  by  large  bleedings,  and  from  the  use  of  certain  drugs  (vera- 
trine,  tartar  emetic),  which  are  even  now  sometimes  employed,  we  should  expect 
harra  rather  than  any  benefit,  yet  under  such  treatment  many  patients  have 
recovered. 

We  do  not  know  of  any  certain  means  favorably  to  influence  the  pneumonic 
process.  Whether  we  are  destined  to  learn  of  some  specific  mode  of  treatment, 
perhaps  by  means  of  some  serum,  after  the  analogy  of  other  infectious  diseases, 
as  diphtheria,  we  can  not  say.  A  few  beginnings  have  already  been  made  in  this 
direction,  but  without  any  practical  results  as  yet.  We  are  at  present  obliged, 
therefore,  to  fall  back  upon  a  purely  symptomatic  and  constitutional  treatment 
of  pneumonia. 

The  symptoms  which  are  usually  prominent  in  pneumonia,  even  in  the  milder 
cases,  and  of  which  the  patient  is  especially  desirous  to  be  relieved,  are  the  pain 
in  the  side,  the  troublesome  cough,  and  the  difiiculty  and  distress  in  breathing. 
Since  the  respiratory  symptoms,  as  we  have  seen,  are  partly  due  to  the  pain, 
as  this  improves  the  patient's  breathing  often  undergoes  a  decided  improvement. 
For  the  pain,  we  may  first  mention  a  number  of  external  applications  to  the 
skin  on  the  affected  side.  An  ice-bag  sometimes  gives  marked  relief.  Many 
patients  can  not  bear  this,  but  prefer  warm  poultices  or  cold  wet  compresses.  The 
application  of  mustard  plasters  or  dry  cups  to  the  skin  may  be  of  advantage. 
Subcutaneous  injections  of  morphine,  however,  are  the  most  effective  remedy,  and 


224  DISEASES    OF    THE    EESPIRATOKY   OEGANS 

are  often  indispensable.  There  is  no  reason  why  we  should  not  use  this  remedy, 
with  care  and  in  moderate  doses,  for  the  relief  of  pain;  and,  as  the  disease  is  of 
short  duration,  we  need  not  particularly  fear  the  morphine  habit.  Small  doses 
of  morphine,  subcutaneously  or  by  the  mouth,  may  also  be  required  to  alleviate 
the  cough. 

Local  blood-letting  is  a  remedy  the  action  of  which  can  not  be  explained 
physiologically,  and  yet  experience  has  shown  that  it  is  of  undoubted  advantage. 
The  relief  which  many  patients  feel  after  the  application  of  eight  or  twelve 
leeches  to  the  affected  side  is  very  striking;  but  we  should  prescribe  them  only 
when  there  are  severe  symptoms  at  the  beginning  of  the  disease,  and  in  persons 
who  were  strong  and  healthj^  before  the  attack.  -Wet  cups  accomplish  the  same 
thing,  but  their  effect  is  somewhat  more  powerful,  and  hence  they  should  be  re- 
served for  strong  and  robust  persons,  such  as  laborers. 

The  tepid  or  cold  bath  serves  as  the  most  effective  means  of  improving  the 
respiration,  of  aiding  expectoration,  and  of  stimulating  and  refreshing  the  whole 
system.  We  hold  it  useless,  if  not  injurious,  to  give  a  patient  baths  if  the  dis- 
ease is  progressing  favorably,  for  almost  every  bath  has  some  disagreeable  feature. 
These  disadvantages,  however,  are  always  less,  in  severe  cases,  than  the  bene- 
fit and  improvement  which  baths  give  the  patient,  and  which  most  patients 
recognize  with  gratitude.  The  main  point  is  that  the  patient  should  make  no 
physical  exertion  while  in  the  bath,  that  he  should  be  lifted  into  it,  held  and  sup- 
ported while  in  it,  and  lifted  into  bed  again  after  it.  Since  the  baths  are  given 
primarily  not  on  account  of  the  fever,  but  to  improve  the  respiration,  and  be- 
cause of  their  favorable  influence  on  the  nervous  system,  their  temperature  need 
not  be  especially  low.  We  give  them  from  82°  to  86°  (22°-24°  E..) ;  somewhat 
warraer  with  sensitive  and  weak  people,  and  cooler,  down  to  77°  or  even  72.5° 
(20°-18°  R.),  with  strong  persons,  or  with  very  high  fever  or  severe  nervous  symp- 
toms. We  need  not  employ  more  than  two  or  three  baths  a  day,  and  at  night 
we  employ  them  only  when  there  are  threatening  symptoms.  The  favorable 
action  of  the  baths  is  seen  especially  in  the  great  relief  and  refreshment  that 
the  patient  feels.  The  respiration  is  quieter  and  slower,  but  deeper.  The  patient 
often  falls  into  a  quiet  sleep  after  the  bath.  Of  late  years  we  have  often  re- 
placed the  baths  by  a  wet  pack,  even  in  adults.  This  has  been  almost  always  very 
well  received,  and  indeed  seemed  to  make  the  patients  quieter,  with  easier  respira- 
tion and  less  discomfort.  We  would  particularly  and  strongly  recommend  the 
pack  for  private  patients,  in  whose  case  the  employment  of  baths  is  associated 
with  many  difficulties. 

Among  internal  remedies  for  pneumonia,  antipyretics  are  frequently  em- 
ployed. We  do  not  believe  they  are  capable  of  exerting  any  decided  infliience 
upon  the  general  course  of  the  disease,  although  we  admit  that  antipyrine  and, 
under  some  circumstances,  also  phenacetine  and  antifebrine  have  a  good  effect, 
since  they  not  only  modify  the  fever,  but  improve  the  nervous  symptoms  and  the 
general  condition.  Antipyrine  is  prescribed  in  doses  of  fifteen  to  thirty  grains 
(grammes  1-2),  particularly  toward  night. 

To  make  the  cough  somewhat  more  effective,  expectorants  are  prescribed.  We 
ourselves  most  frequently  employ  infusion  of  ipecac,  apomorphine,  infusion  of 
senega,  liquor  ammonii  anisatus,  and  benzoin.  The  last  two  remedies  are  espe- 
cially favorable  if  the  heart  is  feeble.  It  also  seems  to  us  of  some  importance, 
with  regard  to  expectoration,  to  prescribe  an  abundance  of  liquid  in  the  form  of 
water,  tea,  lemonade,  and  similar  drinks. 

The  behavior  of  the  heart  should  always  be  watched  with  vigilance,  especially 
in  elderly  and  delicate  persons,  and  in  the  obese  and  alcoholic.  If  the  pulse 
becomes  very  frequent,  an  ice-bag  is  placed  upon  the  heart.  If  the  pulse-rate  is 
remarkably  rapid  from  the  start,  we  may  order  digitalis  at  once,  either  in  infu- 


CROUPOUS   PXEUMOXIA  225 

sion,  or,  still  better,  in  powders  containing  li  to  3  grains  (gramme  0.1-0.2),  re- 
peated several  times  a  day;  and  as  digitalis  acts  slowly,  requiring  twelve  to 
twenty-four  hours  to  make  its  influence  felt,  if  the  weakness  of  the  heart  is  dan- 
gerous, stimulants  which  act  more  promptly  must  be  employed.  As  such,  tinc- 
ture of  strophanthus,  repeated  several  times  a  day,  deserves  to  be  recommended, 
and,  above  all,  subcutaneous  injections  of  oleum  camphoratum  (1  to  4),  of  which 
three  or  four  syringefuls  (tii,  xv),  and  more,  may  be  employed  (oss.  to  5j).  Again, 
ether  injected  subcutaneously  is  a  powerful  cardiac  stimulant,  but  it  should  be 
employed  cautiously  because  of  its  marked  local  effect  (paralysis  of  the  nerves), 
and  the  place  of  injection  should  be  the  skin  of  the  abdomen  or  the  thigh. 

We  have  yet  to  make  some  remarks  upon  the  very  extensive  use  of  large 
amounts  of  alcohol  in  pneumonia.  Without  doubt  a  free  use  of  alcohol  is  neces- 
sary in  drunkards,  especially  when  delirium  tremens  is  beginning  or  is  already 
pronounced.  Since  the  withdrawal  of  any  poison  that  is  taken  habitually,  like 
nicotine  or  morphine,  may  excite  the  severest  symptoms,  the  sudden  withdrawal 
•of  alcohol  from  drunkards  may  have  the  worst  results,  while,  if  we  give  an  abun- 
■dant  supply  of  the  stimulant  to  which  the  nervous  system  is  accustomed,  we  some- 
times succeed  in  avoiding  the  onset  of  severe  nervous  symptoms,  such  as  collapse 
and  failure  of  the  heart  and  respiration.  Likewise  wine  should  certainly  be  given 
to  persons  who  are  accustomed  to  it  and  themselves  desire  it.  It  is  quite  a 
•different  matter  with  patients  who  before  their  illness  have  not  been  accustomed 
to  take  alcohol  at  all,  or  who  took  it  only  in  small  amounts.  It  may  be  true  that 
in  these  cases  moderate  amounts  of  wine  may  have  a  stimulating  and  exciting 
action,  although  we  never  could  satisfy  ourselves  of  the  often  praised  influence 
of  alcohol  upon  the  action  of  the  heart.  We  hold  it,  however,  unjustifiable  to 
:force  large  amounts  of  alcohol  indiscriminately  upon  every  patient  with  pneu- 
monia, perhaps  in  spite  of  great  resistance  on  his  part.  Why  should  we  expect 
sick  persons  to  bear  doses  of  alcohol  which  have  only  bad  results  on  healthy  men 
unaccustomed  to  them?  The  assertion  that  fever  patients  "  bear  "  alcohol  better 
than  healthy  persons  lacks  proof.  It  should  be  admitted  that  perhaps  alcohol 
is  more  rapidly  consumed  in  fever  than  in  health,  but  it  should  also  be  considered 
that  the  toxic  effects  of  alcohol  are  less  easily  noticeable  in  comatose  patients 
than  in  persons  possessing  normal  consciousness. 

[Few  American  physicians  of  any  experience  will  accept  the  reasoning  of 
the  author  on  the  employment  of  alcoholic  stimulants  in  those  not  accustomed 
to  their  use. 

The  toxic  effects  of  alcohol  are  as  undesirable  in  pneumonia  as  in  any  other 
•disease,  but  there  are  few  affections  in  which  so  great  tolerance  is  shown  for  this 
agent.  The  chief  indications  for  its  exhibition  are  derived  from  the  pulse  and 
the  first  cardiac  sound  at  the  apex.  A  fiagging  heart  calls  for  alcohol,  the  effect 
•of  which  on  the  symptoms  and  on  the  circulation  is  to  be  carefully  watched;  the 
quantity  is  to  be  diminished,  increased,  maintained,  or  the  agent  is  to  be  omitted 
'entirely,  according  to  the  conditions  present  in  the  individual  case.  I  am  no  ad- 
vocate of  indiscriminate  alcoholic  stimulation ;  but  I  believe  that  lives  have  been 
frequently  saved  in  the  past,  and  will  be  saved  in  the  future,  by  the  judicious  and 
sometimes  extremely  free  use  of  this  class  of  remedies  in  acute  pneumonia.  In- 
halation of  oxygen  has  won  a  prominent  place  in  the  treatment  of  severe  pneu- 
monia of  late  years,  and  cases  are  reported  in  which  life  seems  unquestionably  to 
have  been  saved  by  it.  In  a  considerable  number  of  cases  the  editor  has  seen  only 
•one  which  could  come  under  this  class.  He  has  seen,  however,  marked  tempo- 
Tary  improvement  in  pulse  and  respiration,  with  diminution  of  cyanosis  and  in- 
duction of  relatively  quiet  sleep.  But  the  oxygen  must  be  given  in  large  quan- 
tities, sometimes  continuously'.  If  its  inhalation  fatigues  the  patient,  the  gas 
may  be  allowed  to  escape  before  the  mouth  or  under  the  nose  of  the  patient.  The 
15 


226  DISEASES    OF   THE   KESPIEATOEY   ORGANS 

objection  to  the  efficient  use  of  oxygen  in  some  cases  is  the  expense  of  perhaps 
some  hundreds  of  gallons  a  day  at  five  cents  a  gallon.] 

We  scarcely  need  to  lay  special  emphasis  on  the  fact  that  the  physican  should 
endeavor,  so  far  as  possible,  to  maintain  the  bodily  strength  by  means  of  appro- 
priate and  sufficient  nourishment.  Soups,  bouillon  with  toast  or  rusk,  milk,  and 
eggs  are  the  most  suitable  articles  of  diet,  and  it  is  sometimes  proper  to  give 
small  amounts  of  finely  minced  meat.  Care  should  be  taken  that  the  patient 
has  an  abundance  of  refreshing  beverages.  Wine  and  also  moderate  amounts  of 
good  beer  may  be  allowed  without  hesitation. 

The  treatment  of  complications  follows  the  ordinary  rules  which  have  been 
given  under  the  individual  affections.  We  must  also  mention  that,  in  delirium 
tremens,  tepid  baths  with  cold  douches  sometimes  have  a  very  good  efl;ect.  Be- 
sides this,  we  may  try  subcutaneous  injections  of  strychnine,  seven  to  fifteen 
minims  of  a  one-per-cent.  solution,  once  or  twice  a  day.  We  can  not  wholly  dis- 
pense with  narcotics,  such  as  morphine  and  chloral,  but  we  must  warn  against  the 
imprudent  use  of  large  doses  of  chloral,  above  thirty-five  grains  (grammes  2.5)^ 


CHAPTER   VI 

TUBERCULOSIS    OF    THE    LUNGS 

(^Pulmonary  Phthuif.     Pulmonary  Consmnption) 

General  Pathology  and  Etiology  of  Tuberculosis 

Ever  since  Bayle,  in  1810,  demonstrated  the  extensive  distribution  of  peculiar- 
nodules  in  the  various  organs,  and  their  relation  to  pulmonary  consumption,  few 
questions  have  so  taxed  clinical  observers  and  pathologists  as  those  relating  to  the 
cause  and  nature  of  tuberculosis.  Harmony  could  not  be  reached,  however,  so 
long  as  the  criterion  for  the  decision  of  the  questions  was  sought  in  the  presence  of 
definite  anatomical  changes,  which  were  regarded  as  specific  of  tuberculosis. 
Laennec  considered  the  peculiar  change  in  the  tubercular  products,  which  later 
was  named  caseation  by  Virchow,  to  be  characteristic,  and  called  everything- 
tubercular  in  which  it  was  found.  He  distinguished  the  isolated  tubercle  from 
diffuse,  tubercular,  cheesy  infiltration.  Thus  Laennec  recognized  that  many  pro- 
cesses were  allied  whose  affinity  was  often  disputed  afterward,  and  which  has  only 
recently  been  established,  such  as  the  affinity  between  "  scrofulous  "  enlargement 
of  the  glands  and  tuberculosis.  Another  opinion  became  quite  prevalent,  after' 
Virchow  discovered  that  precisely  the  same  anatomical  process  as  tubercular  case- 
ation was  also  found  in  inflammatory  products,  which  were  certainly  not  tubercu- 
lar, and  in  cancerous  ulcerations.  Hence  Virchow  made  a  sharp  distinction  be- 
tween tubercle  and  those  new  growths  and  inflammatory  processes  which  had 
become  cheesy.  The  anatomical  criterion  of  tuberculosis  was,  in  his  view,  the 
presence  of  the  miliary  tubercle,  a  gray  nodule,  the  size  of  a  millet-seed  at  the- 
largest,  made  up  of  cells  like  lymph-corpuscles.  The  study  of  the  finer  structure- 
of  the  miliary  tubercle  was  now  pushed  most  eagerly  by  Wagner,  Schiippel,  Lang- 
hans,  and  others,  but  they  were  unable  to  reach  perfect  harmony  regarding  its 
origin  and  significance. 

As  long  ago  as  1865,  however,  a  discovery  was  made  which  pointed  unequivo- 
cally to  the  only  way  which  could  lead  to  a  correct  knowledge  of  tubercvilosis.  It 
was  the  fact,  discovered  by  Villemin,  that  tuberculosis  can  be  produced  artificially 
by  inoculating  healthy  animals  with  small  amounts  of  tubercular  and  cheesy  sub- 
stances.    Although  doubted  and  misinterpreted  at  first  in  various  quarters,  the- 


TUBERCULOSIS    OF   THE   LUNGS  22Y 

fact  that  tuberculosis  can  be  transmitted,  and  consequently  the  fact  of  its  infec- 
tious character,  must  now  be  regarded  as  proved  beyond  a  doubt.  In  the  general 
change  which  our  opinions  upon  the  nature  of  infectious  diseases  have  undergone, 
especially  in  the  last  few  years,  the  existence  of  a  specific,  organized  cause  of 
tuberculosis,  too,  had  to  be  assumed.  Klebs,  and  later  Cohnheim,  had  already 
without  reserve  defined  tuberculosis  as  a  specific,  infectious  disease  and,  sooner 
than  we  dared  to  hope,  R.  Koch  discovered  the  special  carriers  of  the  disease  in 
the  shape  of  the  tubercle  bacilli,  in  the  year  1881.  The  definition  of  tuberculosis 
no  longer  rests  upon  any  external  anatomical  character.  Every  disease  is  tuber- 
cular which  is  excited  by  the  pathogenic  action  of  a  specific  kind  of  bacteria,  the 
tubercle  bacilli  discovered  by  Koch. 

The  pathogenic  bacteria  of  tuberculosis  belong  to  the  group  of  bacilli.  The 
tubercle  bacilli  are  rod-like,  of  small  diameter,  slightly  rounded  at  their  extremi- 
ties, and  either  straight  or  somewhat  bent.  Their  length  is  perhaps  a  fourth  or  a 
half  that  of  the  diameter  of  a  red  blood-corpuscle.  In  the  interior  of  these  rods  it 
is  not  infrequently  possible  to  distinguish  very  minute  colorless  spots  which  are 
probably  to  be  regarded  as  endogenous  spores.  The  tubercle  bacilli  have  no  inde- 
pendent motion  whatever.  Their  reaction  to  certain  coloring  matters  is  very  char- 
acteristic, and  of  the  highest  importance  with  regard  to  their  recognition  (vide 
infra).  We  know  with  absolute  certainty  that  the  tubercle  bacilli  are  always 
present  in  all  the  different  forms  of  pulmonary  tuberculosis,  both  in  the  lung  itself 
and  in  the  expectoration  (vide  infra),  and  also  in  tubercular  diseases  of  other 
organs,  the  brain,  the  intestines,  the  spleen,  the  liver,  and  the  kidneys,  and 
also  in  "  scrofulous  lymph-glands,"  in  "  fungous  "  diseases  of  the  bones  and  joints, 
and  in  the  so-called  lupus,  which  is  nothing  but  a  local  tuberculosis  of  the  skin. 
Precisely  the  same  bacilli  are  also  found  in  the  "  spontaneous  "  tuberculosis  of 
animals,  such  as  monkeys,  puppies,  and  guinea-pigs,  and  in  every  tuberciilosis 
that  is  artificially  produced  in  animals  by  inoculation.  Finally,  by  the  discov- 
ery of  tubercle  bacilli  in  the  "  pearly  distemper  "  of  cattle,  the  identity  of  this 
disease  with  tuberculosis — an  identity  which  had  already  been  established  by  ex- 
periments in  inoculation — was  confirmed  anew. 

Koch,  by  his  successful  "  pure  ctiltures  "  and  inoculations  with  the  cultivated 
bacilli,  has  established  the  fact  that  these  bodies,  known  as  tubercle  bacilli,  are  to 
be  regarded  as  organized,  and  as  the  special  cause  of  tuberculosis.  Bacilli  coming 
from  any  fresh  product  of  tubercular  disease  may  be  cultivated  at  a  constant  tem- 
perature of  98°  to  100°  (37°-38°  C.)  upon  blood-serum  which  has  been  stiffened 
by  heating,  and  upon  several  other  artificially  prepared  soils.  In  this  cultivation 
they  show  certain  characteristic  properties  in  their  growth,  which  can  not  be 
fully  described  here,  and  they  multiply  to  an  unlimited  extent.  In  this  way  we 
can  keep  up  perfectly  pure  cultures  of  tubercle  bacilli.  Inoculation  experi- 
ments tried  with  them  on  all  sorts  of  creatures  always  give  a  positive  result.  The 
animals  fall  ill,  lose  flesh,  and  finally  die,  and  at  the  autopsy  we  find  undoubted 
tubercular  disease  of  the  internal  organs,  which  may  be  more  or  less  extensive. 
The  most  instructive  inoculations  are  those  into  the  anterior  chamber  of  the  eye 
in  puppies  or  guinea-pigs,  which  were  first  tried  by  Cohnheim  and  Salomonsen. 
After  an  incubation  of  two  or  three  weeks  we  see  here  very  plainly  an  eruption  of 
the  first  nodules  of  tubercle  in  the  iris,  and  the  tuberculosis  spreads  to  the  other 
organs  of  the  body  later. 

By  these  experiments  it  was  first  demonstrated  that  tuberculosis  is  always,  at 
the  start,  a  purely  local  disease,  and  that  its  further  extension  depends  upon  the 
spread  of  its  germs. 


228  DISEASES    OF   THE   KESPIEATORY   ORGANS 


^Etiology  of  Tuberculosis  in  Man 

The  distribution  of  tubercle  bacilli  must  be  remarkably  extensive,  for  tuber- 
cular diseases  occur  in  almost  every  country  on  earth.  The  predisposition  of 
mankind  to  the  disease  is  also  very  great,  and  thus  we  understand  the  frightful 
fact,  which  statistics  show,  that  nearly  one  seventh  of  all  deaths  are  from  tuber- 
culosis !  It  has  neither  been  proved,  nor  is  it  probable,  that  tubercle  bacilli  multi- 
ply outside  of  the  human  body,  like  the  bacilli  of  splenic  fever,  since  they  can 
develop  only  in  a  constant  and  uniformly  warm  temperature  between  85°  and 
104°  (30°-4:0°  C).  We  must  therefore  regard  them  as  true  parasites,  which  can 
live — that  is,  which  can  propagate  and  multiply — only  in  the  bodies  of  animals, 
but  they  (or  their  spores)  seem  to  preserve  their  virulence  and  their  ability  to 
multiply  outside  of  the  body  for  a  long  time.  Phthisical  sputum  may  be  used  for 
inoculation  with  success,  even  if  it  has  been  dried  for  several  weeks.  The  tuber- 
cle bacilli  also  resist  most  chemical  reagents,  such  as  nitric  acid,  very  decidedly. 

If  the  body  becomes  infected,  then,  with  tubercle  bacilli,  it  is  always  probable 
that  they  have  come  from  some  other  individual — ^man  or  beast — with  tubercular 
disease.  We  need  not  mention  how  numerous  the  opportunities  for  infection  may 
be,  considering  the  present  general  distribution  of  tuberculosis.  The  chief  stress 
in  this  respect  is  to  be  laid  upon  the  expectoration  of  phthisical  patients,  which 
contains  the  bacilli.  This  dries  on  the  floor,  on  the  linen,  and  on  other  objects, 
and  then  the  small  particles  which  contain  the  germs  of  infection  are  carried  off 
by  the  air.  The  extensive  investigations  of  Cornet  have  well  shown  how  fre- 
quently it  is  possible  to  obtain  tuberculous  material,  which  is  capable  of  causing 
infection,  from  the  dust  in  the  neighborhood  of  phthisical  patients  who  carelessly 
deposit  their  expectoration  upon  the  floor  and  in  handkerchiefs  and  elsewhere. 
On  the  other  hand,  Fliigge  has  lately  emphasized  the  fact  that,  as  shown  by 
experiments,  the  inhalation  of  dry  sputiun  in  the  form  of  dust  is  far  less  dan- 
gerous than  the  breathing-in  of  fine  particles  of  liquid  expectoration.  He  points 
out  that  the  consumptive  with  a  cough  can  be  shown  to  defile  the  surrounding  air 
with  numerous  minute  drops  of  sputum  containing  tubercle  bacilli.  These  hover 
for  a  time  in  the  air,  and  may  be  inhaled  by  other  persons.  This  mode  of  infec- 
tion may  actually  be  important  as  causing  the  direct  transmission  of  tubercu- 
losis, and  that  such  direct  transmission  is  possible  is  shown  by  the  cases  of  tuber- 
culosis in  married  couples,  in  nurses,  and  in  patients  who  for  a  long  time  occupy 
a  ward  in  which  are  many  consumptives.  Still,  the  experience  of  physicians 
proves  that  such  direct  infection  with  tuberculosis  is  of  very  infrequent  occur- 
rence (vide  infra).  There  are  very  many  who  fall  sick  with  tuberculosis  who 
have  never  been  in  close  contact  with  other  consumptives.  In  such  cases  it  must 
be  that  the  tubercle  bacilli  enter  the  body  indirectly. 

The  material  which  contains  the  bacilli  or  spores  is  taken  into  the  body,  in  the 
majority  of  cases,  along  with  the  inspired  air.  This  is  probable,  because,  in  most 
cases,  tuberculosis  has  its  starting-point  in  the  air-passages,  the  lungs,  or  the  lar- 
ynx. Inoculation  experiments  show  that  the  first  extension  of  the  process  depends 
upon  the  point  of  inoculation.  If  it  be  in  the  anterior  chamber  of  the  eye,  the  first 
nodules  appear  in  the  iris,  as  we  have  said ;  if  it  be  in  the  abdominal  cavity,  we 
have  first  a  tuberculosis  of  the  peritonexun;  if  the  infectious  matter  be  inhaled, 
we  have  first  a  tuberculosis  of  the  lungs.  Hence  it  seems  very  probable  that,  in 
tuberculosis  in  man,  the  infectious  matter  is  taken  directly  into  the  air-passages 
by  the  breath.  In  this  way  it  sometimes,  though  rarely,  attacks  the  upper  air- 
passages,  as  in  primary  tuberculosis  of  the  nose,  the  pharynx,  and  the  larynx,  but 
more  frequently  it  affects  the  deeper  portions  of  the  respiratory  apparatus,  as  in 
primary  tuberculosis  of  the  lungs  and  bronchi. 


TUBEECULOSIS    OF    THE   LUNGS  229 

We  must  also  consider  other  modes  of  infection,  first  among'  wliich  is  tlie 
possibility  of  infection  of  the  intestinal  canal,  from  swallowing  the  infectious 
material.  The  transmission  of  tuberculosis  from  domestic  animals  to  man  plays 
a  part  in  this  connection  which  perhaps  is  not  unimportant.  Since  the  pearly 
distemper  of  cattle  is  identical  with  tuberculosis  in  man,  the  use  of  the  flesh  of 
such  animals  as  food  furnishes  a  possible  means  of  infection.  It  is  a  still  more 
important  circumstance  that,  when  pearly  nodules  are  present  on  the  udder, 
the  milk  of  the  diseased  animal  may  be  polluted  by  tubercle  bacilli,  and  that  the 
use  of  such  milk  as  food,  when  it  is  uncooked,  certainly  involves  the  danger  of  the 
transmission  of  tuberculosis.  Primary  tuberculosis  of  the  intestines,  however,  is 
not  very  frequent,  probably  because  the  tubercle  bacilli  which  have  been  swallowed 
are  usually  destroyed  in  the  stomach.  Still,  it  is  to  be  noticed  that  primary  tuber- 
culosis of  the  intestine  and  of  the  abdominal  lymph-glands  (vide  infra)  is  far 
more  frequent  in  children  than  in  adults,  and  that  it  is  children  who  drink  the 
most  milk. 

In  some  eases  the  tubercular  infection  may  probably  arise  from  little  fissures 
and  excoriations  of  the  skin.  In  this  way  either  we  get  a  local  tuberculosis  of  the 
skin,  such  as  lupus,  or  the  bacilli  are  carried  by  the  Ijonphatics  to  the  neighboring 
glands  of  the  neck  or  axilla,  establish  themselves  there,  and  set  up  a  tubercular 
disease  in  them.  It  should  be  stated  that  even  when  the  tubercle  bacilli  are 
taken  into  the  body  through  the  lungs  or  the  intestine,  the  infectious  material 
often  passes  the  primary  seat  of  infection  without  fastening  itself  there,  and  does 
not  take  root  until  it  reaches  the  nearest  lymph-glands;  or  perhaps,  often,  still 
more  distant  regions,  such  as  the  kidneys  or  the  bones  (?).  Thus  arises  the  so- 
called  primary  tuberculosis  of  the  bronchial  or  mesenteric  glands,  leading  some- 
times, as  we  shall  see  later,  to  various  severe  tubercular  diseases  in  other  parts, 
such  as  the  pleura  or  peritoneum. 

It  remains  to  mention  the  possibility  of  a  primary  genito-urinary  tubercu- 
losis. Primary  infection  of  the  uterus  and  ovaries  might  be  referable  to  direct 
infection  from  without;  but  it  is  questionable  whether  genito-urinary  tubercu- 
losis of  the  male,  affecting  the  kidneys,  testicles,  and  prostate,  arises  in  this  man- 
ner. In  such  cases  we  may  be  dealing  with  infection  due  to  the  excretion  by  the 
kidneys  of  tubercle  bacilli  which  have  got  into  the  body  in  some  other  way. 

Considering  the  wide  distribution  of  the  tubercle  bacilli,  and  the  many 
chances  for  infection,  it  seems  wonderful  that  in  spite  of  it  so  many  men  escape 
the  disease.  One  factor,  which  has  been  already  mentioned  by  Koch,  must  be 
borne  in  mind,  however,  and  that  is  the  extremely  slow  growth  of  the  tubercle 
bacilli.  This  is  the  reason  why  the  bacilli  do  not  always  remain  in  the  body,  but 
in  many  cases  are  eliminated  again  before  they  have  gained  a  definite  foothold. 

Individual  predisposition,  however,  is  another  factor  which  is  probably  still 
more  important — a  factor  which  we  can  not  well  explain,  but  which  we  can  not 
get  on  without,  at  the  present  time,  in  the  pathology  of  many  infectious  diseases. 
In  our  conception  of  most  of  the  other  infectious  diseases,  as  well  as  of  tubercu- 
losis, we  must  assume  provisionally  an  unequal  predisposition  to  disease  in  differ- 
ent individuals.  Only  a  part  fall  ill  of  all  who  are  exposed  to  the  action  of  the 
poison.  These  are  persons  in  whom  it  is  particularly  easy  for  the  poison  to  estab- 
lish and  propagate  itself. 

It  is  very  striking  that  the  existence  of  the  tendency  to  tuberculosis  is  often 
expressed  in  the  general  constitutional  debility  of  the  individual,  and — still  more 
remarkable — in  certain  peculiarities  of  his  bodily  frame,  e.  g.,  the  shape  of  his 
thorax.  This  phthisical  habitus  (vide  infra)  is  especially  common  in  persons 
who  come  from  f-amilies  with  a  tendency  to  tuberculosis,  and  it  is  a  peculiar  and 
quite  inexplicable  expression  of  the  predisposition  to  tuberculosis,  due  to  family 
and  hereditary  influence  (vide  infra).    It  should  be  said  that  the  hereditary  tend- 


230  DISEASES    OF    THE   EESPIRATOEY   ORGAl^S 

ency  to  tuberculosis  is  not  invariably  associated  with  any  striking  and  self-evident 
weakness  of  the  constitution.  Persons  who  spring  from  tuberculous  families 
may  have  a  vigorous  frame  and  yet  fall  victims  to  the  disease;  and  likewise 
also,  when  there  is  no  hereditary  tendency,  the  most  powerful  build  does  not  by 
any  means  render  one  invulnerable  to  the  disease. 

We  now  believe  that  many  evil  influences  which  were  once  thought  to  be 
causes  of  tuberculosis  act  only  in  increasing  the  predisposition  to  the  disease.  In- 
sufficient food,  bad  air,  severe  illness,  childbirth,  want,  and  care — these  alone,  of 
course,  can  never  produce  tuberculosis;  but  we  can  easily  imagine  that  the  body 
which  has  become  weakened  affords  less  resistance  to  the  injurious  influence  of 
the  tubercular  poison  than  does  the  strong  and  healthy  body.  Thus  it  seems  to 
us,  from  our  own  observations,  to  be  in  the  highest  degree  probable  that  chronic 
alcoholism  increases  the  liability  of  the  individual  to  tuberculosis.  It  is  surpris- 
ing how  often  drunkards,  possessed  of  a  naturally  most  vigorous  constitution, 
fall  victims  to  tuberculosis;  although  in  this  connection  we  ought  also  to  con- 
sider that  drunkards  are  so  often  and  so  long  in  filthy  and  ill-ventilated  saloons 
that  they  are  particularly  exposed  to  the  danger  of  infection. 

People  used  often  to  speak  of  the  transition  of  other  affections  of  the  lungs 
into  pulmonary  consumption — that  is,  into  tuberculosis.  It  was  imagined  that 
an  old  bronchial  catarrh,  croupous  inflammation  of  the  lungs,  or  the  catarrhal 
pneumonia  accompanying  measles,  or  whooping-cough,  could  readily  become 
"  tubercular."  Of  course  the  proper  interpretation  of  such  a  connection  is  that 
the  precedent  disease  prepares  a  favorable  soil  for  infection  with  the  tuberculous 
virus,  and  that  consequently  the  tubercle  bacilli  fasten  more  readily  upon  the 
mucous  membrane,  which  has  been  previuosly  affected,  than  under  normal  con- 
ditions. Moreover,  many  of  the  infections  which  we  formerly  supposed  to  be 
apt  to  change  into  tuberculosis  are  themselves  tuberculous.  This  is  true  in 
most  of  the  so-called  scrofulous  diseases  of  the  lymph-glands,  bones,  etc.,  and 
also,  as  we  shall  see  later,  in  the  overwhelming  majority  of  cases  of  apparently 
primary  pleurisy.  No  one  will  now  admit  the  truth  of  the  theory,  which  Nie- 
meyer  once  vigorously  defended,  that  a  primary  pulmonary  haemorrhage  could 
cause  the  development  of  pulmonary  phthisis.  Certainly,  in  the  cases  which 
apparently  support  such  an  opinion,  the  pulmonary  haemorrhage  is  not  the  cause, 
but  a  symptom,  of  pulmonary  tuberculosis. 

IsTo  single  factor,  however,  of  those  which  favor  the  predisposition  to  tuber- 
culosis, plays  so  manifest  and  so  visible  a  part  as  does  the  hereditary  tendency 
above  mentioned — that  is,  the  inborn  predisposition  of  the  individual.  The  fact 
of  the  heredity  of  phthisis  meets  us  with  such  uncommon  frequency  that  it  must 
have  forced  itself  upon  the  notice  of  the  older  physicians.  In  the  great  majority 
of  all  cases  of  phthisis  we  can  make  out,  by  close  questioning,  that  in  the  family, 
either  among  the  older  members  or  among  the  brothers  and  sisters,  one  or  more 
cases  of  tubercular  disease  have  already  occurred.  The  closer  we  investigate,  and 
the  more  we  search  for  some  one  of  the  different  forms  in  which  tuberculosis 
can  show  itself,  like  pleurisy,  or  affections  of  the  bones  and  joints,  the  more 
frequently  we  can  make  out  this  hereditary  predisposition.  Some  persons  are 
indeed  of  the  opinion  that  the  hereditary  transmission  of  the  disease  is  often 
merely  apparent,  and  not  real,  from  the  fact  that  the  close  relations  between  the 
children  and  their  diseased  parents,  or  brothers  and  sisters,  greatly  increases  the 
danger  of  infection  of  the  ordinary  kind.  Certainly  this  consideration  should  not 
be  forgotten  with  regard  to  the  occasional  appearance  of  tuberculosis  in  families, 
but  yet  it  would  be  impossible  to  explain  in  this  way  alone  the  extremely  fre- 
quent development  of  tuberculosis  in  special  families. 

There  can  be,  therefore,  scarcely  any  doubt  as  to  the  inheritance  of  tubercu- 
losis, but  the  explanation  of  this  fact  is  far  from  clear.     The  hereditary  charac- 


TUBERCULOSIS    OF   THE   LUNGS  231 

ter  of  tuberculosis  may  very  well  harmonize  with  its  infectious  character.*  We 
might  assume  in  this  case  a  perfect  analogy  with  syphilis — namely,  a  transition  of 
the  infectious  material  itself  from  the  parent  to  the  child  before  birth.  There  is 
only  one  striking  difference  between  syphilis  and  tuberculosis — that  the  children 
of  syphilitic  parents  very  often  come  into  the  world  with  definite  signs  of  infec- 
tion, while  congenital  tuberculosis  in  this  sense  is  an  extremely  rare  occurrence. 
We  must  accordingly  compare  tuberculosis  to  that  form  of  hereditary  syphilis 
(lues  hereditaria  tarda)  in  which  the  first  symptoms  of  the  affection  come  on  at  a 
late  period. 

Since  certain  considerations,  however,  constantly  oppose  such  a  theory,  we  are 
of  late  disposed  to  assume  that,  as  a  rule,  tuberculosis  in  itself  is  not  inherited,  but 
only  the  predisposition  to  tubercular  disease.  This  opinion  agrees  with  the  facts 
that  members  of  a  family  in  which  tuberculosis  prevails  very  often  show  the  so- 
called  tubercular  habit  even  without  any  real  tubercular  disease;  and  that  they 
often  have  "  weak  lungs  " — that  is,  that  they  easily  get  out  of  breath,  and  mani- 
fest a  distinct  tendency  to  catarrh  of  the  respiratory  organs.  Another  fact, 
which  to  a  certain  extent  may  be  regarded  as  an  argument  against  the  assump- 
tion of  a  direct  hereditary  transmission  of  the  disease,  is  that,  in  cases  of  appar- 
ently hereditary  tuberculosis,  as  a  rule  those  organs  first  show  evidences  of  disease 
which  are  most  exposed  to  an  infection  from  the  outer  world— namely,  the  lungs 
and  larynx. 

The  age  of  the  patient  has  an  important  influence  upon  the  predisposition  to 
tubercular  disease.  Pulmonary  tuberculosis  occurs  with  special  frequency  in 
youth,  between  fifteen  and  thirty.  It  is  not  rare  in  children.  After  forty  it  is 
much  rarer  in  its  pronounced  and  rapid  forms,  but  it  is  seen  even  in  the  most 
advanced  age.  Slight  tuberculous  changes  are  very  frequently  found  at  autopsy 
in  the  lungs  of  old  persons.  These  changes  have,  as  a  rule,  no  clinical  sig- 
nificance. They  are  simply  due  to  the  inhalation  of  tuberculous  germs  with 
scarcely  any  tendency  to  further  extension  because  of  the  lack  of  individual  pre- 
disposition to  the  disease.  It  has  not  yet  been  shown  that  sex  has  a  special  influ- 
ence upon  liability  to  the  disease. 

Pathological  Anatomy  of  Tuberculosis,  especially  op  Pulmonary 

Tuberculosis 

If  now  we  inquire  wherein  consists  the  injury  which  the  tubercle  bacilli  in- 
flict upon  the  body,  the  first  point  to  emphasize  is  that  the  action  of  the  tubercle 
bacilli  is  at  first  invariably  purely  local.  Tuberculosis  does  not  belong  to  the 
■*'  general  infectious  diseases,"  in  which  the  infection  of  the  whole  organism,  the 
general  infection  of  the  body,  predominates  over  the  local  disturbances.  The 
essence  of  tuberculosis,  at  least  in  the  great  majority  of  cases,  is  the  local  disease. 
The  tubercle  bacilli  give  rise  to  definite  anatomical  changes  in  the  organs  where 
they  settle,  and  the  consequent  disturbance  of  function  in  the  organ  has  an  effect 
on  the  rest  of  the  body.  In  many  cases  the  whole  body  may  be  so  little  affected 
that  we  may  be  justified  in  saying  that  there  is  a  purely  "  local  tuberculosis." 

The  danger  of  tubercular  diseases,  however,  consists  in  the  fact  that  the  local 
affection  often  attacks  the  most  important  organs,  as  the  lungs  and  the  brain, 
and  sets  up  such  extensive  anatomical  changes  in  them  that  because  of  these 
changes  alone  it  becomes  impossible  for  life  to  continue  longer.  Besides  this,  the 
infection  in  many  cases  does  not  always  confine  itself  to  one  organ,  but  the  infec- 

*  Jani  has  made  the  interesting  observation,  that  a  few  tubercle  bacilli  may  be  found  in  phthisis  in 
the  vas  deferens  and  the  prostate,  or  in  the  folds  of  the  lining  membrane  of  the  tubes,  without  appar- 
ent disease  of  these  parts.  Whether  this,  however,  explains  the  hereditary  transmission  of  tuberculo 
sis,  is  as  yet  doubtful. 


232  DISEASES    OE   THE   KESPIEATOEY   ORGANS 

tious  material  extends  over  the  body  by  ways  and  means  which  we  shall  learn 
in  part  later  on,  and  attacks  one  organ  after  another,  or  even  many  at  once. 
Finally,  it  is  to  be  said  that  the  peculiar  character  of  the  changes  caused  by  tuber- 
culosis explains  why  these  are  often  the  cause  of  manifold  secondary  processes, 
such  as  toxic  effects  and,  particularly,  secondary  infections.  Thus  arise  fever,, 
suppuration,  secondary  inflammation,  and  other  important  phenomena,  which 
will  be  minutely  considered  later. 

The  entire  local  action  of  the  tubercle  bacilli — that  is,  the  pathological  anat- 
omy of  tuberculosis — is  almost  wholly  independent  of  the  organ  attacked.  Tu- 
berculosis belongs  to  the  group  of  so-called  "  infectious  tumors  " — that  is,  the 
local  action  of  the  tubercle  bacilli  consists  chiefly  in  the  production  of  a  prolifer- 
ation and  accumulation  of  cells  at  their  place  of  settlement,  which  is  termed  a 
tubercular  new  growth.  Without  going  into  histological  details  we  may  say, 
briefly,  that  the  whole  process  consists  in  a  primary  injury  of  the  tissue,  due  tO' 
the  invasion  of  the  tubercle  bacilli,  followed  by  a  hyperplasia  of  the  cells  peculiar 
to  the  tissue  itself,  and  involving  not  only  the  connective-tissue  cells  but  also 
those  of  the  epithelium.  In  this  way  are  developed  the  so-called  epithelioid  cells 
and  the  giant  cells.  The  next  step  in  the  process  is  the  migration  of  numerous- 
leucocytes  from  the  surrounding  blood-vessels.  The  leucocytes,  or  round  cells, 
collect  about  the  above-mentioned  new-formed  cells,  and  may  finally  completely 
cover  them.  A  network,  or  reticulum,  is  found  between  the  individual  new- 
formed  cells  and  the  wandering  cells.  This  probably  represents  the  remains  of 
the  original  interstitial  tissue,  crowded  apart  by  the  increased  number  of  cells. 
There  is  no  new  formation  of  vessels.  The  tubercle  contains  no  blood-vessels. 
The  tubercle  bacilli  lie  especially  inside  the  giant  cells,  but  also  in  their  vicinity. 

If  these  changes  have  progressed  far  enough,  they  become  visible  to  the  naked 
eye  as  a  small,  circumscribed  grayish  point,  which  is  called  a  miliary  tubercle. 
From  these  minute  nodules  the  disease  itself  obtained  its  name  of  tuberculosis. 
By  approximation  and  coalescence  of  neighboring  tubercles — for  these  keep  devel- 
oping because  of  the  spread  of  the  local  infection — the  tuberculous  formation 
continually  extends  itself,  and  thus  are  gradually  formed  the  large  tubercular 
nodules,  and  finally  the  diffuse  tuberculous  new  growth  or  the  diffuse  tubercu- 
lous infiltration. 

The  tuberculous  new  growth,  as  such,  can  scarcely  ever  be  distinguished  histo- 
logically from  other  infectious  tumors,  such  as  those  seen  in  syphilis  and  leprosy. 
Tuberculosis,  however,  has  a  characteristic  difference  in  its  final  stages  of  cheesy 
degeneration  and  eventual  disintegration  of  the  new-formed  tissue,  processes 
which  are  apparently  connected  with  the  absence  of  blood-vessels  and  the  conse- 
quent deficiency  of  nutrition  of  the  new  formation.  Both  the  tuberculous  infil- 
tration and  also  the  portions  of  the  original  tissues  inclosed  by  it  perish,  lose  their 
nuclei,  and  finally  become  disintegrated.  The  manner  in  which  they  are  de- 
stroyed— namely,  "  fatty  degeneration  " — belongs  in  the  group  of  the  so-called 
coagulation  necroses.  This  process  is  recognizable  to  the  naked  eye,  because  the 
tuberculous  infiltration  when  it  becomes  thus  degenerated  takes  on  a  pronounced 
yellowish  color.  Wherever  the  necrotic  portions  of  tissue  are  superficially  situ- 
ated they  are  cast  off,  giving  rise  to  tuberculous  ulcers. 

Alongside  the  tuberculous  new  formation  there  are  found  in  the  organs 
affected  with  tuberculosis  various  inflammatory  processes,  either  simple  or  sup- 
purative or  hemorrhagic.  We  may  therefore  surmise  that  the  tubercle  bacilli 
(or  the  chemical  toxines  formed  by  them),  besides  their  characteristic  effects,  act 
simultaneously  in  another  role  as  excitants  of  inflammation;  but  it  is  very 
probable,  and  especially  so  in  pulmonary  tuberculosis,  that  many  of  the  inflam- 
matory changes  which  arise  are  not  peculiar  to  the  tuberculosis  as  such,  but  are 
to  be  regarded  as  secondary  processes  (vide  infra),  for  the  development  of  which 


TUBEECULOSIS    OF   THE   LUNGS  233 

the  preceding  tuberculous  new  growth,  as  it  disintegrates,  furnishes  a  suit- 
able soil. 

As  regards  the  special  anatomical  processes  and  appearances  in  pulmonary 
tuberculosis,  the  tubercular  change  usually  begins  in  the  walls  of  the  smallest 
bronchi,  or  not  rarely  in  the  alveoli  themselves.  The  disease  does  not  begin, 
however,  in  many  different  parts  of  the  lung  at  once,  but  probably  in  one  or  two 
circimiscribed  spots  only,  and  in  a  great  majority  of  cases  in  one  apex.  We  do 
not  know  why  the  apices  are  so  often  the  starting-point  of  phthisis,  but  perhaps 
it  is  because  of  their  relatively  slight  expiratory  power,  which  renders  them  a 
favorable  lodging-place  for  the  tubercle  bacilli. 

The  tuberculous  infiltration  begins  in  the  walls  of  the  bronchi,  and  thence 
gradually  extends  toward  the  periphery.  The  original  tuberculous  bronchitis 
becomes  a  tuberculous  peribronchitis.  The  infectious  material  extends  from  its 
original  focus  by  means  of  the  lymph-  and  blood-channels  out  into  the  sur- 
rounding tissue;  and  also  as  soon  as  superficial  ulceration  takes  place,  the  in- 
fectious matter  is  liable  to  be  carried  by  the  inspired  air  into  other  bronchi.  Thus 
the  diseased  spot,  small  at  first,  keeps  gradually  extending.  Tubercular  peribron- 
chitis is  usually  easily  recognized  with  the  naked  eye.  We  notice  the  little  lumen 
of  the  bronchus  in  the  middle  of  the  "  cheesy  "  nodule,  which  at  first  is  gray  and 
later  yellowish.  Many  of  the  adjacent  nodules  run  together  in  part,  and  even 
entirely.  The  lumen  of  the  bronchus  is  either  wholly  plugged  by  the  infiltra- 
tion, or  the  destruction  of  the  necrotic  cells  begins  in  the  midst  of  the  peri- 
bronchitis. In  the  latter  case  the  lumen  is  enlarged  to  a  little  irregular  hole — 
the  first  beginning  of  the  formation  of  a  cavity. 

The  alveolar  tissue  of  the  lung  can  not  long  remain  unaffected,  with  such  a 
disease  of  the  smaller  bronchi.  Lobular  atelectasis,  the  necessary  result  of 
every  permanent  bronchial  obstruction,  miist  arise,  but  this  soon  passes  (by  pene- 
tration or  aspiration  of  the  germs)  into  a  lobular  pneumonia,  which  from  its 
specific  nature  later  becomes  caseous.  We  can  not  go  into  the  histological  de- 
tails here.  The  alveoli  are  filled  with  pus-corpuscles  and  large  epithelioid  cells, 
which  are  considered  by  many  authors  to  be  the  offspring  of  the  alveolar  epithe- 
lium. The  alveolar  walls  are  also  infiltrated.  This  finally  results  in  the  destruc- 
tion of  the  cheesy  and  necrotic  tissue,  and  consequently  in  the  formation  of 
cavities.  At  other  times  the  neighboring  nodules  run  together,  and  the  tuber- 
cular infiltration  thus  extends,  giving  rise  to  a  diffuse  caseous  pneumonia.  These 
processes  may  all  be  readily  recognized  by  the  naked  eye.  The  earlier  stages  of 
atelectasis  and  infiltration  correspond  to  the  jelly-like,  gray  coloring  seen  in  the 
so-called  gelatinous  infiltration  of  Laennec,  and  the  transition  to  caseation  is 
recognized  by  the  eye  from  the  yellowish  color. 

Although  all  the  processes  thus  far  described  are  destructive  in  their  nature, 
changes  are  also  found  in  the  lungs  in  tuberculosis  which  seem  to  have  a  tendency 
toward  circumscribing  the  disease  and  toward  healing.  Prominent  among  these 
are  the  chronic  interstitial  processes.  We  meet  with  the  formation  of  new  con- 
nective tissue,  partly  about  the  tubercular  infiltration,  but  especially  where  there 
is  already  destruction  of  tissue,  and  this  leads  to  contraction  and  the  formation  of 
a  firm  cicatrix.  The  encapsulated  cheesy  masses  may  then  be  in  part  reab- 
sorbed; in  part  they  undergo  calcification.  The  possibility  of  such  a  halt  in  the 
tuberculous  process  depends,  however,  upon  certain  conditions.  The  tuberculous 
new  growth  and  its  destruction  must  not  advance  too  rapidly,  and  the  new-formed 
tissue  must  not  itself  be  destroyed  before  it  becomes  cicatrized.  We  see  the 
cicatricial  formation,  therefore,  more  especially  in  chronic  cases;  we  find  it  in 
places  which  have  been  affected  the  longest,  and  where  the  tubercular  process, 
perhaps,  has  finally  come  to  a  standstill  of  its  own  accord.  Macroscopically,  this 
cicatricial  connective  tissue  is  composed  of  a  thick,  firm  substance,  usually  pig- 


234  DISEASES    OF    THE   KESPIKATORY   ORGANS 

mented— the  so-called  pigment  induration.  If  the  cicatricial  formation  follows  a 
previous  extensive  destruction  of  the  pulmonary  tissue,  the  affected  portion  of  the 
lung  may  thus  be  diminished  to  less  than  half  its  original  bulk.  Cavities  and 
firm  cicatricial  tissue  form  the  anatomical  basis  of  such  an  extensive  "  pulmonary 
contraction."  Either  the  cavities  are  formed  in  the  usual  way  from  the  destruc- 
tion of  lung  tissue,  or  they  may  be  simple  bronchial  dilatations  due  to  the  trac- 
tion of  the  contracted  tissue — bronchiectatic  cavities. 

The  contractile  changes  in  pulmonary  tuberculosis  teach  us  that  the  tuber- 
cular process  is  in  itself  capable  of  healing.  The  incurability  of  most  cases  of 
phthisis  is  due  to  the  fact  that  the  infectious  material  from  every  existing  tuber- 
cular nodule  is  carried  into  other  bronchi,  and  there  sets  up  a  new  tuberculosis. 
Thus  the  disease  is  constantly  extended.  The  original  tuberculosis,  which  was 
localized  in  one  apex  only,  gradually  spreads  to  the  lower  portion  of  the  lung. 
The  infectious  material  is  carried  by  coughing  into  the  trachea,  and  from  this 
point  may  be  carried  by  inspiration  into  the  other  lung.  This  becomes  diseased, 
and  finally  there  is  such  an  extensive  destruction  of  the  lungs  as  to  make  the 
further  continuance  of  life  impossible. 

Besides  the  specific  tuberculous  lesions  in  phthisical  lungs,  there  are  very  often 
found  simple  inflammatory  processes,  such  as  bronchitis  and  lobular  catarrhal 
pneumonia;  sometimes,  also,  although  seldom  of  great  extent,  croupous  pneu- 
monia; and  finally,  in  exceptional  instances,  limited  foci  of  gangrene.  These 
secondary  diseases  not  specifically  tuberculous,  and  yet  almost  always  associated 
with  tuberculosis,  are  of  the  greatest  clinical  importance.  They  probably  are  due 
in  most  instances  to  the  influence  of  secondary  pathogenic  germs  (particularly 
streptococci,  less  often  diplococci,  etc.),  for  which  the  tuberculosis  has  merely 
prepared  a  favorable  soil.  Many  clinical  phenomena  (particularly  most  of  the 
febrile  exacerbations  of  the  disease)  depend  upon  these  secondary  inflammatory 
processes  which,  in  their  turn,  promote  the  further  extension  of  the  tuberculosis. 
Thus,  frequently,  inflammatory  lesions  which  are  due  to  secondary  infection 
finally  are  transformed  by  the  invasion  of  tubercle  bacilli  into  foci  of  tuberculosis. 

If  we  consider  the  list  of  anatomical  processes  which  are  found  in  tuberculosis 
of  the  lungs,  and  which  may  be  combined  in  the  most  manifold  ways,  we  can 
understand  the  great  diversity  in  the  anatomical  picture  in  different  cases.  Pri- 
mary tuberculosis  of  the  bronchial  wall  and  tubercular  peribronchitis,  diffuse 
cheesy  pneumonia,  and  destruction  of  the  tubercular  new  growths,  with  the  for- 
mation of  cavities,  on  the  one  hand;  contracting  interstitial  pneumonia,  cicatri- 
cial formation,  and  pigment  induration  on  the  other — these  are  the  compara- 
tively simple  anatomical  lesions  from  which  the  whole  process  of  pulmonary 
tuberculosis  in  its  most  varied  forms  is  composed.  Besides  this,  we  often  find  here 
and  there  one  or  more  miliary  tubercles  scattered  through  the  lungs,  which  are 
probably  due  very  largely  to  an  extension  of  the  infectious  material  by  means  of 
the  blood  or  lymph  current;  and  finally  the  already  mentioned  processes  of  sec- 
ondary infiammation,  such  as  bronchitis  and  pneumonia. 

The  secondary  tubercular  diseases  of  the  pleura,  the  bronchial  glands,  and 
other  organs,  will  receive  a  special  description. 

Clinical  History  of  Tuberculosis  in  General  and  of  Pulmonary  Tuberculosis 

IN  Particular 

In  judging  of  the  various  appearances  in  the  clinical  picture  of  tuberculosis 
we  must  especially  consider  the  following  points :  The  place  of  the  first  infec- 
tion is  of  the  chief  importance — that  is,  the  place  where  a  local  affection,  set 
up  by  the  tubercular  poison,  first  arises.  One  can  readily  understand  why  all  those 
organs  which  are  directly  exposed  to  infection  from  without  are  most  frequently 


TUBEECULOSIS    OF   THE   LUNGS  235 

affected  with  primary  tuberculosis.  Very  often,  as  we  have  said,  the  lungs  are  the 
organs  first  attacked.  Less  often  the  upper  respiratory  passages — viz.,  the  larynx 
and  nose.  In  other  cases  the  tubercle  bacilli  fasten  first  upon  the  digestive  tract 
(the  intestines,  less  often  the  pharynx  and  the  tongue).  In  many  other  cases,  how- 
ever, it  can  not  be  that  the  tubercle  bacilli  directly  reach  the  organ  which  seems 
to  be  first  affected.  This  is  true  of  the  so-called  tuberculosis  of  serous  membranes, 
of  the  tuberculosis  of  lymph-glands,  of  bones  and  joints,  of  the  brain  and  of  the 
genito-urinary  tract.  Investigators  have  yet  to  determine  the  paths  by  which 
the  tubercle  bacilli  reach  the  respective  organs  in  these  cases.  The  glance  which 
we  have  just  taken  at  the  organs  most  frequently  attacked  by  tuberculosis  shows 
the  great  clinical  variety  of  tuberculous  diseases  viewed  from  this  aspect. 

Another  reason  for  the  great  variation  in  the  course  of  tuberculosis  is  found 
in  the  fact  that  the  extension  of  the  local  tubercular  process  may  vary  very 
greatly  as  regards  time.  Tuberculosis  in  one  case  may  produce  the  most  exten- 
sive destruction  in  both  lungs  in  a  few  months  or  even  weeks,  and  in  another  case 
it  may  remain  almost  quiescent  for  years,  or  advance  only  very  slowly.  We  do 
not  know  fully  on  what  these  differences  depend,  but  much  is  certainly  due  to  the 
hygienic  influences  under  which  the  patient  lives.  In  the  last  analysis,  however, 
we  are  often  led  to  think  of  individual  differences  of  constitution,  which  now 
check  and  now  favor  the  rapid  extension  of  the  disease. 

This  predisposition  is,  in  most  cases,  congenital  but  sometimes  acquired.  This 
is  particularly  true  of  alcoholic  subjects,  who  often  evince  a  feeble  power  of  re- 
sistance to  tuberculosis,  although  originally  of  vigorous  constitution,  so  that  the 
rapidly  spreading  or  "  galloping  "  forms  of  tuberculosis  are  particularly  common 
in  drunkards. 

A  third  and  final  reason  for  the  differences  in  the  course  of  tubercular  infec- 
tion is  the  manner  of  the  further  extension  of  the  tubercular  poison  in  the  body. 
As  we  shall  see  in  the  description  of  tuberculosis  in  single  organs,  there  are  differ- 
ent ways  in  which  tuberculosis  may  pass  from  one  organ  to  another.  Many  con- 
tingencies are  involved  here,  and  we  can  easily  comprehend  how  greatly  the  whole 
clinical  course  of  the  disease  must  be  modified  by  the  rapidity  and  the  degree 
in  which  individual  organs  are  affected. 

After  these  preliminary  remarks  we  will  pass  on  to  the  description  of  the 
clinical  course  of  pulmonary  tuberculosis. 

The  onset  of  pulmonary  tuberculosis  is  quite  slow  and  gradual  in  the  majority 
of  cases.  The  patient  can  give  only  an  approximate  idea  of  the  time  when  he 
began  to  be  ill.  The  symptoms  are  referred  directly  to  the  respiratory  organs 
The  cough  and  its  attendant  expectoration  are  the  chief  things  which  affect  him. 
Moreover,  there  is  often  pain  in  the  chest,  either  the  pleuritic  stitch,  or  pain 
in  the  sternal  region,  or  pain  between  the  shoulder-blades.  The  patient  is  also 
apt  to  complain  of  shortness  of  breath,  especially  on  severe  physical  exertion. 

Besides  these  symptoms,  which  point  pretty  directly  to  disease  of  the  respira- 
tory organs,  there  are  often  quite  striking  general  symptoms.  The  patient's  ema- 
ciation is  especially  noticeable.  This  may  be  partly,  though  not  wholly,  explained 
by  his  loss  of  appetite.  Besides  the  emaciation  there  is  a  steadily  increasing  pallor 
of  the  skin.  The  patient  also  shows  a  general  dullness,  weakness,  and  disinclina- 
tion to  work.  There  is  not  infrequently  a  slight  rise  of  temperature  in  the 
first  stages  of  the  disease,  which  causes  subjective  feelings  of  chilliness  and  fever. 
Severe  night-sweats  may  also  be  noticed  early. 

Any  such  constitutional  disturbance  should  lead  the  physician  not  to  regard 
the  mild  thoracic  symptoms,  which  are  also  present,  as  insignificant,  but  to  think 
of  the  possibility  of  incipient  tuberculosis.  It  is  very  important  to  remember  that 
the  pulmonary  symptoms  may  be  entirely  subordinate  to  the  general  symptoms 
mentioned,  and  that  the  patient  himself  is  apt  to  pay  little  or  no  attention  to 


236  DISEASES    OF    THE   EESPIRATORY   OEGANS 

them.  Incipient  phthisis  is  therefore  frequently  diagnosticated  as  simple  "  chlo- 
rosis "  or  "  gastric  catarrh  "  for  a  long  time,  and  is  treated  as  such.  An  early  and 
careful  physical  examination  of  the  lungs  and  of  the  expectoration  is  the  only 
protection  against  such  an  error. 

Both  the  pulmonary  and  the  general  symptoms  assume  significance,  if  we 
have  to  do  with  a  patient  in  whom  we  suspect  a  "  tubercular  predisposition."  We 
very  often  meet  persons  in  whose  family,  either  in  the  parents  or  the  brothers  and 
sisters,  several  cases  of  phthisis  have  occurred.  They  are  persons  who  are  always 
pale  and  weak,  and  who  have  previously  shown  a  special  liability  to  catarrh  and 
other  diseases  of  the  respiratory  organs — e.  g.,  pneumonia.  They  have  perhaps 
had  diseases  which  our  present  theories  bring  into  direct  relation  with  tuber- 
cular infection.  We  refer  to  those  quite  frequent  cases  of  pulmonary  tuberculosis 
in  individuals  who  have  previously  siiffered  from  "  scrofulous  diseases,"  such  as 
chronic  swelling  of  the  lymph-glands,  chronic  affections  of  the  eye  or  ear,  or 
fungous  diseases  of  the  bones  and  joints,  pleurisy,  etc.  (vide  supra,  page  230). 

Although  the  first  symptoms  of  pulmonary  tuberculosis  often  develop  in  those 
who  were  not  quite  well  before,  this  is  true  in  only  a  part  of  the  cases.  We 
often  see  precisely  the  same  symptoms,  both  the  pulmonary  and  the  general, 
occurring  in  persons  who  previously  seemed  quite  well  and  strong.  ISTo  consti- 
tution is  perfectly  protected  against  the  disease.  We  have  even  seen  the  her- 
culean athlete  of  a  circus  die  of  phthisis. 

In  distinction  from  the  slow  and  gradual  method  of  the  development  of  tuber- 
culosis which  has  just  been  described,  the  first  symptoms  in  other  cases  may  be 
more  sudden.  A  definite  exposure  is  often  given  as  a  cause,  after  which  the  first 
symptoms  of  the  disease  have  speedily  developed.  It  goes  without  saying  that  we 
must  consider  these  harmful  influences — a  chilling  of  the  body,  a  cold  draught, 
over-exertion,  or  marked  mental  excitement — at  most,  as  exciting  causes. 
When  pulmonary  tuberculosis  begins  somewhat  abruptly,  either  the  initial 
symptoms  are  from  the  start  directly  referable  to  the  respiratory  organs 
(cough,  thoracic  pain,  dyspnoea),  or  the  chest  symptoms  may  be  obscured  by  the 
severity  of  the  constitutional  disturbance.  Thus  we  recall  a  number  of  cases  in 
which  young  persons  fell  sick  rather  suddenly  with  somewhat  severe,  febrile  con- 
stitutional disturbance.  At  first  no  cause  of  the  fever  could  be  found,  so  that 
the  diagnosis  was  doubtful,  or  was  supposed  to  be  typhoid  or  some  other  disease. 
Then  after  a  time,  thoracic  symptoms  developed  and  pulmonary  tuberculosis 
could  be  recognized.  In  most  cases  the  illness  would  take  a  rather  rapid  course. 
That  form  of  pulmonary  tuberculosis  which  is  termed  "  pneumonic  "  (vide  infra) 
also  exhibits  a  decidedly  acute  onset. 

Those  cases  of  pulmonary  tuberculosis  which  begin  with  hsemoptysis  are  of 
special  practical  importance.  Of  course,  it  must  be  understood  that  the  tuber- 
cular process  in  the  lung  has  existed  for  some  time  before  the  blood  appears 
(vide  supra,  page  230).  But  in  the  midst  of  apparent  health,  or  after  some 
slight  constitutional  disturbance,  comes  a  cough  with  bloody  expectoration. 
Very  often  the  further  symptoms  of  pulmonary  tuberculosis  follow  directly  upon 
this  initial  hsemoptysis  (vide  infra). 

In  conclusion,  those  cases  are  to  be  mentioned  in  which  the  first  signs  of 
tuberculosis  appear  not  in  the  lungs  but  in  the  larynx.  The  full  description  of 
these  cases  has  already  been  given  in  the  chapter  on  laryngeal  tuberculosis. 

The  further  course  of  pulmonary  tuberculosis  may  vary  so  much  that  it  is  im- 
possible to  give  a  complete  enumeration  of  all  the  possibilities. 

In  some  cases  it  advances  rapidly.  We  can  make  out  the  extension  of  the  dis- 
ease objectively,  almost  from  week  to  week.  At  first  the  apex  of  one  lung  alone 
is  attacked,  soon  after  the  lower  lobe  of  the  same  lung,  then  the  other  lung,  either 
at  the  apex  first  or  in  the  lower  part.    Besides  the  pulmonary  symptoms,  there  is 


TUBERCULOSIS    OF    THE   LUNGS  237 

quite  a  high  fever,  rapidly  increasing  emaciation,  and  general  loss  of  strength. 
Death  ensues  in  a  few  months.  We  term  such  cases  florid  phthisis,  or  "  gallop- 
ing consumption." 

In  other  cases,  however,  the  disease  has  a  remarkably  chronic  course.  Its 
onset  is  very  gradual,  or  else,  after  rather  an  acute  onset,  there  is  a  comparative 
cessation  of  all  symptoms.  The  thoracic  symptoms  do  not  disappear,  but  they  are 
only  trifling,  and  do  not  disturb  the  patient.  Physical  examination  of  the  lungs 
does  not  show  any  extension  of  the  process  for  months.  The  fever  which  accom- 
panies it  is  slight,  if  there  be  any.  The  patient  remains  quite  well  nourished,  but 
in  some  cases  there  is  a  good  deal  of  weakness.  He  feels  better  and  worse  by 
turns,  his  condition  being  greatly  influenced  by  the  care  and  nursing  he  receives. 

Unilateral  contracting  phthisis  especially  has  this  comparatively  favorable 
course  (vide  supra).  The  affection  remains  confined  to  one  lung  for  a  long  time. 
The  occurrence  of  contraction  shows  the  slight  tendency  of  the  tubercular  process 
to  advance,  ^nd  with  satisfactory  care  the  patient  may  remain  quite  well  for  years. 

In  cases,  too,  which  have  had  severe  symptoms  for  a  long  time,  a  temporary 
standstill  of  the  affection  may  take  place,  or  an  actual  improvement  in  all  the 
symptoms.  At  other  times,  in  eases  which  have  made  no  advance  for  a  long  time, 
the  symptoms  suddenly  grow  worse. 

There  are  all  possible  varieties  between  the  extremes  of  florid  phthisis  and  the 
very  chronic  cases  which  last  for  years  and  decades.  If  we  recall  the  further 
modifications  which  the  course  of  the  disease  may  assume  if  complications  arise, 
we  can  appreciate  the  manifold  character  of  the  clinical  picture  of  phthisis. 

Most  cases  with  definite  signs  of  somewhat  extensive  disease  terminate  fatally. 
Death  ensues,  either  with  the  signs  of  general  exhaustion,  or  as  a  result  of  the 
final  failure  of  respiration ;  or  it  is  due  to  the  occurrence  of  complicatiorLS,  such  as 
tubercular  meningitis,  miliary  tuberculosis,  pulmonary  haemorrhage,  or  pneu- 
mothorax. Yet,  on  the  other  hand,  if  the  tuberculosis  is  not  extensive,  the  disease 
may  terminate  in  complete  recovery.  To  say  how  frequent  recovery  is,  is  diffi- 
cult, for  it  is  probable  that  many  insignificant  cases  escape  diagnosis.  Further- 
more, a  distinction  should  be  drawn  between  recovery  from  a  standpoint  of  patho- 
logical anatomy,  meaning  complete  cicatrization,  with  disappearance  of  all  tuber- 
cular new  growth,  and  recovery  from  a  clinical  standpoint  [arrest],  meaning  dis- 
appearance of  all  symptoms.    Often  apparent  recovery  proves  deceptive. 

Special  Symptoms  and  Complications 

1.  Symptoms  on  the  Part  of  the  Lungs. — Pain  in  the  Chest. — Extensive  de- 
struction of  the  lungs  may  occur  without  any  feeling  of  pain.  Many  cases  of 
phthisis  are  painless  throughout  their  course.  In  other  cases,  however,  the  pa- 
tient's chief  complaint  is  of  severe  pains  in  the  side  or  in  the  front  of  the 
chest.  These  are  probably  always  due  to  co-existing  affections  of  the  pleura,  such 
as  pleurisy,  or  pleuritic  adhesions.  In  patients  who  suffer  from  severe  cough, 
pains  sometimes  arise  in  the  abdominal  muscles  and  at  the  insertion  of  the  dia- 
phragm, due  to  the  excessive  muscular  contraction. 

Cough. — In  the  majority  of  instances  cough  is  one  of  the  most  distressing 
symptoms  of  phthisis,  but  its  severity  varies  very  much  in  different  individuals, 
and  at  different  times  in  the  same  patient.  We  sometimes  see  cases,  particularly 
in  senile,  insensitive  individuals,  in  which,  in  spite  of  advancing  phthisis,  cough  is 
remarkably  slight,  or  entirely  absent.  In  cases  with  severe  cough,  it  is  often 
worst  at  night,  but  paroxysms  of  coughing  of  long  duration  are  also  apt  to 
come  on  in  the  morning  or  evening  hours,  which  are  painful  and  very  distressing, 
and  exhausting  for  the  patient.  The  cough  is  usually  associated  with  a  more  or 
less  abundant  expectoration,  but  sometimes  there  is  chiefly  a  dry  cough.     The 


238  DISEASES    OF   THE   EESPIRATORY   ORGAITS 

cough  becomes  very  severe  if  the  tubercular  affection  attacks  the  larynx  and 
trachea  (see  laryngeal  tuberculosis). 

Expectoration. — The  amount  of  expectoration  differs  very  much  in  different 
cases.  It  is  most  abundant  when  there  is  extensive  formation  of  cavities  in  the 
lungs.  In  such  cases  it  is  often  evacuated  in  the  morning  by  persistent  coughing. 
The  consistency  of  the  great  part  of  the  sputum  is  muco-purulent,  and  it  differs 
little  from  that  of  simple  bronchitis ;  in  fact,  a  large  part  of  the  phthisical  expec- 
toration comes  from  the  catarrhal  inflammation  of  the  bronchial  mucous  mem- 
brane. Usually,  however,  the  amount  of  mucus  as  compared  with  the  amount 
of  pus  is  less  in  phthisical  sputum  than  in  that  of  simple  bronchitis.  The 
sputum  is  therefore  less  viscid  and  more  fluid.  The  amount  of  mucus  in  the  ex- 
pectoration is  also  apt  to  be  greater  in  chronic  bronchitis  than  in  tuberculosis, 
although  mucus  is  seen  in  the  latter.  The  expectoration  which  comes  from  cav- 
ities is  almost  pure  pus,  with  only  a  slight  amount  of  serum  and  mucus  inter- 
mixed. Such  sputum  consists  often  of  large  separate  masses  described  as  num- 
mular, or  coin-shaped.  If  received  in  water,  the  uneven,  rough  surface  of  these 
masses  is  often  evident,  and  suggests  their  formation  in  the  irregular  pulmonary 
cavities. 

The  admixture  of  blood  with  the  sputum  is  of  great  diagnostic  and  practical 
importance.  Since  no  other  disease  so  often  gives  rise  to  the  presence  of  blood 
in  the  expectoration,  coughing  of  blood  (hsemoptysis)  is  almost  synonymous  with 
consumption  among  the  laity.  Little  streaks  of  blood  in  the  expectoration  are 
quite  frequent.  They  have  no  great  significance,  but,  of  course,  they  may  some- 
times be  the  precursors  of  severe  haemorrhages.  Profuse  haemoptysis  takes  place 
when  the  wall  of  a  little  pulmonary  vessel— almost  always  a  branch  of  the  pul- 
monary artery — is  infiltrated,  destroyed,  and  finally  eroded,  by  the  tubercular  new 
growth.  The  reason  why  haemoptysis  is  not  more  frequent  is  because  the  con- 
tents of  the  vessels  usually  undergo  thrombosis.  Severe  haemorrhages  very  often 
have  their  origin  in  little  aneurisms  of  the  branches  of  the  pulmonary  artery, 
which  penetrate  into  the  interior  of  the  cavities.  In  the  cases  of  fatal 
haemoptysis  we  frequently  succeed  in  finding  the  little  aneurism  and  its  point 
of  rupture. 

Pulmonary  haemorrhage  occurs  in  all  stages  of  phthisis.  The  initial  haemopty- 
sis has  already  been  mentioned  (page  236).  This  may  be  followed  by  other  symp- 
toms of  pulmonary  tuberculosis,  or  the  haemoptysis  may  cease  without  any  imme- 
diate sequels.  Pulmonary  haemorrhage  may  also  occur  at  any  time  in  the  further 
progress  of  the  disease.  The  amount  of  blood  raised  is  variable.  There  may  be 
one  or  more  tablespoonfuls,  or  one  or  more  pints.  The  blood  is  bright  red,  usually 
quite  frothy,  but  little  clotted,  and  in  part  mixed  with  other  constituents  of  the 
sputum.  After  the  first  well-marked  haemoptysis,  the  expectoration  usually  is 
mixed  with  blood  for  several  days.  Again,  there  may  be  repeated  haemorrhages  in 
a  short  time.  Sometimes  the  haemoptysis  begins  abruptly,  not  infrequently  at 
night,  without  any  occasion.  In  other  cases,  the  haemorrhage  is  referable  to  some 
distinct  cause,  such  as  bodily  exertion,  a  violent  paroxysm  of  coughing,  strain- 
ing at  stool,  mental  excitement,  and  the  like.  Many  cases  of  phthisis  are  char- 
acterized by  a  special  tendency  to  haemorrhage,  while  in  many  others  haemoptysis 
never  occurs.  Severe  haemoptyses  are,  of  course,  always  an  undesirable  and  dan- 
gerous complication,  since  they  weaken  the  patient  very  much,  and  also  depress 
his  spirits.  Many  patients  maintain  their  peculiar  careless  indifference,  which 
is  almost  characteristic  of  the  disease,  despite  the  spitting  of  blood.  The  haemop- 
tysis may  sometimes  be  the  direct  cause  of  death,  but,  as  a  rule,  the  patients  sur- 
vive it.  We  have  no  better  means  of  determining  with  certainty  the  influence 
which  haemoptysis  has  upon  the  progress  of  tuberculosis  than  by  the  bodily  tem- 
perature.   If  there  was  no  fever  before,  and  the  haemoptysis  also  has  an  afebrile 


TUBEKCULOSIS    OF   THE   LUNGS 


239 


course,  or  only  a  very  brief  rise  of  temperature,  then  we  may  hope  in  general  that 
the  patient  may  fully  recover  from  the  haemorrhage  and  be  as  well  as  before.  If, 
however,  the  haemoptysis  is  followed  by  persistent  fever,  or  if  the  fever  which 
may  have  previously  existed  becomes  higher  and  more  persistent,  we  have  every 
reason  to  suppose  that  the  tuberculous  process  is  making  more  rapid  advances 
subsequently  to  the  haemoptysis.    We  here  append  a  temperature  chart  (Fig.  30) 

*  Haemoptysis. 


Fig.  30.— Influence  of  a  pulmonary  haemorrhage  upon  the  bodily  temperature.    (Erlangen  medical  clinique.) 


illustrating  the  temporary  influence  of  a  haemoptysis  upon  the  temperature  in  a 
stationary  afebrile  case  of  pulmonary  tuberculosis.  The  fact  that  the  fever 
preceded  the  haemorrhage  by  a  few  days  is  probably  due  to  the  tuberculous  arte- 
ritis, because  of  which  material  capable  of  exciting  fever  entered  the  circulation 
before  the  process  had  caused  complete  destruction  and  bursting  of  the  arterial 
wall,  and  consequent  pulmonary  haemorrhage. 

A  purulent  sputum  intimately  mixed  with  blood  is  quite  frequent  and  charac- 
teristic in  many  cases  of  phthisis  with  extensive  formation  of  cavities.  This  is 
formed  in  the  cavities  from  the  mixture  of  the  purulent  secretion  with  little 
capillary  haemorrhages.  In  this  way  the  sputum,  which  is  often  nummular, 
assumes  a  greasy  character  and  a  reddish-brown  or  chocolate  color. 

If  foetid  or  gangrenous  processes  develop  in  the  lungs,  the  sputum  becomes 
foetid.  In  some  cases  we  see  temporarily  in  phthisis  the  characteristic  sputum 
of  croupous  pneumonia,  which  comes  from  portions  of  the  lung  attacked  with 
secondary  pneumonia. 

Microscopic  examination  of  the  sputum  may  show — besides  the  ordinary  mor- 
phological elements,  such  as  pus-corpuscles,  red  blood-corpuscles,  and  epithelium 
— two  constitutents  which  are  of  decided  diagnostic  importance:  elastic  fibers 
and  tubercle  bacilli. 

The  demonstration  of  elastic  fibers  in  the  expectoration  permits  us  to  decide 
with  certainty  that  there  is  a  destructive  process  in  the  lungs,  and  thus  it  usually 
is  direct  proof  of  tuberculosis.  Elastic  fibers  are  also  found  in  pulmonary  gan- 
grene, and  in  the  very  rare  cases  of  pulmonary  abscess,  as  well  as  in  tuberculosis, 
but  gangrene  is  easily  recognized  by  the  other  peculiarities  of  the  sputum.  The 
search  for  elastic  fibers  in  the  expectoration  of  tubercular  patients  demands  a  cer- 
tain amount  of  practice.  We  are  most  sure  to  find  them  if  we  look  in  the  sputum, 
when  it  is  sprend  out,  for  little  lentiform  particles,  which  can  easily  be  discerned 
with  the  naked  eye.  These  consist  of  necrotic  shreds  of  tissue  torn  off  from  th« 
walls  of  cavities.  If  we  press  one  of  these  "  kernels  "  under  a  cover-glass  we  find, 
in  the  midst  of  the  granular  detritus,  beautifully  twisted  elastic  fibers,  which 
often  have  quite  a  definite  alveolar  arrangement  (see  Fig.  31).  The  elastic  tissue 
is  the  only  one  spared  in  the  general  destruction.  There  is  a  special  method  of 
looking  for  elastic  fibers.     The  sputum  is  boiled  in  sodic  hydrate,  diluted  with 


240 


DISEASES    OE    THE   KESPIEATOEY   OEGAXS 


water,  and  we  look  for  elastic  fibers  in  the  precipitate  which  then  forms.  We  are 
never  justified,  however,  in  deciding  that  pulmonary  tuberculosis  is  absent  because 
we  do  not  find  elastic  fibers  in  the  sputum.  Their  presence  is  the  only  thing  that 
has  real  diagnostic  significance. 

The  discovery  of  tubercle  bacilli  in  the  expectoration  of  phthisical  patients  is 
of  much  greater  importance,  and  often  this  alone  is  decisive  (see  Fig.  32).  They 
were  first  demonstrated  by  Koch,  but  Ehrlich  devised  the  first  simple  method  for 
their  discovery,  which  can  be  easily  employed  by  any  physician. 

The  simplest  method  and  the  one  which  we  now  employ  almost  exclusively 
for  staining  the  bacilli,  is  as  follows:  Some  of  the  sputum  is  rubbed  between  two 
cover-glasses,  which  are  then  slowly  separated,  leaving  upon  each  cover-glass  a 


Fig.  31. — Elastic  fibers. 


Fig.  32.— Tubercle  bacilli  in  the  sputum. 


very  thin  layer  of  sputum.  In  order  to  fasten  this  sputum  upon  the  cover-glass, 
the  latter  is  passed  three  times  slowly  through  a  gas  flame.  The  cover-glass  is 
now  held  with  a  pair  of  forceps  and  covered  with  the  following  staining-fluid 
(carbol-fuchsine  solution),  which  was  first  proposed  by  Ziehl  and  jSTeelsen:  Dis- 
tilled water,  100  parts;  crystals  of  carbolic  acid,  5  parts;  fuchsine,  1  part;  mix, 
filter,  and  add  alcohol,  10  parts.  This  staining  solution  upon  the  cover-glass  is 
heated  to  boiling  for  a  short  time,  and  then  the  staining  is  completed.  The  cover- 
glass  is  now  washed,  first  in  absolute  alcohol,  then  in  distilled  water,  then  placed 
for  about  two  minutes  in  a  solution  of  2  parts  of  methyl-blue  in  100  parts  of  a 
twenty-five-per-cent.  solution  of  sulphuric  acid.  The  acid  bleaches  out  the  dif- 
fused fuchsine  stain,  leaving  the  tubercle  bacilli  still  colored,  while  the  pus-cor- 
puscles are  colored  blue.  The  preparation  is  now  rinsed  in  water,  dried  between 
two  pieces  of  filter  paper,  and  examined  in  Canada  balsam.  The  whole  process, 
when  one  has  had  a  certain  degree  of  experience,  requires  four  or  five  minutes. 
The  number  of  bacilli  in  different  cases,  and  at  different  times  in  the  same  case, 
varies  considerably.  The  more  abundant  the  bacilli,  the  more  reason  have  we  to 
suppose  there  is  a  rapidly  advancing  process  of  ulceration,  but  of  course  we 
can  never  draw  a  broad  conclusion  as  to  the  extent  of  the  tuberculous  disease 
from  the  number  of  bacilli  in  the  sputum.  Our  only  information  on  this  point 
must  come  from  the  physical  examination,  and  other  clinical  observations.  On 
the  other  hand,  the  diagnostic  significance  of  the  demonstration  of  bacilli  with 
regard  to  the  recognition  of  a  pulmonary  tuberculosis  can  not  be  overrated. 


TUBERCULOSIS    OF   THE   LUNGS  241 

Every  positive  result  is  absolutely  decisive,  and  the  diagnosis  of  tuberculosis  of 
the  lungs  ought  certainly  never  to  be  made  unless  the  bacilli  have  been  demon- 
strated. Very  frequently  bacilli  may  be  found  in  the  sputum  in  early  cases,  at  a 
time  when  no  other  certain  sign  of  tuberculosis  can  be  detected.  On  the  other 
hand,  we  scarcely  need  to  point  out  that  the  physician  should  be  cautious  in  the 
interpretation  of  negative  results.  In  all  suspicious  cases  we  must  repeat  the  ex- 
amination of  the  sputum  over  and  over  again. 

Dyspnoea. — Many  patients  hardly  ever  complain  of  their  breathing  in  spite  of 
extensive  destruction  in  the  lungs.  A  patient  who  is  much  emaciated  manifestly 
needs  little  oxygen,  and  the  increased  frequency  of  respiration,  which  is  almost 
constant,  can  satisfy  his  needs.  If  there  is  a  greater  demand  upon  the  respiration, 
a  subjective  feeling  of  dyspnoea  may  of  course  very  readily  occur,  especially  on 
a  slight  bodily  exertion.  In  many  cases,  however,  the  patient  complains  of  a  dif- 
ficulty in  breathing  even  when  quiet,  especially  if  pleuritic  pains  or  adhesions 
between  the  surfaces  of  the  pleura  prevent  him  from  taking  a  deep  breath;  and 
in  the  final  stages  the  dyspnoea  may  be  extreme. 

2.  Symptoms  on  Physical  Examination. — In  many  eases  inspection  gives  us 
that  general  impression  of  the  patient  which  we  term  the  "  phthisical  habit."  The 
special  signs  of  this  are  as  follows :  A  slender  but  often  quite  a  tall  frame,  weak 
muscular  development,  a  thin  layer  of  fat,  a  pale  and  perhaps  very  delicate  skin 
with  a  bluish  translucence,  sometimes  a  circumscribed  "  hectic "  flush  in  the 
cheeks,  a  long  and  slender  neck,  a  long  and  flat  thorax,  small,  thin  hands,  etc.  Of 
course  this  characteristic  constitutional  habit  is  not  equally  well  marked  in  all 
cases.  The  inspection  of  the  thorax  is  of  special  value.  The  phthisical  or  "  para- 
lytic "  thorax  is  generally  noticeable  from  its  length,  but  it  is  narrow  and  flat. 
Unustial  width  of  single  intercostal  spaces,  and  acuteness  of  the  epigastric  angle, 
are  associated  with  a  long  thorax.  The  sternum  is  also  long  and  narrow,  and  the 
sternal  angle — Louis's  angle — is  sometimes  particularly  prominent.  The  supra- 
clavicular and  infra-clavicular  fossse  are  sunken,  the  neck  is  Avasted,  and  the 
shoulder-blades  stand  out  from  the  thorax.  On  comparing  the  two  halves 
of  the  thorax  we  very  often  observe  a  distinct  drawing-in  and  flattening  (con- 
traction) on  the  side  most  affected.  This  change  is  most  frequent  in  the  upper 
and  anterior  portions  of  the  chest,  bvit  it  is  not  rare  even  in  the  posterior  and 
lower. 

The  paralytic  form  of  thorax  is  very  often  seen  in  phthisis,  but  it  may  be  en- 
tirely absent. 

The  respiration  is  usually  somewhat  accelerated,  and  sometimes  quite  mark- 
edly so  in  women  with  disease  of  the  apices..  The  feminine  type  of  high  thoracic 
breathing  is  largely  changed  to  low  thoracic  or  diaphragmatic  breathing.  A 
unilateral  impairment  of  respiration  is  of  greater  importance;  in  such  a  case 
the  apex  in  front  or  even  the  whole  side,  if  there  be  phthisis  of  the  lower  lobe, 
lags  in  inspiration.  The  respiration  is  sometimes  irregular,  especially  if  there  be 
pleuritic  pains. 

The  results  of  percussion  are,  of  course,  entirely  dependent  upon  the  sort  of 
anatomical  changes  in  the  lungs,  and  hence  differ  very  greatly  in  different  cases. 
Since  the  phthisical  process  begins  in  the  apices  in  the  majority  of  cases,  our 
chief  attention  is  turned  to  the  condition  of  the  upper  portions  of  the  lungs  on 
percussion.  Slight  changes  in  percussion  may  wholly  escape  discovery.  Only 
when  the  air  contained  in  the  lung-tissue  in  the  part  affected  is  replaced  to  a  cer- 
tain degree  by  the  tubercular  infiltration  does  the  percussion-note  become  dull. 
Unilateral  dullness  at  the  apex  is  therefore  one  of  the  most  frequent  physical 
signs  of  phthisis.  We  can  iisually  make  it  out  most  plainly  in  the  upper  anterior 
intercostal  spaces  first,  and  in  incipient  cases  often  in  the  supra-clavicular  f oss£)e 
only,  but  it  is  also  observed  sometimes  in  the  back  in  the  supra-scapular  fossae. 
16 


242  DISEASES    OF    THE   EESPIEATORY   ORGAIsTS 

As  the  infiltration  advances  the  dulhiess  hecomes  more  extensive.  For  the  accu- 
rate determination  of  the  limits  of  dullness  in  the  upper  portions  of  the  lungs,  we 
recommend  that  percussion  should  be  practiced  in  such  a  way  as  to  proceed  from 
the  normal  resonance  of  the  lower  portions  upward  toward  the  affected  area.  This 
method  is  particularly  useful  for  the  back  of  the  chest.  Often  the  dullness  takes 
a  tympanitic  quality  as  a  result  of  diminished  tension  in  the  lung,  or  more  or  less 
pulmonary  retraction.  Changes  in  tension  may  render  the  resonance,  in  begin- 
ning tuberculosis,  deeply  tympanitic  without  any  accompanying  dullness. 

The  formation  of  cavities  in  tuberculosis  has  a  great  influence  on  the  percus- 
sion-note. The  dullness  on  percussion  may  thus  become  decidedly  less,  the  degree 
of  resonance  depending,  of  course,  upon  the  fullness  of  the  cavity  and  the  char- 
acter of  the  surrounding  tissue.  We  often  find  a  decided  tympanitic  resonance 
or  a  combination  of  dullness  and  tympany  over  a  cavity.  The  different  modifica- 
tions of  the  percussion-note  in  cavities  are  given  feelow.  The  "  cracked-pot  reso- 
nance," or  buckram  sound,  is  met  with  in  percussing  over  cavities,  but  we  also  find 
it  in  many  other  pathological  conditions,  and  in  children  not  infrequently  when 
the  lung  is  normal. 

Auscultation  also  gives  no  special  pathognomonic  signs  of  phthisis.  Varying 
with  the  character  and  extent  of  the  tubercular  changes,  abnonnal  respiratory 
sounds  and  adventitious  sounds  are  heard  in  place  of  the  normal  vesicular  mur- 
mur. With  slighter  changes  the  vesicular  breathing  is  merely  modified;  it  seems 
remarkably  diminished  or  interrupted,  or  sometimes  exaggerated,  with  prolonged 
expiration.  When  the  infiltration  of  the  lungs  increases,  we  find  bronchial  res- 
piration in  place  of  the  vesicular  breathing;  but,  on  the  other  hand,  the  forma- 
tion of  a  cavity  is  a  frequent  cause  of  bronchial  respiration. 

Various  sorts  of  moist  rales  are  among  the  most  frequent  and  diagnostically 
important  of  the  auscultatory  signs  of  phthisis.  They  are  caused  by  the  collection 
of  secretion  in  the  bronchi,  or  in  pulmonary  cavities.  The  more  abundant  and 
liquid  the  secretion  is  which  is  set  in  motion  by  the  air  current  which  traverses 
it,  the  more  abundant  and  moister  the  rales.  The  larger  the  space  is  in  which 
they  develop,  the  coarser  they  are.  Besides  the  true  moist  rales,  there  are  also 
dry  bronchitic  rales  (sibilant  or  sonorous)  occasionally  to  bfe  heard  in  portions  of 
the  tuberculous  lung.  In  general,  we  may  say  that  the  extent  of  the  tuberculous 
disease  in  the  lungs  can  be  determined  by  no  symptom  so  surely  as  by  the  auscul- 
tatory signs  relating  to  the  respiration,  and  the  adventitious  sounds  which  may 
be  present. 

Physical  Diagnosis  of  Incipient  Phthisis. — The  importance  of  the  diagnosis 
of  early  phthisis  is  so  great  that  we  will  briefly  sketch  its  most  important  physical 
signs.  Now  that  the  examination  of  the  sputum  for  tubercle  bacilli  plays  by  far 
the  most  prominent  part  in  the  recognition  of  incipient  tuberculosis,  and  is  the 
only  decisive  evidence,  the  physical  signs  of  this  condition  have  lost  much  of  their 
former  importance.  Still,  even  now,  the  determination  of  the  seat  and  extent 
of  the  early  process  is  extremely  desirable.  The  auscultatory  signs  in  the  begin- 
ning of  the  disease  are  in  general  more  certain  and  easier  to  recognize  than  those 
from  percussion.  He  who  lays  too  much  weight  on  the  so-called  "  slight  dullness 
at  the  apex  "  will  often  make  a  false  diagnosis.  We  will  mention  the  following 
sjonptoms:  1.  Constant  and  evident  diminution  of  the  respiratory  murmur  at 
one  apex,  especially  if  it  is  associated  with  marked  deficiency  of  the  respiratory 
movement  on  the  affected  side.  In  some  cases  the  respiratory  murmur  on  the 
diseased  side  is  not  weaker,  but  it  has  a  more  indefinite  and  harsher  character; 
or  again  it  may  be  rude,  sharp,  and  "  puerile."  2.  Markedly  interrupted  respira- 
tion at  one  apex.  3.  A  prolonged  expiratory  murmur,  which  has  a  harsh  charac- 
ter. 4.  The  discovery  of  dry  rhonchi  or  moist  rales  at  one  apex  is  most  important, 
since  we  know  by  experience  thfvt  "  apex  catarrhs  "  are,  as  a  rule,  tubercular.     5. 


TUBERCULOSIS    OF   THE   LUNGS  243 

Definite  dullness,  apparent  on  repeated  examinations,  or  tympanitic  dullness  or 
tympany  at  one  apex.  6.  Evident  contraction  at  one  apex,  as  revealed  by  inspec- 
tion or  perciission  above  the  clavicles,  7.  Some  authors  lay  stress  upon  a  systolic 
murmur  in  the  subclavian  artery,  especially  loud  on  expiration.  This  may  occur 
in  the  beginning  of  phthisis,  if  the  caliber  of  the  vessel  is  narrowed  by  processes 
of  contraction  in  the  neighboring  apex,  but  this  symptom  is  neither  frequent  nor 
of  great  practical  importance. 

The  chief  rule  in  the  diagnosis  of  incipient  phthisis  must  be  held  to  be  this 
— not  to  give  a  definite  opinion  until  repeated  examinations  have  been  made. 
The  other  portions  of  the  lungs  are  to  be  carefully  examined  as  well  as  the 
apices,  since  in  not  very  rare  cases  tuberculosis  may  begin  in  the  lower  lobes. 
We  must  always  consider  the  patient's  general  symptoms  as  well  as  the  physical 
signs  (vide  infra,  diagnosis). 

Diagnosis  of  Cavities. — The  positive  diagnosis  of  pulmonary  cavities  by 
means  of  physical  examination  is  often  very  difficult.  Any  one  who  will  compare 
the  discoveries  at  autopsies  with  the  results  of  previous  physical  examination  of 
consumptives  will  be  in  a  position  to  confirm  the  truth  of  this  statement.  We 
may  mention  as  the  chief  symptoms  of  a  cavity:  1.  Loud  bronchial  respiration, 
perhaps  of  an  amphoric  character,  in  places  where  the  percussion-note  is  only 
slightly  or  not  at  all  dull,  but  perhaps  tympanitic.  Such  a  condition  means  that 
the  bronchial  respiration  is  not  due  to  an  infiltration  of  lung-tissue.  Bronchial 
respiration,  however,  may  of  course  be  heard  over  cavities  which  are  surrounded 
by  thickened  lung-tissue,  and  hence  give  dullness  on  percussion.  Pure  amphoric 
respiration  is  very  characteristic  of  a  cavity,  particularly  if  there  is  a  clear, 
metallic  quality  to  the  sound;  but  this  sort  of  respiratory  murmur  is  heard  only 
when  the  cavity  is  comparatively  large,  of  regular  shape,  and  with  smooth  walls. 
Under  these  circumstances  the  moist  rales,  if  there  are  any,  also  have  a  clearly 
metallic  sound  (tinkle),  and  the  percussion  resonance  may  also  be  distinctly 
metallic.  This  last  should  be  demonstrated  by  rod  percussion  with  simultaneous 
auscultation.  In  many  cases  of  this  sort  the  differential  diagnosis,  between  a 
large  cavity  and  a  sacculated  pneumothorax  (see  page  298),  is  very  difficult. 
2.  The  so-called  metamorphosing  respiration,  which  begins  as  vesicular  and  sud- 
denly becomes  bronchial,  is  heard  especially  over  cavities,  and  hence  has  a  diag- 
nostic value.  3.  The  different  kinds  of  "  changes  in  the  percussion-note  "  over 
cavities  are  important  signs.  The  most  frequent  and  of  greatest  practical  im- 
portance is  Wintrich's  change  of  note.  This  is  when  the  tympanitic  resonance, 
which  is  obtained  over  the  cavity,  becomes,  on  opening  the  mouth,  more  decided- 
ly tympanitic,  louder,  and  especially,  much  higher.  The  respiratory  change  of 
pitch  of  Friedreich  usually  consists  of  a  higher  pitch  on  inspiration,  but  here 
there  are  numerous  variations.  Gerhardt's  change  of  pitch  (Weil)  consists  in  a 
change  of  the  tympanitic  resonance  when  the  patient  changes  his  position,  the 
pitch  usually  being  higher  when  the  patient  sits  up  than  when  he  is  lying  down. 
4.  Loud,  bubbling  rales  are  one  of  the  most  frequent  signs  of  a  cavity.  They 
are  definite  indications  of  the  occurrence  of  rales  in  a  larger  space  than  is  nor- 
mally present  in  the  apices  of  the  lungs.  If  we  have  coarse  and  metallic  rales  in 
the  apices  of  the  lung,  there  is  considerable  probability  of  the  existence  of  a  cav- 
ity, inasmuch  as  the  normal  apices  can  not  produce  such  sounds. 

Contraction  of  the  Lungs  [Fibroid  Phthisis]. — Unilateral  contraction  of  the 
lungs,  much  more  frequent  on  the  left  than  on  the  right,  is  a  form  of  tuberculosis 
which  is  made  apparent  both  by  special  physical  signs  and  also  by  certain  clinical 
peculiarities.  It  is  usually  recognized  at  once  by  inspection  of  the  thorax,  one 
side  of  the  thorax  being  remarkably  retracted.  The  upper  anterior  portions  of 
the  thorax,  and,  in  all  cases  of  a  high  degree  of  disease,  the  lower  lateral  and 
posterior  portions,  are  much  less  tense  than  the  corresponding  parts  on  the  other 


2i:i  DISEASES    OE    THE   EESPIEATORY   0RGA:NTS 

healthy  side.  The  fossae  and  intercostal  spaces  on  the  affected  side  are  deeper, 
the  shoulder-blade  is  drawn  nearer  the  vertebral  column,  and  the  latter  is  even 
sometimes  drawn  over  to  the  contracted  side  (scoliosis).  The  resonance  is  dimin- 
ished to  a  greater  or  less  degree,  over  the  affected  side,  which  either  lags  behind 
or  remains  almost  wholly  at  rest  on  respiration.  The  respiratory  murmur  is  quite 
loud,  and  bronchial;  and  we  also  hear  many  rales,  which  are  usually  bubbling. 
Exceptionally  the  rales  are  few  and  the  respiratory  murmur  feeble  and  indis- 
tinct. Anatomically,  we  have  to  do  with  a  marked  process  of  contraction  of  the 
interstitial  connective  tissue  in  the  lungs,  which  is  almost  always  associated  with 
extensive  formation  of  cavities,  partly  of  an  ulcerative,  partly  of  a  bronchiectatic 
character.  The  pleura  is  involved  in  the  process  almost  without  exception,  but 
almost  always  secondarily;  it  is  also  thickened  and  contracted.  If  the  pleuritic 
thickening  is  marked,  the  respiratory  murmur  and  the  vocal  fremitus  are  de- 
cidedly weakened. 

The  influence  of  the  contraction  on  the  neighboring  organs  is  very  decided, 
and  usually  it  is  easy  to  discover.  The  heart  especially,  whose  external  peri- 
cardium is  in  most  cases  very  adherent  to  the  pleura,  is  drawn  well  over  to  the  side 
of  the  contraction.  The  apex-beat  and  the  cardiac  dullness  are  correspondingly 
displaced.  With  left-sided  contraction  the  heart  may  be  drawn  over  to  the  line  of 
the  left  axilla,  and  with  right-sided  contraction  it  may  be  drawn  to  the  median 
line,  or  even  to  the  right  of  the  sternum.  With  contraction  of  the  left  upper 
lobe  the  anterior  surface  of  the  heart  comes  into  immediate  contact  with  the  an- 
terior chest-wall  over  a  larger  area  than  normal.  We  therefore  see  the  motions 
of  the  heart  over  an  abnormal  extent,  and  we  can  often  feel  very  plainly  in  the 
second  left  intercostal  space  the  pulsation  and  the  closure  of  the  valves  in  dias- 
tole of  the  pulmonary  artery.  The  upward  traction  of  the  diaphragm  may  be 
recognized  by  the  position  of  the  liver,  or,  in  left-sided  contraction,  by  the  in- 
crease of  the  "  semilunar "  tympanitic  space  on  the  left.  We  usually  find  the 
sound  lung  on  the  other  side  quite  emphysematous,  as  shown  by  the'  downward 
displacement  of  the  lower  boundary  of  the  lung,  and  also  by  the  drawing  over  of 
the  anterior  median  edge  of  the  lung  to  the  contracted  side.  In  a  part  of  the 
cases  we  can  make  out  by  percussion  the  development  of  consecutive  dilatation 
and  hypertrophy  of  the  right  ventricle. 

These  are  the  chief  physical  signs  of  the  so-called  unilateral  form  of  chronic 
pulmonary  contraction.  We  would  add  here  a  few  clinical  remarks.  These 
cases  often,  but  of  course  not  always,  run  a  very  chronic  course,  lasting  for  years. 
The  general  condition  and  the  nutrition  of  the  patient  may  thus  remain  com- 
paratively undisturbed  for  a  long  time.  The  patient  looks  somewhat  pale  and 
cyanotic,  yet  he  is  so  well  nourished  as  to  present  a  very  marked  contrast  to  the 
appearance  of  the  ordinary  cases  of  phthisis.  The  appetite  remains  good,  the 
fever  is  entirely  absent,  or  else  a  slight  degree  of  fever  may  be  at  times  discov- 
ered by  careful  examination.  The  cough  and  expectoration,  too,  though  often 
quite  troublesome,  are  at  other  times  very  slight,  especially  when  the  patient 
has  good  care  and  nourishment.  We  need  not  wonder,  then,  that  formerly 
many  physicians  did  not  consider  that  these  cases  had  anything  to  do  with  phthi- 
sis— "  consumption  " ;  and  yet  we  are  convinced  by  many  clinical  and  anatomical 
observations  that,  setiologically,  they  are  in  by  far  the  greatest  part  tubercular. 
They  represent  a  very  slow  form  of  tuberculosis,  which  has  time  to  develop  inter- 
stitial processes  which  lead  to  contraction — that  is,  to  local  healing.  If  such 
cases  come  to  autopsy,  their  tubercular  character  is  usually  definitely  confirmed. 
We  find  undoubted  tubercular  lesions  in  the  other  lung  and  also  in  the  remaining 
organs — e.  g.,  the  intestines.  Sudden  changes  for  the  worse  may  occur  in  every 
"  pulmonary  contraction,"  even  those  cases  which  seem  favorable ;  the  other  lung 
may  become  highly  tubercular,  a  miliary  tuberculosis  or  a  tubercular  meningitis 


TUBERCULOSIS    OF   THE   LUNGS  245 

may  develop,  etc.  On  the  whole,  however,  the  slow  course  of  this  form  of  chronic 
tuberculosis  is  characteristic  and  of  great  practical  significance,  and  its  prognosis 
is  therefore  comparatively  favorable^ 

We  can  not  deny  that  a  non-tubercular  unilateral  contraction  of  the  lung 
may  occur.  As  a  result  of  bronchitis  (particularly  in  cases  due  to  the  inhalation 
of  dust),  and  also  after  pleurisy,  processes  of  contraction  develop,  which  are 
associated  with  the  formation  of  bronchiectasis,  and  certainly  have  nothing  to  do 
with  tuberculosis.  In  rare  cases  also  croupous  pneumonia  is  followed  by  unilat- 
eral contraction  of  the  lung;  and  finally  there  is  a  rare  and  by  no  means  satis- 
factorily investigated  form  of  unilateral  chronic  interstitial  pneumonia,  with 
contraction,  often  associated  with  the  formation  of  bronchiectasis.  The  differ- 
ential diagnosis  of  these  conditions  from  tuberculous  contraction  rests  in  part 
upon  the  clinical  history,  which  should  be  carefully  taken,  but  mainly  upon  the 
absence  of  tubercle  bacilli  in  the  expectoration. 

In  conclusion,  we  must  mention  that  there  are  very  many  transitional  forms 
between  pulmonary  contraction  and  the  other  varieties  of  pulmonary  tuberculosis. 
We  find  more  or  less  extensive  processes  of  contraction  in  one  apex  in  most  cases 
of  phthisis. 

Disseminated  Pulmonary  Tuberculosis. — There  is  a  form  of  pulmonary  tuber- 
culosis which  it  is  very  hard  to  make  out  on  physical  examination.  In  this  we 
have  to  do  with  numerous  peribronchial  nodules  disseminated  over  the  whole 
lung.  As  there  is  still  a  good  deal  of  normal  tissue,  containing  air,  between  these 
nodules,  percussion  affords  no  dullness,  and  auscultation  gives  at  most  diffuse 
rhonchi ;  hence  this  form  is  often  confused  with  chronic  bronchitis  or  pulmonary 
emphysema.  The  diagnosis  can  seldom  be  made  from  the  physical  signs,  but  only 
from  the  other  symptoms,  such  as  fever,  emaciation,  striking  pallor  of  the  skin, 
and  the  sputum. 

This  form  of  phthisis  sometimes  runs  a  chronic  course,  but  usually  it  is  quite 
rapid.  It  occurs  in  elderly  people,  and  also  in  children.  Many  forms  of  "  dis- 
seminated, coarse  granular  "  tuberculosis  are  transitional  forms  between  this  and 
genuine  acute  miliary  tuberculosis. 

Pneumonic  Form  of  Pulmonary  Tuherciilosis. — A  special  clinical  interest 
attaches  to  that  form  of  pulmonary  tuberculosis  termed  pneumonic,  which 
we  have  already  briefly  mentioned.  The  disease  begins  in  a  decidedly  acute 
manner  with  dyspnoea,  frequent  cough,  and  pain  in  the  side.  Sometimes  we 
observe  even  a  distinct  initial  chill.  The  expectoration  is  scanty,  viscid, 
mucous,  and  often  reddish  or  hsemorrhagic.  It  sometimes  also  has  a  peculiar 
greenish  color.  Even  after  a  few  days  of  illness  we  find,  on  examination,  the 
well-marked  signs  of  lobar  infiltration.  There  is  first  pneumonic  resonance,  then 
a  dull  tympany,  with  fine  moist  rales  and  bronchial  breathing.  In  most  cases, 
but  not  all,  a  lower  lobe  is  involved.  The  disease  is  almost  invariably  regarded 
at  first  as  a  croupous  pneumonia,  but  the  expected  crisis  does  not  appear.  The 
fever  remains  high,  the  infiltration  does  not  undergo  resolution,  the  rales  become 
coarser,  the  patient  looks  pale  and  wretched.  Now,  suspicion  of  tuberculosis 
being  aroused,  the  sputum  is  carefully  examined,  and  soon,  although  perhaps  not 
at  the  first  examination,  tubercle  bacilli  are  found.  All  cases  of  this  sort  take 
a  rapid  and  unfavorable  course.  They  may  be  called  galloping  consumption. 
L"''pon  autopsy  we  find  diffuse  tubercular  infiltration,  and  usually  incipient  cavity 
formation  in  numerous  places.  Other  portions  of  the  h;ngs  than  that  first 
and  most  violently  attacked  ordinarily  present  considerable  tuberculous  change. 
In  these  instances  it  is  evident  that  we  have  to  do  with  an  acute  infection  of  a 
large  portion  of  the  lung  with  tubercle  bacilli,  Avhich  of  themselves  exert  a  pow- 
erful inflammatory  action,  with  unusual  virulence.  In  rare  cases  there  may  also 
be  a  mixed  infection,  due. to  the  pneumococcus. 


246 


DISEASES    OF    THE   EESPIEATOEY   OEGANS 


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Fig.  33.— Sub-febrile  state  iu  chronic  pulmonary- 
tuberculosis. 


3.  General  Symptoms  in  Pulmonary  Tuberculosis. — In  the  description  of  the 
general  course  of  pulmonary  tuberculosis  we  have  already  mentioned  the  value 
of  the  constitutional  symptoms  in  diagnosis  and  prognosis. 

Fever. — Only  a  few  cases  of  phthisis  run  their  course  entirely  without  fever, 
but  it  may  be  absent  for  a  time,  even  for  weeks  and  months;  and  indeed,  in 
cases  with  a  very  slow  and  favorable  course  (e.  g.,  where  there  is  unilateral  con- 
traction), there  may  be  no  fever  at  all  for  years.  The  more  carefully  we  measure 
the  temperature  the  more  often  shall  we  find  a  slight  evening  rise  up  to  100°  or 
101°  (38°  to  38.5°  C),  or  at  least  between  99°  and  100°  (37.5°  to  38°  C),  even 

at  times  when  the  patient  is  doing 
well.  Many  cases  that  pursue  a  com- 
paratively favorable  course  have  for 
a  long  while  a  .  so-called  sub-febrile 
condition.  That  is,  the  bodily  tem- 
perature is  normal  in  the  morning, 
but  in  the  evening  invariably  rises  to 
about  100°  or  100.7°  (37.8°  to  38.2° 
C),  or  even  higher.     (See  Fig.  33). 

Very  often,  particularly  in  the 
more  rapid  cases,  there  is  consider- 
able elevation  of  temperature,  and 
the  varieties  and  course  of  the  fever 
are  more  or  less  characteristic.  We 
should  first  mention  the  "  hectic  fe- 
ver "  (see  Fig.  34)  which  is  often 
observed.  For  months  the  tempera- 
ture chart  may  present  a  uniform  ap- 
pearance with  a  morning  temperature  approaching  or  reaching  the  normal,  while 
there  is  a  regular  elevation  every  evening  to  102°  or  104°  (39°  to  40°  C).  In 
general,  the  higher  the  evening  exacerbations  the  more  unfavorable  the  case. 
In  other  cases  the  temperature  chart  is  quite  irregular;  longer  or  shorter  per- 
sistent periods  of  elevation  alternate  with  periods  when  there  is  no  fever.  Particu- 
larly toward  the  end  of  the  disease,  as  the  bodily  weakness  increases,  the  previously 
regular,  intermitting  temperature  grows 
irregular.  At  this  time  the  intermis- 
sions often  become  more  marked,  and 
not  infrequently  general  collapse  tem- 
peratures—95°  to  93°  (36°  to  34°  C.)— 
are  observed.  Again,  the  fever  may  for 
limited  periods  take  on  a  more  continu- 
ous character,  probably  in  connection 
with  exacerbations  of  the  tuberculous 
process.  In  some  few  cases  with  acute 
onset  (vide  supra)  we  have  also  seen, 
in  the  beginning  of  the  disease,  a  toler- 
ably high  and  approximately  continuous 
fever,  passing  gradually  into  the  ordi- 
nary fehris  hectica.  The  cause  of  the 
fever  in  pulmonary  tuberculosis  is  not 
yet  settled.  The  special  question  is 
whether   the   tubercular   process    causes 

the  fever  of  itself  (by  production  of  toxines),  or  whether  the  fever  is  due  to  the 
secondary  inflammatory  processes,  such  as  the  absorption  of  septic  and  toxic 
material  from  the  decomposing  contents  of  the  bronchi  and  the  pulmonary  cav- 


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36° 

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Fig.  34. 


-Hectic  fever  in  chronic  pulmonary 
tuberculosis. 


TUBEECULOSIS    OF   THE   LUNGS  247 

ities.  The  practical  importance  of  the  fever  in  puhnonary  tuberculosis  is  very 
great.  The  emaciation  and  weakness  of  the  patient  are  caused  mainly  by  fever 
(vide  infra),  as  are  many  subjective  symptoms,  including  headache,  chilliness, 
and  persj)iration.  It  is  important  to  remember  that  in  observations  of  the  fever 
we  possess  one  of  the  most  positive  means  of  forming  an  opinion  as  to  the  course 
of  pulmonary  tuberculosis.  In  cases  which  are  either  completely  stationary  or 
very  chronic  there  is  no  fever  at  all.  The  sub-febrile  condition  shows  a  slow,  but 
still  continuous,  advance  of  the  disease.  Continuous  hectic  fever  is  an  unfavor- 
able sign,  and  indicates  a  comparatively  rapid  march  of  the  disease — the  more 
rapid,  the  higher  the  evening  temperature.  In  the  florid  or  galloping  forms  we 
find  tolerably  high  fever,  at  times  continuous  and  at  times  remittent.  Subnor- 
mal temperatures  are  almost  always  of  bad  omen. 

All  changes  in  the  general  course  of  the  disease  for  better  or  worse  stamp  them- 
selves clearly  on  the  temperature  chart.  The  onset  of  complications  and  secondary 
disease  is  often  first  indicated  by  the  thermometer.  Whether  an  attack  of  hgem- 
optysis  passes  over  witho.ut  permanent  damage,  or  whether  it  is  followed  by  an 
aggravation  of  the  disease,  can  usually  be  told  by  the  temperature  sooner  than  in 
any  other  way  (vide  supra,  page  238).  Thus  we  see  that  the  persistent  and  careful 
observation  of  the  temperature  in  consumption  deserves  to  rank  as  one  of  the 
most  important  means  of  estimating  the  status  and  course  of  the  illness. 

Emaciation. — The  great  emaciation  of  the  patient  is  very  striking  in  most 
cases  of  phthisis.  The  muscular  system  and  the  fatty  tissue  are  affected  in  equal 
degree.  The  soft  parts  of  the  thorax  are  often  especially  involved.  The  emacia- 
tion is  due  in  part  to  the  patient's  loss  of  appetite,  and  to  the  small  amount  of 
food  which  he  takes  in  consequence  thereof,  but  the  chief  cause  lies  in  the  per- 
sistent fever  and  the  increased  metamorphosis  of  tissue.  Quite  a  high  degree  of 
emaciation,  however,  may  appear  in  the  beginning  of  the  disease  with  no  fever. 
This  we  are  wont  to  ascribe  to  the  "  general  illness,"  but  the  special  cause  of  it  is 
unknown.  Under  favorable  external  conditions  phthisical  patients  may  make 
quite  a  decided  gain  in  weight,  especially  at  the  times  when  they  are  free  from 
fever.  In  very  chronic  cases,  which  run  their  course  from  the  first  without  fever, 
the  nutrition  of  the  patient  may  remain  good  for  a  long  time.  Toward  the  end 
of  the  disease  emaciation  sometimes  reaches  its  highest  degree,  and  many  phthis- 
ical patients  die  "  wasted  to  a  skeleton  "  in  the  true  sense  of  the  word. 

Ancemia — Color  of  the  Skin. — In  most  cases  anaemia  appears  in  the  course  of 
the  disease,  to  be  recognized  by  the  pale  and  sallow  color  of  the  skin  and  of 
the  visible  mucous  membranes.  The  anaemia  only  rarely  reaches  that  degree  of 
peculiar  waxy  pallor  that  is  found  in  idiopathic  pernicious  antemia.  If  the  pallor 
is  extreme,  however,  there  is  usually  some  special  reason,  such  as  profuse  haemop- 
tysis or  the  complication  of  amyloid  degeneration.  The  existence  of  the  anaemia 
is  also  the  reason  why  the  phthisical  patient  does  not  look  cyanotic  in  spite  of 
the  respiratory  disturbance.  In  the  more  chronic. forms,  where  the  general  nutri- 
tion suffers  less,  we  often  see  a  cyanotic  coloring  of  the  lips  and  cheeks.  Some- 
times the  skin  of  phthisical  patients  assumes  a  dirty,  dusky  hue.  We  have  already 
spoken  of  the  circumscribed  "  hectic  flush  of  the  cheeks  "  seen  with  the  fever. 

General  WeaJcness — Night-Sweats — Nervous  Disturbances. — We  need  not  say 
that  the  general  emaciation  and  anemia  are  accompanied  by  a  marked  decline  in 
the  patient's  power  of  endurance.  Tie  finally  becomes  so  helpless  that  he  can 
scarcely  move  alone  in  the  bed. 

The  tendency  which  very  many  patients  have  to  severe  night-sweats  is  uni- 
versally acknowledged  but  not  wholly  explained.  It  may  have  some  connection 
with  the  fall  from  the  evening  febrile  temperature  to  the  morning  remission,  and 
perhaps  it  is  due  to  the  greater  accumulation  of  carbonic  acid  in  the  blood  from 
the  disturbance  of  respiration.  i 


218  DISEASES    OF    THE   EESPIEATOEY   OEGANS 

The  disease  has  remarkably  little  influence  upon  the  higher  nervous  functions, 
especially  those  of  the  mind.  Most  patients  have  a  perfectly  clear  intellect  to 
their  latest  breath.  We  all  know  the  contented,  hopeful,  sanguine  disposition  of 
many  patients,  who  do  not  recognize  their  own  danger  until  the  last  stages  of  the 
disease.  Occasionally  the  anaemia  and  the  general  disturbance  of  the  nutrition 
of  the  brain  lead  to  mental  alterations,  such  as  confusion,  distraction,  or  melan- 
cholic conditions. 

We  find,  more  frequently,  disturbances  in  the  peripheral  nerves  and  muscles. 
Among  these  are  neuralgic  pains,  and  pains  of  an  indefinite  character,  which  have 
their  seat  in  the  legs,  or  sometimes  in  the  arms,  especially  in  the  ulnar  region  and 
the  sciatic  nerve.  These  may  be  very  distressing.  Marked  hypersesthesia  of  the 
skin  and  deeper  parts  is  also  not  uncommon.  The  cause  of  such  disturbances  is 
probably  often  to  be  looked  for  in  the  degenerative  changes  in  the  peripheral 
nerves  (Vierordt  and  others).  Well-marked  multiple  neuritis  has  been  repeat- 
edly observed  in  tuberculous  patients  (see  section  on  nervous  diseases). 

We  very  often  see  an  increased  reaction  upon  direct  mechanical  irritation  in 
the  emaciated  muscles,  and  great  liveliness  of  the  so-called  idiomuscular  contrac- 
tions, which  is  shown,  for  example,  on  percussing  the  pectoral  muscles  on  the  an- 
terior wall  of  the  chest.  The  phenomena  grouped  under  the  name  of  tendon  re- 
flexes are  also  much  increased  in  phthisis. 

4.  Symptoms  and  Complications  on  the  Part  of  Other  Organs. — 1.  Pleura.— 
In  pulmonary  tuberculosis  the  pleura  is  also  iuA^olved  as  a  rule.  The  affection  is 
almost  always  the  result  of  a  direct  extension  of  the  process  from  the  lung  to  the 
pleura.  At  the  avitopsy,  we  find  in  the  pleura  a  few  or  many  miliary  tubercles, 
besides  the  simple  inflammatory  process — tubercular  pleurisy. 

In  many  cases,  in  which  we  have  to  do  only  with  an  adhesive  pleurisy  and 
with  pleuritic  contraction,  we  can  merely  suspect  the  disease  of  the  pleura,  but  it 
can  not  be  directly  made  out  and  differentiated  clinically  from  the  pulmonary 
affection.  In  other  cases  we  can  diagnosticate  a  dry  pleurisy  in  phthisis  from  the 
occurrence  of  the  pleuritic  friction-rub.  The  symptoms  of  pleurisy  become  more 
marked  if  there  is  a  pleuritic  effusion,  which  is  usually  readily  discovered  by  a 
physical  examination.  The  patient's  pain  and  dyspnoea  are  usually  much  in- 
creased by  such  a  complication.  Besides  a  simple  sero-fibrinous  effusion  we  quite 
frequently  find  purulent  and  even  heemorrhagic  effusions  in  tuberculosis  of  the 
pleura. 

The  formation  of  pneumothorax  is  an  important  complication  in  the  pleura  in 
phthisis.  This  is  due  to  the  rupture  of  a  superficial  pulmonary  cavity  into  the 
pleural  cavity,  and  the  entrance  of  air  into  the  latter.  The  different  forms  of 
pneumothorax  and  its  symptoms  will  be  described  under  diseases  of  the  pleura. 

2.  Larynx,  Pharynx,  and  Trachea. — The  symptoms  of  laryngeal  tuberculosis 
and  their  relation  to  pulmonary  tuberculosis  have  already  been  given  under  dis- 
eases of  the  larynx  (see  page  148).  We  saw  there  that,  although  there  is  a  primary 
laryngeal  tuberculosis,  most  cases  are  secondary  in  their  development  to  a  pulmo- 
nary tuberculosis. 

The  same  holds  true  in  regard  to  the  much  rarer  tuberculosis  of  the  pharynx. 
In  some  cases  this  may  be  of  primary  origin,  but  it  is  usually  a  result  of  re-inocu- 
lation with  tuberculosis  by  means  of  the  sputum,  or  of  a  direct  extension  of  the 
tubercular  process  from  the  lai-ynx  to  the  pharynx.  Tubercular  ulcers  of  the  phar- 
ynx are  found  most  frequently  on  the  soft  palate,  on  the  tonsils,  on  the  root  of 
the  tongue,  and  on  the  boundary  between  the  pharynx  and  the  larynx;  they 
are  rare  in  other  parts  of  the  pharynx.  In  exceptional  cases  tubercular  affections 
are  seen  in  the  mouth — on  the  tongue.  The  local  discomforts  which  all  these 
ulcers  cause  is  usually  very  considerable.  Disseminated  miliary  tubercles,  too, 
have  been  repeatedly  seen  in  the  mucous  membrane  of  the  pharynx. 


TUBEECULOSIS    OF   THE   LUNGS  249 

3.  Stomach  and  Intestinal  Canal — Peritoneum. — Tubercular  ulcers  in  the 
mucous  membrane  of  the  stomach  are  exceedingly  rare,  but  we  very  often  notice 
some  symptoms  on  the  part  of  the  stomach.  Loss  of  appetite  is  a  particularly 
common  symptom  in  phthisis.  Vomiting  occurs  often  in  phthisical  patients, 
especially  when  the  larynx  is  involved.  It  is  usually  brought  on  by  paroxysms 
of  coughing.  Less  frequently  the  cause  of  the  vomiting  is  gastric  catarrh,  occa- 
sioned by  the  irritation  of  the  sputa  which  have  been  swallowed;  but  in  some 
cases  the  gastric  symptoms  depend  upon  the  general  condition — e.  g.,  the  anaemia. 

Although  the  tubercle  bacilli  swallowed  with  the  sputum  hardly  ever  infect 
the  stomach,  probably  from  the  acid  reaction  of  its  contents,  they  very  often  at- 
tack the  intestinal  canal.  In  the  majority  of  the  cases  of  phthisis  we  find  tuber- 
cular ulcers,  either  singly  or  in  considerable  numbers,  in  the  vicinity  of  Bauhin's 
valves  [the  ileo-ca3cal  valve],  in  the  lower  part  of  the  ileum,  and  the  upper  part 
of  the  large  intestine. 

Intestinal  tuberculosis  does  not  always  cause  very  marked  clinical  symptoms, 
but  as  a  rule  we  find  diarrhoea  in  patients  with  tubercular  ulcers  of  the  intestine. 
They  may  have  three  or  four  stools  in  the  twenty-four  hours,  and  even  more,  but 
the  stools  have  nothing  characteristic.  We  rarely  see  a  slight  admixture  of  pus 
or  blood  in  them.  Tubercle  bacilli  have  been  repeatedly  discovered  in  the  de- 
jections, but  the  search  for  them  is  rather  difficult.  We  must  call  attention,  how- 
ever, to  the  fact  that  many  patients  have  diarrhoea  during  life  in  whom  we  find 
at  the  autopsy  no  intestinal  tuberculosis,  but  only  a  simple  intestinal  catarrh. 
Severe  diarrhoea  of  a  persistent  and  refractory  character  may  also  occur  in  asso- 
ciation with  amyloid  degeneration  of  the  intestine,  which  is  not  infrequently 
seen  in  connection  with  other  amyloid  changes.  Sometimes  tuberculous  ulcera- 
tions of  the  intestine  are  found  at  autopsy  which,  during  life,  had  caused  no 
diarrhoea. 

In  cases  of  severe  intestinal  tuberculosis  we  sometimes  meet  with  meteorism. 
With  deep  ulcers,  extending  to  the  peritoneum,  we  often  see  marked  tenderness 
of  the  abdomen. 

The  peritoneum  may  be  affected  by  the  tubercular  ulcers  of  the  intestine  in  a 
twofold  manner.  Genuine  peritonitis  from  perforation,  with  a  purulent  or  even 
a  sanious  exudation,  is  quite  rare,  and  is  excited  by  the  rupture  of  an  ulcer  and 
the  entrance  of  the  contents  of  the  intestine  into  the  abdominal  cavity.  An  in- 
fection of  the  peritoneum  with  the  tubercular  poison  is  more  frequent.  This 
may  arise  from  deep-seated  ulcers,  which  do  not  reach  actual  perforation,  so  that 
we  have  a  peritoneal  tuberculosis,  or  a  tubercular  peritonitis.  During  life  peri- 
tonitis from  perforation  and  that  from  tuberculosis  are  not  always  to  be  distin- 
guished. We  must  also  mention  that  simple  ascitic  fluid  is  sometimes  found  in 
the  abdominal  cavity  in  phthisis,  which  may  lead  to  a  false  diagnosis  of  peritoneal 
tuberculosis. 

Another  way  in  which  we  may  have  a  peritoneal  tuberculosis  in  the  course  of 
phthisis  is  from  the  extension  of  the  process  in  a  tubercular  pleurisy,  through  the 
diaphragm  to  the  peritoneum. 

4.  Liver  and  Spleen. — We  very  often  find  a  few  or  even  many  tubercles  in  the 
liver  in  phthisis,  but  they  have  no  clinical  significance.  The  liver  is  almost  always 
infected  with  the  tubercular  poison  from  tubercular  ulcers  in  the  intestines,  from 
which  the  poison  passes  to  the  branches  of  the  portal  vein  and  then  to  the  liver. 
Fatty  liver  and  amyloid  or  lardaceous  liver  are  more  important  clinical  changes. 
We  can  sometimes  recognize  the  former  by  making  out  on  physical  examination 
the  increase  in  the  size  of  the  organ,  and  by  feeling  its  characteristic  blunt  lower 
edge.  Moreover,  we  must  emphasize  the  fact  that,  in  our  experience,  fatty  infil- 
tration of  the  liver  is  found  much  more  rarely  at  the  autopsy  of  consumptive 
subjects  than  the  statements  of  many  earlier  authors  wovild  lead  one  to  expect. 


250  DISEASES    OF    THE   EESPIEATOEY   OEGAISTS 

Amyloid  degeneration  of  the  liver  appears  almost  always  in  association  with 
amyloid  change  in  other  organs  (kidneys,  spleen,  intestine).  If  the  amyloid 
degeneration  is  advanced,  the  liver  is  considerably  enlarged,  and  it  is  usually  pos- 
sible to  feel  distinctly  its  sharp  and  resistant  edge;  and,  not  infrequently  also, 
its  firm  upper  surface. 

Miliary  tubercles  or  single  large  tubercular  nodules  in  the  spleen  have  a  patho- 
logical interest  only.  Great  splenic  enlargement  is  found  in  amyloid  degen- 
eration. 

5.  Kidneys,  Urinary  Passages,  and  Sexual  Organs. — The  presence  of  miliary 
tubercles  in  the  kidneys  is  the  first  change  in  them  to  be  mentioned,  but  it  has  no 
clinical  significance.  Extensive  tuberculosis  of  the  genito-urinary  apparatus, 
however,  may  produce  marked  symptoms,  such  as  pyuria.  Genito-urinary  tuber- 
culosis will  be  discussed  in  a  later  part  of  this  work.  In  regard  to  the  symptoms 
of  amyloid  kidney,  which  may  develop  in  the  course  of  phthisis  in  connection 
with  amyloid  disease  in  other  organs,  we  will  refer  to  the  section  on  renal 
diseases. 

Genuine  cases  of  nephritis,  both  acute  and  chronic,  are  also  found  quite  fre- 
quently in  phthisis,  often  combined  with  amyloid  disease.  These  can  not  escape 
notice  if  the  urine  is  carefully  examined.  Their  development  is  probably  always 
referable  to  the  excretion  of  toxic  material,  arising  from  the  disease  in 
the  lung.  , 

6.  Circulatory  Organs. — The  rate  of  the  pulse  is  often  increased  in  consump- 
tion. This  increase  in  frequency  may  be  merely  proportional  to  the  fever,  if  any 
exists.  It  is  also  usually  seen  and  it  may  be  considerable  when  there  is  no 
fever.  A  persistently  rapid  pulse,  when  the  temperature  is  little,  if  at  all,  ele- 
vated, may  therefore  be  an  important  diagnostic  sign  of  pulmonary  (and  all 
other)  tuberculous  diseases.  The  increase  of  the  pulse,  which  readily  comes  on 
from  comparatively  trifling  external  causes,  is  especially  noteworthy.  It  may 
be  seen  after  slight  physical  exertion,  or  upon  mental  excitement,  as  during  the 
physician's  visit. 

Anatomical  changes  in  the  heart  are  rare,  except  that  it  is  often  remarkably 
small  and  flaccid.  Moderate  fatty  degeneration  of  the  heart,  slight  endocarditis 
of  the  valves,  or  occasional  tubercles  in  the  heart,  causes  no  symptoms.  The  oc- 
currence of  tubercular  pericarditis,  however,  is  important.  This  almost  always 
arises  from  the  extension  of  the  tubercular  process  from  the  adjacent  pleura,  but 
in  exceptional  eases  pericarditis  has  been  seen  as  a  result  of  rupture  of  a  tuber- 
culous lymph-gland  or  a  pulmonary  cavity  into  the  pericardium. 

7.  Lymph-glands. — The  lymph-glands  are  a  favorite  seat  for  tubercular 
changes.  We  have  stated  above  that  the  so-called  scrofulous,  cheesy  lymph- 
glands,  which  are  seen  chiefly  in  the  neck  and  the  axillse,  are  afl'ected  with  tuber- 
cle in  the  majority  of  cases.  The  tubercular  infection  probably  develops  here 
from  slight  injuries  and  excoriations  of  the  skin,  by  which  the  bacilli  enter  the 
body  and  reach  the  neighboring  glands  by  means  of  the  lymph-current.  In 
other  cases  the  infection  comes  perhaps  from  the  mucous  membrane  of  the  phar- 
ynx. In  tuberculosis  of  internal  organs,  too,  we  very  often  find  the  corresponding 
lymph-glands  enlarged  and  more  or  less  cheesy.  The  bronchial  lymph-glands 
are  swollen  as  a  result  of  pulmonary  tuberculosis,  the  mesenteric  and  retroperito- 
neal glands  as  a  result  of  intestinal  tuberculosis.  The  tuberculosis  of  the  bron- 
chial lymph-glands  is  of  especial  importance  in  children.  laideed,  the  tubercular 
virus  which  has  gained  access  to  the  lungs  may  apparently  reach  the  bronchial 
glands  by  means  of  the  lymph-channels  even  without  affecting  the  lungs  them- 
selves, and  occasion  a  tuberculous  disease  of  the  glands.  Glands  thus  diseased 
break  down  and  discharge  into  the  lungs,  and  in  this  way  generate  a  secondary 
pulmonary  tuberculosis.     This  is  one  reason  why  the  pulmonary  tuberculosis  of 


TIJBEKCULOSIS    OF    THE   LUNGS  251 

children  so  often  begins  not  in  the  apex  but  in  the  middle  or  lower  portion  of 
the  lung. 

Pressure  from  the  enlarged  glands  may  affect  the  air-passages,  the  branches  of 
the  pulmonary  artery,  the  veins,  the  recurrent  nerve  (paralysis  of  the  vocal  cords), 
and  even  the  aorta.  Perforation  of  the  cheesy  bronchial  glands  into  the  cesoph- 
agus,  the  blood-vessels,  etc.,  has  also  been  observed.  Tuberculosis  of  the  bron- 
chial glands  does  not  present  any  definite  type  of  disease,  however,  and,  although 
we  may  sometimes  suspect  it  when  there  is  pulmonary  tuberculosis,  we  can  only 
rarely  diagnosticate  it  with  certainty.  The  author  himself  observed  a  note- 
worthy case  of  tuberculosis  of  the  bronchial  glands,  with  compression  of  one 
vagus  nerve  in  a  patient  who,  during  life,  for  weeks  coughed  up  large  amounts 
of  a  purely  sero-mucous  expectoration  containing  no  bacilli. 

8.  Nervous  System. — We  have  already  mentioned  various  nervous  symptoms 
in  the  description  of  the  general  symptoms.  We  must  also  add  that  tubercular 
meningitis  is  seen  in  the  course  of  phthisis  (see  page  1059),  and  that  large  soli- 
tary tubercles  may  occasionally  develop  in  the  central  nervous  system. 

9.  Skin. — We  have  spoken  of  the  great  tendency  which  many  patients  have  to 
severe  sweats,  especially  at  night.  The  frequent  appearance  of  pityriasis  versi- 
color, especially  on  the  skin  over  the  thorax,  is  also  worthy  of  note.  We  often 
see  moderate  oedema  of  the  legs  and  ankles,  which  is  due  to  weakness  of  the 
heart.  More  marked  oedema  of  one  leg  sometimes  arises  from  thrombosis  of  the 
femoral  vein.  We  must  also  mention  here,  in  conclusion,  the  specific  tubercular 
disease  of  the  skin — lupus.  This  occurs  alone,  as  a  rule,  without  a  co-existing 
pulmonary  tuberculosis ;  but,  on  the  other  hand,  the  old  term  "  scrofulous  lupus  " 
had  reference  to  the  fact  that  we  often  find  other  tubercular  affections  in  lupus 
besides  the  disease  of  the  skin.  Thus  it  does  not  seem  strange  that  lupus  and 
phthisis  have  been  repeatedly  observed  to  co-exist.  Cutaneous  tuberculosis  may 
develop  not  only  in  the  ordinary  form  of  lupus,  but  also  in  nodules  of  consider- 
able size,  or  in  rather  extensive  ulcers.  Certainly  some  of  the  cases  of  so-called 
corpse-tubercle  belong  to  true  tuberculosis.  We  have  seen  a  similar  tuberculous 
cutaneous  disease  in  a  woman  who  for  a  long  time  had  washed  the  soiled  handker- 
chiefs of  a  consumptive  patient.  We  have  also  seen  a  tuberculous  affection  of 
the  skin  upon  the  chin  of  a  patient  very  ill  with  consumption.  In  this  case,  no 
doubt,  the  skin  became  infected  by  the  sputum. 

Diagnosis. — The  diagnosis  of  pulmonary  tuberculosis  has  become  absolutely 
certain,  since  the  discovery  of  the  tubercle  bacilli,  by  the  demonstration  of  their 
presence  in  the  sputum  (vide  supra).  In  all  incipient  cases,  in  which  the  other 
symptoms  of  the  disease  have  not  yet  made  themselves  manifest,  but  the  sus- 
picion of  incipient  phthisis  has  been  aroused  by  a  persistent  cough,  by  marked 
pallor  and  emaciation,  by  slight  hoarseness,  by  an  evening  rise  of  temperature, 
by  the  appearance  of  night-sweats,  by  the  presence  of  a  hereditary  predisposition, 
and  similar  symptoms,  the  finding  of  tubercle  bacilli  in  the  sputum  is  often  the 
sole  deciding  factor.  Still,  it  must  not  be  forgotten  that  the  examination  for 
bacilli  is  decisive  only  when  its  result  is  positive,  and  that  the  greatest  attention 
should  be  given  also  to  all  the  other  symptoms.  To  form  an  opinion  as  to  the 
severity  of  a  particular  case,  and  as  to  its  exact  distribution  and  the  variety  of 
the  tubercular  process,  is  at  present  possible  only  by  means  of  a  consideration  of 
the  other  symptoms,  and  in  particular  of  the  results  of  physical  examination. 
The  latter,  therefore,  has  lost  none  of  its  importance  by  the  discovery  of  the 
tubercle  bacilli. 

Confusion  between  phthisis  and  other  diseases  is  twofold.  Where  the  consti- 
tutional symptoms  are  predominant,  and  there  are  no  marked  pulmonary  symp- 
toms, an  existing  tuberculosis  may  be  overlooked.  In  the  beginning,  especially, 
many  cases  of  phthisis  are  considered  to  be  merely  anasmia,  chronic  gastric 


252  DISEASES    OF    THE   EESPIRATORY   ORGANS 

catarrh,  or  simple  bronchitis.  If  a  continuous  or  intermitting  fever  appears  in 
an  early  stage  of  phthisis,  before  any  marked  pulmonary  symptoms  have  devel- 
oped, the  disease  may  be  mistaken  for  malaria  or  the  like.  On  the  other  hand, 
it  is  by  no  means  rare  to  consider  patients  phthisical  who  are  suffering  from 
some  entirely  different  affection.  He  who  lays  too  great  stress  .on  the  uncertain 
results  of  percussion  will  often  make  a  false  diagnosis.  Severe  latent  diseases 
of  the  stomach,  or  certain  general  diseases,  such  as  anaemia,  diabetes,  or  chronic 
nephritis,  may  be  mistaken  for  phthisis.  Other  pulmonary  affections,  too,  may 
be  confounded  with  tuberculosis,  especially  chronic  bronchitis,  emphysema, 
bronchiectasis,  foetid  and  gangrenous,  processes,  and  carcinoma  of  the  lungs.  A 
careful,  unprejudiced,  and  complete  examination  of  the  patient  is  the  only  pos- 
sible protection  against  such  errors.  It  is  very  important  for  the  physician  to 
know  that  there  is  such  a  thing  as  hypochondriacal  phthiseophobia.  Some  nerv- 
ous individuals  are  tormented  by  a  constant  dread  of  becoming  consumptive. 
Such  persons  complain  of  thoracic  pain,  dry  cough,  weakness,  and  other  imagi- 
nary symptoms,  which  might  readily  mislead  the  physician  into  supposing  that 
they  actually  have  incipient  pulmonary  tuberculosis.  Of  course,  the  correct 
interpretation  of  such  conditions  is  usually  no  difficult  matter  to  the  experienced 
physician,  who  is  guided  by  the  general  impression  of  "  nervousness,"  and  by  the 
comj)lete  absence  of  any  objective  physical  signs. 

In  this  connection  we  ought,  furthermore,  to  express  our  opinion  of  the  diag- 
nostic value  of  Koch's  tuberculine  (vide  infra).  Koch  made  the  important  dis- 
covery that  tuberculous  patients,  particularly  those  suffering  with  pulmonary 
tuberculosis,  exhibit  a  particular  "  reaction"  after  the  injection  of  small  amounts 
of  tuberculine  (gramme  0.001  to  0.002  of  Koch's  preparation).  When  this  reac- 
tion occurs  there  develops,  some  four  or  five  hours  after  the  injection,  a  fever  of 
102°  to  104°  (39°  to  40°  C),  associated  with  chilliness,  headache,  pain  in  the 
limbs,  nausea,  and  languor.  This  constitutional  reaction  passes  off  after  some 
twelve  or  fifteen  hours.  If  the  tuberculous  process  is  located  in  the  skin,  trachea, 
or  some  other  part  where  it  is  accessible  to  direct  observation,  a  very  decided 
local  reaction  may  usually  be  observed  besides  the  constitutional  disturbance. 
The  tuberculous  tissue  becomes  swollen,  red,  and  finally  in  part  necrotic.  In 
patients  with  tuberculosis  of  the  internal  organs,  also,  this  local  reaction  probably 
takes  place,  but  of  course  it  can  not  be  actu.ally  seen,  although  it  may  perhaps  be 
inferred  because  of  the  secondary  phenomena.  Thus,  in  pulmonary  tuberculosis 
there  may  be  an  increase  in  the  cough  and  expectoration.  On  the  other  hand,  if 
an  injection  of  tuberculine  is  made  in  a  person  who  is  healthy,  or  who  is  suffering 
from  some  disease  other  than  tuberculosis,  then,  according  to  Koch,  there  will 
be  no  reaction  at  all  to  small  doses.  To  obtain  any  reaction  in  persons  who  are 
healthy,  or,  at  any  rate,  not  tuberculous,  it  is  said  that  the  dose  of  Koch's  prepa- 
ration must  be  increased  to  the  amount  of  gramme  0.01.  If  these  statements 
were  true,  the  appearance  or  the  absence  of  a  reaction  after  the  injection  of  a 
small  amount  of  tuberculine  would  be  an  important  and,  indeed,  a  decisive  factor 
in  determining  whether  tuberculosis  did  or  did  not  exist  in  any  given  case. 

These  statements  of  Koch  have  been  shown,  hoAvever,  by  extensive  investiga- 
tions, to  be  true  only  in  general,  and  not  in  every  case.  Other  observers  as  well 
as  the  present  author  have  occasionally  found  that  healthy  persons,  or  persons 
free  from  tuberculosis,  have  reacted  to  doses  of  one  or  two  milligrammes  of  tuber- 
culine ;  while,  on  the  other  hand,  patients  with  indubitable  pulmonary  tuberculo- 
sis have  shown  no  distinct  reaction  even  to  considerable  doses  of  tuberculine. 
Consequently  the  result  of  an  injection  of  tuberculine  can  never  be  completely 
decisive  from  a  diagnostic  point  of  view,  and  in  practice,  therefore,  the  employ- 
ment of  tuberculine  for  diagnosis  has  been  adopted  by  only  a  few;  but  still,  it 
would  be  a  mistake  to  discard  this  means  of  diagnosis  completely.     In  doubtful 


TUBEECULOSIS    OF   THE   LUNGS  253 

cases  when  we  can  not  be  sure  of  the  diagnosis,  the  injection  of  about  two 
milligrammes  of  tuberculine  is  of  real  importance,  and  the  result  of  the  test 
is  certainly  a  valuable  factor  in  summing  up  such  a  case;  yet  the  verdict  is 
never  so  unimpeachable  as  in  cases  in  which  the  tubercle  bacilli  have  been  dis- 
covered. 

Prognosis. — It  is  very  difficult  to  make  a  general  statement  as  to  the  prog- 
nosis of  pulmonary  tuberculosis.  There  is  no  doubt  that  tuberculous  foci  in  the 
lungs,  if  of  limited  extent,  may  become  completely  healed,  at  least  from  a  clinical 
point  of  view.  Indeed,  such  recovery  probably  takes  place  oftener  than  many 
suppose;  at  least,  it  is  not  very  exceptional  to  find  at  the  autopsy  of  elderly 
persons  cicatricial  contractions  in  the  apices  of  the  lungs  which  may,  without 
doubt,  be  regarded  as  healed  tuberculosis.  In  many  of  these  cases  the  previous 
tuberculosis  had  never  come  to  the  knowledge  of  any  physician.  At  the  pres- 
ent day  the  discovery  of  tubercle  bacilli  in  the  sputum  has  rendered  the  diag- 
nosis of  even  very  limited  tuberculous  processes  an  easy  matter,  and,  consequent- 
ly, cases  of  recovery  from  pulmonary  tuberculosis  are  now  recognized  much  more 
often  than  formerly. 

Nevertheless,  the  prognosis  of  pulmonary  tuberculosis  must  always  be  re- 
garded even  now  as  very  serious,  and  when  the  disease  has  made  any  great  prog- 
ress the  prognosis  is  decidedly  unfavorable.  Many  cases  of  apparent  recovery 
exhibit  merely  a  temporary  improvement,  to  grow  worse  again,  and  the  assertion 
that  treatment  is  absolutely  hopeless  in  almost  all  cases  in  which  the  disease  has 
reached  an  advanced  stage  is,  unfortunately,  too  well  established  to  require  elab- 
orate argument. 

There  is,  however,  one  fact  of  extreme  importance  which  should  never  be  dis- 
regarded in  the  prognosis  of  pulmonary  tuberculosis.  There  is  a  great  difference 
in  the  duration  of  the  disease.  It  is  possible  for  the  process  to  go  on  for  years, 
while  the  patient  feels  tolerably  well,  and  yet  the  disease  smoulders.  From  this 
point  of  view  cases  may  be  distinguished  as  "  benign,"  compared  with  those  of 
rapid  progress,  and  this  prognostic  distinction  has  the  greatest  importance  in 
practice,  although  it  is  often  very  difficult  to  recognize.  Many  a  consumptive, 
when  first  examined,  gives  one  the  impression  that  he  can  not  live  a  fortnight 
longer,  and  yet  the  disease  lasts  many  months,  with  improvement  in  most  of  the 
symptoms  and  general  alleviation  of  the  patient's  condition.  Again,  one  believes 
the  disease  to  be  incipient,  encourages  the  family,  and  the  patient  dies  in  a  few 
weeks  of  galloping  consumption. 

Certain  complications  may  occur  which  it  is  impossible  to  foresee,  such  as 
pulmonary  haemorrhage,  pneumothorax,  tubercular  meningitis,  and  miliary  tu- 
berculosis. Apart  from  these,  however,  there  are  certain  conditions  which  lead  us 
to  expect  a  comparatively  favorable  course  for  the  disease :  such  are  a  vigorous 
constitution  unimpaired  by  bad  habits,  of  which  drinking  is  particularly  un- 
favorable ;  a  good  weight ;  freedom  from  hereditary  taint ;  limited  extent  of  the 
local  process ;  later  life ;  the  absence  of  complications ;  and,  finally,  the  persistent 
absence  of  fever.  This  last  factor  is  so  important  that  we  must  lay  special  stress 
upon  it.  If  there  is  no  fever  whatever  in  a  case  of  pulmonary  tuberculosis,  the 
patient  is  at  that  time  in  a  condition  in  which  the  disease  is  quiescent ;  and  a 
decided  improvement,  perhaps  even  cure,  may  Be  expected  if  appropriate  means 
are  employed.  On  the  other  hand,  whenever  fever  appears  we  know  that  the  dis- 
ease is  not  quiescent,  but  is  actively  advancing  with  more  or  less  rapidity.  The 
important  points  about  the  temperature  in  this  regard  have  been  already  empha- 
sized (see  page  246).  It  is  self-evident,  also,  that  the  worldly  circumstances  of 
the  patient,  as  well  as  the  factors  which  we  have  just  alluded  to,  are  of  great 
prognostic  importance.  On  these,  for  instance,  depends  the  possibility  of  i)roper 
care,  of  abundant  nourishment,  and,  it  may  be,  of  a  change  of  climate. 


254  DISEASES    OF    THE   EESPIEATOEY   OEGANS 

Treatment. — 1.  Prophylaxis. — The  question  of  what  prophylactic  measures 
may  effectually  prevent  the  extension  of  the  disease  has  entered  upon  a  new 
stage  since  our  definite  knowledge  as  to  the  infectious  nature  of  tuberculosis.  We 
can  no  longer  doubt  the  contagious  character  of  phthisis,  in  support  of  which 
isolated  examples  were  previously  brought  forward.  Even  if,  according  to  all 
experience,  the  danger  of  contagion  is  not  very  great,  still  it  is  foolish  to  ignore 
it  entirely.  We  must  therefore  call  the  attention  of  the  relatives  of  phthisical 
patients  to  the  possibility  of  this  danger,  and  we  should  not  permit  the  children 
of  such  patients  to  be  uselessly  exposed  to  it.  We  should  take  satisfactory  pre- 
cautions for  isolation,  and  also  for  disinfection  of  the  sputum.  Suitable  sputum 
cups  should  be  employed,  and  care  should  also  be  taken  to  prevent  the  dissemina- 
tion of  the  expectoration,  either  in  its  fresh  state  or  after  it  has  become 
dry.  The  future  will  teach  us  whether  much  evil  may  not  be  averted  by  such 
measures. 

The  "  prophjdaxis "  till  now  employed  was  almost  exclusively  confined  to 
hardening  and  strengthening  the  threatened  individual  as  much  as  possible.  We 
should  ti-y  to  strengthen  the  bodies  of  children  of  a  weak  habit,  with  "  scrofulous  " 
symptoms,  and  children  from  families  in  which  cases  of  tuberculosis  have  already 
occurred,  and  thus  to  arm  them  against  the  enemy  that  threatens  them.  Good 
food,  fresh  air,  and  a  diminxition  of  the  sensitiveness  of  the  body  by  cold  spon- 
ging and  cold  baths — these  are  the  factors  whose  favorable  influence  is  generally 
recognized. 

The  removal  of  certain  foci  of  tubercular  disease,  already  existing,  from  the 
body  may  prove  of  great  prophylactic  importance.  We  refer  to  the  timely  treat- 
ment or  extirpation  of  scrofulous — that  is,  tubercular — swellings  of  the  lymph- 
glands,  healing  or  resection  of  tubercular  bones  and  joints,  etc.  Although  in 
individual  cases  we  can  of  course  never  know  whether  the  part  removed  is  the 
sole  focus  of  disease  in  the  body,  still  we  are  undoubtedly  justified  in  trying 
to  remove  at  least  one  possible  source  of  some  later  general  infection.  A  fuller 
discussion  of  this  important  point  must  be  left  to  the  works  on  surgery. 

2.  Therapeiisis. — Physicians  have  often  thought  that  they  had  discovered  a 
specific  remedy  for  tuberculosis,  but  apparently  they  have  thus  far  been  mistaken. 
Formerly,  the  inhalation  of  antiseptic  substances,  such  as  carbolic  acid,  benzoate 
of  sodium,  and  iodoform,  was  recommended,  but  this  practice  is  now  almost  en- 
tirely given  up.  Arsenic  was  for  a  time  much  used,  best  given  in  pills  containing 
^'^-  To  (g'rm-  0.003)  repeated  several  times  a  day;  but  this  practice,  again,  has 
not  held  its  own.  Arsenic  may  be  tried  in  incipient  cases,  particularly  those 
associated  with  marked  antemia,  but  great  curative  influence  is  not  to  be  expected 
from  it.  Creasote  has  won  far  more  advocates.'  Continued  for  a  considerable 
time  in  large  doses  (fifteen  to  thirty  grains,  grammes  1  to  2,  or  more,  in  the  course 
of  twenty-four  hours),  it  is  regarded  by  many  physicians  as  an  excellent  remedy 
in  incipient  and  even  in  advanced  pulmonary  consumption.  It  is  best  prescribed 
in  gelatine  capsules,  or  in  a  mixture  of  one  part  of  creasote  to  two  parts  of  the 
tincture  of  gentian,  of  which  twenty  to  eighty  drops  may  be  given  three  times  a 
day  in  a  considerable  amount  of  milk,  or  in  wine.  This  remedy  is  usually  fairly 
well  borne,  and  the  patients  are  pleased  with  the  improvement  it  causes  in  their 
appetite  and  general  condition.  Of  late,  physicians  have  employed  guaiacol,  the 
active  ingredient  of  creasote,  instead  of  the  drug  itself,  especially  since  carbonate 
of  guaiacol  has  been  brought  forward,  a  preparation  which  has  very  little  of  the 
disagreeable  odor  and  taste  of  creasote  itself.  Carbonate  of  guaiacol  is  admin- 
istered in  powders  containing  about  eight  grains  (gramme  0.5),  in  daily  doses  at 
first  of  twenty-five  grains  (gramme  1.5),  gradually  increasing  to  thirty  or  forty- 
five  grains  (grammes  2  to  3).  Dyspeptic  disturbance  sometimes  follows  the  use 
even  of  guaiacol,  but  still  this  remedy  is,  in  general,  better  borne  and  more  read- 


TUBEECULOSIS    OF   THE   LU^tgs  255 

ily  taken  than  creasote.  As  to  the  specific  and  therapeutic  use  of  guaiacol  in  pul- 
monary tuberculosis,  it  is  not  easy  to  foitn  a  decided  opinion.  It  is  certain  that 
many  jDatients  praise  these  remedies,  and  improve  considerably  "while  using-  them ; 
but,  on  the  other  hand,  the  indiscriminate  laudation  of  many  authors  is  decidedly 
uiajustifiable.  When  the  disease  is  slowly  progressing-  with  persistent  sub-febrile 
temperatures,  the  author  has  scarcely  ever  felt  sure  of  any  distinct  influence  ex- 
erted by  guaiacol  or  creasote  upon  the  temperature  and  the  disease.  ISTeverthe- 
less,  it  is  often  advisable  in  practice  to  make  trial  of  these  remedies,  particularly 
of  the  carbonate  of  guaiacol.  The  remedy  must  be  employed  for  months  and,  if 
possible,  in  increasing  doses.  Among  the  remedies  which  are  recommended  as 
having  a  specific  influence,  we  will  also  mention  cinnamic  acid,  which  is  con- 
tained in  Peruvian  balsam.  This  has  been  employed  extensively  by  Landerer  in 
the  treatment  of  various  tuberculous  diseases,  and  particularly  in  pulmonary 
tuberculosis.  He  gives  it  in  the  form  of  small  subcutaneous  injections  of  a  five- 
per-cent.  emulsion,  made  up  of  the  sweet  oil  of  almonds  and  the  yolk  of  e^g.  The 
results  obtained  by  Landerer,  in  the  institute  of  Krahenbad,  in  the  Black  Forest, 
appear  very  favorable,  but  as  yet  they  lack  confirmation.  The  method  has  not 
yet  been  generally  adopted. 

At  the  end  of  1890  great  interest  was  excited,  as  is  well  known,  by  the  state- 
ment of  R.  Koch  that  he  had  extracted  from  pure  cultures  of  tubercle  bacilli, 
by  means  of  glycerine,  a  substance  called  tuberculine,  by  Avhich  he  was  able  to 
heal  tuberculous  processes  both  in  animals  and  men.  This  assertion  aroused 
the  thoughtless  enthusiasm  which  is  unfortunately  so  common  with  regard  to  ■ 
therapeutic  questions,  and  which  indeed  in  this  case  was  rendered  excusable  by 
the  high  authority  of  the  discoverer.  In  fact,  within  a  few  weeks  after  the 
remedy  was  made  known,  numerous  reports  were  published  of  cures  due  to  tuber- 
culine. But  the  longer  the  experiments  were  pursued  the  more  evident  it  became 
that  these  extravagant  opinions  were  not  substantiated,  and  there  set  in  a  revul- 
sion of  sentiment  which  has  led  to  many  adverse  criticisms,  perhaps  equally  un- 
justifiable with  the  CTrly  praise.  It  is  absolutely  impossible  to  speak  of  tubercu- 
line as  an  established  remedy  for  tuberculosis.  In  many  patients  there  does  in- 
deed appear  a  decided  improvement  under  treatment,  but  these  cases  are  such  as 
were  favorable  any  way,  and  therefore  they  may.  owe  their  improvement  to  the 
general  sjnuptomatic  treatment  and  regimen  which  they  have  also  enjoyed.  At 
any  rate,  tuberculine  has  done  no  harm  in  such  cases.  Then,  again,  we  have  seen 
numerous  cases  of  rather  severe  disease,  in  which  it  was  not  possible  to  notice  any 
distinct  influence  of  the  tuberculine  upon  the  general  course  of  the  illness.  Per- 
haps the  condition  of  the  patient  improved,  or  remained  unchanged;  or,  again,  it 
grew  worse.  Yet,  whatever  the  change,  it  was  such  as  might  have  occurred  inde- 
pendently. Finally,  there  are,  in  the  third  place,  cases  which  have  been  seen  by 
the  author  as  well  as  other  observers,  in  which  there  was  such  a  decided  change 
for  the  worse  shortly  after  the  commencement  of  treatment,  that  one  might 
really  suppose  that  the  remedy  had  exerted  an  actually  harmful  influence.  We 
refer  especially  to  cases  in  which  the  patient,  previously  without  fever,  exhibited 
after  the  injection  a  persistent  elevation  of  temperature,  Avith  a  more  rapid  ad- 
vance of  the  local  process  in  the  lungs. 

Consequently,  we  may  say  that,  in  all  advanced  cases,  we  can  expect  nothing 
from  tuberculine.  In  incipient  cases  Ave  may  make  trial  of  it,  but  we  should  be  ex- 
tremely careful  in  our  dosage,  so  as  to  avoid  any  chance  of  doing  injuiy.  Koch's 
rule  at  first  was  that  the  physician  should  begin  with  injections  of  gramme 
0.001,  and  gradually  increase.  In  this  way  was  discoA'ered  the  interesting  fact  that 
the  necessary  dose  for  the  production  of  the  "  reaction  "  (vide  supra,  page  252) 
became  greater  and  greater.  Many  patients  would  finally  bear  the  injection  of 
one  hundred  milligrammes  of  tuberculine  without  any  reaction  at  all.     At  first 


256  DISEASES    OF    THE   EESPIEATOEY   OEGAXS 

it  was  regarded  as  the  object  of  treatment  to  reach  this  point  of  tolerance,  but 
the  practice  is  now  abandoned.  One  should  begin  with  very  small  doses,  about  one 
fourth  to  one  half  a  milligramme,  and  increase  so  slowly  and  by  such  minute  gra- 
dations as  to  avoid  any  marked  reaction.  By  such  a  method  we  can  almost  en- 
tirely exclude  any  harmful  effect,  and  it  may  not  be  impossible  that  some  of  the 
patients  who  have  had  a  favorable  result  actually  owe  their  Improvement  to  the 
tubereuline,  but  it  is  extremely  difficult  to  make  sure  of  this.  It  would  require 
the  continuous  observation  of  many  patients  for  years,  to  enable  one  to  form  a 
reliable  opinion  with  regard  to  this  question. 

It  may  be  seen  that  at  present  we  can  only  speak  with  great  reserve  as  to  the 
possible  therapeutic  value  of  tubereuline,  but  nevertheless,  its  discovery  was  an 
event  of  the  greatest  value  and  interest,  regarded  from  a  therapeutical  stand- 
point. There  is  no  doubt  of  the  specific  influence  of  this  substance  upon  tuber- 
culous processes.  There  is  scarcely  any  sight  more  astonishing  to  the  physician 
than  the  reaction  of  a  patch  of  lupus  upon  the  skin  to  a  tiny  dose  of  tubereuline 
introduced  into  the  circulation!  Taken  into  consideration  with  other  bacterio- 
logical facts,  this  affords  us  a  clear  glance  into  a  future  when  we  shall  succeed 
in  making  the  wonderful  influence  of  the  material  produced  by  the  growth  of 
bacteria  available  for  the  cure  of  infectious  disease,  and,  in  particular,  of  tuber- 
culosis. Perhaps  there  are  the  same  possibilities  for  tuberculosis  as  in  the  case 
of  diphtheria,  the  treatment  of  which,  by  means  of  the  antitoxic  serum  pre- 
pared by  Behring,  is  apparently  so  very  successful;  but  with  regard  to  tuber- 
culosis our  methods  are  as  yet  incomplete,  and  a  final  opinion  as  to  their  value 
would  be  premature.  Meanwhile,  therefore,  we  physicians  must  continue  to  lay 
the  greatest  stress  in  the  treatment  of  tuberculosis  upon  those  methods  which  are 
termed  in  the  widest  sense  hygienic  and  constitutional.  It  is  undeniable  that,  by 
the  correct  and  faithful  emplo;vTi:ient  of  such  methods,  many  very  satisfactory 
successes  may  be  obtained.  Eor  the  present,  we  must  be  discreet,  and  seek  to  in- 
fluence the  disease  in  the  old  accustomed  manner  by  those  therapeutic  measures 
which  have  come  down  to  us  from  ordinary  medical  observation  and  expe- 
rience. 

The  hygienic  and  constitutional  method  of  treating  consumption  has  for  its 
object  the  greatest  possible  promotion  of  the  natural  powers  of  healing.  "We 
aim  at  this,  in  the  first  place,  by  avoiding  as  much  as  possible  all  influences  which 
might  cause  a  further  extension  of  the  disease,  and  by  re-enforcing,  so  far  as  we 
can,  all  influences  which  increase  the  resisting  powers  of  the  individual,  and  the 
processes  of  spontaneous  cure.  The  factors  which  are  of  most  importance  in  this 
connection  are,  first,  diet;  second,  rest;  and  third,  the  uninterrupted  enjojTuent 
of  good  air.  To  obtain  these  three  therapeutic  factors  all  at  once  requires  the 
renunciation  by  the  patient  of  his  calling,  and  his  usual  mode  of  life.  The 
treatment  of  tuberculosis,  therefore,  should  begin  with  the  demand  that  the 
patient,  for  as  long  a  time  as  possible,  should  devote  himself  exclusively  to  the 
care  of  his  health.  The  next  point  is  the  choice  of  the  place  in  which  the  "  cure  " 
shall  be  carried  on.  In  many  cases  the  proper  management  of  the  patient  i^iay 
be  pursued  under  the  ordinary  surroundings  of  home.  Often,  however,  this  is 
not  the  case  because  the  last  two,  or  even  all  three,  of  the  essentials  named  can 
not  be  provided  at  home.  It,  therefore,  is  the  duty  of  the  physician  in  every  indi- 
vidual case  to  determine  how  the  desiderata  are  best  to  be  obtained.  According 
to  the  patient's  means  we  consider  respectively  a  residence  in  the  country  (if  pos- 
sible, in  a  picturesque  and  wooded  region);  a  special  health-resort;  or,  finally, 
a  suitable  sanitarium.  Erom  a  therapeutic  standpoint,  there  is  no  doubt  that 
treatment  in  a  specially  adapted  sanitarium  is  chiefly  to  be  recommended.  In 
this  all  the  requirements  for  recovery  can  be  best  carried  out,  and  the  patient 
constantly  remain  under  medical  obseiwation.     In  most  cases  it  is  only  exter- 


TUBEECULOSIS    OF   THE   LUNGS  257 

nal  considerations,  for  instance,  pecuniary,  -vvhicli  keep  the  patient  from  a  sani- 
tarium. It  is  a  true  philanthropy,  therefore,  which  has  of  late  led  everywhere 
to  efforts  to  render  the  benefits  of  institutional  treatment  accessible  to  the  less 
wealthy  classes.  The  requirements  for  proper  treatment  are  also  partially  ful- 
filled in  the  so-called  public  health-resorts  for  pulmonary  consumptives.  These 
resorts,  however,  have  the  disadvantage  that  the  patient  is  left  far  more  to  his 
own  resources,  and  is  consequently  apt  to  be  incautious,  and  hence  jeopardize 
his  recovery.  A  public  health-resort  would,  therefore,  be  especially  chosen  for 
patients  who  have  already  been  in  an  institution,  and  have  learned  what  mode 
of  life  is  proper  for  them;  or  for  those  who  have  already  so  far  recovered  that 
they  may  be  allowed  a  certain  degree  of  freedom. 

With  regard  to  the  minutiae  in  carrying  out  the  above-enumerated  essen- 
tials of  treatment,  we  would  add  as  follows :  1.  Diet.  This  should  be  as  nourish- 
ing and  abundant  as  possible.  Meat,  milk,  eggs,  farinaceous  foods,  and  butter  are 
chiefly  to  be  recommended,  care  being  taken  that  the  body  should  receive  a 
sufficient  amount  of  carbohydrates  and  fats,  as  well  as  an  abundance  of  albumen. 
Many  special  "  cures  "  for  pulmonary  consumption  have  a  value,  in  so  far  as  they 
lead  to  the  ingestion  of  an  abundant  amount  of  easily  assimilated  nourishment. 
Such  are  cures  with  milk,  koumyss,  or  kefir.  It  has  even  been  proposed  to  in- 
troduce large  amounts  of  such  nourishment  as  milk  and  pulverized  meat  into 
the  stomach  by  means  of  a  stomach-tube,  and  thus  accomplish  "  overfeeding." 
This  method  has  not  become  very  popular,  although  it  may  be  indicated  in  some 
cases.  It  is  very  important  to  see  that  the  patient  has  a  diet  that  is  not  only 
abundant,  but  also  palatable  and  varied.  If  pure  milk  is  not  readily  taken,  we 
may  try  the  addition  of  coffee,  tea,  common  salt,  or  brandy.  With  regard  to  the 
prescription  of  alcohol  we  recommend,  unhesitatingly,  moderate  amounts  of  beer, 
and  particularly  such  beer  as  is  rich  in  extractive  matter;  and  perhaps  also 
extract  of  malt,  and  porter.  Small  amounts  of  good  wine  may  contribute  to  the 
improvement  of  the  appetite  and  the  general  condition.  On  the  other  hand,  we 
think  it  useless  and,  in  some  circumstances,  harmful,  to  order  large  amounts  of 
the  stronger  alcoholic  beverages,  such  as  port  wine  and  brandy,  as  prescribed  in 
many  sanitariums.  Artificial  foods,  such  as  various  preparations  of  meat,  soma- 
tose,  neutrose,  and  the  like,  should  be  used  merely  as  makeshifts.  The  employ- 
ment of  cod-liver  oil  to  the  amount  of  two  to  four  tablespoonfuls  a  day  is  some- 
times not  inappropriate,  if  it  is  well  borne. 

2.  The  two  other  factors  of  cure — rest,  and  the  continuous  enjoyment  of  good 
air — are  best  fulfilled  by  the  fresh-air  treatment,  which  is  of  late  gaining  in 
importance  and  popularity.  The  patients  spend  the  greatest  part  of  the  day  lying 
in  the  open  air  on  comfortable  reclining  chairs.  At  the  same  time  they  avoid 
any  unnecessary  bodily  exertion,  any  great  demands  upon  respiration,  and  any 
irritation  of  the  respiratory  passages.  Gain  in  bodily  weight  is  promoted.  The 
limitation  of  the  diseased  processes  in  the  lungs  is  favored.  Of  course,  in  such 
matters  also  the  individual  should  be  considered,  for  moderate  exercise  in  the 
open  air  is  certainly  for  many  patients  not  harmful,  but  rather  beneficial.  Often 
the  methodical  carrying  out  of  the  open-air  treatment  under  suitable  conditions 
demands  the  resources  of  a  sanitarium,  but  we  may  find  in  a  garden  or  on  a 
veranda  a  sunny  spot,  screened  from  the  wind,  where  the  patient  may  lie  com- 
fortably and  pass  the  entire  day  till  near  sunset  in  the  open  air.  In  case  of 
necessity  the  patient  must  content  himself  with  a  place  by  an  open  window.  The 
advantages  of  the  climatic  health-resorts  {vide  infra)  consist  principally  in  the 
fact  that  they  render  possible  a  continuous  enjoyment  of  the  open  air,  even  during 
the  colder  part  of  the  year.  It  has  been  maintained  that  climatic  factors,  par- 
ticularly elevation,  exercise  a  specific  influence  upon  the  healing  of  pulmonary 
tuberculosis;  but  this  has  not  yet  been  proved.  The  best-known  sanitariums  for 
17 


258  DISEASES    OF    THE   EESPIEATORT   OEGANS 

pulmonary  disease  are  found  in  Falkenstein  in  the  T  annus,  Gorbersdorf,  St.  Bla- 
sien,  Eeiboldsgriin,  Hohenhonnef,  and  Andreasberg  in  the  Hartz  Mountains,  and 
Davos  and  Arosa  in  Switzerland.  Of  the  public  health-resorts  which  are  particu- 
larly suitable  for  consumptives,  we  would  name  for  summer  use  the  acidulated, 
alkaline,  and  chloride-of-sodium  waters  of  Ems,  Obersalzbrun,  and  Eeinerz;  the 
chloride-of -sodium  waters  in  Eeichenhall,  Salzungen,  and  Soden;  the  mud  springs 
in  Lippspringe,  Inselbad,  and  Weissenburg  in  Switzerland.  Eor  summer  climate, 
the  following  are  to  be  recommended:  Beatenberg,  Heiden,  Engelberg  in  Switzer- 
land; Badenweiler,  St.  Blasien,  Eippoldsau  in  the  Black  Forest,  and  many  others. 
For  the  colder  portion  of  the  year  we  have,  in  their  lofty  situation,  Davos, 
Arosa,  and  others.  The  more  vigorous  the  constitution  of  the  patient,  the  more 
proper  it  is  to  recommend  him  to  go  to  a  great  elevation  in  the  winter;  while 
delicate  subjects  are  usually  better  suited  in  the  soitthern  resorts. 

Of  course  only  the  very  distant  health-resorts  in  Algiers,  Egypt,  Malta,  and  the 
much-praised  Madeira,  can  furnish  a  certain  guarantee  of  constant  mild  weather. 
The  Sicilian  health-resorts  (Catania  and  Palermo),  and  also  Ajaccio,  afford  fa- 
vorable climatic  conditions;  while  the  health-resorts  of  the  Eiviera,  Meran,  Gries, 
Arco,  Gardone,  Lugano,  Pallanza,  and  Montreux,  are  much  more  uncertain  in 
this  respect,  and  therefore  are  to  be  used  merely  as  stopping-places  by  the  way 
during  the  spring  and  autumn  months. 

We  must  also  state  that,  in  incipient  cases,  a  residence  by  the  sea,  or  a  long 
sea-voyage,  may  sometimes  be  of  great  help.  We  have  ourselves  known  severaj 
young  physicians  who  have  become  ship  surgeons  on  account  of  incipient  phthisis, 
and  who  have  returned  from  the  voyage  much  stronger,  and  some  of  them  appar- 
ently entirely  well. 

We  can  not  go  into  a  full  description  here  of  all  the  health-resorts  mentioned. 
We  can  not  omit,  however,  calling  special  attention  to  the  fact  that  we  should 
always  ask  ourselves,  in  choosing  a  health-resort,  whether  the  expense  and  incon- 
venience thus  imposed  upon  the  patient  can  be  balanced  by  the  possible  benefit. 
The  earlier  the  stage  of  the  disease  and  the  better  the  general  condition  of  the 
patient,  the  more  will  his  physician  be  justified  in  urging  him  to  make  every 
sacrifice  in  order  to  regain  his  health. 

We  must  particularly  insist  with  the  patient  that  no  cure  of  tuberculosis  can 
be  accomplished  by  a  single  visit  to  any  health-resort,  but  that  recovery  must  be 
achieved  by  living  continuously  for  years  in  accordance  with  all  the  demands  of 
hygiene.  On  the  other  hand,  it  is  wrong,  both  from  a  medical  and  from  a  humane 
standpoint,  to  send  away  consumptives  in  the  last  stages  of  their  disease,  to  perish 
far  from  home  and  friends.  Consumptives  with  fever  should  never  be  sent  from 
home,  unless  they  find  refuge  in  a  real  sanitarium  where  they  may  enjoy  the  con- 
stant observation  and  treatment  of  a  physician. 

[Our  own  health-resorts  for  consumptives  are  too  well  known  to  demand  ex- 
tensive consideration  here.  The  prime  object  is  to  secure  for  the  patient  a  pure 
air,  with  such  climatic  conditions  that  he  can  pass  the  largest  amount  of  time  out 
of  doors,  at  the  same  time  that  within  doors  his  comfort  is  provided  for,  and  a 
sufficiency  of  suitable  and  well-cooked  foods  is  attainable.  In  Colorado,  ISTew 
Mexico,  and  California,  large  numbers  of  fonner  consumptives  are  leading  active 
lives.  Florida,  Aiken,  Thomasville,  Asheville,  and  some  other  southern  resorts, 
are  good  winter  asylums  for  many  cases,  but  patients  should  not  return  to  jiSTew 
England  before  June  1st.  An  out-door  life  in  the  Maine  or  Adirondack  woods 
during  the  warmer  months  is  highly  to  be  recommended  for  early  and  otherwise 
suitable  cases.  Saranac,  IST.  Y.,  affords  every  comfort  during  the  colder  months, 
combined  with  the  very  best  medical  attendance,  and  many  people  do  well  there. 
A  relative  disadvantage  under  which  nearly  all  American  health-resorts  labor,  as 
compared  with  those  of  Europe,  consists  in  the  greater  difiiculty  in  providing  oc- 


TUBEECULOSIS    OF   THE   LUNGS  259 

cupation  and  thus  securing  a  mental  attitude  most  favorable  to  recovery.  In  gen- 
eral, the  northern  sea-board  is  much  less  favorable  than  the  interior,  and  early- 
cases  often  do  well  during  the  wint.er  removed  from  the  dampness  of  the  coast, 
with  its  alternations  of  freezing  and  thawing.  A  change  of  climate  is  a  very  im- 
Ijortant  step,  and  should  receive  the  most  careful  consideration  of  the  physician — • 
the  circumstances  of  the  patient,  the  stage  and  character  of  his  disease,  his  tastes, 
etc.,  being  carefully  weighed  before  a  decision  is  reached.] 

Finally,  the  employment  of  hydrotherapy  should  be  mentioned  in  the  hygienic 
treatment  of  tuberculosis.  Although  this  can  not  exert  any  specific  influ- 
ence on  the  disease,  and  therefore  must  not  be  prized  too  highly,  yet  it  is 
often  beneficial  in  the  form  of  cold  sponging,  or  brief  cool  douching  and  the 
like;  and  the  stimulation  of  the  skin  has  a  favorable  influence  upon  the  general 
health.  In  severe  febrile  cases  we  may  order  sponging  and  rubbing  in  bed  with 
cold  water,  brandy,  vinegar,  and  the  like.  Also  for  the  relief  of  symptoms  (vide 
infra),  such  as  pain,  fever,  and  perspiration,  we  may  often  employ  sponging,  cold 
or  warm  compresses,  and  the  wet  pack. 

The  symptomatic  treatment  of  phthisis  is  directed  in  the  first  place  against  the 
pulmonary  symptoms.  We  use  much  the  same  remedies  to  help  the  cough  as  in 
chronic  bronchitis.  We  try  inhalations  with  a  solution  of  common  salt,  or  of  the 
alkaline  carbonates,  or,  if  there  is  much  secretion,  with  solutions  of  tannin  and 
the  balsams,  such  as  turpentine,  or  balsam  of  Peru.  When  there  is  severe,  spas- 
modic cough,  inhalations  with  narcotic  solutions  sometimes  give  some  relief,  such 
as  cherry-laurel  water,  opium,  or  bromide  of  potassium. 

Morphine  stands  first  among  the  drugs  employed  to  check  the  cough.  We 
should  be  cautious  and  sparing  in  its  use  at  first,  but  it  is  an  indispensable  remedy 
in  severe  and  hopeless  cases.  It  relieves  the  irritation  of  coughing,  the  pain  and 
the  oppression  in  the  chest,  and  at  least  gives  the  patient  for  a  time  the  desired 
sleep.  In  chronic  cases,  with  moderately  severe  symptoms,  we  may  use  for  a  long 
time  the  milder  narcotics  with  advantage,  particularly  codeine  (powders  of  gr. 
0.5-1.0,  gramme  0.03-0.05)  or  phosphate  of  codeine;  also  the  extracts  of  hyos- 
cyamus  and  of  belladonna  (extracti  hyoscyami  1,  aquae  lauro-cerasi  20,  fifteen  to 
twenty,  drops  every  two  hours).  [Heroine  is  sometimes  useful  in  doses  of  ^g- 
grain. — ^V.]  It  is  important  that  the  patient  should  learn  to  suppress  his  incli- 
nation to  cough,  at  least  up  to  a  certain  point.  Sips  of  cold  water  often  quiet 
the  cough,  as  may  also  a  "  cough  drop  "  held  in  the  mouth,  or  a  pastille  contain- 
ing the  salts  found  in  Ems  mineral  water. 

If  the  patient  complains  of  difiiculty  in  loosening  the  expectoration,  we  pre- 
scribe expectorants,  the  action  of  which  often  fails  to  meet  our  desires,  but  which 
can  not  be  dispensed  with  in  practice.  The  expectorants  most  frequently  used 
are  carbonate  of  ammonia,  ipecacuanha,  apomorphine,  and  senega.  We  very  often 
combine  expectorants  with  narcotics,  as  in  Dover's  powder. 

If  severe  pain  in  the  chest  comes  on,  we  often  use  local  applications :  mustard 
plasters,  warm  poultices  and  cold  compresses,  painting  with  iodine,  or  embro- 
cations of  chloroform.  ISTarcotics,  such  as  morphine,  are  indispensable  in  severe 
dyspnoea,  which  usually  occurs  only  in  the  last  stages  of  the  disease  or  as  a  result 
of  pneumothorax. 

The  treatment  of  ha3moptysis  is  important.  As  a  slight  admixture  of  blood 
in  the  expectoration  often  precedes  a  severe  haemoptysis,  such  an  appearance 
always  suggests  caution.  When  there  is  any  haemoptysis,  absolute  rest  in  bed  is 
necessary.  We  should  avoid  any  careful  examination  of  the  lungs,  especially 
any  severe  percussion.  We  should  lay  a  flat  and  not  too  heavy  ice-bag  over 
the  lung  on  the  side  from  which  we  suspect  the  haemorrhage;  the  cold  is  usually 
well  borne,  but  sometimes  it  aggravates  the  cough,  and  must  then  be  omitted. 
We  would  also  recommend  SAvallowing  bits  of  cracked  ice.     Narcotics,  such  as 


260  DISEASES    OF    THE   KESPIEATORT   ORGAlSrS 

morphine,  are  tlie  most  suitable  internal  remedies,  since  they  aid  the  cessation  of 
the  hsemorrhag-e  by  suppressing  the  attacks  of  coughing-.  The  more  troublesome 
the  cough  the  more  necessary  is  it,  therefore,  to  administer  morphine  in  solu- 
tion, by  the  mouth  or  even  subcutaneously.  Of  remedies  to  check  the  blood  we 
should  name,  first,  extract  of  ergot  or  ergotine,  which  may  be  given  by  the  mouth, 
or,  still  better,  subcutaneously,  in  doses  of  2  to  8  grains  (grammes  0.1-0.5) 
several  times  a  day.  As  to  sphacelotoxine,  and  other  special  preparations  of  ergo- 
tine, there  has  been  as  yet  no  extended  experience.  We  may  also  try  the  fluid 
extract  of  hydrastis,  with  equal  parts  of  an  elixir,  giving  thirty  to  forty  drops 
of  the  mixture  several  times  a  day;  also,  acetate  of  lead  and  atropine.  The  in- 
fluence of  these  remedies,  particularly  those  last  named,  is,  however,  quite  uncer- 
tain. The  inhalation  of  a  one-  to  two-per-cent.  solution  of  perchloride  of  iron 
usually  excites  cough,  and  is  therefore  more  harmful  than  beneficial.  A  very 
popular  remedy  among  the  laity,  and  one  almost  always  at  hand,  is  common  salt, 
of  which  several  teaspoonfuls  may  be  given  in  water.  When  the  haemorrhage 
recurs  frequently,  it  is  also  advisable  to  "  tie  off "  the  limbs — that  is,  to  apply 
bandages  rather  firmly  around  the  middle  of  the  upper  arms  and  the  thighs. 
This  causes  venous  congestion,  and  hinders  the  return  of  blood  to  the  lungs. 
When  pulmonary  hsemorrhage  has  occurred,  the  diet  should  consist  at  first  of 
nothing  but  cold  milk,  eggs,  and  similar  food.  Hot  food,  alcohol,  and  large 
amounts  of  meat  are  to  be  forbidden.  It  is  a  good  thing  to  give  acids,  such  as 
lemonade,  or  aromatic  sulphuric  acid,  well  diluted. 

Even  when  the  bleeding  has  ceased  we  must  keep  the  patient  several  days  in 
bed,  and  for  a  loiiger  time  be  extremely  cautious,  since  the  hsemorrhage  is  apt 
to  be  repeated. 

The  hectic  fever  of  consumption  is  remarkably  little  influenced  by  antipyretic 
drugs.  It  often  is  entirely  useless,  or  even,  on  account  of  its  evil  effect  upon  the 
stomach,  actually  harmful  to  give  to  feverish  consumptives,  for  long  periods  of 
time,  large  doses  of  such  drugs  as  quinine,  antipyrine,  and  antifebrine,  particu- 
larly as  the  fever  often  of  itself  has  deep  morning  remissions.  The  prescription 
of  antipyretics  is  only  justified  when  they  make  the  patient  feel  better.  On  the 
other  hand,  it  is  very  appropriate  to  give  a  cold  sponging  and  rubbing  to  the 
whole  body  or  chest,  with  water  or  alcohol,  especially  in  the  evening  when  the 
fever  is  high.  The  sponging  is  almost  always  well  borne,  and  makes  the  patient 
feel  brighter  and  easier.     The  cold  pack  may  also  be  tried  occasionally. 

Cold  sponging  often  diminishes  the  troublesome  sweats  in  phthisis,  but  if  this 
does  not  check  them,  we  may  often  prescribe  atropine  to  advantage,  grain  tJt  to 
•gV  (gramme  0.0005-0.001)  at  night,  but  its  action  does  not  usually  last  very  long. 
Lately  agaricine  in  ^f"  to  -g-grain  pills  (gramme  0.005-0.01)  has  been  recom- 
mended for  the  night-sweats  in  phthisis;  also  picrotoxine,  of  which  grain  i  to  J 
(gramme  0.008-0.01)  is  given  in  pill  or  solution  at  bed-time,  and  lately  camphoric 
acid,  grains  20-30  (grammes  1.5-2.0)  in  wafers.  Dusting  the  body  with  a  powder 
of  five  parts  of  salicylic  acid  to  ninety-five  of  French  chalk  is  also  good.  Sage 
tea  is  a  favorite  remedy  for  night-sweats — two  or  three  cups  of  it  cold  at  night — 
and  so  are  milk  and  cognac. 

If  there  is  loss  of  appetite,  small  doses  of  quinine,  compound  tincture  of  cin- 
chona, wine  of  cinchona,  and  other  bitter  remedies,  such  as  tinctura  amara 
(P.  G.),  are  sometimes  of  service.  It  is  also  frequently  a  good  thing  to  prescribe 
a  little  muriatic  acid,  five  to  ten  drops  of  the  dilute  acid,  with  the  meals.  It  is 
often  very  hard  to  check  diarrhoea  in  phthisis.  Opium,  combined  with  tannin  or 
acetate  of  lead,  is  most  effective.  This  subject  will  be  discussed  more  fully  in  the 
chapter  on  intestinal  tuberculosis. 

We  often  prescribe  preparations  of  iron,  combined  sometimes  with  quinine  or 
arsenic  (vide  supra),  in  the  beginning  of  the  disease  to  improve  the  general  con- 


ACUTE   GENEKAL   MILIAEY   TUBERCULOSIS  261 

dition  and  the  anaemia,  but,  as  experience  shows,  iron  is  contra-indicated  in 
patients  who  are  feverish  or  who  have  a  tendency  to  haemoptysis. 

The  treatment  of  the  diseases  complicating  phthisis  is  to  be  found  in  the  appro- 
priate chapters. 


CHAPTEE  YII 
ACUTE  GENERAL  MILIARY  TUBERCULOSIS 

.Sltiolog^. — Acute  miliary  tuberculosis  is  a  form  of  tuberculosis  which  we  are 
justified  in  describing  particularly  because  of  its  anatomical  relations  and  its 
peculiar  clinical  history.  The  disease  is  characterized  anatomically  by  the  ex- 
tremely abundant  development  of  miliary  tubercles  in  a  comparatively  short 
time  in  many  organs  of  the  body.  We  can  not  liken  this  process  to  anything 
but  an  overwhelming  of  the  body  with  tubercle  bacilli,  which  in  some  way  reach 
the  different  organs  simultaneously,  and  in  them  give  rise  to  the  eruption  of 
tubercles.  Buhl  advanced  the  hypothesis  a  long  time  ago,  that  a  cheesy  focus 
could  be  found  somewhere  in  the  body  in  every  case  of  acute  miliary  tuberculosis, 
and  that  the  general  infection  of  the  body  resulted  from  the  absorption  of  these 
cheesy  masses  by  the  blood.  Later  investigations,  however,  have  given  us  a  much 
more  definite  explanation  of  the  nature  and  manner  of  this  general  infection. 
Ponfick  found,  in  some  cases  of  acute  miliary  tuberculosis,  an  extensive  tubercu- 
losis of  the  thoracic  duct  with  breaking  down  of  the  tubercular  new  growth.  It 
is  easy  to  see  how,  in  this  way,  a  large  amount  of  tubercular  material  could  be 
brought  directly  into  the  circulation,  from  the  free  communication  of  the  lymph- 
duct  with  the  subclavian  vein,  and  thus  be  "  disseminated  "  through  the  different 
organs  in  a  short  time.  Still  more  frequently,  however,  the  tuberculosis  of  the 
large  venous  trunks,  discovered  by  Weigert,  especially  the  pulmonary  veins, 
seems  to  be  the  starting-point  for  an  acute  general  miliary  tuberculosis.  Usually 
there  are  tubercular  lymph-glands,  or  sometimes  other  foci  of  tubercular  disease, 
which  involve  the  wall  of  a  neighboring  vein,  gradually  break  through  it,  and 
project  into  its  lumen.  If  caseation  and  ulceration  result  in  this  spot,  the  infec- 
tious material  is  of  course  constantly  washed  off  by  the  blood-current  and  carried 
away,  and  thus  it  reaches  the  other  organs. 

Since  such  a  tubercular  focus — e.  g.,  a  tubercular  bronchial  gland— may  remain 
for  a  long  time  entirely  without  symptoms,  we  can  understand  how  miliary  tuber- 
culosis may  break  out  in  an  acute  form  in  persons  who  previously  seemed  per- 
fectly well.  In  other  cases  the  patient  has  already  suffered  from  some  tubercular 
affection,  and  suddenly  the  conditions  occur  somewhere  in  the  body  which  lead 
to  the  development  of  miliary  tuberculosis.  Thus  we  sometimes  see  it  break  out 
in  a  patient  who  has  ordinary  phthisis,  but  acute  miliary  tuberculosis  is  one  of 
the  rarities  in  advanced  phthisis.  If  we  find,  at  the  autopsy  of  a  case  of  acute 
general  miliary  tuberculosis,  old  phthisical  changes  in  the  lungs,  which  is  by  no 
means  very  common,  they  consist  of  old,  partly  cicatrized  foci,  pigment  indura- 
tions, etc.  We  see  miliary  tuberculosis  rather  frequently  as  a  sequel  to  pleuritic 
effusion.  We  have  already  previously  called  attention  to  the  fact  that  in  such 
cases  the  pleurisy  itself  is  a  tubercular  disease.  Miliary  tuberculosis  is  also  seen 
in  persons  with  old  tubercular  affections  of  the  bones  and  joints,  such  as  coxitis 
and  vertebral  caries,  with  tubercular  swellings  of  the  lymph-glands,  as  in  the 
neck  and  the  axillae,  or  with  tuberculosis  of  the  genito-urinary  organs.  In  such 
cases,  of  course,  the  tubercular  affection  which  is  discovered  during  life,  is  not 
always  the  source  of  the  general  miliary  tuberculosis,  but  the  discovery  of  the 


262  DISEASES    OF   THE   EESPIEATOET   OEGAXS 

existence  of  such  an  afPection  is  of  the  greatest  significance  in  diagnosis,  as  in  this 
way  our  attention  is  strongly  directed  to  the  possibility  of  a  general  tubercular 
affection. 

In  some  cases  an  outbreak  of  miliary  tuberculosis  has  been  seen  to  follow  other 
acute  diseases,  such  as  typhoid,  or  measles. 

Pathological  Anatomy. — Except  for  the  presence  of  an  old  tubercular  affec- 
tion in  some  organ,  and  except  for  the  tuberculosis  of  a  vein  or  of  the  thoracic 
duct,  which  are  as  a  rule  apparent,  and  which  have  been  described  above,  the 
anatomical  lesion  in  acute  miliary  tuberculosis  consists  in  the  dissemination  of 
miliary  tubercles  through  a  large  number  of  the  organs  of  the  body.  The  lungs, 
the  liver,  and  the  spleen  are  constantly  affected;  almost  as  constantly  the  kid- 
neys, the  thyroid  gland,  the  marrow  of  the  bones,  the  heart,  and  the  choroid;  less 
constantly,  but  still  quite  frequently,  the  serous  membranes  and  the  meninges. 
The  miliary  nodules  may  be  found  in  large  numbers  in  all  the  organs  mentioned. 
They  may  in  part  be  easily  recognized  by  the  naked  eye,  and  in  the  kings  they 
may  be  very  plainly  perceived  by  the  touch.  In  many  organs,  however,  especially 
in  the  liver  and  often  in  the  spleen,  they  are  hard  to  recognize  with  the  naked  eye, 
but  they  are  easily  discovered  by  the  microscope.  In  regard  to  the  histological 
structure  of  miliary  tubercles,  and  the  discovery  of  tubercle  bacilli  in  them,  we 
must  refer  to  what  has  been  said  in  the  chapter  on  pulmonary  tuberculosis,  but 
we  must  also  mention  that,  in  some  of  the  more  chronic  cases,  some  of  the  nodules 
may  grow  to  be  large  tubercular  foci,  from  the  size  of  a  lentil  to  that  of  a  pea. 
Less  developed  cases  of  miliary  tuberculosis  are  also  found,  in  which  only  a  lim- 
ited number  of  organs  are  attacked,  and  these  with  less  severity. 

Clinical  History. — The  clinical  symptoms  of  miliary  tuberculosis  depend  upon 
two  factors,  the  first  being  the  general  infection  of  the  body,  and  the  second  the 
local  tubercular  affection  of  certain  organs.  Although  in  many  organs  miliary 
tuberculosis  is  entirely  without  symptoms,  as  in  the  liver,  the  kidneys,  the  heart, 
and  the  marrow  of  the  bones,  in  two  organs — the  lungs,  and  more  especially  the 
brain — it  leads  to  the  most  marked  local  symptoms.  The  miliary  tuberculosis  of 
the  choroid,  discovered  by  Cohnheim  and  Manz,  is  also  without  symptoms,  but  it 
can  be  made  out  with  the  ophthalmoscope,  and  it  is  therefore  of  great  diagnostic 
value. 

Miliary  tuberculosis  affords  quite  different  pictures,  according  to  the  predom- 
inance of  one  or  the  other  of  the  groups  of  symptoms  mentioned.  We  distinguish 
the  four  following  forms : 

1.  Miliary  Tuberculosis,  with  Predominant  Symptoms  of  General  Infection: 
the  so-called  Typhoidal  Form. — This  form  may  in  part  greatly  resemble  typhoid 
fever.  The  patient,  who  previously  seemed  quite  well,  or  in  whom  some  local 
manifestation  of  tuberculosis  was  suspected,  falls  ill  with  gradually  increasing 
general  symptoms,  dullness,  loss  of  appetite,  headache,  and  fever.  Since  there  is 
no  local  affection  to  be  discovered  to  explain  the  symptoms,  the  disease  at  first 
may  well  be  taken  for  typhoid.  The  general  condition  grows  worse  constantly, 
the  fever  is  high  and  continually  rises,  and  cerebral  symptoms  appear.  In  some 
cases  an  exanthematous  eruption,  like  roseola,  may  increase  the  resemblance  to 
typhoid.  With  careful  observation,  however,  symptoms  are  almost  always  de- 
tected later  in  the  disease  which  are,  to  a  certain  degree,  characteristic  of  miliary 
tuberculosis,  and  are  due  to  the  existence  of  that  disease  either  in  the  lungs  or  in 
the  brain.  The  patient's  complexion  assumes  a  peculiar  pallor,  and  with  it  a  defi- 
nite cyanotic  hue.  The  respiration  becomes  remarkably  deep,  and  there  is  dysp- 
noea; or  signs  of  a  tubercular  meningitis  arise,  such  as  rigidity  of  the  neck,  loss 
of  consciousness,  disturbances  in  the  innervation  of  the  ocular  muscles,  etc.,  and 
death  follows  with  these  symptoms.  These  cases  last  from  ten  days  to  three 
weeks,  reckoning  from  the  beginning  of  the  severe  symptoms. 


ACUTE    GEXEEAL   :MILIAEY   TUBEECULOSIS  263 

2.  Miliary  Tuberculosis,  ivith  Predominant  Pulmonary  Symptoms. — These 
cases,  too,  may  begin  quite  suddenly,  almost  like  an  acute  croupous  pneumonia, 
or  they  may  develop  gradually  with  quite  a  long  prodromal  stage.  From  the 
onset  the  symptoms  point  especially  to  disease  of  the  lungs  or  the  pleura.  The 
patient  complains  of  a  stitch  in  the  side,  cough,  and  dyspnoea.  The  expectora- 
tion may  bear  a  decided  resemblance  to  that  of  pneumonia.  Such  cases,  espe- 
cially if  they  begin  abruptly,  are  at  first  often  erroneously  regarded  as  croupous 
pneumonia,  particularly  if  we  find  fine  rales  almost  like  crepitant  rales  over  cer- 
tain portions  of  the  lungs.  But  the  expected  crisis  does  not  occur:  the  fever 
continues;  the  dyspnoea,  general  weakness,  and  anaemia  of  the  patient  increase; 
the  physical  signs  of  pulmonary  disease  (diffuse  bronchitic  rales)  become  more 
and  more  extensive.  The  patient's  face  is  pale,  cyanotic,  and  anxious.  Death 
ensues  with  all  the  signs  of  impaired  respiration.  The  course  is  usually  some- 
what more  protracted  than  in  the  tjTphoidal  form,  lasting  for  three  or  four  weeks 
and  more. 

3.  Miliary  Tulerculosis,  until  Predominant  Cerebral  Symptoms,  due  to  Tuber- 
cular Meningitis. — Tuberculosis  of  the  meninges  does  not  belong  among  the  reg- 
ular lesions  of  general  miliary  tuberculosis.  It  develops  in  about  haK  the  cases, 
according  to  our  estimation;  but  where  it  occurs  it  almost  always  gives  the  whole 
case  the  characteristic  imprint  of  tubercular  meningitis,  by  which  the  other  symp- 
toms are  entirely  concealed.  The  predominant  symptoms  are  headache,  fever, 
stupor  increasing  to  deep  coma,  rigidity  of  the  back  and  neck,  and  disturbances 
in  the  innervation  of  the  ocular  muscles.  In  such  cases  the  tuberculous  menin- 
gitis may  alone  be  diagnosticated,  and  not  the  universal  miliary  tuberculosis. 
In  fact,  all  the  other  signs  of  general  miliary  tuberculosis  are  not  infrequently 
obscured  by  meningeal  symptoms,  and  yet  we  have  repeatedly  observed,  even  in 
the  deepest  coma  of  the  patient,  a  peculiarly  deep  and  hurried  respiration,  which 
was  the  only  noticeable  sign  referable  to  the  miliary  tuberculosis  in  the  lungs. 

The  sjonptoms  of  tubercular  meningitis  in  many  cases  predominate  in  this 
type  of  the  disease  from  the  onset,  but  in  other  cases  they  come  on  during  the 
attack  and  form  its  final  period.  The  duration  of  the  disease  varies  accord- 
ingly. 

4.  Miliary  Tuberculosis  witli  a  Protracted  Course  and  Indefinite  Symptoms 
for  a  Long  Time — Intermitting  Form. — ^Besides  the  forms  already  mentioned, 
cases  occur  which  usually  take  quite  a  protracted  course,  lasting  for  eight  or  ten 
weeks,  and  having  such  indefinite  symptoms  that  an  absolute  diagnosis  is  for  a 
long  time,  or  even  throughout  the  disease,  quite  impossible.  The  patient  com- 
plains of  a  number  of  general  symptoms,  such  as  headache  and  dullness,  and  also 
of  thoracic  symptoms,  for  which,  however,  we  can  find  on  examination  no  sufli- 
cient  basis.  There  is  almost  always  fever,  usually  not  very  high,  and  with  a  very 
irregular  course ;  hut  we  have  seen  a  regular  daily  rise  of  temperature  for  a  time 
in  some  cases,  and  attacks  of  fever  with  quite  a  severe  chill,  so  that  at  first  we 
thought  of  an  irregular  malarial  intermittent  fever — the  intermitting  form. 
Later  on  the  symptoms  gradually  increase.  The  apparently  inexplicable  loss  of 
strength,  and  the  patient's  ansemia  and  emaciation,  are  marked,  and  they  are 
important  in  diagnosis.  Einally,  either  severe  pulmonary  symptoms  or  the  signs 
of  tubercular  meningitis  set  in,  and  to  these  the  patient  succumbs. 

We  must  mention  particularly  that  the  four  forms  of  miliary  tuberculosis  just 
described  are  only  the  types  of  the  disease.  In  individual  cases  we  often  meet 
with  variations  and  transitional  forms  between  these  types. 

Single  Symptoms. — 1.  General  Symptoms. — In  all  c^ses  of  acute  miliary  tu- 
berculosis the  general  condition  of  the  patient  is  very  serious.  Most  patients 
have  a  subjective  feeling  of  severe  illness,  although  they  make  little  special  com- 
plaint of  it  from  the  painless  character  of  the  disease.    As  the  disease  increases, 


264  DISEASES    OF   THE   EESPIRATOET   OEGANS 

there  is  often  a  marked  feeling'  of  anxiety  and  oppression  besides  the  dyspnoea. 
There  is,  especially  in  the  face,  quite  a  peculiar  pallor,  characteristic  of  the 
disease,  and  associated  with  a  marked  cyanosis  of  the  lips  and  cheeks. 

2.  Fever. — Acute  miliary  tuberculosis  almost  always  runs  its  course  with  a 
more  or  less  high  fever,  a  course  without  fever  having  been  observed  in  only  a 
few  instances.  It  often  happens,  in  more  protracted  cases,  that  the  temperature 
may  be  nearly  normal  for  a  time,  or  only  slightly  elevated.  There  is  nothing 
characteristic  or  typical  in  the  course  of  the  fever.  In  the  cases  with  typhoidal 
symptoms  the  fever  is  usually  quite  high,  between  103°  and  105°  (39.5°-40.§°  C), 
so  that  the  temperature-curve  may  be  exactly  like  that  of  typhoid.  In  other  cases 
the  fever  is  irregular  and  is  broken  by  many  remissions,  remitting  or  intermit- 
ting quite  regularly  for  some  time.  Death  ensues  with  a  moderately  high  tem- 
perature or  in  collapse.  In  cases  with  tubercular  meningitis  there  is  also  a 
marked  rise  of  temperature  at  the  close,  up  to  108°  (42°  C.)  and  over. 

3.  Respiratory  Apparatus. — It  goes  without  saying  that  physical  examination 
of  the  lungs  may  give  no  definite  results.  Almost  all  positive  evidence  is  often 
wanting',  and  the  contrast  between  the  labored  breathing  and  dyspnoea  and 
the  insignificance  of  the  physical  signs  in  the  lungs  is  an  important  feature  in 
diagnosis.  Auscultation,  as  a  rule,  gives  the  signs  of  an  intense  bronchial  ca- 
tarrh; we  hear  rhonchi  or  numerous  fine  and  medium  moist  rales  all  over  both 
lungs.  The  respiratory  murmur  itself  is  usually  higher  in  pitch  than  normal, 
and  in  many  cases  it  is  obscure,  rough,  or  harsh.  In  one  of  our  cases  there  was 
heard,  over  a  circumscribed  area  of  the  lung,  a  wholly  peculiar,  sharp,  "  lapping  " 
sound  on  inspiration,  which  we  have  never  heard  under  any  other  circumstances. 
Jiirgensen  describes  a  soft  friction  sound,  due  to  miliary  tuberculosis  of  the 
pleura.  Percussion  usually  gives  no  objective  changes.  At  times  the  resonance 
is  rather  tympanitic,  or  slightly  dull  in  some  places. 

In  some  cases  circumscribed  pneumonic  infiltration  has  been  observed  in  the 
lungs  in  acute  miliary  tuberculosis,  which,  as  we  have  said,  may  give  rise  to  a 
confusion  between  miliary  tuberculosis  and  croupous  pneumonia,  from  the  pres- 
ence of  marked  dullness,  crepitant  rales,  and  bronchial  respiration. 

We  must  mention,  finally,  that  in  some  of  the  eases  physical  examination  of 
the  lungs  shows  old  changes  in  them,  a  phthisical  affection  of  the  apex,  a  former 
pleurisy,  and  the  like.  Positive  evidence  of  such  old  tubercular  affections  may 
be  of  great  diagnostic  value  in  doubtful  cases. 

Dyspnoea  has  been  repeatedly  mentioned  among  the  pulmonary  symptoms. 
The  respiration  is  usually  very  much  accelerated,  especially  during  the  more 
advanced  stage  of  the  disease,  so  that  we  see  in  adults  forty,  sixty,  and  even 
seventy  respirations  a  minute.  The  respiration  is  also  very  deep,  and  is  some- 
times noisy.  As  a  rule  there  is  cough,  but  it  is  usually  troublesome  only  in  the 
cases  with  severe  bronchitis.  It  is  often  very  slight.  The  expectoration  is  usu- 
ally scanty,  and  it  is  not  characteristic.  Special  mention  must  be  made  of  the 
fact  that  tubercle  bacilli  are  absent  in  it,  unless  old  ulcerated  tubercular  foci  are 
present  at  the  same  time  in  the  lungs. 

4.  Circulatory  Apparatus. — The  pulse  is  frequent,  about  100  to  120  a  minute, 
often  weak  and  small,  and  sometimes  irregular,  especially  if  tubercular  menin- 
gitis co-exists.  The  miliary  tubercles,  which  post  mortem  are  almost  always  to 
be  found  in  the  heart,  especially  in  the  endocardium,  cause  no  symptoms.  In 
uncomplicated,  acute,  miliary  tuberculosis  there  is  little  if  any  increase  in  the 
number  of  white  corpuscles  in  the  blood.  The  presence  of  tubercle  bacilli  in  the 
blood  will  be  mentioned  below. 

5.  Digestive  Apparatus. — Vomiting  is  frequent  at  the  onset  of  the  disease. 
The  bowels  are  usually  constipated,  but  in  many  cases  there  is  a  moderate  diar- 
rhoea.    The  loss  of  appetite,  the  thirst,  and  the  dry  tongue  are  due  to  the  general 


ACUTE   GENERAL   MILIARY   TUBERCIJLOSIS  265 

disease  and  the  fever.  The  spleen  is  usually  somewhat,  but  not  very  much, 
enlarged. 

'6.  Nervous  System. — In  many  cases  in  which  the  pulmonary  symptoms  pre- 
dominate the  intellect  remains  quite  clear  until  the  last,  but  in  other  cases  cere- 
bral symptoms,  such  as  headache,  dizziness,  stupor,  and  delirium,  come  on  quite 
early,  and  are  a  part  of  the  general  infection.  As  has  already  been  said,  the 
nervous  symptoms  in  the  cases  combined  with  tubercular  meningitis  become 
quite  prominent,  but  in  individual  instances  it  may  be  hard  to  decide  whether 
they  are  due  to  such  a  complication,  or  are  merely  severe  general  symptoms. 

7.  Eyes. — The  ophthalmoscopic  examination  of  the  retina  is  of  special  diag- 
nostic importance,  since  the  diagnosis  may  be  made  absolutely  certain  by  finding 
miliary  tubercles  in  the  choroid.  A  negative  result,  however,  is  never  decisive 
against  the  diagnosis,  since  the  tubercles  are  sometimes  absent,  or  at  least  are 
very  few  in  number.  Their  discovery  is  almost  always  difficult,  and  demands 
much  practice  in  the  method  of  examination.  In  cases  with  tubercular  menin- 
gitis we  sometimes  find  an  optic  neuritis. 

Diagnosis. — The  diagnosis  of  acute  general  miliary  tuberculosis  is  ordinarily 
and  justly  considered  very  difficult.  It  quite  often  happens  that  at  the  autopsy  a 
miliary  tuberculosis  is  found  which  was  not  even  suspected  during  life.  It  must 
be  confessed  that  frequently,  in  such  cases,  we  might  very  well  have  thought  of 
acute  tuberculosis.  If,  therefore,  the  possibility  of  acute  miliary  tuberculosis  is 
brought  to  our  attention  during  the  patient's  life,  we  can  occasionally  make  an 
absolute  diagnosis. 

The  severe  general  condition,  usually  associated  with  fever,  is  most  important, 
and  for  this  no  local  cause  can  be  found.  Then  come  the  pulmonary  symptoms, 
especially  the  peculiar  dyspnoea,  for  which  there  is  also  no  adequate  corresponding 
physical  change  to  be  discovered.  It  gives  decided  support  to  our  suspicion  if  we 
can  make  out  a  distinct  predisposition  to  tuberculosis,  either  hereditary  or  consti- 
tutional, or  the  history  of  a  previous  tubercular  affection,  especially  pleurisy,  and 
also  chronic  affections  of  the  bones.  The  peculiar  cyanotic  pallor  of  the  patient 
is  very  characteristic. 

On  these  factors  rests  the  differential  diagnosis  between  the  "  typhoidal " 
form  of  miliary  tuberculosis  and  typhoid  fever.  Marked  roseola  and  considerable 
enlargement  of  the  spleen  are  distinct  arguments  for  typhoid,  although  they 
sometimes  occur  in  miliary  tuberculosis,  and  so  are  the  intestinal  symptoms 
of  typhoid,  such  as  meteorism,  the  characteristic,  loose  yellow  stools,  and  possi- 
bly intestinal  hsemorrhage ;  but  we  must  not  forget  that  both  the  roseola  and  the 
intestinal  symptoms  may  be  absent  in  typhoid.  The  course  of  the  fever  must 
always  be  considered  in  the  differential  diagnosis.  It  is  much  more  frequently 
irregular  and  atypical  in  tuberculosis  than  in  typhoid.  Of  course,  the  tempera- 
ture-curve is  not  an  absolutely  decisive  factor.  The  blood  does  not  afford  any 
indubitable  signs  of  distinction  between  the  two,  since  in  neither  disease  is  there 
a  decided  leucocytosis.  If  the  number  of  leucocytes  is  conspicuously  small, 
5,000  or  less,  typhoid  is  strongly  suggested.  The  Widal  serum-reaction  with 
typhoid  bacilli  (see  page  22)  is  very  important,  and,  when  it  turns  out  positively, 
decisive.  On  the  other  hand,  of  course,  the  absolute  demonstration  of  miliary 
tuberculosis  in  the  choroid  is  unequivocal  evidence  in  favor  of  miliary  tuber- 
culosis. 

In  many  cases  the  onset  of  meningeal  symptoms  may  aid  the  diagnosis.  Of 
course,  if  the  patient  is  not  seen  until  the  last  stages  of  meningitis,  especially 
when  there  is  an  incomplete  history,  the  diagnosis  is  next  to  impossible.  In  this 
case,  if  the  fluid  obtained  by  lumbar  puncture  is  found  to  contain  tubercle  bacilli, 
the  diagnosis  may  be  settled  (compare  the  chapter  on  tubercular  meningitis). 

Acute  tuberculosis  is  often  confounded  with  severe  bronchitis,  especially  in  old 


266  DISEASES    OF   THE   RESPIRATOEY   ORGAINTS 

persons  wlio  are  considered  emphysematous.  The  very  severe  general  condition, 
the  pallor,  the  rapid  loss  of  strength,  and  the  fever,  are  the  only  things  here  which 
call  our  attention  to  acute  tuberculosis,  and  render  the  diagnosis  possible.  We 
have  already  indicated  the  possibility  of  confusion  at  the  onset  between  miliary 
tuberculosis  and  croupous  pneumonia. 

Of  decisive  diagnostic  value  in  all  cases  is  the  demonstration  of  tubercle 
bacilli  in  the  blood,  which  is  indeed  a  difficult  matter,  but  it  has  already  been  ac- 
complished more  than  once  (Weichselbaum  and  others). 

Prognosis. — The  cases  described  in  literature  as  "  cured  miliary  tuberculosis  " 
are  so  uncertain  in  their  diagnosis  that  they  can  not  be  regarded  as  convincing. 
We  must  therefore  consider  the  prognosis  as  absolutely  fatal.  The  differences  in 
the  course  of  the  disease  have  been  already  mentioned. 

Treatment. — Although  drugs  are  absolutely  powerless,  still  the  case  in  hand 
must  always  receive  treatment,  especially  if  the  diagnosis  can  not  be  made  with 
absolute  certainty.  Our  prescriptions  are  purely  symptomatic.  The  cases  with 
a  typhoidal  course  are  to  be  treated  just  like  typhoid,  with  baths,  stimulants, 
etc.  Tepid  baths,  and  also  local  applications  to  the  chest,  expectorants,  and  nar- 
cotics, are  indicated  when  the  thoracic  symptoms  predominate.  If  meningeal 
symptoms  set  in,  we  may  try  ice,  perhaps  local  blood-letting,  iodoform  salve,  or 
mercurial  ointment  externally,  and  iodide  of  potassium  internally. 


CHAPTER   VIII 
GANGRENE    OF    THE    LUNGS 

.31tiology. — The  sole  cause  of  pulmonary  gangrene — that  is,  the  death  and 
putrid  decomposition  of  the  lung-tissue — is  the  entrance  of  the  bacteria  of  putre- 
faction into  the  lungs.  The  opportunity  for  inhaling  them  is  certainly  very 
great,  but  the  normal  organism  apparently  possesses  the  property  of  nullifying 
them  and  making  them  powerless.  Under  certain  conditions,  however,  they  take 
root  in  the  lung  and  cause  the  death  of  the  pulmonary  parenchyma,  which  then, 
as  a  result  of  the  presence  of  these  specific  bacteria  of  putrefaction,  succumbs  to 
that  peculiar  form  of  putrid  decomposition  known  as  "  moist  gangrene." 

The  factor  which  most  frequently  gives  rise  to  the  development  of  pulmonary 
gangrene  is  the  entrance  of  organic  foreign  substances,  especially  bits  of  food,  into 
the  lungs.  The  bacteria  of  putrefaction  either  enter  the  lungs  with  the  foreign 
substance,  or  they  settle  there  later  and  set  up  a  putrid  decomposition,  first  in  that 
portion  of  the  lungs,  and  then  in  the  neighboring  lung-tissue.  The  entrance  of 
organic  foreign  substances  into  the  lungs  occurs  in  different  ways.  It  often  hap- 
pens from  swallowing  the  wrong  way,  or  from  an  accidental  inhalation.  In  this 
way  pulmonary  gangrene  may  arise  in  previously  healthy  people,  but  it  occurs 
especially  in  patients  who  are  very  low,  very  stupid,  and  soporose,  and  also  in  the 
insane,  in  patients  who  can  not  swallow  or  cough  well,  and  in  patients  with  paral- 
ysis of  deglutition,  as  in  bulbar  paralysis.  Bits  of  food  may  also  reach  the  lungs 
from  eructations  and  vomiting.  Thus  are  explained  the  cases  of  pulmonary  gan- 
grene which  occur  in  patients  with  cancer  of  the  stomach,  and,  still  more  fre- 
quently, with  cancer  of  the  oesophagus.  Putrid  organic  material  may  also  reach 
the  lungs  from  ulcerative  and  ichorous  processes  in  the  mouth,  the  pharynx,  and 
the  larynx.  In  cancer  of  the  tongue,  the  pharynx,  and  the  larynx,  in  other  ulcer- 
ative processes,  and  in  injuries  or  wounds  from  operations  in  the  mouth  and  phar- 
ynx that  have  become  septic,  pulmonary  gangrene  may  develop  quite  readily. 


GAKGEE^^E    OF    THE   LUNGS  267 

Finally,  septic  foci  in  the  vicinity  may  extend  to  the  kings  or  perforate  into  a 
bronchus.  In  this  way  pulmonary  gangrene  may  arise  from  the  perforation 
through  the  pleura  into  the  lungs  of  an  ulcerated  cancer  of  the  stomach  or  a 
gastric  ulcer,  or  in  rare  cases  from  vertebral  caries,  or  from  sanious  lymph-glands. 

In  some  cases  the  cause  of  the  pulmonary  gangrene  can  not  be  made  out,  since 
the  entrance  of  a  foreign  substance  has  perhaps  been  -wholly  unnoticed,  as  may 
happen  in  children,  or  during  sleep.  We  had  a  grown-up  young  woman  under 
observation  for  a  long  time  with  pulmonary  gangrene,  and  one  day  she  coughed 
up  several  fragments  of  chicken-bones,  but  she  could  give  no  account  of  how  they 
entered  the  lungs. 

Experience  teaches  us  that  pulmonary  gangrene  is  more  apt  to  develop  in 
persons  with  impaired  nutrition,  in  old,  marantic  individuals  and  drunkards,  than 
in  those  who  are  healthy.  The  tendency  of  patients  with  diabetes  mellitus  to 
pulmonary  gangrene  is  remarkable. 

Pulmonary  gangrene  often  develops  secondarily  to  some  other  pulmonary 
affection.  We  have  already  spoken  of  the  relations  between  it  and  foetid  bron- 
chitis. Foetid  bronchitis,  on  the  one  hand,  often  leads  to  pulmonary  gangrene 
through  an  extension  of  the  process  to  the  alveoli ;  and,  on  the  other  hand,  when 
there  is  a  gangrenous  focus  in  the  lungs,  the  bronchi  are  often  infected  to  a  wide 
extent  by  the  putrid  secretion  coming  from  it,  and  then  there  arises  foetid  bron- 
chitis. Both  diseases  often  run  into  each  other  without  any  sharp  boundary;  but 
gangrene  may  develop  secondarily  in  other  affections  of  the  lungs.  A  new  infec- 
tion with  putrid  material,  however,  is  always  requisite,  and  the  affection  of  the 
lungs  that  already  exists  furnishes  merely  a  favorable  soil.  This  is  the  only 
explanation  of  the  process  when  croupous  pneumonia  "  runs  into  gangrene,"  or 
when  gangrene  develops  in  catarrhal  pneumonia,  in  bronchiectasis,  or  in  phthisis. 

Although  the  agents  of  putrefaction  enter  the  lungs  through  the  bronchi  in 
most  of  the  modes  of  origin  of  pulmonary  gangrene  that  have  been  mentioned, 
they  may  also  be  transported  into  the  lungs  by  the  blood-current.  We  call  these 
forms  embolic  gangrene.  We  find  such  gangrenous  nodules  in  the  lungs  in 
connection  with  extensive  gangrenous  bed-sores,  puerperal  processes,  suppurative 
caries  of  the  bones,  etc.  In  these  cases  the  putrid  material  enters  a  vein  from  the 
seat  of  the  primary  process  and  is  brought  to  the  lungs,  and  here  we  find,  as  a 
result  of  the  putrid  character  of  the  embolus,  not  a  simple  infarction,  but  an 
embolic  gangrene. 

Pathological  Anatomy. — We  more  frequently  find  pulmonary  gangrene  in  the 
lower  lobes  than  in  the  upper,  corresponding  to  its  mode  of  origin.  Either  both 
lungs  are  affected  or  only  one,  and  the  right  somewhat  more  freqiiently  than  the 
left.  We  distinguish  a  diffuse  and  a  circumscribed  form,  according  to  the  extent 
of  the  gangrene.  Embolic  gangrene  belongs  to  the  latter  form,  and  its  nodules, 
by  preference,  lie  near  the  pleural  surface. 

We  can  easily  recognize  the  anatomical  changes  in  gangrene.  The  lung-tissue 
is  changed  to  a  discolored,  dirty,  greenish-gray  mass,  Avhich  gradually  and  pro- 
gressively becomes  dissolved,  forming  a  most  foul-smelliug  ichor.  We  find,  left 
in  it,  necrotic  fragments  of  tissue  and  vessels.  Gangrene  cavities,  with  irregular, 
ragged  walls,  are  formed  from  the  partial  expectoration  of  the  softened  gangre- 
nous nodule.  The  lung-tissue  in  the  vicinity  of  the  gangrenous  spot  is  to  a  greater 
or  less  extent  inflamed,  partly  in  the  form  of  catarrhal  pneumonia,  partly  in  the 
form  of  circumscribed  croupous  pneumonia.  The  inflamed  parts  in  the  vicinity 
are  gradually  involved  in  the  gangrene,  so  long  as  the  process  extends,  but  finally 
a  suppurating  line  of  demarkation  may  be  formed  about  the  gangrene,  the  whole 
gangrenous  fragment  is  in  a  measure  sequesti-ated,  encapsuled,  and  gradually 
expelled,  and  so  healing  becomes  possible.  We  have  already  stated  that  fcctid 
bronchitis  may  arise  from  a  gangrenous  nodule. 


268  DISEASES    OF   THE   RESPIEATOET   OEGANS 

Whenever  a  gangrenous  nodule  reaches  the  pleura,  a  purulent  and  usually  a 
sanious  pleurisy  follows  from  direct  infection.  Pneumothorax  may  arise  from 
perforation  of  a  gangrenous  cavity. 

Clinical  History. — The  symptoms  of  gangrene  depend  for  the  most  part  upon 
the  local  affection  in  the  lung.  The  condition  of  the  expectoration  is  characteris- 
tic, and  it  alone  may  decide  the  diagnosis. 

In  many  ways  the  expectoration  greatly  resembles  that  of  foetid  bronchitis, 
and  indeed  a  great  part  of  it  does  not  come  directly  from  the  gangrenous  nodule, 
but  is  the  secretion  of  the  diseased  bronchi.  The  penetrating  stench  of  the 
sputum,  a  most  repulsive,  putrid  odor,  is  very  striking.  The  patient's  breath 
and  cough  also  have  this  stench,  which  infects  the  whole  vicinity.  The  amount 
of  the  sputum  is  usually  large;  it  may  reach  ten  or  twenty  ounces  (200-500  cubic 
centimetres)  in  twenty-four  hours.  If  the  sputum  is  collected  in  a  glass  it  forms 
three  layers,  like  the  sputum  of  foetid  bronchitis — an  upper  layer,  muco-purulent, 
greasy,  consisting  in  part  of  nummular  sputa,  and  covered  with  much  froth;  a 
middle  serous  layer,  in  which  some  firm  masses  from  the  upper  layer  float;  and 
a  lower  layer,  almost  wholly  of  pus,  but  greasy  and  greenish-yellow,  which  usually 
contains  many  large  and  small  plugs  and  shreds  of  tissue.  We  find  in  these 
plugs,  on  microscopic  examination,  beautifully  twisted  needles  of  the  fat  acids 
(see  Fig.  24,  page  168)  imbedded  in  countless  bacteria,  fat-drops,  and  detritus, 
and  often  collected  in  large  bundles ;  but  besides  these  we  find  in  the  sputum  the 
constituents  of  the  parenchyma  of  the  lungs,  and  this  alone  is  the  decisive  factor 
in  distinguishing  between  pulmonary  gangrene  and  simple  foetid  bronchitis. 

Traube's  statement  that  in  pulmonary  gangrene  the  expectoration  contains 
few,  if  any,  elastic  fibers,  because  the  elastic  tissue  itself  is  destroyed  by  gan- 
grene, is  not  correct ;  or,  at  any  rate,  it  is  too  sweeping.  We  have  almost  invariably 
found  in  the  expectoration  an  abundance  of  elastic  tissue,  as  well  as  other  frag- 
ments of  the  parenchyma,  pigment  granules,  and  the  like.  Yet  there  is  a  prob- 
ability, no  doubt,  that  in  pulmonary  gangrene  the  elastic  tissue  is  for  the  most 
part  destroyed.  Filehne  succeeded  in  extracting  from  the  sputum  of  pulmonary 
gangrene,  by  means  of  glycerine,  a  ferment  which  in  alkaline  solution  completely 
dissolved  elastic  tissue  in  a  few  days.  The  sputum  always  contains  in  enormous 
numbers  bacteria  of  various  kinds,  both  cocci  and  bacilli.  Which  of  these  are 
the  special  cause  of  the  gangrene  has  not  yet  been  definitely  settled.  The  chem- 
ical examination  of  the  sputum  shows  the  presence  of  those  substances  which  may 
always  be  found  in  the  putrefaction  of  organic  matter — tyrosine,  leucine,  am- 
monia, sulphuretted  hydrogen,  butyric  acid,  valerianic  acid,  caprylic  acid,  etc. 
The  fresh  sputum  usually  has  an  alkaline  reaction,  but  on  standing  it  becomes 
acid. 

Many  cases  of  gangrene  lead  to  erosion  of  the  vessels  and  severe  haemoptysis. 
Slight  admixtures  of  blood  in  the  sputum  are  not  infrequent. 

The  other  symptoms  on  the  part  of  the  lungs  are  not  especially  characteristic 
of  gangrene.  Most  patients  complain  of  cough,  pain  in  the  side,  and  more  or  less 
severe  dyspnoea.  Physical  examination,  as  a  rule,  permits  us  to  make  out  the  seat 
of  the  nodule,  but  not  always,  since  the  physical  signs,  of  course,  depend  upon  the 
situation  and  extent  of  the  gangrene.  Small  nodules,  situated  centrally,  often 
give  no  objective  evidence  of  their  presence.  Every  extensive  infiltration,  how- 
ever, must  cause  dullness  on  percussion.  Over  the  area  of  dullness  we  hear  bron- 
chial respiration,  and  usually  quite  numerous  moist  rales.  If  a  gangrenous  cavity 
is  formed,  the  physical  examination  may  show  plain  symptoms  of  a  cavity — tym- 
panitic resonance  on  percussion,  amphoric  respiration,  coarse  moist  rales,  etc. 

The  physical  signs  are  sometimes  due  to  the  accompanying  pleurisy ;  the  dull- 
ness is  more  complete,  the  respiratory  murmur  and  the  vocal  fremitus  are  dimin- 
ished, and  the  adjacent  organs  are  displaced  by  the  abundant  effusion;  but  an 


GAK"GKENE   OF   THE   LUNGS  269 

absolute  diagnosis  of  an  accompanying  pleurisy  is  often  to  be  made  only  by  an 
exploratory  puncture.  We  have  already  spoken  of  the  occasional  development 
of  pneumothorax. 

In  many  cases  there  is  fever,  of  quite  an  irregular  character  and  of  very  vary- 
ing intensity.  In  the  cases  in  which  the  gangrenous  nodule  is  sequestrated,  and 
the  secretion  can  be  freely  emptied  through  the  bronchi,  so  that  there  is  no  ab- 
sorption of  septic  material  into  the  blood,  fever  may  be  entirely  absent. 

We  often  see  gastric  and  intestinal  symptoms  injpulmonary  gangrene,  the  dis- 
turbance being  without  doubt  due  to  swallowing  some  of  the  foetid  sputum.  Many 
patients  complain  of  loss  of  appetite,  and  sometimes  of  vomiting  or  diarrhoea. 
In  severe  acute  cases  there  is  sometimes  a  well-marked  typhoidal  state,  with  such 
symptoms  as  stupor,  delirium,  and  great  cardiac  weakness.  This  condition  is 
probably  caused  by  the  absorption  of  septic  material  into  the  blood.  Rheumatic 
pains  in  the  muscles  and  joints  are  seen  in  this  disease,  just  as  in  foetid  bronchitis. 
Finally,  it  should  be  remarked  that  the  appearance  of  secondary  abscesses  in  the 
brain  (see  page  1107)  has  been  repeatedly  observed  in  pulmonary  gangrene.  This 
fact  must  be  borne  in  mind  when,  in  the  course  of  pulmonary  gangrene,  marked 
brain  symptoms  are  developed,  especially  if  we  have  not  only  such  general  symp- 
toms as  coma,  but  also  such  local  symptoms  as  hemplegia  and  other  forms  of 
paralysis,  and  convulsions. 

The  general  course  of  the  disease  shows  very  great  variations.  In  all  cases 
in  which  the  pulmonary  gangrene  is  secondary  to  some  other  affection,  the  course 
and  the  general  type  of  the  disease  depend  very  largely  upon  the  primary  attack, 
but  the  cases  of  idiopathic  gangrene  also  present  great  variations.  The  onset  is 
either  quite  gradual  and  slow,  or  quite  acute,  and  associated  with  fever  and  tho- 
racic symptoms.  The  stinking  expectoration  and  the  bad  odor  from  the  patient's 
mouth  first  direct  the  attention  to  the  existence  of  putrid  processes  in  the  lungs. 
The  disease  is  usually  very  chronic,  lasting  for  months  or  even  years.  Many 
remissions  and  intermissions  occur.  With  proper  care  and  treatment  we  may  see 
a  decided  improvement,  and  often  apparently  a  complete  cessation  of  the  disease. 
The  bad  odor  ceases,  the  expectoration  diminishes  or  disappears  entirely,  and  the 
patient's  strength  and  nutrition  become  almost  normal;  but  relapses  may  occur 
after  long  intervals.  When  the  affection  is  of  slight  extent  we  may  even  see  a 
complete  recovery. 

Pulmonary  gangrene  always  takes  a  worse  course  in  previously  weak  and 
marantic  persons,  and  an  unfavorable  termination  may  follow  in  a  comparatively 
short  time.  Death  ensues  either  from  a  general  loss  of  strength,  as  a  result  of  the 
disease,  or  from  complications,  such  as  pulmonary  haemorrhage,  ichorous  pleurisy, 
pneumothorax,  or  abscess  of  the  brain.  Rupture  of  an  ichorous  empyema  out- 
wardly, or  into  the  peritoneum,  or  into  other  cavities,  is  i*are. 

Special  mention  must  be  made  of  the  fact  that  the  symptoms  of  pulmonary 
gangrene  are  not  always  so  very  pronounced.  In  persons  who  are  weak  and  run 
down  we  often  see  pulmonary  gangrene  at  the  autopsy,  although  during  life  there 
have  been  no  marked  symptoms,  not  even  offensive  sputum  or  foetor  from  the 
mouth. 

Diagnosis. — The  diagnosis  can  not  be  made  with  certainty  unless  the  charac- 
teristic sputum  is  present.  We  can  decide  whether  the  sputum  comes  from  a 
foetid  bronchitis  or  from  the  foetid  contents  of  a  bronchiectasis,  or  from  actual 
gangrene,  only  by  finding  under  the  microscope  the  remains  of  lung-tissue  in  the 
expectoration.  Physical  examination  in  gangrene,  at  least  in  part  of  the  cases, 
also  gives  the  signs  of  infiltration  or  of  cavity-formation  in  the  lungs. 

Prognosis. — The  prognosis  depends  first  upon  the  nature  of  the  underlying 
disease,  and  then  upon  the  extent  of  the  affection,  the  strength  of  the  patient,  and 
the  possibility  of  sufficient  care  and  proper  treatment.     If  the  process  in  the  lung 


270  DISEASES    OF   THE   EESPIEATOKY   OEGAI^S 

becomes  sequestrated,  marked  improvement  may  follow,  even  in  tlie  severest  con- 
ditions; but  we  must  always  remember  that  a  relapse  is  possible.  Complete  re- 
covery from  pulmonary  gangrene  is  certainly  extremely  rare,  if  it  ever  occurs. 
We  have  already  mentioned  the  dangers  which  may  cause  a  fatal  termination  in 
pulmonary  gangrene. 

Treatment.- — Prophylaxis  plays  an  important  part  in  those  cases  in  which 
there  is  danger  of  the  entrance  of  bits  of  food  into  the  air-passages  from  de- 
fective deglutition.  We  must  think  of  the  possibility  of  this  with  all  patients 
who  show  great  stupor,  and  also  with  patients  who  have  pharyngeal  paralysis,  in 
order  to  watch  them  while  taking  food,  and  eventually  to  try  artificial  feeding 
with  the  oesophageal  tube. 

The  treatment  of  already  existing  pulmonary  gangrene  has,  as  its  chief  aim,  to 
check  the  putrid  processes  of  decomposition  in  the  lungs.  Unfortunately,  the 
remedies  at  our  colnmand  are  not  in  all  cases  sufficient  for  this.  The  different 
disinfecting  inhalations  are  the  most  effective.  They  are  used  in  the  same  way  as 
in  foetid  bronchitis  (vide  supra).  Turpentine  deserves  the  most  confidence,  and 
it  may  also  be  given  internally  with  good  results.  According  to  Lepine,  however, 
terpine  acts  even  better  than  turpentine.  We  may  also  call  attention  to  inhala- 
tions with  carbolic  acid,  Curschmann's  carbolic  mask,  inhalations  with  salicylic 
and  boraeic  acids  (4  parts  of  salicylic  and  20  of  boracic  acid  to  1,200  of  distilled 
water),  bromine  (bromine  and  bromide  of  potassium,  2  parts  of  each  to  1,000  of 
water),  and  similar  substances. 

Besides  oil  of  turpentine,  other  internal  remedies  are  recommended:  half  a 
grain  to  a  grain  (gramme  0.03-0.06)  of  acetate  of  lead  every  two  hours,  creasote, 
carbolic  acid,  etc.  Their  action  is  uncertain.  Of  late,  myrtol  has  been  greatly 
extolled.  It  is  given  in  capsules  containing  gr.  ijss.  (grm,  0.15),  of  which  two  or 
three  are  to  be  taken  every  two  hours. 

The  general  treatment  of  the  patient  is  very  important — he  should  have  good 
food,  and  live  in  as  good  air  as  possible.  We  must  treat  the  pain  in  the  chest  and 
the  cough  symptomatic  ally,  local  applications  and  morphine  being  most  useful. 
The  fever  seldom  gives  occasion  for  direct  interference.  We  may  try  to  relieve 
the  g'astric  and  intestinal  symptoms  by  giving  antiseptics  internally,  especially 
by  small  doses  of  muriatic  acid,  salicylic  acid,  or  creasote,  as  well  as  by  the  ordi- 
nary remedies,  such  as  bitters  and  opium. 

If  a  secondary  ichorous  pleurisy  develops,  with  or  without  pneumothorax, 
removal  of  the  fluid  by  operation  is  necessary,  if  the  patient  has  sufficient  strength 
to  bear  it. 

In  some  few  cases  trial  has  been  made  of  opening  up  the  foci  of  gangrene  by 
surgical  means.  As  yet,  it  must  be  confessed,  the  results  have  not  been  very 
encouraging. 


CHAPTEE   IX 

DISEASES    FROM    THE    INHALATION    OF    DUST 

(P/ie^mwnoconiosis) 

Although  there  are  a  number  of  important  contrivances  in  the  respiratory 
apparatus  to  prevent  the  entrance  of  foreign  substances  into  the  lungs,  still,  if  a 
person  remains  in  a  dusty  atmosphere,  so  many  particles  of  dust  may  be  inhaled 
that  they  are  not  without  effect  on  the  lung-tissue.  The  diseases  arising  from 
the  inhalation  of  dust  are  usually  purely  professional  diseases,  which  occur  espe- 
cially in  workmen  whose  occupation  involves  the  continual  inhalation  of  some 


DISEASES   FROM   THE   I^TIALATIOIT   OF   DUST  271 

kind  of  dust.  In  earlier  chapters  of  this  book,  particularly  while  considering 
chronic  bronchitis,  we  have  already  emphasized  the  harmful  influence  of  the 
inhalation  of  dust.  We  have  seen  how  the  habitual  respiration  of  organic  dust 
in  particular  (from  grain,  wool,  wood,  and  tobacco)  is  very  apt  to  lead  to  severe 
forms  of  bronchitis  and  bronchiolitis.  We  must  now  draw  attention  to  certain 
specific  diseases  similarly  caused. 

We  must  first  mention,  however,  a  condition  of  the  lungs  which  can  scarcely 
be  regarded  as  pathological,  although  it  has  its  origin  in  the  constant  inhalation 
of  dust,  especially  of  coal-dust — the  ordinary  black  pigmentation  of  the  lungs. 
There  can  now  no  longer  be  any  doubt,  although  there  was  once  a  long  dispute 
about  it,  that  the  black  pigment  in  the  lung  comes,  in  large  part  at  least,  from  the 
inhalation  of  carbon.  The  particles  of  carbon  pass  into  the  lungs  themselves,  and 
thence  into  the  bronchial  glands  by  means  of  the  lymphatics.  A  certain  part  of 
the  coal-dust  inhaled  is  removed  with  the  expectoration,  and  it  may  easily  be 
found  in  it  microscopically,  and  often  by  the  naked  eye,  as  we  see  it  in  the  well- 
known  black  expectoration  which  we  often  have  in  the  morning,  if  we  have  spent 
the  previous  evening  in  a  room  filled  with  smoke.  In  Germany,  Traube  was  the 
first  to  discover  the  particles  of  carbon  in  the  expectoration  of  a  charcoal-burner. 
In     the     man's     lungs,     aftei 

death,  the  vegetable  origin  of  •'^'^'?^^   "'.";.-7i^9% 

these   particles   could   be   rec-  ^.,/    ^-,3^ 

ognized,  and  Traube  gave  the  ,■-■■'•:;-'"  .,  • 

.  ■■■'''■.  jf 

correct    exi^lanation    of    them.  -if^^^^f       *^       ■^•r  ' 

In  workmen  who  inhale  large  *^^^v,  f^  '     ~  m'    ' 

amounts  of  charcoal-dust,  an-  ^    '  ''■'•''   ;/*-;;,           .r' 

thracite     coal-dust,     soot,     or  v^-.                /^"~ '^  '#/     "^ 

graphite,    the    "normal"    pig-  v,!"     *«»::         ■              '_^  . 

mentation  of  the  lung  passes  '*?'!              ^      4-""-' 

into     a     pathological     condi-  -l::*;:.--              .■^^£_,. 

tion,      anihracosis     pulmonum.        Fig.  35.— Expectoration  of  a  man  who  worked  on  graphite. 

With  this  is  usually  associated  meS  clinfqlfe.f '"'^  '"'^  ^^''"''^'' '''  ""■^°°'   ^^'■^^°^^° 

an     extensive     chronic     bron- 
chitis.    In  the  expectoration  of  such  patients  are  found  many  cells,  filled  with 
black  particles  of  coal,  even  long  after  they  have  left  the  dusty  atmosphere.    The 
pigmented  cells  are  leucocytes,  or  perhaps  some  of  them  epithelial  cells   (see 
Fig.  35). 

Zenker  first  discussed  comprehensively  the  fact  of  the  entrance  of  the  different 
sorts  of  dust  into  the  lungs  and  the  consequent  results.  Besides  the  anthracosis 
already  mentioned,  the  pulmonary  disease  from  inhaling  the  dust  of  flint  and 
other  stones  is  of  especial  importance,  the  so-called  stone-cutter's  lung — chaUcosis 
pulmonum — and  also  that  from  inhaling  metallic  dust,  especially  oxide  of  iron — 
siderosis  pulmonum.  The  "  stone-lungs  "  have  been  observed  in  workmen  in  the 
stamping-rooms  of  glass-factories,  in  mill-stone  cutters,  stone-polishers,  stone- 
hammerers,  plasterers,  workers  in  porcelain,  masons,  slate-quarrymen,  potters, 
etc.  "  Metal-dust  lungs  "  occur  in  file-cutters,  iron-workers,  mirror-polishers,  and 
especially  in  grinders,  who  inhale  a  mixture  of  stone-  and  iron-dust.  The  first 
case  of  a  "  red  iron  lung  "  was  observed  by  Zenker,  in  a  girl  who  had  inhaled  a 
thick  dust  of  iron  for  ten  or  twelve  hours  a  day.  Her  work  was  to  color  blotting- 
paper  with  a  powder  of  red  oxide  of  iron.  During  the  inhalation  of  all  these 
and  similar  kinds  of  dust,  a  portion  of  the  inspired  particles  of  dust  are  taken 
up  by  the  leucocytes,  and  perhaps  also  by  the  epithelial  cells,  finally  reaching  the 
lymph-channels  of  the  lungs.  Some  of  the  particles  of  dust  remain  in  the  inter- 
stitial connective  tissue  of  the  lungs.  Others  find  their  way  to  the  bronchial  and 
retro-bronchial  lymph- glands. 


2Y2  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

If  the  inlialation  of  dust  is  long  continued,  it  causes  not  only  this  abnormal 
pigmentation  of  the  lungs,  but  also  macroscopic  auatomieal  lesions.  These  con- 
sist, partly,  in  a  more  or  less  severe  and  extensive  chronic  bronchitis,  and  partly 
in  an  interstitial  inflammation  which  is  due  to  the  chronic  irritation  of  the  for- 
eign matter  (e.g.,  flinty  particles),  and  leads  to  the  formation  of  connective 
tissue.  The  lungs  are  studded  with  nodules,  which  feel  hard  to  the  touch,  and 
grate  on  section  with  a  knife.  All  of  these  nodules  consist  of  firm  connective 
tissue,  in  which  the  particles  of  stone  or  iron  are  encapsuled.  By  the  union 
of  single  nodules  we  may  get  more  extensive  induration  and  cicatricial  forma- 
tion. Chemical  examination  of  such  lungs  gives,  as  might  be  supposed,  a  large 
amount  of  silicic  acid,  iron,  etc. 

In  most  of  the  cases  which  come  to  autopsy  we  find  further  changes  in  the 
lungs,  which  are  not  the  immediate  result  of  the  inhalation  of  dust,  but  consist  of 
sequelae  and  complications.  Chronic  diffuse  bronchitis  in  the  worker  in  dust, 
like  any  other  chronic  bronchitis,  may  give  rise  to  pulmonary  emphysema,  and 
later  to  cardiac  hypertrophy,  etc.  We  very  often  find  in  the  lungs  co-existing 
and  pronounced  tubercular  changes.  It  need  hardly  be  emphasized  that  these 
changes  are  not  the  direct  result  of  the  inhalation  of  dust,  but  that  the  changes  in 
the  lungs  set  up  by  such  an  inhalation  furnish  merely  a  favorable  soil  for  infec- 
tion with  tuberculosis.  In  most  cases,  the  "  dust-lungs  "  acquire  a  marked  clinical 
significance  chiefly  from  the  sequelae  mentioned — namely,  emphysema  and  tuber- 
culosis. The  circumscribed  nodules  of  interstitial  pneumonia  have  no  very 
marked  symptoms  following  them.  In  all  cases  in  which  there  is  a  fatal  termina- 
tion, with  pulmonary  symptoms,  we  should  regard  the  immediate  action  of  the 
dust  as  much  less  the  cause  of  death  than  are  the  secondary  diseases. 

The  actual  points  to  be  considered  in  judging  of  the  clinical  symptoms  of  the 
diseases  from  inhaling  dust  are  contained  in  what  has  been  said.  The  symptoms 
are  those  of  chronic  bronchitis,  pulmonary  emphysema,  or  chronic  phthisis, 
and  attention  to  the  injurious  influences  associated  with  the  patient's  calling  is 
the  only  possible  way  of  making  a  diagnosis,  but  in  individual  cases  it  may  always 
be  a  matter  of  doubt  how  far  other  accidental  causes  of  disease  may  come  into 
play. 

The  prognosis  depends,  in  the  first  place,  upon  whether  the  patient  can  be 
removed  from  the  action  of  these  injurious  influences  or  not,  but  we  must  also 
mention  the  fact,  which  has  been  often  observed,  that  many  individuals  get  some- 
what used  to  the  dust.  After  they  have  once  recovered  from  the  initial  bi'on- 
chitis,  such  persons  can  live  in  an  atmosphere  of  dust  for  a  long  time  without 
any  noticeable  injury. 

The  prophylaxis  of  diseases  from  inhaling  dust  forms  an  extended  chapter  in 
the  hygiene  of  occupations,  which  we  can  not  dwell  upon  here.  The  workman 
must  be  taught  the  danger  to  which  he  is  exposed,  and  the  danger  itself  must  be 
diminished  as  much  as  possible  by  sufficient  ventilation  of  the  work-rooms,  by 
cleanliness,  and,  under  some  circumstances,  by  a  change  in  the  teclniicalities  of 
the  business. 

We  need  not  give  any  special  directions  regarding  the  treatment  of  diseases 
from  inhaling  dust.  It  is  founded  on  the  same  principles  as  the  treatment  of 
chronic  bronchitis,  emphysema,  and  chronic  pulmonary  tuberculosis. 


EMBOLIC   PEOCESSES   IN   THE   LUNGS 


CHAPTER   X 

EMBOLIC    PROCESSES    IN    THE    LUNGS 

(IltemorrJiai/ic  I/tfarctio7t  of  the  Lvngn) 

Etiology. — The  sources  from  which  the  material  for  an  embolic  plugging  of 
branches  of  the  pulmonary  artery  comes  lie  either  in  the  right  side  of  the  heart  or 
in  the  veins  of  the  body.  Pathological  anatomj^  teaches  us  how  often  thrombi  are 
formed  in  the  veins,  especially  in  the  veins  of  the  lower  extremities  and  in  the 
pelvic  veins,  and  in  the  right  side  of  the  heart,  in  the  recesses  between  the  tra- 
beculse,  in  the  auricles,  on  the  valves  and  the  chordse  tendinge,  and  at  the  apex  of 
the  ventricle.  The  particles,  torn  loose  from  thrombi  so  situated,  are  carried  on 
by  the  blood-current,  reach  the  lungs,  plug  a  larger  or  a  smaller  branch  of  the 
pulmonary  artery,  according  to  the  size  of  the  particles,  and  thus  cause  further 
changes  in  the  lung-tissue.  Since  the  branches  of  the  pulmonary  artery  are  "  ter- 
minal arteries,"  and  since  thus  the  vascular  territory  belonging  to  each  branch 
can  not  be  supplied,  or  can  be  supplied  only  to  a  small  amount,  with  blood  by 
collateral  circulation  from  other  vessels,  the  closure  of  a  branch  of  the  artery 
shuts  the  territory  supplied  by  it  out  of  the  circulation.  The  pressure,  in  the  part 
of  the  vessel  lying  peripherally  to  the  point  of  plugging,  becomes  almost  nil,  and, 
as  a  result,  there  is  a  collateral  or  backward  current  into  the  region  shut  off,  flow- 
ing from  the  capillaries  in  the  vicinity,  and  probably  even  from  the  veins  belong- 
ing to  it.  Yet  the  blood  which  flows  in  is  under  so  slight  a  pressure  that  it  does 
not  flow  throiigh,  but  stagnates  in  the  affected  area.  The  walls  of  the  capillaries 
and  veins,  in  which  the  normal  blood-current  has  ceased,  lose  their  natural  con- 
sistency as  a  result  of  this.  The  vascular  walls  become  abnormally  pervious. 
The  fluid  of  the  blood,  the  white  blood-corpuscles,  and  also  very  many  red  blood- 
corpuscles,  penetrate  through  the  walls  of  the  vessel  into  the  surrounding  tissue, 
and  change  it  into  the  so-called  hsemorrhagic  infarction. 

Every  embolic  closure  of  a  branch  of  the  pulmonary  artery  does  not  necessarily 
result  in  the  formation  of  an  infarction.  Upon  the  sudden  plugging  of  a  main 
trunk,  or  of  several  large  branches  of  the  pulmonary  artery,  death  may  ensue  at 
once,  so  that  naturally  all  further  changes  in  the  lung-tissue  cease.  We  also  find 
quite  frequently,  especially  in  central  portions  of  the  lung,  embolism  of  single 
branches  of  the  pulmonary  artery  without  the  formation  of  an  infarction.  In 
such  cases  there  must  necessarily  be  a  little  circulation  in  the  vascular  territory 
which  has  been  shut  off,  either  by  anastomoses  between  the  territory  of  the  pul- 
monary artery  and  that  of  the  bronchial  or  mediastinal  artery,  or  by  the  neigh- 
boring capillaries,  whose  arteries  of  supply  remain  open. 

The  changes  thus  far  described  are  the  result  of  a  purely  mechanical  closure  of 
a  pulmonary  artery.  We  have  noticed  this  especially  when  simple  fibrinous 
plugs  have  given  the  occasion  for  the  embolic  process.  Pulmonary  infarctions 
are  most  frequent  in  chronic  heart  disease,  in  all  forms  of  primary  and  secondary 
dilatation  of  the  heart,  but  especially  in  disease  of  the  mitral  orifice,  most  oftel^ 
mitral  stenosis.  Thrombus  formation  is  frequent  in  the  dilated  right  side  of  the 
heart,  and  furnishes  material  for  pulmonary  emboli ;  but  these  emboli  are  seen  in 
all  other  possible  conditions  of  disease,  in  which  thrombosis  in  the  right  side  of 
the  heart  or  in  the  veins  may  occur. 

The  changes  in  the  lungs  assume  quite  a  different  appearance  if  the  embolic 
material  is  not  simple  fibrine,  but  if  it  contains  at  the  same  time  some  specific 
infectious  matter.  If  emboli  reach  the  lungs  from  an  acute  malignant  endocar- 
ditis in  the  right  side  of  the  heart,  or,  as  is  most  frequently  the  case,  from  a  puru- 
lent (septic)  phlebitis  anywhere  in  the  body,  giving  rise  to  a  puriform,  liquefying 
18 


274  DISEASES    OF   THE   EESPIEATOET   OEGAE"S 

thrombus,  the  specific  factors  in  inflartmiation — that  is,  bacteria — get  into  the 
lungs.  Thus  arise  embolic  abscesses  and  embolic  gangrenous  nodules  in  the  lungs. 
We  have  already  spoken  of  the  latter,  and  the  former  are  among  the  most  constant 
lesions  in  every  typical  case  of  pyaemia. 

The  fundamental  facts  as  to  the  occurrence  and  significance  of  embolic  pro- 
cesses in  general,  and  those  located  in  the  lungs  in  particular,  were  discovered  by 
Virchow.  Eor  a  fuller  understanding  of  the  results  of  embolic  closure  of  the 
vessels  ve  must  thank  chiefly  Cohnheim. 

Pathological  Anatomy. — ^Hgemorrhagic  infarctions  may  involve  one  or  more 
lobules,  or  almost  a  vhole  lobe  of  the  lung,  according  to  the  situation  of  the 
embolus.  Most  infarctions  are  situated  at  the  periphery  of  the  lung,  and  have 
approximately  a  conical  shape,  corresponding  to  the  extent  of  the  region  of  the 
vessel.  The  base  of  the  cone  lies  against  the  surface  of  the  pleura.  It  generally 
projects  a  little  above  that  surface,  and  its  dark  color  can  usually  be  plainly  rec- 
ognized through  it.  The  pleura  itself  is  the  seat  of  a  fibrinous  inflammation  at 
the  point  to  which  the  infarction  reaches,  and  sometimes  for  a  large  space  around 
it.  The  conical  shape  of  the  infarction  is  plainly  recognized  on  section.  The 
lung-tissue  is  changed  to  a  firm,  fragile,  uniformly  black-red  tissue,  devoid  of  air. 
The  embolus  can  usually  be  readily  found  in  the  branch  of  the  pulmonary  artery 
leading  to  the  infarction.  Under  the  microscope  we  see  a  diffuse  infiltration  of 
tissue,  with  red  blood-corpuscles  in  the  infarcted  portion.  The  alveoli  and  finer 
bronchi  are  also  filled  with  coagulated  blood.  Under  favorable  circumstances,  in 
cases  of  longer  standing,  the  blood  may  be  reabsorbed  in  part ;  so  that  the  lung 
again  contains  air,  but  it  remains  much  pigmented  in  that  place,  and  more  or 
less  indurated  from  the  development  of  interstitial  connective  tissue.  In  excep- 
tional cases  there  is  complete  destruction  of  the  pulmonary  tissue  where  the  in- 
farction is  situated.  This  brcken-do^wn  material  is  either  discharged  or  absorbed ; 
then  cicatrization  with  contraction  takes  place. 

Hsemorrhagic  infarctions  are  usually  situated  in  the  lower  lobes,  and  more 
frequently  on  the  right  side  than  on  the  left. 

The  smaller  embolic  abscesses  are  sometimes  very  numerous,  and  are  dissemi- 
nated over  the  whole  lung.  In  larger  abscesses  the  conical  shape  may  often  be 
plainly  recognized.  When  an  abscess  extends  to  the  pleura,  a  purulent  pleurisy 
arises  from  direct  infection.  Combinations  and  transitional  forms  between  the 
ordinary  heemorrhagic  infarction  and  embolic  abscesses  are  occasionally  found  in 
the  lungs. 

Symptoms. — We  often  find  at  the  autopsy  embolism  of  single  branches  of  the 
pulmonary  artery,  with  or  without  infarction,  which  has  caused  no  symptoms  at 
all  during  life. 

Embolism  of  the  main  trunk,  or  of  a  large  branch  of  the  pulmonary  artery, 
may  cause  sudden  death,  as  has  been  repeatedly  observed  in  patients  with  heart 
disease,  or  with  venous  thrombosis.  If  death  be  not  immediate,  sudden  severe 
dyspnoea  and  oppression  arise.  The  diagnosis  may  at  least  be  suspected  in  such  a 
case  if  we  know  of  a  possible  source  for  an  embolus.  In  some  instances,  when  an 
embolus  is  situated  in  a  large  branch  of  the  pulmonary  artery,  but  has  not  com- 
pletely filled  it,  we  can  hear  a  systolic  vascular  murmur  over  the  affected  spot,  as 
has  been  observed  by  Litten.  The  diagnosis,  however,  becomes  certain  if  the 
further  signs  of  infarction  appear  later. 

The  most  characteristic  symptom  of  infarction  in  the  lungs  is  the  bloody 
expectoration.  If  we  see  quite  suddenly  bloody  sputum  in  a  patient  with  mitral 
stenosis,  we  are  usually  right  in  assuming  a  hsemorrhagic  infarction  of  the  lung. 
Either  the  sputum  consists  almost  entirely  of  dark  blood,  or  the  blood  is  mixed 
with  more  or  less  mucus;  but  there  is  never  much  air  in  it.  The  bloody  expecto- 
ration often  lasts  for  several  days. 


BROWN   INDUEATION   OE    THE   LUKGS  275 

We  try  to  learn  more  of  the  size  and  situation  of  the  lesion  by  a  physical  ex- 
amination of  the  lungs.  Of  course  this  often  gives  a  negative,  or  at  least  a  doubt- 
ful, result.  It  goes  without  saying  that  small  infarctions,  and  also  those  which 
are  central,  can  not  be  made  out  by  physical  examination.  Large  peripheral 
infarctions  may  give  rise  in  many  cases  to  dullness  on  percussion,  crepitant  rales, 
and  harsh  or  bronchial  respiration,  but  it  is  often  hard  to  decide  in  an  individual 
case  whether  the  physical  signs  which  we  meet  with  are  not  due  to  other  patho- 
logical changes  in  the  lungs,  such  as  bronchitis  or  hydrothorax.  We  sometimes 
hear  a  pleuritic  friction-sound  in  some  part  of  the  chest  a  few  days  after  we  sus- 
pect that  an  infarction  has  occurred,  by  which  the  diagnosis  gains  additional  cer- 
tainty. We  have  already  mentioned  the  subjective  symptoms  in  embolism  of  a 
large  pulmonary  vessel — sudden  dyspnoea  and  oppression.  Small  nodules  often 
cause  no  special  symptoms,  but  in  other  cases  the  patient  feels  a  severe  pleuritic 
pain,  due  to  irritation  of  the  pleura. 

Eever  may  be  wholly  absent,  though  we  sometimes  see  a  moderate  rise  of  tem- 
perature at  the  onset. 

The  embolic  abscesses  in  the  lungs  hardly  ever  give  rise  directly  to  clinical 
symptoms.  They  form  a  part  of  the  general  picture  of  pyaemia  and  similar  gen- 
eral infectious  processes.  Marked  symptoms  on  the  part  of  the  respiratory  appa- 
ratus are  seen  only  when  the  abscesses  are  present  in  very  large  number.  If  an 
empyema  develops  from  a  focus  which  extends  to  the  pleura,  it  sometimes  occa- 
sions definite  physical  signs. 

It  follows  from  all  that  has  been  said,  that  in  the  diagnosis  of  embolic  pro- 
cesses the  chief  stress  must  always  be  laid  on  the  presence  of  an  ^etiological 
factor.  We  must  regard  the  bloody  sputum  as  the  main  direct  symptom  in 
hsemorhagic  infarction.  Embolic  abscesses  in  the  lungs  may  often  be  suspected 
in  pysemic  diseases,  but  they  can  hardly  ever  be  diagnosticated  with  certainty. 

The  prognosis  is  entirely  dependent  upon  the  underlying  disease.  In  heart 
disease  the  occurrence  of  a  hsemorrhagic  infarction  is  usually  on  the  whole  an 
unfavorable  sign,  since  it  points  to  weakness  of  the  right  ventricle,  and  hence  to 
the  formation  of  a  thrombus  in  it ;  yet  it  often  happens  that  the  symptoms  of  a 
pulmonary  infarction  may  pass  away  entirely. 

We  need  not  give  special  directions  for  treatment.  It  is  in  part  purely  symp- 
tomatic, and  in  part  coincident  with  treatment  of  the  underlying  affection.  As 
regards  prophylaxis,  we  must  bear  in  mind  the  absolute  necessity  of  as  perfect  rest 
as  possible  for  those  patients  in  whom  the  presence  of  venous  thrombi — e.  g.,  in 
the  femoral  veins,  suggests  the  possibility  of  pulmonary  embolism. 


CHAPTER  XI 

BROWN    INDURATION    OF    THE    LUNGS 

{Lungs  of  Heart  Disease) 

In  heart  disease,  especially  in  mitral  stenosis,  we  often  find  a  peculiar  change 
in  the  lungs,  whose  origin  must  be  sought  in  the  long-persisting  engorgement  of 
the  pulmonary  circulation.  The  lungs  are  hard  and  dense,  and  show  on  a  fresh 
section  an  abnormal  brownish-yellow  color.  In  the  larger  pulmonary  vessels,  both 
arteries  and  veins,  there  is  a  thickening  and  cloudiness  of  the  intima  as  a  result  of 
the  stasis.  We  see  here  and  there  on  the  surface  of  the  section,  and  beneath  the 
pleura,  little  dark  spots  of  pigment  and  fresh  htemorrhages.  We  term  this  condi- 
tion brown  induration  of  the  lungs. 


276 


DISEASES    OF   THE   EESPIRATOEY   OEGANS 


Microscopic  examination  shows  that  the  capillaries  are  evidently  dilated  and 
twisted  as  a  result  of  the  persistent  stasis.  They  even  extend  a  good  way  into  the 
alveoli,  whose  lumen  is  thus  actually  diminished.  The  interstitial  connective  tis- 
sue seerris  somewhat  thickened,  and  we  find  in  it  many  brown  pigment-granules, 
the  remains  of  the  extravasated  and  decomposed  red  blood-corpuscles.  The  pig- 
ment-granules are  some  of  them  free,  and  some  contained  in  cells  (escaped  leuco- 
cytes). In  the  intima  of  the  larger  vessels  we  often  find  fatty  degeneration  of  the 
endothelium. 

With  regard  to  the  clinical  importance  of  the  pulmonary  changes  due  to  heart 
disease,  we  should  say  that  it  is  very  probable  that  the  dyspnoBa  of  such  patients 
is  aggravated  by  the  diminution  of  the  alveolar  spaces  throughout  the  lungs,  as  a 
result  of  their  being  crowded  with  desquamated  pulmonary  epithelium.  Clin- 
ically, however,  we  can  not  well  distinguish  this  factor  from  the  other  causes  of 
dyspnoea. 

We  have  no  positive  factors  by  which  to  diagnosticate  brown  induration  of 
the  lungs  during  life.     The  anatomical  lesions,  too,  show  a  certain  variation,  not 

always  to  be  explained,  in  that,  under 
apparently  the  same  conditions,  the 
brown  induration  is  often  very 
marked,  and  often  extremely  slight. 
In  cases .  in  which  we  find  this  in- 
duration in  the  cadaver  we  have  re- 
peatedly heard,  during  the  patient's 
life,  a  very  sharp,  puerile  respiratory 
murmur,  which  seems  to  be  character- 
istic of  many  cases  of  the  "  heart-dis- 
ease lung."  We  might  lay  still  more 
stress  upon  the  presence  of  large, 
characteristic  cells  in  the  expectora- 
tion, which  are  thickly  filled  with 
large  and  small  yellow  or  bro-mi 
pigment  -  granules  (see  Fig.  36). 
These  large  pigmented  cells  ("  cells 
of  heart  disease")  are  especially 
abundant  in  the  expectoration  of 
patients  with  extreme  mitral  stenosis. 
They  are  identical  with  the  above- 
mentioned  pigment-cells  which  are  found  in  the  lymph  of  the  alveoli  after  death. 
Many  investigators  regard  them  as  alveolar  epithelium,  while  we  are  more  in- 
clined to  regard  them  as  mainly  leucocytes  which  have  taken  up  the  pigment  of 
the  disintegrated  red  blood-corpuscles.  Besides  these  pigment-cells  we  also^  fre- 
quently see  the  still  intact  red  blood-corpuscles  in  the  expectoration  of  patients 
with  heart  disease. 

The  prognosis  and  treatment  coincide  with  those  of  the  underlying  cardiac 
disease. 


Fig.  36.— Sputum  of  a  patient  with  mitral  stenosis, 
containing  the  so-called  "cells  of  heart  disease." 
(.Personal  observation.) 


CHAPTER  XII 

TUMORS  OF  THE    LUNGS.      CANCER    OF    THE    LUNGS.     ECHINOCOCCUS 
OF    THE    LUNGS.      PULMONARY    SYPHILIS 

1.  ISTew  Growths  in  the  Lungs.  Cancer  of  the  Lungs. — Most  of  the  new 
growths  which  are  met  with  in  the  lungs  are  of  a  secondary  nature.  Secondary 
cancers  are  sometimes  found  in  the  lungs,  with  carcinoma  of  other  organs,  whose 


TUMOES    OF   THE   LUNGS— PULMONAEY   SYPHILIS  277 

origin  may  always  be  explained  by  supposing  a  growth  of  the  primary  tumor  into 
a  vein,  and  the  consequent  carriage  of  the  germs  of  the  growth  to  the  lungs. 
These  secondary  nodules  in  the  lungs  usually  cause  no  special  clinical  symptoms, 
unless  they  are  very  numerous  and  extensive,  when  they  give  rise  to  dyspna3a, 
and  physical  signs.  There  once  came  to  the  clinique  in  Leipsic  a  case  of  sec- 
ondary, and  very  extensive,  miliary  carcinosis  of  the  lungs,  which  ran  a  brief  and 
fatal  course,  simulating  acute  miliary  tuberculosis  with  predominant  pulmonary 
symptoms. 

Other  secondary  new  growths  deserving  mention  are  enchondroma  and  sar- 
coma. We  have  seen  an  extensive  development  of  secondary  pulmonary  sarcoma, 
following  primary  sarcoma  of  the  bronchial  lymph-glands,  and  also  following 
lympho-sarcoma  of  the  lymph-glands  of  the  neck,  which  grew  into  the  jugular 
vein.  We  have  also  seen  secondary  deposits  of  sarcoma  repeatedly  in  connection 
with  primary  congenital  sarcoma  of  the  kidney  (see  page  644). 

Enchondroma,  sarcoma,  and  endothelioma  appear,  also,  as  primary  new 
growths  in  the  lung.  Pulmonary  cancer  is,  however,  the  only  primary  tumor 
which  has  any  great  clinical  importance.  In  its  clinical  relations  we  can  also 
rank  with  it  certain  malignant,  metastatic  forms  of  alveolar  sarcoma.  The 
typical  cancer  of  the  lungs  is  always  a  cylindrical-celled  carcinoma,  which  un- 
doubtedly arises  from  the  bronchial  epithelium.  It  is  especially  common  in 
elderly  persons,  over  forty,  and  seems  to  be  found  somewhat  more  frequently  in 
the  right  lung  than  in  the  left,  and  in  the  upper  lobes  than  in  the  lower.  By  its 
diffusion  the  lung-tissue  in  the  parts  affected  by  cancer  is  changed  to  a  yellow- 
ish-gray and  quite  soft  and  crumbling  mass,  devoid  of  air.  We  can  usually 
scrape  away  from  the  section  the  characteristic  cancer-juice,  in  which  the  micro- 
scope shows  the  typical  cancerous  elements.  The  pleura  is  very  often  involved. 
The  new  growth  has  either  extended  directly  into  it,  or  single,  and  more  circum- 
scribed, secondary  nodules  have  formed  in  it.  The  lymph-glands  are  almost 
invariably  affected,  especially  the  bronchial  glands,  and  also  the  axillary  and 
cei'vical  glands.  Secondary  carcinoma  of  other  organs  is  rare,  but  it  is  found 
in  some  cases  in  the  other  lung,  the  liver,  the  brain,  and  elsewhere. 

It  is  almost  always  difficult  to  interpret  correctly  the  clinical  symptoms  of 
cancer  of  the  lungs  at  the  beginning  of  the  disease.  They  are  referred  to  some 
other,  more  common  chronic  pulmonary  disease,  such  as  chronic  bronchitis,  phthi- 
sis, or  pleurisy,  but  in  the  further  course  of  the  disease  we  succeed,  at  least  in  a 
number  of  cases,  in  making  a  correct  diagnosis.  In  other  cases,  especially  in  old 
people,  the  growth  may  remain  latent. 

The  general  pulmonary  symptoms  have  little  that  is  characteristic.  The 
patient  complains  of  gradually  increasing  difficulty  in  respiration,  and  of  pressure 
and  distress  in  the  chest,  which  may  finally  increase  to  the  most  intense  dyspnoea. 
Most  patients  suffer  very  much  from  the  labored,  frequent,  and  spasmodic  cough. 
The  expectoration  in  some  cases  has  no  peculiarity,  but  it  often  assumes,  at  least 
for  a  time,  a  characteristic  consistency  which  is  extremely  important  for  diagno- 
sis. It  contains  blood,  and  also  has  a  peculiar  "  currant-jelly-like  "  appearance. 
Under  the  microscope  we  can  sometimes  make  out  the  characteristic  elements  of 
the  tvimor  in  it.     Severe  haemoptysis  is  also  seen  in  cancer  of  the  lungs. 

Physical  examination  of  the  lungs  gives  positive  results  in  many  cases,  such 
as  dullness,  bronchial  respiration,  diminished  respiration,  rales,  and  sometimes 
pleuritic  friction-sounds,  none  of  which  has  anything  characteristic  in  itself, 
although  these  signs  may  be  of  distinct  significance  in  making  out  the  seat  and 
the  extent  of  the  new  growth.  Yet  sometimes  the  area  and  peculiar  limitations  of 
the  dullness — for  example,  if  confined  to  the  sternum — are  so  different  from  usual 
that  from  these  factors  alone  suspicion  of  a  new  growth  is  excited.  Thfe  sense  of 
resistance  upon  percussion  is  quite  considerable;  the  respiratory  murmur  over  the 


2T8  DISEASES    OF   THE   KESPIEATOKT   OEGANS 

tumor  is  often  inaudible  or  concealed  by  tlie  stridor  due  to  encroachment  on  tlie 
lumen  of  the  larger  bronchi.  Finally  should  be  noted  the  not  infrequent  appear- 
ance of  a  diffuse  swelling,  and  sometimes  of  a  slight  oedema  of  the  skin  over  the 
affected  spot. 

The  occurrence  of  certain  sequelse  is  of  great  diagnostic  significance.  The 
chief  one  is  swelling  of  the  lymph-glands  in  the  neck  or  axilla,  and  also  certain 
symptoms  of  compression,  which  either  are  produced  directly  by  the  new  growth, 
or  are  due  to  the  secondary  enlargement  of  the  lymph-glands.  Pressure  on  the 
superior  vena  cava,  or  a  large  branch  of  it,  causes  oedema  in  the  face,  neck,  over 
the  wall  of  the  chest,  or  in  one  arm.  The  subcutaneous  veins  in  the  regions 
named  appear  dilated  and  tortuous.  Pressure  on  the  oesophagus  causes  diffi- 
culty in  deglutition;  pressure  on  the  brachial  plexus,  intense  neuralgic  pains 
and  paresis  of  one  arm;  pressure  on  the  recurrent  nerve,  paralysis  of  the  vocal 
cords  and  hoarseness;  pressure  on  the  trachea  or  a  primary  bronchus,  the 
symptoms  of  tracheal  or  bronchial  stenosis.  The  pleura  is  often  involved  so 
that  the  signs  of  a  pleuritic  effusion  associate  themselves  with  the  other  symp- 
toms. It  is  of  diagnostic  importance  that  in  such  cases  the  exudation  is  not 
infrequently  hasmorrhagic  (vide  infra,  new  growths  of  the  pleura).  Besides  the 
symptoms  already  mentioned  we  must  consider  the  general  symptoms.  As  in 
carcinoma  in  general,  so  in  pulmonary  carcinoma,  the  well-known  cancerous 
cachexia  gradually  develops.  The  patient  grows  dull,  loses  his  appetite  more  and 
more,  disturbances  of  digestion  and  sometimes  moderate  elevations  of  tempera- 
ture develop,  until  he  finally  succumbs  to  general  marasmus. 

The  whole  duration  of  the  disease  is  from  six  months  to  two  years.  The  prog- 
nosis is  fatal.  The  treatment  can  be  only  symptomatic,  and  we  employ  the  same 
remedies  as  in  other  pulmonary  affections. 

We  must  still  briefiy  consider  a  new  growth  in  the  lungs  which  is  extremely 
interesting  from  a  theoretical  point  of  view.  In  workmen  in  the  cobalt  mines  of 
Schneeberg,  in  the  Saxon  Voigtland,  the  development  of  malignant  lympho- 
sarcomata  in  the  lungs,  with  the  occasional  formation  of  metastases  in  the  glands, 
the  liver,  the  spleen,  etc.,  is  of  frequent  occurrence.  The  disease  runs  its  course 
under  the  type  of  a  chronic  pulmonary  affection,  and  almost  always  ends  fatally. 
The  endemic  occurrence  seems  to  point  to  an  infectious  origin  for  the  tumor. 

2.  EcHiNOCOCCUS  OF  THE  LuNGS. — Primary  echinococcus  of  the  lungs  is  very 
rare.  In  most  cases  the  echinococci  are  brought  to  the  lungs  secondarily  from 
other  organs,  either  by  way  of  the  blood-current,  or,  as  is  far  oftener  the  case,  by 
perforation  of  an  echinococcus  of  the  liver  through  the  diaphragm. 

The  symptoms  of  echinococcus  of  the  lungs  are  manifold.  The  parasite  some- 
times remains  entirely  concealed.  In  other  cases  a  more  or  less  severe,  and  often 
febrile,  affection  of  the  lungs,  is  developed,  with  pain  in  the  chest,  cough,  and 
sometimes  bloody  expectoration,  and  dyspnoea.  Physical  examination  of  the 
lungs  gives  in  some  cases  dullness,  absence  of  respiratory  murmur,  and  diminished 
vocal  fremitus,  while  after  the  expectoration  of  the  echinococcus  (vide  infra) 
symptoms  of  a  cavity  may  ensue.  A  correct  interpretation  of  all  these  symptoms 
is  possible  only  when,  as  has  often  been  observed,  the  echinococcus  cysts  are 
coughed  up,  or  at  least  when  parts  of  them,  like  the  membranes  or  the  booklets, 
are  found  in  the  expectoration. 

The  termination  of  the  disease  may  be  favorable  if  the  echinococci  are  expec- 
torated, or  if  we  succeed  in  removing  them  by  operative  means.  We  can  hardly 
hope  to  be  able  to  kill  the  parasite  by  inhalations  of  turpentine  or  benzine.  Some- 
times the  echinococcus  cyst  becomes  gangrenous,  or  suppurates.  Rupture  into  the 
pleura,  into  the  peritoneum,  into  the  pericardium,  and  externally,  has  also  been 
observed.  This  last  termination  is  the  most  favorable,  since  otherwise,  if  the 
affection  progresses,  a  fatal  result  may  be  caused  by  the  sequelae,  or  rarely  by  the 


PLEUEISY  279 

occurrence  of  suffocation.  The  details  of  the  natural  history  of  the  echinococcus 
are  given  in  the  chapter  on  echinococcus  of  the  liver. 

3.  Pulmonary  Syphilis. — This  would  also  be  the  place  to  speak  of  syphilitic 
new  growths  in  the  lungs,  but,  in  our  opinion,  in  spite  of  the  quite  abundant  lit- 
erature of  this  subject  in  recent  times,  no  definite  clinical  description  of  pulmo- 
nary syphilis  can  be  made.  Those  physicians  who  are  disposed  to  consider  every 
pulmonary  disease  in  a  previously  syphilitic  subject  to  be  of  a  syphilitic  nature, 
certainly  regard  many  things  as  pulmonary  syphilis  which  have  nothing  at  all  to 
do  with  syphilis.  At  least,  we  have  found  that  all  those  cases  which  at  first  sug- 
gested a  diagnosis  of  pulmonary  syphilis,  finally,  upon  more  accurate  examina- 
tion and  after  longer  observation,  have  turned  out  to  be  something  else,  usually 
tuberculosis.  There  are  a  few  indubitable  cases  of  chronic  indurative  contrac- 
tion of  the  lungs  following  primary  syphilitic  infiltration.  The  clinical  picture 
here  does  not  differ  in  any  characteristic  manner  from  that  of  ordinary  chronic 
interstitial  pneumonia.  A  probable  diagnosis  may  be  made  from  the  knowledge 
of  the  syphilitic  taint,  the  simultaneous  existence  of  other  syphilitic  lesions — 
e.  g.,  of  the  liver — the  physical  signs  of  chronic  pulmonary  disease,  and  the  fail- 
ure to  find  tubercle  bacilli  in  the  sputum  on  repeated  examinations.  It  is  also 
well  established  that  there  may  be  syphilis  of  the  larger  and  medium-sized 
bronchi,  which  is  recognized  at  the  autopsy  by  extensive  radiating  cicatrices  in 
the  bronchial  mucous  membrane,  which  sometimes  lead  to  stenosis.  Single  gum- 
matous nodules  in  the  lungs  are  of  the  greatest  rarity.  We  sometimes  find  in 
the  pleura  peculiar  radiating  cicatrices,  which  probably  are  of  syphilitic  origin. 
The  pulmonary  syphilis  of  the  new-born,  which  occurs  in  the  form  of  single  nod- 
ules or  as  a  diffuse  syphilitic  infiltration,  the  so-called  pneumonia  alba,  has  only 
a  pathological  interest. 

If  the  existence  of  a  syphilitic  disease  of  the  lungs  is  suspected,  of  course 
specific  treatment  should  be  employed.  Iodide  of  potassium  must  be  adminis- 
tered and  perhaps  also  a  course  of  mercurial  inunctions.  The  results  are  not  apt 
to  be  brilliant,  however,  because  it  is  of  course  impossible  to  restore  the  portions 
which  have  been  cicatrized. 


SECTION  T 

Diseases  of  the  Pleura 

CHAPTER   I 

PLEURISY 

{Pleuintis) 

.31tiology. — Pleurisy  is  divided  into  primary  and  secondary.  In  a  strict  sense, 
the  only  cases  of  pleurisy  which  can  be  termed  primary  are  those  in  which  the 
pathogenic  organisms  penetrate  into  a  healthy  body,  and  become  localized  in  the 
pleura  without  any  previous  organic  lesion  elsewhere,  l^o  doubt  many  a  case  of 
pleurisy  seems  primary  from  a  clinical  standpoint,  which  is  really  not  so.  The 
disease  antecedent  to  the  pleurisy  may  be  so  slight  as  to  present  no  symptoms  and 
attract  no  attention.  The  pleurisy  appears  as  an  apparently  independent  dis- 
ease, and  is  the  first  thing  which  attracts  attention  to  the  previously  existing 
affection. 

Exclusive  of  traumatic  pleurisy,  resulting  from  such  injuries  as  a  penetrating 


280  DISEASES    OF   THE   EESPIRATOEY   OEGAKS 

thoracic  wound,  xve  know  positively  of  only  one  form  of  pleurisy — viz.,  the  rheu- 
matic— ^whicli  is  primary.  This  is,  from  an  astiological  point  of  view,  most 
closely  allied  with  acute  articular  rheumatism  (Fiedler).  In  polyarthritis  (see 
page  680)  it  is  not  very  exceptional  to  have  pleurisy  develop  secondarily.  In 
many  cases  the  rheumatic  affection  attacks  the  pleura  at  first,  without  any  great 
involvement  of  the  joints.  Then  often  follow  articular  trouble,  endocarditis, 
and  the  like,  confirming,  or  for  the  first  time  disclosing,  the  setiology  of  the 
attack.  Whether  still  other  pathogenic  influences  may  produce  primary  pleurisy 
is  not  settled.  Some  cases  of  acute  pleurisy,  setting  in  with  high  fever,  we  have 
felt  justified  in  referring  to  diplococcus  infection,  as  suggested  by  the  association 
of  herpes  and  other  symptoms.  In  such  instances  it  is  scarcely  possible  to  ex- 
clude with  certainty  the  presence  of  a  small  focus  of  pneumonia.  In  genuine 
primary  pleurisy  the  pathogenic  germs  must  first  enter  the  circulation,  and  by 
that  means  reach  the  pleura.  It  is  frequently  impossible  to  find  out  any  special 
exciting  cause  for  the  attack.    Often  it  is  ascribed  to  catching  cold. 

Among  those  varieties  of  pleurisy  which  appear  from  a  clinical  standpoint  as 
primary,  while  their  existence  is  really  referable  to  a  previous  lesion  of  the  body, 
by  far  the  most  frequent  and  important  is  the  tubercular.  On  this  point  it  was 
only  gradually  and  by  means  of  long  experience  that  physicians  obtained  a  cor- 
rect conception  of  the  truth.  We  believe  it  right  to  say  that  the  great  major- 
ity of  all  cases  of  apparently  primary  pleurisy  are  tubercular.  The  infection  of 
the  pleura  is  due  to  the  invasion  of  it  by  germs  from  some  tuberculous  focus, 
situated  near  by.  Either  there  are  small  tuberculous  patches  in  the  lungs  which 
extend  to  the  pleura,  or,  probably  yet  more  frequently,  bronchial  or  retro-bron- 
chial lymph-glands,  being  tubercular,  break  into  the  pleural  cavity  and  promptly 
excite  pleurisy.  In  many  of  these  cases  the  further  course  of  this  disease  clearly 
shows  that  the  pleurisy  was  tuberculous  at  the  start,  and  not  infrequently  the 
physican  is  justified,  even  at  the  very  beginning  of  the  illness,  in  expressing  his 
suspicion  of  tuberculosis  (vide  infra,  diagnosis).  In  many  other  cases  of  pleu- 
risy its  secondary  character  is  clear  from  the  start.  Most  of  these  occur  from 
the  direct  extension  of  the  inflammatory  process,  from  some  neighboring  organ, 
to  the  pleura.  When  considering  pulmonary  diseases,  we  had  occasion  to  point 
out  that  the  various  pathological  changes  in  the  lungs,  when  they  extend  to  the 
pleura,  involve  it  in  the  disease.  Thus  we  see  pleurisy  associated  with  croupous 
pneumonia,  lobular  catarrhal  pneumonia,  pulmonary  gangrene,  haamorrhagic  in- 
farction, embolic  abscesses,  and,  most  important  of  all,  pulmonary  tuberculosis. 
Many  of  the  diseases  just  enumerated  are  frequent  complications  of  the  most 
diverse  diseases.  Hence,  it  is  easy  to  understand  that  pleurisy  is  a  not  infre- 
quent phenomenon  in  all  sorts  of  severe  illnesses.  ^ 

Inflammation  from  other  neighboring  organs  beside  the  lungs  may  extend  to 
the  pleura.  Inflammation  of  the  contiguous  serous  membranes  may  spread  to  the 
pleura  by  continuity;  thus  pleurisy  complicates  pericarditis  and  peritonitis.  In- 
asmuch as  the  pleura  and  the  outer  surface  of  the  pericardium  lie  in  direct  appo- 
sition and,  furthermore,  the  pleural  cavity  and  the  peritoneal  cavity  are  directly 
connected  by  the  lymph-channels  of  the  diaphragm,  we  can  easily  understand 
that  not  only  serous  and  purulent,  but  also  diplococcus,  inflammation  of  the  peri- 
cardium and  peritoneum  may  have  pleurisy  for  a  sequel. 

Another  variety  of  secondary  pleurisy  is  due  to  the  conveyance  of  the  inflam- 
matory organisms  not  from  the  immediate  neighborhood,  but  from  other  parts, 
by  way  of  the  circulation.  Here  should  be  mentioned  pleurisy  due  to  general 
sepsis,  to  polyarthritis,  to  nephritis  (see  page  632),  and  to  genuine  gout  (which 
see).  The  factors  which  give  rise  to  the  inflammation  are  either  organic  or.  in 
the  case  of  gout  and  nephritis,  chemical  in  their  nature.  The  inflammation  they 
excite  in  the  pleura  is  most  varied  in  its  kind  and  degree. 


•  PLEUEISY  2S1 

Of  late  years  bacteriological  investigations  have  been  made  by  E.  Levy,  Prince 
Ludwig  Ferdinand,  and  others,  to  obtain  a  more  accurate  knowledge  as  to  the 
special  variety  of  germs  in  the  various  forms  of  pleurisy,  due  to  infection  with 
org-anized  material.  It  must  not  be  forgotten,  however,  that  these  bacteriological 
investigations  have  been,  for  the  most  part,  directed  not  to  the  diseased  tissue, 
but  to  the  inflammatoiy  pleuritic  exudation.  This,  however,  in  many  cases  con- 
tains no  bacteria  whatever.  In  particular,  the  exudation  in  most  cases  of  tuber- 
culous pleurisy,  whether  serous  or  purulent,  is  absolutely  sterile,  and  in  the  sec- 
ondary pleuritic  exudations,  in  acute  polyarthritis  and  nephritis,  the  search  for 
bacteria  has  failed  again  and  again.  In  other  cases  of  pleiirisy,  however,  staphy- 
lococci have  been  found  in  the  exudate,  and  in  empyema  streptococci  also.  Meta- 
pneumonic pleurisy,  whether  serous  or  purulent,  is  often,  though  not  always, 
characterized  by  the  presence  of  genuine  pneumococci.  In  general,  the  question 
with  regard  to  the  special  cause  of  the  disease  will  have  to  be  whether  the  pleu- 
risy, in  each  case,  is  a  part  of  the  original  primary  disease — that  is,  whether  we 
find  tubercle  bacilli  in  tuberculosis  and  diploeocci  in  pneumonia,  or  whether  thej 
pleurisy  is  a  secondary  complication,  so  that,  for  example,  we  find  streptococci 
in  typhoid  fever.  Further  investigations  are  needed  for  complete  enlightenment 
with  regard  to  all  these  matters. 

Pathological  Anatomy. — The  inflamed  pleura  is  markedly  injected,  it  has  lost 
its  normal  luster,  and  instead  has  a  dull  surface.  This  dullness  is  due  to  the 
coagulated  fibrinous  exudation  upon  the  pleura,  the  exudation,  in  mild  cases, 
forming  only  a  thin  layer.  In  more  advanced  cases,  however,  the  surface  of  the 
pleura  is  covered  with  thick,  rough,  and  shaggy  masses  of  fibrine.  As  long  as  the 
fluid  in  the  pleura  is  little  or  not  at  all  increased,  we  speak  of  a  simple  fibrinous 
or  dry  pleurisy  (pleuritis  fihrinosa  vel  sicca). 

In  other  cases,  however,  besides  the  layer  of  fibrine  there  is  an  abundant  exu- 
dation of  fluid  from  the  capillaries  of  the  pleura,  forming  a  pleuritic  effusion. 
This  is  ordinarily  of  a  simple  serous  character — serous  and  sero-fibrinous  effu- 
sions. The  fluid  collects  between  the  surfaces  of  the  pleura,  or,  if  there  is  at  the 
same  time  an  abundant  coating  of  fibrine,  between  the  gaps  and  in  the  meshes  of 
the  fibrinous  exudation.  In  such  cases  there  are  often  many  flakes  of  fibrine 
floating  in  the  fluid. 

Upon  microscopic  examination  there  are  invariably  found  a  few  leucocytes 
even  in  serous  exudations,  and  also  sometimes  a  very  few  blood-corpuscles  and 
endothelial  cells  (often  swollen  or  fatty-degenerated),  and  plates  of  choles- 
terin. 

If  the  number  of  pus-corpuscles  in  the  exudation  becomes  much  increased,  we 
have  a  sero-purulent,  or  a  purulent  exudation.  This  is  always  due  to  the  presence 
of  a  specific  organized  poison  which  excites  the  suppuration.  The  pleurisies 
which  come  from  embolic  abscesses,  from  gangrenous  foci  in  the  lungs,  and  from 
carious  ribs,  and  those  which  arise  from  the  rupture  of  tubercular  cavities  into 
the  pleura,  are  almost  always  of  a  suppurative  character.  We  call  the  purulent 
pleuritic  effusion  empyema.  If  putrefactive  agencies  enter  the  pleural  cavity  at 
the  same  time  with  the  pus  poison,  as  in  the  pleurisies  which  develop  in  pulmonary 
gangrene,  the  purulent  exudation  assumes  an  ichorous,  putrid  character — ichorous 
effusion. 

Under  certain  circi^mstances  the  effusion  assumes  a  hsemorrhagic  character — • 
haemorrhagic  effusion — especially  if  hsemorrhages  occur  from  the  old  or  newly 
formed  capillaries  dilated  by  the  inflammation.  They  arise  partly  by  diapedesis 
and  partly  from  rupture  of  the  walls  of  the  vessels.  The  exact  cause  of  the  hsem- 
orrhages is  usually  unknown.  We  know  by  experience  that  haemorrhagic  effu- 
sions are  most  frequent  in  tubercular  pleurisy,  a  fact  which  is  of  diagnostic  im- 
portance.    The   exudation  may   also   be  hasraorrhagic   in   connection  with  new 


282  DISEASES    OE   THE   KESPIEATOEY   OKGANS 

growths  of  the  pleura,  after  severe  croupous  pneumonia,  in  septic  disease  (e.  g., 
puerperal  fever),  and  finally  when  there  is  a  general  hsemorrhagic  diathesis,  as 
seen  in  scurvy,  purpura  hsemorrhagica,  and  leukaBmia.  In  all  these  last-men- 
tioned cases  it  should,  of  course,  be  considered  that  we  are  not  always  dealing 
with  a  true  inflammatory  exudation,  but  merely  with  a  haemorrhage  into  the 
pleural  cavity. 

The  amount  of  fluid  collected  in  one  pleural  cavity  is,  in  the  majority  of  cases, 
somewhere  between  a  pint  and  a  quart  (500-1,000  cubic  centimetres),  but  it  may 
reach  three  or  four  quarts.  Every  large  effusion  must  influence  the  position  of 
the  yielding  walls  of  the  pleural  cavity,  the  chest-wall,  the  lungs,  the  medias- 
tinum, and  the  diaphragm,  through  the  consequent  increase  of  pressure  in  the 
affected  pleural  cavity ;  and  the  resultant  symptoms  of  pressure  on  the  neighbor- 
ing organs  are  of  the  greatest  clinical  significance.  Attention  is  first  called  to 
the  lungs  themselves.  Since  the  normal  lung  is  expanded  in  the  thorax  beyond 
its  elastic  equilibrium,  it  will  retract  as  soon  as  a  part  of  the  pleural  cavity  is 
occupied  with  fluid.  Until  it  has  reached  its  position  of  elastic  equilibrium  there 
can  be  no  question  of  a  positive  pressure  on  the  lung.  The  lung  floats  on  the  effu- 
sion, in  a  certain  way,  if  there  be  no  adhesions,  but,  as  the  amount  of  the  fluid 
further  increases,  compression  of  the  lung  follows.  With  a  very  large  effusion  the 
lung  is  pushed  wholly  up  and  back  against  the  vertebral  column,  and  is  changed 
to  an  almost  bloodless,  airless,  flat  mass.  It  is,  however,  possible  that  the  atelec- 
tasis of  the  lung  is  not  caused  exclusively  by  compression  from  without,  but  that, 
after  the  normal  respiratory  movements  have  ceased,  a  part  of  the  air  in  the  lung 
may  be  absorbed  by  the  vessels,  or  even  by  the  effusion. 

We  also  see  the  results  of  the  pressure  exerted  by  the  pleuritic  effusion  on  the 
mediastinum  and  diaphragm,  as  well  as  on  the  lungs.  Displacements  of  the  heart 
arise  from  the  lateral  pressure  on  the  mediastinum,  which  must  take  place  if  the 
pressure  in  the  diseased  pleural  cavity  is  equal  to  that  of  the  atmosphere,  for  a 
greater  and  positive  pressure  is  unnecessary,  since  a  negative  pressure  prevails  on 
the  healthy  side. 

The  downward  pressure  of  the  diaphragm,  which  usually  affects  both  halves  of 
it,  although  in  unequal  degree,  makes  itself  manifest  on  the  right  by  the  low  posi- 
tion of  the  liver,  and  on  the  left  by  the  downward  displacement  of  the  stomach 
and  large  intestine.  It  must  be  particularly  noticed,  however,  that  adhesions 
may  prevent  all  the  pressure-displacements  which  we  have  mentioned,  both  of  the 
lungs  and  of  the  neighboring  organs. 

As  regards  the  further  changes  and  terminations  of  the  pleuritic  processes, 
they  depend  upon  the  amount  and  character  of  the  effusion.  Favorable  cases  may 
result  in  complete  recovery  and  absorption  of  the  effusion.  The  fluid  contents 
are  taken  up  directly  by  the  lymphatics  of  the  pleura,  and  the  solid  constituents, 
the  fibrine  and  the  white  blood-corpuscles,  are  decomposed,  dissolved,  and  ab- 
sorbed. Old  fibrinous  patches  sometimes  become  impregnated  with  lime  salts, 
so-called  "pleuritic  ossification." 

Whenever  a  case  of  extensive  pleurisy,  with  an  abundant  fibrinous  or  fluid 
exudation,  gets  well,  there  is  a  marked  cicatricial  contraction  of  the  pleura, 
in  which  the  whole  thoracic  wall  is  involved.  It  requires  months  for  the  lungs 
and  the  thorax  to  regain  their  normal  expansion,  if  they  can  ever  do  so. 

That  recovery  from  large  pleuritic  exudation  is  so  often  incomplete,  is  ex- 
plained for  the  most  part  by  the  nature  of  the  original  disease.  We  often  find 
that  temporary  improvement  is  followed  by  a  fresh  relapse  of  pleurisy,  or  by  the; 
appearance  of  extensive  and  usually  tuberculous  disease  of  the  lungs  or  other 
organs. 

In  the  case  of  purulent  exudations,  also,  final  absorption  of  the  fluid  is  possi- 
ble.    This  is  especially  likely  when  the  empyema  is  meta-pneuraonic  and  benign. 


PLEUEIST  283 

but  this  demands  much  time,  and  thick,  cheesy  masses  of  pus  are  often  left  in  the 
pleural  sac.  In  most  cases  of  empyema,  if  there  is  not  timely  operative  interfer- 
ence, the  pus  seeks  an  outlet  for  itself.  It  may  break  through  the  visceral  pleura 
into  a  bronchus,  and  be  emptied  externally,  thus  giving  rise  to  a  pyo-pneumo- 
thorax ;  but  in  many  cases  the  pleura  seems  to  be  destroyed  only  superficially,  and 
the  pus  is  pressed  into  the  alveoli  as  into  a  sponge,  especially  by  the  movements 
of  coughing,  and  thence  reaches  the  bronchi,  without  letting  the  air  enter  the 
pleural  cavity  (Traube).  In  other  cases  the  empyema  breaks  externally  through 
the  chest-wall — empyema  necessitatis.  The  point  of  rupture  is  usually  found  in 
the  vicinity  of  the  sternum,  where  the  chest-wall  is  thinnest.  In  very  rare  cases 
the  empyema  breaks  into  the  deeper  parts  of  the  trunk,  or  into  the  abdominal 
cavity. 

Course  of  the  Disease. — We  will  speak  in  what  follows  especially  of  the  course 
and  symptoms  of  ordinary,  apparently  primary  {vide  supra),  fibrinous  or  sero- 
fibrinous pleurisy,  the  so-called  simple  pleuritic  effusion.  What  is  said  of  it 
obtains  in  large  measure  in  the  other  form  of  pleurisy  also.  The  physical  signs, 
of  course,  are  almost  wholly  independent  of  the  character  of  the  effusion.  As  far 
as  the  different  forms  of  pleurisy  differ  clinically,  we  will  mention  their  peculiari- 
ties below. 

Only  rarely  is  the  onset  of  pleurisy  quite  acute  and  sudden,  beginning  with  a 
rigor.  In  such  cases  we  must  guard  against  confusing  it  with  croupous  pneu- 
monia. Pleurisy  usually  begins  slowly  and  gradually.  The  symptoms,  which 
the  patient  himself  feels,  are  in  many  cases  to  be  referred  directly  to  the  disease  of 
the  pleura.  One  of  the  most  constant  is  the  pleuritic  pain,  the  stitch  in  the  side. 
A  more  or  less  severe  pain  comes  on  in  the  side  at  every  deep  breath,  and  hence 
upon  any  physical  exertion;  also  upon  movements  of  the  body,  in  stooping, 
coughing,  or  gaping.  Shortness  of  breath  soon  appears,  and  constantly  increases. 
There  is  often  a  frequent,  dry  cough.  Sometimes  there  ar'e  scarcely  any  cough 
and  expectoration.  Such  expectoration  as  there  may  be  is  usually  simply  mu- 
cous. Besides  that,  severe  general  symptoms  almost  always  develop;  the  patient 
feels  dull,  looks  pale,  and  has  no  appetite.  Patients  who  can  endure  a  good  deal 
often  keep  at  work  for  a  long  time,  until,  after  feeling  miserable  for  three  or  four 
weeks,  they  are  forced  to  stay  at  home  and  summon  a  physician.  It  is  very  impor- 
tant to  know  that  in  not  a  few  cases  the  general  symptoms  are  much  more  promi- 
nent, at  the  beginning  of  pleurisy,  than  the  local  ones.  The  patient  comes  to  the 
physician  complaining  only  of  weakness,  loss  of  appetite,  or  headache,  and  the 
physical  examination  is  the  first  thing  that  shows  the  presence  of  perhaps  a  large 
pleuritic  effusion. 

In  most  of  the  severe  cases  the  further  course  is  slow  like  the  beginning,  but 
sometimes  the  severest  symptoms,  most  intense  dyspnoea,  marked  cyanosis,  etc., 
may  come  on  in  a  short  time,  owing  to  a  sudden  increase  of  the  effusion.  On  the 
other  hand,  in  mild  cases  the  symptoms  may  disappear  again  in  a  few  weeks,  but 
the  objective  signs  in  such  cases  are  generally  to  be  made  out  for  a  longer  time. 
The  disease  ordinarily  lasts  for  at  least  five  or  six  weeks,  and  often  much  longer. 
Gradual  recovery  follows,  or  the  onset  of  some  new  disease,  usually  tubercular 
{vide  infra). 

Single  Symptoms. — The  pleuritic  pain,  the  stitch  in  the  side,  is  one  of  the 
most  frequent  subjective  symptoms.  We  have  previously  mentioned  that  in  pri- 
mary diseases  of  the  lungs,  too,  as  in  croupous  pneumonia,  the  stitch  in  the  side 
is  due  to  the  accompanying  pleurisy.  It  is  remarkable  that  the  intensity,  of  the 
pain  in  no  way  corresponds  to  the  apparent  intensity  of  the  disease.  There  is 
often  the  severest  pain  in  the  side  when  the  physical  examination  shows  almost 
nothing.  On  the  other  hand,  we  often  hear  a  decided  pleuritic  rub  without  the 
patient's  complaining  of  any  special  pain.     Pressure  on  the  chest-wall  on  the 


284  DISEASES    OF   THE   EESPIRATORT   ORGAK^S 

affected  side  is  often  very  painful.  With  severe  pain  we  may  consider  the  possi- 
bility of  an  invasion  of  the  intercostal  nerves  by  the  inflammation.  We  have 
never  observed  cases,  like  those  described  by  some  authors,  of  "  crossed  pleuritic 
pain  " — that  is,  cases  in  which  the  pain  is  localized  on  the  side  not  affected. 

Cough  and  Expectoration. — The  cough  is  probably  excited  directly  by  the  dis- 
ease of  the  pleura.  We  often  find  that  the  pain  in  the  side  and  also  the  cough 
are  brought  on  by  a  deep  inspiration.  Expectoration  is  entirely  absent  in  uncom- 
plicated pleurisy,  or  it  is  scanty,  and  consists  simply  of  mucus.  Much  expectora- 
tion always  means  a  pulmonary  complication.  A  large  amount  of  purulent 
sputum  is  evacuated  if  a  purulent  effusion  breaks  into  the  lungs  {vide  supra). 

Dyspnoea. — The  respiration  is  usually  shallow,  and  consequently  frequent,  be- 
cause of  the  pleuritic  pain.  In  every  large  effusion  which  prevents  respiration 
in  one  lung  the  dyspnoea  becomes  more  severe,  and  may,  with  a  very  extensive 
effusion,  reach  the  highest  degree  of  orthopncea.  The  stronger  the  patient  was 
before  the  disease,  and  the  more  rapidly  the  effusion  develops,  the  more  severe,  as 
a  rule,  is  the  dyspnosa. 

Fever. — Most  severe  pleurisies  are  associated  with  fever,  but  its  height  is  not 
very  great,  so  that  it  quite  rarely  reaches  104°  (40°  C).  The  fever  has  no  typical 
course.  In  cases  with  an  acute  beginning  it  is  sometimes  quite  continuous,  or 
slightly  remitting  at  first.  If  improvement  takes  place,  the  fever  goes  down  in 
about  two  or  three  weeks  by  lysis,  so  that  this  part  of  the  temperature-curve  may 
be  precisely  like  the  period  of  defervescence  in  typhoid. 

In  the  more  protracted  cases  the  fever  gradually  becomes  more  remitting,  vary- 
ing between  100°  and  101°  (38°-38.5°  C),  and  it  assumes  more  and  more  the 
form  of  hectic  fever.  The  longer  the  evening  rise  of  temperature  lasts,  the  more 
we  are  justified  in  suspecting  tuberculosis.  In  empyema  we  see  a  higher,  irregu- 
lar fever,  sometimes  associated  with  severe  chills. 

The  pulse  is  constantly  rapid,  up  to  100  and  over.  In  all  severe  cases  the 
strength  and  tension  of  the  pulse  are  much  diminished.  Irregularity  of  the  pulse 
is  not  infrequent.  All  these  changes  are  probably  due  in  great  part  to  the  pres- 
sure of  the  effusion  on  the  heart  and  large  vessels.  Lichtheim  has  discovered 
experimentally  that  it  is  not  the  compression  of  the  vessels  in  the  compressed 
lung  which  lowers  the  arterial  tension. 

General  Symptoms. — Pleurisy  is  almost  always  associated  with  a  pronounced 
general  malaise,  muscular  weakness,  and  dullness.    The  patient  is  pale,  and  often 
markedly  cyanotic   in   cases  with  much  disturbance   of   respiration.     There   is' 
great  emaciation  if  the  disease  is  of  long  duration. 

The  appetite  declines  from  the  outset.  There  is  often  occasional  vomiting, 
especially  in  the  first  period  of  the  disease.  The  bowels  are  usually  constipated. 
Many  patients  complain  of  headache. 

The  condition  of  the  urinary  secretion  is  very  important.  In  every  pleuritic 
effusion  the  amoimt  of  urine  is  decidedly  diminished  so  long  as  the  effusion 
increases  or  remains  at  the  same  height.  The  daily  amount  is  sometimes  only 
eight  or  ten  ounces  (200-400  cubic  centimetres).  The  urine  is  also  concentrated, 
its  specific  gravity  being  about  1020-1028,  Sediments  of  urates  often  form. 
This  diminution  of  the  excretion  of  water  by  the  kidneys  is  largely  the  result  of 
the  diminished  arterial  pressure.  An  increase  of  the  amount  of  urine  is  always  a 
favorable  symptom,  often  the  first  sign  of  beginning  absorption  of  the  effusion. 
If  a  large  effusion  is  rapidly  absorbed,  the  amount  of  urine  may  increase  to 
eighty  or  a  hundred  ounces  (2,500-3,000  cubic  centimetres)  daily.  The  urine, 
then,  of  course,  is  abnormally  clear  and  of  low  specific  gravity. 


PLEUEIST  285 

Physical  Signs 

1.  Fibrinous  Pleurisy — Pleuritis-  Sicca. — Simple  fibrinous  pleurisy  sometimes 
gives  rise  to  no  physical  signs  at  all.  If  it  develops  as  a  result  of  some  pulmonary 
affection,  the  physical  signs  present  are  often  dependent  upon  the  latter  alone. 

In  many  cases,  however,  dry  pleurisy  may  cause  marked  objective  signs.  On 
inspection,  we  are  struck  by  the  impaired  mobility  of  the  affected  side  on  respira- 
tion, which  is  due  to  the  pain  caused  by  breathing.  Because  of  this  same  tender- 
ness the  patient  at  first  often  lies  on  the  sound  side.  Percussion  gives  no  qualita- 
tive change  of  resonance  as  yet.  With  the  beginning  of  exudation  slight  dullness 
appears,  at  first  almost  always  in  the  posterior  portion  of  the  lungs.  Sometimes 
the  resonance  becomes  tympanitic  as  a  result  of  retraction  of  the  lung.  We  can 
almost  constantly  make  out,  especially  in  the  back,  that  the  lower  edge  of  the 
lung  moves  less  than  usual  on  respiration.  Auscultation  gives  a  respiratory  mur- 
mur that  is  either  qualitatively  unchanged  or  indefinite,  but  it  is  always  dimin- 
ished. The  peculiar  pathognomonic  sign  of  dry  pleurisy,  however,  is  the  pleuritic 
friction-rub,  that  characteristic  rubbing,  grating,  creaking  sound,  which  arises 
from  the  sliding  of  the  rough  pleural  surfaces  over  each  other,  and  is  detected 
especially  in  the  lateral  portions  of  the  thorax.  We  can  hear  it  both  on  inspira- 
tion and  on  expiration.  It  is  often  jerky,  one  rub  following  another  after  a  con- 
siderable interval.  If  we  are  sure  we  hear  a  pleuritic  rub,  it  is  direct  evidence  of 
the  existence  of  a  dry  pleurisy,  but  its  absence  will  not  let  us  exclude  pleurisy. 
The  friction-sound  must  be  absent  if  there  are  pleuritic  adhesions.  We  can  often 
feel  a  marked  rub  by  laying  the  hand  on  the  chest.  Sometimes  the  patient  feels 
it  himself,  but  in  other  cases  he  has  no  sensation  of  it.  We  may  confound  a  slight 
rub  with  fine  crepitant  rales.  Eepeated  examinations  before  and  after  the 
patient  has  coughed  usually  confirm  the  diagnosis,  since  the  rales  are  often 
changed  by  coughing. 

To  be  distinguished  from  the  mild  form  of  dry  pleurisy  just  described  is  that 
variety  in  which  there  is  an  extensive  and  abundant  fibrinous  exudation,  with 
scarcely  any  liquid.  We  have  repeatedly  seen  severe  cases  following  pneumonia, 
or  even  apparently  primary  cases,  which  displayed  marked  dullness  and  sense  of 
resistance  on  percussion  over  the  whole  of  one  side  of  the  chest,  with  diminished 
or  absent  respiration,  and  yet  upon  exploratory  puncture  only  a  few  drops  of 
serous  exudation  could  be  obtained.  Evidently  we  had  to  do  with  the  forma- 
tion of  large  amounts  of  coagulated  fibrine.  Attacks  of  this  sort  usually  run  a 
severe  and  tedious  course,  but  they  may,  nevertheless,  get  well  at  last. 

2.  Pleuritic  Effusion. — Small  amounts  of  fluid  in  a  pleural  cavity  escape 
discovery.  Physical  signs  first  appear  when  the  amount  of  effusion  reaches  eight 
or  ten  ounces  (200-300  cubic  centimetres). 

Inspection  shows  first  the  more  or  less  marked  impairment  of  motion  on  the 
affected  side  on  respiration.  If  the  amount  of  the  effusion  is  large,  there  is  an 
evident  distention  of  the  affected  side  in  the  lower  posterior  and  lateral  portions 
of  the  thorax.  The  intercostal  spaces  are  flattened  or  even  a  little  convex.  The 
nipples  and  shoulder-blades  are  farther  removed  from  the  median  line  on  the 
affected  side  than  on  the  healthy  side.  The  hj-pochondrium  on  the  affected  side 
is  more  prominent.  In  an  extraordinarily  large  effusion  on  the  left  side  we  have 
seen  and  felt,  in  the  left  hypochondrium,  the  lower  surface  of  the  diaphragm, 
which  was  actually  arched  downward.  By  direct  measurement  in  severe  cases  we 
can  make  out  that  the  affected  side  is  expanded  several  centimetres. 

With  every  large  effusion  there  is  marked  dyspncca  and  accelerated  respira- 
tion. The  slight  excursions  of  the  affected  side  on  respiration  are  usually  very 
striking,  while  the  sound  side  moves  so  much  the  more.  In  this  stage  of  pleurisy 
the  patient  often  lies  upon  the  affected  side,  in  order  to  breathe  with  the  healthy 


286  DISEASES    OE   THE   EESPIEATORY   OEGAITS 

lung  with  as  little  restraint  as  possible.  With  large  effusions  complete  orthopnoea 
may  develop. 

The  signs  due  to  displacement  of  the  neighboring  organs,  which  are  noticeable 
on  inspection,  will  be  mentioned  below  in  the  appropriate  connection. 

Everywhere  that  a  layer  of  fluid  comes  between  the  lung  and  the  chest-wall 
there  is  a  loss  of  clearness  in  the  percussion-note.  If  the  thickness  of  the  layer 
of  effusion  is  five  or  six  centimetres,  the  resonance  seems  completely  dull  or  flat. 
The  pleuritic  dullness  is  almost  always  made  out  first  in  the  lower  posterior  por- 
tions of  the  thorax,  more  rarely  in  the  lower  lateral  portions.  With  a  slight 
effusion  the  height  of  the  dullness  is  only  a  few  centimetres,  but,  with  much 
effusion,  it  rises  higher  in  the  back  and  the  lateral  portions  of  the  thorax ;  and  on 
the  right,  resonance  gradually  grows  dull  anteriorly  and  inferiorly,  above  the 
liver.  With  very  large  effusions  the  dullness  may  begin  in  front  at  the  second  or 
third  rib,  or  in  rare  cases  even  the  whole  half  of  the  chest,  front  and  back,  may 
give  a  totally  flat  percussion-note.  Pleuritic  dullness  is  always  attended  with  a 
marked  feeling  of  resistance  on  percussion. 

With  medium-sized  effusions,  when  the  dullness  does  not  extend  over  the 
whole  back,  the  upper  boundary  of  the  dullness  usually  forms  an  oblique  line, 
highest  at  the  vertebral  column  and  thence  running  obliquely  downward  to  the 
side  of  the  thorax.  Exceptionally  the  line  runs  the  other  way.  On  the  right  it 
is  not  possible  to  distinguish  by  percussion  the  lower  limit  of  the  exudation  from 
the  liver.  On  the  left  we  can  often  distinguish  its  lower  limit  from  the  tympa- 
nitic resonance  of  the  stomach,  and  are  thus  aided  in  diagnosis  {vide  infra,  dis- 
placement of  organs). 

[In  moderate  effusion  without  adhesions  or  pneumonic  complications,  the  line 
of  flatness  in  the  back,  the  patient  being  in  the  vertical  position,  is  lowest  near 
the  spinal  column,  and  rises  in  a  curve  like  the  letter  S  as  it  passes  outward 
toward  the  axillary  region.  The  experiments  by  Dr.  Garland,  of  Boston,  with 
reference  to  this  point  are  well  known.  Before  attempting  to  mark  out  this  line 
the  patient  should  be  told  to  take  several  deep  inspirations,  in  order  to  inflate  the 
triangular  portion  of  lung  which  dips  down  near  the  vertebrae.] 

The  percussion-note  above  a  pleuritic  effusion  deserves  attention.  The  begin- 
ning of  pleuritic  dullness  is  almost  always  relative,  gradually  passing  to  an  abso- 
lute flatness.  The  pulmonary  resonance  above  the  beginning  of  dullness  is  usu- 
ally tympanitic,  from  retraction  of  the  lung-tissue.  We  find  the  tympanitic 
resonance  beautifully  distinct  in  large  effusions  in  the  first  and  second  intercostal 
spaces  in  front.  It  is  loud  and  deep,  and  remains  imchanged  with  the  mouth 
open — Skoda's  resonance.  With  very  large  effusions,  which  cause  an  actual  com- 
pression of  the  lung,  we  sometimes  find,  in  the  second  intercostal  space,  a  dull 
tympanitic  resonance,  which  becomes  higher  on  opening  the  mouth.  This  reso- 
nance arises  from  the  vibrations  of  air  in  a  large  bronchus  surrounded  by  com- 
pressed lung — "Williams's  tracheal  tone."  With  large  effusions  we  sometimes 
hear  over  the  retracted  lung,  in  the  upper  anterior  intercostal  spaces,  a  distinct 
buckram  sound — the  "  cracked-pot  sound." 

Displacement  of  the  neighboring  organs,  which  is  made  out  chiefly  by  percus- 
sion, forms  one  of  the  most  important  physical  signs  in  pleurisy  with  effusion. 

In  right-sided  effusions  the  liver,  especially  the  right  lobe,  is  displaced  down- 
ward. We  find  the  lower  border  of  the  liver  dullness  extending  several  centi- 
metres below  the  ribs.  In  very  large  effusions  the  liver  may  be  pushed  down  to 
the  level  of  the  umbilicus.  The  pushing  of  the  mediastinum  to  the  left  in  large 
effusions  may  be  recognized  upon  percussing  from  the  right  toward  the  left,  by 
dullness  over  the  upper  part  of  the  sternum,  reaching  to  or  beyond  the  left  border 
of  the  sternum.  The  displacement  of  the  heart  to  the  left  in  the  majority  of  well- 
marked  cases  is  associated  with  a  displacement  of  the  apex  of  the  heart  upward. 


PLEUEISY  287 

This  is  easily  explained  by  considering  the  position  of  the  heart  and  the  direction 
of  the  pressure,  which  first  acts  from  below.  We  recognize  the  displacement  of  the 
heart  chiefly  by  the  position  of  the  apex-beat,  which  is  seen  and  felt  at  or  outside 
the  left  mammillary  line  in  the  fifth  space,  or  often  higher,  as  we  have  said — in 
the  fourth.  Percussion  gives  a  corresponding  displacement  of  the  left  boundary 
of  the  cardiac  dullness  to  the  left. 

In  left-sided  effusions  the  displacement  of  the  heart  to  the  right,  which  can 
usually  be  made  out  even  in  moderate  effusions,  is  especially  noticeable.  Reso- 
nance over  the  lower  part  of  the  sternum  is  diminished,  the  heart's  dullness 
extends  to  the  right  border  of  the  sternum  or  several  centimetres  beyond  it.  In 
the  most  marked  cases  the  heart  is  pushed  to  the  right  mammillary  line.  The 
displacement  of  the  mediastinum  is  also  to  be  made  out  over  the  upper  part  of  the 
sternum,  the  dullness  reaching  to  the  right  border  of  the  sternum  or  beyond. 
The  low  position  of  the  diaphragm  is  made  out  by  a  depression  of  the  left,  and  in 
marked  cases  of  the  right,  lobe  of  the  liver.  It  is  an  especially  important  sign, 
however,  that  dullness  occurs  in  the  zone,  about  a  hand-breadth  wide,  of  normal 
tympanitic  resonance  above  the  left  border  of  the  ribs — the  "  semilunar  space  " 
of  Traube.  The  normal  tympanitic  resonance  here  comes  from  the  stomach  or 
large  intestine.  As  the  diaphragm  is  pressed  downward  the  pleuritic  effusion 
presses  on  these  organs.  The  semilunar  space  is  therefore  diminished,  and  finally, 
with  large  effusions,  there  is  absolute  dullness  down  to  the  edge  of  the  ribs. 

Changes  in  dullness  in  pleuritic  effusions  may  occur  with  a  change  of  the 
patient's  position,  but  they  may  often  be  absent  on  account  of  adhesions.  As  a 
rule  the  normal  change  in  the  position  of  the  lower  border  of  the  lung  corre- 
sponding with  respiration  is  abolished. 

Auscultation  always  gives  a  diminished  respiratory  murmur  over  the  pleuritic 
effusion.  With  a  beginning  effusion  it  may  sound  approximately  vesicular,  but 
later  it  becomes  indefinite,  harsh,  and  finally  bronchial,  if  the  larger  bronchi  re- 
main open  for  the  respiratory  current  of  air.  The  bronchial  respiration  sounds 
distant  and  low,  and  has  the  character  of  the  sharp  German  ch,  but  in  rare  cases 
it  also  assumes  a  distinct  amphoric  tone,  so  that  it  sounds  almost  like  a  cavernous 
respiration.  The  respiratory  murmur  may  finally  disappear  entirely  over  very 
large  effusions.  Above  the  upper  boundary  of  the  effusion  the  respiration  almost 
always  sounds  harsh.  Among  the  adventitious  sounds  we  must  mention  the 
pleuritic  friction  sound,  which  of  course  can  be  heard  only  at  the  upper  boundary 
of  the  effusion,  where  the  two  pleural  surfaces  meet.  Moist  rales  and  rhonchi 
signify  a  co-existing  disease  in  the  lungs.  With  slight  effusions  we  often  hear, 
on  deep  breathing,  pure  crepitant  rales  on  inspiration,  as  the  walls  of  the  alve- 
oli and  bronchioles  in  the  atelectatic  lung,  which  were  stuck  together,  are  torn 
apart. 

On  auscultation  of  the  voice  we  sometimes  hear  bronchophony,  and  sometimes 
that  bleating,  nasal  sound  known  as  segophojiy.  Baccelli  advanced  the  theory 
that  auscultation  of  the  whispered  voice  might  be  of  service  in  diagnosticating 
the  character  of  the  effusion.  With  a  serous  effusion  we  can  understand  a  whisper 
distinctly  through  the  thorax,  but  not  with  a  purulent  effusion,  since  theoret- 
ically the  cell-elements  destroy  the  waves  of  resonance.  This  theory  holds  true  in 
many  cases,  but  by  no  means  in  all. 

On  auscultation  of  the  heart  we  notice,  as  a  result  of  its  displacement,  an  ab- 
normal extension  of  the  region  over  which  the  heart-sounds  are  audible.  If  the 
inflammation  spreads  from  the  pleura  to  the  outer  surface  of  the  pericardium, 
we  can  sometimes  hear  an  extra-pericardial  friction-rub,  accompanying  both  the 
respiration  and  the  action  of  the  heart. 

The  vocal  fremitus  is  always  diminished  over  the  pleuritic  effusion,  and  in 
marked  cases  is  entirely  absent. 


288  ^  DISEASES    OF   THE   EESPIEATOEY   0EGA:N'S 

3.  Absorption  of  the  Effusion — Pleuritic  Contraction. — The  beginning  ab- 
sorption of  the  effusion  is  usually  first  made  evident  by  the  percussion-note  in  the 
upper  part  of  the  dullness  becoming  clearer  and  sometimes  tympanitic.  The 
respiratory  murmur  is  also  plainer.  Where  it  was  bronchial  it  becomes  in- 
definite and  gradually  vesicular  again.  The  vocal  fremitus  is  again  to  be  felt. 
All  these  improvements  take  place  gradually  but'slowly.  It  is  usually  a  very  long 
time  before  the  percussion-note  resumes  its  normal  clearness. 

The  changes  in  the  form  of  the  thorax  are  especially  striking.  Only  in  pleu- 
risies with  slight  effusion  does  the  somewhat  expanded  thorax  resume  its  old  form 
without  further  change.  After  every  severe  pleurisy  with  large  effusion  there  is, 
during  its  absorption,  a  marked  contraction  of  the  affected  half  of  the  chest.  In 
cases  of  moderate  intensity  the  contraction  affects  only  the  lower  lateral  portions 
of  the  thorax,  in  severe  cases  the  upper  and  anterior  portions  as  well.  "We  find 
the  most  marked  contractions  in  children  and  young  persons  with  a  yielding 
thorax.  The  circumference  of  the  affected  side  is  much  less  than  that  of  the 
sound  side.  The  ribs  are  pressed  together  and  the  intercostal  spaces  become 
very  narrow.  The  fossae  are  deepened  and  the  nipples  and  shoulder-blades  are 
drawn  nearer  the  vertebral  column,  which  takes  on  an  abnormal  lateral  curva- 
ture, in  which  its  convexity  is  directed  usually  toward  the  affected  side,  but  some- 
times to  the  sound  side.  Dullness  and  diminution  of  the  respiratory  murmur  and 
vocal  fremitus  continue  with  the  contraction  of  the  pleura,  but  they  no  longer 
depend  upon  the  presence  of  a  fluid  effusion,  but  are  due  to  the  pleuritic  thick- 
ening. 

The  process  of  marked  contraction  always  lasts  for  months,  or  even  longer. 
In  favorable  cases  the  contraction  of  the  thorax  may  be  readjusted  very  much 
later,  often  after  years.  The  thickening  is  absorbed,  and  the  lungs  and  thorax 
gradually  expand,  but  in  other  cases  there  are  extensive  adhesions  between  the 
pleural  surfaces,  especially  over  the  lower  lobe,  which  result  in  a  permanent  dis- 
turbance of  respiration.  In  almost  all  cases  of  pleurisy  with  contractions  there 
arises  a  vicarious  emphysema  in  the  lung  on  the  sound  side. 

Complications. — Peculiar  complications  of  pleurisy  are  rare.  Where  such 
occur  they  are  due  either  to  the  primary  disease  v\-hich  has  led  to  the  pleurisy,  or 
to  the  simultaneous  action  of  the  same  cause  of  disease,  such  as  tuberculosis. 
Hence  it  happens  that  we  speak  of  the  frequent  "  complication  "  of  pleurisy  with 
chronic  bronchitis  or  with  tuberculosis  of  the  lungs  or  other  organs.  It  is  impor- 
tant to  bear  in  mind  that,  by  a  direct  advance  of  the  inflammation,  the  pleurisy 
may  also  invade  the  pericardium,  and  rarely  the  peritoneum,  through  the  dia- 
phragm; but  we  see  this  extension  of  the  process  almost  solely  in  tubercular  and 
purulent  pleurisies.  We  must  mention,  finally,  that  we  have  seen  several  cases 
with  a  large  serous  effusion,  in  which  an  acute  hsemorrhagic  nephritis  occurred. 
For  the  paralysis  of  the  arm  on  the  corresponding  side  observed  in  some  cases  of 
empyema,  compare  what  is  said  in  regard  to  reflex  paralyses  on  page  833. 

Various  Forms  of  Pleurisy 

1.  Primary  Rheumatic  Pleurisy. — As  we  have  already  pointed  out,  when  con- 
sidering the  aetiology  of  pleurisy,  clinical  observations  have  lately  led  to  the 
belief  that  some  of  the  cases  of  acute  primary  pleurisy  are  due  to  the  same  cause 
as  acute  articular  rheumatism  (which  see).  Although  there  are  as  yet  no  suffi- 
cient number  of  decisive  bacteriological  investigations,  we  are,  nevertheless, 
strongly  inclined,  from  our  present  experience,  to  acknowledge  the  correctness  of 
this  view,  even  if  we  do  not  estimate  the  frequency  of  rheumatic  pleurisy  nearly 
so  high,  as,  e.  g.,  does  Fiedler,  on  the  ground  of  his  observations  in  Dresden. 

Rheumatic  pleurisy  usually  develops  rather  suddenly  in  persons  previously 
healthy.     Sometimes  it  is  preceded  by  mild  rheumatic  pains  in  the  muscles  or 


PLEUKISY  289 

some  of  the  joints.  The  local  discomforts,  such  as  pain  in  the  side,  are  often 
very  severe,  the  fever  is  moderately  high,  though  rarely  over  104°  (40°  C.) ; 
and  as  the  case  progresses  such  rheum^itic  symptoms  as  swelling  of  the  joints  and 
endocarditis  may  associate  themselves  with  the  pleurisy,  and  confirm  the  diag- 
nosis. In  general,  however,  the  course  of  the  disease  is  favorable.  The  fever 
lasts,  as  a  rule,  only  a  week  or  two,  and  even  when  there  is  a  large  exudation  it 
finally  undergoes  complete  absorption  with  recovery. 

2.  Tubercular  Pleurisy. — In  an  setiologieal  sense  we  must  declare  the  larger 
part  of  the  ordinary  "  pleuritic  effusions,"  which  clinically  seem  primary,  to  be 
tubercular.  The  further  course  of  the  cases,  if  we  can  watch  them  long  enough, 
almost  always  permits  us  finally  to  recognize  the  tubercular  nature  of  the  dis- 
ease; yet  we  can  not  say  that  some  other  tubercular  disease,  particularly  phthisis, 
is  always  the  immediate  sequel  of  the  pleurisy. 

In  a  comparatively  small  number  of  cases  do  the  symptoms  of  acute  tubercu- 
losis, or  more  frequently  of  chronic  phthisis,  appear  as  an  immediate  result  of  the 
pleurisy,  which  at  that  time  is  usually  still  present  or  in  the  contracting  stage. 
The  objective  changes  of  phthisis  are  evident  either  in  the  apex  or  in  the  lower 
lobe  of  the  affected  side.  The  fever  continues,  the  pulmonary  affection  advances, 
the  other  lung  is  also  attacked,  and  the  disease  takes  a  fatal  course  under  the 
type  of  an  ordinary  phthisis,  now  more  acute  and  now  more  chronic. 

In  other  cases  acute  tubercular  aifections  arise  sooner  or  later  as  a  result 
of  the  pleurisy — tubercular  meningitis,  or  general  miliary  tuberculosis.  In  other 
cases  still  the  disease  develops  under  the  form  of  tuberculosis  of  the  serous  mem- 
branes, to  which  we  will  return  again  in  the  description  of  tubercular  pericar- 
ditis and  tubercular  peritonitis.  We  often  have  to  do  with  a  double  pleurisy 
with  no  evident  complication  in  the  lungs.  In  varying  succession  are  added  the 
symptoms  of  chronic  tubercular  peritonitis,  with  pain,  swelling,  and  effusion  of 
fluid  into  the  abdomen,  or  the  symptoms  of  tubercular  pericarditis.  Death  finally 
ensues  with  persistent  hectic  fever  and  increasing  general  emaciation  and  weak- 
ness. The  whole  affection  usually  runs  a  chronic  course,  lasts  for  months,  and 
often  shows  marked  remissions  and  temporary  improvements. 

In  very  many  instances,  on  the  other  hand,  the  pleuritic  effusion  has  through- 
out an  apparently  favorable  course.  After  some  weeks  the  fever  ceases,  the  effu- 
sion is  absorbed,  the  patient  gets  up,  and  is  finally  discharged  as  nearly  well. 
Of  course,  some  dullness  and  retarded  motion  often  remain  in  the  affected  side, 
but  even  these  may  gradually  disappear.  These  cases,  too,  very  often  turn  out 
in  the  end  to  be  tubercular.  After  a  longer  or  shorter. period  of  apparent  health, 
sometimes  after  the  lapse  of  years,  a  "  new  "  disease  appears — that  is,  either  a 
return  of  the  pleurisy,  a  pleurisy  on  the  other  side,  or  some  other  acute  or  chronic 
tubercular  affection.  In  such  cases,  too,  we  must  look  upon  the  former  pleurisy,  in 
an  setiological  sense,  as  tubercular.  It  is  not  impossible,  however,  for  even  a  tuber- 
cular pleurisy  to  recover,  and  for  the  recovery  to  be  permanent,  if  no  other  organ 
is  at  the  same  time  affected  by  tuberculosis,  especially  if  the  lungs  remain  intact. 

Finally  we  must  mention  the  cases  in  which  a  pleuritic  effusion  develops  sec- 
ondarily to  an  already  pronounced  phthisis.  Here  too  we  almost  always  have  to 
do  with  a  tubercular  pleurisy. 

The  anatomical  changes  in  tubercular  pleurisy  consist  in  the  ordinary  signs 
of  inflammation,  and  also  the  presence  of  the  specific  nodules  of  tubercle.  The 
number  of  tubercles  differs  very  much  in  different  cases.  The  pleura  is  in  some 
cases  completely  studded  with  miliary  nodules,  and  in  others  we  find  the  tuber- 
cles, at  least  with  the  naked  eye,  only  in  single  spots.  The  effusion  is  usually  of 
a  sero-fibrinous  character.  Sometimes  it  is  ha9morrhagic,  as  the  majority  of  cases 
of  apparently  primary  "  haemorrhagic  pleurisy ''  are  generally  of  a  tubercular 
nature.  Empyema  also  (vide  infra)  occurs  not  infrequently  in  association  with 
19 


290  DISEASES    OF   THE   EESPIEATOEY   OEGANS 

tuberculosis;  and  finally,  in  a  few  cases  the  exudation  has  been  of  a  peculiar 
milky  character,  and  has  contained  numerous  oil-globules,  probably  originating 
from  fatty-degenerated  and  disintegrated  leucocytes  and  endothelium, 

3.  Purulent  Pleurisy— Empyema.— A  purulent  exudation  is  developed  in  the 
pleura  when  the  inflammation  of  that  organ  is  due  to  a  specific  cause  which 
excites  suppuration.  So  far  as  is  yet  known,  the  streptococcus  pyogenes  seems 
to  be  the  most  frequent  factor  in  producing  empyema.  It  is  found  in  the  pus 
of  empyema,  due  to  such  causes  as  external  injury,  caries  of  the  ribs,  pulmonary 
tuberculosis,  pneumonia,  and  pyaemia.  Less  often  empyema  is  excited  by  staphy- 
lococci. This  is  almost  always  a  rather  favorable  form  of  the  disease.  Likewise 
comparatively  benign  is  meta-pneumonic  empyema,  which  in  most  instances  is 
caused  by  the  pneumococcus.  The  empyema  of  tuberculosis  is,  as  has  been 
already  pointed  out,  in  most  cases  devoid  of  bacteria  (A.  Frankel  and  others), 
and  here  we  may  have  to  do  with  the  formation  of  chemical  poisons  capable  of 
exciting  suppuration. 

Empyema  usually  causes  severe  symptoms.  The  fever  is  higher  than  in  the 
other  forms  of  pleurisy,  but  it  is  irregularly  intermittent,  and  is  often  associated 
with  chills.  There  are  severe  general  symptoms  besides  the  fever,  such  as  great 
languor,  headache,  a  dry  tongue,  and  a  rapid  pulse.  We  sometimes  notice  a  slight 
oedema  of  the  chest-wall  on  the  affected  side.  Otherwise  the  local  symptoms  and 
disturbances  are,  of  course,  the  same  as  in  the  other  forms  of  pleurisy.  If  the 
pus  is  not  evacuated  artificially,  the  empyema  may  finally  break  externally  or  into 
the  lungs  (vide  supra).  In  the  latter  case  a  very  large  expectoration  of  pus  sud- 
denly occurs,  and  is  usually  followed  by  pneumothorax. 

Diagnosis. — Our  chief  attention  in  regard  to  diagnosis  is  directed  to  the  dis- 
tinction between  pleurisy  and  acute  or  chronic  pneumonia,  which  is  not  very  easy 
in  all  cases.  We  will  briefly  contrast  the  distinctive  features  as  made  out  on 
physical  examination. 

Inspection. — A  marked  distention  of  the  affected  side  points  to  effusion;  it 
does  not  occur  in  pneumonia. 

Percussion. — The  dullness  in  pleurisy  is  complete,  and  the  feeling  of  resistance 
on  percussion  is  very  marked;  in  pneumonia,  however,  the  dullness  is  rarely  so 
marked,  and  there  is  often  a  tympanitic  sound.  The  discovery  by  percussion  of 
signs  of  displacement  of  the  neighboring  organs  is  of  especial  weight,  as  these 
signs  are  always  absent  in  uncomplicated  pneumonia,  while  with  few  exceptions 
they  can  be  easily  demonstrated  in  every  case  of  pleurisy  when  the  exudation  is 
at  all  considerable. 

Auscultation. — Diminished  or  suppressed  respiratory  murmur  points  to  pleu- 
risy, loud  bronchial  breathing  and  rales  to  pneumonia;  but  we  must  not  forget 
that  in  pneumonia  auscultation  may  give  the  same  signs  as  in  pleurisy,  if  a 
bronchus  is  plugged. 

Vocal  Fremitus. — Marked  vocal  fremitus  over  dullness  is  direct  evidence  of 
pneumonia,  diminished  or  absent  vocal  fremitus  of  pleurisy ;  but  the  vocal  fremi- 
tus may  also  be  diminished  in  pneumonia  if  a  bronchus  is  plugged. 

Besides  the  physical  signs,  other  phenomena  to  be  observed  are  the  mode  of 
commencement,  the  course  of  the  disease,  the  fever,  the  expectoration,  and  the 
appearance  of  herpes.  The  most  reliable  means  of  deciding  in  all  doubtful  cases 
is  exploratory  puncture,  although  even  then  we  may  of  course  be  left  in  doubt 
whether  an  infiltration  of  the  corresponding  portion  of  the  lung  may  not  exist,  in 
addition  to  pleurisy.  If  the  exudation  is  largely  fibrinous,  or  if  there  is  an 
abundant  new  growth  of  inflammatory  connective  tissue,  the  results  of  aspira- 
tion may  be  negative.  Hence,  in  doubtful  cases  we  should  always  make  re- 
peated trials. 

If  we  have  diagnosticated  a  pleuritic  effusion,  the  next  question  is  always  as 


PLETJKISY  291 

to  the  character  of  the  effusion,  because  the  prognosis  and  treatment  are  to  a  large 
degree  dependent  upon  this.  Although  certain  well-known  astiological  circum- 
stances, and  the  severity  of  the  fever  and  the  general  symptoms,  often  permit  us 
to  suspect  the  nature  of  the  effusion,  whether  serous  or  purulent,  the  only  certain 
information  comes  from  an  exploratory  puncture  with  a  hypodermic  syringe. 
If  the  syringe  is  carefully  disinfected,  and  the  operation  is  cautiously  conducted, 
this  procedure  is  entirely  devoid  of  danger,  and  we  must  urgently  advise  its 
employment  in  all  doubtful  cases  in  order  to  settle  the  diagnosis.  It  is  indeed  of 
practical  importance  to  know  that  there  is  a  likelihood  in  empyema  of  obtaining 
no  fluid  by  means  of  exploratory  puncture  (vide  supra),  even  when,  upon  incision, 
pus  is  found.  We  have  had  this  experience  repeatedly.  In  doubtful  and  severe 
cases  in  which  there  is  suspicion  of  empyema,  it  is  therefore  decidedly  advisable, 
when  life  is  threatened,  to  make  an  incision  of  the  pleura.  Besides  a  macro- 
scopic inspection,  a  careful  microscopic  examination  of  the  fluid  withdrawn  is 
sometimes  of  importance.  Besides  the  ordinary  constituents — red  and  white 
blood-corpuscles,  endothelial  cells,  and  cholesterine  crystals — ^we  may  sometimes 
find  something  of  special  diagnostic  significance,  such  as  bacteria  in  septic  pleu- 
risy, carcinoma-cells  in  cancerous  pleurisy,  etc. 

We  can  not  always  judge  from  the  beginning  whether  a  pleurisy  is  tuber- 
cular or  not;  but  we  should  never  forget,  as  has  already  been  affirmed,  that  in 
every  case  of  pleurisy,  even  if  it  is  apparently  primary,  there  is  a  strong  sus- 
picion of  tuberculosis.  We  must  observe  in  particular  the  general  habit  and 
the  nutrition  of  the  patient,  and  inquire  into  the  hereditary  predisposition  and 
any  previous  illnesses.  In  the  further  course  of  the  disease  persistent  hectic 
fever,  slowly  increasing  emaciation  and  pallor,  fresh  relapses,  and  the  onset  of 
pulmonary  symptoms,  point  to  the  tubercular  character  of  the  pleurisy.  Every 
double  pleurisy,  and  every  pleurisy  associated  with  pericardial  symptoms,  leads 
us  most  decidedly  to  suspect  tuberculosis.  A  hsemorrhagic  effusion,  as  we  have 
said,  points  strongly  to  tuberculosis.  Tubercle  bacilli  are  usually  not  present  in 
the  exudation  of  tuberculous  pleurisy,  because  the  tubercular  nodules  of  the 
serous  membrane  scarcely  ever  ulcerate.  On  the  other  hand,  we  have  often  been 
able  to  demonstrate  tubercle  bacilli  in  the  scanty  expectoration  of  such  patients, 
even  when  there  were  scarcely  any  pulmonary  symptoms.  The  peculiarities  of 
rheumatic  pleurisy  have  been  already  detailed. 

Prognosis. — The  prognosis,  as  regards  the  immediate  danger  of  the  disease, 
depends  entirely  upon  the  severity  of  the  symptoms,  and  especially  upon  the 
dyspnoea.  The  prognosis,  as  regards  the  further  course  of  the  disease,  depends 
chiefly  upon  the  nature  of  the  pleurisy.  Many  secondary  and  also  many  appar- 
ently primary  pleurisies,  although  extensive,  recover  completely  and  permanently 
after  weeks  or  months.  Unfortunately,  we  only  too  frequently  have  to  give  a 
doubtful  or  an  unfavorable  prognosis,  especially  if  the  tubercular  nature  of  the 
pleurisy  be  probable  or  certain.  The  prognosis  of  empyema  depends  partly  upon 
the  underlying  disease,  but  especially  upon  judicious  and  timely  operative  inter- 
ference. In  benign  cases  of  empyema  recovery  is  usually  complete  in  a  few  weeks 
after  operation,  but  sometimes  months  are  required.  The  possibilities  of  a  spon- 
taneous rupture  of  empyema,  internally  or  externally,  have  been  mentioned  above. 
With  incomplete  healing,  which  leaves  a  pleural  fistula,  we  must  fear  the  appear- 
ance of  general  amyloid  disease  in  various  organs. 

In  rare  instances  with  large  effusions  sudden  death  occurs,  an  event  which  can 
not  always  be  satisfactorily  explained.  Probably  there  are  different  factors  in 
different  cases,  such  as  pulmonary  embolism,  cerebral  embolism,  sudden  cerebral 
anaemia,  weakness  of  the  heart,  or  the  onset  of  pulmonary  cedema. 

Treatment. — In  the  beginning  of  the  disease  the  treatment  is  purely  symp- 
tomatic.    We  try  to  alleviate  the  patient's  symptoms,  the  pain  and  dyspnoea,  by 


292  DISEASES    OF   THE   EESPIEATORY   ORGANS 

local  applications,  especially  by  mustard  plasters,  warm  poultices,  which  are 
usually  more  grateful  than  cold  applications,  sometimes,  too,  by  dry  cups,  also  by 
embrocations  with  chloroform  liniment,  and,  with  severe  symptoms,  by  mor- 
phine internally  or  subcutaneously.  Unfortunately,  we  have  but  few  remedies  to 
check  the  inflammatory  process  in  the  pleura.  If  an  ice-bag  is  well  borne,  it  may 
be  of  service.  The  efficacy  of  the  much-used  painting  with  iodine  is  doubtful,  but 
it  may  always  be  tried  if  there  is  a  severe  pleuritic  pain.  Perhaps  more  efficient 
is  the  application  of  iodized  vasogen,  or  of  iodoform  ointment  (1  to  15). 

If  a  large  serous  effusion  has  formed,  it  is  the  universal  custom  to  prescribe 
diuretics.  The  idea  is  to  cause,  or  at  any  rate  promote,  the  absori)tion  of  the 
exudation  by  increasing  the  excretion  of  urine.  It  is,  however,  very  difficult  to 
obtain  any  real  proof  of  the  usefulness  of  diuretics  in  pleurisy  with  effusion. 
They  often  are  of  no  use  whatever,  but  again,  the  absorption  of  the  fluid  may 
follow  the  administration  of  a  diuretic,  so  tha't  it  does  not  seem  impossible  that 
the  latter  has  a  therapeutic  influence.  With  regard  to  a  choice  of  the  diuretics  to 
be  employed  we  would  name,  first,  salicylate  of  sodium,  75  to  120  grains  (grammes 
5  to  8)  a  day,  because  a  specific  influence  has  been  ascribed  to  this  drug  in  pleu- 
risy. This  applies  particularly  to  cases  of  supposed  rheumatic  origin  (vide 
supra).  Many  good  observers  assert  that  primary  pleuritic  exudations  often  run 
a  remarkably  rapid  and  favorable  course,  when  treated  with  salicylate  of  sodium. 
Moreover,  the  drug  has  a  direct  diuretic  effect.  Besides  this,  the  acetates  of  potas- 
sium and  of  sodium  are  frequently  prescribed,  as  well  as  squills,  and,  of  late,  diu- 
retine  (sodio-salicylate  of  theobromine),  given  in  doses  of  thirty  grains  (grammes 
2)  two  or  three  times  a  day.  We  have  sometimes  found  this  remedy  apparently 
very  efficient.  If  there  are  signs  of  cardiac  weakness  and  diminished  arterial 
tension,  digitalis  must  be  prescribed,  alone  or  with  a  diuretic.  Other  internal 
remedies  are  at  present  seldom  employed  in  pleurisy  with  effusion.  The  influence 
of  iodide  of  potassium  as  an  "absorbent "  is  extremely  doubtful.  Drastic  purga- 
tives and  such  diaphoretic  remedies  as  hot  packs  and  pilocarpine  usually  affect 
the  general  condition  unfavorably,  and  are  of  little  use.  Probably  there  are  to- 
day few  advocates  of  the  so-called  Schroth  method  of  treatment,  according  to 
which  the  amount  of  fluid  ingested  is  reduced  to  a  minimum,  so  as  to  promote  the 
absorption  of  the  exudation.  In  many  cases  the  operative  treatment  of  pleu- 
risy (introduced  by  Trousseau) — the  evacuation  of  the  effusion  by  puncture — is 
of  the  greatest  importance.  Many  cases  of  pleurisy  with  effusion  run  a  favor- 
able course  without  it,  and  we  consider  it  at  least  superfluous  to  puncture  every 
effusion  without  sufficient  grounds,  but  puncture  is  often  one  of  the  most  service- 
able therapeutic  influences  at  our  command.  The  first  and  most  important  indi- 
cation for  puncture  is  present  when  the  effusion  becomes  so  large  as  to  be  directly 
dangerous  to  life.  As  soon  as  the  patient's  dyspnoaa  reaches  a  dangerous  degree, 
and  the  cyanosis  becomes  marked  and  the  pulse  weaker,  a  puncture  must  be 
made  as  a  direct  vital  indication.  When  the  exudation  is  of  considerable  size 
there  may  be  a  very  sudden  aggravation  of  the  symptoms,  so  that  in  such  cases 
one  should  not  wait  too  long.  It  is  much  better  to  puncture  too  early  than  too 
late!  Trousseau  urged  that  tapping  should  invariably  be  performed  when  the 
dullness  caused  by  the  exudation  involves  not  only  the  back,  but  also  the  whole 
or  nearly  all  of  the  anterior  wall  of  the  thorax,  a  rule  which  the  author  almost 
always  follows.  The  benefit  of  such  a  puncture  is  often  pronounced.  The  sec- 
ond indication  is  a  too  protracted  absorption  of  the  effusion.  Puncture  is  indi- 
cated if  the  effusion  does  not  disappear  after  an  apparent  remission  of  the  in- 
flammatory symptoms,  especially  after  the  fever  has  gone.  We  often  see  the 
further  absorption  stimulated  by  such  a  puncture.  It  has  been  said  that,  if  pos- 
sible, tapping  should  be  delayed  until  the  fever  has  ceased,  but  to  us  this  does 
not  seem  at  all  necessary.     When  the  exudation  was  large,  or  the  absorption  was 


PLEURISY 


293 


delayed,  Ave  have  repeatedly  aspirated  even  when  the  patient  was  still  feverish, 
and  have  not  infrequently  found  that  the  fever  diminished  remarkably  upon  the 
removal  of  the  exudation  (see  the  temperature  chart,  Fig.  37). 


*  Puncture 
(1200  Ccm.) 


40.' 


39.° 


ifiiiaiiiiiiniiiiiiiii 

HinHaiiRiBeiiiiii 


"Bailiriaii 


Fig.  37. — Temperature-curve  in  pleurisy  witli  effusion  before  and  after  tappiufr.    (Erlangen  medical 

clinique.) 

[There  is  considerable  danger  in  delaying  interference  with  a  large  effusion, 
especially  if  it  has  come  on  pretty  rapidly,  however  comfortable  the  patient  may 
be.  The  liability  to  sudden  and  fatal  dyspnoea  under  these  circumstances  is  now 
well  recognized.] 

As  regards  the  performance  of  the  puncture,  we  can  not  here  go  into  all  the 
numerous  methods  and  forms  of  apparatus  proposed.  The  distinctions  are  imma- 
terial. The  simpler  the  method,  the  easier  it  is  to  perform,  and  hence  the  better 
it  is. 

Every  puncture  must  be  preceded  by  an  exploratory  puncture  in  order  to  settle 
the  diagnosis  as  to  the  presence  and  character  of  the  exudation.  A  medium-sized 
trocar  with  a  lateral  openiug,  to  which  a  rubber  catheter  can  be  fastened,  senses  to 
evacuate  the  fluid.  Billroth's  and  Frantzel's  trocars  are  useful.  Aspiration 
can  be  performed  still  more  conveniently  with  a  hollow  needle,  and  best  of  all, 
according  to  our  experience,  with  that  proposed  by  Fiedler,  which  is  now  exclu- 
sively employed  in  the  author's  wards,  because  the  point  of  this  needle  is  guarded 
so  that  it  can  not  scratch  the  tissues,  and  also,  if  it  becomes  plugged  with  clots  of 
fibrine,  these  can  be  pushed  out.*  The  instruments  and  the  chest-wall  at  the 
point  of  puncture  must  be  carefully  disinfected.  We  usually  choose  a  point  for 
puncture,  somewhere  about  the  sixth  intercostal  space,  in  the  middle  or  poste- 
rior axillary  line.  The  patient  sits  up  in  bed,  but  is  held  and  supported  by 
another  person,  when  it  is  possible.  Before  and  during  the  puncture  he  takes 
a  little  strong  wine,  strophanthus,  or  similar  stimulant.  The  pain  of  the  opera- 
tion may  be  mitigated  by  previously  injecting  morphine  [or  still  better,  by  caus- 
ing local  anaesthesia  with  a  half-  to  one-per-cent.  solution  of  cocaine].  In  the 
overwhelming  majority  of  cases,  and  especially  if  the  exudation  is  abundant,  we 
can  remove  a  large  part  of  the  fluid  by  simple  puncture  with  siphonage.  With 
few  exceptions,  the  pleuritic  exudation  is  under  a  positive  pressure  of  10  to  25 
millimetres  of  mercury.  The  evacuating  tube  of  the  trocar  must  be  previously 
filled  with  carbolized  water  and  conducted  under  a  layer  of  the  same  into  the 
vessel  prepared  to  receive  the  effusion.  The  evacuation  of  the  effusion  should 
always  be  slow  and  gradual.  Many  physicians  advise  stopping  when  1,500 
cubic  centimetres  have  been  removed,  but  if  the  fluid  is  allowed  to  escai^e  slowly 
and  everything  is  going  well,  this  quantity  may  often  be  exceeded  with   im- 

*  [Fiedler's  instrument  consists  essentially  of  a  sharp  lioUovv  needle,  with  anoutor  jacket,  which  can 
be  moved  so  as  to  cover  the  sharp  point  after  the  chest-wall  has  been  penetrated.  If  the  lumen  is 
stopped  up,  a  pointed  steel  wire  thrust  directly  tlirough  the  attached  rubber  tubing  displaces  tlie 
obstruction. — Tkans.] 


294  DISEASES    OF   THE   EESPIRATOEY   ORGANS 

punity  in  the  case  of  large  exudations.  While,  as  we  have  said,  in  most  in- 
stances the  exudation  may  be  satisfactorily  removed  by  simple  puncture  and 
siphonage,  it  will  sometimes  prove  necessary  to  employ  aspiration.  Hence  some 
physicians  invariably  do  so,  and  to  this  there  is  no  objection,  even  if  it  is  unne- 
cessary. The  forms  of  apparatus  most  used  for  this  are  those  invented  by 
Dieulafoy  and  Potain.  In  puncture  with  aspiration  we  proceed  more  slowly  and 
cautiously. 

[The  necessity  for  two  punctures — one  exploratory,  the  other  distinctly  opera- 
tive— does  not  seem  clear.  The  two  can  be  perfectly  combined,  a  fair-sized  trocar 
or  needle  being  as  easy  of  introduction  and  producing  really  no  more  pain  than  a 
very  fine  one,  and  being  more  sure  to  give  results  on  which  reliance  can  be  placed. 
An  ordinary  Davidson's  syringe  makes  a  very  satisfactory  pump  and  can  always 
be  obtained.] 

Unpleasant  incidents  which  may  cause  a  cessation  of  the  process  are  rare. 
If  the  patient  complains  of  dizziness  or  faintness  we  must  cease,  or  at  any  rate, 
pause.  Usually  everything  goes  well  until  the  needle  begins  to  rub  against  the 
pleura:  then  there  is  pain  and  generally  a  violent  cough.  It  is  well,  then,  to 
remove  the  needle  at  once.  The  cough  can  usually  be  promptly  quieted  by  rest 
and  a  little  morphine,  but  sometimes  after  aspiration  there  will  develop  a  sort  of 
pulmonary  oedema,  with  the  expectoration  of  a  large  amount  of  frothy  serous 
sputum  (expectoration  albumineuse).  This  is  perhaps  due  to  the  increased  per- 
meability of  the  vascular  wall,  or  to  feebleness  of  the  left  ventricle. 

When  the  process  is  over,  we  close  the  little  opening  with  a  bit  of  sticking- 
plaster  or  with  iodoform  collodion.  A  regular  surgical  dressing  is  scarcely  ever 
necessary. 

If  the  exploratory  puncture  has  shown  a  purulent  effusion,  we  can  first  evacu- 
ate the  pus  by  puncture,  if  the  vital  indication  exists;  but  a  permanent  cure 
from  tapping  is  exceptional.  The  pus  almost  always  reappears.  Empyema  is  like 
an  abscess,  which  can  not  be  cured  until  a  permanent,  free  exit  for  the  pus  has 
been  provided.  We  must,  therefore,  not  only  remove  the  pus,  but  institute 
drainage  of  the  pleural  cavity.  The  best  method,  and  the  one  which  is  almost 
exclusively  practiced  in  the  surgical  wards  in  Erlangen,  is  by  incision  of  the 
pleural  cavity,  preceded  by  resection  of  a  portion  of  a  rib  for  the  purpose  of  com- 
pletely emptying  out  the  pus,  and  obtaining  a  better  final  result.  This  compara- 
tively simple  method  gives  results  so  good  and  so  entirely  satisfactory  that,  to  be 
frank,  we  can  not  understand  why  there  has  been  so  much  discussion  over  the 
treatment  of  empyema.  We  are  perfectly  willing  to  allow  that  good  results  are 
likewise  obtained  with  other  methods,  and  in  particular  with  the  drainage  by 
siphon  action,  advocated  by  Biilau.  Yet  there  is  not,  in  our  opinion,  any  satis- 
factory ground  for  abandoning  the  ordinary  surgical  principles,  relating  to  the 
treatment  of  internal  suppuration,  in  the  case  of  empyema.  With  regard  to  the 
minutiae  of  the  operation,  we  must  refer  to  text-books  on  surgery. 

In  treating  the  chronic,  contracted  pleurisies  with  thickening,  but  without 
fluid  effusion,  methodical  respiratory  efforts,  "  lung-gymnastics,"  are  of  use.  Be- 
sides these  we  should  strengthen  the  general  condition  as  much  as  possible.  We 
should  advise  the  patient  to  breathe  deeply,  and  prescribe  cold  sponging  of  the 
chest  daily.  Inspiration  of  compressed  air  by  means  of  a  pneumatic  apparatus  is 
often  accompanied  by  good  results.  Well-to-do  patients,  who  have  had  a  severe 
pleurisy,  should  be  sent  to  a  suitable  climatic  health-resort. 


PEEIPLEUKITIS  295 

CHAPTER  II 
PERIPLETJRITIS 

Under  the  name  of  "  peripleuritis  "  Wvinderlich  was  the  first  to  describe  a  rare 
form  of  disease,  which  consists  of  an  inflammation  of  the  connective  tissue 
between  the  costal  pleura  and  the  ribs,  and  which  terminates  in  the  formation  of 
an  abscess.  Similar  cases  have  since  been  repeatedly  observed,  and  all  were  char- 
acterized by  the  lack  of  any  discoverable  aetiology.  There  is  neither  a  previous 
injury,  nor  a  primary  disease  of  the  ribs  or  the  pleura.  Nevertheless  the  cause 
must  be  sought  in  an  invasion  of  micrococci,  which  excite  the  suppuration.  A 
knowledge  of  the  particulars,  however,  can  only  be  gained  from  future  investiga- 
tions. They  will  determine  whether  peripleuritis  can  be  regarded  as  an  inde- 
pendent disease  or  not. 

The  disease  occurs  chiefly  in  men.  It  usually  begins  suddenly  with  a  chill, 
and  runs  its  course  with  quite  a  high  fever.  In  pronounced  cases  the  local  symp- 
toms have  the  greatest  similarity  to  those  of  an  empyema,  but  the  greater  protru- 
sion of  the  chest-wall  is  striking.  The  ribs  are  crowded  apart  by  the  abscess,  and 
there  is  often  spontaneous  rupture  externally,  scarcely  ever  into  the  pleura.  Per- 
cussion gives  no  symptoms  of  displacement  of  the  neighboring  organs,  a  distin- 
guishing point  from  empyema.  It  is  of  diagnostic  significance  that  we  can  often 
discover  normal  lung-tissue  containing  air  below  the  abscess.  The  mobility  of  the 
lower  border  of  the  lung  is  also  usually  retained,  contrary  to  what  is  the  case  in 
empyema.  Another  important  sign  was  first  brought  to  notice  by  Bartels:  the 
wall  of  the  abscess  relaxes  on  inspiration  and  becomes  tense  on  expiration.  We 
may  also  mention  that  acute  nephritis  has  often  been  observed  among  the  com- 
plications. 

From  these  points  we  may  be  able  to  make  the  diagnosis  during  life,  at  least  in 
many  cases.  The  prognosis  is  quite  unfavorable,  but  recovery  does  occur.  The 
treatment  can  be  only  operative,  and  it  is  quite  analogous  to  that  for  empyema. 


CHAPTER   III 

PNEUMOTHORAX 

{Pyv-pneumothoraz.     Hydro-pneumotliora'x.) 

.31tiology. — Pneumothorax^ — that  is,  a  collection  of  air  or  gas  in  the  pleural 
cavity — arises,  in  an  overwhelming  majority  of  cases,  from  the  penetration  of  air 
into  the  pleural  cavity  through  an  opening  in  the  pleura.  The  opening  may  be 
in  the  external  chest-wall  from  a  penetrating  wound  of  the  chest  or  an  empyema 
operation,  or  it  may  be  in  the  pulmonary  pleura.  Pneumothorax  is  by  far  most 
frequently  associated  with  phthisis,  when  a  cavity  lying  beneath  the  pulmonary 
pleura  perforates  into  the  pleural  cavity.  This  is  more  apt  to  happen  in  compara- 
tively acute  phthisis  than  in  very  chronic  forms,  because  the  extensive  adhesions 
and  contractions  in  the  latter  hinder  its  development.  It  usually  apj^ars  in 
quite  far  advanced  cases,  but  it  may  sometimes  arise  with  but  slight  changes^  in 
the  lung. 

Pulmonary  gangrene  or  abscess,  as  well  as  phthisis,  may  cause  pneumothorax 
by  perforation  into  the  pleural  cavity.  It  may  also  arise  from  the  rupture  of  an 
empyema  into  the  lung.    In  some  cases  a  perforation  of  the  oesophagus  or  stom- 


296  DISEASES    OF   THE   EESPIRATOEY   ORGAl^S 

acli  into  the  pleura,  as  in  gastric  nicer,  has  been  observed,  with  the  formation  of 
pneumothorax. 

The  development  of  this  condition  from  severe  injuries,  as  from  laceration 
of  the  previously  healthy  lung,  without  injury  to  the  chest-wall,  is  rare.  Forced 
respiratory  movements,  associated  with  physical  exertion,  seem  especially  capable 
of  exciting  svTch  a  process.  We  have  ourselves  seen  pneumothorax  develop  sud- 
denly in  a  previously  healthy  woman  while  hanging  out  her  washing,  and  another 
time  in  a  young  man  during  very  labored  rowing.  Both  cases  recovered  rapidly 
and  completely. 

All  the  last-named  causes,  however,  are  far  less  important  than  pulmonary 
tuberculosis.  We  should  mention  that  in  phthisis,  too,  there  is  sometimes  a  defi- 
nite exciting  cause — severe  coughing,  vomiting,  or  muscular  exertion — which 
may  favor  the  development  of  the  pneumothorax. 

•  Many  authors  maintain  that,  by  decomposition  of  a  putrid  pleuritic  effusion, 
gas  may  be  produced,  and  thus  we  may  have  pneumothorax ;  but  such  an  event  is 
extremely  rare,  if  it  ever  happens. 

Pathological  Anatomy. — On  opening  the  pleural  cavity  a  part  of  the  air  usu- 
ally rushes  out,  sometimes  with  an  audible  noise.  We  then  look  into  a  large 
cavity  filled  with  air,  and  find,  in  total  pneumothorax,  the  lung  completely  re- 
tracted and  lying  compressed  against  the  vertebral  column.  If,  however,  the  air 
fills  only  a  part  of  the  pleural  cavity,  as  a  result  of  extensive  adhesions  of  the 
pleurse,  we  speak  of  a  circumscribed  or  sacculated  pneimiothorax.  The  amount 
of  air  contained  in  the  pleural  cavity  may  reach  2,000  cubic  centimetres.  The 
pressure  which  it  is  under  is  almost  always  positive — on  an  average  five  or  ten 
centimetres  of  water. 

In  the  cases  of  pneumothorax  arising  from  perforation  of  the  pulmonary 
pleura  we  can  usually  make  out  the  point  of  perforation  in  the  lungs.  This  is 
more  frequently  situated  in  the  upper  lobe  than  in  the  lower.  Sometimes  it  is 
already  grown  over  or  is  covered  by  a  layer  of  fibrine,  and  can  no  longer  be  found. 
The  opening  is  usually  quite  small,  but  it  may  reach  the  size  of  a  ten-cent  piece. 
Left-sided  pneumothorax  seems  to  be  somewhat  more  frequent  than  right-sided. 

The  pleura  itself  is  only  rarely  normal.  Usually  agents  of  inflammation  have 
entered  it  with  the  air,  and  hence  it  is  found  in  a  state  of  inflammation.  A  part 
of  the  cavity  is. then  filled  with  effusion.  This  is  usually  wholly  purulent — pyo- 
pneumothorax— or  sero-purulent,  but  it  may  even  be  serous  or  sero-fibrinous — 
sero-pneumothorax,  or  hydro-pneumothorax. 

The  neighboring  organs,  especially  the  heart  and  liver,  are  found  pushed  out 
of  their  normal  position,  as  in  large  pleuritic  effusions. 

Symptoms  and  Course. — The  onset  of  pneumothorax  (we  speak  in  what  fol- 
lows especially  of  pneumothorax  in  connection  with  pulmonary  tuberculosis)  is 
quite  often  made  known  by  a  sudden  pain,  usually  associated  with  an  increase  of 
the  dyspnoea  and  of  the  general  symptoms.  There  is  sometimes  collapse.  The 
temperature  sinks  below  normal,  the  pulse  rises  to  140  and  over.  The  patient 
looks  pale  and  cyanotic.  He  usually  sits  upright  or  is  in  a  half -sitting  position 
in  bed,  either  more  on  the  aft'ected  side,  in  order  to  use  the  normal  lung  as  much 
as  possible  for  breathing,  or  more  on  the  sound  side  on  account  of  the  tenderness. 
If  the  pneumothorax  has  come  on  as  a  result  of  the  rupture  of  an  empyema  into 
the  lungs,  there  is  at  the  same  time  a  veiy  abundant  expectoration  of  pus. 

Although  in  many  cases  the  symptoms  mentioned  lead  to  a  suspicion  of  pneu- 
mothorax, yet  a  positive  diagnosis  can  be  made  only  after  a  physical  exami- 
nation. 

Inspection  gives  a  very  marked  distention  of  the  affected  side.  The  inter- 
costal spaces  are  stretched  out,  or  even  protruded.  In  some  cases,  as  we  have  our- 
selves noticed,  there  is  a  marked  elastic  "  air-cushion  feeling  "  on  palpating  the 


PNEUMOTHOEAX  297 

intercostal  spaces.  On  respiration,  the  afFeeted  side  is  almost  entirely  motionless, 
while  the  excursions  of  the  other  side  are  the  more  marked.  The  displacement  of 
the  heart  is  often  evident  from  the.  visible  displacement  of  the  apex-beat. 

Percussion  gives  over  the  pneumothorax  a  remarkably  loud,  full  note,  abnor- 
mally deep,  but  usiTally  not  tympanitic,  on  account  of  the  tension  of  the  walls. 
It  is  especially  important  to  note  that  this  resonance  extends  beyond  the  normal 
limits  of  the  lung  on  the  right  down  to  the  seventh  or  eighth  rib,  and  on  the 
left  to  the  fifth  or  sixth  rib,  and  sometimes  even  to  the  edge  of  the  thorax.  The 
lower  limit  of  this  abnormally  loud  percussion  resonance  shows  no  change  of 
position  with  respiration. 

The  displacement  of  the  neighboring  organs  can  also  be  made  oi;t  by  percus- 
sion. With  right-sided  pneumothorax  we  find  the  lower  border  of  the  liver  dull- 
ness abnormally  low,  and  the  left  border  of  the  cardiac  dullness  pushed  over  to 
the  anterior  axillary  line.  In  left-sided  pneumothorax  the  cardiac  dullness  is 
usually  entirely  absent  from  its  normal  place,  and  is  found  instead  to  the  right  of 
the  sternum.  The  left  lobe  of  the  liver  is  pressed  downward,  and  in  the  "  semilu- 
nar space  "  we  find,  instead  of  the  normal  tympanitic  resonance,  the  same  deep, 
loud,  and  usually  non-tympanitic  note  as  in  the  upper  parts  of  the  thorax. 

Upon  auscultation  we  are  struck  by  the  entire  absence  of  respiratory  murmur. 
This  is  in  special  contrast  to  the  clear  resonance  on  percussion.  In  other  cases, 
however,  we  hear  a  number  of  metallic  sounds,  at  least  in  many  places  and  at 
many  times,  which  are  very  characteristic  of  pneumothorax.  First  among  these 
is  amphoric,  metallic  respiration.  This  arises  in  open  pneumothorax  (vide 
infra)  from  the  direct  passage  of  the  air  in  and  out,  but  in  all  other  cases  it  is  the 
ordinary  respiratory  murmur,  which  has  acquired  a  metallic  timbre  from  reso- 
nance in  the  pneumothorax.  In  an  analogous  way  arise  the  metallic-sounding 
rales  ["metallic  tinkling''],  and  the  metallic  resonr.nce  of  the  cough  and  voice. 
Heubner  has  devised  a  particularly  beautiful  and  practically  important  method 
for  demonstrating  the  metallic  sound  in  pneumothorax.  If  we  strike  lightly  on 
a  pleximeter  with  a  little  rod,  usually  the  handle  of  a  percussion  hammer,  while 
we  auscult  near  it — "  rod  percussion  " — we  very  often  hear  quite  a  distinct  high 
metallic  sound. 

The  vocal  fremitus  over  a  pneumothorax  is  usually  diminished,  but  it  may  be 
felt  in  spite  of  quite  a  large  collection  of  air. 

A  number  of  special  physical  signs  are  found  if  a  purulent  or  serous  effusion 
be  added  to  the  pneumothorax.  In  the  first  place,  the  resonance  is  thereby  ren- 
dered dull,  to  a  greater  or  less  extent,  in  the  lower  parts  of  the  chest.  The  bound- 
aries of  the  fluid  by  percussion  show  a  very  evident  change  with  the  patient's 
change  of  position,  because  the  fluid  in  pneumothorax  can  move  easily  in  all 
directions.  Inasmuch  as  the  shape  of  the  remaining  air  space  must  change  cor- 
respondingly, there  is  not  infrequently  a  change  in  the  pitch  of  any  metallic 
sounds  which  may  be  produced,  whether  by  percussion  or  respiration,  varying 
with  the  posture  of  the  patient  (Biermer's  change  of  note).  In  many  cases,  if 
the  ear  is  applied  to  the  chest-wall  there  is  heard,  on  every  motion  of  the  fluid, 
produced,  e.  g.,  by  gently  shaking  the  patient,  a  metallic  gurgling  sound,  so- 
called  Hippocratic  succussion. 

Forms  of  Pneumothorax. — According  to  the  condition  of  the  perforation  dur- 
ing life,  we  distinguish  three  kinds  of  pneumothorax  (Weil).  We  speak  of  an 
"  open  pneumothorax,"  if  the  point  of  perforation  remains  open,  so  that  the  air 
on  respiration  constantly  passes  in  and  out  of  the  pleural  cavity.  If  the  perfora- 
tion is  completely  closed,  we  have  a  "  closed  pneumothorax."  The  third  and  most 
frequent  form  is  the  "  valvular  pneumothorax,"  in  which  air  enters  the  pleural 
cavity  at  each  inspiration,  but  on  expiration  there  is  a  valve-like  closure  of  the 
perforation,  and  thus  the  air  can  not  escape  again;  but  as  soon  as  the  pressure 


298  DISEASES    OF   THE   RESPIRATOEY   ORGAITS 

in  the  pleural  cavity  increases  so  that  no  more  air  can  enter  it  on  inspiration, 
the  valvular  pneumothorax  becomes  closed.  In  open  pneumothorax  the  pressure 
in  the  pleural  cavity  must  be  the  same  as  the  atmospheric  pressure.  A  positive 
pressure  in  the  pleural  cavity  can  exist  only  in  a  closed  or  a  valvular  pneumo- 
thorax. 

A  clinical  diagnosis  of  the  form  of  pneumothorax  is  not  always  possible,  and 
has  usually  no  great  practical  importance.  The  very  loud,  metallic,  amphoric 
respiratory  murmur,  which  may  be  heard  in  open  pneumothorax,  must  be  men- 
tioned, and  Wintrich's  change  of  pitch  (see  page  243)  can  sometimes  be  heard 
in  this  form.  It  is  worthy  of  mention  that  symptoms  of  displacement  of  the 
neighboring  organs  must  also  arise  in  open  pneumothorax.  The  predominant 
atmospheric  pressure  here  is  positive  in  contrast  to  the  negative  pressure  in  the 
other  pleural  cavity,  and  to  the  normal  negative  pressure  which  previously 
acted  on  the  upper  surface  of  the  diaphragm.  A  very  marked  protrusion  of  the 
affected  side,  and  great  displacement  of  the  heart  and  liver,  however,  speak  most 
strongly  against  an  open  pneumothorax.  Some  authors  have  tried  to  find  a  point 
of  distinction  for  the  different  forms  of  pneumothorax  in  the  composition  of  the 
gas  in  the  pleural  cavity,  but  the  results  of  chemical  analysis  are  still  contradic- 
tory. According  to  Ewald,  we  find  in  open  pneumothorax  not  over  five  per  cent. 
of  carbonic  acid  and  about  twelve  to  eighteen  per  cent,  of  oxygen ;  in  closed  pneu- 
mothorax, however,  fifteen  to  twenty  per  cent,  of  carbonic  acid  and  ten  per  cent, 
at  most  of  oxygen.  If  in  an  open  pyo-pneumothorax  or  hydro-pneumothorax  the 
point  of  perforation  lies  below  the  level  of  the  fluid,  there  sometimes  arise  on 
every  inspiration  metallic  sounds,  since  the  bubbles  of  air  drawn  in  rise  and  come 
up  through  the  fluid — "  the  water-pipe  sound,"  "  metallic  tinkling."  A  peculiar 
sipping  and  short  snapping  sound  on  inspiration,  heard  by  us  in  one  case,  seems  to 
point  directly  to  the  existence  of  a  valvular  pneumothorax. 

Course  of  the  Disease. — In  many  cases  the  occurrence  of  pneumothorax  causes 
such  a  high  degree  of  respiratory  disturbance  that  death  ensues  in  a  few  hours  or 
days.  In  other  cases  the  patient  improves,  and  may  feel  quite  well  for  a  long  time 
in  spite  of  the  condition.  We  have  ourselves  frequently  observed  patients  who 
passed  the  entire  day  out  of  bed  with  scarcely  any  inconvenience.  Usually,  how- 
ever, the  disease  which  gives  rise  to  the  pneumothorax,  most  often  pulmonary 
tuberculosis,  leads  in  a  shorter  or  longer  time  to  death.  Sometimes,  again,  the 
patient  recovers.  This  almost  always  occurs  in  those  rare  cases  above  mentioned, 
when  a  healthy  lung  has  been  torn,  but  sometimes,  also,  in  cases  of  pulmonary 
tuberculosis.  The  healing  takes  place  in  this  way,  that  the  air  is  first  replaced  by 
a  fluid  effusion,  and  then  the  latter  is  gradually  absorbed,  but  the  air  may  also  be 
directly  absorbed  in  whole  or  in  part.  It  depends  upon  the  origin  of  the  lesion, 
then,  and  upon  the  intensity  of  the  underlying  disease,  whether  the  recovery  is 
permanent  or  not. 

Diagnosis. — The  diagnosis  of  pneumothorax  is  usually  easy  with  careful  ex- 
amination, but  the  symptoms  may  sometimes  be  of  so  little  prominence  as  to 
excuse  overlooking  it.  It  is  very  difficult  and  often  quite  impossible  to  make  a 
differential  diagnosis  between  very  large  cavities  and  a  saccular  pneumothorax, 
since  both  conditions  must  have  in  part  precisely  the  same  symptoms.  We  may 
mention  as  the  chief  points  in  distinction :  A  cavity  is  apt  to  be  situated  in  the 
apex,  pneumothorax  in  the  lower  part  of  the  thorax ;  over  a  cavity  the  chest-wall 
is  often  sunken  in,  over  pneumothorax  it  is  prominent ;  the  vocal  fremitus  is  usu- 
ally marked  over  a  cavity,  weak  over  pneumothorax.  Signs  of  the  displacement 
of  organs  point  to  pneumothorax,  as  does  distinct  succussion,  while  a  metallic 
respiratory  sound  and  metallic  resonance  on  rod  percussion  may  also  be  heard 
over  large  cavities  with  smooth  walls.  Besides  the  above  signs,  we  should  also 
carefully  regard  the  general  course  of  the  disease.     On  careful  questioning  we 


HYDKOTHOEAX.    H^MATOTHOEAX  299 

shall  almost  always  find  that  the  severe  symptoms  depending  upon  the  develop- 
ment of  a  pneumothorax,  set  in  with  more  or  less  suddenness. 

Treatment. — Whenever  pneumothorax  has  developed  we  must  seek  to  obtain 
perfect  quiet  for  the  patient,  as  well  as  diminution  of  his  sufferings,  by  means  of 
morphine  given  subcutaneously  or  internally.  The  results  of  the  administration 
of  this  drug,  in  a  sufficient  though  careful  dosage,  is  often  very  satisfactory. 
We  must  also  stimulate  cardiac  activity,  if  it  is  impaired,  by  means  of  stro- 
phanthus  or  camphor.  It  is  exceptional  to  find  operative  interference  necessary 
because  of  the  danger  to  life  in  the  first  days  of  the  attack;  and  even  later  on  we 
should  usually  wait  to  see  how  much  spontaneous  improvement  of  the  condition 
may  take  place.  If  the  symptoms  remain  severe  and  the  displacement  of  organs 
is  great,  we  should  try  to  remove  by  aspiration  as  much  air  as  possible  from  the 
pleural  cavity.  Likewise  if  there  is  an  abundant  exudation  it  is  always  useful 
to  puncture  and  remove  the  fluid,  repeating  the  operation  if  necessary.  If  the 
exudation  is  purulent,  the  treatment  is  precisely  the  same  as  for  empyema,  ex- 
cept that  in  hopeless  cases  of  far-advanced  tuberculosis  we  may  limit  our  efforts 
to  purely  symptomatic  treatment,  or  to  the  simple  evacuation  of  the  pus  by 
puncture. 


CHAPTEE   IV 
HYDROTHORAX.      H^MATOTHORAX 

1.  Hydrothorax. — We  term  the  occurrence  of  a  serous  transudation  into  the 
pleural  cavity,  independent  of  an  inflammation  of  the  pleura,  hydrothorax,  or 
thoracic  dropsy.  The  cause  of  hydrothorax  is  in  rare  cases  a  local  hindrance  to 
the  outflow  of  venous  blood  or  lymph  from  the  thorax,  as  in  compression  of  the 
veins  or  of  the  thoracic  duct  by  tumors;  but  in  the  great  majority  of  cases  the 
hydrothorax  is  part  of  a  general  dropsy,  occurring  especially  in  cardiac  or  renal 
disease.  Hydrothorax  is  often  first  developed  after  marked  oedema  of  the  sub- 
cutaneous cellular  tissue  and  ascites,  but  it  may  sometimes  be  one  of  the  first 
symptoms  of  dropsy,  particularly  in  renal  cases.  It  is  usually  bilateral,  but  it  is 
often  unilateral,  or  at  least  much  greater  on  one  side  than  on  the  other.  The 
pleura  itself  is  normal  or  else  oedematous.  We  often  find  it  traversed  v/ith  a  net- 
work of  dilated  lymphatics.  The  serous  fluid  in  hydrothorax  is  distinguished 
from  an  inflammatory  serous  effusion  by  the  smaller  amount  of  albumen  in  it, 
and  a  correspondingly  low  specific  gravity  (usually  below  1018),  by  the  scanty 
number  of  cell-elements,  and  by  the  absence  of  or  the  slight  tendency  to  spon- 
taneous coagulation. 

The  clinical  importance  of  hydrothorax  lies  in  the  hindrance  to  respiration 
which  it  causes.  As  a  result  of  this  the  hydrothorax  may  be  regarded  in  many 
cases,  especially  in  renal  disease,  as  the  chief  cause  of  death.  The  objective  evi- 
dence of  it  comes  from  the  physical  examination,  which  must,  in  general,  give 
dullness,  diminished  vocal  resonance,  and  dislocation  of  neighboring  organs,  the 
same  as  in  pleuritic  effusion.  We  desire  to  emphasize  also  the  bronchial  res- 
piration from  compression  in  hydrothorax,  which  is  often  very  loud,  although 
at  the  same  time  usually  high  and  sharp,  and  which  may  even  given  rise  to 
a  confusion  with  pneumonic  infiltration  in  the  lungs.  This  very  loud  respira- 
tory murmur,  contrasting  with  that  of  pleuritic  effusion,  is  explained  by  the  nor- 
mal condition  of  the  lungs  and  the  absence  of  all  adhesions.  For  the  same  rea- 
son, too,  the  change  in  the  boundary  of  the  dullness,  as  a  result  of  the  patient's 
change  of  position,  is  usually  more  marked  in  hydrothorax  than  in  pleuritic 


300  DISEASES    OF   THE   EESPIEATOEY   ORGANS 

effusion.  We  often  hear  a  few  fine  crepitant  rales  over  the  hydrothorax,  which 
arise  in  the  retracted  and  partly  atelectatic  lung.  The  main  factor,  however,  in 
distinguishing  hydrothorax  from  a  pleuritic  exudation  is,  in  every  case,  the  con- 
sideration of  the  primary  disease.  It  should  also  be  noticed  that  hydrothorax 
is  usually  bilateral,  while  pleuritic  exudation  is  usually  unilateral. 

Treatment  is  directed,  first  of  all,  to  the  primary  disease.  If  we  succeed  in 
strengthening  and  regulating  the  action  of  the  heart,  or  in  restoring  the  secre- 
tion of  urine,  the  hydrothorax  often  disappears  with  the  other  dropsical  symptoms. 
If  the  dyspnoea  caused  by  it  reaches  a  dangerous  degree,  we  often  see  great  relief 
from  aspirating  the  fluid.  The  nature  of  the  underlying  condition,  of  course, 
renders  the  benefit  in  many  cases  only  transitory. 

2.  Hsematotliorax. — Effusions  of  blood  into  the  pleural  cavity  (hsemato- 
thorax.)  arise  most  frequently  from  traumatic  lacerations  of  blood-vessels,  rarely 
from  the  bursting  of  an  aneurism  of  the  aorta  into  the  pleural  cavity,  from  ero- 
sion of  an  intercostal  artery  in  caries  of  the  ribs,  from  the  rupture  of  a  cavity  into 
the  pleura  in  phthisis,  if  it  simultaneously  opens  a  blood-vessel,  etc.  In  many 
such  cases  a  typical  exudative  pleurisy  follows  the  effusion  of  blood.  The  physical 
signs  are  the  same  as  in  other  pleural  effusions.  Severe  dyspnoea  may  demand 
the  removal  of  the  blood  by  puncture,  or  even  by  an  incision. 


CHAPTER   V 
NEW    GROWTHS    OF    THE    PLEURA 

The  majority  of  new  growths  occurring  in  the  pleura  are  of  a  secondary  na- 
ture. We  sometimes  find  single  metastatic  nodules  of  cancer  in  the  pleura  after 
primary  carcinoma  of  other  organs,  especially  of  the  mammary  gland  and  the 
lungs,  but  most  carcinomata  of  the  pleura  arise  from  primary  carcinomata  of  the 
lungs  and  are  due  to  a  direct  invasion  of  the  pleura  by  the  new  growth. 

Of  the  primary  new  growths  in  the  pleura,  only  one  is  of  great  importance — ■ 
the  endothelial  carcinoma,  first  described  by  E.  Wagner.  This  develops  de  novo, 
in  a  diffuse  manner,  from  a  proliferation  of  the  endothelial  cells  of  the  lymphatics 
and  the  connective  tissue.  Metastases  occur  in  the  lungs,  in  the  lymph-glands,  in 
the  liver,  in  the  muscles,  etc. 

Single  secondary  nodules  of  cancer  in  the  pleura  cause  no  special  clinical 
symptoms,  but  the  cases  of  diffuse  cancer  of  the  pleura  as  a  result  of  primary  can- 
cer of  the  lungs  are  important,  inasmuch  as  the  sjmiptoms  of  disease  of  the  pleura 
often  quite  predominate  over  the  pulmonary  disease.  The  dullness  is  intense,  the 
respiratory  murmur  and  the  vocal  fremitus  diminished.  In  one  such  case  we  saw 
a  proliferation  of  the  cancer  upon  the  ribs  in  front  so  that  there  was  externally  a 
very  marked  circumscribed  swelling.  The  character  of  the  sputum  is  the  only 
thing  that  can  give  ns  definite  information  as  to  the  origin  of  the  new  growth 
in  the  lungs  (see  the  chapter  on  cancer  of  the  lungs). 

Primary  endothelial  carcinoma  of  the  pleura  runs  a  course  similar  to  chronic 
pleurisy.  As  we  sometimes  find  a  co-existing  fluid  effusion  in  the  pleural  cavity, 
displacement  of  the  neighboring  organs  may  occur.  The  affection  goes  on  for  a 
long  time  without  fever,  or  with  slight  and  irregular  elevations  of  temperature. 
Most  cancers  of  the  pleura  are  associated  with  severe  pain. 

The  diagnosis  of  new  growths  in  the  pleura  can  usually  be  made,  if  at  all,  only 
in  the  more  advanced  stages  of  the  disease.  At  first  almost  all  the  cases  are 
regarded  as  simple  or  tubercular  chronic  pleurisy.     The  diagnosis  is  founded  less 


MEDIASTINAL   TUMOES  301 

upon  the  physical  signs  than  upon  the  general  course  of  the  disease,  the  habit  of 
the  patient,  and  the  evidence  of  metastases  in  the  glands  and  other  organs.  In 
some  cases  characteristic  elements  of  the  new  growth  can  be  found  by  the  micro- 
scope in  the  cloudy  fluid  obtained  by  an  exploratory  puncture. 

The  prognosis  is  absolutely  unfavorable,  the  treatment  purely  symptomatic. 
In  endothelial  carcinoma  we  might  perhaps  try  the  long-continued  use  of  arsenic. 


CHAPTER   YI 
MEDIASTIlSrAL    TUMORS 

Ix  the  anterior  mediastinum,  in  quite  rare  cases,  extensive  new  growths  occur, 
which  are  of  importance  on  account  of  their  severe  clinical  symptoms.  The 
point  of  origin  for  the  tumor  is  either  the  mediastinal  lymph-glands,  or  the 
connective  tissue,  or  sometimes  the  remains  of  the  thymus  gland.  In  their 
anatomical  character  the  tumors  are  almost  always  sarcomata,  usually  lympho- 
sarcoma, rarely  alveolar  sarcoma.  They  usually  occur  in  youth  or  middle  age, 
and  are  somewhat  more  frequent  in  men  than  in  women.  The  special  setiological 
factors  are  unknown.  In  some  cases  an  injury  is  stated  to  be  the  cause  of  their 
development. 

The  first  clinical  symptoms  are  usually  of  a  very  indefinite  nature.  The 
patient  complains  of  general  languor,  headache,  pain  in  the  chest,  and  slight  diffi- 
culty in  breathing,  and  only  gradually  do  severe  subjective  and  objective  symp- 
toms develop  in  the  chest. 

The  symptoms  are  in  part  due  directly  to  the  tumor,  but  in  larger  part  they 
are  symptoms  of  compression  from  the  gradually  increasing  pressure  of  the 
tumor  on  a  number  of  neighboring  organs. 

The  pain  in  the  chest,  which  is  located  chiefly  in  the  sternal  region,  and  is 
associated  with  a  marked  feeling  of  oppression,  may  be  very  severe.  It  sometimes 
shoots  into  the  lateral  portions  of  the  chest  and  into  the  arms,  showing  pressure 
on  the  brachial  plexus. 

The  dyspnoea  may  finally  increase  to  an  extreme  degree.  A  patient  with 
lympho-sarcoma  under  our  observation  could,  in  the  last  days  of  her  life,  breathe 
only  while  standing.  The  dyspncea  is  due  to  a  compression  of  the  heart  and 
lungs,  and  sometimes  to  actual  stenosis  of  the  trachea  or  a  primary  bronchus. 
Paralysis  of  the  dilators  of  the  glottis  may  also  occur  from  a  pressure  paralysis 
of  the  recurrent  nerves.  Paralysis  of  one  vocal  cord  has  been  repeatedly  observed. 
In  the  case  mentioned  above  a  marked  goitre  developed,  as  a  result  of  vascular 
stasis,  which  further  increased  the  dyspnoea  by  pressure  on  the  trachea.  A  hydro- 
thorax  from  local  venous  stasis  may  also  aid  in  increasing  the  dyspnoea. 

Pressure  on  the  oesophagus,  and  disturbances  of  deglutition  due  to  it,  are  rare. 
Pressure  on  the  vagus  nerve  and  the  sympathetic  sometimes  causes  anomalies  in 
the  rate  of  the  pulse — either  marked  acceleration  or  slowing  of  the  pulse.  If 
the  sympathetic  is  involved  there  is  inequality  of  the  pupils.  In  some  cases,  by 
pressing  on  the  tumor,  an  artificial  dilatation  of  the  pupil  can  be  excited  at  will. 
By  pressure  on  the  vessels,  especially  on  the  superior  vena  cava,  the  subcla- 
vian vein,  etc.,  oedema  and  cyanosis  may  arise  in  the  coiTCsponding  parts  of  the 
body. 

Objective  examination  of  the  chest  gives  a  marked  diffuse  prominence  of  the 
sternal  region  in  a  part  of  the  advanced  cases;  in  other  cases  this  swelling  is 
absent.    The  discovery  of  an  abnormal  dullness  in  the  anterior  part  of  the  chest 


502 


DISEASES    OF   THE   EESPIEATORY   ORGANS 


is  of  diagnostic  importance;  this  usually  joins  the  cardiac  dullness  on  the  left, 
and  on  the  right  it  extends  a  varying  distance  beyond  the  right  border  of  the 
sternum.  The  heart  is  often  pushed  somewhat  to  the  left.  We  heard  over  the 
pulmonary  artery  in  our  case  a  marked  systolic  murmur,  caused  by  compression 
of  the  vessel.    A  dissimilarity  of  the  pulse  on  the  two  sides  is  not  infrequent. 

The  diagnosis  of  a  mediastinal  tumor  is  usually  possible  in  cases  with  well- 
marked  symptoms,  but  in  other  cases  it  is  difficult  and  uncertain.  The  differential 
diagnosis  between  mediastinal  tumors  and  aneurism  of  the  aorta  (g.  v.)  causes 
especially  great  difficulty.  Tumors  may  also  be  confounded  with  abscesses  in  the 
anterior  mediastinum. 

The  prognosis  is  in  all  cases  absolutely  unfavorable.  The  disease  terminates 
fatally,  sometimes  after  a  duration  of  six  months  or  a  year. 

The  treatment  can  be  merely  symptomatic.  Internally  we  may  try  iodide  of 
potassium  or  arsenic.  In  the  last  stages  of  the  disease  we  must  try  to  alleviate 
the  patient's  great  distress  by  narcotics. 


CHAPTER   YII 
ACTINOMYCOSIS    OF    THE    THORACIC    CAVITY 


Bollinger  and  others  have  described  a  peculiar  tumor  affecting  the  jaw-bones 
of  cattle,  and  occasioned  by  the  presence  of  a  special  form  of  fungus,  known  as  the 

actinomyces  or  ray-fimgus.  More  recently 
a  class  of  diseases  has  been  studied  in 
human  beings,  occasioned  by  the  same 
fungus  (Ponfick,  Israel,  and  others). 
These  diseases  may,  as  in  cattle,  affect  the 
jaws,  the  floor  of  the  mouth,  and  the 
neck;  but  in  these  cases  they  are  mainly 
of  surgical  interest.  The  actinomycotic 
diseases  of  the  internal  organs,  however, 
possess  a  great  clinical  importance;  and, 
inasmuch  as  the  lungs  and  pleura  are  the 
most  frequently  affected  organs,  it  will 
be  well  to  present  briefly  here  the  most 
important  facts  which  have  as  yet  been 
learned  with  regard  to  actinomycosis. 
The  botanical  position  of  actinomyces  has 
not  yet  been  definitely  settled.  Cohn  and 
O.  Israel  regard  it  as  a  mould  fungus. 
Bostrom,  on  the  other  hand,  classes  it  with 
the  algse,  and  namely  with  the  variety 
eladothrix.  In  its  growth,  the  fungus 
forms  small  or  moderate-sized  gray  or  sul- 
phur-yellow nodules  which  may  be  dis- 
tinguished with  the  naked  eye  in  the  pus 
of  the  diseased  tissue  (see  below),  and  which  upon  microscopic  examination  re- 
solve themselves  into  a  tangle  of  mycelium.  It  is  an  especial  characteristic  that 
many  of  these  mycelia  bear  on  their  ends  a  club-shaped  swelling.  These  are 
placed  for  the  most  part  like  radii  on  the  periphery  of  a  nodule,  and  so  surround 
the  entire  mass  like  a  circlet  of  rays  (see  Fig.  38).     In  nature  actinomyces  seems 


Fig.  38.— Classes  of  actinomycosis. 
(From  Johne.j 


ACTDTOMYCOSIS    OF    THE    THOEACIC    CAVITY  303 

to  appear  especially  upon  plants,  for  example  upon  the  beard  of  spikes  of  wheat. 
Thus  is  explained  the  frequency  of  infection  in  the  plant-eating  cattle,  and  a 
similar  direct  infection  seems  occasionally  to  be  possible  in  man.  It  is  worthy 
of  note  that  the  fungus  seems  to  locate  itself  often  in  carious  teeth.  Thus  appar- 
ently arises  the  above-mentioned  disease  in  the  buccal  cavity;  while  on  the  other 
hand,  the  fungus  may  be  carried  from  its  nidus  in  the  mouth  by  inspiration  into 
the  respiratory  tract,  or  by  swallowing  into  the  primce  vice.  Of  course  it  may 
also  be  directly  swallowed  or  inhaled. 

Wherever  the  fungus  fastens  itself  in  the  body  it  occasions  first  a  new  growth 
of  granulation-tissue,  which  hp^  a  tendency  to  break  down  into  a  whitish  or 
brownish  pasty  mass.  The  brown  color  is  occasioned  by  the  haemorrhage  which 
frequently  occurs.  Very  often  actinomycosis  goes  on  to  suppuration;  still,  this 
probably  depends  upon  the  influence  of  pathogenic  germs  which  have  secondarily 
infected  the  part.  Of  especial  importance  is  the  tendency  of  the  disease  to  extend 
from  the  lungs  to  the  pleura  and  from  the  pleura  to  the  peripleuritic  connective 
tissue,  and  still  further  to  the  wall  of  the  thorax.  Thus  arise  not  only  extensive 
abscesses  and  wide-branching  fistulous  tracts,  but  also  a  very  characteristic, 
extremely  tough  cicatricial  infiltration  of  the  affected  part.  Not  infrequently 
there  is  at  last  a  perforation  reaching  the  outer  surface  of  the  body. 

The  entire  process,  as  a  rule,  is  slow  and  insidious,  but  constantly  progressive. 
The  symptoms  consist  at  first  in  slight  thoracic  discomfort,  pain,  cough,  and  ex- 
pectoration. Physical  examination  will  often  detect  changes  in  the  lungs,  but  the 
correct  interpretation  of  the  signs  found  is  of  course  at  first  difficult,  if  not  impos- 
sible. The  more  the  disease  spreads  the  greater  is  the  distress.  Usually  there  is 
hectic  fever,  which  may  assume  a  pysemic  character  if  there  is  extensive  suppura- 
tion. The  patient  gradually  loses  flesh,  and  in  repeated  instances  amyloid  degen- 
eration of  the  liver,  spleen,  and  kidneys  has  been  observed.  If  a  focus  breaks  into 
a  pulmonary  vein,  the  disease  may  be  developed  by  metastasis  in  other  internal 
viscera.  Moreover,  there  may  be  a  direct  extension  of  the  disease  to  the  pericar- 
dium, or  through  the  diaphragm  into  the  peritoneal  cavity. 

The  diagnosis  of  actinomycosis  is  at  first  difficult.  It  is  established  when  the 
characteristic  fungus  is  found  in  the  sputum,  but  this  has  occurred  in  only  a  few 
cases  as  yet.  If  very  extensive  peripleuritic  and  pericostal  suppuration  has  taken 
place,  and  the  process  has  spontaneously  broken  outward  or  been  laid  open  by 
surgical  means,  the  demonstration  above  described  in  reference  to  the  fungus 
is  easy. 

The  treatment  can  be  only  symptomatic,  unless  the  diseased  spot  can  be 
reached  by  operation,  and  then  the  treatment  becomes  surgical.  Permanent  cure 
has  so  far  been  attained  in  but  rare  instances.  [Iodide  of  potassium  has  proved 
curative  in  a  considerable  number  of  cases,  and  it  should  certainly  be  tried,  in 
doses  of  forty  to  sixty  grains  a  day. — V.] 


DISEASES   OF    THE   CIRCULATORY   ORGANS 


SECTION"  I 
Diseases  of  the  Heart 


CHAPTER   I 

ACUTE    ENDOCARDITIS 

{Endocarditis  verrucosa.     Endocarditis  ulcerosa) 

etiology. — Organized  excitants  of  inflammation  of  different  sorts,  whicli  cir- 
culate in  the  blood,  may  settle  on  the  endocardium,  especially  on  the  valves  of  the 
heart,  and  there  give  rise  to  an  acute  endocarditis.  Endocarditis,  therefore,  in 
its  fetiological  relations,  is  not  to  be  regarded  as  a  single  disease.  Pathogenic 
micro-organisms  have  been  injected  into  the  blood  (the  streptococcus  pyogenes, 
staphylococcus  aureus,  and  others),  and  in  this  way  an  artificial  endocarditis  has 
been  set  up  in  animals.  The  experiments  are  more  apt  to  succeed  if  the  valves 
or  the  inner  coat  of  the  vessels  have  been  subjected  to  some  slight  injury  before 
the  injection,  thus  promoting  the  settling  of  the  germs  upon  them  (Orth  and 
Wyssokowitsch,  Ribbert).  Most  cases  of  endocarditis  in  man,  both  the  vegeta- 
tive and  ulcerative  forms,  appear  to  be  caused  by  the  staphylococcus  pyogenes 
aureus.  Streptococci  are  much  less  frequent  than  staphylococci,  and  it  is  only 
in  rare  cases  that  endocarditis  is  occasioned  by  the  pneumococcus,  gonococcus,  and 
perhaps  the  diphtheria  bacillus. 

In  accord  with  these  statements  is  the  fact  that  in  human  beings  acute  articu- 
lar rheumatism,  which  is  probably  to  be  regarded  as  a  staphylococcus  infection,  is 
that  one  of  the  infectious  diseases  which  is  especially  apt  to  have  acute  endocar- 
ditis as  a  frequent  and  important  complication.  The  staphylococcus  infection 
need  not  appear,  however,  in  the  first  place,  as  a  typical  acute  polyarthritis. 
An  acute  endocarditis  may  appear  as  a  sequel  of  many  cases  of  apparently  pri- 
mary pleurisy,  tonsillitis,  or  other  disease.  Indeed,  it  is  sometimes  impossible 
to  determine  the  gate  of  entry  of  the  infection,  and  the  whole  disease  takes  the 
shape  of  an  apparently  primary  endocarditis.  In  such  cases  the  nature  of  the 
disease  is  made  evident  by  the  later  appearance  of  multiple  articular  swellings. 
We  also  regard  as  allied  to  polyarthritis  certain  forms  of  infection  called  the 
"acute  hsemorrhagic  diseases"  (e.g.,  purpura  rheumatica),  and  also  chorea 
(which  see).  It  is  therefore  not  surprising  that  acute  endocarditis  is  not  infre- 
quently observed  in  association  with  these  affections. 

There  are  other  acute  infectious  diseases  with  which  acute  endocarditis  may 
be  associated.  Probably  in  these  it  is  usually  the  result  of  a  secondary  mixed 
infection,  generally  with  the  staphylococcus.  This  explains  the  appearance  of 
acute  endocarditis  in  scarlet  fever,  small-pox,  diphtheria,  measles,  and  typhoid. 
Not  infrequently  mild  cases  of  acute  endocarditis,  without  clinical  significance, 
are  found  in  association  with  primary  tuberculosis  and  ulcerating  carcinoma. 
Again,  acute  and  chronic  nephritis  may  sometimes  occasion  a  development  of 
304 


ACUTE   ENDOCAEDITIS  305 

endocarditis.  An  especially  important  role  in  producing  endocarditis  is  dis- 
played by  grave  septic  and  pyaemic  conditions  (vide  supra).  In  these  cases  the 
acute  endocarditis  appears  as  one  symptom,  but  it  is  often  so  prominent  that  the 
whole  attack  is  called  endocarditis  (;vide  infra).  In  such  severe  diseases  we  have 
often  to  do  with  a  streptococcus  disease,  although  it  may  be  a  staphylococcus  in- 
fection of  especial  virulence.  The  ajtiology  of  gonorrhoeal  endocarditis  is  not 
yet  fully  determined.  Endocarditis  as  a  sequel  of  gonorrhoea  is  fortunately  very 
rare.  It  often  seems  to  be  an  actual  gonococcus  infection,  but  in  other  instances 
is  occasioned  by  some  secondary  germ. 

Finally,  we  have  still  to  mention  the  important  fact  that  acute  endocarditis 
quite  frequently  develops  on  the  soil  of  an  already  existing  chronic  endocarditis — 
the  so-called  acute  recurrent  endocarditis.  In  women,  pregnancy  and  the  puer- 
peral state  sometimes  seem  to  give  the  occasion  for  a  recrudescence  of  the  endo- 
carditis. 

Pathological  Anatomy. — We  usually  distinguish  an  endocarditis  verrucosa, 
with  the  formation  of  large  or  small  papillary  nodules  on  the  endocardium,  and 
an  endocarditis  ulcerosa  (endocarditis  diphtheritica) ,  with  ulcerations  as  a  result 
of  the  destruction  and  wasting  away  of  the  superficially  necrosed  tissue.  The 
malignant,  invariably  fatal  form  of  severe  septic  endocarditis  is  chiefly  ulcerative 
endocarditis.  Endocarditis  verrucosa  is  the  milder  form,  which  is  seen  especially 
in  acute  polyarthritis  and  allied  diseases,  but  we  can  not  draw  either  a  sharp  ana- 
tomical or  a  sharp  clinical  distinction  between  the  two,  since  malignant  cases  of 
endocarditis  verrucosa  are  also  observed. 

The  endocardial  growths  are  usually  situated  on  the  valves,  especially  on  their 
edges  of  closure.  More  rarely  we  find  them  on  the  chordas  tendinese  and  on  the 
endocardium  of  the  ventricle  and  auricle.  In  the  mildest  cases  they  are  scarcely 
as  large  as  the  head  of  a  pin,  but  in  severe  cases  they  may  increase  to  quite  large 
warty  and  glandular  masses.  Microscopically,  the  base  of  the  nodule  consists  of 
a  newly  formed  vascular  tissue,  infiltrated  with  small  cells,  which  on  its  surface 
changes  to  a  granular,  coagulated  mass.  This  last  is  formed  partly  of  coagulated 
albumen,  dead  cells,  and  fibrine  deposited  from  the  blood,  and  partly  of  micrococci 
(vide  supra).  The  micrococci  are  found  without  exception  in  all  cases  of  ulcera- 
tive endocarditis — having  been  first  discovered  by  Eberth.  The  endocardial  ulcers 
arise  from  the  destruction  of  the  superficially  necrosed  nodules.  If  the  thin 
valve  in  any  place  yields  to  the  blood-pressure,  we  have  the  so-called  acute  val- 
vular aneurism.  Complete  perforation  of  a  valve,  and  tearing  off  of  fragments 
of  a  valve  and  of  the  chordae  tendinese,  are  also  seen. 

The  great  majority  of  cases  of  acute  endocarditis  are  confined  to  the  valves  of 
the  left  side  of  the  heart — the  mitral  and  aortic  valves.  Endocarditis  on  the  tri- 
cuspid valve  is  seldom  seen  except  as  a  secondary  affection  in  old  cases  of  heart 
disease.  In  a  case  of  acute  ulcerative  endocarditis  in  a  grown  man  seen  by  us,  the 
process  was  confined  exclusively  to  the  tricuspid  valve,  and  there  were  very  many 
embolic  abscesses  in  the  lungs.  This  may  be  considered  a  great  rarity.  In  con- 
trast to  the  ordinary  localization  of  endocarditis  we  find  foetal  endocarditis  most 
frequently  in  the  right  side  of  the  heart. 

Many  other  organs  may  be  affected  by  the  endocarditis,  through  embolism.  In 
the  benign  endocarditis  verrucosa,  the  masses  of  fibrine  deposited  on  the  irregu- 
larities of  the  valve  furnish  the  embolic  material.  They  cavise  large  or  small  in- 
farctions in  the  kidneys  and  spleen,  embolic  softening  of  the  brain,  etc.  In  the 
malignant,  ulcerative  forms,  however,  large  numbers  of  bacteria  get  into  the  cir- 
culation at  the  same  time  with  the  necrotic  masses  of  tissue  which  have  been  torn 
off.  Here,  then,  we  have  to  do  not  merely  with  simple  mechanical  obstruction  but 
with  infectious  emboli.  The  emboli  in  ulcerative  endocarditis,  therefore,  either 
give  rise  to  embolic  abscesses  in  the  cardiac  muscles,  the  kidneys,  the  spleen,  the 
20 


306  DISEASES    OF   THE   CIRCULATOKY   ORGAIsTS 

lungs,  the  retina,  etc.,  or  they  result  in  haemorrhages,  especially  into  the  skin,  but 
also  into  the  kidneys,  the  brain,  the  retina,  and  the  serous  membranes.  It  is  not 
yet  known  why  in  some  cases  abscesses  are  more  frequent  and  in  others  haemor- 
rhages. The  two,  however,  may  be  combined.  In  general,  we  may  suppose  that 
the  development  of  abscesses  is  everywhere  connected  with  the  presence  of  bac- 
teria, while  haemorrhages  may  also  arise  from  toxic  influences ;  but  again  changes 
in  the  vascular  walls  caused  by  bacteria  might  give  rise  to  haemorrhages.  Em- 
bolic abscesses  belong  almost  exclusively  to  the  severe  form  of  septic  endocarditis. 
Haemorrhages  are  seen  in  this  form,  and  also — without  co-existing  abscesses — in 
certain  severe  forms  of  endocarditis  occurring  in  the  course  of  acute  rheumatism 
and  allied  diseases. 

Clinical  History. — Since  acute  endocarditis  is  not  aatiologically  a  distinct  dis- 
ease, and  since  its  clinical  course  is  very  different  in  different  cases,  it  seems  ad- 
visable to  us  to  describe,  in  what  follows,  the  most  important  varieties  separately ; 
but  it  must  be  expressly  noted  that  the  separate  classes  can  by  no  means  be  sharply 
defined,  and  that  there  are  many  intermediate  forms. 

1.  Slight  endocarditis  verrucosa  is  quite  frequently  found  in  the  cadaver, 
without  the  slightest  signs  of  any  affection  of  the  heart  during  life.  The  little 
papillary  excrescences  on  the  valves  of  the  heart  in  phthisis,  and  carcinoma,  whose 
aetiology  has  been  explained  above,  are  to  be  classed  under  this  head. 

2.  The  typical  form  of  henign  acute  endocarditis  is  most  frequent,  clinically, 
in  the  course  of  acute  articular  rheumatism.  It  is  much  rarer  in  other  infectious 
diseases  (vide  supra).  In  a  few  cases  it  is  also  seen  as  an  apparently  primary 
disease.  Here  there  is  a  constitutional  rheumatic  infection  which  has  taken 
place  in  some  way,  and  which  settles  directly  on  the  valves  of  the  heart  instead  of 
in  the  joints  (so-called  primary  rheumatic  endocarditis).  Careful  questioning 
will  sometimes  reveal,  or  at  least  render  probable,  the  place  of  infection  (a  mild 
case  of  tonsillitis  or  some  slight  external  injury).  Very  often  there  will  be  later 
the  symptoms  of  articular  rheumatism.  It  is  seldom  that  endocarditis  as  such  is 
associated  with  special  local  disturbances,  such  as  pain  in  the  region  of  the  heart, 
palpitation,  and  dyspnoea.  Ordinarily  the  heart  disease  is  discovered  only  by 
physical  examination.  The  impulse  of  the  heart  in  many  cases  is  abnormally 
strong  and  diffuse;  the  pulse  is  accelerated,  but  strong,  often  somewhat  jerky 
(pidsus  celer),  and  usually  regular,  but  sometimes  a  little  irregular.  Percussion 
at  first  shows  no  deviations  from  the  limits  of  normal  dullness.  On  auscultation, 
we  hear  at  the  apex,  more  rarely  at  the  base,  a  loud  blowing,  systolic  souffle. 
Diastolic  murmurs  are  rare  in  acute  endocarditis.  The  pulmonic  second  sound  is 
often  accentuated.  The  physical  signs  referable  to  the  heart  are  only  slightly 
marked  in  many  cases  of  acute  endocarditis.  This  is  understood  if  we  remember 
that  the  occurrence  of  a  heart-murmur  depends  wholly  on  the  localization  of  the 
endocarditis,  on  the  development  of  some  valvular  insufficiency,  etc. 

Besides  the  direct  symptoms  pointing  to  the  cardiac  affection,  the  onset  of  an 
acute  endocarditis  is  often,  but  not  always,  associated  with  fever,  or,  if  fever  be 
already  present,  with  an  increase  of  it,  and  with  a  slight  aggravation  of  the  gen- 
eral disturbance.  Embolic  processes  may  occur  in  the  brain,  the  spleen,  the  kid- 
neys, and  the  extremities,  but  they  are  comparatively  rare.  Sometimes  a  peri- 
carditis develops  as  a  result  of  the  endocarditis  (vide  infra). 

It  is  hard  to  make  any  accurate  statements  as  to  the  duration  of  this  form  of 
endocarditis.  The  physical  signs  may  last  for  days,  or  for  several  weeks.  Com- 
plete recovery  is  possible,  but  in  the  majority  of  cases  this  variety  passes  into 
chronic  valvular  disease  of  the  heart. 

3.  Malignant,  non-septic  form  of  acute  endocarditis  ("  rheumatoid  endocar- 
ditis" of  Litten).  In  many  cases  this  form  is  perhaps  only  a  quantitative  in- 
crease of  the  preceding  form,  but  in  other  cases  it  is  probably  distinct  from  it 


ACUTE   ENDOCAEDITIS  307 

setiologically.  The  severe  general  infection  is  usually  quite  prominent  here,  and 
the  disease  resembles  in  many  particulars  grave  septic  endocarditis.  The  ob- 
jective signs  in  the  heart  are  the  same  as  in  the  preceding  form,  but  more  intense 
and  extensive.  The  subjective  cardiac  symptoms,  such  as  palpitation  and  distress, 
may  be  quite  pronounced,  but  they  may  also  be  almost  wholly  absent  in  this  form. 
The  general  condition,  however,  is  usually  bad.  There  is  sometimes  high  fever 
with  an  irregular  or  intermitting  course,  but  in  many  cases  the  fever  is  remark- 
ably low  in  spite  of  quite  severe  constitutional  symptoms. 

The  constitutional  infection  is  very  often  manifested  in  these  cases  by  the 
appearance  of  small  or  large  haemorrhages  in  the  skin,  sometimes  in  the  mucous 
membranes,  as  in  the  conjunctiva  and  the  soft  palate,  and  rarely  in  the  retina. 
Secondary  articular  swellings  often  develop;  they  are  always  of  a  serous  charac- 
ter, and  never  purulent.  Renal  haemorrhages  and  acute  haemorrhagic  nephritis 
are  quite  frequent.  Large  emboli  may  also  occur  in  the  different  organs  in  this 
as  in  every  other  form  of  endocarditis. 

The  duration  of  the  disease  extends  over  many  weeks.  In  severe  cases  death 
ensues  with  a  gradual  aggravation  of  the  general  condition,  and  often  with  severe 
cerebral  symptoms,  such  as  stupor  and  delirium.  In  milder  cases,  however,  the 
patient  may  finally  get  well. 

Regarding  the  occurrence  of  this  form,  we  see  it  most  frequently  in  acute 
articular  rehumatism;  also,  in  rare  cases,  in  gonorrhoea,  when  it  comes  on  some 
three  or  four  weeks  after  the  beginning  of  the  urethral  affection;  also  in  ne- 
phritis, chorea,  peliosis  rheumatica,  etc.  The  apparently  primary  cases  of  this 
sort  usually  belong  to  the  recurrent  form  of  acute  endocarditis. 

4.  The  recurrent  form  of  acute  endocarditis  consists  of  an  acute  increase  of 
the  endocardial  process,  brought  on  by  some  exciting  cause,  in  a  patient  already 
suffering  from  chronic  endocarditis.  The  acute  disease  may  show  all  the  grada- 
tions from  the  mildest  to  the  severest.  The  mild  cases  often  run  their  course 
without  any  special  symptoms.  To  this  form  we  may  frequently  refer  the  more 
or  less  temporary  elevations  of  temperature  which  we  often  see  in  patients 
with  chronic  valvular  disease  of  the  heart.  In  rarer  cases  the  recurrent  endo- 
carditis comes  on  quite  suddenly  in  the  form  of  a  severe  acute  attack.  This 
sometimes  seems  to  be  clinically  a  primary,  independent  disease,  especially  if  the 
previous  chronic  heart  disease  has  up  to  that  time  caused  no  special  symptoms. 
The  patient  has  general  malaise,  headache,  chills,  and  fever.  The  last  may  be 
quite  high — 104°  (40°  C.)  and  over — or  moderate,  varying  between  100°  and  102° 
(38°-39°  C),  or  it  may  be  entirely  absent.  In  many  cases  it  is  intermittent, 
when  the  return  of  fever  is  often  associated  with  a  chill.  The  cardiac  symp- 
toms may  be  quite  pronounced,  but  in  this  form,  too,  they  may  be  obscure  and 
indefinite.  In  the  further  course  of  the  disease  we  meet  with  cutaneous  htBmor- 
rhages,  retinal  haemorrhages,  articular  swellings,  large  renal  haemorrhages,  or 
typical  haemorrhagic  nephritis — in  short,  just  the  same  general  type  of  disease  as 
in  the  other  malignant  forms  of  acute  endocarditis.  The  course  is  rarely  rapid, 
and  often  lasts  for  weeks.    Severe  cases  almost  always  end  fatally. 

5.  The  severe  septic  ulcerative  endocarditis  has  already  been  described  as  a 
complication  of  a  general  septic  state.  We  therefore  refer  to  the  appropriate 
chapter  (see  page  116)  for  all  particulars.  Septic  endocarditis  is  probably  en- 
tirely distinct  aetiologically  from  the  forms  thus  far  described,  and  is  manifested 
by  quite  a  rapid  fatal  course,  with  severe  typhoidal  or  pyaemic  symptoms.  It  is 
characterized  anatomically,  apart  from  the  cardiac  affection,  by  the  appearance 
of  metastatic  abscesses  in  the  various  organs,  but  in  many  cases,  as  we  have  said, 
abscesses  and  haemorrhages  are  combined. 

Diagnosis. — The  diagnosis  of  an  endocarditis,  coming  on  secondarily  in  the 
course  of  articular  rheumatism  and  other  diseases,  can  be  made  only  by  a  physical 


308  DISEASES    OE   THE    CIECULATORY   ORGAITS 

examination  of  tlie  heart.  We  must  therefore  give  constant  attention  to  the  con- 
dition of  the  heart  in  diseases  which  we  know  may  give  rise  to  endocarditis. 

The  diagnosis  of  the  malignant  form  of  endocarditis  often  causes  great  diffi- 
culty, especially  if  the  patient  is  not  seen  until  the  later  stages.  It  is  confused 
with  typhoid,  meningitis,  or  acute  miliary  tuberculosis.  Examination  of  the 
heart  may  furnish  positive  evidence,  but  sometimes,  as  we  have  said,  there  are 
no  physical  signs  of  cardiac  disturbance,  or  the  signs  present  are  indefinite.  Of 
other  factors  in  diagnosis  a  special  importance  attaches  to  the  secondary  swelling 
of  the  joints,  and  also  to  the  haemorrhages  into  the  skin  and  retina,  for  these  are 
much  more  infrequent  in  the  diseases  with  which  this  form  of  endocarditis 
may  be  confounded.  The  acute  hsemorrhagic  nephritis,  too,  in  connection  with 
the  other  symptoms,  is,  at  least  to  a  certain  degree,  characteristic  of  malignant 
endocarditis.  The  course  of  the  fever  is  of  diagnostic  value  only  when  it  is 
decidedly  intermittent.  A  careful  search  for  some  setiological  factor  is  very 
important  for  diagnosis  in  all  cases.  Eor  other  points  the  reader  is  referred  to 
the  consideration  of  septic  diseases  (page  116). 

Prognosis. — In  the  description  of  the  course  of  the  disease  we  have  already 
mentioned  the  prognosis  of  the  different  forms.  The  severe  cases  of  acute  endo- 
carditis usually,  and  the  cases  of  severe  septic  endocarditis  always  end  fatally. 
Here,  however,  the  cause  of  death  is  to  be  sought  rather  in  the  accompanying 
systemic  infection  than  in  the  endocarditis  itself.  In  mild  cases  recoverj^  is  pos- 
sible, but  the  process  of  repair  is  often  so  incomplete  that  chronic  valvular  disease 
of  the  heart  develops  from  the  acute  endocarditis. 

Treatment. — The  chief  requisite  in  the  treatment  of  every  endocarditis  is  as 
complete  rest  as  possible  for  the  patient.  If  ice  is  well  borne,  the  continuous 
application  of  an  ice-bag  to  the  cardiac  region  is  of  service.  If  there  are  signs 
of  cardiac  weakness,  such  as  a  small,  rapid,  and  irregular  pulse,  we  must  employ 
cardiac  stimulants,  strophanthus,  camphor,  and,  above  all,  digitalis.  It  must  be 
eonfessed  that  the  effect  of  these  is  not  very  great.  If  there  are  marked  sub- 
jective symptoms  (such  as  dyspncea)  narcotics,  particularly  morphine,  are  indis- 
pen-sable.  Effort  is  made  to  combat  the  systemic  infection  by  salicylic  acid, 
salicylate  of  sodium,  and  similar  remedies,  including  phenacetine  and  salipyrine. 
Quinine  is  usually  entirely  without  effect,  even  when  the  fever  is  of  an  inter- 
mittent character.  Arsenic,  however,  seems  to  be  useful,  particularly  in  the  more 
protracted  cases. 

[Eor  remarks  upon  the  alkaline  treatment  of  rheumatism,  see  page  686.] 


CHAPTEE   II 


VALVULAR    DISEASE    OF    THE    HEART 

(Clironie  Endocarditis) 

.31tiology. — A  large  number  of  cases  of  chronic  valvular  disease  of  the  heart 
proceed  from  acute  endocarditis.  Hence  the  frequent  statement  in  the  history  of 
chronic  valvular  disease  that  the  patient  has  had  articular  rheumatism,  once  or 
many  times.  In  a  collection  of  163  cases  of  undoubted  valvular  heart  disease,  we 
were  able  to  ascribe  86  to  a  previous  attack  of  acute  articular  rheumatism.  Fol- 
lowing the  acute  valvular  endocarditis,  which  is  often  associated  with  this  dis- 
ease, marked  thickening  of  the  valves  occurs,  due  to  the  growth  of  connective  tis- 
sue. There  are  also  changes  in  the  way  of  contraction,  adhesion,  and  finally  often 
of  considerable  calcification.    The  unavoidable  result  of  all  these  processes  is  that 


VALVULAE   DISEASE   OF   THE   HEAET  309 

the  altered  valves  are  rendered  incapable  of  fulfilling  their  physiological  function 
of  regulating  the  circulation.  Inasmuch  as  the  mitral  valve  is  most  often 
attacked  by  endocarditis  when  associated  with  acute  articular  rheumatism,  we 
find  mitral  disease  predominating  among  rheumatic  valvular  troubles ;  but  lesions 
of  the  aortic  valves,  rheumatic  in  their  origin,  are  by  no  means  rare. 

If  we  find  a  valvular  lesion  in  a  patient  who  has  never  sufi'ered  from  articular 
rheumatism  we  may,  in  some  cases,  be  able  to  refer  the  origin  of  the  valvular 
trouble  to  a  previous  attack  of  acute  endocarditis,  excited  by  one  of  the  other 
causes  above  mentioned.  Thus  it  is  well  known  that  acute  endocarditis  may 
occur  in  the  course  of  scarlet  fever,  diphtheria,  and  typhoid  fever,  and  eventuate 
in  chronic  disease,  but  this  is,  according  to  our  experience,  very  rare. 

In  quite  a  large  number  of  cases  of  heart  disease,  however,  we  can  not  obtain 
a  history  of  acute  endocarditis.  We  have  to  do  here  with  an  endocarditis  which 
is  chronic  from  the  start,  which  also  leads  gradually  to  thickening,  contraction, 
adhesion,  and  calcification  of  the  valves. 

The  causes  of  this  chronic  fibrous  endocarditis  are  probably  the  same  as  of 
acute  articular  rheumatism,  but  in  such  cases  they  act  from  the  start  in  a 
chronic  manner.  Perhaps  often  there  may  have  been  an  incipient  acute  endo- 
carditis, whose  course  was  unperceived.  We  not  infrequently  learn  from  patients 
with  chronic  heart  disease,  who  have  never  had  an  attack  of  acute  articular  rheu- 
matism, that  in  former  years  they  did  suffer  repeatedly  from  mild  rheumatic 
pains,  to  which  they  paid  little  attention.  Furthermore,  it  is  by  no  means  excep- 
tional to  observe  that  such  patients  with  a  well-developed  cardiac  valvular  lesion 
later  on  undergo  one  or  more  attacks  of  acute  polyarthritis.  Heart  disease  is 
also  rarely  associated  with  genuine  chronic  arthritis  deformans.  In  other  cases 
of  valvular  disease  we  must  consider  the  possibility  of  other  lesions,  some  infec- 
tious, some  perhaps  of  a  chemical  and  mechanical  nature.  Here  belong,  in  the 
first  place,  those  cases  of  cardiac  disease  which  are  associated  with  general  arterio- 
sclerosis (atheroma  of  the  blood-vessels).  Indeed,  atheromatous  degeneration  of 
the  aorta  seems  sometimes  to  extend  directly  to  the  aortic  valves,  and  thus  cause 
a  valvular  lesion.  Every  setiological  factor  favorable  to  general  arterio-sclerosis 
is,  therefore,  important  in  the  aetiology  of  valvular  disease.  This  includes  ad- 
vanced life,  excessive  physical  labor,  alcoholism,  and  genuine  gout.  Another 
important  cause  is  syphilis.  Of  late  years,  since  we  have  paid  more  attention  to 
this  last  factor  than  formerly,  we  have  observed  many  cases  of  valvular  disease 
which  were  almost  certainly  of  syphilitic  origin.  In  particular,  lesions  of  the 
aortic  valves,  when  there  is  no  evidence  of  other  causation,  must  awaken  our 
suspicion  of  syphilis.  There  remains  to  be  mentioned  the  influence  of  chronic 
nephritis  upon  the  development  of  cardiac  valvular  disease,  although  in  the  not 
infrequent  cases  in  which  chronic  nephritis,  particularly  of  the  interstitial  vari- 
ety, is  associated  with  chronic  endocarditis,  it  is  not  always  easy  to  determine 
whether  both  conditions  are  related  in  the  way  of  cause  and  effect,  or  whether 
they  are  both  secondary,  and  both  alike  the  result  of  some  third  unfavorable 
influence.  A  hereditary  predisposition  to  heart  disease  is  not  very  frequent,  but 
yet  it  can  be  made  out  with  certainty  in  many  cases.  We  have  ourselves  seen 
five  members  of  the  same  family  who  have  suffered  from  chronic  heart  disease, 
some  from  pure  valvular  disease  and  some  from  severe  so-called  idiopathic  hyper- 
trophy. Perhaps  the  very  frequent  occurrence  of  heart  disease  in  many  families 
is  also  connected  with  a  special  family  predisposition  to  rheumatic  affections,  the 
occurrence  of  which  predisposition  can  not,  in  our  opinion,  be  denied.  Finally, 
a  small  number  of  cases  of  heart  disease,  especially  in  the  right  side  of  the  heart, 
depend  upon  anomalies  of  development  of  the  heart — congenital  heart  disease. 

Valvular  disease  of  the  heart  occurs  at  every  age  of  life.  The  time  of  origin 
of  most  cases,  corresponding  in  part  to  the  occurrence  of  acute  articular  rheuma- 


310  DISEASES    OF   THE   CIRCULATORY   ORGAITS 

tism,  falls  in  youth  and  middle  age,  somewhere  between  eighteen  and  forty; 
but  severe  valvular  disease  is  not  infrequent  even  in  children;  while  late  in  life 
the  clinical  picture  of  valvular  disease  is  often  confused  by  the  simultaneous 
presence  of  general  arterio-sclerosis,  pulmonary  emphysema,  or  kidney  trouble. 
Heart  disease  is  said  to  be  rather  more  frequent  in  the  female  sex  than  in  the 
male.  Women  with  heart  disease  not  infrequently  date  their  symptoms  from 
pregnancy  and  the  puerperium. 

General  Pathology  of  Valvular  Disease  of  the  Heart. — Every  valve  of  the 
heart,  in  order  to  fulfill  its  physiological  task,  must,  on  the  one  hand,  open  per- 
fectly at  the  right  time  in  order  to  furnish  a  free  passage  to  the  blood-current 
through  the  appropriate  orifice,  and  must,  on  the  other  hand,  close  firmly  and 
perfectly  at  the  right  time  in  order  to  make  any  abnormal  backward  flow  of  blood 
impossible.  In  both  relations  the  function  of  the  valves  may  be  disturbed  by 
chronic  endocarditis,  the  disturbance  being  the  result  of  their  anatomical 
changes.  If  the  tips  of  the  valves  are  shortened  on  their  free  edges  by  contrac- 
tion, or  if  the  complete  unfolding  of  the  auriculo-ventricular  valves  is  hindered 
by  a  shortening  of  their  chordse  tendinese,  the  closure  of  the  valve  can  not  be 
complete.  At  the  moment  when  the  closure  of  the  valve  is  necessary  a  fissure 
remains  open  between  its  apices.  We  call  this  condition  an  insufficiency  of  the 
valve.  On  the  other  hand,  the  valves  may  lose  their  capability  of  free  and  suffi- 
cient separation  from  one  another,  as  a  result  of  thickening  and  calcification  of 
the  connective  tissue,  and  also  as  a  result  of  adhesions  of  the  points  of  the  valves 
with  one  another.  At  the  moment  when  the  blood-current  should  pass  freely 
through  the  open  orifice,  the  valve  remains  a  stiff,  narrow  ring,  through  which 
the  blood  must  force  its  way — stenosis  of  the  orifice.  The  changes  in  the  valves 
are  often  of  such  a  sort  that  they  cause  at  the  same  time  both  an  insufficiency  of 
the  valve  and  a  stenosis  of  the  orifice.  The  thickening  and  calcification  of  the 
valves  in  stenosis  cause,  as  a  rule,  a  valvular  insufficiency  at  the  same  time;  but 
an  insufficiency,  set  up  by  a  contraction  of  the  edges  of  the  valves,  may  occur 
without  a  coincident  stenosis  of  the  orifice. 

The  abnormal  and  injurious  effect  of  a  valvular  lesion  upon  the  circulation 
in  the  heart  is  felt  in  two  directions.  Either  the  obstacles  to  the  circulation  are 
increased  in  certain  places,  or  there  is  a  greater  diastolic  distention  of  certain 
portions  of  the  heart.  Both  circumstances  of  course  demand  greater  cardiac 
effort.  If  the  heart  were  to  labor  with  only  the  same  degree  of  energy  as  under 
normal  conditions,  in  spite  of  the  increased  resistance,  or  in  spite  of  the  greater 
distention,  there  would  speedily  be  an  impairment  of  circulation,  incompatible 
with  the  continuance  of  life ;  for,  if  the  increased  resistance  were  not  overcome, 
or  if  the  abnormally  distended  cavity  were  not  properly  emptied,  there  would  at 
once  be  a  rapidly  increasing  congestion  behind  the  diseased  valve,  and  beyond 
it  a  constantly  diminishing  pressure.  We  can  speak  of  a  circulation  of  the  blood 
only  when,  in  a  given  interval  of  time,  exactly  as  much  blood  is  driven  out  of  the 
heart  as  flows  into  it.  The  slightest  difference  in  this  regard  would,  in  a  very 
brief  period,  produce  such  a  congestion  of  blood  in  the  veins  and  such  a  diminu- 
tion of  blood  in  the  arteries  that  the  demand  of  the  tissues  for  oxygen  could  no 
longer  be  satisfied,  and  death  would  be  the  necessary  result.  A  normal  circulation 
is  maintained  so  long  as  the  amount  of  arterial  blood,  which  flows  into  the  organs 
in  a  given  interval  of  time,  is  sufficiently  great  and  also  capable  of  immediate 
increase,  proportional  to  any  temporary  increase  in  the  demands  of  the  organs, 
as,  for  example,  when  there  is  bodily  exertion.  The  amount  of  blood  flowing 
through  the  organs  in  a  given  time  depends  upon  the  degree  of  distention,  the 
frequency  of  contraction,  and  the  complete  emptying  of  the  left  side  of  the  heart. 
This  amount  ("  the  size  of  the  circulation  ")  may  be  diminished,  and  yet  the 
circulation  continue  as  such;  but  that  the  circulation  can,  in  spite  of  the  dis- 


VALVULAR   DISEASE    OF   THE   HEART  311 

turbance  occasioned  by  a  valvular  lesion,  still  be  maintained  in  a  satisfactory 
manner  is  due  to  the  capability  of  the  heart  of  overcoming  the  obstacles  to  the 
circulation  by  means  of  increased  work.  It  is  one  of  the  wisest  contrivances  in 
our  organism,  that  the  heart  has  control  of  a  reserve  fund  of  strength,  which 
comes  into  action,  if  need  be,  in  a  way  to  compensate  as  far  as  possible  for  any 
disturbance  of  the  circulation.  This  explains  why  a  man  with  valvular  disease 
of  the  heart  may  be  almost  perfectly  well  for  a  long  time,  while  the  increased 
work  of  certain  portions  of  his  heart  suffices  to  keep  up  an  approximately  normal 
circulation  in  spite  of  the  existing  valvular  disease.  We  call  a  heart  disease,  in 
which  there  is  at  least  no  marked  disturbance  of  circulation,  a  compensated  heart 
disease. 

The  abnormal  increase  in  functional  activity  of  certain  portions  of  the  heart, 
associated  with  every  cardiac  lesion,  and  referable  in  every  case,  as  we  have  said, 
either  to  increased  resistance  or  to  increased  distention,  results  in  a  hypertrophy 
of  those  particular  portions  of  the  heart,  just  as  in  the  case  of  any  other  muscle. 
This  hypertrophy  does  not  consist  of  an  increase  in  thickness  of  the  individual 
muscular  fibers,  but  chiefly  of  an  increase  in  number.  The  total  bulk  of  the 
cardiac  muscle  increases,  and  thus  its  capacity  for  work  naturally  becomes  greater. 
It  goes  without  saying  that  increased  nutritive  processes  and  a  large  supply  of 
nourishment  for  the  heart  are  necessary  to  bring  about  such  a  hypertrophy,  by 
which  alone  a  compensation  of  the  heart  disease  is  possible  for  any  length  of  time. 
Hence  we  find  the  secondary  hypertrophy  of  the  heart  absent,  or  at  least  only 
imperfectly  developed,  in  feeble  individuals,  especially  in  those  who  have  suffered 
from  some  other  chronic  wasting  disease  besides  the  heart  disease,  such  as  phthi- 
sis or  carcinoma. 

Although  the  compensatory  processes  in  the  heart  may  prevent  for  a  long  time 
any  marked  disturbance  of  the  circulation,  the  already  overburdened  heart  can  no 
longer  completely  satisfy  any  excessive  demands  upon  it,  even  in  a  compensated 
heart  disease.  Hence  patients  with  a  compensated  heart  disease  are  free  from  sub- 
jective disturbance  only  when  they  remain  at  rest,  while  the  signs  of  a  disturbed 
circulation  usually  become  quite  apparent  on  slight  physical  exertion. 

The  hypertrophied  cardiac  muscle  can  seldom  supply  permanently  the  ab- 
normally great  drafts  made  upon  it.  There  finally  comes  a  condition  of  "  fa- 
tigue," of  "  cardiac  insufficiency."  The  cause  lies  either  in  the  increase  of  the 
valvular  disease,  so  that  the  hindrance  to  the  blood-current  caused  by  it  can  no 
longer  be  completely  overcome,  or  in  the  fact  that  the  nervous  and  muscular  ele- 
ments in  the  heart  have  their  powers  gradually  impaired  by  a  disturbance  of 
circulation  in  the  heart  itself.  In  short,  in  every  heart  disease  the  moment  may 
finally  come  when  the  capacity  of  the  heart  has  reached  its  limit,'%nd  hence  the 
compensation  of  the  heart  disease  ceases.  The  results  of  stasis  now  appear  with 
increasing  severity  in  the  different  organs,  as  we  shall  learn  to  recognize  later  on, 
and  the  patient  finally  succumbs  to  them,  unless  some  intercurrent  event  puts  an 
end  to  life. 

After  these  general  remarks,  which  will  be  understood  better  on  reading  what 
follows,  we  will  pass  on  to  the  special  description  of  the  different  forms  of  heart 
disease  and  their  physical  signs. 

1.  Insufficiency  of  the  Mitral  Valve 

Mitral  insufficiency  is  one  of  the  most  frequent  forms  of  heart  disease.  It 
develops  in  acute  or  chronic  endocarditis  of  the  mitral  valve,  from  contraction  of 
the  free  edges  of  the  valve  or  from  shortening  of  the  chordte  tendineas.  In  rare 
cases  it  comes  on  from  partial  adhesion  of  the  valves  to  the  walls  of  the  ventricle. 

The  closure  of  the  mitral  valve  occurs  normally  at  each  systole  of  the  left  ven- 


312  DISEASES    OF   THE    CIKCULATOEY   ORGANS 

tricle.  It  prevents  the  return  of  blood  from  the  left  ventricle  to  the  left  auricle. 
If  the  mitral  valve  is  insufficient  and  its  closure  is  incomplete,  at  every  systole  of 
the  left  ventricle  a  part  of  the  blood  is  thrown  back  from  it  into  the  left  auricle 
through  the  open  space  of  the  ostium  venosum.  This  abnormal  backward  wave 
encounters  the  blood-current  coming  in  an  opposite  direction  into  the  left  auri- 
cle from  the  pulmonary  veins.  The  meeting  of  these  two  opposing  currents,  as 
well  as  the  stream  of  regurgitant  blood  pressing  through  the  open  chink  in  the 
mitral  valves,  sets  the  blood  in  a  whirl,  and  this  impinging  upon  the  tense  edges 
of  the  valves  produces  a  loud,  blowing,  systolic  murmur.  We  hear  this  murmur 
loudest  at  the  apex  of  the  heart,  corresponding  to  the  laws  of  conduction  in  the 
thorax ;  yet  it  usually  is  propagated  so  far  that  it  may  often  be  heard  at  the  other 
cardiac  orifices,  although  not  so  distinctly.  A  loud  systolic  mitral  murmur  cau 
also  be  heard  sometimes  in  the  back,  on  the  left,  and  occasionally  on  the  right. 
Tn  some  few  cases  the  systolic  murmur  of  mitral  insufficiency  is  heard  best  in  the 
second  left  intercostal  space.  This  is  probably  because  the  murmur  occasioned  by 
the  commotion  in  the  left  ventricle  is  conducted  by  the  left  auricular  appendix  to 
the  anterior  chest- wall  (Naunyn).  Curschmann  has  pointed  out  that  this  is  par- 
ticularly apt  to  happen  in  cases  of  incipient  mitral  insufficiency;  but,  as  a  rule, 
even  in  these  cases,  the  murmur  is  found  at  the  apex  of  the  heart.  In  most 
instances  the  systolic  muscle-sound  of  the  left  ventricle,  the  so-called  first  sound 
of  the  heart,  can  also  be  heard  besides  the  systolic  murmur.  It  can  be  heard 
rather  better  if  the  ear  is  slightly  removed  from  the  ear-piece  of  the  stethoscope 
[meaning  the  mon-aural  instrument].  Exceptionally  the  sound  may  be  com- 
pletely obscured  by  the  murmur.  The  second  sound  is  often  not  to  be  heard  at 
the  apex,  probably  because  it  is  obscured  by  the  relatively  protracted  murmur. 

Since  the  left  auricle,  at  each  systole  of  the  ventricle,  receives  blood  from  two 
sides — its  normal  quantity  from  the  pulmonary  veins,  and,  besides  that,  the  abnor- 
mal blood-wave  from  the  left  ventricle — it  becomes  much  dilated.  At  the  next 
diastole  of  the  left  ventricle  the  whole  amount  of  blood  collected  in  the  auricle 
under  increased  pressure  pours  into  the  left  ventricle  through  the  mitral  valve, 
which  is  now  wide  open  (supposing  a  pure  insufficiency  of  the  valve  without  any 
stenosis).  We  see,  then,  that  in  pure  mitral  insufficiency  the  left  ventricle  must 
be  filled  beyond  the  normal  amount  during  the  diastole.  The  left  ventricle  must 
also  expel  in  the  following  systole  an  abnormally  large  amount  of  blood.  Al- 
though by  this  contraction  only  a  part  of  the  blood  reaches  the  aorta  in  the 
direction  of  the  normal  blood-current  while  a  part  pours  back  into  the  auricle, 
the  work  of  the  left  ventricle  is  of  course  excessive.  Thus,  in  pure  mitral  insuffi- 
ciency, the  left  ventricle  is  dilated  as  a  result  of  its  increased  filling  in  diastole, 
and  is  hypertrophied  as  a  result  of  its  increased  labor.  The  general  arterial 
tension  remains  approximately  normal.  It  is  not  increased,  since  a  part  of  the 
abnormal  amount  of  blood,  which  pours  out  of  the  left  ventricle  at  every  systole, 
flows  backward  into  the  auricle.  So  long  as  the  left  ventricle  is  completely  emp- 
tied by  vigorous  contractions,  the  aorta  receives  about  the  normal  amount  of 
blood,  and  the  radial  pulse  remains,  therefore,  in  cases  of  pure  mitral  insuffi- 
ciency, of  about  the  normal  strength  and  tension. 

The  anomalies  in  the  movements  of  the  blood  in  mitral  insufficiency  produce 
still  other  effects.  We  have  already  seen  that  the  left  auricle  is  dilated  from  its 
overfilling.  It  also  becomes  hypertrophied,  so  far  as  its  weak  muscular  structure 
permits,  but  it  is  not  in  itself  capable  of  compensating  for  the  disturbance  which 
the  pulmonary  circulation  suffers  from  the  mitral  insufficiency,  for  the  back  cur- 
rent from  the  left  ventricle,  and  the  consequent  high  pressure  in  the  left  auricle, 
must  plainly  offer  an  abnormal  hindrance  to  the  flow  of  blood  from  the  pulmo- 
nary veins.  This  stasis  sets  back  through  the  pulmonary  capillaries  and  arteries 
into  the  right  ventricle.     This  may  be  recognized,  on  physical  examination,  by 


VALVULAE   DISEASE    OF   THE   HEART  313 

the  change  in  the  pulmonic  second  sound,  which  is  louder,  more  valvular,  and 
"  accentuated,"  since  the  closure  of  the  semilunar  valves  in  the  pulmonary  artery 
now  takes  place  under  the  abnormally  high  pressure  which  prevails  in  the  arteries 
of  the  lungs.  The  right  ventricle  has  the  task  of  overcoming  this  abnormal  stasis 
in  the  pulmonary  circulation.  It  can  overcome  the  abnormal  resistance  in  the 
pulmonary  circulation  by  increased  work,  and  as  a  result  it  becomes  hyper- 
trophied.  So  long  as  the  hypertrophy  of  the  right  ventricle  suffices  to  maintain 
the  normal  pulmonary  circulation,  the  stasis  extends  no  farther  backward,  but  in 
the  later  stages  of  heart  disease  we  see  the  right  ventricle  becoming  paralyzed, 
and  more  and  more  dilated  as  a  result  of  stasis.  The  flow  of  venous  blood  from 
the  body  into  the  right  auricle  and  ventricle  is  now  rendered  more  difficult.  The 
signs  of  venous  stasis  become  manifest;  the  patient  has  a  cyanotic  hue,  con- 
gestive oedema  appears  in  the  face  and  the  extremities,  symptoms  of  passive 
congestion  of  the  liver,  spleen,  and  kidneys  appear,  and,  in  short,  there  is  devel- 
oped the  picture  of  an  uncompensated  heart  disease. 

If  we  now  sum  up  the  physical  signs  of  mitral  insufficiency,  the  different 
methods  of  investigation  give  the  following  results: 

Inspection. — The  cardiac  region  often  seems  rather  prominent,  as  a  result  of 
the  hypertrophy  of  the  heart.  This  protrusion  is  most  marked  in  young  persons 
with  a  yielding  thorax.  The  apex-beat  is,  as  a  result  of  the  dilatation  and  hyper- 
trophy of  the  left  ventricle,  displaced  toward  the  left  and  sometimes  downward 
into  the  sixth  intercostal  space.  It  is  more  extensive  and  stronger  than  normal 
("heaving").  The  apex-beat  is  somewhat  displaced  toward  the  left  as  a  result 
of  the  hypertrophy  and  dilatation  of  the  left  ventricle,  and  it  is  quite  marked. 
Besides  that,  we  often  see  a  diffuse  pulsation  in  the  whole  cardiac  region.  In 
the  epigastrium  we  sometimes  see  an  epigastric  pulsation  proceeding  from  the 
hypertrophied  right  ventricle.  In  cases  which  are  no  longer  perfectly  compen- 
sated the  stasis  in  the  veins  of  the  body  is  rendered  apparent  by  the  general 
cyanotic  appearance  of  the  patient  and  the  marked  filling  of  the  jugular  veins  in 
the  neck,  Undulatory  or  pulsating  movements  often  occur  in  the  latter  (see  tri- 
cuspid insufficiency,  below). 

Palpation. — By  palpation  likewise  we  perceive  the  abnormal  vigor  and  extent 
of  the  apex-beat,  and  the  displacement  of  the  same  toward  the  left;  and  often, 
also,  an  extensive  diffuse  pulsation  over  the  cardiac  region,  and  in  particvilar  a 
distinct  epigastric  pulsation,  due  to  the  right  ventricle.  We  often  feel  a  systolic 
thrill  at  the  apex  of  the  heart — a  "  cat's  purr  " — by  laying  the  hand  flat  on  the 
chest.  The  same  whirl  of  blood,  which  is  audible  as  a  murmur,  may  be  per- 
ceived as  a  fine  tremor  of  the  chest-wall. 

The  radial  pulse  is  quite  strong  and  usually  regular.  The  sphygmographic 
tracing  of  it  shows  nothing  characteristic  in  mitral  insufficiency. 

Percussion. — This  usually  gives  at  first  only  a  moderate  increase  of  the  heart's 
dullness  to  the  left,  and  a  little  upward  dilatation  of  the  left  auricle  and  left 
ventricle,  but  in  the  later  stages  there  is  at  the  same  time  an  increase  of  the 
heart's  dullness  to  the  right,  caused  by  hypertrophy  and  dilatation  of  the  right 
ventricle.  The  whole  area  of  cardiac  dullness  may  finally  extend  two  fingers' 
breadth  beyond  the  right  edge  of  the  sternum,  and  to  the  left  it  may  reach  the 
mammillary  line,  or  even  pass  far  beyond  it. 

Auscultation. — At  the  apex  of  the  heart  we  hear  a  loud,  quite  long,  pure  sys- 
tolic blowing  murmur,  limited  to  the  systole,  either  replacing  the  first  sound  or 
accompanying  it.  The  second  sound  is  often  obscure  or  inaudible  at  the  apex, 
but  the  pulmonic  second  sound  is  increased  and  accentuated.  Auscultation  of  the 
vessels  gives  nothing  characteristic. 


314  DISEASES    OF   THE   CIRCULATOEY   ORGANS 


2.  Stenosis  of  the  Mitral  Orifice  (Mitral  Stenosis) 

Mitral  stenosis  often  develops  in  chronic  endocarditis  of  the  mitral  valve,  as  a 
sequel  to  a  previous  insufficiency.  The  valve  constantly  grows  stiffer  and  more 
rigid,  and  the  signs  of  stenosis  gradually  predominate  over  those  of  insufficiency. 
Hence  we  very  often  find  stenosis  and  insufficiency  of  the  mitral  valve  combined, 
but  often  the  signs  of  stenosis  are  so  much  more  prominent  that  we  can  properly 
speak  of  a  pure  mitral  stenosis. 


Fig.  39. — Pulse  curve  in  marked  mitral  stenosis. 

The  disturbance  which  the  circulation  suffers  in  mitral  stenosis  is  much 
greater  than  in  mitral  insufficiency.  In  mitral  stenosis  the  orifice  may  finally 
become  so  narrow  that  it  scarcely  admits  an  ordinary  lead-pencil.  The  influx  of 
blood  into  the  left  ventricle  is  accordingly  much  impeded.  During  the  diastole 
of  the  left  ventricle  the  blood  must  force  its  way  through  the  stiff  and  narrow 
ring  of  the  mitral  valve.  In  this  way,  again,  are  caused  irregular  whirling  move- 
ments in  the  blood,  and  abnormal  vibrations  of  the  mitral  valve,  giving  rise  in 
most  cases  to  an  audible  diastolic  murmur.  In  mitral  stenosis  the  left  ventricle 
receives  less  than  its  normal  amount  of  blood,  and  therefore  it  has  no  direct  occa- 
sion for  hypertrophy,  and  in  fact  it  is  sometimes  found  at  the  autopsy  to  be  com- 
paratively small  and  to  be  crowded  backward  by  the  enormously  dilated  and 
hypertrophied  right  heart.  ISTevertheless,  we  do  often  find  hypertrophy  of  the 
left  ventricle  in  cases  of  mitral  stenosis,  and  for  this  reason,  that  mitral  stenosis 
usually  develops  gradually  from  a  previous  insufficiency  of  the  valves.  That  is, 
the  chronic  endocarditis  occasions,  probably  in  every  case,  first,  an  insufficiency  of 
the  valve,  which  is  later  followed  by  stenosis  as  the  change  progresses.  We  have 
already  seen  that  insufficiency  of  the  mitral  valve  always  leads  to  hypertrophy 
of  the  left  ventricle,  and  so  we  find  it  to  persist  even  at  a  time  when  stenosis 
has  become  the  prominent  lesion.  In  other  cases  of  stenosis,  hypertrophy  of  the 
left  ventricle  is  due  to  certain  associated  conditions,  such  as  arterio-sclerosis  or 
chronic  nephritis.  And  finally  we  should  also  consider  Friedreich's  theory,  that 
severe  venous  congestion  may  extend  into  the  capillaries,  and  thence  finally 
occasion  abnormal  resistance  to  the  arterial  circulation. 

The  radial  pulse  in  mitral  stenosis  is  approximately  normal,  as  long  as  the 
ventricle  is  sufficiently  filled  with  blood  during  diastole.  In  spite  of  the  stenosis 
of  the  mitral  valve,  the  left  ventricle  may  be  satisfactorily  filled,  and  this  is 
more  likely  if  the  action  of  the  heart  is  slow,  allowing  a  longer  diastole;  and  if, 
also,  the  left  auricle  is  still  capable  of  vigorous  contraction.  If,  however,  the 
action  of  the  heart  is  hurried,  and  the  left  ventricle  is  no  longer  sufficiently  dis- 
tended with  blood  during  the  diastole,  the  radial  pulse  becomes  small  and  of  low 
tension.  Marked  arhythmia  is  very  often  present  in  mitral  stenosis,  probably 
because  of  the  insufficient  amount  of  arterial  blood  supplied  to  the  myocardium 
and  its  ganglia. 

The  hindrance  to  the  flow  into  the  left  ventricle  in  mitral  stenosis  soon  lends 
to  a  marked  stasis,  which  extends  to  the  right  side  of  the  heart  through  the  left 
auricle,  and  the  pulmonary  veins,  capillaries,  and  arteries.  The  left  auricle  is 
dilated  first  (often  to  an  enormous  extent),  and  its  walls  are  hypertrophied,  but  it 
can  overcome  only  a  very  small  part  of  the  resistance  at  the  mitral  orifice.  The 
right  ventricle  can,  by  more  work,  so  increase  the  pressure  in  the  pulmonary  ves- 


VALVULAE   DISEASE   OF   THE   HEART  315 

sels  that,  in  spite  of  the  narrowed  orifice,  an  approximately  sufficient  quantity 
of  blood  may  pour  into  the  left  ventricle.  Hence  we  find  in  mitral  stenosis  a 
very  marked  hypertrophy  and  dilatation  of  the  right  ventricle.  The  stasis  in 
the  pulmonary  circulation,  manifested  objectively  by  the  accentuation  of  the 
pulmonic  second  sound,  has  as  a  result  a  gradually  developing  ectasis  of  the 
pulmonary  capillaries.  Thickening  of  the  intima  of  the  pulmonary  arteries 
and  veins  also  usually  develops.  (See  the  chapter  on  brown  induration  of  the 
lungs.) 

The  results  of  physical  examination  are  as  follows : 

Inspection. — The  whole  cardiac  region  may  seem  slightly  prominent,  as  a  re- 
sult of  the  hypertrophy  of  the  heart.  This  protuberance  is  most  marked  in  chil- 
dren with  their  yielding  thoracic  walls.  The  heart's  action  is  usually  extended 
over  a  larger  area,  but  in  pure  mitral  stenosis  the  apex-beat  is  no  stronger  than 
usual,  though  often  displaced  to  the  left.  We  have  frequently  noticed  a  marked 
pulsation  in  the  epigastrium,  produced  by  the  right  side  of  the  heart.  The  jugu- 
lar veins  are  apt  to  be  prominent,  and  show  the  different  forms  of  undulatory  and 
pulsating  movement. 

Palpation. — This  also  gives  signs  corresponding  to  the  more  extended  action 
of  the  heart.  We  sometimes  feel  the  pulsation  of  the  dilated  right  ventricle  even 
to  the  right  of  the  sternum.  In  some  cases  we  feel  a  diastolic  thrill  at  the  apex 
of  the  heart,  which  alone  may  almost  establish  the  diagnosis  of  mitral  stenosis. 
This  thrill  arises  from  the  same  vertiginous  currents  in  the  blood  which  form  the 
basis  of  the  diastolic  murmur  (vide  infra).  The  radial  pulse  is  small  in  every 
case  of  severe  mitral  stenosis,  and  is  very  often  irregular. 

Percussion. — Percussion  shows,  in  the  first  place,  an  extension  of  cardiac  dull- 
ness toward  the  right,  reaching  to  the  right  edge  of  the  sternum,  or  far  beyond. 
Dullness  also  extends  as  a  rule  further  to  the  left  than  normal.  This  is  in  part 
due  to  the  hypertrophy  of  the  left  ventricle  (vide  supra),  in  part  to  a  dilatation 
of  the  right  side  of  the  heart,  so  great  as  to  push  the  left  ventricle  backward  and 
to  the  left.  The  great  distention  of  the  left  auricle  causes  an  enlargement  of  the 
cardiac  dullness  upward.  We  observed  one  case  in  which  the  left  auricle  was 
so  enormously  dilated  that  it  extended  behind  and  beyond  the  right  auricle 
toward  the  right,  and  was  one  factor  in  the  increase  of  cardiac  dullness  toward 
the  right,  as  observed  during  life. 

Auscultation. — The  characteristic  auscultatory  sign  of  mitral  stenosis  is  the 
diastolic  [pre-systolic]  murmur  at  the  apex.  This  is  never  so  loud  and  blowing  as 
the  systolic  murmur  of  insufficiency,  but  it  usually  sounds  more  rolling  or  rippling. 
It  is  loudest  at  the  apex,  and  it  is  transmitted  only  slightly  toward  the  base. 
Since,  as  has  been  said,  the  left  ventricle  in  mitral  stenosis  is  sometimes  pushed 
to  the  left  and  backward  by  the  very  much  enlarged  right  ventricle,  in  looking 
for  the  murmur  we  must  often  go  far  to  the  left,  in  order  not  to  auscult  the  right 
ventricle  only. 

The  origin  of  the  murmur  is  easily  explained.  In  the  diastole  of  the  left 
ventricle  the  blood-current  must  force  its  way  through  the  narrow  mitral  orifice, 
whence  vertiginous  movements  arise  in  the  blood,  and  produce  the  murmur. 
Since  the  blood  flowing  through  the  narrow  orifice  has  a  current  of  relatively 
slight  intensity,  the  murmur  produced  by  it  can  not  be  very  loud.  Indeed,  in  the 
most  extreme  cases  of  mitral  stenosis,  the  murmur  is  particularly  apt  to  be  very 
faint,  and  when  the  heart's  action  is  hurried  and  irregular,  entirely  inaudible. 
Not  infrequently  the  murmur  is  not  heard  until  the  second  half  of  diastole.  That 
is,  when  the  contraction  of  the  left  auricle  gives  a  fresh  impulse  to  the  current 
of  blood  streaming  through  the  stenosed  orifice.  A  murmur  of  this  sort,  which 
is  audible  only  at  the  end  of  diastole,  and  passes  with  a  distinct  crescendo  directly 
into  the  loud  systolic  sound  and  terminates  with  this,  is  called  a  pre-systolic 


316  DISEASES    OF   THE   CIECULATOEY   OEGANS 

murmur.  This  murmur  can  often  be  plainly  felt  if  the  hand  is  laid  upon  the 
apex  of  the  heart,  as  a  pre-systolic  thrill. 

It  is  not  very  exceptional  to  find  no  murmur  audible  in  cases  of  extreme  mitral 
stenosis.  If  such  cases  do  not  come  under  observation  till  the  last  stage  of  the 
disease,  the  mitral  stenosis  may  readily  be  overlooked.  We  have  ourselves  re- 
peatedly found,  in  cases  of  mitral  stenosis,  that  as  the  lesion  grew  worse  the  dis- 
tinct diastolic  or  pre-systolic  murmur  gradually  and  completely  disappeared. 
This  is  explained  by  the  fact  that  as  the  chink  in  the  valve  grows  narrower  and 
the  weakness  of  the  heart  greater,  the  blood  is  not  forced  through  the  narrow 
orifice  with  siifiicient  vigor  to  cause  audible  vibrations  of  the  thickened  valves. 
If  the  left  ventricle  is  wholly  displaced  backward  by  the  enormous  increase  in 
size  of  the  right  ventricle,  we  have  also  less  favorable  conditions  for  the  propa- 
gation of  the  waves  of  sound  from  the  mitral  valve  to  the  ear. 

The  first  sound  at  the  apex  is  maintained  in  pure  mitral  stenosis.  Indeed,  it 
is  often  noticeably  loud  and  valvular.  All  the  later  observations  confirm  the 
view  that  the  systolic  sound  is  a  muscle  sound,  and  consequently  it  is  probable 
that  this  vigorous  first  sound  is  due  to  the  contraction  of  the  left  ventricle,  which, 
as  we  have  seen  above  (page  314),  is  often  hypertrophied,  and  also,  as  a  result  of 
the  stenosis,  only  imperfectly  filled.  The  strength  of  the  first  ventricular  sound 
in  mitral  stenosis  affords,  at  any  rate,  a  marked  contrast  to  its  weakness  in  aortic 
insufficiency  (vide  infra).  We  have  a  strong  sound  when  the  ventricle  is  ill- 
filled,  diminution  and  dullness  of  sound  when  the  ventricle  is  over-filled.  If  in- 
sufficiency of  the  valve  co-exists,  we  may  hear  a  systolic  murmur  with  the  first 
sound  or  instead  of  it. 

The  very  marked  accentuation  of  the  pulmonic  second  sound,  the  result  of 
the  abnormally  high  tension  in  the  pulmonary  artery,  is  almost  constant.  It 
fails  only  in  very  anasmic,  weak  people,  or  in  co-existing  insufficiency  of  the 
tricuspid  valve  (vide  infra).  The  second  sound  at  the  base  is  very  often  "di- 
vided "  or  reduplicated.  The  closure  of  the  semilunar  valves  in  diastole  does  not 
happen  at  the  same  time  in  the  pulmonary  artery  and  in  the  aorta,  on  account  of 
the  unequal  tension  in  the  two  vessels,  so  that  consequently  the  two  sounds  are 
heard,  one  shortly  after  the  other.  Although  this  division  of  the  second  sound  is 
particularly  frequent  in  mitral  stenosis,  it  is  by  no  nieans  a  pathognomonic  sign 
of  it. 

Mitral  stenosis  is  one  of  the  severest  forms  of  heart  disease.  It  almost  always 
causes  greater  subjective  disturbance  than  mitral  insufficiency.  Hypertrophy  of 
the  right  ventricle  may,  indeed,  maintain  for  a  time  an  approximately  complete 
cornpensation,  but  the  signs  of  marked  stasis  in  the  pulmonary  circulation,  and 
further  in  the  veins  of  the  body,  are  apt  to  appear  quite  early.  It  must  be 
admitted  that  the  disturbances  of  compensation  which  occur  in  mitral  stenosis 
are  particularly  susceptible  of  treatment,  so  that  for  many  years  there  may  be 
times  of  improvement,  alternating  with  times  of  aggravation  of  the  symptoms; 
but  finally  the  time  comes  when  it  is  impossible  to  regulate  the  circulation.  The 
dyspnosa  grows  worse,  and  finally  death  occurs,  usually  preceded  by  dropsy. 

3.  Insufficiency  of  the  Semilunar  Valves  of  the  Aorta 

Insufficiency  of  the  aortic  valves  is  due  most  frequently  to  contraction  of  the 
free  edges  of  the  valves.  Tears,  perforations,  or  adhesions  of  the  valve  to  the 
wall  of  the  vessel  more  rarely  lead  to  insufficiency.  The  cause  of  all  these 
changes  is  either  a  valvular  endocarditis,  which  is  usually  a  sequel  of  articular 
rheumatism,  or  a  general  arterial  atheroma,  which  extends  gradually  from  the 
intima  of  the  aorta  to  the  valves.  We  have  already  referred  to  syphilis  as  a  not 
very  infrequent  cause  of  aortic  lesions.     A  question  of  practical  importance  is 


VALVULAR   DISEASE    OF    THE   HEAET  317 

whether  violent  bodily  exertion  may  suddenly  occasion  the  partial  laceration  of 
an  aortic  valve.  Many  clinical  observations,  including  a  recent  case  of  the 
author's,  seem  to  show  the  possibility  of  this  extremely  rare  occurrence. 

The  function  of  the  aortic  valves  is  to  close  tightly  at  the  time  of  diastole  of 
the  left  ventricle,  in  order  to  prevent  any  return  of  blood  from  the  aorta  into  the 
ventricle.  If  these  valves  are  insufficient — that  is,  if  they  do  not  close  perfectly 
at  each  diastole — there  is  a  return  current  of  blood  from  the  aorta  into  the  left 
ventricle. 

This  regurgitant  diastolic  wave  sets  the  tense  edges  of  the  valve  in  vibration 
as  it  passes  over  them.  Furthermore,  the  two  currents  of  blood  impinging  upon 
each  other  in  the  left  ventricle,  the  one  an  abnormal  regurgitation  from  the 
aorta,  the  other  the  normal  stream  from  the  left  auricle,  produce  irregular  whirl- 
ing motions  in  the  blood.  All  these  vibrations  are  propagated  to  the  surround- 
ing structures,  and  produce  the  long-continued,  blowing,  diastolic,  and  remark- 
ably characteristic  murmur  of  aortic  insufficiency. 

Aortic  insufficiency  causes  an  immediate  and  great  increase  in  the  demands 
upon  the  left  ventricle,  because  of  its  abnormal  distention,  for  it  receives,  as  we 
have  already  said,  not  merely  its  normal  quantum  of  blood  from  the  left  ven- 
tricle, but  also  the  blood  which  regurgitates  through  the  leaking  valves  of  the 
aorta.  It  is  consequently  overfilled  at  every  diastole,  and  finally  becomes  per- 
manently distended.  Dilatation  of  the  left  ventricle  forms  a  constant  anatom- 
ical lesion  in  every  case  of  aortic  insufficiency,  and  is  shown  not  only  in  the  dila- 
tation of  the  whole  ventricular  cavity,  but  also  in  the  very  characteristic  flatten- 
ing of  the  trabeculte  and  of  the  papillary  muscles.  There  is  iisually  some  fibrous 
thickening  of  the  endocardium  at  the  spot  upon  which  the  regurgitant  blood-cur- 
rent is  continally  impinging.  The  left  ventricle  possesses  sufficient  reserve 
strength  to  discharge  its  contents  completely  for  a  long  period  by  means  of  in- 
creased effort.  This  is  indeed  a  task  like  that  of  Sisyphus,  since  the  portion  of 
the  blood  which  is  thrown  into  the  aorta  is  constantly  rolling  back  into  the  ven- 
tricle. The  increased  demands,  however,  lead  necessarily  at  last  to  a  hypertrophy 
of  the  left  ventricle,  often  greater  than  is  seen  under  any  other  conditions. 

From  the  facts  enumerated  we  can  easily  understand  the  physical  signs  of 
insufficiency  of  the  aortic  valves. 

Inspection. — Great  hypertrophy  of  the  left  ventricle  often  causes  a  marked 
protrusion  of  the  whole  cardiac  region.  The  diffuse  and  very  strong  apex-beat, 
displaced  downward  and  to  the  left,  is  especially  striking.  It  may  usually  be 
seen  in  the  sixth  intercostal  space,  outside  the  left  mammillary  line,  and  some- 
times even  at  the  anterior  axillary  line.  Besides,  we  often  see  a  marked  diffuse 
tremor  of  the  whole  cardiac  region.  There  is  marked  pulsation  of  the  carotid 
arteries  in  the  neck.  The  jugular  veins  show  undulation  and  pulsation,  when  at 
last  compensation  begins  to  fail. 

Palpation. — ^We  can  appreciate  the  heart's  action  to  a  still  greater  extent  by 
palpation  than  by  inspection.  The  apex-beat  is  very  resistant,  massive,  and 
plainly  heaving — that  is,  the  finger  or  stethoscope  applied  to  the  apex  is  lifted  by 
the  beat  at  every  systole.  In  rare  cases  a  diastolic  thrill,  corresponding  to  the 
diastolic  murmur,  can  be  felt  over  the  base  of  the  heart.  In  two  such  cases 
observed  by  us  the  murmur  had  a  marked  musical  character  (vide  infra).  The 
appearances  in  the  arteries  are  given  below. 

Percussion. — Percussion  gives  an  extension  of  the  cardiac  dullness  to  the  left, 
beyond  the  left  mammillary  line  and  even  to  the  anterior  axillary  line,  caused  by 
the  hypertrophy  and  dilatation  of  the  left  ventricle.  The  upper  boundary  of 
the  cardiac  dullness  is  normal,  or  it  may  extend  up  to  the  third  rib.  The  right 
boundary  is  in  its  normal  place  at  the  left  border  of  the  sterniun,  but  it  may  also 
be  pushed  farther  to  the  right,  either,  because  the  large  left  ventricle  of  itself 


318  DISEASES    OF   THE   CIECULATOEY   OEGANS 

causes  an  extension  of  the  "whole  heart  to  the  right,  or  because  the  right  ventricle 
is  also  hypertrophied.  The  latter  change  occurs  in  pure  aortic  insufficiency  "when 
the  compensation  is  no  longer  complete,  and  the  stasis  extends  back"ward  from  the 
left  ventricle,  through  the  pulmonary  circulation,  into  the  right  side  of  the  heart. 

It  may  also  be  remarked  here  that,  in  insufficiency  of  the  aortic  valves,  the 
ascending  aorta  is  often  considerably  dilated  by  the  marked  impulse  frora  the 
amount  of  blood  pouring  into  it.  A  moderate  degree  of  dullness  is  found  over 
the  dilated  aorta,  "n-hich  may  sometimes  be  made  out  at  the  sternal  end  of  the 
second  right  intercostal  space. 

Auscultation.— rlnsufficiency  of  the  aortic  valves  is  characterized  by  a  long- 
dra"wn,  loud,  blowing  diastolic  murmur,  the  origin  of  "^'hich  has  been  explained 
above.  The  place  in  "which  the  murmur  is  heard  loudest  is  not  the  sternal  end 
of  the  second  right  intercostal  space,  the  ordinary  point  for  auscultation  of  the 
aorta,  but  it  almost  al"ways  lies  farther  to  the  left.  Corresponding  to  the  back- 
"ward  current  of  blood  to"ward  the  left  ventricle,  which  begets  the  murmur,  "we 
hear  the  latter  loudest  over  the  upper  part  of  the  sternum  or  even  at  its  left  bor- 
der. In  some  eases  the  murmur  assumes  a  marked  "  musical  character  " — that 
is,  there  is  a  definite  high  musical  tone,  "which  is  due  to  a  tendinous  fiber  arising 
from  a  "wearing  a"way  of  the  valve,  and  set  in  vibration  by  the  diastole,  or  to  some 
similar  cause.  The  diastolic  murmur  is  often  audible  at  the  apex,  but  it  is  faint 
there.  It  is  only  in  a  few  exceptional  cases  that  there  is  no  diastolic  murmur 
in  aortic  insufficiency.  Sometimes  we  hear  not  only  the  murmur,  but  also  the 
diastolic  sound  of  the  closing  valve.  During  systole  we  scarcely  ever  hear  over 
the  aorta  a  pure,  loud,  first  soimd,  but  almost  always  a  short  systolic  murmur. 
This  may,  of  course,  be  due  to  accompanying  stenosis  of  the  aortic  valves,  but 
yet  is  very  common  when  there  is  insufficiency  alone.  It  is  explained  by  O. 
Eosenbach  as  being  due  to  the  fact  that  at  the  beginning  of  the  systole  of  the  left 
ventricle,  the  diastolic  flow  of  blood  has  not  yet  completely  ceased,  so  that  the 
emerging  blood-stream  encounters  this  opposing  current.  This  meeting  of  the 
two  blood-currents  in  the  root  of  the  aorta  during  systole  causes  the  vibrations 
which  give  rise  to  the  short  systolic  murmur.  It  is  to  be  noted  that  this  circum- 
stance also  may  perhaps  have  some  influence  upon  the  development  of  the  hyper- 
trophy of  the  left  ventricle. 

It  is  very  interesting  and  important  that,  as  Traube  pointed  out,  we  find  the 
first  sound  at  the  apex  scarcely  ever  loud  and  pure,  but  often  very  indistinct  and 
muffled;  or  else  we  hear  a  short  systolic  murmur  instead  of  it.  This  veiling  of 
the  first  sound  at  the  apex  of  the  heart  has  theoretic  interest,  because  it  has  been 
employed  as  an  argument  against  the  view  that  the  first  mitral  sound  is  a  mus- 
cular sound;  for  it  is  not,  in  fact,  at  once  apparent  why  the  hypertrophied  left 
ventricle  should  so  often  fail  to  produce  a  distinctly  audible  tone  by  its  contrac- 
tion. But,  as  "we  have  already  pointed  out  (see  page  316),  the  probable  explana- 
tion lies  in  the  previous  over-distention  of  the  left  ventricle  during  diastole. 
This  renders  the  systolic  contraction  difficult  and  somewhat  slow,  and  may  be  the 
cause  of  the  indistinctness  of  the  muscle-sound.  In  later  stages  of  the  disease 
we  may  also  adduce  parenchymatous  degeneration  of  the  myocardium,  as  an  ex- 
planation of  its  feebleness.  The  systolic  murmur,  often  heard  at  the  apex  in 
aortic  insufficiency,  may  depend  upon  a  co-existing  true  mitral  insufficiency,  but 
it  is  probably  often  due  to  a  relative  insufficiency  of  the  mitral,  since  the  valves, 
which  are  normal  in  themselves,  can  no  longer  cause  a  perfect  closure  of  the  left 
mitral  orifice  now  that  the  left  ventricle  is  dilated. 

Sympto5IS  in  the  Peripheral  Arteries. — Such  remarkable  symptoms  are 
found  in  the  peripheral  arteries  in  aortic  insufficiency  that  they  demand  a  brief 
special  description.  The  first  striking  symptom  is  the  strong  pulsation  not  only 
of  the  larger  but  also  of  the  smaller  arteries,  even  those  the  pulsation  of  which  is 


VALVULAE   DISEASE    OF   THE   HEART 


319 


not  generally  visible.  We  see  and  feel  not  only  a  strong  pulsation  in  the  carotids, 
but  also  in  the  tortuous  brachial  artery,  in  the  radial,  ulnar,  temporal,  dorsalis 
pedis,  etc.  We  sometimes  feel  an  arterial  pulse  in  the  liver  through  the  ab- 
dominal walls. 

The  rapid  decline  of  the  pulse — the  pulsus  celer  [Corrigan's  pulse] — is  most 
characteristic  of  aortic  insuiEciency,  and  is  to  be  felt  especially  in  the  radial 
artery,  but  also  in  the  femoral,  dorsalis  pedis,  and  other  vessels.  An  abnormally 
large  quantity  of  blood  is  thrown  into  the  arteries  from  the  hypertrophied  and 
dilated  left  ventricle;  hence  the  high  ascent  of  the  pulse;  but  since  the  distended 
artery  quickly  contracts  again,  and  particularly  as  at  the  next  diastole  of  the 
ventricle  the  blood  escapes  in  two  directions,  into  the  capillaries  and  back  into 
the  ventricle,  an  abnormally  rapid  and  deep  decline  of  the  pulse  follows  the 
high  ascent  of  its  wave — a  condition  which  explains  the  "  jumping,"  "  springing  " 
pulse  (pulsus  celer)  of  aortic  insufficiency.  The  quality  of  the  pulse  may  be 
plainly  recognized  also  in  the  sphygmographic  tracing  (see  Fig.  40).  The  abnor- 
mal backward  wave 
may  even  be  detected 
in  the  capillaries.  We 
often  see  a  marked 
pallor  of  the  finger- 
nails at  every  diastole 
of  the  heart  in  pa- 
tients with  aortic  insuf- 
ficiency— Quincke's  ca- 
pillary pulse. 

The  auscultatory 
phenomena  over  the  ar- 
teries are  connected 
partly  with  the  chang- 
ing conditions  of  tension  of  the  arterial  walls.  We  very  often  hear  a  short, 
rough,  systolic  murmur  in  the  carotid.  The  second  sound,  which  is  well  known 
to  be  the  transmitted  aortic  second  sound,  is  absent.  Instead  of  it  we  sometimes 
hear  faintly  transmitted  the  aortic  diastolic  murmur.  The  sound  of  the  medium- 
sized  and  smaller  arteries  is  very  characteristic.  By  applying  the  stethoscope 
lightly  we  hear  over  the  femoral,  the  brachial,  and  often  over  the  radial,  the 
ulnar,  the  palmar  arch,  and  the  dorsalis  pedis,  a  marked  valvular  sound,  which 
is  changed  by  pressure  on  the  artery,  especially  in  the  larger  arteries,  to  a  loud 
stenotic  murmur.  The  quicker  the  pulse,  the  more  certain  are  we  to  hear  these 
sounds  in  the  arteries.  In  the  most  marked  cases  of  Corrigan's  pulse  these  vas- 
cular sounds  are  so  loud  that  we  may  hear  almost  any^vhere  below  the  knee,  by 
means  of  a  stethoscope,  a  valvular  sound.  The  double  sound  in  the  femoral 
(Traube's  double  sound)  is  quite  a  frequent  phenomenon,  about  the  origin  and 
significance  of  which  there  has  been  much  discussion.  The  double  sounds  either 
follow  each  other  shortly,  so  that  the  first  seems  something  like  a  preparatory 
blow  for  the  second,  or  they  are  separated  from  each  other  by  a  longer  interval, 
like  the  two  sounds  of  the  heart.  Traube  explained  the  origin  of  the  first  sound 
by  the  sudden  tension  of  the  vessel-wall,  as  in  the  simple  femoral  sound,  and  the 
second  sound  by  the  sudden  relaxation  of  it.  Friedreich  has  pointed  out  in  regard 
to  this  that,  in  co-existing  tricuspid  insufficiency,  a  sound  may  also  be  produced 
in  the  femoral  vein  by  tension  of  the  venous  valves.  The  double  sound  in  the 
femoral  may  probably  have  different  causes  of  origin.  It  is,  of  course,  by  far  the 
most  frequent  in  aortic  insufficiency,  but  it  has  also  been  repeatedly  observed  in 
other  forms  of  heart  disease,  as  in  mitral  stenosis.  The  so-called  Duroziez's  double 
murmur  in  the  femoral  is  more  rare,  and  it  is  noticed  almost  exclusively  in  aortic 


Fig.  40.— Pulse  curve  in  aortic  insufficiency. 


320  DISEASES    OF   THE   CIECULATOEY   OEGAKS 

insufficiency.  This  is  when  we  hear,  by  pressing  the  stethoscope  on  the  femoral, 
two  murmurs  plainly  distinct  from  each  other,  of  which  the  first  comes  from  the 
passage  of  the  systolic  blood-wave,  and  the  second  from  the  passage  of  the  abnor- 
mal backward  wave  coming  from  the  periphery  of  the  vascular  system  through 
the  artificially  contracted  vessel.  While  the  well-marked  Corrigan's  pulse  and 
the  arterial  sounds  associated  with  it  are  so  characteristic,  they  do  not  appear 
with  great  distinctness  in  every  case  of  aortic  insufficiency,  but  only  in  many; 
while  in  other  and  apparently  similar  cases  they  are  indistinct  or  quite  absent. 
Probably  this  difference  depends  at  least  in  part  upon  a  diiference  in  the  elasticity 
of  the  arterial  walls.  At  any  rate,  we  have  seen  well-marked  Corrigan's  pulse  and 
sounding  arteries  in  youthful  patients;  while  in  elderly  persons  with  accompany- 
ing arterio-sclerosis  or  similar  changes,  these  phenomena  are  not  apt  to  be  striking. 
Aortic  insufficiency  is  a  comparatively  favorable  form  of  heart  disease,  since 
it  may  be  almost  perfectly  compensated  for  years  by  hypertrophy  of  the  left 
ventricle.  Many  patients  with  moderate  aortic  insufficiency  feel  perfectly  well, 
and  are  even  capable  of  quite  hard  work.  They  have  not  the  slightly  cyanotic 
hue  which  almost  all  patients  with  mitral  disease  exhibit,  but  they  have  a  nor- 
mal or  even  a  pale  complexion.  If,  however,  the  signs  of  disturbed  compensa- 
tion once  appear  in  aortic  insufficiency  the  severest  sequelae  may  develop  quite 
rapidly.  In  aortic  insufficiency  it  is  exceptional  to  see  such  repeated  changes 
from  bad  to  good,  and  good  to  bad,  as  are  often  observed,  for  instance,  in  mitral 
stenosis.  If  the  left  ventricle  becomes  enfeebled,  it  can  no  longer  satisfy  the 
excessive  demands  made  upon  it.  Passive  congestion  ensues,  extending  back- 
ward through  the  pulmonary  circuit  into  the  systemic  veins,  even  while  the  pulse 
may  still  seem  to  be  powerful.  The  average  arterial  tension  becomes  subnormal, 
dyspnoea  increases,  and  there  are  attacks  of  cardiac  asthma.  CEdema  appears, 
and  the  patient  dies  with  the  sjonptoms  of  anasarca.  We  will  speak  more  fully 
below  of  certain  intercurrent  events  in  aortic  insufficiency,  such  as  cerebral  haem- 
orrhage and  pericarditis. 

4.  Stenosis  of  the  Aortic  Orifice 

Except  for  the  mild  forms  of  aortic  stenosis,  which  often  come  on  with  aortic 
insufficiency,  aortic  stenosis  is  a  rare  disease.  It  arises  from  marked  thick- 
enings and  calcifications,  and  especially  from  adhesions  of  the  aortic  valves  to 
one  another.  The  stenosis  may  become  so  considerable  that  the  orifice  is  finally 
reduced  to  a  mere  fissure,  through  which  the  left  ventricle  must  force  the  blood 
at  its  systole.  The  fluttering  of  the  valves  and  the  vertiginous  movements  in  the 
blood  thus  arising  produce  a  loud  systolic  murmur.  The  left  ventricle  is  com- 
pelled to  do  greater  work  in  consequence  of  the  increased  resistance  of  the  aortic 
orifice,  and  hence  becomes  hypertrophied.  In  spite  of  the  increased  effort,  how- 
ever, comparatively  little  blood  reaches  the  arterial  system,  and  consequently  the 
radial  pulse  is  small  and  the  arteries  contracted. 

Inspection  and  Palpation. — Upon  physical  examination  of  the  heart  we  find, 
in  the  first  place,  the  apex-beat  displaced  outward  as  a  result  of  the  hypertrophy 
of  the  left  ventricle,  and  also  often  more  powerful  than  normal.  It  may,  how- 
ever, be  noticeably  feeble,  perhaps  because  of  the  slowness  of  the  systole.  A 
former  explanation  of  this  feebleness  was  the  diminution  of  the  recoil  of  the 
apex  (the  Gutbrod-Skoda  theory  of  the  apex-beat). 

Percussion. — Percussion  gives  an  extension  of  the  heart's  dullness  to  the  left. 
The  right  ventricle  is  also  dilated  and  hypertrophied  to  a  moderate  degree  in  the 
later  stages,  if  the  stasis  extends  backward  through  the  pulmonary  circulation. 

Auscultation. — On  auscultation,  we  hear  over  the  aorta  a  very  loud  "  sawing," 
long-drawn,  systolic  murmur,  which  is  usually  transmitted  to  the  right,  corre- 


VALVULAE   DISEASE    OF   THE   HEART  321 

sponding  to  the  course  of  the  aorta,  in  distinction  from  the  diastolic  murmur  of 
aortic  insufficiency.  It  is  usually  to  be  heard  loudest  at  the  sternal  end  of  the 
second  right  intercostal  space,  but  it  is  audible  to  a  lesser  extent  over  almost  the 
whole  heart.  It  is  usually  quite  loud  over  the  carotids.  The  systolic  sound  at 
the  apex  is  apt  to  be  feeble.  The  second  aortic  sound  is  likewise  faint  or  even 
inaudible.  If  there  is  co-existing  insufficiency  of  the  valve,  the  second  aortic 
sound  is  replaced  by  a  diastolic  murmur. 

The  pulse  has  been  already  described.  It  is  small,  and  often  surprises  one  by 
its  contrast  with  the  strength  of  the  apex-beat.  In  well-compensated  cases  it  is 
regular,  and  often  moderately  or  even  extremely  slow.  This  slow  pulse  of  aortic 
stenosis  is  often  explained  as  a  compensatory  change  in  the  heart's  action,  appro- 
priate to  the  existing  lesion — the  systole  being  lengthened,  an  increased  amount 
of  blood  can  be  driven  through  the  narrow  aortic  orifice.  But  the  slowing  of  the 
cardiac  action  is  really,  in  main  part,  a  prolongation  of  the  diastole,  and  there- 
fore the  slow  pulse  is  probably  due  chiefly  to  the  fact  that  the  wall  of  the  left  ven- 
tricle is  ill-supplied  with  blood,  just  as  in  the  case  of  sclerosis  of  the  coronary 


Fig.  41. — Pulse  curve  in  stenosis  of  the  aortic  orifice. 

arteries.     The  sphygmographic  tracing  of  the  radial  pulse  (see  Eig.  41)  shows  a 
low  wave  and  a  comparatively  slow  rise  and  fall. 

Aortic  stenosis  of  slight  or  moderate  degree  may  be  tolerably  well  borne  by 
the  patient.  We  have  even  seen  a  man  with  well-marked  aortic  stenosis  who 
for  years  did  not  have  the  slightest  subjective  symptoms  of  heart-disease,  until 
he  finally  died  with  an  acute  recurrent  endocarditis.  When  the  stenosis  is  more 
complete  we  sometimes  have  a  most  peculiar  clinical  picture.  The  pulse  is  very 
infrequent,  as  low  as  thirty  to  twenty-four  beats  in  a  minute.  From  time  to 
time  there  are  attacks  of  vertigo  or  syncope,  the  patient  often  falls,  and  has  epi- 
leptiform attacks.  These  seizures,  which  may  be  repeated  for  months  or  even  for 
some  years,  are  probably  connected  with  a  sudden  ansemia  of  the  heart  and  brain. 
We  have  observed  this  remarkable  group  of  symptoms  particularly  in  elderly  per- 
sons with  aortic  stenosis,  due  to  arterio-sclerosis.  In  other  respects  the  course  of 
aortic  stenosis  is  similar  to  that  of  the  acute  valvular  diseases,  and  in  the  same 
way  terminates  in  general  circulatory  derangement  with  its  results. 

5.  Insufficiency  of  the  Tricuspid  Valve 

Insufficiency  of  the  tricuspid  valve  is  extremely  rare  as  an  independent  dis- 
ease of  the  heart,  but  a  secondary  insufficiency  of  the  tricuspid  is  quite  fre- 
quent, and  is  therefore  of  practical  interest,  as  it  complicates  other  already-exist- 
ing valvular  diseases  in  the  left  side  of  the  heart.  It  arises  either  from  a  sec- 
ondary endocarditis,  affecting  the  tricuspid,  in  quite  an  analogous  manner  with 
mitral  insufficiency,  or  it  is  a  so-called  relative  insufficiency.  This  name  we  give 
to  that  form  of  insufficiency  which  develops  when  the  edges  of  the  tricuspid  valve, 
normal  in  themselves,  at  last  fail  to  meet  one  another,  from  the  increasing  dilata- 
tion of  the  right  ventricle,  or  at  any  rate  from  the  inability  of  the  enfeebled  right 
ventricle  properly  to  close  the  valve. 

The  necessary  result  of  tricuspid  insufficiency  is,  that  in  every  systole  of  the 
right  ventricle  a  backward  current  passes  through  the  open  tricuspid  orifice  into 
the  right  auricle,  and  thence  into  the  veins  of  the  body.  The  tricuspid  insuffi- 
ciency ensuing  in  other  forms  of  heart  disease  must  therefore  increase  the  stasis 
21 


322  DISEASES    OF   THE   CIECULATORY   ORGAIsTS 

in  the  reins  of  the  body,  and  it  is  thus  far  an  unfavorable  complication.  It  has  a 
compensatory  significance  only  as  it  affords  relief  to  the  pulmonary  circulation. 
Since  a  part  of  the  blood  passes  back  from  the  right  ventricle  into  the  veins, 
less  blood  than  usual  must  reach  the  pulmonary  arteries.  The  decrease  in  ten- 
sion thus  produced  in  these  arteries  makes  itself  apparent  on  auscultation,  since 
the  accentuation  of  the  pulmonic  second  sound  in  valvular  disease  of  the  mitral 
orifice  diminishes  "R-hen  tricuspid  insufliciency  takes  place. 

That  tricuspid  insufliciency  must  result  in  a  hypertrophy  of  the  right  ven- 
tricle is  explained  in  just  the  same  "way  as  the  hypertrophy  of  the  left  ventricle 
in  mitral  insufliciency,  from  the  increased  influx  of  blood  at  increased  tension 
into  the  right  ventricle  during  diastole;  but  this  effect  of  tricuspid  insufficien- 
cy can  rarely  be  made  out  in  any  individual  case,  since  the  right  ventricle  is  usu- 
ally already  hypertrophied  as  a  result  of  the  disease  in  the  left  side  of  the 
heart. 

The  most  important  symptom  from  vhich  we  can  diagnosticate  tricuspid  in- 
sufliciency is  the  venous  pulse.  The  cause  of  this  is  the  backward  wave  of  blood 
produced  at  each  systole  of  the  right  ventricle.  So  long  as  the  venous  valve 
above  the  bulbus  jugularis  is  closed,  we  usually  see  only  a  "  bulbar  pulse,"  but 
very  soon  this  valve  also  yields  to  the  continued  impulse  of  the  blood,  and  then 
a  strong,  purely  venous  pulse  is  visible  along  the  whole  course  of  the  jugular 
vein  up  to  the  vicinity  of  the  mastoid  process.  The  contraction  of  the  right 
auricle  very  often  causes  a  decidedly  weaker  elevation  of  the  vein,  which  just 
precedes  the  marked  pulsation  caused  by  the  ventricular  systole  (anadicrotic 
venous  pulse) .  On  account  of  the  straighter  course  of  the  right  innominate  vein, 
the  jugular  venous  pulse  is  often  stronger  on  the  right  side  than  on  the  left.  We 
must  state,  however,  that  the  jugular  venous  pulse  is  not  an  absolutely  certain 
sign  of  tricuspid  insufficiency,  since  it  may  arise  in  hypertrophy  of  the  right  side 
of  the  heart  without  any  insufficiency  of  the  tricuspid,  from  the  closure  of  the 
valves. 

If  there  is  pulsation  in  the  bulb  of  the  jugular  vein  and  the  jugular  valve  is 
still  capable  of  closing,  a  low,  audible,  venous,  valvular  sound  may  be  produced  by 
its  closure.  A  sound  may  also  arise  in  tricuspid  insufficiency,  as  has  been  already 
said,  from  the  tension  of  the  valves  in  the  femoral  vein.  A  visible  pulsation  in 
the  larger  veins  of  the  extremities  is  very  rare,  but  in  tricuspid  insufficiency  we 
quite  frequently  feel  a  venous  pulsation  in  the  liver,  which  organ  is  usually  en- 
larged by  passive  congestion.  This  may  be  quite  apparent  even  in  many  cases 
in  which  the  jugular  venous  pulse  is  absent,  because  the  veins  in  the  liver  are 
without  valves.     [It  is  best  appreciated  by  means  of  bimanual  palpation. — V.] 

Auscultation  over  the  right  side  of  the  heart  gives  a  systolic  murmur  in  insuffi- 
ciency of  the  tricuspid,  arising  from  the  regurgitating  blood-current.  This  may 
be  heard  loudest  over  the  lower  part  of  the  sternum,  or  at  the  sternal  end  of  the 
right  fifth  rib.  The  significance  of  this  murmur  in  diagnosis,  however,  is  im- 
paired by  the  fact  that  it  can  not  always  be  separated  from  the  systolic  mitral 
murmur  that  often  co-exists. 

6.  Stenosis  of  the  Tricuspid  Orifice 

Stenosis  of  the  tricuspid  orifice  is  an  extremely  rare  disease,  and  hence  it  is 
without  practical  significance.  It  has  usually  been  observed,  up  to  the  present 
time,  as  a  congenital  form  of  heart  disease,  almost  always  combined  with  other 
anomalies  of  development  in  the  heart. 

The  physical  signs  of  tricuspid  stenosis  can  easily  be  constructed  theoretically. 
The  first  result  must  be  a  marked  dilatation  of  the  right  auricle,  and  the  occur- 
rence of  a  diastolic  or  presystolic  murmur  over  the  right  side  of  the  heart.    From 


VALVULAE   DISEASE    OF   THE   HEART  323 

the  rarity  and  complex  character  of  the  cases,  however,  we  have  so  far  seldom 
had  an  opportunity  to  confirm  these  theories  at  the  bedside. 

The  prognosis  of  this  form  of  heart  disease  is  veiy  unfavorable,  since  a  long- 
continued  compensation  by  increased  labor  on  the  part  of  the  right  auricle  is 
scarcely  conceivable. 

[Seventy  cases  of  tricuspid  stenosis  have  been  collected  by  Bedford  Fenwick, 
whose  analysis  affords  good  grounds  for  thinking  that  the  lesion  is  often  ac- 
quired. In  fifty  per  cent,  of  the  cases  there  was  a  clear  history  of  rheumatism, 
and  nearly  all  of  the  patients  were  more  than  twenty  years  of  age  at  the  time  of 
death. 

This  lesion  is  never  found  alone,  but  invariably  combined  with  mitral  stenosis ; 
all  but  eight  of  the  cases  were  in  women.  Fenwick  thinks  that  the  influence  of 
sex  lies  in  the  less  onerous  nature  of  the  work  of  women  than  of  men,  the  granu- 
lating edges  of  the  valves  being  kept  more  in  apposition,  thus  healing  with  adhe- 
sion and  causing  obstructions  at  the  orifice.] 

7.  Insufficiency  of  the  Pulmonary  Valve 

Insufficiency  of  the  pulmonary  valve  is  also  a  very  rare  form  of  heart  disease. 
It  occurs  as  a  congenital  anomaly,  often  combined  with  other  failures  of  develop- 
ment, or  as  a  disease  acquired  after  birth.  The  anatomical  changes  in  the  valve, 
which  lead  to  insuificiency,  are  precisely  analogous  to  those  which  cause  insuffi- 
ciency of  the  aortic  valve. 

The  physical  signs  of  this  form  of  valvular  disease  consist  chiefly  of  a  marked 
dilatation  and  hypertrophy  of  the  right  ventricle,  to  be  made  out  by  percussion, 
and  of  a  loud  diastolic  murmur  over  the  pulmonary  valve.  These  signs  are 
explained  in  just  the  same  way  as  the  precisely  analogous  signs  in  the  left  ven- 
tricle in  aortic  insufficiency. 

In  general,  pulmonary  insufficiency,  like  aortic  insufficiency,  seems  to  be  com- 
pensated quite  well  for  a  long  time  by  hypertrophy  of  the  right  ventricle.  In 
many  cases  a  co-existing  patency  of  the  foramen  ovale  also  seems  to  be  of  favor- 
able influence,  as  it  lessens  the  stasis  in  the  right  auricle  and  the  veins  of  the 
body,  while  it  renders  easier  the  filling  of  the  left  ventricle. 

8.  Stenosis  of  the  Pulmonary  Orifice   (Pulmonary  Stenosis)   and  the  other 
Congenital  Diseases  of  the  Heart 

1.  Congenital  Pulmonary  Stenosis.— While  the  stenosis  of  the  pulmonary 
orifice  acquired  in  later  life  is  so  rare  that  it  has  only  slight  practical  signifi- 
cance, the  congenital  pulmonary  stenosis  is  of  far  greater  importance.  It  is, 
on  the  whole,  the  most  frequent  of  the  congenital  forms  of  heart  disease.  Its 
origin  is  to  be  referred  either  to  an  endocarditis  of  the  pulmonary  valves  during 
fcBtal  life,  or  to  anomalies  in  the  development  of  the  heart.  The  stenosis  is  often 
situated  not  merely  at  the  pulmonary  orifice  itself,  but  farther  back  in  the  conus 
arteriosus,  which  seems  to  be  narrowed  by  the  formation  of  myocardial  cicatrices. 
The  pulmonary  artery  is  often  also  narrowed  as  a  whole.  In  the  majority  of 
cases  we  find,  in  addition,  other  anomalies  of  development  in  the  heart,  espe- 
cially patency  of  the  foramen  ovale,  great  defects  in  the  ventricular  septum,  and. 
in  about  half  the  cases,  patency  of  the  ductus  Botalli,  etc. 

The  symptoms  of  congenital  pulmonary  stenosis  sometimes  appear  soon  aftet 
the  birth  of  the  child.  The  first  thing  that  strikes  us  is  the  marked  cyanosis, 
which  is  constant,  or  else  comes  on  with  crying,  or  with  movements  of  the  body. 
Many  children,  however,  reach  a  fair  age,  five  or  ten  years,  or  even  fifteen.  In 
some  cases  the  heart  disease  may  be  so  perfectly  compensated  that  the  child  may 


324:  DISEASES    OF   THE   CIECULATOEY   OEGANS 

be  comparatively  well  for  a  time,  and  severe  disturbances  may  not  appear  for 
several  years. 

As  a  rule,  children  with  congenital  pulmonary  stenosis  present  a  very  strik- 
ing appearance.  The  cyanosis  is  especially  noticeable  in  the  face,  the  lips,  the 
nose,  and  the  hands  and  nails.  The  parts  mentioned  feel  cool.  The  eyes  are 
often  somewhat  prominent,  and  there  is  a  slight  cedematous  swelling  about  them. 
The  peculiar  club-like  thickening  of  the  terminal  phalanges  of  the  fingers  and 
toes,  a  result  of  stasis,  as  seen  also  in  many  cases  of  bronchiectasis,  is  very  char- 
acteristic.    The  nails  also  present  a  characteristic  claw-like  curvature. 

The  whole  development  of  the  child  is  remarkably  retarded.  It  often  seems 
several  years  younger  than  it  is.  The  muscles  and  fatty  layer  are  slight.  The 
gums  are  sometimes  very  spongy  and  disposed  to  bleed.  In  severe  cases  the  child 
suffers  from  faintness,  vertigo,  etc. 

On  physical  examination  of  the  heart,  we  usually  find  the  cardiac  region 
rather  prominent.  Percussion  gives  an  increase  of  the  heart's  dullness,  especially 
toward  the  right.  This  extension  of  the  dullness  is  due  to  the  hypertrophy  of  the 
right  ventricle,  which  must  arise  in  the  same  way  as  hypertrophy  of  the  left  ven- 
tricle in  aortic  stenosis.  On  auscultation,  we  hear  a  loud  systolic  murmur,  which 
is  perceptible  over  the  whole  heart,  but  which  has  its  greatest  intensity  at  the 
sternal  end  of  the  second  left  intercostal  space.  The  eddies  of  blood,  which  pro- 
duce the  murmur,  may  also  often  be  felt  by  the  hand  as  a  systolic  thrill.  In  some 
cases,  however,  we  miss  the  murmur  in  pulmonary  stenosis,  just  as  in  mitral  ste- 
nosis. The  pulmonic  second  sound  is  weak  or  inaudible,  or  it  is  replaced  by  a 
murmur  if  there  is  also  insufficiency  of  the  valve. 

The  course  of  congenital  pulmonary  stenosis  is  always  unfavorable.  As  has 
been  implied,  few  children  get  beyond  the  age  of  fifteen  years.  Death  ensues, 
either  with  general  disturbances  of  compensation  evidenced  by  dyspnoea  and 
dropsy,  as  in  every  other  form  of  heart  disease,  or  from  complications.  Among 
the  latter,  we  may  mention  especially  the  very  frequent  development  of  phthisis. 

2.  The  Remaining  Congenital  Lesions  of  the  Heart. — Inasmuch  as  other  con- 
genital lesions  than  pulmonary  stenosis  have  but  slight  clinical  importance,  we 
will  limit  ourselves  here  to  a  brief  review  of  the  same.* 

(a)  Patency  of  the  foramen  ovale  is  a  comparatively  frequent  lesion,  whether 
alone  or  combined  with  others.  Physical  signs  are  mostly  absent.  In  a  few 
cases  a  presystolic  murmur  has  been  heard.  When  mitral  insufficiency  co-exists 
with  a  patent  foramen  ovale,  venous  pulsation  may  be  caused. 

(&)  Defects  in  the  septum  between  the  ventricles.  These  are  most  frequently 
situated  in  the  posterior  section  of  the  anterior  septum,  and  they  likewise  are 
associated  with  other  anomalies,  such  as  abnormal  distribution  of  the  arteries, 
pulmonary  stenosis,  or  defects  in  the  septum  between  the  auricles.  Sometimes  the 
patency  of  the  septum  gives  rise  to  a  systolic  murmur,  but  a  diagnosis  of  the  con- 
dition during  life  is  scarcely  ever  possible. 

(c)  Persistence  of  the  ductus  Botalli.  Inasmuch  as  this  contributes  blood 
from  the  aorta  to  the  pulmonary  circulation  the  pressure  in  the  latter  is  raised, 
hence  there  is  to  be  observed  accentuation  of  the  second  pulmonic  sound  and 
hypertrophy  of  the  right  ventricle.  There  is  sometimes  also  a  loud  systolic 
murmur. 

(d)  We  have  already  spoken  of  congenital  stenosis  of  the  tricuspid  valve. 
Congenital  narrowing  of  the  mitral  valve  and  of  the  aortic  valves  may  also  occur, 
but  they  are  extremely  rare. 

*  A  more  extensive  ^j .  ntation  of  the  subject  can  be  found  in  the  article  by  Eauehfuss  in  Ger- 
hardt's  "  Ilandbuch  dor  Kinderlvrankheiten,"  vol.  iv,  and  in  text- books  on  pathological  anatomy  — 
for  example,  Orth's. 


VALVULAR  DISEASE   OF   THE   HEART 


325 


9.  Combined  Valvular  Diseases  of  the  Heart 

Although  in  what  has  preceded  we  have  dealt  with  the  several  forms  of  valvu- 
lar disease  of  the  heart  separately,  in  order  to  present  them  in  a  general  way, 
yet  in  reality  combinations  of  them  often  occur  in  great  variety.  We  find 
especially,  as  has  already  been  mentioned,  stenosis  of  an  orifice  co-existing  with 
insufficiency  of  the  accompanying  valve;  but  diseases  of  two  or  more  different 
valves  are  not  infrequent,  combined  in  the  most  diverse  manners.  The  physical 
signs  of  these  "  combined  forms  of  heart  disease  "  may,  of  course,  be  inferred  from 
the  signs  of  anomalies  of  single  valves,  but  the  phenomena  are  often  so  compli- 
cated that  the  diagnosis  of  combined  heart  disease  is  generally  much  harder  than 
that  of  the  simple  forms.  Sometimes  the  single  forms  neutralize  one  another  in 
their  action.  For  example,  the  left  ventricle  is  usually  small  in  pure  mitral  ste- 
nosis, but,  if  aortic  insufficiency  be  also  present,  it  is  nevertheless  found  dilated,  at 
least  to  a  certain  degree.  The  influence  of  an  absolute  or  relative  tricuspid  insuf- 
ficiency on  the  action  of  mitral  disease,  especially  the  decrease  in  tension  in  the 
pulmonary  vessels  caused  by  it,  and  also  the  diminished  accentuation  of  the  pul- 
monic sound,  have  been  mentioned  above. 

In  reference  to  the  clinical  symptoms  of  combined  heart  disease  we  may  say, 
on  the  whole,  that,  in  a  large  number  of  cases,  the  disease  of  o?ie  valve  stands  out 
as  predominant  in  the  whole  picture  of  the  disease.  The  other  anomalies  are  only 
slightly  noticeable,  and  often  of  later  date.  Hence,  we  may  find  at  the  autopsies 
of  patients,  who  during  life  have  shown  the  symptoms  of  disease  of  only  one 
particular  valve,  unimportant  changes  on  the  other  valves,  which  have  been  with- 
out clinical  significance. 

General  Comparison  of  the  most  Important  Physical  Signs  in  Valvul.aji  Disease 

OF  THE  Heart 


Form  of 
Heart  Disease 


1.  3Iitral  in- 
sufficiency. 


2.  3Iifral 
stenosis. 


3.  Aortic  in- 
sufficiency. 


Inspection. 


4.  Aortic 
stenosis. 


Strong  apex-beat, 
often  somewhat 
displaced  out- 
ward. 

Area  of  cardiac  im-  i  Diastolic 
pulse     enlarged,  !     at     the 
epigastric  pulsa- 
tion. 


Palpation. 


Systolic       thrill 

at    the    apex. 

Quite     strong 

radial  pulse. 

■"      thrill 


Apex  -  beat  very 
strong,  displaced 
downward  and  to 
the  left.  Visible 
pulsation  of  the 
medium  -  sized 
and  smaller  ar- 
teries. 


Apex  -  beat  dis- 
placed to  the 
left. 


apex. 
Small  and  oft- 
en irregular 
pulse. 


Very  strong, 
heaving  apex- 
beat.  Pulsus 
celer. 


Heart's  action 
not  very  strong. 
Pulse  small,  in- 
frequent,some- 
times slow. 


Percussion. 


Hypertrophy  of 
the  left,  later 
of  the  right 
ventricle. 

Hypertrophy  of 
the  right  ven- 
tricle. 


Marked  hyper- 
trophy of  the 
left  ventricle. 


Hypertrophy  of 
the  left  ven- 
tricle. 


Auscultation. 


Loud  systolic  murmur 
at  the  apex.  Pul- 
monic second  sound 
accentuated. 

Diastolic  or  presys- 
tolic murmur  at  the 
apex.  First  sound 
sometimes  loud. 

Pulmonic  second 
sound  accentuated, 
and  sometimes  dou- 
ble. 

Loud  diastolic  aortic 
murmur,  especially 
over  tlie  upper  part 
of  the  sternum. 
Sounds  in  the  ar- 
teries (femoral  and 
brachial  sounds, 
etc.).  Sometimes  a 
double  sound  or 
double  murmur  in 
the  femoral. 

Loud  systolic  aortic 
murmur,  transmitted 
to  the  right. 


326  DISEASES    OF   THE   CIKCULATOEY   OEGAl^S 

[Bramwell  reports  that  of  131  cases  with  macroscopic  valvular  lesion,  the  tri- 
cuspid was  implicated  in  33.58  per  cent.;  in  all  but  12  per  cent,  of  these  the 
changes  were  recent.  Hence  he  thinks  that  tricuspid  endocarditis  is  generally 
recovered  from,  and  this  he  attributes  to  the  relatively  small  strain  to  which  that 
valve  is  subjected.  The  obvious  therapeutic  deduction  is  the  importance  of  rest 
in  mitral  endocarditis.] 

General  Sequels  and  Complications  of  Valvular  Disease  op  the  Heart 

After  having  discussed,  in  what  precedes,  the  mechanism  of  the  single  forms  of 
valvular  disease,  and  the  physical  signs  derived  from  it,  we  must  now  describe  a 
number  of  symptoms  and  sequelae  which  may  be  present  to  a  greater  or  less  degree 
in  all  forms  of  valvular  disease.  With  them  we  must  also  mention  certain  pecul- 
iarities of  the  individual  forms. 

1.  Subjective  Symptoms. — Fully  compensated  heart  disease  may  exist,  at  least 
for  a  long  time,  without  any  subjective  symptoms.  This  is  especially  the  case  in 
aortic  insufficiency,  more  rarely  in  mitral  insufficiency.  Stenosis  of  the  mitral 
or  of  the  aortic  valves  almost  always  causes  subjective  symptoms.  These  symp- 
toms often  do  not  exist  so  long  as  the  patient  keeps  perfectly  quiet  physically  and 
mentally,  but  they  develop  under  appropriate  circumstances,  especially  upon  bod- 
ily exertion. 

The  existing  subjective  symptoms  in  heart  disease  are  by  no  means  always 
referred,  in  the  first  place,  to  the  heart  itself.  It  sometimes  happens  that  the 
patient  comes  to  the  physician  complaining  of  various  digestive  disturbances,  or 
in  other  cases  of  headache,  vertigo,  etc.  The  physical  examination  alone  leads  us 
to  recognize  the  heart  disease.  As  a  rule,  the  patient's  first  and  chief  complaint 
is  directed  toward  his  difficulty  in  breathing.  The  shortness  of  breath,  which 
increases  on  any  physical  exertion,  comes  on  quite  early  in  many  cases.  In  the 
later  stages  it  is  almost  always  the  most  distressing  symptom.  The  causes  of 
dyspnoea  in  heart  disease  are  manifold.  In  the  first  place  dyspnoea  results  from 
congestion  of  the  pulmonary  circuit,  with  consequent  slowing  of  the  circulation 
in  the  lungs,  and  limitation  of  the  exchange  of  gases  in  those  organs.  In  later 
stages  the  anatomical  changes  in  the  lungs  contribute  also  to  an  increase  of  the 
dyspnoea  (vide  supra,  the  chapter  on  brown  induration  of  the  lungs).  Basch 
ascribes  special  importance  to  the  fact  that  the  distended  capillaries  encroach 
upon  the  alveoli,  as  a  result  of  the  passive  congestion.  This  broadens  the  alveoli 
("swelling  of  the  lungs"),  but  at  the  same  time  impairs  the  mobility  of  the 
lungs  ("  rigidity  of  the  lungs  "),  and  thus  embarrasses  the  exchange  of  gases  in 
the  lungs,  just  as  in  emphysema.  Further  investigations  are  necessary  in  order  to 
determine  the  clinical  importance  of  these  conditions. 

The  secondary  bronchitis  of  heart  disease  is  a  very  great  factor  in  the  dysp- 
noea. This  bronchitis  is  a  frequent  result  of  the  pulmonary  stasis.  Often  the 
respiratory  distress  increases  and  decreases  simultaneously  with  corresponding 
variations  in  the  bronchitis.  A  purely  mechanical  cause  of  dyspnoea  is  the  com- 
pression of  the  lower  portion  of  the  left  lung  by  great  cardiac  hypertrophy.  The 
highest  grade  of  dyspnoea  is  reached  when  finally  hydrothorax,  hydropericardium, 
and  pulmonary  oedema  are  developed.  From  what  has  already  been  stated,  it  is 
easy  to  see  why  lesions  of  the  mitral  valve  which  directly  impair  the  pulmonary 
circulation  lead  sooner  to  shortness  of  breath  than  do  lesions  of  the  aortic 
valves.  Finally,  it  is  self-evident  that  the  condition  of  the  heart  has  the  great- 
est influence  upon  the  degree  of  dyspnoea  present,  for  all  the  phenomena  of 
pulmonary  congestion  must  increase  or  diminish,  according  to  the  functional 
integrity  of  the  heart,  and  particularly  of  the  left  ventricle.  If  the  contractile 
power  of  the  left  ventricle  grows  less,  dyspnoea  must  at  once  increase.  ISTot 
infrequently   conditions    of   cardiac    weakness    develop    with    considerable    sud- 


VALYULAE   DISEASE   OF   THE   HEART  327 

denness,  and  occasion  attacks  of  dyspnoea  which,  are  termed  cardiac 
asthma. 

Palpitation  is  the  first  subjective  symptom  to  be  mentioned  of  those  which 
are  referred  directly  to  the  heart.'  It  is  not  yet  accurately  determined  under 
what  circumstances  the  action  of  the  heart  is  perceived  by  the  patient  himself. 
We  sometimes  see  an  uncommonly  strong  action  of  the  heart,  as  in  aortic  insuffi- 
ciency, which  is  not  perceived  at  all  subjectively.  In  other  eases,  where  objec- 
tivelj"  the  heart  is  not  especially  active,  palpitation  forms  the  patient's  chief 
complaint.  It  usually  first  appears  when  the  heart  disease  ceases  to  be  fully 
compensated.  It  is  increased  or  first  excited  by  physical  exertion  or  mental 
excitement.  In  many  patients  attacks  of  palpitation  occur  without  any  discover- 
able external  cause,  due  apparently  to  nervous  disturbance.  They  are  sometimes 
associated  with  a  striking  acceleration  of  the  pulse,  the  so-called  tachycardia. 

Pain  in  the  cardiac  region  is  only  rarely  present  in  heart  disease.  The  patients 
more  frequently  complain  of  an  indefinite  feeling  of  pressure  and  oppression  in 
the  chest,  but  still  there  do  occur,  particularly  in  aortic  insufficiency,  attacks  of 
violent  pain  in  the  front  part  of  the  chest  and  the  region  of  the  heart,  radiating 
to  the  shoulders  and  arms,  and  associated  with  a  general  feeling  of  extreme  anx- 
iety and  weakness.  Such  conditions  are  termed  angina  pectoris,  or  attacks  of 
stenocardia  (vide  infra).  Pains  in  the  epigastrium  and  abdomen,  which  some- 
times form  the  chief  annoyance  of  the  patient,  usually  depend  upon  passive  con- 
gestion of  the  liver  (vide  infra),  or  upon  the  tension  of  the  abdominal  walls  from 
ascites,  oedema,  etc. 

We  must  finally  mention  here  the  rheumatoid  pains  in  the  joints  and  muscles, 
from  which  many  patients  with  heart  disease  suffer. 

The  greatest  subjective  distress  occui's  in  the  last  stages  of  heart  disease,  when 
general  dropsy  develops.  The  patient's  helplessness  usually  culminates.  All 
motions  of  the  body  are  difficult,  the  dyspnoea  and  oppression  in  the  chest  con- 
stantly increase,  until  death  finally  releases  the  patient  from  his  mournful  con- 
dition. 

2.  Sequelae  in  the  Heart  Itself. — We  have  already  discussed  the  most  impor- 
tant sequelse  of  valvular  disease  in  the  heart  itself,  its  hypertrophies  and  dilata- 
tions. It  remains  for  us  to  describe  the  influence  of  the  cardiac  disease  on  the 
frequency  and  regularity  of  the  heart's  action,  and  also  to  discuss  some  secondary 
diseases  of  the  cardiac  muscle  and  of  the  pericardium. 

In  every  well-compensated  heart  disease  the  heart's  action  may  for  a  long  time 
be  of  approximately  normal  frequency  and  regularity.  We  often  find  a  constant 
and  moderate  acceleration  of  the  pulse,  which  is  easily  increased  from  temporary 
causes.  Obviously  this  increase  in  the  number  of  heai't-bcats  is  often  compensa- 
tory. If  the  left  ventricle  receives  during  diastole  less  blood  than  normal — for 
example,  in  stenosis — there  is  such  an  increase  in  the  frequency  of  the  cardiac 
contractions  that  the  same  amount  of  blood  reaches  the  various  organs  in  a  given 
interval  of  time  as  before.  Diminution  of  the  pulse-rate  (bradycardia)  is  ex- 
ceptional in  valvular  heart  disease,  except  when  it  is  artificially  caused  by  large 
doses  of  digitalis.  It  is  most  frequent  in  aortic  stenosis,  and  here  perhaps  it 
has  a  compensatory  effect  (vide  supra).  Marked  changes  in  the  rate  of  the  pulse 
are  due  to  severe  disturbances  of  the  nervous  apparatus  of  the  heart,  and  hence 
they  are  often  associated  with  arhythmia.  Under  such  circumstances,  the  pulse- 
rate  may  be  as  high  as  120-140  beats  per  minute.  A  rare  but  interesting  symptom 
is  the  sudden  onset  of  attacks  of  enormous  rapidity  of  the  pulse,  up  to  160-200 
beats  and  more  (tachycardia).  This  is  especially  connected  with  mitral  lesions. 
In  the  intervals  the  action  of  the  heart  is  quiet,  with  approximately  complete 
compensation  of  the  cardiac  lesion.  The  acceleration  of  the  pulse  occurs  rather 
suddenly,  and  is  usually  associated  with  a  subjective  sensation  of  palpitation  and 


328  DISEASES    OF   THE   CIRCULATORY   ORGANS 

distress.  It  may  last  several  Lours  and  then  vanisli,  -usually  with  the  same  sudden- 
ness. The  exact  cause  of  these  attacks  is  unknown.  They  suggest  a  temporary 
paralysis  of  the  inhibitory  apparatus  of  the  heart.  Very  often  a  well-marked 
acute  dilatation  may  be  demonstrated  by  percussion,  during  the  attack  of  tachy- 
cardia. 

Arhythmia  of  the  heart  is  of  still  greater  importance  than  anomalies  of  the 
pulse-frequency.  It  always  points  to  a  severe  disturbance  of  the  nervous  appa- 
ratus of  the  heart.  The  general  circulatory  disturbance  which  follows  every  valv- 
ular disease  must  of  course  make  itself  felt  in  the  heart  itself,  and  the  nerves  and 
ganglia  of  the  heart  can  not  remain  undisturbed  by  it.  Hence  we  generally  see 
marked  variations  in  the  frequency  and  rhythm  of  the  heart's  action  along  with 
the  other  signs  of  beginning  disturbance  of  compensation;  but  daily  clinical 
experience  teaches  us  that  there  is  not  a  perfect  parallelism  between  the  two  symp- 
toms. We  find  often  enough  in  heart  disease  a  considerable  irregularity  of  the 
pulse  without  any  of  the  other  signs  of  marked  disturbance  of  compensation,  and, 
on  the  other  hand,  we  see  in  many  patients  an  almost  perfect  regularity  of  the 
pulse  up  to  death.  In  mitral  disease,  especially  in  mitral  stenosis,  arhythmia  of 
the  heart  is  much  more  frequent  than  in  aortic  disease. 

We  can  not  enter  here  into  a  complete  discussion  of  the  special  varieties  and 
symptoms  of  arhythmia.  A  distinction  is  made  between  the  irregular  pulse,  in 
which  the  successive  beats  are  separated  by  irregular  intervals,  and  the  unequal 
pulse  in  which  the  sepai-ate  waves  are  of  unequal  height.  In  reality,  both  phe- 
nomena are  often  associated,  for  when  the  pulse  is  more  rapid  the  left  ventricle 

is  imperfectly  filled  during  diastole,  and  the  pulse 
is  consequently  smaller.  The  irregularity  of  the 
cardiac  activity  may  be  extreme  (delirium  cordis) ; 
or  it  may  be  so  modified  as  to  have  a  certain  pe- 
riodic regularity  of  its  own  (allorhythmia).  One 
of  the  most  important  and  frequent  forms  of 
allorhythmia  is  the  pulsus  higeminus  (see  Fig. 
Fig.  42.— Pulsus  bigeminus.  42).     In  this  there  is  first  a  vigorous  systole  and 

then,  before  the  ventricular  diastole  is  completely 
finished,  a  second  weaker  contraction,  followed  by  a  pause.  We  feel  alter- 
nately a  strong  and  quite  weak  pulse.  The  latter  may  be  imperceptible,  so 
that  it  can  be  made  out  only  by  the  sphygmograph.  In  such  cases,  with  co-ex- 
isting tricuspid  insufiiciency,  we  sometimes  find  the  number  of  the  venous  pul- 
sations twice  as  great  as  the  number  of  the  radial  pulsations,  because  the  sec- 
ond weaker  contraction  of  the  heart  produces  a  visible  venous  pulse,  but  not 
an  appreciable  radial  pulse.  It  is  possible  that  in  such  cases  we  may  have 
to  do  with  an  unequal  contraction  of  the  two  halves  of  the  heart,  the  right 
ventricle  contracting  vigorously,  and  the  left  feebly.  If  we  listen  to  the  heart 
when  there  is  a  pulsus  bigeminus  we  hear  four  sounds  in  quick  succession,  the 
first  two  corresponding  to  the  distinct  radial  pulse,  the  next  two  to  the  close- 
following  systole  of  the  heart  which  does  not  give  rise  to  a  distinguishable  pulse. 
Continuous  and  regular  pulsus  bigeminus,  as  depicted  in  the  preceding  figure,  is 
an  infrequent  phenomenon,  but  we  very  often  have  a  few  beats  of  this  character 
at  brief  irregular  intervals.  It  is  certainly  the  most  frequent  cause  of  the  inter- 
mittent ptilse.  The  fingers  on  the  radial  artery  from  time  to  time  fail  to  distin- 
guish any  pulse  whatever,  or  else  they  perceive  it  merely  as  a  short  wave,  closely 
following  the  preceding  pulse ;  but  if  we  listen  to  the  heart  at  the  same  time,  we 
recognize  that  four  audible  heart  sounds  correspond  to  every  intermission  of  the 
pulse.  On  the  whole,  the  pulsus  bigeminus  is  a  bad  sign,  since  it  always  points  to 
a  marked  disturbance  of  the  cardiac  innervation ;  but  it  may  also  pass  away  again 
and  give  place  to  a  regular  action  of  the  heart. 


VALVULAE   DISEASE    OF   THE   HEART  329 

Chronic  valvular  disease  of  the  heart  is  often  combined  with  anatomical 
changes  in  the  cardiac  muscle,  and  sometimes  in  the  pericardium. 

Among  the  changes  in  the  cardiac  muscle,  cloudy  swelling,  and  especially  fatty 
degeneration  of  the  muscular  fibers,  are  the  most  frequent.  The  fatty  degenera- 
tion of  the  muscle  occurs  either  in  a  diffuse  form,  or  in  little  yellowish  spots, 
which  are  plainly  visible  on  the  papillary  muscles  and  trabeculse.  The  opinion 
has  often  been  expressed  that  fatty  degeneration  of  the  muscles  is  the  cause  of 
the  disturbance  of  compensation;  that  the  cardiac  muscle  performs  its  increased 
work  until  fatty  degeneration  ensues  and  reduces  its  strength.  This  theory  does 
not  entirely  correspond  to  the  facts.  We  have  often  seen  the  greatest  disturbance 
of  compensation  in  valvular  disease  when  section  of  the  cardiac  muscle  showed 
no  fatty  degeneration ;  and,  on  the  other  hand,  we  have  seen  great  fatty  degenera- 
tion of  the  heart,  as  in  pernicious  ansemia,  when  there  were  no  signs  of  cardiac 
weakness  during  life.  Anatomically,  with  our  present  aids  to  research,  we  can 
hardly  ever  decide  with  certainty  whether  the  cardiac  muscle  is  still  capable  of 
performing  its  normal  functions  or  not.  The  usual  state  of  the  case  is  probably 
this,  that  fatty  degeneration  of  the  cardiac  muscle  is  a  result  of  the  disturbance 
of  compensation,  and  especially  of  the  deficient  supply  of  arterial  oxygenated 
blood  to  the  muscle  (see  the  chapter  on  ansemia). 

There  is  as  truly  a  passive  congestion  of  the  heart  as  there  is  a  passive  con- 
gestion of  the  liver  and  kidneys.  The  circulatory  disturbance  in  the  heart  itself 
is  the  chief  cause  of  cardiac  insufficiency,  and  the  phenomena  of  disturbed  com- 
pensation. 

A  frequent  affection  of  the  cardiac  muscle  in  valvular  disease  is  the  presence 
of  cicatricial  changes  and  so-called  myocarditic  nodules  in  the  substance  of  the 
heart.  Chronic  endocarditis  may  directly  invade  the  subjacent  parts  of  the  car- 
diac muscles  and  set  up  a  chronic  inflammation  there,  but  the  cardiac  cicatrices 
usually  have  another  origin.  The  connective-tissue  thickening  beneath  the  endo- 
cardium is  the  result  of  a  simple  atrophy  of  the  superficial  muscular  fibers  due  to 
the  increased  internal  pressure  of  the  blood,  as  in  mitral  or  aortic  insufficiency. 
The  connective-tissue  nodules  within  the  cardiac  muscle,  however,  depend  in  part 
upon  a  deficiency  in  the  local  supply  of  arterial  blood.  Simple  sclerotic  thickening 
of  the  coronary  arteries,  or  complete  embolism  or  thrombosis  of  a  small  branch 
of  one  of  them,  is  the  evident  cause  of  these  circumscribed  cicatrices.  On  the 
other  hand,  it  is  also  probable  that  disease  of  the  myocardium  is  associated  with 
the  endocarditis,  and  is  referable  to  the  simultaneous  action  of  the  same  causes, 
such  as  the  infection  of  articular  rheumatism,  diphtheria,  and  syphilis.  On  care- 
ful microscopic  examination  we  find,  in  almost  all  cases  of  valvular  disease,  quite 
extensive  changes  in  the  myocardium  (Krehl),  and  in  many  cases  these  may  cer- 
tainly impair  the  functional  powers  of  the^heart.  Still,  we  often  find  cicatrices 
of  myocarditis  without  any  signs  of  a  previous  disturbance  in  the  compensation 
of  the  heart.    A  fuller  discussion  of  this  subject  will  be  found  in  the  next  chapter. 

Pericarditis  is  not  very  rare  as  a  result  of  chronic  valvular  disease.  It  is 
always  a  dangerous  complication,  and  it  may  cause  death.  Regarding  its  origin, 
we  have  found  that  almost  all  the  cases  of  heart  disease  complicated  with  peri- 
carditis show  changes  in  the  aortic  valves.  Hence  it  does  not  seem  improbable  to 
us  that  the  secondary  pericarditis  in  such  cases  is  sometimes  due  to  a  direct 
invasion  of  the  pericardium,  by  the  excitants  of  inflammation  passing  from  the 
aortic  valves  through  the  walls  of  the  blood-vessel. 

3.  Symptoms  of  Stasis  in  the  Different  Organs  of  the  Body. — As  has  fre- 
quently been  mentioned  in  what  precedes,  the  results  of  stasis  of  the  blood  make 
themselves  manifest  in  heart  disease  in  various  organs.  We  have  already  spoken 
of  the  important  results  of  blood  stasis  in  the  heart  itself  and  the  lungs.  It  re- 
mains for  us  to  discuss  the  symptoms  of  stasis  in  the  systemic  veins. 


330  DISEASES    OF   THE   CIECULATORY   ORGA^Tg 

As  soon  as  the  flow  of  venous  blood  into  tlie  right  side  of  the  heart  is  hindered, 
the  venous  stasis  is  shown  by  the  cyanotic  appearance  of  the  patient.  This 
cyanosis  may  exhibit  any  degree.  In  heart  disease  which  is  still,  on  the  whole, 
well  compensated,  it  is  recognized  only  by  the  practiced  eye  of  the  physician  as 
a  slight  bluish  tinge  of  the  lips,  the  alse  of  the  nose,  the  cheeks,  or  the  nails. 
With  the  increase  of  the  disturbance  of  compensation  the  cyanosis  increases,  if 
it  be  not  modified  by  the  co-existence  of  general  anaemia.  In  mitral  disease, 
especially  in  mitral  stenosis,  the  cyanosis  is  usually  more  marked  than  in  aortic 
disease.  The  large  veins,  also,  become  plainly  visible  as  a  result  of  their  complete 
filling,  especially  the  large  external  jugulars. 

A  further  important  symptom  which  follows  the  venous  stasis  is  the  oedema, 
the  dropsy  of  heart  disease.  As  we  know  from  general  pathology,  every  venous 
stasis,  if  it  reaches  a  certain  grade,  leads  to  a  transudation  of  the  fluid  of  the 
blood  from  the  capillaries.  If  the  lymphatics  can  no  longer  carry  this  transuda- 
tion away,  it  collects  in  the  meshes  of  the  tissues  and  leads  to  cedema.  The 
oedema  of  heart  disease,  therefore,  does  not  appear  until  the  venous  stasis  has 
reached  a  certain  degree,  and  the  compensation  of  the  heart  disease  has  become 
impaired.  It  first  appears  in  those  parts  where  there  is  a  particularly  loose 
tissue,  as  in  the  scrotum,  or  where  mechanical  conditions  favor  its  development. 
The  legs  usually  swell  first,  especially  about  the  ankles,  because  here  the  stasis 
of  the  venous  blood  is  increased  by  gravity.  At  first,  slight  cedema  appears  only 
temporarily  and  by  day,  and  disappears  again  while  the  patient  is  in  bed  at  night ; 
but,  as  the  disturbance  of  compensation  increases,  the  oedema  also  constantly  grows 
worse,  especially  in  the  dependent  parts  of  the  body,  until  finally  it  may  reach  the 
highest  degree  of  dropsy.  Besides  the  cedema  of  the  skin,  transudations  into  the 
internal  cavities  occur,  especially  into  the  abdomen  and  the  pleural  cavity. 

The  relation  between  the  degree  of  cutaneous  oedema  and  the  amount  of  drop- 
sical transudation  is  variable ;  thus,  in  particular,  we  may  have  a  large  amount  of 
ascites,  with  only  moderate  swelling  of  the  legs.  This  is  probably  occasioned  in 
most  cases  by  special  secondary  changes  in  the  liver  {vide  infra) . 

The  patient's  distress  is  decidedly  increased  by  marked  oedema,  as  has  already 
been  said.  All  the  motions  of  the  swollen  extremities  are  considerably  impeded. 
Hydrothorax  and  ascites  increase  the  dyspnoea,  the  former  by  compression  of  the 
lungs,  the  latter  by  upward  pressure  on  the  diaphragm.  The  passage  of  urine  may 
be  rendered  very  difficult  by  oedema  of  the  prepuce.  Besides  that,  we  must  men- 
tion that  the  skin,  when  very  oedematous,  is  quite  apt  to  become  the  seat  of 
furuncular  and  erysipelatous  inflammations. 

The  .results  of  stasis  in  the  internal  organs  may  be  best  seen  in  the  liver, 
spleen,  and  kidneys. 

Passive  congestion  of  the  liver  is  manifested  by  quite  a  considerable  increase 
in  the  size  of  the  organ.  The  lower  boundary  of  the  liver  dullness  extends 
several  fingers'  breadth  beyond  the  edge  of  the  ribs,  and  the  anterior  surface  and 
lower  border  of  the  liver  may  often  be  plainly  felt.  The  liver  may  also  be 
enlarged  in  cases  in  which  there  are  no  other  marked  signs  of  passive  congestion, 
such  as  dropsy.  Quite  severe  pain  in  the  hepatic  region  sometimes  arises  from  the 
tension  of  the  capsule  of  the  liver.  In  later  stages  the  liver  may  grow  smaller 
again  through  a  partial  atrophy  of  the  liver  cells  (atrophic  nutmeg-liver).  In- 
deed, there  may  even  develop,  as  a  result  of  the  chronic  congestion,  a  secondary 
cirrhosis  of  the  liver,  with  a  distinctly  granulated  surface.  These  are  the  cases 
in  which  marked  ascites  is  especially  apt  to  occur  (vide  supra). 

Slight  jaundice  often  develops  in  heart  disease,  as  a  result  of  passive  congestion 
of  the  liver,  or  perhaps  sometimes  from  a  secondary  duodenal  catarrh.  The 
peculiar  mixture  of  a  cyanotic  and  slightly  jaundiced  hue  of  the  skin  is  very  char- 
acteristic in  many  cases,  especially  in  mitral  disease.     It  should  be  added  that 


VALVULAR   DISEASE    OF   THE   HEART  331 

the  yellowish  discoloration  of  the  skin  in  heart  disease  is  probably  not  always 
a  genuine  icterus,  but  it  may  be  occasioned  by  the  deposit  of  other  pigments  in 
the  skin. 

Passive  congestion  of  the  spleen  arises  if  the  stasis  of  the  blood  extends  to 
the  splenic  vein.  The  spleen  increases  in  size  and  becomes  firm  and  dense.  It  is 
often  hard  to  make  out  the  congestion  from  the  increase  of  the  splenic  dullness, 
because  percussion  of  the  spleen  is  uncertain  if  there  be  also  ascites,  hydrothorax, 
etc.  We  can  often,  however,  plainly  feel  the  enlarged  spleen  under  the  edge  of 
the  ribs  on  the  left. 

In  the  kidneys  we  find  .passive  congestion,  with  the  final  development  of 
"  cyanotic  induration."  The  slowness  of  the  circulation  and  the  diminution  of 
the  arterial  tension  in  these  organs  lead  to  marked  changes  in  the  ui'ine.  In 
particular,  there  is  a  diminution  in  the  quantity,  especially  if  the  patient  is  at 
the  same  time  dropsical.  The  amount  of  urine  falls  as  low  as  800-500  cubic  centi- 
metres (27-17  ounces),  or  even  less,  in  twenty-four  hours.  It  becomes  dark,  con- 
centrated, of  high  specific  gravity,  and  abnormally  acid,  and  hence  it  usually  has 
an  abundant  sediment  of  urate  of  sodium.  In  marked  degrees  of  stasis  there  is 
albumen  in  the  urine  as  a  result  of  the  damage  done  to  the  glomerular  epithe- 
lium. The  amount  of  albumen  is  usually  slight,  but  it  may  equal  one  third  or 
one  fourth  of  the  volume  of  urine.  Under  the  microscope  we  find,  in  the  urine 
of  simple  passive  congestion,  only  an  occasional  hyaline  cast,  and  a  few  red  and 
white  blood-corpuscles. 

Careful  examination  of  the  urine  in  cases  of  severe  heart  disease  is  of  the 
greatest  practical  importance,  for  the  character  of  the  urine  as  shown  by  the 
color,  specific  gravity,  and  amount  of  albumen,  is  an  excellent  index  of  the  vigor 
of  the  heart  and  the  condition  of  the  circulation.  Any  change  for  the  worse  in 
the  circulation  is  directly  shown  in  a  diminution  of  the  amount  of  urine,  and  an 
increase  in  its  specific  gravity,  or,  it  may  be,  in  the  appearance  of  albuminuria. 
Any  improvement  in  the  circulation,  whether  spontaneous  or  due  to  remedies,  is 
shown  first  and  clearest  by  an  increase  in  the  daily  excretion  of  urine,  and  a  cor- 
responding diminution  in  its  specific  gravity. 

We  not  infrequently  meet  with  acute  and  chronic  nephritis,  particularly 
arterio-sclerotic  nephritis,  complicating  heart  disease.  It  is  often  no  easy  matter 
clinically  to  form  a  correct  opinion  about  such  cases. 

We  may  in  part  refer  the  numerous  gastric  and  digestive  disturbances,  such 
as  loss  of  appetite,  vomiting,  constipation,  and  diarrhoea,  from  which  such  pa- 
tients often  sufl^er,  to  the  stasis  in  the  blood-vessels  of  the  stomach  and  intestines; 
but  of  course  there  are  not  infrequently  diseases  such  as  acute  and  chronic  catarrh 
of  these  organs,  which  are  to  be  regarded  as  complications. 

4.  Embolic  Processes. — The  slowing  of  the  circulation,  and  the  disturbances  in 
the  nutrition  of  the  walls  of  the  vessels,  which  result  from  it,  often  give  rise  in 
heart  disease  to  the  formation  of  thrombi.  These  are  situated  in  the  heart  itself, 
on  the  diseased  valves,  in  the  recesses  between  the  trabeculse,  in  the  auricles, 
etc.,  or  else  they  form  in  the  veins,  especially  in  those  of  the  lower  extremity. 
From  these  thrombi  fibrinous  plugs  may  easily  be  set  loose  and  enter  the  circu- 
lation, and  thus  give  rise  to  embolic  processes  in  distant  organs.  Some  of  the 
embolisms,  whose  clinical  relations  are  especially  important,  have  been  more  fully 
described  elsewhere,  and  will  be  mentioned  only  briefly  here. 

Embolism  of  the  pulmonary  arteries,  proceeding  from  venous  thrombi  or  from 
thrombi  in  the  right  side  of  the  heart,  gives  rise  to  hasmorrhagic  infarction  of  the 
lungs.  Its  pathogenesis  and  symptoms  have  already  been  discussed  in  a  pre- 
vious section  (see  page  273). 

Embolism  of  the  cerebral  arteries  is  a  common  cause  of  apoplectic  attacks, 
which  are  not  infrequent  in  heart  disease,  and  usually  lead  to  hemiplegia.     The 


332  DISEASES    OF   THE   CIECULATOEY   OKGANS 

anatomical  cause  of  the  hemiplegia  in  these  cases  is  the  embolic  softening  of 
the  brain  which  ensues.  The  details  of  this  are  given  in  the  section  on  cerebral 
diseases  (see  page  1103). 

Embolism  of  the  larger  arteries  of  the  extremities,  such  as  the  femoral  and  the 
brachial,  is  much  rarer  than  the  forms  mentioned.  It  leads  to  embolic  gangrene 
of  the  extremities,  unless  an  adequate  collateral  circulation  can  be  established. 
The  skin  of  the  peripheral  parts,  the  fingers  or  toes,  first  becomes  cool,  bluish, 
and  at  last,  if  the  circulation  be  wholly  checked,  almost  black.  The  gangrene 
advances  slowly,  usually  occupying  weeks.  Ulcerations  develop  as  the  necrotic 
portions  are  thrown  off.  The  affection  is  extremely  painful.  The  patient  soon 
becomes  very  miserable  from  the  pain  and  the  septic  fever  that  usually  attend 
the  ulcerations,  and  extensive  gangrene  almost  always  ends  fatally.  Sometimes 
there  is  embolism  of  the  abdominal  aorta.  This  is  usually  located  at  its  bifurca- 
tion, and  occasions  a  sudden  and  almost  complete  paraplegia,  speedy  disturbance 
of  sensation,  abolition  of  the  reflexes,  and  loss  of  electrical  excitability.  No  pulse 
can  be  felt  in  the  peripheral  arteries;  the  feet  are  pale  and  cold,  and  soon  there 
are  signs  of  gangrene  in  both  legs.     The  condition  is  probably  invariably  fatal. 

Embolism  of  the  renal  arteries,  with  consequent  anaemic  or  haemorrhagic  in- 
farctions in  the  kidneys,  may  have  no  clinical  symptoms  at  all,  but  it  is  sometimes 
indicated  by  sudden  pains  in  the  region  of  the  kidneys  and  marked  hsematuria 
(see  page  644). 

Embolic  infarction  of  the  spleen  is  often  marked  by  swelling  of  the  spleen 
and  by  severe  perisplenitic  pains.    In  other  eases  it  is  wholly  without  symptoms. 

Embolism  of  a  mesenteric  artery  is  a  very  rare  event.  Its  symptoms  consist  of 
a  sudden  intestinal  haemorrhage,  of  severe  colicky  pains,  general  collapse,  and 
peritonitis. 

5.  Complications  on  the  Part  of  the  Nervous  System. — The  most  important 
complication  on  the  part  of  the  nervous  system — embolic  softening  of  the  brain — 
has  already  been  mentioned.  We  must  also  state  that  cerebral  haemorrhage  may 
occur  in  heart  disease.  It  is  especially  frequent  in  aortic  insufficiency,  either 
as  a  result  of  co-existing  atheroma  of  the  cerebral  arteries,  or  perhaps  of  the  ab- 
normally high  tension  of  the  vessels  during  systole. 

Mental  disorders  have  been  repeatedly  observed  in  chronic  valvular  disease. 
They  are  the  result  of  the  disturbance  of  the  circulation,  and  the  consequent  im- 
pairment of  nutrition  in  the  brain.  Hence  they  usually  make  their  first  appear- 
ance in  the  last  stages  of  heart  disease,  at  the  same  time  with  the  other  disturb- 
ances of  compensation.  The  psychoses  in  heart  disease  most  frequently  have  the 
character  of  melancholia,  but  conditions  of  confusional  insanity  and  excitement 
also  occur. 

6.  Secondary  Affections  of  the  Joints  are  not  rare  in  heart  disease.  As  acute 
endocarditis  develops  in  the  course  of  acute  articular  rheumatism,  so,  on  the  other 
hand,  rheiimatic  pains  in  the  muscles  and  joints,  and  even  acute  swelling  of  the 
joints,  associated  with  fever,  appear  in  the  course  of  chronic  heart  disease.  Some- 
times we  have  the  complete  picture  of  acute  articular  rheumatism.  Probably  no 
fresh  infection  from  without  is  requisite  for  the  development  of  these  second- 
ary lesions  in  the  joints,  but  under  certain  circumstances  there  is  an  unusual 
development  of  infectious  germs  (staphylococci?)  on  the  diseased  valves,  and 
large  numbers  of  them  passing  into  the  circulation  occasion  a  fresh  constitutional 
infection. 

Y.  Constitutional  Symptoms.  Fever. — In  congenital  and  early  acquired  val- 
vular disease,  the  general  development  of  the  child  is  ordinarily  much  retarded. 
In  heart  disease  in  adults,  however,  we  by  no  means  always  see  an  injurious  influ- 
ence on  the  general  nutrition.  In  many  patients  we  even  find  a  remarkably  good 
development  of  fat.     A  marked  general  disturbance  of  nutrition,  such  as  great 


VALVULAR   DISEASE    OF   THE   HEART  333 

ansemia  and  general  emaciation,  often  develops  in  the  later  stages,  especially  in 
aortic  insufficiency.     The  wasting  is  of  course  often  hidden  by  the  oedema. 

In  general,  chronic  heart  disease  runs  its  course  without  fever,  but  periods 
often  occur  in  the  course  of  the  disease  when  there  is  a  moderate  and  usually 
irregular  fever.  Marked  disturbances  of  the  general  condition  may  or  may  not  be 
associated  with  it.  The  basis  of  the  fever  is  probably  an  acute  exacerbation  of 
the  endocarditis,  except,  of  course,  in  accidental  complications.  All  variations 
occur,  from  a  mild  febrile  movement  without  further  symptoms  to  a  severe  acute 
recurring  endocarditis  (q.  v.).  In  other  cases  the  fever  is  connected  with  second- 
ary swelling  of  the  joints,  or  with  embolic  processes. 

General  Course  and  Prognosis  of  Valvular  Disease  of  the  Heart 

The  course  of  valvular  disease  of  the  heart  is  in  most  cases  very  chronic.  It 
may  last  for  years.  So  long  as  there  is  a  complete  compensation,  the  patient  feels 
almost  perfectly  well;  sometimes  he  even  has  no  misgivings  as  to  his  trouble. 
The  slight  difficulty  in  respiration  and  the  incapacity  for  physical  exertion  are 
noticed,  but  little  attention  is  paid  to  them,  because  the  patient  is  used  to  them. 
In  other  cases  there  is  a  moderate  disturbance  for  a  long  time,  but  it  may  be  borne 
quite  easily  if  the  patient  is  rational  and  prudent  in  his  conduct. 

We  can  not  make  any  general  statement  as  to  the  length  of  the  stage  of  com- 
pensation, because  cases  differ  very  greatly  in  this  resjject.  It  depends  in  part 
upon  the  intensity  of  the  heart  disease,  in  part  upon  the  external  conditions 
under  which  the  patient  lives,  and  in  part,  certainly,  upon  the  different  indi- 
vidual capacity  for  work  and  power  of  resistance  of  the  heart.  Thus  it  happens 
that  many  cases  last  for  decades,  while  in  others  severe  sequelae  appear  within  a 
few  months.  External  injurious  agencies,  acting  on  the  patient,  are  of  great 
influence  on  the  course  of  heart  disease.  Severe  physical  exertion,  an  injudicious 
manner  of  living,  intercurrent  febrile  disease,  mental  distux'bances,  care,  and 
anxiety  are  often  followed  by  unhappy  consequences. 

If  the  first  signs  of  disturbed  compensation  appear,  if  severe  dyspnoea,  slight 
cedema  of  the  ankles,  etc.,  develop  for  the  first  time,  these  symptoms  may  disap- 
pear again  completely  under  proper  treatment.  Severe  disturbances  of  compen- 
sation even,  great  general  dropsy,  associated  with  very  weak  and  irregular  action 
of  the  heart,  may  abate,  after  a  few  weeks'  duration,  and  the  patient  may  feel 
quite  well  again.  Exacerbations  of  the  disease  may  come  on  several  times  and 
as  often  improve.  Finally,  of  course,  the  improvement  is  incomplete.  Persistent 
oedema  and  the  other  results  of  venous  stasis  ensue,  the  symptoms  constantly 
increase  in  severity,  especially  the  dyspnoea,  until  the  patient  dies  after  a  long 
and  distressing  illness.  Immediately  before  death  in  heart  disease,  certain  irregu- 
larities in  the  innervation  of  the  heart  and  in  the  respiration  sometimes  develop. 
Among  these  the  so-called  Cheyne-Stokes  phenomenon  deserves  especial  mention. 
It  consists  in  a  peculiar  periodical  variation  in  the  respiratory  movements.  There 
will  be,  first,  a  complete  pause  in  the  respiration  (apnoea),  and  this  will  be  suc- 
ceeded by  feeble  breathing  gradually  becoming  stronger,  then  gradually  abating, 
and  finally  ending  in  another  complete  cessation  of  the  respiration.  The  patient 
usually  becomes  more  comatose  during  the  cessation  of  respiration;  his  pupils 
contract.  During  the  hard  breathing  the  patient  recovers  somewhat,  and  his 
pupils  dilate  again.  The  chief  cause  of  this  rhythmical  breathing  is  probably  to 
be  sought  in  the  decided  lowering  of  the  excitability  of  the  respiratory  center. 
During  the  apnoea  a  considerable  amount  of  carbonic  acid  collects  in  the  blood 
before  the  respiratory  center  is  sufficiently  stimulated  to  resume  its  activity. 

We  have  seen  the  heart  behave  in  a  precisely  analogous  manner,  but  independ- 
ently of  any  Cheyne-Stokes  respiration.  There  was  a  series  of  rapid  but  regular 
pulsations,  alternating  with  a  series  of  slower  contractions. 


334  DISEASES    OE   THE   CIRCULATOEY   OEGANS 

In  regard  to  the  particular  forms  of  valvular  disease,  aortic  insufficiency  gener- 
ally gives  the  best  prognosis,  inasmuch  as  it  may  be  very  perfectly  compensated 
for  many  years,  but  if  severe  disturbance  of  compensation  once  occurs  in  this  form 
of  heart  disease,  it  gives  a  very  unfavorable  prognosis,  since,  as  a  rule,  we  can  not 
reinvigorate  the  heart.  Mitral  insufficiency  is  also  quite  a  favorable  form  of 
heart  disease,  which  may  be  compensated  for  a  long  time.  Mitral  stenosis  is  de- 
cidedly inore  unfavorable  in  its  prognosis,  and  is  associated  with  more  disturb- 
ance ;  but  in  all  mitral  diseases  very  severe  conditions  may  improve  once  or  even 
repeatedly.  Aortic  stenosis  is  also  capable  of  quite  good  compensation,  and  in  this 
respect  it  is  even  more  favorable  for  the  patient  than  mitral  stenosis,  but  it  often 
causes  persistent  cerebral  symptoms,  such  as  headache  and  vertigo,  depending  on 
anaemia  of  the  brain,  or  very  likely  upon  simultaneous  changes  in  its  blood-vessels. 

Whether  established  valvular  disease  of  the  heart  is  curable  is  a  question  which 
can  not  be  answered  unconditionally  in  the  negative.  Of  course  in  the  great 
majority  of  cases  it  is  in  itself  incurable;  only  its  sequelae  can  be  prevented  or 
removed  to  a  certain  degree.  In  children  and  young  people,  however,  cases  some- 
times do  occur,  as  we  ourselves  have  seen,  in  which  there  are  all  the  signs  of  a 
pronounced  heart  disease,  but  after  a  long  time  recovery  is  complete.  Of  course 
it  is  very  hard  to  decide  whether  we  really  have  to  do  with  a  valvular  disease  that 
has  been  cured,  because  simple  dilatation  of  the  heart,  relative  insufficiency  of 
the  valves,  anaemic  cardiac  murmurs,  etc.,  may  easily  be  confounded  with  pure 
valvular  disease  of  the  heart. 

Among  the  dangerous  intercurrent  accidents  in  valvular  disease  we  must  make 
especial  mention  of  embolic  processes,  which  may  occur  suddenly  and  without 
warning.  The  different  forms  of  embolism  have  been  mentioned  above,  and  also 
the  possibility  of  cerebral  haemorrhage  in  heart  disease.  Intercurrent  acute  dis- 
eases, such  as  typhoid  and  pneumonia,  often,  but  not  invariably,  take  a  very 
severe  and  dangerous  course  in  patients  with  heart  disease,  because  they  make 
increased  demands  upon  the  heart. 

Treatment  of  Valvular  Heart  Disease 

1.  Prophylaxis. — Our  means  for  preventing  the  development  of  heart  disease 
are  very  limited.  To  avert  endocarditis  in  articular  rheumatism  by  the  present 
method  of  treating  acute  rheumatism  with  salicylic  acid  is  impossible.  The  proba- 
bility of  the  onset  of  endocarditis  may  be  lessened  only  so  far  as  the  whole  dura- 
tion of  the  disease  is  often  considerably  shortened  by  salicylic  acid. 

We  can  also  do  little  in  the  way  of  prophylaxis  against  the  development  of 
heart  disease  that  is  chronic  from  the  start,  since  the  cause  of  the  disease  is  in 
many  cases  wholly  unknown  to  us.  Those  injurious  influences  deserve  the  most 
attention  which  may  favor  the  development  of  arterial  atheroma  and  its  conse- 
quent chronic  valvular  disease.  The  chief  factors  in  this  connection  are  exces- 
sive physical  exertion  and  high  living,  including  the  use  of  too  much  alcohol 
and  tobacco;  but  the  role  which  these  play  in  the  development  of  genuine  val- 
vular disease  is  certainly  much  less  important  than  their  influence  upon  certain 
myopathic  and  nervous  diseases  of  the  heart  (see  the  following  chapter). 

[There  is  evidence  that  the  alkaline  treatment  of  acute  rheumatism  lessens  the 
danger  of  cardiac  complications  (see  page  686).] 

2.  Treatment  of  Compensated  Heart  Disease. — If  we  have  to  treat  a  heart 
disease  which  already  exists,  but  which  is  at  the  same  time  fully  compensated,  our 
treatment  must  be  chiefly  hygienic.  The  patient  must  be  made  aware  of  his  heart 
disease  without  making  him  needlessly  anxious.  He  must  be  told  that  his  further 
good  health  depends  in  great  part  upon  his  own  conduct,  his  discretion,  and  his 
perseverance.  The  patient  must  avoid  everything  which  makes  great  demands 
upon  the  heart,  or  which  may  have  a  directly  injurious  influence  on  it.     All 


VALVULAR  DISEASE    OF   THE   HEART  335 

violent  bodily  exertion,  too  intense  mental  work,  and  also  all  excesses  in  eating, 
drinking,  smoking,  etc.,  must  be  avoided.  That  the  physician's  directions  will 
often  collide  with  the  demands  of.  the  patient's  occupation,  as  well  as  with  his 
favorite  amusements  and  his  habits,  should  not  deter  the  physician  from  demand- 
ing the  fulfillment  of  his  prescriptions,  at  least  so  far  as  possible. 

Treatment  by  drugs  is  usually  unnecessary  in  compensated  heart  disease.  We 
do  not  know  a  remedy  which  has  a  directly  favorable  action  on  heart  disease. 
The  protracted  use  of  iodide  of  potassium,  Fowler's  solution,  arsenite  of  antimony 
("granules  of  antimony"),  etc.,  has  been  recommended.  The  efficacy  of  these 
remedies  is  very  questionable.  We  can  always  try  them,  if  a  mild  disturbance 
makes  a  prescription  desirable  and  other  remedies  are  not  especially  indicated. 
Beyond  this,  the  physician  is  usually  contented  with  an  endeavor  to  improve 
the  appetite  and  nutrition  of  the  patient  by  means  of  iron,  quinine,  and  bitters. 
If  there  is  a  suspicion  that  the  heart  disease  may  be  due  to  syphilis,  a  trial  of 
iodide  of  potash  may  be  made,  but  a  brilliant  result  from  the  employment  of  anti- 
syphilitic  measures  is  hardly  to  be  expected,  because  the  mechanical  imperfections 
of  the  valves,  leading  to  regurgitation  and  stenosis,  can  scarcely  be  remedied. 

The  employment  of  baths  in  heart  disease  deserves  special  consideration.  ISTu- 
nierous  experiences  go  to  prove  that  they  are  not  only  well  borne  by  patients 
with  heart .  disease,  but  that  they  exercise  a  peculiarly  beneficial  and  invig- 
orating influence  upon  the  action  of  the  heart.  In  this  regard,  the  greatest 
reputation  is  possessed  by  the  warm  mud  baths,  which  are  rich  in  carbonic  diox- 
ide, particularly  those  at  Nauheim.  Even  where  there  is  incipient  failure  of 
compensation,  there  will  be  marked  improvement  upon  the  use  of  these  or  similar 
baths  (e.  g.,  Kissingen).  Patients  may  also  employ  at  home  either  simple,  or,  still 
better,  salt  baths,  at  a  temperature  of  88°-90°  (25°-26°  R.).  Where  there  is  no 
marked  disturbance  of  compensation,  the  methodical  employment  of  gymnastic 
exercises,  the  so-called  Swedish  movements,  has  a  certain  value  in  the  treatment  of 
heart  disease.  Regular  muscular  movements  certainly  promote  the  circulation  of 
the  blood,  and  thus  lighten  the  task  of  the  heart.  If  they  are  carried  out  cau- 
tiously and  with  a  proper  consideration  of  the  individual  case,  they  are  not  infre- 
quently beneficial.  The  best  measure  for  the  amount  of  bodily  exercise  for  pa- 
tients with  heart  disease  seems,  to  the  author,  to  be  the  subjective  sensation  of 
dyspnoea.  Any  patient  who  has  no  special  signs  of  failing  compensation  may 
walk  at  a  slow  pace  until  he  experiences  distinct  dyspnoea.  As  soon  as  this  hap- 
pens he  must  stand  still  and  rest.  The  author  regards  it  as  a  great  mistake  to 
encourage  patients  to  persist  in  their  efforts  regardless  of  difficulty  in  breathing. 
We  should  not  forget  that  any  disturbance  of  the  circulation  which  occurs  must 
involve  the  myocardium  itself  in  its  influence.  That  a  change  of  climate  may 
prove  beneficial  is  self-evident.  It  is  particularly  appropriate  that  patients  with 
a  tendency  to  bronchitis  or  rheumatism  should  spend  the  winter  South. 

3.  Treaiment  of  Ruptured  Compensation. — As  soon  as  the  compensatory 
activity  of  the  heart,  in  a  case  of  valvular  trouble,  begins  to  be  impaired,  as  soon 
as  there  is  marked  dyspnoea,  diminution  in  the  excretion  of  urine,  and  oedema,  we 
must  promptly  lighten  the  burden  of  the  heart  by  complete  bodily  rest.  Many 
cases,  particularly  of  mitral  disease,  are  completely  restored,  even  when  there  are 
marked  symptoms  of  cardiac  embarrassment,  by  mere  rest  in  bed  with  simple  diet 
and  without  any  other  therapeutic  measures;  but  if  the  disturbance  of  com- 
pensation is  more  marked  and  persistent,  the  physician  must  have  recourse  to 
digitalis,  a  remedy  which  possesses  undoubted  value  when  the  powers  of  the  heart 
are  impaired.  Digitalis  has  the  properties  of  making  the  separate  beats  more 
powerful,  of  lowering  the  pulse-rate  by  lengthening  the  diastole,  and  above  all  of 
heightening  the  arterial  tension.  Digitalis  is  thei'efore  indicated  in  every  case 
of  heart  disease  when  there  is  persistent  disturbance  of  compensation,  and  if  the 


336  DISEASES    OF   THE   CIECULATOKT   OKGANS 

pulse  is  small,  of  low  tension,  and,  above  all,  frequent  and  irregular;  tlie  desired 
effect  of  digitalis  is  to  make  the  pulse  slower,  more  regular,  and  especially  of 
higher  tension.  Under  the  influence  of  the  increase  in  tension  thus  produced 
and  of  the  acceleration  of  the  circulation,  the  disturbances  of  compensation  often 
disappear  in  a  surprising  fashion;  there  is  more  abundant  diuresis,  the  scanty, 
dark,  concentrated  urine  of  passive  congestion  disappears,  the  daily  amount  of 
urine  increases,  and  the  urine  therefore  becomes  clear  and  of  lower  specific  grav- 
ity. The  oedema  then  disappears,  the  dyspnoea  ceases,  the  head  becomes  free,  the 
general  condition  improves,  and,  in  brief,  there  may  again  ensue  a  complete  com- 
pensation of  the  heart  disease.  This  change  is  sometimes  accomplished  in  a  com- 
paratively short  time,  in  a  few  days  or  weeks. 

It  is  very  important  to  prescribe  digitalis  in  a  correct  manner  in  order  for  it 
to  be  efficient.  Much  experience  has  shown  that  it  is  best  to  give  it  at  regular 
intervals  of  two  hours,  in  doses  of  one  grain  and  a  half  (gramme  0.1)  of  the 
powdered  leaves,  either  in  capsules  or  simply  in  water ;  so  that  the  patient  receives 
in  the  course  of  a  day  some  five  or  six  powders — that  is,  eight  or  ten  grains 
(gramme  0.5-0.6)  of  digitalis.  If  the  remedy  is  well  borne  we  may  continue  it  in 
this  manner,  but  usually  it  is  omitted  during  the  night,  to  be  resumed  in  the  same 
way  on  the  next  day.  As  a  rule,  the  distinct  specific  influence  of  digitalis  is 
evident  after  the  employment  of  ten  to  fifteen  powders  in  the  course  of  two  or 
three  days.  This  is  recognized  by  the  marked  diminution  in  pulse-rate,  the  in- 
creasing strength  and  regularity  of  the  pulse,  and  the  improvement  in  the  general 
symptoms.  Instead  of  the  powder  we  may  employ  an  infusion  of  the  strength  of 
1  or  2  parts  to  150  of  water.  Of  this  a  tablespoonful  must  be  given  regularly 
every  one  or  two  hours.  In  some  cases,  particularly  if  the  patient  has  already 
become  accustomed  to  the  remedy,  we  may  prescribe  still  larger  doses,  up  to  thirty 
or  forty-five  grains  (grammes  2-3)  and  even  more,  daily.  But  in  every  case 
digitalis  should  be  given  in  regularly  repeated  doses,  so  as  to  obtain  by  their  com- 
bined action  the  full  effect  of  the  drug.  It  is  entirely  useless  to  prescribe  digitalis 
in  small  doses  at  long  intervals.  The  remedy  must  never  be  prescribed  unless 
we  can  accurately  watch  the  pulse  and  the  heart's  action,  for  only  thus  can  we 
obtain  clear  indications  as  to  the  further  employment  or  the  omission  of  the  drug. 

Often  some  unpleasant  incidental  effects  appear  simultaneously  with  the  bene- 
ficial influence  upon  the  heart's  action.  Among  these  are  nausea,  vomiting,  and 
specks  before  the  eyes.  If  the  digitalis  is  omitted  these  symptoms  usually  cease, 
while  the  beneficial  effect  upon  the  heart  may  last  for  a  long  time.  "With  regard 
to  these  incidental  and  disagreeable  symptoms,  different  patients  vary  greatly. 
Many  bear  digitalis  very  well,  others  very  ill.  From  a  therapeutic  point  of  view 
it  is  particularly  embarrassing  if  the  nausea,  vomiting,  and  other  disagreeable 
symptoms  appear  before  the  digitalis  has  produced  an  effect  upon  the  heart ;  but 
in  such  eases  we  should  not  be  too  hasty  in  abandoning  the  drug,  especially  if 
it  is  urgently  indicated.  If  the  patient  can  not  bear  the  infusion  we  should 
administer  the  digitalis  in  powders,  or  vice  versa.  If  the  drug  absolutely  can  not 
be  given  by  the  mouth,  it  should  be  injected  into  the  rectum  in  the  form  of  an 
infusion  of  the  strength  of  1  or  2  parts  to  100  of  water.  This  should  be  warmed 
to  the  temperature  of  the  body  and  given,  after  a  cleansing  enema  has  been  em- 
ployed, once  or  twice  a  day.  The  subcutaneous  employment  of  digitalis  has  also 
been  recommended,  in  the  form  of  an.  infusion  of  the  strength  of  3  parts  to  100,  of 
which  two  or  three  syringefuls  may  be  injected  daily  (lU  25-40),  but  with  this  we 
have  had  no  personal  experience.  Sometimes,  especially  if  the  patient  has  not 
been  carefully  watched,  the  cumulative  effect  of  digitalis  is  shown  in  severe  symp- 
toms of  poisoning,  such  as  collapse,  very  frequent  pulse,  disturbance  of  vision,  and 
dilated  pupils.  Then  such  stimulants  must  be  employed  as  camphor,  ether,  wine, 
and  strong  black  coffee.    How  often  digitalis  is  to  be  used  in  the  case  of  heart 


VALVULAE   DISEASE    OF   THE   HEAET  337 

disease  can  be  determined  by  experience  alone.  Many  patients,  particularly  cases 
of  mitral  disease,  may  undergo  treatment  with  digitalis  twenty  to  thirty  times 
or  more,  with  the  best  results.  Eve-ry  time  that  signs  of  impaired  compensation 
return,  we  must  try  digitalis  again.  It  must  be  confessed  that  it  will  often  be 
necessary  gradually  to  increase  the  dose.  As  is  the  case  with  so  many  other  rem- 
edies, the  patient  becomes  habituated  to  the  drug.  There  is  no  maximum  dose, 
and  we  must  find  out  by  experience  in  each  case  what  the  satisfactory  amount  may 
be.  Some  patients  become  at  last  genuine  "  digitalis  eaters,"  and  are  unable  to 
exist  without  large  doses  of  digitalis.  We  have  ourselves  seen  a  patient  take 
seventy-five  grains  (grammes  5)  of  the  powder  daily.  In  very  many  cases,  how- 
ever, the  beneficial  effect  of  digitalis  even  in  the  larger  doses  fails  at  last  to 
appear.  The  remedy  is  no  longer  borne  and  it  must  be  abandoned.  This  usually 
marks  the  last  stage  of  the  disease. 

JSTot  infrequently  we  see  patients  with  distinct  symptoms  of  passive  conges- 
tion, in  whom  the  character  of  the  pulse  seems  at  first  to  contraindicate  the 
administration  of  digitalis :  the  pulse  is  perhaps  frequent,  but  regular  and  strong ; 
in  other  cases  it  is  not  rapid  at  all,  but  yet  somewhat  irregular;  or  it  may  be 
even  infrequent  and  regular.  Particularly  in  cases  of  aortic  insufficiency  is  it 
often  very  difficult  to  determine  whether  we  should  give  digitalis  or  not.  With 
all  patients  of  this  sort  it  is,  in  general,  worth  while  to  make  a  proper  trial  of 
digitalis,  since  it  may  often  be  beneficial,  and  yet  we  should  exercise  especial 
caution  and  vigilance  with  regard  to  its  effects. 

The  attempt  to  employ  the  active  ingredients  of  digitalis  in  a  pure  form 
(viz.,  digitaline,  digitaleine,  and  digitoxine)  instead  of  the  drug  itself,  have  not 
yet  proved  very  successful.  We  should  admit  that  we  ourselves,  in  common  with 
other  observers,  have  seen  good  results  follow  the  use  of  digitoxine.  This  has  been 
introduced  quite  recently,  and  is  to  be  given  in  tablets  containing  j^-q  of  a  grain 
(one  quarter  of  a  milligramme)  every  one  or  two  hours.  It  has  no  special  advan- 
tages over  digitalis,  but  certainly  deserves  to  be  recommended  as  a  substitute  for 
digitalis  when  that  drug  is  ill  borne  or  ineffectual.  Tincture  of  digitalis,  vinegar 
of  digitalis,  and  other  preparations  are  far  less  efficient  than  digitalis  leaves,  and, 
in  our  opinion,  may  be  disregarded.  The  best  opportunity  for  their  employment 
is  when  patients  with  slight  disturbance  of  compensation  need  to  take  small 
amounts  of  digitalis  persistently. 

[Digitalis  is  used  more  commonly  in  this  country  in  the  form  of  the  tincture. 
The  urine  affords  a  good  guide  as  to  the  safety  of  the  continuance  of  the  drug ;  as 
long  as  the  renal  secretion  is  sufficient  in  quantity,  and  increasing  rather  than 
diminishing,  th,ere  is  no  danger  of  the  toxic  effects.  It  is,  consequently,  a  good 
plan  to  follow  carefully  the  twenty-four-hour  quantity  of  urine  when  this  can 
be  done. 

There  are  cases  in  which  digitalis  must  be  taken  for  long  periods,  but  it  should 
then  be  given  only  twice  a  day,  with  twelve  hours'  interval  between  the  doses, 
unless  the  patient  has  ready  access  to  his  physician;  there  is  then  less  risk  of 
toxic  symptoms. 

In  mitral  cases,  with  or  without  secondary  tricuspid  regurgitation,  where  the 
cyanosis  and  other  symptoms  show  that  the  right  heart  is  engorged  with  blood 
which  it  can  not  propel  onward,  the  relief  afforded  by  venesection,  or  by  a  dozen 
leeches  in  the  hepatic  region,  may  be  very  great.  Until  the  veins  are  relieved 
either  in  this  way  or  by  free  purgation,'  digitalis  and  stimulants  iire  useless,  and  a 
resort  to  them  results  merely  in  a  loss  of  time,  and  perhaps  in  the  loss  of  a  life 
which  might  be  saved.] 

Caffeine  deserves  the  first  mention  among  the  substances  having  a  similar 
action,  which  have  of  late  been  recommended  as  substitutes  for  digitalis  by  Le- 
pine,  Riegel,  and  others.  Given  in  repeated  small  doses,  a  total  of  fifteen  to 
22 


338  DISEASES    OF   THE    CIECULATOKY   OEGAl!TS 

twenty  grains  a  day  (gramme  1.0  to  1.  5),  it  often  slows,  regulates,  and  strength- 
ens the  activity  of  the  heart,  and  also  increases  the  arterial  pressure.  The  salicy- 
late of  caffeine  and  sodium  is  chiefly  used,  three  to  five  grains  (gramme  0.2  to  0.3) 
of  the  powder,  and  also  the  benzocitrate  of  caffeine  in  the  same  or  smaller  doses. 
The  latter  is  also  given  subcutaneously.  Besides  caffeine,  we  may  also  mention 
here  adonis  vernalis,  convallaria  majalis,  and  sulphate  of  sparteine;  but  none  of 
these  drugs  is  as  reliable  as  digitalis. 

On  the  other  hand,  in  cases  of  simple  acute  or  chronic  weakness  of  the  heart, 
the  tincture  of  strophanthus  sometimes  proves  decidedly  beneficial.  It  is  given 
in  doses  of  ten  drops  several  times  a  day.  In  many  cases  it  is  an  excellent  way 
to  combine  digitalis  with  some  of  the  drugs  already  named,  or  with  others,  par- 
ticularly diuretics.  Thus,  for  example,  we  may  often  with  advantage  add  one  or 
two  parts  of  the  tincture  of  strophanthus  to  the  infusion  of  digitalis,  or  we  may 
prescribe  powders  containing  a  grain  and  a  half  (gramme  0.1)  of  digitalis  and  of 
diuretine  fifteen  grains  (gramme  1.0)  in  each  dose,  or  digitalis  and  calomel  (vide 
infra) ;  or  digitalis  and  caffeine.  A  combination  of  this  sort  which  is  often  very 
efficient  is  the  following:  Infusion  of  digitalis,  30  grains  to  5  ounces  of  water 
(grammes  2  to  grammes  150) ;  sodio-salicylate  of  caffeine,  30  grains  (grammes 
2) ;  tincture  of  strophanthus,  1  drachm  (grammes  4)  ;  liquor  potassii  acetatis,  2 
ounces  (grammes  60);  syrupi  aurantii,  1  ounce  (grammes  30).  M.  S.  A  table- 
spoonful  every  two  hours. 

4.  Symptomatic  Treatment. — Some  symptoms  which  often  occur  in  heart  dis- 
ease demand  a  special  description. 

Dropsy  is  a  symptom  of  venous  stasis,  and  disappears  if  compensation  be 
restored  spontaneously  or  by  the  use  of  digitalis.  Complete  rest  in  bed  and  eleva- 
tion of  the  swollen  parts  serve  as  the  chief  aid  in  removing  the  dropsy.  Dropsical 
patients  ought  also  to  change  their  position  in  bed  frequently,  if  possible,  that 
there  m'ay  not  be  too  much  oedema  collected  in  the  dependent  portions  of  the  body. 
It  is  a  good  plan  to  wrap  up  the  swollen  arms  and  legs  with  flannel  bandages  under 
gentle  pressure.  Mild  massage  of  the  oedematous  parts  may  sometimes  be  of 
advantage.  The  amount  of  liquid  ingested  is  to  be  limited,  if  possible.  Of  in- 
ternal remedies,  besides  digitalis,  which  should  invariably  be  first  employed,  and 
drugs  of  similar  action,  the  true  diuretics  are  to  be  considered,  such  as  acetate  of 
potassium,  acetate  of  sodium,  and  diuretine.  They  are  sometimes  ordered  in 
combination  with  digitalis  and  sometimes  alone,  particularly  when  digitalis  can 
not  be  borne  or  it  is  not  indicated.  Calomel  is  sometimes  especially  efficient  in 
cardiac  dropsy.  Its  diuretic  influence  has  lately  been  emphasized  by  Jendrassik 
and  others.  It  is  prescribed  in  powders  of  three  grains  (0.2  gramme)  three  to  flve 
times  a  day.  Often  a  very  marked  diuresis  will  be  caused  after  one  or  two  days, 
with  rapid  abatement  of  the  dropsy.  The  administration  of  the  remedy  is  stopped 
as  soon  as  the  diuresis  begins.    It  is  also  omitted  if  stomatitis  develops. 

We  have  already  mentioned  the  advantageous  combination  of  calomel  wifh 
digitalis  (digitalis,  one  grain  and  a  half,  gramme  0.1;  calomel,  three  grains, 
gramme  0.2),  five  such  powders  daily. 

In  the  last  stages  of  heart  disease  the  patient's  condition  may  be  particularly 
distressing  from  the  severe  general  oedema.  It  is  then  justifiable  to  remove  the 
ascites  or  hydrothorax  by  puncture,  or  to  let  the  oedema  drain  out  by  scarifica- 
tion of  the  skin — long  incisions  into  the  subcutaneous  cellular  tissue— in  order 
to  procure  relief  for  the  patient.  The  scarification  of  the  skin,  however,  is  dan- 
gerous, and  is  not  to  be  employed  without  urgent  indications,  because  erysipel- 
atous inflammation,  etc.,  is  apt  to  ensue  at  the  point  of  incision.  We  can  recom- 
mend little  silver  capillary  trocars  (the  so-called  Southey's  trocars),  to  which  a 
thin  rubber  tube  is  attached.  By  the  aid  of  these  trocars  we  can  drain  off  large 
amounts  of  serum.    We  must  always  use  great  cleanliness,  however,  and  the  utmost 


VALVULAE  DISEASE   OE   THE   HEAKT  339 

disinfection  of  the  skin,  wrapping  the  parts  in  sterilized  gauze.  In  patients  with 
heart  disease  it  is  not,  as  a  rule,  advisable  to  attack  the  dropsy  by  sweating,  by  hot 
packs,  or  pilocarpine. 

The  dyspnoea  of  heart  disease  is  usually  the  most  distressing  symptom  of  all. 
Here,  too,  our  chief  task  is  of  course  to  restore  the  compensation;  but  this  failing, 
we  must  try  to  relieve  the  dyspnoea  symptomatically.  Morphine  is  most  efficient 
in  this  respect.  In  general,  morphine  is,  next  to  digitalis,  the  most  indispensable 
remedy  in  the  treatment  of  severe  heart  disease.  It  is  usually  well  borne,  and 
procures  great  relief,  especially  if  given  subcutaneously.  If  we  have  to  do  with 
the  last  stage  of  the  disease,  we  need  not  spare  large  doses.  Otherwise,  of  course, 
caution  is  necessary. 

Chloral  hydrate  should  be  cautiously  employed  in  heart  disease.  It  is  often, 
however,  well  borne  and  gives  the  patient  rest  and  comfort.  We  have  also  pre- 
scribed chloralamide  in  cardiac  cases,  with  good  results. 

In  practice  we  must  often  prescribe  external  applications  to  the  chest,  mus- 
tard-plasters, hot  poultices,  and  also  hot  foot-baths  with  mustard,  ashes,  etc.  In 
severe  cases  their  action  is  slight.  Acetate  of  lead  in  large  doses  sometimes 
seems  to  have  a  favorable  influence  in  severe  dyspnoea,  especially  with  threatening 
pulmonary  oedema.  We  give  the  powder,  up  to  a  grain  and  a  half  (gramme  0.1), 
every  two  or  three  hours,  and  it  is  often  a  good  plan  to  add  half  a  grain  or  a  grain 
(gramme  0.03  to  0.05)  of  opium.  We  can  also  frequently  obtain  decided  relief 
for  the  patient,  particiilarly  if  constipated,  by  a  vigorous  drastic  purge,  with  com- 
pound infusion  of  senna  or  gamboge.  Inhalations  of  nitrite  of  amyl  seldom  have 
a  beneficial  effect. 

Palpitation,  constant  or  paroxysmal,  is  treated  by  applying  ice  to  the  cardiac 
region;  the  "heart-bottles,"  made  of  tin,  act  very  well.  In  patients  with  aortic 
insufficiency  and  very  excited  action  of  the  heart,  we  may  recommend  the  pro- 
tracted use  of  ice.  Hot  poultices  also  are  sometimes  beneficial.  The  narcotics  are 
the  most  efficient  internal  remedies,  especially  morphine,  which,'  of  course,  we 
should  reserve  for  severe  cases.  If  the  palpitation  is  of  a  lesser  degree,  we  may 
try  bromide  of  potassium,  or  bitter-almond  water. 

The  subcutaneous  use  of  morphine  is  again  by  far  the  most  potent  remedy  in 
the  anginous  attacks,  associated  with  pain  and  a  feeling  of  distress.  We  may 
also  use  cutaneous  irritation,  mustard-plasters,  etc.,  hot  compresses  or  poultices, 
and  perhaps  strophanthus,  nitrite  of  amyl,  or  nitroglycerine. 

We  may  prescribe  bitter  remedies — tinctura  amara  (P.  G.),  or  compound  tinc- 
ture of  cinchona — and  muriatic  acid  for  the  loss  of  appetite,  in  case  this  is  not 
improved  by  regulating  the  activity  of  the  heart.  In  addition,  we  must  always 
endeavor  to  get  a  regular  evacuation  of  the  bowels. 

For  the  attacks  of  f  aintness  and  vertigo,  occurring  especially  in  aortic  stenosis, 
as  a  result  of  cerebral  anaemia,  we  may  prescribe  a  horizontal  position,  and  stimu- 
lants— wine,  ether,  and  Hoffmann's  anodyne.  If  the  cerebral  symptoms  depend 
upon  venous  stasis,  we  try  to  remove  it  by  ice,  mustard-plasters  to  the  neck,  and 
thorough  derivation  to  the  intestines. 

Especial  accidents  and  complications,  like  pulmonary  oedema,  infarctions,  or 
apoplexy,  are  to  be  treated  according  to  the  usual  rules. 


340  DISEASES    OF   THE   CIECULATOET   OEGANS 

CHAPTEE  III 

DISEASES    OF    THE    MYOCARDIUM: 

Preliminary  Remarks.— In  valvular  disease  of  the  heart  a  disturbance  of  the 
circulation  takes  place  because  of  the  functional  impairment  of  the  valves,  or  the 
obstruction  of  the  orifices  of  the  heart ;  but  in  the  diseases  which  we  are  now  to 
consider  we  have  to  deal  with  impairment  of  the  structure  and  functional  activity 
of  the  cardiac  muscle  itself,  while  the  valvular  apparatus  of  the  heart  remains  in- 
tact. The  expression  myocardial  diseases  of  the  heart,  in  a  strict  sense,  is  too 
narrow,  inasmuch  as  we  probably  have  diseases  of  the  ganglia  and  nerves  of  the 
heart  associated  with  the  muscular  diseases.  Indeed  these  nervous  lesions  may 
often  be  the  essential  change,  but  as  yet  our  knowledge  with  regard  to  the  patho- 
logical changes  in  the  nervous  apparatus  of  the  heart  is  extremely  limited;  and, 
on  the  other  hand,  most  of  the  organic  diseases  of  the  cardiac  nerves  probably  in- 
volve some  secondary  changes  in  the  cardiac  muscle.  We  may  therefore,  in  the 
classification  and  consideration  of  these  conditions  of  the  heart,  limit  ourselves 
provisionally  to  the  disturbances  of  the  cardiac  function  observed  during  the  life 
of  a  patient,  and  the  anatomical  changes  in  the  muscle  of  the  heart  found  after 
death.  It  remains  to  be  discovered  later  what  is  the  part  which  the  degenerations 
of  the  nerves  and  ganglia  of  the  heart  have  in  the  development  of  these  disturb- 
ances. We  must  also  point  out  that  in  what  follows  we  shall  consider  merely  the 
primary  muscular  diseases  of  the  heart,  in  which  the  change  in  the  heart  is  the 
cause  of  all  the  essential  symptoms.  We  shall  quickly  find  how  difficult  it  is  in 
these  matters  invariably  to  draw  a  sharp  distinction  between  secondary  and  pri- 
mary disease. 

1.  Interstitial  Myocarditis 

{Fibrinous  Degeneration  of  the  Myocardium.     Sclerosis  of  the  Coronary  Arteries) 

.31tiology  and  Pathological  Anatomy. — The  anatomical  changes  of  inter- 
stitial myocarditis  result  in  irregular-shaped  spots  of  a  whitish  luster,  often  very 
numerous,  interspersed  through  the  cardiac  muscle  and  corresponding  to  a  par- 
tial or  complete  destruction  of  the  muscle-fibers  and  the  substitution  for  them 
of  a  firm,  fibrinous,  cicatricial  connective  tissue.  These  places,  which  are  best 
found  by  making  horizontal  sections  of  the  myocardium,  occur  particularly  in 
the  left  ventricle,  and  especially  at  its  apex  and  in  its  anterior  wall;  but  they 
may  also  be  found  everywhere,  and  especially  in  the  papillary  muscles.  Often 
we  may  observe  them  as  somewhat  glistening  retracted  spots  on  the  endocardial 
or  pericardial  surface  of  the  heart.  The  origin  of  this  interstitial  myocarditis 
was  explained  by  the  researches  of  Weigert,  Ziegler,  Tluber,  and  others.  In  a 
great  majority  of  cases,  though  perhaps  not  in  all,  the  changes  just  sketched  are 
directly  associated  with  changes  in  the  coronary  arteries  and  their  branches.  In 
almost  every  case  we  find  in  these  vessels  marked  changes  due  to  endarteritis, 
or  arterio-sclerosis.  In  places  where  this  change  in  the  vessel  causes  marked 
diminution  of  its  lumen,  the  corresponding  portion  of  the  myocardium  is  imper- 
fectly supplied  with  arterial  blood,  and  in  consequence  the  muscular  fibers  grad- 
ually degenerate,  lose  their  nuclei,  and  change  into  a  friable,  cheesy  detritus. 
In  place  of  the  destroyed  muscular  fiber  there  is  a  new  growth  of  connective  tis- 
sue. With  ordinary  endarteritis  these  processes  are  slow  and  gradual,  but  under 
certain  circumstances  there  may  be  a  somewhat  rapid  occlusion  of  the  branches 
of  the  coronary  arteries,  because  of  thrombosis  or  embolism  of  proximal  origiii. 
In  such  cases  we  have  a  genuine  cardiac  infarction,  presenting  a  spot  of  ansemic 
necrosis,  or  sometimes  a  rather  fresh  brownish-yellow  haamorrhagic  infiltratic«l. 


INTEESTITIAL  MYOCAEDITIS  341 

Of  course,  this  limited  necrosis  and  interstitial  new  growth  will  not  occur  if, 
in  spite  of  the  existence  of  arterio-sclerosis,  the  direct  supply  of  blood  remains 
suflficient,  or,  if  insufficient,  is  eked  out  by  the  collateral  circulation. 

If  the  formation  of  connective  tissue  is  extensive,  the  entire  heart  wall  may 
become  decidedly  thinner,  so  that  it  yields  to  the  internal  pressure  of  the  blood. 
This  sometimes  occasions  in  the  left  ventricle  the  bulging  of  a  limited  portion 
of  the  wall  of  the  heart,  so-called  cardiac  aneurism.  A  cardiac  aneurism  of 
this  sort,  and  also  an  extensive  fresh  infarction,  may  exceptionally  result  in 
rupture  of  the  heart  with  escape  of  blood  into  the  pericardium,  and  sudden  death. 
Of  still  greater  importance,  because  far  more  frequent,  is  the  formation,  in 
places  where  the  fibrinous  process  reaches  to  the  endocardium,  of  parietal 
thrombi  inside  the  heart.  These  sometimes  give  rise  to  embolism  in  distant 
organs. 

As  to  further  pathologic  changes  in  the  heart  we  find  that  certain  portions  of 
the  heart  are  not  infrequently  dilated  or  hypertrophied.  The  dilatation  may,  at 
least  in  part,  be  due  to  the  diminished  resistant  power  of  the  cardiac  walls,  but 
in  case  of  hypertrophy  we  must  always  seek  for  special  causes,  inasmuch  as  sclerosis 
of  the  coronary  arteries  as  such  can  not  lead  to  hypertrophy  of  a  portion  of  the 
heart.  As  a  rule,  the  cause  is  easily  discovered,  either  in  an  associated  arterio- 
sclerosis, or  in  those  factors,  such  as  dissipation,  which  may  occasion,  simultane- 
ously with  arterio-sclerosis,  an  idiopathic  hypertrophy  of  the  heart.  Of  course, 
we  must  also  bear  in  mind  the  possible  but  exceptional  presence  of  such  compli- 
cating diseases  as  interstitial  nephritis,  or  pulmonary  emphysema.  With  regard 
to  the  right  ventricle  we  know,  also,  that  this  portion  of  the  heart  must  hyper- 
trophy as  a  result  of  congestion  in  the  pulmonary  circuit,  when  the  left  ventricle 
is  permanently  weakened. 

The  causes  of  this  most  important,  and  by  no  means  rare,  fonn  of  myocarditis 
which  we  have  just  described,  and  which  is  due  to  sclerosis  of  the  coronary 
arteries,  must  be  the  same  as  the  causes  of  this  latter  affection.  Often  the  sclerosis 
of  the  coronary  arteries  is  merely  a  part  of  a  general  arterio-sclerosis,  but  we 
sometimes  find  comparatively  marked  changes  in  the  poronaries,  although  there 
are  no  specially  extensive  atheromatous  changes  in  the  other  arteries  of  the  body, 
and  again,  when  there  is  well-marked  arterio-sclerosis  elsewhere,  the  coronary  ar- 
teries may  show  slight  symptoms  of  disease,  if  any.  In  general,  howevei%  we  have 
the  same  setiological  factors  to  explain  sclerosis  of  the  coronary  arteries  as  arterio- 
sclerosis in  general.  Often  we  shall  find  the  cause  in  high  living,  and  particularly 
in  chronic  alcoholism.  In  other  cases,  habitual  muscular  overstrain  seems  to 
favor  the  development  of  arterio-sclerosis,  and  clinical  experience  shows  that  an 
important  cause  of  sclerosis  of  the  coronary  arteries,  particularly,  lies  in  great 
mental  effort  and  excitement,  which  indeed  are  not  infrequently  combined  with 
the  above-mentioned  factors — for  example,  in  the  case  of  extraordinarily  active 
business  men,  speculators,  high  officials,  and  physicians.  All  these  considera- 
tions go  to  explain  the  fact  that  sclerosis  of  the  coronary  arteries  is  seen  far  more 
often  in  the  male  than  in  the  female  sex.  That  age  plays  an  important  part  is  uni- 
versally aclaiowledged.  It  is  true  of  interstitial  myocarditis,  as  of  arterio-sclero- 
sis in  general,  that,  as  a  rule,  persons  are  attacked  in  the  second  half  of  life, 
from  forty  years  of  age  on.  Finally,  we  must  add  that  hereditary  tendencies  to 
the  development  of  arterio-sclerosis  in  general,  and  sclerosis  of  the  coronary 
arteries  in  particular,  can  not  be  denied. 

That  form  of  disease  of  the  coronary  arteries  deserves  special  mention  which 
is  of  syphilitic  origin,  and  therefore  somewhat  distinct  from  ordinary  arterio- 
sclerosis, although  the  number  of  proved  cases  is  not  great.  It  is  scarcely  possible 
to  doubt  that  there  is  a  specific  syphilitic  endarteritis  of  the  coronary  arteries, 
giving  rise  to  almost  exactly  the  same  symptoms  as  ordinary  arterio-sclerosis.    At 


342  DISEASES    OF   THE   CIECULATOET   OEGAifS 

any  rate,  tliis  point  should  in  every  ease  be  considered,  for  tlierapentic  reasons 
if  for  none  other  (vide  infra). 

Finally,  it  is  to  be  added  that  there  may  be  another  form  of  chronic  myocar- 
ditis not  associated  with  primary  chronic  disease  of  the  arteries,  but  ^vith  an 
antecedent  acute  myocarditis  as  a  sequel  of  severe  constitutional  infectious  dis- 
ease, such  as  typhoid,  diphtheria,  sepsis,  or  scarlet  fever.  The  careful  histological 
examination  of  the  myocardium  by  Krehl,  Romberg,  and  others,  in  eases  of  dis- 
ease of  this  sort,  has  demonstrated  acute  inflammatory  processes  in  the  cardiac 
muscle.  It  might  very  well  be  that  chronic  interstitial  myocarditis,  with  all  its 
results,  should  gradually  develop  from  acute  processes  of  this  sort.  Still,  the 
matter  needs  further  clinical  study. 

There  is  a  secondary  chronic  myocarditis  as  a  sequel  of  chronic  endocarditis 
(valvular  disease),  but  this  is  only  exceptionally  of  any  importance  in  itself.  The 
endocarditic  process  may  extend  directly  to  the  neighboring  muscular  layers  of 
the  heart,  or  there  may  occur,  especially  in  association  with  aortic  endocarditis, 
embolic  infarctions,  the  development  of  which  is  the  same  as  of  the  previously 
described  thrombotic  infarctions  of  the  heart.  Finally,  there  is  the  possibility 
that  myocarditis  and  endocarditis  might  appear  simultaneously.  It  has  been 
maintained  that  myocarditis  may  develop  as  a  sequel  of  acute  articular  rheuma- 
tism. The  development  of  myocarditis  in  this  way,  if  it  ever  occurs,  is  probably 
very  exceptional. 

Clinical  History. — ^We  must  first  mention  that  sometimes  quite  extensive  cica- 
tricial formation  may  be  found  in  the  cardiac  muscle  post  mortem,  without  the 
occurrence  of  any  manifest  symptoms  referable  to  the  heart  during  life.  We  see, 
then,  that  the  heart  may,  under  some  circumstances,  undergo  quite  a  considerable 
loss  in  its  contractile  substance  without  injury. 

In  many  other  cases,  however,  the  heart's  capacity  for  work  suffers  so  much 
that  the  same  s\T3iptoms  arise  as  in  valvular  disease.  The  course  of  such  cases 
may  be  very  chronic.  The  symptoms  begin  quite  gradually.  The  patient  first  has 
a  slight  dyspnoea  or  palpitation,  and  a  feeling  of  distress  in  the  chest,  but  only 
from  external  causes,  such  as  slight  physical  exertion.  Sometimes  there  is  marked 
general  weakness  and  languor.  The  patients  have  an  unhealthy  sallow  look.  They 
become  easily  tired,  feel  depressed,  and  scarcely  capable  of  any  great  bodily  or 
mental  exertion.  The  symptoms  gradually  increase,  and  just  the  same  results  of 
disturbance  of  the  circulation  appear  as  in  all  the  other  forms  of  heart  disease. 
The  difficulty  in  breathing  becomes  more  marked,  oedema  occurs,  signs  of  stasis  in 
the  liver,  intestines,  and  kidneys  appear — in  short,  the  well-known  type  of  general 
circulatory  disturbance  develops. 

Physical  examination  of  the  heart  shows  marked  anomalies  of  the  heart's 
action  in  all  severe  cases.  The  pulse  is  often  irregular  in  regard  to  its  rhythm 
and  the  intensity  of  its  single  beats,  but  the  arhytlnnia  may  also  be  wholly  absent 
in  spite  of  the  degeneration  of  the  myocardium,  as  we  have  often  convinced  our- 
selves. The  pulse  is  at  first  quite  strong  and  full,  later  it  becomes  weaker,  of 
lower  tension,  and  at  last  sometimes  very  small  and  scarcely  perceptible.  It  may 
be  increased  in  frequency,  but  we  quite  often  notice  in  chronic  myocarditis,  espe- 
cially in  the  early  stages,  a  very  characteristic  and  persistent  slowing  of  the  pulse 
to  60,  50,  or  even  less,  in  a  minute.  With  this  slowness  of  the  pulse  there  is  also 
frequently  irregularity  of  the  heart's  action,  especially  the  appearance  of  occa- 
sional double  beats  (pulsus  bigeminus).  Percussion  usually  shows  an  increase 
of  the  heart's  dullness,  due  to  dilatation  or  hypertrophy  of  the  heart,  the  increase 
being  either  general  or  chiefly  on  one  side.  Auscultation  shows  the  absence  of 
any  murmur,  and  hence  the  absence  of  valvular  disease.  The  heart-sounds  are 
distinctly  audible,  and  sometimes  quite  loud  and  valvular,  but  in  the  later  stages 
often  low  and  obscure.     The  pulmonic  second  sound  is  accentuated,  when  there 


INTERSTITIAL   MYOCAEDITIS  343 

is  stasis  of  the  pulmonary  circulation.  In  several  cases  we  found  the  second  sound 
for  a  long  time  very  plainly  divided — reduplicated.  We  must  also  mention  that 
sometimes  in  pure  myocarditis  a  sj^tolic  murmur  is  heard  at  the  apex  which  is 
due  either  to  a  relative  insufficiency  of  the  mitral  valve,  or  to  its  incomplete 
closure,  as  a  result  of  defective  musciilar  action  of  the  left  ventricle. 

We  must  make  particular  mention  of  one  symptom  of  sclerosis  of  the  coronary 
arteries,  which,  although  it  is  not  pathognomonic,  is  by  far  most  often  seen  in 
association  with  it  and  therefore  has  an  important  diagnostic  significance.  We 
refer  to  the  attacks  of  so-called  angina  pectoris  (stenocardia,  heart-pang).  These 
attacks  of  genuine  angina  pectoris  (compare  also  the  following  chapter)  consist  in 
the  sudden  occurrence  of  pain  in  the  region  of  the  heart,  extending  into  the 
back,  the  left  shoulder,  and  the  left  arm  even  to  the  tips  of  the  fingers.  In  severe 
cases  the  pain  is  extremely  violent.  It  is  as  if  the  chest  were  squeezed  in  a  vise. 
At  the  same  time  there  is  a  decided  feeling  of  anxiety  and  oppression,  as  well  as 
complete  loss  of  strength — a  sense  of  impending  death.  The  patient  seeks  some 
support,  he  can  scarcely  move,  scarcely  utter  a  few  words  in  a  whisper;  the  ex- 
tremities grow  cool,  the  brow  moist  and  cold.  The  attack  may  be  directly  fatal, 
but  this  is  the  exception.  As  a  rule,  the  symptoms  pas  away  in  a  few  hours,  and 
the  patient  gradually  recovers.  In  many  cases  of  sclerosis  of  the  coronary  arteries 
attacks  of  this  sort  occur  very  often,  in  varying  severity.  ISTot  infrequently  an 
attack  may  be  due  to  some  special  cause,  such  as  the  bodily  exertion  of  a  long 
walk  or  climb,  errors  in  diet,  or  mental  excitement.  In  such  cases  bad  news  may 
cause  death. 

With  regard  to  the  true  essence  of  angina  pectoris,  we  are  confined  to  hypoth- 
esis. The  ordinary  supposition  of  a  sudden  paralysis  of  the  left  ventricle  explains 
many  symptoms,  but  not  all.  The  intense  pain  indicates  irritation  of  the  sensory 
nerves.  Sometimes  during  an  attack  the  pulse  grows  small  and  irregular,  but  often 
also,  as  we  have  learned  by  experience,  it  may  not  be  very  greatly  disturbed.  There 
may  or  may  not  be,  during  an  attack,  acute  dilatation  of  the  heart. 

Besides  genuine  angina  pectoris,  attacks  of  cardiac  asthma  are  not  infrequent 
in  chronic  myocarditis.  This  differs  from  angina  pectoris  in  that  the  peculiar 
pain  and  constriction  are  not  present,  while  the  distress  for  breath,  the  parox- 
ysmal dyspncea,  is  prominent.  In  most  cases  of  this  sort  we  probably  have  really 
to  do  with  sudden  weakness  of  the  heart.  Another  symptom  that  has  been  re- 
peatedly observed  in  sclerosis  of  the  coronary  arteries  is  simple  syncope,  due  to 
acute  anaemia  of  the  brain,  and  perhaps  also  referable  to  simultaneous  sclerosis  of 
the  cerebral  arteries. 

The  general  course  of  the  disease  varies  considerably  in  different  cases.  Much 
depends  upon  the  patient — e.  g.,  upon  his  ability  to  take  good  care  of  himself. 
Sometimes  dyspncea,  a-dema,  and  other  general  symptoms  of  passive  congestion 
are  prominent,  and  in  such  cases  the  patient  is  alternately  better  or  worse.  Other 
cases  are  characterized  by  attacks  of  angina  pectoris.  The  termination  is  in- 
variably unfavorable.  It  may  either  occur  gradually  with  increase  in  the  circu- 
latoiy  disturbance,  or  with  complete  suddenness  like  a  stroke. 

This  important  clinical  fact  of  sudden  apoplectiform  death  ("paralysis  of 
the  heart ")  in  patients  with  sclerosis  of  the  coronary  arteries,  demands  consid- 
eration. It  usually  happens  in  elderly  persons  in  comfortable  circumstances  and 
good  livers,  who  up  to  that  time  have  not  regarded  themselves  as  really  ill;  but 
they  have  repeatedly  had  slight  attacks  of  vertigo,  of  oppression,  etc.  Suddenly  a 
sort  of  apoplectic  attack  comes  on,  often  after  some  definite  cause,  after  a  ban- 
quet, or  after  some  physical  exertion  or  mental  excitement.  Death  follows  in 
a  few  moments,  or  after  a  deep  coma  that  lasts  for  several  hours  or  even  days. 
The  diagnosis  often  remains  in  doubt  in  such  cases,  especially  if  we  have  not 
known  the  patient  previously.    The  autopsy  shows,  as  the  sole  pathological  lesion, 


344  DISEASES    OE   THE   CIRCULATOEY   OEGANS 

a  sclerosis  of  the  coronary  arteries,  with  a  more  or  less  extensive  cicatricial  f  orma-'^ 
tion  in  the  heart.  Apparently  in  these  cases  the  moment  must  suddenly  arise 
when  the  supply  of  blood  to  the  heart  is  insufficient,  and  thus  death  is  caused. 
Experiments  upon  artificial  closure  of  the  coronary  arteries,  by  Cohnheim  and 
others,  agree  perfectly  with  the  clinical  facts  above  mentioned.  Artificial  narrow- 
ing of  the  coronary  arteries  may  also  be  well  borne  for  a  long  time,  until  suddenly 
both  halves  of  the  heart  stand  still  in  a  condition  of  diastole.  In  such  cases,  also, 
the  heart  seems  to  stop  suddenly,  but  sometimes  there  are  frequent  anginous  at- 
tacks, and  death  occurs  in  one  of  them.  Finally,  it  should  be  mentioned  that  sud- 
den death  in  sclerosis  of  the  coronary  arteries  may  also  be  caused  by  embolism  of 
the  trunk  of  the  coronary  artery,  or,  as  in  one  case  seen  by  the  author,  by  the 
bursting  of  a  focus  of  myocarditis  with  haemorrhage  into  the  pericardial  cavity. 

Diagnosis. — The  diagnosis  of  chronic  myocarditis  is  by  no  means  always  easy 
and  certain.  We  must  first  determine  that  there  is  a  cardiac  lesion  of  some  kind. 
This  is  usually  evident  from  the  secondary  symptoms  of  stasis,  the  condition  of 
the  pulse,  the  area  of  cardiac  dullness,  etc.  Then  the  question  arises  whether  we 
have  to  do  with  a  valvular  disease  or  with  a  myopathic  disease  of  the  heart.  Here 
auscultation  must  chiefly  decide.  The  absence  of  a  heart  murmur,  in  spite  of 
other  definite  signs  of  heart  disease,  speaks  against  valvular  disease,  but  not  with 
complete  certainty.  All  murmurs  may  be  absent  in  the  last  stages,  especially 
with  a  high  degree  of  mitral  stenosis,  and  hence  we  may  easily  confuse  mitral 
stenosis  with  myocarditis,  particularly  when  there  is  marked  arhythmia  of  the 
heart.  On  the  other  hand,  we  have  already  stated  that  in  pure  myocarditis,  with 
the  valves  intact,  functional  murmurs  may  be  present,  which  may  lead  to  an 
erroneous  opinion  as  to  valvular  disease.  If  continued  study  of  the  case  has  en- 
abled us  to  exclude  valvular  disease,  it  remains  to  distinguish  between  chronic 
myocarditis  or  sclerosis  of  the  coronary  arteries  on  the  one  hand,  and  the  other 
diseases  of  the  myocardium  (vide  infra)  on  the  other.  We  regard  it  as  impos- 
sible to  make  this  distinction  with  absolute  certainty.  All  the  diseases  named 
present  the  same  clinical  picture  of  cardiac  insufficiency,  but  what  the  anatomical 
conditions  may  be  which  occasion  this  cardiac  insufficiency  we  can  at  present 
only  conjecture  with  more  or  less  probability,  during  life.  The  following  symp- 
toms are  most  characteristic  of  coronary  sclerosis :  persistent  inf requency  (slow- 
ness) of  the  pulse,  particularly  if  associated  with  arhythmia;  attacks  of  genuine 
angina  pectoris;  and  the  evidence  of  arterio-sclerosis  in  the  brachial,  radial,  tem- 
poral, and  other  peripheral  arteries.  Persistent  rapidity  and  arhythmia  of  the 
pulse  occur  in  interstitial  myocarditis,  just  as  in  other  myopathic  diseases  of 
the  heart;  but  arhythmia  is,  in  general,  far  more  common  when  there  is  actual 
myocarditis  than  when  there  is  simple  muscular  weakness  of  the  heart.  There 
is  self-evident  difficulty  in  the  diagnosis  of  cases  with  sudden  apoplectiform 
paralysis  of  the  heart,  and  in  distinguishing  them  from  apoplexy,  embolism,  pan- 
creatic haemorrhage,  and  similar  causes  of  sudden  death. 

Prognosis. — The  prognosis  is  evident  frora  what  has  been  already  said.  Re- 
covery is  impossible,  but  even  extensive  cicatricial  formation  in  the  heart  may 
probably  last  for  years  without  causing  much  disturbance.  We  must  always  be 
prepared  for  disturbances  of  compensation,  and  the  manifold  sudden  accidents  to 
which  patients  with  myocarditis  are  exposed,  but  we  can  not  foretell  the  time  of 
their  occurrence. 

Treatment. — The  treatment  of  chronic  myocarditis  must  be  directed  first  to 
the  dietetic  and  hygienic  care  of  the  patient.  This  is  of  the  greatest  importance. 
Eor  obese  persons  accustomed  to  high  living,  a  moderate,  simple  diet  must  be 
accurately  prescribed.  Alcoholic  beverages  must  be  greatly  limited  or  wholly 
forbidden,  and  not  more  than  two  or  three  cigars  allowed  per  diem.  Moderate 
bodily  exercise  is  beneficial,  and  indeed  necessary,  for  the  promotion  of  the  circuia- 


SO-CALLED  IDIOPATHIC  HYPERTROPHY  OF  THE  HEART  34:5 

tion  and  the  more  rapid  diminution  of  the  obesity,  but  the  patient  must  be  ear- 
nestly warned  against  too  violent  exertion,  nor  can  great  mental  effort  be  per- 
mitted. In  summer,  a  quiet  life  injhe  country  or  some  mountain  region  is  to  be 
advised,  or,  under  suitable  circumstances,  the  cautious  use  of  the  waters  of  Carls- 
bad, Kissingen,  Marienbad,  or  ISTauheim.  Frequent  tepid  baths  or  mud  baths  may 
usually  be  employed  even  at  home  with  advantage.  Of  internal  remedies,  iodide  of 
potassium  has  been  specially  recommended  to  be  used  persistently,  in  the  amount 
of  eight  to  fifteen  grains  (gramme  0.5-1.0)  or  more  daily.  Iodide  of  potassium 
enjoys  a  reputation  for  an  especial  specific  action  upon  arterio-sclerosis  in  general, 
and  ought  therefore  to  have  a  beneficial  effect  upon  arterio-sclerosis  of  the  coro- 
nary arteries.  We  have  ourselves  seldom  seen  very  striking  results  from  its  use. 
Probably  iodide  of  potassium  is  of  benefit  in  cases  of  syphilitic  origin,  and  we 
therefore  recommend  it  particularly  when  there  is  any  suspicion  of  a  syphilitic 
taint.  With  disturbance  of  compensation,  and  with  abnormally  frequent,  weak, 
and  irregular  action  of  the  heart,  digitalis  and  similar  remedies  are  indicated,  just 
as  in  valvular  disease.  In  cases  with  an  abnormally  slow  pulse,  we  may  use  them, 
provided  great  caution  is  exercised,  but  we  must  also  be  governed  by  the  other  pre- 
vailing symptoms.  In  attacks  of  angina  pectoris  (see  the  following  chapter)  the 
subedit aneous  injection  of  morphine  is  by  far  the  most  efiicient,  and  often  an  in- 
dispensable remedy.  Also,  the  frequently  enumerated  cardiac  stimulants,  such  as 
strophanthus,  camphor,  ether,  and  wine,  ought  to  be  borne  in  mind,  and,  finally, 
one  may  make  trial  of  nitro-glycerine  (-^V  to  ^V  oi  a  grain,  gramme  0.001-0.002) 
in  alcoholic  solution,  and  of  nitrite  of  sodium  (two  or  three  teaspoonfuls  daily  of 
a  solution  containing  1  or  2  parts  to  120  of  water).  The  inhalation  of  a  few  drops 
of  nitrite  of  amyl  is  also  sometimes  beneficial,  but  more  often  it  has  no  effect. 
In  cardiac  asthma,  stimulants  are  indicated,  but  often  narcotics  as  well.  Mus- 
tard-plasters, the  application  of  cold  and  of  heat,  hot  foot-baths,  etc.,  are  also 
employed.  Sometimes  even  in  the  worst  cases  we  see  good  results  from  the  use  of 
digitalis. 

With  regard  to  regimen  and  mechanical  treatment  compare  the  following 
section  on  idiopathic  hypertrophy  of  the  heart. 

2.  So-called  Idiopathic  Hypertrophy  of  the  Heart 

(Mechanical  Strain  of  the  Heart) 

.^Etiology  and  Greneral  Pathology. — ISTot  infrequently  cases  during  life  pre- 
sent all  the  symptoms  of  an  uncompensated  cardiac  lesion,  and  yet  the  autopsy 
discloses  merely  hypertrophy  of  the  heart  with  a  greater  or  less  degree  of  accom- 
panying dilatation.  There  is  no  lesion  of  valves,  coronary  arteries,  or  myo- 
cardium. The  cardiac  hypertrophy,  which  involves  the  left  ventricle  chiefly, 
but  often  both  ventricles,  can  not  be  regarded  as  secondary  in  the  ordinary  sense 
of  the  word,  for  in  the  heart  itself  and  in  the  other  organs  we  find  nothing  which 
can  call  forth  a  secondary  hypertrophy  of  the  cardiac  muscle — no  valvular  disease, 
no  chronic  nephritis,  no  general  arterio-sclerosis,  and  no  pulmonary  emphysema. 
Hence  we  term  these  cases  "  primary  idiopathic "  cardiac  hypertrophy,  in  the 
sense  that  we  can  not  discover  any  other  primary  disease. 

Notwithstanding,  we  must  in  these  cases  also  seek  the  cause  of  the  cardiac 
hypertrophy  in  some  excessive  demand  upon  the  cardiac  muscle,  and  as  there  are 
no  macroscopic  anatomical  or  mechanical  changes  involving  an  increase  in  the 
cardiac  activity,  we  must  seek  other  circumstances  occasioning  a  functional  over- 
strain of  the  heart.  Careful  observation  and  investigation  of  cases  of  this  sort 
have  taught  us  a  number  of  such  causes. 

Among  the  most  frequent  is  habitual  embarrassment  of  the  circulation  by 
excess  in  eating  and  drinking.    There  can  be  no  doubt  that  every  time  food  is 


346  DISEASES    OF   THE   CIECULATOEY   OKGANS 

taken  in  large  amount  there  is  a  temporary  increase  in  the  activity  of  the  heart, 
the  frequency  of  the  pulse,  and  the  tension  in  the  arteries.  This  is  in  part  because 
the  specific  gravity  of  the  blood  is  temporarily  increased  by  the  material  taken  into 
it,  and  in  part  because  the  products  of  metabolism  in  the  blood  have  a  direct 
stimulating  action  upon  the  heart  or  the  blood-vessels,  and  finally,  because  an  ex- 
cessive ingestion  of  liquids  temporarily  increases  the  total  amount  of  blood.  In 
brief,  there  are  numerous  persons  of  the  more  favored  classes  who  indulge  too 
freely  in  eating  and  drinking,  and  for  years  go  to  excess  in  the  pleasures  of  the 
table;  and  in  the  case  of  such  persons  there  is,  during  a  great  part  of  their  life, 
although  not  all  the  time,  that  condition  which  the  older  physicians  termed 
plethora.  All  these  circumstances  which  we  have  mentioned  occasion  an  increase 
in  the  demands  upon  the  heart,  especially  its  left  ventricle.  The  heart  performs 
this  extra  work  laid  upon  it,  and  consequently  becomes  gradually  hypertrophied. 
Erom  what  has  been  said,  it  is  easy  to  understand  why  this  form  of  cardiac 
hypertrophy  is  especially  frequent  in  the  obese,  and  particularly  in  men  from 
forty  to  fifty  years  old,  though  sometimes  much  younger.  We  have  seen  by  far 
the  most  frequent  examples  of  it  in  great  beer-drinkers,  and  so  in  persons  whose 
business  tempts  them  to  excessive  indulgence  in  beer,  such  as  landlords,  brewers, 
hop-dealers,  butchers,  and  many  others.  Persons  of  this  sort  often  drink  for  years, 
almost  daily,  four  or  five,  or  even  eight  or  ten,  litres  (quarts)  of  beer.  Let  the 
reader  consider  what  an  amount  of  liquid,  and  at  the  same  time  of  nourishment 
(for  one  litre  of  beer  contains  about  fifty  or  sixty  grammes  [two  ounces]  of  carbo- 
hydrates), is  in  this  way  alone  introduced  into  the  blood.  This  explains  the 
great  frequency  of  cardiac  hypertrophy  which  Bollinger  has  shown  to  exist  at 
Munich ;  but  the  "  Munich  beer-heart "  is  seen  with  unfortunate  frequency  in  other 
towns  than  Munich.  The  alcohol  is  probably  not  a  factor  in  the  development  of 
the  hypertrophy  of  the  heart,  but  we  may  well  suppose  that  it  promotes,  or  at 
least  hastens,  the  degenerative  changes  in  the  cardiac  muscle,  and  particularly  in 
the  cardiac  nerves,  which  at  last  render  the  heart's  action  inadequate  and  the 
circulation  imperfect.  Eor  the  development  of  cardiac  hypertrophy  in  itself  is  a 
circumstance  which  does  not  impair  the  health,  but  rather  preserves  it ;  only,  ex- 
perience teaches  us  that  no  heart  can  uninterruptedly  perform  an  amount  of  work 
which  is  physiologically  excessive,  and  escape  final  exhaustion — the  point  of  time 
depending  upon  the  individual  vigor  and  other  associated  factors. 

A  second  cause  of  idiopathic  hypertrophy  is  persistent  muscular  strain.  Every 
muscular  exertion  increases  the  demands  upon  the  cardiac  activity.  There  is  an 
increase  in  the  frequency  of  the  pulse  and  in  the  amount  of  blood  passing  through 
the  heart.  If  excessive  bodily  exertion  is  habitual  for  a  considerable  period  of 
time,  there  finally  develops  hypertrophy  of  the  heart,  usually  affecting  both  ven- 
tricles, but  especially  the  left.  Thus  is  explained  the  hypertrophy  sometimes  seen 
in  blacksmiths,  locksmiths,  baggage-carriers,  laborers  in  vineyards  ("  Tiibingen 
heart"),  and  soldiers  after  severe  campaigns.  Why  this  hypertrophy  should 
sometimes  occur  and  sometimes  be  absent,  under  apparently  similar  conditions, 
must  be  explained  by  the  difference  in  the  physiological  capacity  of  the  individ- 
ual. Here,  too,  the  abnormality  of  the  condition  does  not  become  evident  till  the 
functional  ability  of  the  heart  begins  to  fail  ("  heart  overstrain,"  "  irritable 
heart"). 

In  the  third  place,  it  seems  that  in  some  few  cases  of  idiopathic  hypertrophy 
of  the  heart,  in  which  none  of  the  causes  yet  named  are  operative,  it  is  abnor- 
mal nervous  irritation  of  the  heart  which  increases  its  activity,  and  hence, 
finally  leads  to  its  hypertrophy.  This  is  perhaps  the  explanation  of  many  cases 
of  cardiac  hypertrophy  in  persons  Avho  have  long  been  exposed  to  many  sorts  of 
psychical  excitement.  The  cardiac  hypertrophy  of  exophthalmic  goitre  (q.  v.) 
may  also  be  put  in  this  category.     ISTot  infrequently  we  may  conjecture  in  an 


SO-CALLED  IDIOPATHIC  HYPERTEOPHY  OF  THE  HEAET   347 

individual  case  that  several  of  the  causes  mentioned  have  been  operative  simul- 
taneously in  the  development  of  the  hypertrophy.  Thus,  idiopathic  hypertrophy 
of  the  heart  is  seen  particularly  oft.en  in  individuals  who  have  to  undergo  great 
mental  strain  and  excitement,  and  at  the  same  time  are  heavy  drinkers. 

There  is  usually  associated  with  the  hjiDcrtrophy  a  dilatation,  referable  to  the 
persistent  over-distention  of  the  ventricles  during  diastole.  The  weaker  and 
more  yielding  the  myocardium  becomes  with  the  course  of  time,  and  the  more 
passive  congestion  affects  the  heart  itself  (particularly  the  auricles  and  right  ven- 
tricle), the  more  the  dilatation  increases;  and  with  it  comes  degeneration  of  the 
cardiac  muscle,  or,  at  any  rate,  functional  weakness  of  the  same,  giving  rise  to 
symptoms  of  cardiac  insufficiency. 

Clinical  History. — Idiopathic  hypertrophy  of  the  heart  may  certainly  exist  for 
a  long  time  without  causing  the  patient  any  subjective  disturbance.  We  have 
already  emphasized  the  fact  that  it  is  precisely  the  cardiac  hypertrophy  which 
protects  the  patient  for  a  time  from  the  onset  of  marked  symptoms.  Prodromata 
may  occur  for  a  long  time  before  severe  disturbance  sets  in.  Among  these  are 
palpitation,  a  certain  sense  of  discomfort  in  the  cardiac  region,  and  slight 
dyspnoea.  The  symptoms  begin  when  the  heart  can  no  longer  respond  to  the  de- 
mands made  upon  it,  and  when  it  begins  to  fail.  Then  all  the  symptoms  of 
cardiac  insufficiency  arise,  in  just  the  same  way  as  in  valvular  disease  and  in 
chronic  myocarditis.  Hence  we  need  not  go  into  the  details  of  the  disturbances 
of  compensation  again.  The  whole  series  of  symptoms  of  stasis,  as  well  as  the 
attacks  of  angina  pectoris  and  cardiac  asthma,  described  in  the  preceding  chapter, 
also  occur  in  idiopathic  hypertrophies  and  dilatations  of  the  heart. 

Another  subjective  disturbance  is  the  peculiar  and  often  very  annoying  feel- 
ing of  "  fluttering  "  of  the  heart — that  is,  a  momentary  feeling  of  fluttering  con- 
traction of  the  heart.  This  symptom  indicates,  probably,  abnormal  conditions  of 
contraction,  and  must  by  no  means  be  confounded  with  the  numerous  sensations 
which  hypochondriacal  and  neurasthenic  patients  refer  to  the  heart.  If  the  action 
of  the  heart  is  irregular,  and  especially  if  there  is  a  tendency  to  bigeminal  pulsa- 
tion, many  patients  feel  every  bigeminal  contraction  as  a  jolt  or  stopping  of  the 
heart. 

The  general  course  of  the  disease  differs  considerably  in  individual  cases. 
Sometimes  there  is  moderate  difficulty  in  breathing  for  a  long  time,  especially  on 
any  physical  exertion.  The  patient  often  complains  of  great  languor,  or  nervous 
irritability,  and  sometimes  of  attacks  of  vertigo  and  faintness,  and  a  tendency  to 
perspiration.  The  appetite  is  poor,  and  there  is  very  apt  to  be  constipation.  The 
condition  may  become  quite  suddenly  worse  after  any  marked  injurious  influence, 
especially  after  great  physical  exertion  or  mental  excitement.  Physical  examina- 
tion discloses  all  the  signs  of  hypertrophy  of  the  heart.  In  the  first  place,  the 
left  ventricle  is  usually  enlarged,  corresponding  to  the  direct  causes  of  the  con- 
dition. This  enlargement  is  often  better  appreciated  by  accurate  observation  of 
the  apex-beat  than  by  percussion.  Later  the  right  side  of  the  heart  also  becomes 
hypertrophied ;  dullness  on  percussion  then  extends  over  the  lower  part  of  the 
sternum,  with  epigastric  pulsation  and  undulatory  movements  in  the  veins  of 
the  neck.  The  heart-sounds  are  pure,  at  first  valvular,  later  sometimes  muffled 
and  feeble.  We  lay  especial  value  on  the  characteristics  of  the  first  sound  of  the 
heart.  A  dull,  indistinct  sound  is  probably  a  sign  of  considerable  dilatation,  while 
a  normal  valvular  sound  indicates  a  vigorous  systole.  In  general,  there  is  per- 
sistent frequency  of  the  pulse,  at  least  in  patients  Avho  are  led  to  seek  the  physician 
because  of  beginning  symptoms.  Infrequency  of  the  pulse  probably  indicates,  in 
most  cases,  co-existent  sclerosis  of  the  coronary  arteries  (vide  supra).  The  fre- 
quent pulse  may  for  a  long  time  remain  regular,  but  it  is  not  always  so.  So  long 
as  the  left  ventricle  does  its  work  well  the  pulse  may  be  tense,  and  the  second 


348  DISEASES    OF   THE   CIECULATOET   0KGA:N"S 

aortic  sound  valvular;  but  if  the  heart  becomes  insufficient  the  pulse  grows  small, 
feeble,  often  irregular;  the  heart-sounds  grow  faint,  and  not  infrequently  that 
bad  sign  appears  which  is  known  as  hruit  de  galop  or  gallop  rhythm,  and  con- 
sists in  a  peculiar  reduplication  of  the  first  sound  of  the  heart ;  *  for  each  beat  of 
the  pulse  we  hear  three  sounds  over  the  heart.  At  the  same  time  the  dyspncea 
and  oppression  in  the  chest  increase,  the  amount  of  urine  diminishes,  and  oedema 
appears  in  the  legs.  We  now  have  the  complete  picture  of  an  uncompensated 
heart  disease.  With  proper  treatment  the  symptoms  may  disappear  again;  but, 
sooner  or  later,  they  return.  Death  finally  ensues  from  general  dropsy  or  from 
some  complications  or  intercurrent  attacks,  among  which  we  may  mention  em- 
bolic processes. 

Cases  of  sudden  death  (paralysis  of  the  heart)  from  heart-failure  occur  not 
very  infrequently,  as  we  know  from  experience,  in  idiopathic  hypertrophy  of  the 
heart  independently  of  chronic  myocarditis. 

Diagnosis. — It  is  by  no  means  an  easy  task  for  the  physician  to  make  an 
absolute  diagnosis  of  idiopathic  hj^pertrophy  of  the  heart.  Sometimes,  when  the 
subjective  symptoms  suggest  an  examination  of  the  heart,  it  is  easy  to  make  out 
an  increase  in  the  cardiac  dullness  and  a  displacement  of  the  apex-beat;  but  in 
other  cases  the  presence  of  emphysema,  or  obesity,  or  even  of  dropsy,  makes  the 
physical  examination  very  difficult.  If  an  enlargement  of  the  heart  has  been 
demonstrated,  we  must  then  exclude  valvular  disease,  especially  mitral  stenosis, 
and  also  secondary  hypertrophy,  as  a  result  of  chronic  interstitial  nephritis,  or 
other  causes.  It  may  be  difficult  to  rule  out  nephritis  if  the  patient  is  suffering 
from  passive  congestion  when  he  first  comes  under  observation,  for  then  it  is  often 
hard  to  say  whether  the  albuminuria  which  may  be  present,  is  to  be  referred 
to  actual  renal  disease,  or  to  passive  congestion.  Even  if  we  can  exclude  nephritis 
we  have  still  to  determine  whether  there  is  simple  hypertrophy  of  the  heart,  or 
an  interstitial  myocarditis.  To  settle  this  question  is,  as  we  have  already  said 
(page  344),  very  difficult.  ^Etiology  is  always  important — for  example,  if  there 
has  been  an  excess  in  beer,  or  in  muscular  exertion.  Frequent  attacks  of  angina 
pectoris,  arhythmia,  and  a  lowering  in  the  rate  of  the  pulse,  suggest  sclerosis  of 
the  coronary  arteries.  Xot  infrequently  diseases  of  the  myocardium  are  eon- 
founded  with  chronic  obliterative  pericarditis.  When  we  consider  this  latter  con- 
dition we  shall  refer  again  to  the  differential  diagnosis. 

Treatment. — The  main  points  in  the  treatment  of  idiopathic  hypertrophy  of 
the  heart  are,  in  general,  exactly  the  same  as  for  valvular  disease  and  interstitial 
myocarditis.  We  may,  therefore,  refer  the  reader  for  these  to  the  preceding  chap- 
ters. There  is,  however,  one  point  which  we  would  like  to  discuss  in  more  detail 
here,  because  it  is  especially  prominent  in  the  treatment  of  diseases  of  the  myo- 
cardium. We  refer  to  the  so-called  dietetic  and  mechanical  treatment  of  circu- 
latory disturbances.  Much  of  what  we  shall  say  here  applies  also  to  other  forms 
of  chronic  heart  disease. 

Efforts  have  long  been  made,  but  with  fresh  zeal  of  late  years,  because  of 
Oertel's  recommendation,  to  promote  and  improve  the  circulation  by  mechanical 
means  as  well  as  by  such  internal  remedies  as  digitalis.  The  following  considera- 
tions lead  one  to  regard  such  an  influence  as  possible : 

1.  Diminution  of  the  Amount  of  Fluid  in  the  Body,  and  particularly  in  the 
Blood  {^^  Desiccation^^). — This  is  the  point  upon  which  Oertel  lays  the  greatest 

*  This  sign  is  not  infrequently  found  in  idiopathic  hypertrophy  of  the  heart,  iu  myocarditis,  and 
particularly  in  secondary  cardiac  hypertrophy  following  chronic  nephritis.  It  has  not  yet  been  fully 
and  definitely  explained.  Perhaps  we  have  to  do  with  an  audible  muscle-sound  originating  in  the 
auricle,  perhaps  with  peculiar  irregularities  in  the  contraction  of  the  heart  [for  example,  the  contraction 
of  the  right  and  left  ventricles  not  being  simultaneous. — V.]. 


SO-CALLED  IDIOPATHIC  HYPEETEOPHY  OF  THE  HEAET   349 

Stressi  He  believes  that  he  can  diminish  the  amount  of  blood  in  the  body  by  with- 
drawing liquids,  and  thus  lighten  the  task  of  the  heart  and  restore  the  normal  cir- 
culation. On  this  view  rest  the  proscription  of  excessive  drinking  and  the  limita- 
tion of  liquid  nourishment,  such  as  soup.  We  must  confess  that  it  is  difficult  for 
us  to  decide  upon  this  point.  Numerous  well-known  physiological  experiments 
prove  that  the  body  maintains  its  amount  of  blood  with  great  tenacity  at  a  cer- 
tain constant  ratio.  Inasmuch  as  the  body  is  able  by  means  of  numerous  ways 
(secretion  and  absorption  of  liquids)  to  make  speedy  compensation  for  variations 
arising  through  changes  in  the  amoiint  of  water  ingested,  it  is  by  no  means  proved 
that  the  total  amount  of  blood  in  patients  with  circulatory  derangements  is  in- 
creased; and  if  actually  there  is  a  retention  of  fluid  in  the  body  (as  indeed  is 
certainly  the  case  where  oedema  has  developed),  yet  the  liquid  does  not  collect  in 
the  vessels,  but  in  the  lymph-spaces  of  the  interstitial  tissue,  or  possibly  in  the 
cells  of  the  parenchyma  itself.  That  the  total  amount  of  water  in  the  system  may 
be  subjected  to  great  variations  must  certainly  be  admitted;  but  this  assumption, 
that  in  circulatory  disturbances  there  is  an  increase  in  the  amount  of  water  con- 
tained in  the  blood,  is  not  proved.  On  the  other  hand,  there  are  facts  which  con- 
tradict it,  such  as  the  actual  number  of  blood-corpuscles  and  the  specific  gravity 
of  the  blood.  That  there  should  be  any  increase  in  the  labor  demanded  of  the 
heart,  requires  that  a  large  amount  of  fluid  should  be  added  to  the  blood  in  a 
relatively  short  space  of  time,  so  that  an  actual,  although  extremely  temporary, 
hydrsemic  plethora  should  exist.  If  this  process  is  very  frequently  repeated,  it 
"will  surely  result  in  a  permanent  hindrance  to  the  circulation.  These  circum- 
stances are,  however,  actually  found  only  in  certain  patients,  particularly  in  great 
beer-drinkers.  In  them,  of  course,  to  forbid  the  ingestion  of  fluid  means  to  forbid 
the  drinking  of  beer,  and  is  therefore  of  the  greatest  benefit ;  and  we  can  not  in- 
sist too  strongly  upon  the  necessity  of  this  injunction  in  the  case  of  corpulent 
beer-drinkers  who  are  beginning  to  have  some  dyspnoea.  It  is  not,  however,  in 
our  opinion,  permissible  to  apply  this  rule  about  liquids,  as  is  sometimes  done,  to 
every  patient  without  individualizing.  For  those  who  live  temperately  and  are  of 
spare  figure,  the  amount  of  fluid  ingested  needs  no  special  attention  from  the 
physician. 

2.  Strengthening  of  the  Cardiac  Muscle  and  Promotion  of  Compensatory 
Hypertrophy  ty  Increased  Physical  Exertion. — That  the  fulfilling  of  this  indica- 
tion may  be  of  great  importance  is  certain,  and  Oertel  lays  the  greatest  stress 
upon  inciting  the  heart  to  more  vigorous  contractions  by  means  of  suitable  bodily 
exertion,  and  especially  by  methodical  mountain-climbing,  in  order  by  these  means 
to  promote  as  much  as  possible  the  development  of  cardiac  hypertrophy.  This 
view  is  probably  fully  justified  and  of  obvious  utility  in  many  cases  of  simple 
muscular  cardiac  weakness.  If,  however,  we  apply  it  to  those  cases  of  circulatory 
disturbance  in  Avhich  there  is  valvular  disease,  or  some  other  actual  mechanical 
hindrance  to  the  circulation,  or  in  which  the  heart  is  already  suffering  from  func- 
tional strain,  the  matter  seems  to  be  entirely  different.  For  we  must  consider  that 
we  can  not  transfer  unreservedly  to  the  cardiac  muscle  our  current  views  relating 
to  the  voluntary  muscles  of  the  body  with  regard  to  exercise  and  invigoration. 
The  functional  activity  of  the  heart  is  minutely  regulated  by  means  of  an  especial 
reflex  apparatus,  independently  of  our  volition.  We  know  that  every  increased 
demand  upon  the  heart's  activity  is  in  most  cases  directly  fulfilled  by  an  increased 
cardiac  effort.  Under  proper  conditions  the  most  marked  cardiac  hypertrophy 
may  develop  in  a  completely  bedridden  patient.  We  must  therefore  consider 
carefully  whether,  in  cases  of  this  sort,  the  further  increase  of  the  demands  upon 
the  heart  is  judicious;  whether  it  may  not,  on  the  contrary,  contribute  to  a 
pjemature  exhaustion  of  the  myocardium.  It  certainly  seems  to  us,  and  our 
opinion  is  fortified  by  practical  experience,  that  the  prescription  of  increased 


350  DISEASES    OF   THE   CIECULATOEY   OKGAITS 

bodily  exertion,  such  as  mountain-clinibing',  should  always  be  given  with  great 
caution,  and  with  consideration  of  the  individual  circumstances,  if  the  physician 
desires  to  avoid  unhappy  consequences.  It  may  indeed  be  claimed  that  a  cer- 
tain measure  of  bodily  exercise  is  very  suitable  for  many  patients  with  valvular 
and  other  similar  cardiac  lesions,  but  we  hold  that  the  benefit  lies  less  in  the  re- 
sultant "  invigoration  of  the  cardiac  muscle "  than  in  the  promotion  of  the 
venous  circulation  occasioned  by  the  motion  of  the  extremities  and  the  deeper 
inspirations;  or,  in  the  obese,  in  the  increased  metabolism  of  fat  occasioned 
by  the  increased  muscular  effort.  Nevertheless,  the  inconsiderate  prescription 
of  muscular  exertion  has  worked  much  harm.  Long  mountain  trips  have  a  great 
and  unique  value  for  those  circulatory  disturbances  alone  which  are  occasioned 
by  obesity,  or  associated  with  simple  weakness  and  slight  dilatation  of  the  heart. 

3.  Promotion  of  the  Circulation  hy  Massage,  Passive  Movements,  Gymnastics, 
and  Baths.- — It  can  not  be  doubted  that  the  first  three  of  these  are  siiitable  means 
for  the  promotion  of  the  circulation,  especially  in  the  veins.  We  ought  not  to 
overestimate  their  value,  but  we  are  fully  justified  in  the  assertion  that  they  may 
sometimes  be  employed  with  decided  benefit  in  circulatory  derangements.  There 
are  patients  whom  we  dare  not  permit  to  take  general  bodily  exercise,  and  for 
these  there  is  sometimes  great  benefit  in  Swedish  movements  methodically  and 
regularly  pursued,  especially  in  the  form  of  what  is  called  resisted  movements 
with  the  arms  and  legs.  The  employment  of  massage  is  likewise  useful  in  appro- 
priate cases,  in  which  there  are  such  symptoms  as  slight  oedema  and  moderate 
dyspnoea. 

Thermic  stimulation  and  baths  are  considered  to  have  a  strengthening  influ- 
ence upon  the  heart.  About  this  we  have  as  yet  little  physiological  knowledge, 
but  we  can  not  ignore  the  fact  of  the  beneficial  influence  upon  many  cardiac 
patients,  from  the  use  of  lukewarm,  or  warmer  baths,  and  in  particular  the  salt 
baths  and  natural  brine  baths,  containing  carbonic-dioxide  gas,  as  employed  at 
ISTauheim  and  Kissingen,  and  other  places. 

To  sum  up  what  has  been  said,  we  must,  in  every  case  of  beginning  impairment 
of  the  circulation,  give  full  weight  to  the  considerations  just  enumerated.  We 
must  find  out  the  patient's  mode  of  life,  and  determine  and  regulate  his  diet 
and  exercise  according  to  the  individual  circumstances.  In  this  we  must  always 
pay  great  regard  to  the  patient's  constitution,  whether  he  is  obese  or  spare; 
whether  he  is  full-blooded  or  angemic ;  whether  his  muscular  strength  is  great  or 
small.  It  scarcely  seems  necessary  to  go  into  every  detail  in  this  place,  since  all 
the  points  are  repeatedly  discussed  in  other  portions  of  this  book.  We  would 
refer  particularly,  however,  to  the  chapter  on  obesity. 

3.  Hypertrophy  of  the  Heart,  Associated  with  Congenital  Smallness  of  the 

Systemic  Arteries 

{Hypoplasia  of  the  Aorta) 

For  a  considerable  time,  physicians  have  occasionally  noticed  cases,  of  the  sort 
to  be  described,  in  which  weakness  of  the  heart  and  disturbance  of  the  circulation 
appear  at  a  comparatively  early  age.  The  patient  complains  of  palpitation,  dysp- 
noea, and  slight  oedema.  On  examination  we  usvially  observe  ansemia,  combined 
with  more  or  less  cyanosis.  The  cardiac  dullness  is  extended  toward  the  left,  and 
the  apex  of  the  heart  is  displaced  in  the  same  direction.  There  is  no  marked  dila- 
tation of  the  right  ventricle  till  the  later  stages  of  the  disease.  The  heart-sounds 
are  perfectly  clear,  unless  there  may  be  a  murmur  due  to  relative  insufficiency  of 
the  mitral  valve,  or  due  to  imperfect  muscular  contraction.  The  heart's  action  is 
usually  regular,  but  considerably  accelerated;  the  pulse  small  and  the  arteries 
contracted,  but  often  of  high  tension.    We  observe  the  ordinary  symptoms  of  in- 


HYPOPLASIA   OF   THE   AOETA  351 

creasing  circulatory  disturbance,  and  finally  death.  Upon  autopsy  we  find  the 
heart  hypertrophied  and  usually  dilated.  The  valves  are  normal,  but  the  entire 
aorta  and,  in  most  cases,  probably,  the  other  large  arteries,  are  hypoplastic,  though 
otherwise  of  normal  structure.  Such  cases  are  termed  congenital  hypoplasia  of 
the  systemic  arteries,  and  it  is  believed  that  the  hypertrophy  of  the  heart  is  due  to 
the  increased  effort  to  drive  the  blood  through  these  small  vessels. 

In  our  opinion,  this  condition  of  the  blood-vessels  deserves  full  consideration 
in  forming  an  opinion  about  idiopathic  hypertrophy  of  the  heart ;  but,  ordinarily, 
still  other  factors  are  potent  at  the  same  time,  for  we  sometimes  find  this  hypo- 
plasia at  the  autopsy  of  persons  who  showed  no  material  disturbance  of  the  cir- 
culation during  life,  and  in  whom  the  heart  is  of  normal  or  even  less  than  normal 
size.  Virchow  has  called  special  attention  to  the  fact  that  this  sort  of  hypoplasia 
of  the  aorta  and  its  branches  is  sometimes  found  in  association  with  chlorosis,  or, 
perhaps  more  correctly,  with  constitutional  anaemia.  In  these  cases  the  smallness 
of  the  reservoir  diminishes  the  volume  of  blood*  contained  in  it,  but  it  does  not 
have  any  marked  influence  upon  the  heart,  which  indeed  has  a  less  than  normal 
burden  rather  than  an  excessive  one ;  so  that  we  believe  that  in  those  instances  of 
congenital  hypoplasia  of  the  aorta  in  which  there  is  severe  circulatory  disturbance 
there  is  either  coincident  smallness  and  feebleness  of  the  heart  itself  (vide  infra), 
or  an  association  of  the  hypoplasia  with  other  influences  unfavorable  to  the  heart. 
There  have  been  repeatedly  observed  cases  of  cardiac  hypertrophy  due  to  muscular 
strain  (for  instance,  in  soldiers),  or  due  to  excessive  drinking,  in  which  congen- 
ital hypoplasia  of  the  aorta  and  its  branches  has  been  found  in  association  with 
the  hypertrophy  of  the  heart ;  and  in  the  cases  which  we  have  ourselves  seen  and 
in  which  the  diagnosis  was  confirmed  by  autopsy,  there  have  almost  always  been 
some  Other  factors  unfavorable  to  the  heart  besides  this  congenital  abnormality 
of  the  blood-vessels.  Indeed,  one  can  easily  understand  that  the  same  injurious 
influences  which  a  normal  circulatory  apparatus  might  endure  for  a  considerable 
time  without  much  damage,  would  occasion  premature  symptoms  if  the  vascular 
system  were  abnormally  developed. 

The  recognition  of  hypoplasia  of  the  systemic  arteries  during  life  is  probably 
in  every  case  difficult,  and  scarcely  ever  absolutely  certain.  Important  factors 
would  be  the  existence  of  anaBmia  and  a  tendency  to  shortness  of  breath  and  palpi- 
tation from  early  youth;  and  also  the  discovery  by  palpation  that  the  circum- 
ference of  the  arteries  was  less  than  normal.  The  condition  of  the  heart  is  to  be 
determined  in  the  ordinary  manner. 

Prognosis  and  treatment  must  likewise  be  governed  by  the  same  principles  as 
in  other  forms  of  heart  disease. 

4.  Primary  Weakness  of  the  Myocardium 

(Congenital  Weakness  of  the  Heart;    Weakened  Heart;  Acute  Muscular  Strain  of  the  Heart; 

Toxic  Weakness  of  the  Heart) 

If  there  is  a  myopathic  heart  disease,  and  the  heart  is  at  the  same  time  hyper- 
trophied, this  indicates  that  for  a  considerable  time  the  heart  has  done  an  un- 
usual amount  of  work.  In  such  cases,  therefore,  it  can  not  be  that  the  heart 
has  been  feeble  from  the  start.  It  must  indeed  have  been  able  to  do  more  than 
is  normally  demanded  of  it.  It  is  not  until  a  later  period,  when  its  power  is 
impaired,  that  we  can  say  that  the  heart  is  relatively  or  finally  absolutely  feeble. 
There  are  cases,  however,  in  which  the  heart  is  originally  feeble — that  is,  its 
functional  powers  are  below  normal.  This  weakness  is  certainlj^  in  many  in- 
stances, congenital.  It  may  be  expressed  in  the  structure  of  the  heart,  the  organ 
being  tmusually  small  with  thin  walls,  or  merely  in  physiological  incapacity,  the 
organ  being  apparently  of  normal  structure.     In  either  case  the  heart  can  not 


352  DISEASES    OF   THE   CIECULATOEY   OEGAI^S 

satisfy  even  the  ordinary  demands  made  upon  it.  Patients  of  this  sort  complain, 
upon  the  least  exertion,  of  palpitation,  shortness  of  breath,  and  a  sense  of  pres- 
sure over  the  heart.  The  pulse  is  usually  frequent  or,  at  any  rate,  very  easily 
accelerated;  a  short  but  rapid  walk,  for  instance,  may  raise  the  pulse-rate  to 
120  or  140  beats  per  minute. 

In  many  cases  there  are  never  any  severer  symptoms.  The  patient  remains 
through  life  feeble,  and  "  with  a  weak  heart " ;  but  if  his  mode  of  life  is  favorable 
the  heart  manages  to  maintain  the  circulation.  Not  so,  however,  if  unusual 
demands  are  made  upon  it — as,  for  example,  in  the  course  of  military  service,  or 
in  mountain  climbing,  or  in  unsuitable  raodes  of  life.  Then  more  threatening 
symptoms  of  cardiac  insufficiency  appear,  either  suddenly  or  gradually,  and  ex- 
press themselves  objectively  in  dilatation  (or  stretching)  of  the  heart.  In  some 
cases  the  heart  is  not  able  permanently  to  satisfy  even  the  ordinary  demands  made 
upon  it.  We  observe  all  the  symptoms  of  circulatory  disturbance,  and  at  last  upon 
autopsy  find  a  heart  which  is  dilated,  but  not  much  hypertrophied.  Cases  of 
this  sort  are  not  very  frequent,  but  they  certainly  do  occur ;  their  recognition  dur- 
ing life,  however,  is  not  easy,  for  it  is  difficult  to  distinguish  simple  dilatation 
from  insufficiency  which  is  subsequent  to  hypertrophy.  We  shall  probably  be  able 
to  determine  that  there  is  some  muscular  heart  disease  because  of  the  increase  in 
cardiac  dullness,  the  smallness  and  frequency  of  the  pulse,  and  the  ordinary 
tokens  of  disturbed  circulation,  such  as  dyspnoea,  palpitation,  osdema,  and  the 
urine  of  passive  congestion.  If  we  consider  carefully  the  history  of  the  case  and 
the  presence  or  absence  of  special  ^etiological  factors,  we  may  be  able  while  the 
patient  is  still  alive  to  make  a  probable  diagnosis  of  simple  dilatation  of  the 
heart,  as  a  result  of  muscular  weakness. 

Acquired  muscular  weakness  of  the  heart  should  be  distinguished  from  the  con- 
genital variety.  It  is  occasioned  by  the  action  upon  an  originally  normal  heart 
of  influences  which  damage  the  myocardium  or  its  nervous  apparatus.  We  often 
see  temporary  conditions  of  muscular  weakness  of  the  heart  in  anajmia,  or  fol- 
lowing severe  attacks  of  acute  disease.  Even  in  these  cases  there  are  such  differ- 
ences as  to  indicate  a  difference  in  the  original  vigor  of  the  heart.  The  same  is 
true  of  acute  muscular  strain  of  the  heart.  Acute  attacks  of  cardiac  weakness 
are  seen  in  the  case  of  soldiers  at  maneuvers,  or  in  laborious  mountain  climb- 
ing, such  as  has  of  late  been  so  often  undertaken  in  an  ill-considered  manner;  and 
these  attacks  are  usually  associated  with  acute  dilatation.  There  is  a  sudden  and 
enormous  increase  in  the  demands  made  upon  the  heart;  the  amount  of  blood 
which,  in  a  given  period  of  time,  must  pass  through  the  muscles  is  increased; 
and  the  heart  is  unequal  to  the  task.  It  yields  to  the  increased  tension  and  dilates. 
The  pulmonary  circulation  becomes  congested,  the  pressure  in  the  arteries  falls, 
and  we  have  all  the  clinical  phenomena  of  cardiac  insufficiency,  including  dyspnoea, 
cardiac  asthma,  and  sometimes  angina  pectoris.  If  there  is  prompt  cessation  of 
the  effort  and  medical  assistance,  the  condition  may  be  restored  to  normal  and 
so  remain.  This,  for  example,  we  lately  saw  in  the  case  of  a  young  and  healthy 
person  who  escaped  drowning  only  by  desperate  efforts.  But  sometimes  there  re- 
mains behind  a  permanent  weakness  of  the  heart,  whether  because  the  single  ex- 
cessive strain  caused  a  permanent  damage  to  the  heart,  or  because  the  heart  was 
already  of  less  than  normal  vigor,  and  betrayed  its  weakness  for  the  first  time 
when  this  excessive  demand  was  made  upon  it. 

Certain  forms  of  chronic  intoxication  are  among  the  causes  which  frequently 
lead  to  acquired  weakness  of  the  myocardium,  or  its  nerves.  The  most  important 
of  these,  from  a  clinical  standpoint,  is  chronic  alcoholism,  the  noxious  influence 
of  which  upon  the  heart  is  universally  recognized.  Less  frequent,  but  still  of 
practical  importance,  is  chronic  nicotine  poisoning,  or,  to  speak  in  a  more  general 
and  perhaps  more  correct  manner,  the  influence  of  excessive  smoking.     This  is 


FATTY   HEAET  353 

especially  evident  in  persons  who  have  smoked  many  strong-flavored  Havana 
cigars.  The  symptoms  consist  of  an  unpleasant  subjective  sensation  in  the  re- 
gion of  the  heart  (fluttering,  pressure,  or  palpitation),  of  slight  dyspnoea,  and  ob- 
jectively of  a  frequent,  irregular,  or  intermittent  pulse.  Other  objective  cardiac 
signs  are  not  present,  at  least  at  first;  but  there  may  be  still  other  symptoms  of 
chronic  nicotine  poisoning,  such  as  specks  before  the  eyes,  disturbance  of  vision, 
and  dyspepsia.  If  smoking  is  stopped  in  due  time,  the  symptoms  may  vanish. 
Otherwise,  there  follow  severer  disturba.nces  of  the  heart,  although  in  most  cases 
there  are  other  etiological  factors  also  present,  such  as  alcoholism  and  mental 
strain. 

With  regard  to  prognosis  and  treatment,  there  are  few  special  statements  to 
be  made.  If  there  are  signs  of  congenital  weakness  of  the  heart  we  must 
strengthen  the  constitution  in  every  way  possible,  and  we  must  seek  to  give  the 
patient,  on  the  one  hand,  the  proper  amount  of  protection,  and,  on  the  other 
hand,  cautious  and  moderate  exercise  of  the  cardiac  muscle,  by  means  of  medical 
gymnastics;  and  in  other  respects  regimen  and  hygienic  precautions  are  of  first 
importance,  from  a  prophylactic  and  therapeutic  point  of  view.  The  treatment 
of  acute  and  chronic  weakness  of  the  heart  by  such  remedies  as  cardiac  stimulants 
and  digitalis  is  controlled  by  the  ordinary  rules.  Finally,  we  may  mention  in 
this  connection  that  obliteration  of  the  pericardial  sac  by  chronic  pericarditis,  or 
as  a  sequel  of  antecedent  acute  pericarditis  (vide  infra),  sometimes  occasions 
atrophy  of  the  myocardium,  with  resultant  feebleness  and  dilatation  of  the  heart. 
Oases  of  this  sort  may  readily  be  confused  with  primary  cardiac  dilatation. 

5.  The  So-called  Fatty  Heart 

.^Itiology  and  Pathological  Anatomy. — By  the  name  of  "  fatty  heart "  we 
often  mean,  at  present,  two  quite  distinct  conditions  of  the  heart — the  one  an 
abnormal  deposit  of  fat  in  the  heart,  and  the  other  a  fatty  degeneration  of  the 
muscular  fibers  of  the  heart. 

Fatty  overgrowth  and  fatty  infiltration  of  the  heart  are  usually  merely  symp- 
toms of  great  general  obesity.  At  the  autopsy  of  very  fat  people  we  sometimes 
find  the  heart  entirely  inclosed  in  a  thick  capsule  of  fat.  The  fat  is  situated  chiefly 
in  the  external  pericardium  and  beneath  the  visceral  pericardium.  It  is  usually 
abundant  along  the  course  of  the  larger  vessels  within  the  grooves  of  the 
heart,  but  in  marked  cases  the  fat  also  involves  the  muscular  substance,  so  that 
many  groups  of  fat-cells  are  interspersed  between  the  muscular  fibers.  The  heart 
itself  is  otherwise  quite  normal  or  somewhat  hypertrophied  or  dilated.  There  are 
in  some  instances  also  present  sclerosis  of  the  coronary  arteries  and  indurations 
due  to  myocarditis. 

We  have  already  mentioned  fatty  degeneration  of  the  muscular  substance  of 
the  heart  as  a  frequent  result  of  valvular  disease.  In  myocarditis  and  idiopathic 
cardiac  hypertrophy,  and  in  the  hypertrophy  secondary  to  chronic  nephritis 
and  pulmonary  emphysema,  we  also  meet  with  fatty  degeneration.  We  often  find 
fatty  degeneration  of  the  heart,  as  well  as  of  other  organs,  in  severe  acute  infec- 
tious diseases,  in  phosphorus  poisoning,  and  in  all  marked  primary  and  secondary 
anaemias.  Under  the  microscope  we  find  the  muscular  fibrillse  studded  with  little 
drops  of  fat,  which  may  be  so  numerous  that  the  nuclei  and  the  transverse  stria- 
tion  of  the  fibers  are  quite  concealed  by  them.  We  often  find,  besides  the  fatty 
granules,  albuminous  granules,  which  disappear  on  the  addition  of  acetic  acid 
("cloudy  swelling"  of  the  cardiac  muscle).  If  the  fatty  degeneration  is  of  high 
degree,  we  can  easily  recognize  it  with  the  naked  eye.  Beneath  the  endocardium, 
especially  on  the  trabeculae  and  papillary  muscles,  we  see  very  fine  and  delicate 
yellow  points  and  strife.  With  great  fatty  degeneration,  as  in  phosphorus  poison- 
23 


354  DISEASES    OF   THE    CIECULATOEY   OEGAl^TS 

ing  and  pernicious  anaemia,  the  whole  cardiac  muscle  is  manifestly  yellow,  and 
also  soft  and  flabby.  It  is  claimed  that  rupture  of  the  heart  may  occur  as  a  result, 
of  marked  fatty  degeneration. 

In  fatty  degeneration  of  .the  heart  the  fat  comes  from  the  decomposition  of 
albumen  in  the  muscular  cells.  The  occasion  of  it  is  probably  a  defective  supply 
of  oxygen,  which  has  either  a  general  cause,  as  in  ansemia  and  phosphorus  poison- 
ing, or  a  local  cause,  as  disturbed  circulation  in  the  heart  in  heart  disease.  The 
details  of  this  are  given  in  the  chapter  on  ansemia  (page  708). 

Clinical  Symptoms. — Fatty  degeneration  of  the  heart  has  no  characteristic 
clinical  symptoms.  In  the  conditions  under  which  we  know  it  is  apt  to  occur,  we 
can  usually  suspect  it  during  the  lifetime  of  the  patient,  but  we  can  not  diagnos- 
ticate it.  We  must  also  mention  that  the  frequently  expressed  opinion,  that  fatty 
degeneration  of  the  heart  invariably  occasions  general  cardiac  weakness,  is  very 
often  incorrect.  In  pernicious  anemia  there  may  be  quite  a  strong  and  a  per- 
fectly regular  pulse  up  to  death  in  spite  of  the  most  marked  fatty  degeneration,, 
and  many  pei-sonal  observations  lead  us  earnestly  to  dispute  the  view  that  fatty 
degeneration  of  the  heart  is  to  be  regarded  as  the  regular  cause  of  cardiac  insuf- 
ficiency, and  the  consequent  disturbances  of  compensation.  We  have  made  micro- 
scopic examinations  in  many  cases,  and  failed  to  find  any  sign  of  fatty  degenera- 
tion in  the  myocardium,  although  during  life  the  signs  of  cardiac  insufliciency 
were  well  developed.  In  general,  with  our  present  knowledge,  it  is  impossible- 
to  establish  definite  relations  between  the  histological  condition  of  the  muscular 
tissue  of  the  heart  and  its  functional  activity  during  life. 

We  can  not  say  much  that  is  certain  in  regard  to  the  clinical  synaptoms  of  a 
deposit  of  fat  in  the  heart.  "  Fatty  degeneration  of  the  heart  "  always  plays  a  far 
larger  part  in  popiilar  speech  than  it  does  in  reality.  It  is  certainly  a  fact  that 
difficulty  with  the  heart  and  respiration  is  very  often  observed  in  fat  people.  Ex- 
amination of  the  heart,  which,  however,  is  decidedly  impeded  by  the  thick  pannicu- 
lus  adiposus,  often  shows  in  such  cases  an  increase  of  the  cardiac  dullness,  a  small 
and  sometimes  irregular  pulse,  and  faint  but  clear  heart-sounds.  The  disturbance- 
may  be  very  considerable,  attacks  of  angina  pectoris  and  cardiac  asthma  may 
come  on,  and  death  may  follow  with  increasing  dyspnoea  and  general  oedema. 

If  one  has  opportunity  to  make  an  autopsy  in  such  cases,  there  will  be  found 
no  single,  constant  anatomical  change  as  the  cause  of  the  cardiac  disturbance,  but 
usually  idiopathic  hypertrophy  (vide  supra),  or,  less  often,  myocarditic  changes 
with  sclerosis  of  the  coronary  arteries,  and  the  like.  Sometimes,  but  by  no  means 
invariably,  there  is,  of  course,  a  marked  deposit  of  fat  upon  the  heart  itself,  but 
the  question  arises  whether  this  can  directly  and  seriously  embarrass  the  cardiac- 
activity.  The  fact  is  that  we  often  have  seen  similar  well-marked  cases  of  fatty 
heart  which  during  life  presented  no  special  cardiac  symptoms.  There  would  be- 
more  reason  in  ascribing  an  unfavorable  influence  to  the  fatty  infiltration  of  the 
cardiac  muscle;  but  in  such  cases  there  is  almost  always  a  coincident  atrophy  of 
the  muscular  structure,  so  that  it  is  questionable  whether  the  fatty  infiltration 
is  to  be  regarded  as  actually  the  primary  pathological  process.  We  ourselves  are 
far  more  inclined  to  the  view  that  there  is  primary  atrophy  of  the  myocardium, 
with  this  fatty  infiltration  as  a  secondary  phenomenon,  similar  to  the  frequent 
and  well-known  occurrence  of  secondary  lipomatosis  of  atrophic  voluntary  mus- 
cles. At  any  rate,  we  are  as  yet  entirely  unable  to  recognize  cases  of  this  sort 
of  fatty  heart  during  life,  and  it  is  certain  that  they  are  much  less  frequent 
than  the  other  myopathic  diseases  of  the  heart. 

Therefore  we  can  not  associate  with  the  term  "  fatty  heart "  any  uniform- 
anatomical  and  clinical  conception.  It  would  be  better  to  speak  of  the  "  heart- 
of  obesity" — that  is,  of  all  the  manifold  injuries  to  which  the  heart  of  obese  per- 
sons is  exposed. 


CAEDIAC   IsTEUEOSES  355 

According  to  our  experience,  simple  idiopathic  hypertrophy  of  the  heart  is 
certainly  the  most  frequent  of  these  conditions,  and  it  would  be  very  desirable 
if  physicians  would  have  more  reg^ard  to  the  facts  of  pathology,  when  they  are 
inclined  to  make  an  off-hand  diagnosis  of  fatty  heart. 

Treatment. — A  great  part  of  the  disturbance  of  respiration  in  fat  people  de- 
pends not  upon  the  cardiac  weakness,  but  on  the  corpulency  itself.  The  great 
bulk  of  the  body,  and  the  hindrance  to  the  activity  of  the  respiratory  muscles,  are 
very  important  factors.  Treatment  directed  against  the  respiratory  disturbance 
must  hence  attack  the  obesity  chiefly,  and  thus  in  many  cases  we  also  assist  the 
action  of  the  heart.  The  detailed  description  of  the  hygienic  methods  of  cure  to 
be  employed  here  is  to  be  found  in  the  chapter  on  obesity  (page  784). 

In  regard  to  the  special  treatment  of  the  cardiac  symptoms  in  the  obese,  this 
does  not  differ  from  the  rules  that  obtain  in  other  forms  of  heart  disease. 


CHAPTER   lY 
CARDIAC    NEUROSES 

1.  Angina  Pectoris  (Stenocardia). — Angina  pectoris  is  not  an  independent 
disease,  but  a  group  of  symptoms,  to  which  we  have  had  frequent  occasion  to  re- 
fer already;  but  for  a  considerable  time  this  symptom-complex  may  be  the  only 
sign  of  disease.  It  is  the  paroxysmal  occurrence  of  an  extremely  violent  pain 
below  the  sternum  and  in  the  region  of  the  heart,  associated  with  a  feeling  of  the 
greatest  distress  and  oppression  ("  prjecordial  anxiety,"  "  sense  of  impending 
death").  The  pain  is  usually  described  as  cramp-like,  boring,  and  constricting 
It  not  infrequently  radiates  from  the  heart  into  the  shoulders  and  the  left  arm, 
sometimes  as  far  as  the  tips  of  the  fingers.  The  beginning  of  the  attack  is  usually 
absolutely  abrupt.  It  may  last  a  few  minutes  or  half  an  hour,  or  longer.  The 
attacks  may  be  infrequent  with  intervals  of  weeks  or  months,  or  they  may  be 
repeated  several  times  a  day.  Respiration  during  the  attack  is  often  unaffected, 
in  which  point  genuine  angina  pectoris  differs  from  cardiac  asthma.  Many 
patients  indeed  seek  to  lessen  their  pain  by  holding  the  breath,  and  sometimes 
even  in  angina  pectoris  the  respiration  is  hurried  and  irregular.  It  must  be 
pointed  out  that  the  symptoms  of  "  pure  "  angina  pectoris  and  the  symptoms  of 
cardiac  asthma  may  be  clinically  much  intermixed  and  confused.  The  pulse  is 
usually  rapid  and  small  during  an  attack,  and  not  infrequently  irregular.  Some- 
times, however,  we  find  that,  in  spite  of  the  most  violent  pain  and  distress,  the 
pulse  remains  strong,  quiet,  and  apparently  normal.  If  the  hand  is  placed  upon 
the  heart  a  peculiar  wavy  motion  and  "  fluttering  "  is  felt  in  a  few  cases,  and  this 
symptom  the  patient  also  perceives  subjectively.  The  countenance  is  usually  pale 
during  an  attack;  the  hands  feel  cool.  Toward  the  end  of  an  attack  there  is  often 
abundant  perspiration. 

We  are  as  yet  entirely  ignorant  as  to  the  internal  processes  which  are  the 
foundation  of  angina  pectoris.  The  condition  is  often  compared  Avith  neuralgia, 
and  spoken  of  as  "  cardiac  neuralgia."  Other  investigators  suspect  that  there  is 
a  painful  contraction  of  the  blood-vessels  of  the  heart.  It  is  certain  that  angina 
pectoris  rarely  occurs  as  an  independent  disease,  or  pure  neurosis.  Xothnagel 
described  a  vaso-motor  form  of  angina  pectoris  ("  angina  pectoris  vasomotoria  "), 
in  which  there  were  at  the  same  time  distinct  signs  of  vascular  contraction  in 
the  extremities,  as  indicated  by  pallor,  cyanosis,  and  parsesthesife.  In  the  case 
of  excessive   smoking,   also,   angina  pectoris  sometimes   appears   as   a   result   of 


356  DISEASES    OF   THE    CIRCULATORY   ORGAl^S 

chronic  tobacco  poisoniBg,  without  any  other  demonstrable  change  in  the  heart. 
Similar  attacks  may  occur  after  strong  mental  excitement,  but  these  have  more 
or  less  connection  with  certain  forms  of  hysterical  and  neurasthenic  attacks, 
bearing  a  merely  superficial  resemblance  to  angina  pectoris.  The  true  angina 
pectoris  is  most  often  seen  as  a  symptom  in  association  with  certain  diseases  of 
the  heart  and  aorta,  particularly  sclerosis  of  the  coronary  arteries,  insufficiency  of 
the  valves,  aneurism  of  the  root  of  the  aorta;  less  often,  idiopathic  hypertrophy 
of  the  heart,  and  hypertrophy  secondary  to  interstitial  nephritis.  The  way  in 
which  the  other  symptoms  of  these  conditions  may  be  conjoined  with  the  anginous 
attacks  is  sufficiently  clear  from  their  presentation  in  a  previous  chapter. 

We  can  not  speak  of  the  prognosis  of  angina  pectoris  as  a  distinct  entity. 
In  general  angina  pectoris  is  certainly  of  evil  omen,  and  occasionally  death  may 
occur  during  the  attack. 

With  regard  to  the  symptomatic  treatment  of  angina  pectoris,  there  is  no 
doubt  that  in  severe  cases  the  greatest  relief  is  obtained  from  a  subcutaneous  in- 
jection of  morphine.  We  confess  that  the  employment  of  morphine  in  severe 
heart  disease  always  demands  the  greatest  caution,  but  yet  experience  shows  that 
in  numerous  instances  this  remedy  is  excellently  borne,  and  most  beneficial. 
Among  other  remedies  should  be  named  chloral  and  chloralamide,  which  also  are 
to  be  employed  with  caution,  but  which  sometimes  have  a  good  effect ;  nitroglyc- 
erine to  the  amount  of  A  to  A  of  a  grain  (gramme  0.001-0.005),  which  is  highly 
praised  by  many  physicians;  also  nitrite  of  sodium,  and  inhalations  of  amyl 
nitrite,  ether,  or  chloroform.  If  there  are  decided  signs  of  cardiac  weakness, 
camphor,  strophanthus,  and  alcohol  are  to  be  employed  as  stimulants.  An  ice- 
bag  may  be  placed  over  the  heart,  and  sometimes,  also,  hot  applications  are  of 
benefit;  mustard-poultices,  hot  foot-baths,  and  the  like  are  also  frequently  pre- 
scribed in  practice. 

We  must  always  bear  in  mind  the  general  treatment  of  the  underlying  condi- 
tion, as  well  as  the  employment  of  purely  sym.ptomatic  remedies.  Special  atten- 
tion should  be  directed  to  any  setiological  factors,  such  as  muscular  strain,  men- 
tal excitement,  alcoholism,  or  excessive  smoking.  If  we  have  to  do  with  the 
"  purely  nervous  "  form  of  angina  pectoris,  without  any  physical  signs  of  change 
in  the  heart,  we  must  of  course  avoid  the  use  of  the  stronger  narcotic  remedies 
so  far  as  possible,  and  lay  the  main  emphasis  upon  the  general  treatment  of  the 
nervous  system  by  means  of  electricity,  cold-water  cures,  and  psychical  influences. 

[In  well-marked  angina  sudden  death  during  a  paroxysm  is  not  very  rare.  In 
Dr.  Arnold,  of  Rugby,  the  first  attack  proved  fatal.  The  patient  may,  however, 
live  for  years — cases  of  survival  for  upwards  of  twenty,  and  one  even  of  thirty, 
years  being  recorded.  Flint  has  known  recovery  to  occur.  The  prognosis  depends 
somewhat  on  the  condition  of  the  cardiac  valves  and  walls;  but  changes,  espe- 
cially in  the  latter,  may  escape  detection  by  any  save  a  very  skillful  observer. 
Walshe  states  that  in  every  one  of  twenty-four  cases  he  examined  during  life  he 
found  physical  signs  of  changes  either  in  the  heart,  the  aorta,  or  both.  The 
experience  of  Balfour  and  Latham  is  similar.] 

2.  Nervous  Palpitation. — By  "  palpitation "  we  understand  the  subjective 
perception  of  the  movements  of  the  heart.  It  is  usually  excited  by  increased  ac- 
tion of  the  heart,  but  there  is  no  constant  relation  between  the  intensity  of  the 
cardiac  pulsations  and  the  subjective  feeling  of  them.  We  sometimes  observe 
that  patients  with  aortic  insufficiency  do  not  perceive  the  very  strong  action  of 
their  hypertrophied  hearts,  while  in  other  cases  a  patient  complains  of  a  trouble- 
some feeling  of  palpitation,  although  the  action  of  the  heart  does  not  appear 
objectively  to  be  especially  increased. 

We  term  cases  "  nervous  palpitation  "  if  the  patient  complains  of  palpita- 
tion when  a  physical  examination  of  the  heart  shows  no  anatomical  change  in  it. 


CAEDIAC   NEUROSES  357 

As  a  rule,  in  these  cases  we  really  have  to  do  with  a  heart  whose  action  is  increased 
by  abnormal  nervous  influences.  In  many  cases  the  palpitation  arises  from  slight 
external  causes,  which  may  give  rise  to  little  or  no  palpitation  in  a  healthy  per- 
son, as,  for  example,  after  the  slightest  mental  excitement,  after  any  slight  phys- 
ical exertion,  after  taking  food,  after  indulging  in  certain  drinks,  such  as  tea, 
coffee,  wine,  or  beer,  or  after  assuming  certain  positions,  as  in  lying  on  the  left 
side.  Here,  then,  we  have  to  do  with  an  abnormal  sensitiveness  of  the  heart  to 
external  irritation.  Usually  the  increase  in  vigor  of  the  heart's  action  is  associ- 
ated with  a  decided  increase  in  its  frequency.  We  have  often  seen  patients  with 
nervous  palpitation  who  had  a  pulse-rate  of  140  to  160  beats  a  minute  after  com- 
paratively slight  exertion;  but  in  other  cases  there  is  apparently  a  sort  of  hyper- 
sesthesia  of  the  patient  w^ith  regard  to  the  motions  of  the  heart,  so  that  contrac- 
tions of  normal  strength  and  rapidity  give  rise  to  disagreeable  sensations. 

The  patient  rarely  complains  of  continuous  palpitation;  it  usually  occurs  in 
more  or  less  sharply  defined  paroxysms.  Very  commonly  in  pure  nervous  palpi- 
tation we  have  to  do  with  persons  who,  in  general,  suffer  from  nervous,  hysterical, 
and  neurasthenic  symptoms,  or  they  are  anaemic  persons,  chlorotic  girls,  etc. ;  but, 
on  the  other  hand,  nervous  palpitation  may  occur  in  very  full-blooded,  "  plethoric  " 
subjects. 

Often  hypochondriasis  plays  an  important  part,  and  dread  of  heart  disease 
and  the  thought  of  its  possible  consequences  excite  a  palpitation  which  confirms 
the  patient  in  his  delusion. 

The  diagnosis  of  nervous  palpitation  can  be  made  only  when  repeated  careful 
examination  shows  no  objective  abnormality  in  the  heart.  In  many  cases,  as 
when  there  are  anaemic  murmurs,  the  decision  may  be  quite  difiicult.  We  must 
always  pay  particular  attention  to  the  whole  constitution  and  the  general  impres- 
sion which  the  patient  makes. 

It  is  often  especially  difficult  to  distinguish  between  purely  nervous  palpita- 
tion in  a  heart  otherwise  functionally  normal,  and  conditions  of  congenital  or 
acquired  weakness  of  the  heart  (vide  supra). 

The  prognosis  is  so  far  favorable  in  that  the  disease  is  not  dangerous.  In 
many  cases  improvement  and  final  recovery  may  be  effected,  but  other  cases,  of 
course,  resist  all  therapeutic  efforts  very  obstinately. 

The  treatment  must  first  be  directed  to  improving  the  patient's  general  con- 
stitution. The  antemic  are  to  be  given  iron,  quinine,  and  strengthening  diet. 
We  put  full-blooded  persons,  however,  on  scanty  fare,  and  prescribe  for  them 
bitter  waters,  or  a  bath  cure  at  Marienbad  or  Kissingen.  When  there  is 
hysteria  or  neurasthenia,  it  requires  special  treatment.  If  the  patient  is  hypo- 
chondriacal, of  course  the  main  thing  is  for  the  physician  to  reassure  him.  We 
should  avoid  all  the  influences  which  seem  to  excite  palpitation.  As  a  symptom- 
atic indication  during  an  attack  we  should  recommend  the  patient  especially  to 
keep  quiet.  The  use  of  cold  to  the  cardiac  region — cold  compresses  and  ice-bags 
— often  acts  beneficially.  On  the  other  hand,  however,  it  is  to  be  noted  that  a 
tendency  to  palpitation  associated  with  cardiac  weakness  may  often  be  allayed 
by  methodical  exercise  and  the  invigoration  of  the  cardiac  muscle  consequent 
thereupon  (see  the  preceding  chapter).  Among  internal  remedies  we  must  employ 
nervines,  and  in  severer  cases  even  narcotics.  Among  the  former  we  would  men- 
tion especially  ethereal  tincture  of  valerian  and  bromide  of  potassium,  which  have 
repeatedly  done  us  good  service.  Digitalis  is  lasually  of  little  value  in  pure  nevi- 
roses  of  the  heart,  but  we  may  give  it  as  an  experiment,  say  fifteen  to  twenty  drops 
of  the  tincture  with  the  same  amount  of  cherry-laurel  water. 

3.  Tachycardia  (Paroxysmal  Tachycardia). — A  peculiar  and  quite  rare  neu- 
rosis of  the  heart,  tachycardia,  consists  of  an  enormous  frequency  of  the  pulse, 
coming  on  in  paroxysms,  up  to  160-200  beats  and  more  a  minute. 


358  DISEASES    OF   THE    CIRCULATORY   ORGAN'S 

We  have  already  mentioned  these  attacks  as  a  rare  symptom  in  mitral  and 
aortic  valvular  disease  and  in  diseases  of  the  myocardium,  but  precisely  similar 
attacks  occur  as  a  pure  neurosis  without  demonstrable  lesion  of  the  heart,  particu- 
larly in  anaemic,  nervous,  or  obese  individuals.  We  saw  one  very  well-marked  case 
in  a  lady  with  extreme  neurasthenic  melancholia.  The  attacks  occurred  many 
times  a  day,  each  lasting  only  a  few  minutes.  We  were  often  able  while  feeling 
the  pulse  to  notice  that  it  suddenly  became  extremely  rapid,  and  then  in  a  brief 
time  almost  with  equal  suddenness  resumed  its  approximately  normal  rate.  We 
have  seen  many  similar  attacks  of  genuine  tachycardia,  although  not  so  extreme, 
in  young  and  neurasthenic  individuals,  following  muscular  exertion — for  example, 
in  soldiers.  Similar  states  develop  sometimes  after  diphtheria  {q.  v.),  and  after 
other  acvite  infectious  diseases ;  but  in  such  instances  the  tachycardia  is  usually 
more  continiTOUS  and  not  so  distinctly  paroxysmal. 

In  men  we  must  consider  the  possibility  of  the  action  of  injurious  habits,  such 
as  drinking  and  smoking.  The  individual  attack  usually  begins  quite  suddenly, 
by  day  or  by  night,  sometimes  without  any  cause,  but  often  it  is  apparently  pro- 
duced by  certain  exciting  causes,  especially  at  times  by  overdistention  of  the 
stomach.  The  patient  feels  that  the  attack  is  coming,  he  becomes  anxious  and 
restless,  and  looks  pale ;  but  there  are  not,  as  a  rule,  at  least  according  to  our 
experience,  any  symptoms  like  precordial  anxiety,  dyspnoea,  or  attacks  of  faint- 
ness.  We  notice  in  the  heart  itself,  during  the  attack,  chiefly  a  great  acceleration 
of  the  heart-sounds.  We  sometimes  hear  indefinite,  functional  murmurs.  The 
action  of  the  heart  is  often  quite  regular,  but  there  is  not  infrequently  manifest 
arhythmia  during  the  attack.  Acute  increase  of  the  heart's  dullness  has  been 
observed  during  the  attack.  We  have  repeatedly  been  able  to  verify  a  marked 
temporary  dilatation  of  this  sort,  particularly  in  patients  with  heart  disease,  and 
also  in  one  case  of  paroxysmal  tachycardia  affecting  a  sufferer  from  cirrhosis  of 
the  liver.  In  other  instances  and  especially  when  the  tachycardia  is  a  mere  neu- 
rosis, no  such  dilatation  of  the  heart  can  be  made  out. 

We  know  little  that  is  definite  as  to  the  nature  of  the  attacks.  The  affection 
is  usually  regarded  as  a  temporary  paralysis  of  the  vagus. 

We  may  also  state  here  that  paroxysmal  and  constant  tachycardia  have  also 
been  repeatedly  observed  in  anatomical  lesions  of  the  cardiac  nerves  and  their 
centers,  in  tumors  and  other  affections  in  the  vicinity  of  the  medulla  oblongata, 
and  in  compression  of  the  vagus  in  the  neck  from  new  growths,  and  aneurisms. 

The  prognosis  of  tachycardia  depends  first  upon  the  nature  of  the  underlying 
disease.  We  do  not  know  whether  a  permanent  recovery  is  possible  in  idiopathic 
cases,  but  we  can  always  succeed  in  improving  the  condition.  The  treatment  dur- 
ing the  attack  consists  in  enjoining  complete  bodily  rest,  and  in  applying  ice  to 
the  heart.  Such  sedatives  as  bromide  of  potassium,  water  of  bitter  almonds,  and 
tincture  of  valerian  are  particularly  beneficial  in  the  '•'  purely  nervous "  cases. 
Sometimes  the  physician  may  even  be  consti^ained  to  the  cautious  injection  of 
small  amounts  of  morphine.  In  other  respects  our  treatment  is  determined  mainly 
by  the  underlying  condition,  if  known.  [If  there  is  reason  to  think  that  the 
stomach  is  overloaded,  gentle  measures  should  be  taken  to  empty  it. — V.]  The 
best  way  to  guard  against  the  return  of  the  attacks  is  to  give  precise  hygienic 
directions,  suited  to  the  patient's  constitution  and  manner  of  life.  The  contin- 
ued use  of  iodide  of  potassium  has  sometimes  seemed  to  us  to  be  of  service. 


PERICARDITIS  359 

SECTION   II 

Diseases  of  the  Pericabdiuai 

CHAPTER  I 

PERICARDITIS 

{Inflammation,  of  the  Pericardiu7)i) 

etiology. — Pericarditis  seldom  appears  as  a  primary  idiopathic  disease.  It  is 
usually  merely  a  sequel  or  a  complication  of  other  diseases.  Thus,  it  is  observed 
with  particular  frequency  in  the  course  of  acute  articular  rheumatism,  where  it 
appears  sometimes  alone,  sometimes  in  combination  with  acute  endocarditis.  It 
is  not  impossible  that  some  few  cases  of  apparently  primary  acute  pericarditis 
belong,  from  an  setiological  standpoint,  to  acute  articular  rheumatism — that  is, 
they  are  excited  by  the  same  pathogenic  factors  which  exceptionally  attack  the 
pericardium  alone,  without  simultaneous  participation  of  the  joints  in  the  disease. 
This  supposition  is  rendered  probable  from  the  later  course  of  many  such  cases. 
Eor  instance,  arthritis  may  ensue.  Cases  of  secondary  pericarditis,  unassociated 
with  articular  rheumatism,  occur,  although  much  less  often,  in  other  acute  infec- 
tious diseases,  among  which  scarlet  fever,  measles,  and  septico-pysemic  processes, 
as  well  as  scurvy  and  purpura  haemorrhagica,  deserve  especial  mention.  In  sepsis 
and  pyaemia  the  pericarditis  is  purulent,  and  in  purpura,  hsemorrhagic.  Among 
the  chronic  diseases  in  the  course  of  which  pericarditis  sometimes  appears  we 
must  mention  especially  chronic  nephritis.  We  have  seen  hsemorrhagic  peri- 
carditis in  association  with  leukaemia.  Pericarditis  sometimes  occurs  also  in  the 
victims  of  carcinoma,  but  here  it  is  probably  dependent  upon  a  secondary  septic 
infection.  Finally,  it  should  be  mentioned  that  severe  hsemorrhagic  pericarditis 
is  seen  comparatively  often  in  alcoholic  subjects,  and  apparently  as  a  primary 
•disease.  Often  it  is  really  tubercular,  but  by  no  means  always;  and  if  not,  the 
author  is  inclined  to  regard  it  as  a  primary  hsemorrhagic  inflammation,  analogous 
to  hsemorrhagic  pachymeningitis  or  hsematoma  of  the  dura  mater. 

A  large  number  of  cases  arise  from  an  extension  of  the  inflammation  from  the 
vicinity.  Thus  we  not  infrequently  see  pericarditis  as  a  result  of  pleurisy,  espe- 
cially on  the  left  side,  and  in  pneumonia  complicated  with  pleurisy.  New  growths 
and  ulcerative  processes  in  the  oesophagus,  in  the  vertebrse,  in  the  bronchial  glands, 
or  in  the  lungs,  also  lead  at  times  to  perforation  into  the  pericardium  and  a  con- 
sequent inflammation.  It  is  not  settled  whether  the  pericarditis,  which  appears  in 
the  course  of  chronic  valvular  disease,  is  also  to  be  regarded  as  arising  from  ex- 
tension by  contiguity.  We  have  thought  of  this  possibility,  because  we  have  been 
struck  with  the  fact  that  secondary  pericarditis  is  especially  frequent  in  valvular 
disease  of  the  aorta,  suggesting  a  direct  propagation  of  the  inflammatory  genus 
through  the  aortic  wall  to  the  pericardium.  Still,  it  must  of  course  be  allowed 
that  this  form  of  pericarditis  may  have  an  independent  origin,  particularly  in 
cases  of  mitral  disease.  Pericarditis  may  also  develop  as  a  result  of  myocarditis, 
abscess  of  the  heart,  etc. 

Tuberculosis  plays  a  very  important  part  in  the  setiology  of  pericarditis.  No 
small  number  of  apparently  primary  cases  of  pericarditis  turn  out  at  the  autopsy 
to  be  tubercular.  This  seems  to  come  on  in  quite  an  isolated  way,  or  as  one 
symptom  of  a  special  localized  form  of  tuberculosis,  which  we  term  tuberculosis 
of  the  serous  membranes.  In  many  cases  we  can  discover  the  origin  of  a  tuber- 
cular pericarditis  in  the  direct  extension  of  a  tubercular  pleurisy.  In  apparently 
primary  cases  the  occurrence  of  the  infection  may  sometimes  be  explained  bj^  the 


360  DISEASES    OF   THE   CIECULATOEY   OEGANS 

discovery  of  a  tubercular  lymph-gland,  which  has  broken  through  into  the  peri- 
cardium. 

Pericarditis  is  usually  a  disease  of  youth  and  middle  life,  but  it  may  also  occur 
in  advanced  age. 

Pathological  Anatomy. — Ordinary  pericarditis  involves  the  internal  surface 
of  the  pericardium  in  either  a  circumscribed  or  diifuse  manner.  Inflamma- 
tion of  the  outer  surface  of  the  pericardial  sac  is  distinguished  as  external 
pericarditis  (vide  infra).  The  anatomical  processes  in  pericarditis  are  precisely 
analogous  to  those  in  inflammations  of  the  serous  membranes  in  general,  especially 
of  the  pleura. 

We  usually  divide  pericarditis  into  fibrinous,  sero-fibrinous,  hsemorrhagic,  and 
purulent  (or  ichorous)  forms,  according  to  the  character  of  the  exudation.  The 
fibrinous  and  sero-fibrinous  forms,  with  an  abundant  fluid  effusion  into  the  peri- 
cardial cavity,  are  the  most  frequent,  occurring  in  articular  rheumatism,  in  valvu- 
lar disease  of  the  heart,  etc.  Both  layers  of  the  pericardium  are  covered  with 
masses  of  fibrine,  which  often  show  a  reticular  or  villous  arrangement  (cor 
villosum).  Besides  this,  we  find  more  or  less  of  a  fluid  effusion  which  distends 
the  pericardium.  The  fluid  is  of  a  serous  nature,  contains  more  or  less  numer- 
ous flakes  of  fibrine,  and  is  turbid  from  the  admixture  of  cells — pus-corpuscles, 
and,  in  part,  desquamated  endothelium.  A  purulent  pericarditis  is  always  the 
expression  of  a  specific  infection  of  the  pericardium.  It  is  seen  in  pysemic  dis- 
eases, as  a  result  of  empyema,  and  in  perforation  of  abscesses,  cancers  of  the  oesoph- 
agus, etc.,  into  the  pericardium.  A  hsemorrhagic  effusion  is  seen  chiefly  in  tuber- 
cular pericarditis.  In  this  we  flnd  miliary  tubercles,  and  little  cheesy  nodules  in 
the  inflammatory  new  growths,  besides  all  the  signs  of  inflammation.  The  specific 
tubercular  changes  are  sometimes  recognizable  with  the  naked  eye,  but  at  other 
times  we  have  to  use  the  microscope  to  find  them.  Hsemorrhagic  pericarditis  also 
occurs  in  general  hsemorrhagic  diseases,  such  as  scurvy,  and  in  weak  and  debili- 
tated persons,  especially  drunkards  (vide  supra). 

In  long-continued  pericarditis  the  cardiac  muscle  almost  invariably  undergoes 
changes.  The  heart  is  usually  flabby  and  dilated,  and  the  muscle  often  shows 
fatty  degeneration.  After  the  pericarditis  has  lasted  a  long  time  there  is  often 
considerable  atrophy  of  the  cardiac  muscle,  which  is  partly  replaced  by  fat  tissue. 
We  have  already  mentioned  the  occurrence  of  pericarditis  in  connection  with 
valvular  disease  and  degenerations  of  the  myocardium. 

In  favorable  cases  of  pericarditis  we  may  have  a  perfect  recovery.  The  so- 
called  maculcB  tendinece  sometimes  remain  in  the  pericardium  as  residua  of  a 
past  circumscribed  pericarditis.  In  some  cases  the  pericarditis  leads  to  an  adhe- 
sion of  the  two  layers  of  the  pericardium  to  each  other,  and  obliteration  of  the 
pericardial  cavity  (vide  infra).  In  many  cases  a  chronic  pericarditis  finally  de- 
velops from  the  acute  form,  or  the  whole  affection  takes  a  more  chronic  course 
from  the  outset.  In  this  way  chronic  adhesions  of  connective  tissue  arise,  and 
great  thickening  of  the  pericardium,  but  the  amount  of  fluid  is  usually  small. 
Sometimes  the  chronic  pericarditis  is  interrupted  by  an  acute  exacerbation  of  the 
disease. 

Clinical  Symptoms. — 1.  SuhjecUve  Symptoms,  General  Symptoms,  and  Fever. 
— Mild  forms  of  pericarditis  may  develop,  as  in  the  course  of  an  acute  articular 
rheumatism,  without  causing  any  subjective  symptoms.  They  are  discovered  only 
by  a  careful  physical  examination  of  the  heart.  In  severe  cases,  however,  the  peri- 
carditis causes  violent  subjective  symptoms,  which  of  course  have  in  themselves 
little  that  is  characteristic. 

On  careful  questioning  we  often  find  that  there  is  pain  in  the  cardiac  region, 
or  not  infrequently  in  the  epigastrium.  This  pain  is  of  decided  diagnostic  impor- 
tance, but  it  does  not  always  exist. 


PEEICAEDITIS  361 

A  general  feeling  of  constraint  and  distress  is  almost  constant  in  all  acute  cases 
of  any  severity,  and  so  is  a  feeling  of  dyspnoea,  which  may  increase  to  the  highest 
degree  of  orthopnoea.  The  patients,  often  complain  of  headache.  In  severe  cases 
they  become  stupid  and  comatose. 

It  is  easy  to  understand  that  extensive  pericarditis  must  impede  the  motions 
of  the  heart.  Probably  the  most  important  way  in  which  it  does  this  is  by  in- 
creasing the  tension  in  the  pericardium,  and  thus  embarrassing  the  diastole  of  the 
ventricles,  so  that  the  cavities  of  the  heart  are  not  normally  filled  and  general  dis- 
turbance of  the  circulation  ensues.  Furthermore,  the  pericarditic  deposits  and 
adhesions,  and  such  changes  in  the  myocardium  as  may  occur,  interfere  with  the 
cardiac  systole.  Thus  are  explained  the  early  signs  of  diminution  in  the  amount 
of  blood  received  by  the  arteries,  as  shown  by  pallor  and  cerebral  anaamia;  the 
distention  of  the  systemic  veins,  as  shown  by  cyanosis ;  and  the  disturbance  of  the 
pulmonary  circulation,  causing  dyspnoea. 

The  dyspnoea  is  also  increased  in  large  pericardial  effusions  by  the  mechanical 
pressure  of  the  distended  pericardium  on  the  left  lung. 

Acute  pericarditis  is  usually  associated  with  fever.  This  has  no  special  type, 
and  usually  keeps  at  a  moderate  height— 102°  to  103.5°  (39°-39.8°C.)— but  it 
often  exhibits  considerable  variations.  In  cases  of  recovery  the  fever  declines  by 
lysis.    Chronic  pericarditis  may  run  its  whole  course  without  fever. 

2.  Physical  Signs — Inspection. — The  general  hne  of  a  patient  with  severe 
pericarditis  is  pale,  but  also  more  or  less  cyanotic.  He  has  an  anxious  expression. 
He  lies  with  the  upper  part  of  the  body  raised,  or  he  sits  up  in  bed.  The  breath- 
ing is  usually  rapid,  labored,  and  somewhat  irregular.  The  veins  in  the  neck  are 
swollen  and  prominent.  We  very  often  see  marked  undulating  or  pulsating 
movements  in  the  jugular  veins,  as  a  result  of  stasis.  The  cardiac  region  seems 
unusually  prominent  in  all  cases  with  much  effusion,  and  the  intercostal  spaces 
there  are  flattened  out.  We  sometimes  detect  a  slight  oedematous  swelling  of  the 
chest-wall  itself. 

If  the  action  of  the  heart  is  powerful  and  the  exudation  small,  the  heart's 
movements  may  be  distinctly  visible.  In  other  cases  they  are  seen  only  faintly, 
and  they  may  be  noticeably  diffuse.  If  the  exudation  is  abundant,  or  if  adhesions 
occur  (vide  infra),  they  may  disappear  altogether. 

Palpation  in  the  milder  cases  shows  the  apex-beat  in  its  normal  position  and 
of  about  normal  strength ;  but  if  the  amount  of  the  pericardial  effusion  increases, 
the  heart  is  pushed  away  from  the  chest-wall  by  it,  and  hence  the  heart-beat 
grows  weaker  until  it  disappears  entirely.  In  such  cases  it  is  sometimes  to  be  felt 
again  if  the  patient  bends  forward  or  lies  on  his  left  side.  In  the  rest  of  the  car- 
diac region  we  sometimes  feel  the  movements  feebly,  but  they  entirely  disappear 
as  the  effusion  increases.  There  is  diagnostic  importance  in  the  contrast  between 
the  great  extent  of  cardiac  dullness  (inde  infra)  and  the  faintly  distinguishable 
motions  of  the  heart,  with  absence  of  a  distinct  apex-beat  and  any  marked  epi- 
gastric pulsation.  In  some  cases,  by  laying  the  hand  flat  on  the  chest,  we  can 
feel  the  rub  of  the  rough  pericardial  surfaces  against  each  other. 

The  pulse  is  usually  accelerated,  and  in  severe  cases  it  becomes  irregular.  In 
every  large  effusion,  as  we  have  already  said,  the  tension  and  height  of  the  pulse 
are  diminished.  In  severe  cases  the  pulse  sometimes  becomes  very  small  and  weak, 
but,  when  the  heart  is  otherwise  normal  and  strong,  it  may  also  remain  quite 
strong — and  indeed  this  condition  of  the  pulse,  in  contrast  to  the  gi'eat  weaken- 
ing of  the  heart-beat,  is  sometimes  of  diagnostic  significance.  In  some  eases  with 
a  large  pericardial  effusion  we  have  seen  a  manifest  pulsus  paradoxus — that  is,  a 
diminution  or  a  complete  disappearance  of  the  radial  pulse  on  every  inspiration. 

Changes  in  percussion-resonance  are  evident  as  soon  as  the  pericardial  sac  is 
distended  with  exudation.     The  so-called  triangular  shape  of  cardiac  dullness  is 


362  DISEASES    OF   THE    CIECULATORY   ORGANS 

regarded  as  especially  characteristic  of  large  pericardial  exudations.  The  blunt 
apex  of  the  triangle  is  found  above  in  the  second  or  third  left  intercostal  space, 
near  the  edge  of  the  sternum.  The  lateral  boundaries  run  obliquely  to  the  right 
and  downward  to  about  the  right  parasternal  line,  and  to  the  left  and  downward 
to  the  left  mamniillary  line,  or  beyond.  The  broad  base  of  the  triangle  which  lies 
below  is  usually  not  to  be  defined  by  percussion,  on  account  of  the  adjacent  left 
lobe  of  the  liver.  On  the  border  of  the  dullness  we  often  find  a  tympanitic  reso- 
nance due  to  the  retraction  of  the  adjacent  lung. 

In  general,  the  author's  personal  experience  forces  him  to  say  that  we  must 
not  be  too  dogmatic  in  the  establishment  of  special  shapes  of  cardiac  dullness, 
as  peculiar  to  pericarditis.  The  fact  of  enlargement  of  the  area  of  cardiac  dull- 
ness, and  the  marked  sense  of  resistance  upon  percussion,  are  important  signs,  but 
there  is  a  considerable  variety  in  the  shapes  of  the  dull  area,  although  extension 
of  the  dullness  upward  and  to  the  right  may  be  regarded  as  particularly  frequent. 
According  to  Ebstein's  observations,  the  first  change  in  percussion  in  incipient 
•exudation  is  usually  an  extension  to  the  right  of  the  heart's  apex,  in  a  triangle 
between  the  heart  and  the  liver. 

The  area  of  the  dullness  depends,  of  course,  in  the  first  place,  upon  the  amount 
■of  the  effusion,  but  we  must  take  special  notice  that  in  regard  to  this  the  relation 
is  not  constant.  In  old  cases  of  pericarditis  especially  we  sometimes  fijid  the 
cardiac  dullness  very  extensive,  while  the  autopsy  detects  only  a  little  fluid  in  the 
pericardium.  This  is  explained  partly  by  a  secondary  dilatation  of  the  heart,  and 
partly  by  a  persistent  retraction  of  the  lung. 

It  is  an  often-mentioned  but  seldom  available  diagnostic  sign  of  pericarditis 
that  in  many  cases  the  still  perceptible  apex-beat  lies  within  the  cardiac  dullness, 
since  the  pericardial  effusion  extends  farther  to  the  left  than  the  heart  itseK.  It 
is  also  worthy  of  note  that  the  dullness  in  pericarditis  often  shows  very  great 
changes  when  the  patient  changes  his  position.  The  dullness  is  more  extensive 
when  the  body  is  erect  than  when  lying  down,  and  when  the  patient  lies  on  his 
side  it  sometimes  shows  a  lateral  displacement  of  several  centimetres.  The  same 
changes,  however,  though  rarely  so  marked,  also  occur  in  a  hypertrophied  heart. 

The  characteristic  pathognomonic  auscultatory  sign  of  pericarditis  is  the  peri- 
cardial friction-rub.  This  arises  during  the  movements  of  the  heart  from  the 
rubbing  of  the  rough  and  inflamed  pericardial  surfaces  against  each  other.  The 
friction-rub  is  absent  in  pericarditis  if  the  rough  surfaces  of  the  two  layers  of  the 
pericardium  are  separated  from  each  other  by  a  considerable  fluid  effusion,  or  if 
they  can  no  longer  rub  against  each  other  from  an  adhesion  of  the  layers  of  the 
pericardium.  We  usually  hear  the  friction-rub  loudest  in  the  neighborhood  of 
the  base  of  the  heart,  but  it  may  also  be  heard  at  other  parts  of  the  heart.  In 
general  the  adventitious  sounds  of  pericarditis  are  not  transmitted  to  any  great 
■distance.  The  quality  of  the  sound  is  described  as  rubbing,  grating,  or  scratching. 
The  friction-rub  may  be  heard  chiefly  either  during  the  systole  or  during  the 
diastole  of  the  heart,  but  it  is  in  general  not  often  closely  associated  with  the 
phases  of  the  heart's  action.  We  sometimes  find  it  intermitting  frequently,  and 
jerky.  The  intensity  of  the  friction-rub  sometimes  varies  with  the  phases  of  the 
respiration.  It  is  usually  louder  on  inspiration,  but  sometimes  on  expiration.  If 
the  patient  changes  his  position,  the  intensity  of  the  sound  is  sometimes  altered. 
It  is  louder  when  sitting  up  than  Ijing  down,  etc.  The  friction-rub  often  sounds 
louder  if  the  stethoscope  is  pressed  fimily  against  the  chest,  since  in  this  way  the 
layers  of  the  pericardium  are  approximated  to  each  other. 

The  heart-sounds,  when  the  valves  are  intact,  may  sometimes  be  heard  as  well 
as  the  friction-rub,  or  they  may  be  completely  drowned  by  the  loud  rub,  at  least 
in  some  parts  of  the  heart.  In  general,  they  are  faint  in  every  case  of  pericardial 
effusion,  since  their  conduction  to  the  ear  is  impaired.     In  large  effusions  where 


PERICAEDITIS  363 

no  friction-rub  is  to  be  heard,  we  hear  the  heart-sounds,  especially  the  first,  but 
only  very  faintly  and  obscurely.  This  condition,  in  connection  with  the  increase 
of  the  cardiac  dullness,  is  of  diagnostic  importance.  If  there  is  also  valvular  dis- 
ease with  the  pericarditis,  the  pericardial  and  endocardial  murmurs  are  some- 
times hard  to  distinguish  from  each  other,  but  usually  the  former  greatly  pre- 
ponderate. 

3.  Sequelce  of  Pericarditis. — A  large  pericardial  effusion  may  excite  special 
symptoms  from  pressure  on  the  neighboring  organs.  Thus  we  have  already  said 
that  compression  of  the  left  lung  must  increase  the  dyspnoea.  In  many  cases  we 
also  notice  a  moderate  dullness  over  the  left  lower  back,  from  compression  of  the 
left  lower  lobe.  Not  infrequently  there  is  a  combination  of  pericarditis  and  left- 
sided  pleurisy  with  effusion.  In  rare  cases  difficulty  in  deglutition  has  been  ob- 
served as  a  result  of  pressure  on  the  oesophagus,  and  paralysis  of  one  vocal  cord 
from  pressure  on  the  recurrent  nerve. 

In  cases  of  long-continued  pericarditis  the  same  sequelae  may  develop  as  in  any 
<ihronic  disease  of  the  heart.  The  amount  of  urine  diminishes  as  a  result  of  the 
low  arterial  pressure.  The  venous  stasis  finally  leads  to  general  dropsy  and  to 
symptoms  of  passive  congestion  in  the  liver,  spleen,  and  kidneys.  We  would  also 
state  that  we  have  repeatedly  met  with  large  effusions  in  the  cavities  of  the  body, 
especially  hydrothorax,  without  any  oedema  of  the  skin.  All  the  symptoms  of 
stasis  mentioned,  however,  are  often  due  much  less  to  the  pericarditis  itself  than 
to  the  atrophy  and  dilatation  of  the  heart  which  frequently  follow  it  (vide 
supra). 

Special  Forms  of  Pertcarditis 

1.  Pericarditis  externa  and  Mediastino-pericarditis  (Pleuro-pericarditis). — 
By  pericarditis  externa  we  mean  an  inflammation  of  the  external  surface  of  the 
pericardial  sac,  which  is  usually  combined  with  an  inflammation  of  the  mediastinal 
connective  tissue  and  the  neighboring-  pleura,  especially  over  the  lingula  of  the  left 
lung.  This  form  of  pericarditis  may  exist  by  itself,  or  it  may  be  combined  with 
internal  pericarditis.  It  is  a  rare  disease,  and  is  most  frequently  seen  as  a  result 
of  tubercular  pleurisy. 

The  physical  signs  must  differ  so  much,  according  to  the  localization  and  extent 
of  the  process,  that  we  can  give  few  general  data  in  regard  to  them.  There  are 
only  a  few  peculiar  signs,  which  must  be  noted  as  characteristic  of  many  cases.  In 
the  vicinity  of  the  apex-beat,  or  at  the  left  border  of  the  cardiac  dullness,  we  some- 
times hear  a  so-called  extra-pericardial  (pleuro-pericardial)  friction-rub.  This 
depends  both  upon  the  cardiac  movements  and  upon  the  respiratory  movements. 
The  friction  sound  often  becomes  louder  during  inspiration,  or,  again,  it  may  be 
aiidible  only  when  the  lungs  are  fully  inflated.  On  holding  the  breath  we  hear 
merely  the  sound  due  to  the  pulsations  of  the  heart,  while  on  deep  breathing-  the 
pleuritic  friction-sound  is  also  to  be  heard.  In  individual  cases  there  are  many 
modifications,  which  can  not  all  be  mentioned.  Another  interesting-  sign,  first 
found  by  Griesinger  and  Kussmaul  in  a  cicatricial  mediastino-pericarditis,  is  the 
so-called  pulsus  paradoxus.  This  consists  of  a  diminution  of  the  pulse  at  each 
inspiration.  This  condition  arises,  in  part  of  the  cases  at  least,  from  the  fact  that 
the  bands  and  adhesions  of  connective  tissue  at  the  origin  of  the  aorta  mechan- 
ically nick  into  and  contract  its  lumen  at  every  inspiratory  movement  of  the 
thorax.  This  explanation,  of  course,  does  not  suffice  for  all  cases,  since  the  pulsus 
paradoxus  also  occurs  under  other  conditions,  as  with  large  pericardial  effusions. 
In  some  cases  there  may  be  seen  a  marked  swelling  of  the  jugular  veins  in  the 
neck  at  each  inspiration,  at  the  same  time  with  the  pulstis  paradoxus,  since 
the  large  venous  trunks  also  undergo  a  mechanical  nicking  and  constriction  at 
each  inspiration.    We  have  ourselves  seen  a  very  pronounced  slowing  of  the  pulse 


364  DISEASES    OF   THE   CIECULATOEY   OEGANS 

at  every  inspiration,  in  a  complicated  case  of  extra-pericardial  adhesions  (vagus 
irritation?).  We  must  also  mention  that  Eiegel  observed  a  disappearance  of  the 
apex-beat  on  expiration  in  some  cases  where  there  were  bands  of  connective  tissue 
between  the  lungs  and  the  outer  surface  of  the  heart.  At  every  expiration  the 
bands  were  stretched  more  tightly,  and  hence  checked  the  movements  of  the  heart. 

2.  Obliteration  of  the  Pericardial  Cavity  (Adhesive  Pericarditis;  Adhesions 
of  the  Layers  of  the  Pericardium;  Concretio  seu  Synechia  pericardii). — ^We  may 
have  a  more  or  less  complete  adhesion  of  the  two  layers  of  the  pericardium  with 
each  other  as  a  result  of  pericarditis.  We  can  sometimes  observe  the  occurrence 
of  this  condition  during  the  course  of  a  pericarditis.  Quite  frequently,  however, 
we  meet  with  extensive  adhesions  of  the  two  layers  of  the  pericardium  at  autopsies, 
without  being  able  to  gather  any  history  of  a  previous  acute  pericarditis.  The 
pericarditis  must  have  occurred  here  in  a  chronic  way,  and  without  symptoms  from 
the  outset. 

Even  extensive  adhesions  of  the  pericardial  surfaces  may  develop  and  remain 
entirely  without  symptoms,  and  be  met  with  accidentally  at  the  autopsy.  In 
other  cases,  however,  the  obliteration  of  the  pericardial  sac  causes  special  physical 
signs  and  severe  clinical  sequelae.  Of  the  physical  signs,  one  of  the  best-known  and 
most  discussed  is  the  systolic  retraction  of  the  chest,  either  limited  to  the  apex  or 
involving  a  larger  area.  This  is  most  comprehensible  if  there  is  an  adhesion  of 
the  pericardium  with  the  heart,  and  also  with  the  chest-wall  (Skoda)  ;  but  we  cer- 
tainly find  this  retraction  at  the  systole  without  co-existing  extra-pericardial  adhe- 
sions. It  is  not,  however,  an  absolutely  certain  sign  of  an  intra-pericardial  adhe- 
sion, especially  if  we  have  to  do  with  a  systolic  retraction  at  the  apex  alone,  or 
limited  to  the  third  or  fourth  intercostal  space,  since  systolic  retractions  may  some- 
times occur  in  other  disturbances  of  the  heart's  motions,  or  even  under  normal 
conditions;  but  systolic  retractions  of  the  whole  cardiac  region  are,  in  the  major- 
ity of  cases,  a  certain  sign  of  pericardial  adhesion.  The  amount  of  this  retraction 
is  often  dependent  upon  the  respiration,  it  being  usually  more  marked  on  inspira- 
tion. 

On  the  other  hand,  it  must  be  noted  that  very  often  there  is  no  retraction  of 
the  prsecordia  during  systole,  in  many  cases  of  undoubted  obliterative  pericar- 
ditis. In  brief,  the  symptom  under  consideration  is  extremely  ambiguous,  and  it 
must  always  be  viewed  with  considerable  reserve  in  forming  a  diagnosis.  Of  at 
least  equal  importance,  in  our  opinion,  is  the  obscurity  or  absence  of  any  cardiac 
motion  either  to  sight  or  touch.  We  can  lay  great  diagnostic  value  upon  the 
absence  of  a  normal  cardiac  impulse,  when  the  cardiac  dullness  is  increased,  al- 
though the  heart-sounds  are  normal;  and  when  the  adjacent  borders  of  the  lung 
do  not  move  with  respiration,  because  of  the  adhesions  due  to  the  associated 
pleurisy  (vide  infra)  ;  and  finally,  when  the  history  of  the  case  and  the  general 
course  of  the  illness  are  confirmatory,  for  instance,  if  there  are  indications  of  a 
previous  acute  pericarditis. 

The  other  symptoms  of  obliteration  of  the  pericardial  cavity  are  more  rare  and 
in  their  diagnostic  significance  still  more  uncertain.  Friedreich  observed  a  sudden 
collapse  of  the  jugular  veins  at  each  diastole — the  "  diastolic  collapse  " — while 
they  became  well  filled  agaiii  at  the  next  systole.  He  explained  this  phenomenon 
by  supposing  that  the  conditions  for  emptying  the  veins,  at  the  moment  of  the 
diastole  of  the  ventricle,  were  especially  favorable,  since  the  chest -wall,  which  had 
previously  been  drawn  in  by  the  systole,  went  back  again  quickly.  But  we  have 
ourselves  seen  distinct  diastolic  collapse  of  the  veins  in  a  case  of  adhesive  peri- 
carditis, the  diagnosis  of  which  was  confirmed  by  autopsy,  in  which  there  was 
no  systolic  retraction  of  the  prfecordia.  Riess  described  some  cases  of  pericardial 
adhesions  in  which  the  heart-sounds  had  a  metallic  character  from  the  resonance 
of  the  stomach,  Avhich  had  been  drawn  up.     All  things  considered,  we  must  say 


PERICARDITIS  365 

that  although  the  diagnosis  of  pericardial  adhesions  can  be  correctly  made  in 
many  cases,  yet  the  signs  given  for  it  are  more  or  less  uncertain,  since  they  may 
be  absent  in  obliteration  of  the  pericardial  sac,  and  they  may  also  be  caused  by 
other  conditions  without  such  an  obliteration.  In  a  word,  it  is  no  easy  matter  to 
establish  the  diagnosis  of  obliterative  pericarditis,  and  in  cases  of  this  sort  the 
autopsy  not  infrequently  brings  surprises,  as  our  own  experience  has  shown. 

The  general  constitutional  symptoms  of  obliterative  pericarditis  are  also  sub- 
ject to  great  variations.  In  many  cases  the  affection,  as  we  have  said,  has  no 
symptoms  at  all  or  at  least  no  grave  results.  In  other  cases,  however,  there  is 
distinct  evidence  of  circulatory  disturbance.  This  disturbance  is  sometimes  due 
directly  to  the  mechanical  embarrassment  of  the  heart,  but  more  often  to  sec- 
ondary changes  in  the  myocardium.  We  find  atrophy,  fatty  infiltration,  and 
fatty  degeneration,  with  consequent  dilatation.  In  such  cases  the  pulse  becomes 
small  and  frequent,  and  the  ordinary  picture  of  ruptured  compensation  is  dis- 
played, characterized  by  oedema,  dyspnoea,  and  congestion  of  the  liver  and  kidneys. 
In  these  cases  the  diagnosis  is  often  very  difiicult.  It  is  scarcely  possible  to  dis- 
tinguish between  this  form  of  pericarditis  and  chronic  myocarditis,  or  the  "  idio- 
pathic "  enlargement  of  the  heart. 

There  is  another  symptom-complex,  somewhat  different  from  the  above,  which 
deserves  special  mention.  We  have  been  acquainted  with  it  for  years,  but  it 
has  only  lately  received  general  attention.  Sometimes,  when  there  is  obliteration 
of  the  pericardial  sac,  there  is  developed  a  condition  so  like  that  of  hepatic  cir- 
rhosis {q.v.),  that  the  name  of  "  pericarditic  pseudo-cirrhosis  of  the  liver"  has 
been  applied  to  it.  There  are  increasing  dyspnoea  and  great  ascites,  with  subse- 
quent oedema  of  the  lower  extremities,  so  that  we  have  dropsy  of  the  lower  half 
of  the  body,  while  the  upper  half  remains  free  from  oedema  (see  Fig.  43).  There 
may  be,  however,  a  serous  effusion  demonstrable  in  one  or  both  pleural  cavities. 
At  the  autopsy  we  do  not  find  the  hepatic  cirrhosis  which  has  in  many  cases  been 
supposed  to  exist,  but  instead,  a  total  obliteration  of  the  pericardial  sac,  with 
which  is  often  associated  a  nutmeg  liver  (sometimes  atrophic,  vide  supra,  page 
330),  and  often,  also,  chronic  peritonitis  and  chronic  pleurisy.  The  peritonitis 
causes  a  marked  fibrous  thickening  of  the  peritoneum,  apt  to  be  especially  marked 
on  the  surface  of  the  liver,  in  the  form  of  what  is  called  "  frosted  liver."  This 
condition,  therefore,  in  many  cases,  should  be  classed  as  one  of  "  chronic  inflam- 
mation of  the  serous  membranes"  {vide  supra,  page  289).  We  may  have  a 
similar  group  of  symptoms  not  associated  with  inflammation  of  the  peritoneum, 
if  the  circulatory  disturbance  resulting  from  the  obliteration  of  the  pericardium 
affects  chiefly  the  portal  circulation.  We  have  also  observed  a  combination  of 
obliterative  pericarditis  with  genuine  hepatic  cirrhosis.  In  a  word,  the  cases  are 
not  all  after  one  pattern.  The  diagnosis  can  not  be  correctly  made  unless  one 
is  acquainted  with  the  symptom-complex,  and  pays  special  attention  not  only 
to  the  history  of  the  case  but  to  the  cardiac  signs,  such  as  increase  in  the  area  of 
•dullness,  absence  of  apex -beat,  or  presence  of  systolic  retraction. 

3.  Tubercular  Pericarditis. — Tubercular  pericarditis  is  an  important  disease 
clinically,  since  in  many  cases  it  is  apparently  primary.  It  may  be  either  quite 
acute  or  chronic.  The  patient  falls  ill  suddenly,  or  more  gradually,  with  indefi- 
nite thoracic  symptoms,  dyspnoea,  general  weakness,  moderate  fever,  etc.  If  the 
■disease  is  of  long  duration,  there  is  more  or  less  oedema.  When  we  find  on  phys- 
ical examination,  in  such  cases,  the  signs  of  pericarditis,  the  diagnosis  of  tubercu- 
lar pericarditis  is  probable,  if  we  discover  a  general  "  phthisical  habit,"  hereditary 
predisposition,  and  also  co-existing  disease  of  other  serous  membranes,  especially 
pleurisy,  or  more  rarely  chronic  peritonitis.  In  the  latter  case  the  tubercular 
pericarditis  forms  one  symptom,  of  the  so-called  tuberculosis  of  the  serous  mem- 
branes, but,  as  has  been  said  before,  apparently  isolated  primary  tubercular  peri- 


366 


DISEASES    OE   THE    CIECULATOEY   OEGANS 


carditis  does  occur  (vide  supra).  We  have  seen  such  cases  repeatedly,  especially 
in  old  people.  In  these  cases  the  disease  is  not  easy  to  diagnosticate.  The  patient 
gives  one  the  impression  of  having  heart  disease,  but  the  physical  signs  in  the 
heart  are  sometimes  of  a  very  indefinite  nature.     Eriction-rubs  may  be  entirely 


Fig.  43.— Pseudo-hepatic  cirrhosis  due  to  pericarditis.    (Personal  observation.) 

absent,  on  account  of  adhesions  or  of  large  effusions.  This  leads  to  confusion 
with  myocarditis  or  mitral  stenosis.  In  other  cases,  of  course,  all  the  physical 
signs  of  pericarditis  mentioned  above  may  be  manifest,  and  a  correct  diagnosis 
can  be  made. 

Diagnosis. — Erom  what  precedes,  it  follows  that  the  diagnosis  of  pericarditis  is 
very  easy  in  many  cases,  but  is  very  difficult  or  impossible  in  others.  The  most 
unequivocal  sign  is  the  characteristic  friction-rub.  The  practiced  ear  can  often 
distinguish  it  from  an  endocardial  sound  by  its  quality.  The  pericardial  sound 
is  a  rubbing,  grating  noise,  near  the  ear;  the  endocardial  is  blowing,  distant  from 
the  ear.  The  following  features  may  serve  as  marks  of  distinction  in  doubtful 
cases:  1.  We  hear  the  pericardial  sounds  at  first,  and  also  later,  over  the  base  of 
the  heart  in  the  vicinity  of  the  pulmonary  valve ;  the  endocardial  are  often  loudest 


PEEICAEDITIS  367 

at  the  apex.  2.  The  pericardial  murmurs  are  not  so  closely  associated  with  the 
phases  of  the  heart's  action,  with  systole  and  diastole,  as  the  endocardial.  3. 
We  find  that  the  pericardial  sounds  are  not  transmitted  far.  A  loud  rub  may  be 
audible  at  one  spot  which  can  not  be  heard  a  few  centimetres  away.  Loud  endo- 
cardial murmurs,  however,  are  audible  over  almost  the  whole  heart.  4.  Some- 
times the  peculiarity  of  the  pericardial  murmur — that  it  becomes  louder  when 
the  patient  sits  up,  on  pressure  with  the  stethoscope,  etc. — may  be  of  diagnostic 
value.  In  many  cases  the  loud,  functional,  so-called  anaemic  murmurs  over  the 
base  of  the  heart  may  give  rise  to  confusion  with  pericarditis. 

If  no  pericarditic  friction  has  been  heard  during  any  part  of  the  illness,  it  is 
seldom  possible  to  make  an  absolute  diagnosis  of  pericarditis.  At  least,  we  must 
confess  that  we  have  made  many  errors  in  the  diagnosis  of  such  cases.  Important 
factors  to  be  considered  are  the  general  course  of  the  disease,  including  the  acute 
onset  and  precordial  pain,  and  also  the  shape  of  the  cardiac  dullness  (triangular)  ,^ 
and  the  signs  furnished  by  the  apex-beat,  the  pulse,  and  the  heart-sounds.  We 
have  already  pointed  out  the  possibility  of  confusion  between  pericarditis  and 
myopathic  disease  of  the  heart,  and  mitral  stenosis  if  unattended  by  murmur.  No 
rules  of  universal  application  in  these  cases  can  be  laid  down.  It  is  very  often 
advisable,  and  absolutely  devoid  of  danger,  to  make  an  exploratory  puncture  in 
doubtful  cases  with  a  hypodermic  syringe.  This  is  done  at  the  left  edge  of  the 
sternum,  or  a  little  way  in  from  the  left  limit  of  cardiac  dullness. 

Course  and  Prognosis. — Many  cases  of  pericarditis  in  articular  rheumatism, 
pneumonia,  or  heart  disease,  and  also  many  of  the  rare  and  apparently  primary 
forms,  may  recover  completely.  The  disease  lasts,  in  the  mild  cases,  only  about 
a  week,  in  severe  cases  much  longer. 

Many  cases  of  pericarditis,  however,  terminate  fatally.  The  unfavorable  issue 
depends  either  upon  the  severity  of  the  primary  disease,  or  upon  the  intensity 
of  the  pericarditis  itself.  In  extensive  croupous  pneumonia,  in  valvular  disease 
of  the  heart,  or  in  severe  chronic  nephritis,  an  attack  of  pericarditis  is  often  the 
terminal  affection — the  immediate  cause  of  death.  In  otherwise  healthy  persons,, 
however,  a  severe  pericarditis  with  a  large  eifusion  may  be  the  direct  cause  of 
death,  as  a  result  of  the  impairment  of  the  movements  of  the  heart.  Yet  one  need 
not  wholly  despair,  particularly^ in  rheumatic  pericarditis,  even  in  cases  which 
seem  very  bad.  The  prognosis  of  tubercular  pericarditis  is  always  very  unfa- 
vorable. This  form  may,  indeed,  run  quite  a  chronic  course,  but  it  is  hardly 
ever  capable  of  definite  recover^".  The  prognosis  of  pysemic  pericarditis  is  also 
unfavorable. 

In  one  class  of  cases  pericarditis  takes  a  chronic  course  from  the  start,  or 
chronic  pericarditis  develops  from  an  acute  attack.  The  ultimate  prognosis  of 
these  cases  is  usually  unfavorable,  since  the  secondary  atrophy  and  dilatation  of 
the  heart  gradually  lead  to  severe  disturbances  of  the  circulation.  We  have 
spoken  above  of  the  termination  of  pericarditis  in  obliteration  of  the  pericar- 
dial sac. 

Treatment. — Since  pericarditis  is  a  severe  affection  under  all  circumstances,  we 
must  see  especially  that  the  patient  has  perfect  rest  and  care.  Extreme  caution 
must  be  enjoined  upon  him,  especially  in  the  cases  in  which  at  first  the  subjective 
symptoms  are  slight.  We  must  keep  the  patient  strictly  confined  to  the  bed,  and 
not  let  him  leave  it  even  temporarily. 

The  remedies  which  are  used  against  pericarditis  aim  partly  at  keeping  the 
inflammation  in  check,  and  partly  at  aiding  the  action  of  the  heart.  For  the  first, 
the  continued  application  of  ice  to  the  cardiac  region  deserves  especially  to  be 
recommended.  Local  blood-letting,  ten  or  twelve  leeches  to  the  cardiac  region 
— formerly  very  often  but  now  more  rarely  used — may,  in  otherwise  strong  and 
healthy  persons,  aiford  great  relief  in  cases  with  marked  subjective  symptoms^ 


368  DISEASES    OF   THE    CIECULATOEY   OEGAIsTS 

Painting  with,  tincture  of  iodine  and  blistering,  however,  deserve  little  confi- 
dence. Digitalis  is  our  chief  means  to  bring  down  an  accelerated  pulse,  and  to 
strengthen  the  heart's  action.  It  is  a  drug  which  is  most  active  and  most  fre- 
quently used  in  pericarditis,  and  is  always  indicated  when  the  pulse  is  rapid  and 
of  diminished  tension.  Of  course,  the  action  of  the  remedy  must  be  carefully 
watched,  as  in  all  cases  where  digitalis  is  prescribed.  Tincture  of  stroj)hanthus  is 
also  useful.  As  a  palliative,  morphine  often  does  indispensable  service  when  the 
subjective  symptoms  are  marked  and  the  patient  is  very  restless.  Diuretics  are 
also  employed,  as  in  pleurisy  with  effusion  (g.  v.). 

If  the  symptoms  are  threatening,  the  question  arises  whether  a  large  fluid  peri- 
cardial effusion  is  the  cause  of  the  severe  symptoms.  In  this  case  the  evacuation 
of  the  exudation  is  of  course  imperatively  indicated.  The  difficulty  of  forming 
a  correct  opinion,  however,  is  very  great,  because  in  any  individual  case  it  is  rarely 
possible  to  determine  the  amount  of  fluid  that  may  be  present.  In  the  first  place, 
we  must  consider  the  size  of  the  cardiac  dullness  and  the  weakening  of  the  move- 
ments of  the  heart,  but  both  factors  may  give  rise  to  deception.  Hence  we  always 
first  make  an  exploratory  puncture  with  a  Pravaz's  hypodermic  syringe.  The  best 
point  for  insertion  is,  in  general,  the  sternal  end  of  the  fourth  or  fifth  [left]  inter- 
costal space  with  the  patient  on  his  back,  partially  raised  in  bed.  If  the  explora- 
tory puncture  gives  a  positive  result,  we  make  a  puncture  with  Billroth's,  Fraent- 
zel's,  or  some  similar  trocar.  With  regard  to  the  details,  we  will  refer  to  the 
description  of  puncture  of  the  pleura.  Puncture  of  the  pericardium  is  always 
performed  by  the  aid  of  aspiration.  It  is  less  dangerous  than  might  be  feared. 
Even  injuries  to  the  heart  during  the  operation  have  scarcely  ever  had  grave  re- 
sults. The  temporary  relief  to  the  patient,  in  cases  of  successful  puncture,  is 
usually  very  striking,  but  the  permanent  results  of  pericardial  puncture  are,  of 
course,  much  less  favorable  than  those  of  puncture  of  the  pleura,  which  is  chiefly 
due  to  the  character  of  the  underlying  disease.  In  some  cases  of  purulent  peri- 
carditis, incision  of  the  pericardium  has  also  been  practiced  after  the  analogy  of 
the  treatment  of  empyema.  In  other  forms  of  pericarditis  with  an  abundant 
fibrino-serous  exudation,  it  might  often  be  preferable  to  make  an  incision  rather 
than  to  aspirate,  but  there  has  not  yet  been  much  experience  with  the  former 
method. 

[The  experiments  of  Eotch  show  that  pericardial  effusion  causes  dullness  in  the 
fifth  right  interspace,  a  sign  which  he  thinks  is  not  produced  in  cardiac  enlarge- 
ment. So  far  as  is  known  to  the  editor,  he  is  the  only  person  who  has  acted  on 
this  observation,  and  punctured  on  the  right  of  the  sternum  for  pericardial  effu- 
sion. In  the  case  referred  to,  the  signs  pointed  to  a  very  large  acute  effusion  of 
rheumatic  origin.  The  first  puncture  was  made  in  the  fiith  left  interspace,  but 
only  about  an  ounce  and  a  half  of  bloody  serum  was  obtained.  The  needle  was 
then  withdrawn  and  immediately  inserted  in  the  fourth  right  space  near  the  sternar 
border  with  absolutely  negative  result.  The  gravity  of  the  symptoms  led  to  two  ■ 
more  punctures  on  the  left  some  days  later,  one  with  small  though  positive  result, 
the  other  with  negative.    Absoi'ption  and  recovery  ultimately  took  place. 

The  recommendation  of  the  author  to  make  a  preliminary  puncture  with  a'  • 
hypodermic  syringe  for  diagnostic  purposes  seems  unnecessary,  just  as  with  pleural  ^ 
effusions.] 

If  there  is  a  condition  of  cardiac  weakness,  stimulants  are  indicated — strong 
w;ine,  subcutaneous  injections  of  ether  or  camphor,  or  wine  of  musk.  We  try  to 
keep  up  the  patient's  strength  by  the  best  of  nourishment.  ,      "[; 

The  resulting  conditions  of  disturbance  of  the-  circulation,  such  as  (»dema,  .iii^2 
chronic  pericarditis,  are  treated  in  the  same  way  as  in  valvular  disease  in^if^etif 
supra).     Digitalis  and  diuretics  are  the  chief  remedies.  -.,,!  ,^-,:-;jO 


HYDEO-PERICAEDIUM  '  369 


CHAPTER  II 

HYDRO-PERICARDIUM,   HiEMO-PERICARDIUM,  AND  PNEUMO- 
PERICARDIUM 

1.  Hydro-Pericardium 

{Dropsy  of  the  Pericardium) 

The  collection  of  a  serous  transudation  in  the  pericardial  sac,  without  any  in- 
flammatory symptoms  in  the  serous  membrane  itself,  we  term  hydro-pericardium, 
or  dropsy  of  the  pericardium.  Dropsy  of  the  pericardium,  which  formerly  played 
quite  a  great  role  in  pathology,  is  never  a  disease  of  itself,  but  is  always  a  sec- 
ondary condition.  It  may  occur  in  ansemic  and  cachectic  persons  as  a  result  of 
hydrsemia,  but  it  usually  depends  upon  a  local  or  general  venous  stasis  in  the 
pericardium.  In  the  latter  case  the  hydro-pericardium  is  one  symptom  of  general 
dropsy,  and  hence  is  found  chiefly  in  heart  disease,  renal  disease,  or  pulmonary 
emphysema. 

The  clinical  symptoms  of  hydro-pericardium  are  only  exceptionally  distinct, 
being  obscured  by  the  underlying  affection.  Large  amounts  of  fluid  in  the  peri- 
cardial sac,  which  may  amount  to  a  quart  (a  litre)  or  more,  must  of  course  impair 
the  action  of  the  heart,  weaken  the  heart-beat  objectively,  and  cause  an  increase  in 
the  cardiac  dullness.  The  distinction  from  pericarditis  is  rendered  possible  by 
the  absence  of  a  friction-rub,  but  especially  by  attention  to  the  existence  of  an 
underlying  disease.  In  other  respects  the  distinction  between  a  pericardial  tran- 
sudation and  an  effusion  during  life  is  not  always  easy. 

The  prognosis  and  treatment  depend  wholly  upon  the  nature  of  the  underlying 
disease.  Only  exceptionally  do  we  need  to  puncture,  when  the  exudation  is  very 
large. 

2.  Hsemo-Pericardium 

{Blood  in  the  Pericardial  Sac) 

In  rare  cases  haemorrhages  occur  into  the  pericardial  sac.  The  source  of  the 
haemorrhage  is  most  frequently  an  aneurism  of  the  aorta,  which  perforates  into 
the  pericardium.  Other  causes  of  haemorrhage  are  the  bursting  of  aneurisms  of 
the  coronary  arteries  and  rupture  of  the  heart.  The  latter  has  been  seen  after 
injuries,  and  also  as  a  result  of  cardiac  aneurism  and  the  cicatricial  formations 
in  myocarditis  (see  myocarditis).  Finally,  direct  injuries  to  the  heart,  especially 
bullet-wounds,  may  also  cause  haemorrhages  into  the  pericardial  sac. 

In  most  cases  death  occurs  in  a  few  moments  from  compression  of  the  heart, 
when  a  haemo-pericardium  comes  on.  Hence  the  amount  of  blood  poured  out  into 
the  pericardial  sac  is  usually  not  very  considerable.  Only  in  the  cases  in  which 
the  blood  oozes  out  more  slowly  can  a  great  distention  of  the  pericardial  sac  be 
reached.  The  diagnosis  is  rarely  possible.  With  regard  to  treatment  we  can 
merely  note  that,  in  some  traumatic  cases,  the  aspiration  of  the  blood  has  been 
performed  with  success. 

3.  Pneumo-Pericardium 

{Air  in  the  Pericardial  Sac) 

'The  entrance  of  air  or  gas  into  the  pericardial  sac  has  been  obseiwed  in  rare 
cases,  apart  from  external  wounds,  as  a  result  of  the  perforation  of  a  pyo-pneumo- 
thorax,  or  of  some  other  suppurating  process  in  organs  that  contain  air.  Thus 
cases  are  known  in  which  the  rupture  into  the  pericardial  sac  comes  from  the 
oesophagus,  as  in  cancer ;  from  the  stomach,  in  cancer  or  ulcer ;  or  from  the  lungs, 
24 


370  DISEASES    OF   THE   CIECULATOEY   OEGANS 

in  tubercular  or  gangrenous  cavities.  Since  the  agents  of  inflammation  enter  the 
pericardium  along  with  the  air,  a  purulent  pericarditis  almost  always  develops, 
besides  the  pneumo-pericardium,  or  it  may  rarely  be  simply  a  sero-iibrinous  peri- 
carditis. 

The  most  characteristic  and  striking  sign  of  pneumo-pericardium  is  the  pres- 
ence of  a  metallic  sound,  due  to  the  movements  of  the  heart.  Either  the  heart- 
sounds  themselves,  or  some  existing  friction-rub,  may  acquire  a  metallic  timbre 
from  the  increased  resonance,  or  splashing  metallic  sounds  may  be  produced  in 
the  pericardial  sac  from  the  movements  of  the  air  and  the  fluid,  which  may  often 
be  heard  at  a  distance  from  the  patient.  In  regard  to  diagnosis,  however,  it  is 
important  to  know  that  signs  similar  to  those  of  metallic  resonance  in  the  heart 
may  arise  from  the  stomach,  when  it  is  drawn  or  pushed  upward. 

In  true  pneumo-pericardium  percussion  gives  a  more  or  less  complete  absence 
of  the  cardiac  dullness.  On  rod-percussion  (see  page  297)  a  metallic  sound  is  some- 
times heard,  whose  pitch  may  vary  somewhat  with  the  phase  of  the  heart's  action. 
If  fluid  is  also  present  in  the  pericardial  sac  besides  the  air,  the  dullness  caused 
by  this  will  rise  on  raising  up  the  patient. 

The  other  symptoms  of  the  disease  and  the  treatment  are  the  same  as  in  a 
severe  pericarditis.  The  prognosis,  however,  corresponding  to  the  primary  dis- 
ease, is  wholly  unfavorable. 


SECTIOIST  III 
Diseases  of  the  Vessels 

CHAPTEE  I 

ARTERIO-SCLEROSIS 

(Endafteritis  clironica  deformans.     Atheroma  of  the  Vessels) 

.3]tiology. — Atheromatous  degeneration  is  probably  in  most  cases  an  expres- 
sion of  the  wearing  out  of  the  arteries,  because  of  the  many  ways  in  which  the 
intima  of  the  arteries  is  damaged  during  life,  both  chemically  and  mechanically. 
Atheroma  of  the  arteries  is  then  inainly  a  change  incident  to  age,  and  as  such 
is  often  regarded  as  not  a  true  disease. 

On  the  other  hand,  if  arterio-sclerosis  appear  in  earlier  life,  say  before  the 
fortieth  year,  we  must  look  for  such  circumstances  as  would  tend  to  make  the 
ordinarily  efficient  causes  unusually  active.  We  must  not  forget  that  there  is 
an  apparent  predisposition  to  the  condition,  which  often  seems  to  be  hereditary; 
but  without  doubt  there  are  more  appreciable  causes.  The  reason  that  arterio- 
sclerosis is  so  common  and  occurs  comparatively  so  early  in  hard  laborers,  is  the 
great  mechanical  strain  which  the  arteries  tmdergo  during  persistent,  severe,  bodily 
exertion.  Again,  in  diseases  which  are  associated  with  a  persistent  elevation  of 
arterial  tension,  such  as  hypertrophy  of  the  left  ventricle  in  interstitial  nephritis, 
arterio-sclerosis  develops  probably  as  a  result  of  the  constant  high  tension.  It 
must  be  confessed  that  here  a  decision  is  often  very  difficult,  inasmuch  as  the  ar- 
terial disease  may  be  simultaneous  with  the  nephritis,  or  even  the  actual  cause  of 
it.  Again,  excessive  chemical  irritation  must  be  considered,  as  experience  shows 
that  a  continued  excess  in  eating  and  drinking,  particularly  in  the  use  of  alcohol, 
is  apt  to  occasion  arterio-sclerosis;  and  in  the  same  connection  are  to  be  named 
such  constitutional  diseases  as  syphilis,  gout,  and  chronic  nephritis,  and  perhaps 
also  definite  poisons  such  as  lead.    Nor  can  we  disregard  the  possibility  that  the 


AETEEIO-SCLEEOSIS  371 

'disease  may  follow  persistent  mental  strain  and  excitement.  All  these  circum- 
stances explain  why  well-marked  atheroma  is  far  more  frequent  in  men  than  in 
women. 

Pathological  Anatomy. — Atheroma  is  almost  exclusively  confined  to  the  arte- 
ries ;  only  exceptionally  do  like  processes  occur  in  the  veins.  Among  the  arteries 
the  aorta  is  almost  always  the  most  intensely  and  extensively  diseased;  we  also 
find  disease  in  the  iliac  and  femoral  arteries,  the  brachial,  radial,  and  ulnar,  the 
coronaiy  arteries  of  the  heart,  and  the  arteries  of  the  brain.  In  some  of  the  other 
arteries,  however,  like  the  gastric  artery,  the  hepatic,  and  the  mesenteric,  we  very 
rarely  find  atheromatous  changes. 

The  atheromatous  process  is  easy  to  recognize  macroscopically.  Instead  of  the 
normal  smooth  internal  surface,  we  find  more  or  less  numerous  irregularities  and 
thickenings  on  the  intima,  which  appear  either  more  or  less  gelatinous  and  trans- 
lucent, or  dense  and  fibrous,  or  ossified  as  a  result  of  calcification,  in  which  case 
they  also  feel  perfectly  hard.  In  many  cases  we  find  the  surface  of  the  thicken- 
ings destroyed^atheromatous  ulcers — and  covered  with  masses  of  fibrine. 

The  wall  of  the  arteries  is  usually  increased  in  thickness,  making  the  vessel 
feel  stiff  and  hard.  Very  frequently  the  calcareous  plates  may  be  felt  by  the 
finger.  The  frequently  associated  increase  in  arterial  tension  gradually  stretches 
the  walls  of  the  arteries,  rendering  them  tortuous.  This  is  best  seen  in  those 
of  medium  size,  such  as  the  brachial  and  radial. 

Microscopic  examination  shows  that  the  chief  changes  are  situated  in  the 
intima  of  the  arteries.  This  appears  three  or  four  times  as  thick  as  normal, 
partly  from  the  swelling  of  its  elements  and  partly  from  the  new  growth  of  con- 
nective tissue  and  the  deposit  of  round  cells.  In  the  connective-tissue  cells  of  the 
intima,  and  in  the  endothelial  cells  of  its  surface,  we  usually  find  a  marked  fatty 
and  hyaline  degeneration,  to  which  the  yellowish,  translucent  appearance  of  the 
surface  is  due.  Finally,  in  the  deeper  layers  there  is  a  complete  breaking  down  of 
the  tissue  into  a  mixture  of  fat,  detritus,  and  cholesterine  crystals,  which  has 
given  the  whole  process  the  name  of  atheroma  [  =  pulp] .  If  this  destruction  ex- 
tends to  the  surface,  an  atheromatous  ulcer  is  formed.  In  other  places,  however, 
it  does  not  reach  ulceration,  but  the  superficial  layers  of  the  intima  become  scle- 
rosed, and  are  finally  changed  to  lamellae  of  bony  hardness  from  the  deposition  of 
lime-salts.  The  atheromatous  spots  on  the  intima  of  the  vessels  often  give  rise 
to  the  formation  of  parietal  thrombi. 

The  media  and  adventitia  of  the  arteries  also  show  changes,  in  the  later  stages 
of  the  process.  Here,  too,  we  may  finally  get  fatty  degeneration  and  calcification. 
In  other  cases,  however,  there  is  a  marked  atrophy  of  the  media. 

The  immediate  result  of  the  atheromatous  changes  is  a  loss  of  elasticity  in  the 
walls  of  the  vessels.  The  ability  to  resist  the  blood-pressure  is  reduced,  and  this 
is  why  diffuse  or  circumscribed  aneurismal  dilatations  of  the  vessels  so  often  arise 
as  a  result  of  arterio-sclerosis  (see  the  following  chapters). 

Another  result  of  extensive  atheromatous  degeneration  of  the  vessels  is  an 
increase  of  the  resistance  to  the  blood-current,  and  a  consequent  elevation  of  the 
arterial  pressure.  Furthermore,  the  loss  of  elasticity  in  the  coats  of  the  medium- 
sized  and  smaller  arteries  removes  an  important  factor  for  the  propulsion  of  the 
blood.  The  left  ventricle,  in  consequence  of  these  additions  to  its  task,  becomes 
almost  invariably  hypertrophied  in  cases  of  extensive  arterio-sclerosis,  provided 
:  the  general  nutrition  of  the  patient  is  still  well  maintained. 

We  see,  therefore,  how  close  the  mutual  relations  are  between  increased 
arterial  tension,  hypertrophy  of  the  left  side  of  the  heart,  and  arterio-sclerosis. 

The  thickening  of  the  intima  in  the  smaller  vessels  often  causes  so  marked  a 
diminution  of  the  blood-supply  that  secondary  disturbances  of  nutrition  are  not 
wanting  in  the  various  organs.  .  The  lumina  of  the  vessels  may  be  still  further 


372  DISEASES    OF   THE   CIKCULATOEY   OKGANS 

narrowed,  or  even  completely  closed,  by  ttie  formation  of  thrombi  on  such  por- 
tions of  the  wall  of  the  vessels  as  have  undergone  atheromatous  changes.  We 
have  already  in  part  learned  to  recognize  the  sequelae  which  necessarily  arise  in 
the  various  organs,  such  as  indurations  in  the  heart  as  a  result  of  atheroma  of 
the  coronary  arteries,  and  we  will  return  later  on  to  the  analogous  changes  in 
some  other  organs,  such  as  cerebral  softening  and  certain  forms  of  contracted 
kidney.  " 

Clinical  Symptoms. — In  order  to  decide  whether  an  arterio-sclerosis  is  prese:pt 
in  the  living  subject,  we  are  of  course  restricted  exclusively  to  the  examination-  of 
those  peripheral  arteries  that  are  accessible  to  palpation.  We  must  examine,  first 
of  all,  the  radial,  brachial,  femoral,  and  temporal  arteries.  If  there  is  atheroma, 
we  feel  the  hard  and  partly  calcified  vascular  tube.  In  marked  cases  we  have  a 
feeling,  especially  in  the  radial,  as  if  we  had  hold  of  a  goose's  neck.  We  some- 
times notice  a  diffuse  dilatation  of  the  femoral  arteries.  In  many  cases  i]ie 
marked  spiral  form  of  the  vessels  is  very  striking,  and  it  is,  as  we  have  said,rff 
direct  result  of  the  loss  of  elasticity  of  their  walls  and  of  the  increased  blood,- 
pressure.  The  spiral  form  is  most  frequently  observed  in  the  temporal,  brachial^ 
and  radial  arteries. 

Although  we  can  often  directly  demonstrate  atheroma  in  the  vessels  men^ 
tioned,  we  must  always  be  cautious  in  deciding  from  this  that  there  is  also  an 
atheroma  of  the  internal  arteries,  for  the  radial  arteries  often  feel  very  rigid^ 
while  the  autopsy  later  on  shows  little  or  absolutely  no  atheroma  of  the  internal 
arteries.  In  other  cases,  however,  we  find  at  the  autopsy  marked  atheromatous 
changes  in  the  arteries  of  the  brain,  the  kidneys,  the  heart,  etc.,  although  the 
external  arteries  during  life  felt  perfectly  normal.  We  see  from  this  how  hard  it 
is  to  make  an  absolute  diagnosis  of  general  arterio-sclerosis. 

It  is  impossible  to  give  a  uniform  picture  of  arterio-sclerosis,  since  its  results 
appear  now  chiefly  in  this  organ  and  now  chiefly  in  that,  whereby  entirely  dis- 
tinct types  of  disease  arise.  Hence  we  must  confine  ourselves  here  only  to  men- 
tioning briefiy  the  most  important  sequelse.  For  the  most  part,  they  are  described 
separately  in  other  portions  of  this  work. 

In  the  heart  we  find  a  hypertrophy  of  the  left  ventricle  as  a  result  of  the  in- 
creased resistance  to  the  arterial  circulation.  This  is  often  apparent  during  life 
from  the  strength  of  the  apex-beat  and  its  displacement  to  the  left,  and  also  from 
the  extension  of  the  area  of  cardiac  dullness  to  the  left.  On  auscultation,  the 
increased  tension  in  the  aortic  system  is  made  manifest  by  the  strength  of  the 
aortic  second  sound.  The  examination  of  the  heart,  however,  is  often  rendered 
difficult  by  the  presence  of  pulmonary  emphysema.  On  the  other  hand,  we  some- 
times can  not  decide  how  far  a  manifest  hypertrophy  of  the  left  ventricle  is  due 
to  an  arterio-sclerosis,  and  not  to  other  co-existing  processes,  such  as  contracted 
kidney.  We  often  find  other  anatomical  changes  in  the  heart  besides  hypertrophy 
of  the  left  ventricle.  We  have  already  spoken  of  the  important  and  interesting 
results  of  atheroma  of  the  coronary  arteries,  the  formation  of  the  so-called  indura- 
tions of  myocarditis  in  the  heart  (see  page  340  et  seq.).  Sometimes,  from  an 
invasion  of  the  aortic  valves  by  the  atheromatous  process,  we  get  an  insufficiency, 
or  much  more  rarely  a  stenosis  of  the  aortic  orifice.  Finally,  we  may  also  mention 
here  that  atheroma,  especially  of  the  ascending  aorta  or  the  arch,  is  the  commoB- 
est  cause  of  the  formation  of  aneurism  of  the  aorta. 

We  have  already  described  the  character  of  the  peripheral  arteries.  The  radial 
pulse  is  hard  and  tense,  and  the  wave  is  either  quite  large,  or,  when  the  tube  is 
very  narrow,  small.  Since  the  wall  of  the  vessel  contracts  only  slowly,  in  conse- 
quence of  its  loss  of  elasticity,  the  radial  pulse  is  usually  sluggish — pulsus  tardus. 
This  condition  is  also  pronounced  in  the  sphygmographic  tracing,  which  shw-S 
a  slow  ascent,  and  a  still  slower  descent,  of  the  pulse-curve,  and  an  absence  oi^tia^ 


AETEEIO-SCLEKOSIS  373 

elevation  in  the  descending  limb  of  the  curve,  due  to  the  normal  elasticity.  The 
frequency  of  the  pulse  is  quite  different  in  different  cases ;  it  is  often  rather  slow 
as  a  result  of  sclerosis  of  the  coronary  arteries.  The  pulse  is  very  often  irregular 
as  a  consequence  of  changes  in  the  heart.  We  sometimes  find  an  abnormal  delay 
in  the  radial  pulse,  or  in  the  pulse  in  other  arteries,  in  comparison  with  the  heart- 
beat, from  the  lessened  rapidity  of  transmission  of  the  pulse-wave. 

Besides  the  heart,  the  brain  is  the  chief  place  in  which  we  observe  definite 
results  of  arterial  sclerosis.  The  increased  tendency  to  rupture  which  the  athe- 
romatous vessel-walls  show,  and  the  co-existing  heightened  blood-pressure,  explain 
the  comparatively  frequent  occurrence  of  cerebral  hsemorrhages.  Cerebral  haemor- 
rhages often  result  from  little  miliary  aneurisms,  which  have  formed  in  the  athe- 
romatous cerebral  arteries.  Atheroma  is  also  the  most  frequent  cause  for  the 
formation  of  foci  of  softening  in  the  brain,  since  the  arterial  changes  may  give 
rise  to  a  closure  of  the  cerebral  arteries  from  thrombosis  or  embolism.  Finally, 
so-called  senile  dementia,  or,  at  any  rate,  many  cases  of  that  condition,  are  ref- 
erable to  cerebral  atrophy,  resulting  from  the  faulty  nutrition  of  the  brain 
through  the  sclerosed  arteries. 

In  the  kidneys,  too,  atrophic  processes  often  develop  from  the  diminution  of 
the  blood-supply  owing  to  the  narrowed  lumina  of  the  vessels,  and  they  lead  to 
a  special  form  of  contracted  kidney.  The  origin  of  the  granulated  "  senile  kidney  " 
is  in  large  part  atheroma  of  the  renal  arteries. 

The  lower  extremities  display  symptoms  of  arterio-sclerosis  less  often  than 
the  parts  already  mentioned,  but  if  present  the  symptoms  may  be  very  striking. 
Here  belongs  a  peculiar  group  of  symptoms,  which  has  been  specially  studied  by 
Charcot,  Erb,  and  others.  It  is  termed  intermittent  claudication  or  lameness,  or 
dyshasia  intermittens  angiosclerotica  (Erb).  It  is  sometimes  associated  with 
lesions  of  one  or  both  femoral  or  iliac  arteries,  more  often  with  obliterative  arter- 
itis of  the  distal  arteries  of  the  lower  leg  and  foot.  It  usually  begins  with  dis- 
agreeable paraisthesise  of  crawling,  tickling,  or  coldness  in  the  feet  and  calves.  If 
the  patient  walks  even  for  a  short  time  the  symptoms  increase,  the  feet  grow  cold 
and  blue,  there  is  actual  pain,  and  the  patient  becomes  completely  incapable  of 
walking  farther.  After  a  short  pause  he  can  resume  his  walk,  but  soon  he  has  to 
stop  again.  Upon  examination  we  find  the  feet  and  legs  cold  and  bluish-red.  If 
we  palpate  the  arteria  dorsalis  pedis,  or  the  tibialis  postica,  we  can  detect  no  pul- 
sation whatever.  This  is  the  diagnostic  sign.  The  course  of  the  trouble  is  chronic, 
biit  decided  improvement  may  ensue  under  correct  treatment  (vide  infra).  From 
•a  prognostic  point  of  view  there  is  an  unfavorable  tendency  to  the  development  of 
gangrene  of  the  toes,  as  the  arteritis  increases.  With  regard  to  causation,  an  im- 
portant part  in  the  development  of  intermittent  lameness  is  played  by  syphilis, 
excess  in  tobacco,  glycosuria,  damage  from  thermic  influences,  and  other  causes. 
''^!  Sometimes  gangrene  of  the  lower  extremities  occurs  as  a  result  of  marked 
•Atheroma  without  any  previous  appearance  of  intermittent  lameness.  So-called 
■^-'fepontaneous  gangrene,"  senile  gangrene,  and  diabetic  gangrene  are  probably, 
,*with'out  exception,  due  to  primary  lesions  from  arteritis  and  consequent  impair- 
'inent  in  the  arterial  blood-supply. 

^- '-''•'  'Air  this  shows  how  different  the  symptoms  of  arterio-sclerosis  may  be  in  differ- 
"eife^* 'eases.  The  symptoms  in  the  vascular  apparatus  often  predominate  over  all 
others.  The  heart,  which  is  simply  hypertrophied,  or  which  has  undergone  in  part 
'^feafricial  degeneration,  is  finally  paralyzed,  and  then  all  the  symptoms  of  a 
^hl'onic  heart  disease  develop — dyspnoea,  oedema,  etc.  If  there  is  also  albumi- 
"fMria,  a  type  of  disease  is  produced  which  resembles  that  of  contracted  kidney. 
"I^  dtlier  cases,  however,  the  symptoms  in  the  brain  are  especially  manifest,  either 
■Mbiife  OT  in  combination  with  the  other  symptoms  mentioned,  and,  finally,  in  rare 
'■^'asds- We  have  the  above-described  symptoms  relating  to  the  lower  extremities. 


374:  DISEASES    OE   THE   CIECTJLATOEY   OEGAl^S 

We  must  remark,  however,  in  conclusion,  tliat  all  tlie  results  of  arterio- 
sclerosis mentioned  may  be  absent  for  a  long  time  or  altogether.  Many  persons 
have  pi-actically  no  symptoms  at  all  from  their  arterio-sclerosis,  and.  reach  an 
advanced  age,  but  we  must  always  consider  the  possibility  of  the  sudden  occur- 
rence of  severe  symptoms,  and  make  our  prognosis  accordingly. 

Treatment. — If  we  recall  the  above-mentioned  causes  of  arterial  sclerosis,  we 
see  at  once  the  possibility  and  iraportance  of  prophylaxis,  and  of  course  if  the 
disease  already  exists  we  must  endeavor  to  avert  these  injurious  influences,  so  as 
to  limit  the  progress  of  the  disease  as  far  as  possible.  There  is  little  direct  influ- 
ence upon  the  arterio-sclerotic  process  to  be  expected  from  drugs.  Iodide  of 
potassium  has  won  the  highest  reputation  in  this  regard,  and  it  is  employed 
extensively  in  all  cases  of  arterio-sclerosis.  Probably  it  is  most  efiicient  in  those 
cases  which  are  associated  with  a  syphilitic  taint.  In  general,  treatment  must  be 
symptomatic,  according  to  the  indications  in  each  instance.  In  the  symptom- 
complex  known  as  intermittent  lameness,  Erb  recommends  iodide  of  potassium,  or 
iodide  of  sodium;  local  applications  of  warmth  (for  instance,  by  means  of  the 
warm  pack) ;  galvanic  foot-baths ;  such  cardiac  tonics  as  strophanthus ;  and 
careful  regulation  of  bodily  exercise.  If  gangrene  has  set  in,  prompt  amputa- 
tion of  the  necrotic  part  is  necessary,  for  we  have  no  means  of  influencing  the 
process  itself.  In  each  case  treatment  must  be  adapted  to  the  sequelae  which 
ensue.  Prophylaxis  is  important.  It  may  hinder,  or  at  least  delay,  the  develop- 
ment of  the  process  if  the  patient  avoids  the  causes  already  enumerated. 


CHAPTER  II 
ANETJIIISM  OF  THE  THORACIC  AORTA 

.Sltiology  and  Pathological  Anatomy. — The  circumscribed  dilatation  of  an 
artery  is  termed  an  aneurism.  The  cause  of  its  formation  is  almost  always  to 
be  sought  in  a  primary  disease  of  the  vessel-wall,  which  weakens  its  resistance  to 
the  blood-pressure.  As  we  have  already  said  in  the  previous  chapter,  it  is  chiefly 
arterio-sclerosis  which  lies  at  the  foundation  of  aneurisms  in  many  cases.  The 
same  factors,  therefore,  which  favor  the  origin  of  arterio-sclerosis  belong  to  the 
aetiology  of  aneurism.  This  explains  why  the  root  of  the  aorta,  where  arterio- 
sclerosis is  most  marked,  is  also  the  most  common  seat  of  aneurism,  and  further, 
why  aneurisms  are  especially  seen  in  advanced  life  and  in  men.  Still,  the  develop- 
ment of  aneurism  is  a  rare  occurrence  in  comparison  with  the  great  frequency 
of  arterio-sclerosis ;  so  that  there  are  probably  other  circumstances  of  importance 
which  we  shall  some  day  know  more  about.  Possibly  there  is  a  congenital  weak- 
ness of  certain  portions  of  the  arterial  wall.  Traumatic  influences,  also,  are  not 
wholly  out  of  the  question.  Lately  many  authors  have  laid  special  weight 
on  syphilis  affecting  the  intima  of  the  aorta.  Indeed,  syphilis  is  said  by  some 
to  be  by  far  the  most  frequent  factor  in  the  aetiology  of  aneurism  of  the  aorta. 
This  seems  to  us  an  exaggerated  view,  but  certainly  the  point  deserves  consid- 
eration. 

[The  occurrence  of  aneurism  in  early  middle  rather  than  in  advanced  life  shows 
that  too  much  stress  can  be  laid  on  atheroma  as  a  cause.  That  sudden  strain  often 
plays  an  important  part  in  the  aetiology  can  scarcely  be  doubted,  though  the  cases 
in  which  a  perfectly  healthy  aorta  yields  locally  to  internal  pressure  must  be  very 
rare.  It  is  highly  probable  that  violent  exertion  tends  to  produce  changes  in  the 
walls  of  the  aorta.     The  far  greater  frequency  of  aneurism  in  the  male  sex  is  : 


ANEURISM  OF  THE  THOEACIC  AOETA        375 

notable.  Syphilis,  gout,  alcoliolic  excess,  and  lead-poisoning  appear  to  be  factors 
in  some  cases.] 

The  size  of  aneurisms  of  the  aorta  varies  very  much,  of  course,  in  different 
cases.  They  most  frequently  are  about  the  size  of  an  apple  or  the  fist ;  but  in  rare 
cases  much  larger  aneurisms  are  observed.  According  to  their  shape  we  distin- 
guish the  more  diffuse  or  spindle-shaped  dilatations  from  the  saccular  aneurisms 
{aneurisma  diifusum  seu  cylindricum,  aneurisma  fusiforme,  et  aneurisma  sac- 
ciforme).  Intermediate  forms  and  combinations  of  the  different  forms  occur  in 
manifold  ways. 

As  we  should  expect  from  its  origin,  we  never  find  the  wall  of  the  aneurism 
formed  of  a  normal  vessel  wall.  The  intima  almost  always  shows  the  same 
changes  that  are  characteristic  of  arterio-sclerosis,  only  in  a  much  higher  degree. 
The  media,  too,  is  usually  changed,  and  its  muscular  structure  often  shows  fatty 
degeneration.  The  adventitia  is  usually  thickened  by  chronic  inflammatory  pro- 
cesses. The  media,  and  sometimes  the  intima,  are  in  many  cases  so  much  atro- 
phied that  the  wall  of  the  aneurism,  at  least  in  part,  is  formed  only  of  the  adven- 
titia. 

In  the  cavity  of  the  aneurism  the  blood  is  only  partly  fluid.  We  usually  find 
it  more  or  less  full  of  new  and  old  masses  of  thrombi.  The  oldest  thrombi,  which 
lie  upon  the  wall  of  the  aneurism,  are  firm,  yellowish,  adherent  to  the  wall,  and 
sometimes  calcified.  At  other  points  the  thrombi  are  softened  and  broken  down. 
The  most  marked  coagulation  is  usually  found  in  the  saccular  aneurisms  with  a 
narrow  entrance,  because  in  this  form  of  aneurism  the  blood  is  almost  completely 
stagnant  in  the  aneurismal  sac. 

Aneurisms  of  the  aorta  usually  have  their  seat  in  the  ascending  aorta,  or  in 
the  arch.  Aneurisms  of  the  descending  thoracic  and  of  the  abdominal  aorta  are  far 
more  rare.  The  following  description  refers  principally  to  aneurisms  at  the  be- 
ginning of  the  aorta. 

We  do  not  give  separate  consideration  to  aneurism  of  the  ascending  aorta  and 
of  the  arch  of  the  aorta,  respectively,  for  it  is  impossible  clinically  to  draw  a  sharp 
distinction  between  them.     Other  aneurisms  will  be  considered  further  on. 

Clinical  Symptoms. — The  subjective  sensations  of  the  patient,  relating  directly 
to  the  aneurism,  are  of  a  very  uncertain  nature,  and  are  often  entirely  absent.  In 
other  cases  there  is  pain  in  the  region  of  the  aneurism,  either  only  a  slight  sense 
of  pressure,  or  very  sevei'e  and  subject  to  paroxysmal  increase,  sometimes  rather 
localized,  sometimes  radiating  into  the  back,  the  shoulders,  and  the  extremities. 
Sometimes,  too,  the  patient  feels  the  beating  and  pulsation  of  the  aneurism. 
The  remaining  symptoms  of  aneurism  may  be  divided  into  two  groups.  The  first 
group  embraces  those  symptoms  which  are  directly  related  to  the  aneurism  itself, 
and  most  prominent  in  this  group  are  the  physical  signs.  The  second  group  of 
symptoms  inckides  the  resultant  phenomena  which  the  aneurism  occasions  in  the 
circulatory  apparatus  and  by  pressure  upon  the  neighboring  parts. 

1.  Physical  Signs. — It  depends  entirely  upon  the  position  of  an  aneurism  of 
the  aorta  whether  it  causes  physical  signs  or  not.  Deep  aneurisms,  which  no- 
where approach  the  chest-wall,  may,  of  course,  be  quite  inaccessible  to  direct  ex- 
amination. 

Aneurisms  of  the  ascending  aorta,  however,  and  of  the  arch,  often  extend  so 
near  to  the  anterior  wall  of  the  chest  that  they  cause  an  abnormal  pulsation.  We 
feel  this  most  frequently  at  the  sternal  end  of  the  second  right  intercostal  space, 
or  over  the  upper  part  of  the  sternum.  The  pulsation  of  an  aneurism  of  the  arch 
of  the  aorta  may  sometiraes  be  felt  in  the  root  of  the  neck.  It  often  occurs  a 
moment  later  than  the  systole  of  the  heart.  In  many  cases  the  pulsation  is  clearly 
double,  analogous  to  the  normal  dicrotism  of  the  pulse.  We  sometimes  feel  a 
slight  systolic  thrill  with  the  flat  of  the  hand.     In  the  rare  aneurism  of  the  de- 


376  DISEASES    OF   THE   CIECULATOEY   OEGAITS 

scending  thoracic  aorta  the  pulsating  swelling  may  make  its  appearance  in  ther 
back,  between  the  vertebral  column  and  the  left  scapula.  If  the  aneurism  has : 
reached  a  certain  size,  the  pulsating  part  protrudes  as  a  tumor.  The  protrusion  is , 
either  merely  slight,  or  in  many  cases  it  forms  a  large  prominent  swelling.  It. 
then  shows  usually  a  marked  pulsation,  not  only  from  below  upward,  but  also  in  a) 
lateral  direction,  which  is  of  diagnostic  significance.  In  large  aneurisms,  how-a 
ever,  the  pulsation  sometimes  is  only  very  weak,  and  scarcely  perceptible,  from 
the  formation  of  many  coagula.  ;     ,  r.'^a 

[The  Roentgen  ray  furnishes  a  most  valuable  means  of  searching  for  thoracies. 
aneurism,  as  the  latter  casts  a  shadow  which  dilates  with  each  cardiac  sys^-:? 
tole.— V.J 

The  marked  prominence  of  large  aneurisms  is  possible  only  because  the  cover-:  i 
ing  parts,  not  only  the  muscles  and  skin,  but  also  the  cartilages  and  bones, \the.; 
ribs  and  sternum,  are  brought  to  a  gradual  atrophy  and  wasting  by  the  persistentt 
pressure.  The  skin  over  large  aneurisms  gradually  becomes  thinner  and  thinn^i.i 
until  finally  it  may  even  become  necrotic.  i  . 

There  is  of  necessity  more  or  less  dullness  on  percussion  over  every  aneurism;* 
of  any  size.  The  dullness  is  usually  evident  in  the  upper  right  intercostal  spaces,.: 
or  the  adjacent  parts  of  the  sternum.  Sometimes  it  even  precedes  the  palpable, 
pulsation,  although  then  its  significance  is  usually  still  very  uncertain.  In  rare  [ 
eases  of  aneurisms  of  the  ascending  aorta  and  of  the  arch,  dullness  and  abnormal  ; 
pulsation  have  been  observed  to  the  left  of  the  sternum. 

Auscultation  gives  varying  results.  In  some  cases  (probably  chiefly  when-r 
many  coagula  form)  we  hear  nothing  at  all  over  the  aneurism.  In  other  cases  we 
hear  one  or  two  sounds,  which  are  usually  the  audible  heart-sounds  transmitted. 
Perhaps  a  systolic  sound  may  also  arise  from  vibration  of  the  wall  of  the  aneu- 
rism. In  other  cases,  we  hear  a  murmur  over  the  aneurism.  A  dull  and  usually 
not  very  loud  systolic  murmur  often  arises  from  the  formation  of  eddies  in  the 
aneurismal  sac.  If  we  also  hear  a  diastolic  murmur,  it  is  almost  always  due  to  a 
co-existing  insuflficiency  of  the  semi-lunar  valves  of  the  aorta  {vide  supra). 

2.  Sequelw. — ^An  aneurism  of  the  aorta  by  itself  probably  never  causes  such  an 
increased  resistance  to  the  blood-current  as  to  give  rise  to  the  development  of 
a  hypertrophy  of  the  left  ventricle.  In  the  quite  frequent  cases  in  which  hyper- 
trophy of  the  left  side  of  the  heart  exists,  it  may  almost  always  be  referred  to  a 
co-existing  insufiiciency  of  the  aortic  valves,  and  sometimes  to  very  extensive 
atheroma  of  the  arteries.  During  life  a  hypertrophy  of  the  heart  may  be  simu- 
lated, because  the  heart  is  pushed  to  the  left  by  the  aneurism. 

In  many  cases  the  signs  in  the  peripheral  arteries  are  important.     Marked 
inequality  of  the  pulse  in  symmetrical  arteries  is  often  an  especially  valuable 
diagnostic  sign.     Either  the  trunk  of  an  efferent  vessel  is  compressed  by  the 
aneurism,  or  the  lumen  of  the  exit  of  the  vessel  is  itself  involved  in  the  aneurism, 
and  hence  the  opening  of  the  vessel  is  distorted  or  contracted,  or  partly  stopped  : 
by  a  coagulum.     This  readily  explains  why,  in  aneurism  of  the  ascending  aorta,  . 
the  radial,  and  sometimes  the  carotid  pulse,  are  plainly  weaker  on  the  right  than 
on  the  left,  as  a  result  of  implication  of  the  trunk  of  the  innominate,  while  in 
aneurism  of  the  arch  or  of  the  beginning  of  the  descending  aorta  the  oppositer: 
condition  may  obtain.    Abnormal  differences,  too,  in  the  intensity  of  the  pulse  in  o 
the  upper  and  lower  halves  of  the  body  may  arise  under  some  circumstances.    .  :o"t 

[W.  S.  Oliver  has  described  a  valuable  sign  to  which  he  gives  the  name  of  "x 
"  tracheal  tugging."  In  aneurism  of  the  transverse  arch  with  pressure  on  the",!; 
left  primary  bronchus,  a  distinct  downward  pull,  synchronous  with  the  heart«.I 
beat,  can  be  felt  by  the  thumb  and  forefinger  on  either  side  of  the  inferior  borfl'i 
der  of  the  cricoid  cartilage,  when  the  patient,  in  the  erect  or  sitting  posture  aridci 
with  the  mouth  shut,  raises  the  chin  as  far  as  he  can.    The  late  E.  L.  MaGDoB^o: 


ANEUEISM  OF  THE  THORACIC  AORTA        377 

nell,  of  Montreal,  lias  shown  that  non-aneurismal  tumors  in  this  region  are  not 
accompanied  by  this  sign,  and  that  pressure  on  the  trachea,  from  whatever  cause, 
does  not  produce  it.  It  may  be  the  sole  sign  of  aneurism  present,  and  may  then 
possess  the  double  diagnostic  value  of  indicating  both  the  nature  and  exact  seat  of 
the  disease. — Editor.  Very  exceptionally,  tracheal  tugging  is  caused  by  other 
conditions  than  thoracic  aneurism. — V.] 

A  marked  delay  of  the  pulse  in  the  arteries  arising  below  the  aneurism  is  a 
symptom  that  is  occasionally  seen.  Thus,  we  see  in  aneurism  of  the  arch  of  the 
aorta  that  the  left  radial  pulse  is  later  than  the  right,  and  that  in  aneurism  of  the 
descending  aorta  the  pulse  in  the  lower  extremities  is  later  than  the  radial  pulse. 

We  see  very  striking  signs  in  the  veins  if  the  large  venous  trunks  in  the 
thorax,  the  superior  vena  cava,  or  an  innominate  vein,  are  compressed  by  the 
aneurism.  The  veins  swell  in  the  neck,  in  the  upper  extremities,  or  upon  the  sur- 
face of  the  thorax,  according  to  the  seat  of  the  compression.  Local  oedema  may 
also  be  produced  in  this  way. 

The  respiratory  organs  are  exposed  to  the  pressure  of  aortic  aneurisms  in  many 
ways.  Compression  of  the  lungs  by  large  aneurisms  actually  contributes  toward 
increasing  the  dyspnoea  in  many  cases.  This  may  be  still  more  distressing  if  the 
trachea  be  compressed.  Of  the  two  main  bronchi,  the  left  bronchus,  which  lies 
beneath  the  arch  of  the  aorta,  is  more  apt  to  be  compressed.  This  produces  the 
symptoms  of  a  unilateral  bronchial  stenosis  (vide  supra).  The  comparatively  fre- 
quent compression  of  one  recurrent  nerve,  especially  the  left,  is  also  of  diagnostic 
importance,  as  it  results  in  jjaralysis  of  one  vocal  cord. 

Pressure  on  the  vagus  may  occasion  changes  in  the  rate  of  the  pulse,  and  per- 
haps sometimes  attacks  of  dyspnoea.  The  dyspnoea  in  most  cases,  however,  takes 
the  form  either  of  angina  pectoris  or  of  cardiac  asthma,  and  is  referable  to  the 
other  coincident  lesions  of  the  heart  and  the  coronary  arteries. 

Very  prominent  symptoms  sometimes  arise  from  compression  of  the  intercostal 
nerves  or  branches  of  the  brachial  plexus  by  the  aneurism.  As  a  result  of  this 
pressure,  extremely  severe  and  distressing  neuralgias  are  felt  in  the  nerve  terri- 
tories affected,  and  sometimes  we  see  motor  paresis  in  the  arm. 

Finally,  disturbances  of  deglutition  arise  in  many  cases  from  compression  of 
the  oesophagus.  If  this  be  falsely  interpreted,  it  may  lead  to  a  mischievous  use  of 
the  oesophageal  sound.  Cases  have  repeatedly  occurred  in  which  perforation  of 
the  aneurism  has  been  caused  by  passing  a  sound  into  the  oesophagus.  Hence  we 
must  always  remember  this  possibility  in  practice. 

Course  and  Termination  of  the  Disease. — Aneurisms  may  remain  latent  for  a 
long  time  without  causing  any  symptoms.  In  such  cases  a  sudden  perforation  may 
lead  to  a  speedy  and  unexpected  death. 

In  the  cases  which  have  shown  the  above  symptoms  to  a  greater  or  less  extent 
for  a  long  time,  and  often  for  years,  sudden  death  quite  frequently  results  from 
rupture  of  the  aneurismal  sac  and  perforation  into  a  neighboring  organ.  In  per- 
foration into  the  pericardium  death  follows  almost  instantly  from  cessation  of  the 
heart's  action.  In  perforation  into  the  oesophagus  a  fatal  hsemorrhage  occurs. 
In  perforation  of  the  aneurism  into  the  air-passages  (the  trachea  or  bronchi)  or 
into  one  pleural  cavity,  two  factors,  haemorrhage  and  suffocation,  unite  in  causing 
death.  In  aneurisms  which  gradually  erode  the  anterior  wall  of  the  chest,  the  per- 
foration is  in  rare  cases  external;  but  here  a  sudden,  immediately  fatal  htemor- 
rhage  seldom  ensues ;  much  more  commonly  a  slowly  increasing  anaemia  develops 
as  a  result  of  repeated  slight  haemorrhages  which  may  sometimes  go  on  for  weeks. 
Death  then  is  due  to  the  gradually  increasing  weakness,  or  to  a  final  severe  haemor- 
rhage. Perforation  of  an  aneurism  into  the  right  side  of  the  heart,  into  the 
pulmonary  arteries,  or  the  vena  cava,  is  a  rare  termination.  Here  death  does 
nat  fdillow  at  once,  but  severe  general  disturbances  of  the  circulation,  such  as 


378  DISEASES    OF   THE    CIRCULATOEY   ORGAINTS 

dropsy,  soon  arise.  In  many  of  these  rare  eases  peculiar  physical  signs  also  appear 
• — a  venous  pulse,  a  loud  systolic  murmur  over  the  point  of  perforation,  etc. 

If,  in  patients  with  aneurism  of  the  aorta,  death  does  not  ensue  from  a  sudden 
perforation,  the  general  type  of  the  disease  takes  a  form  similar  to  chronic  heart 
disease.  The  aneurism,  as  we  have  said,  is  often  also  combined  with  aortic  insuffi- 
ciency. The  left  ventricle  gradually  becomes  paralyzed,  and  the  well-known  dis- 
turbances of  compensation  set  in — increasing  dyspnosa,  oedema,  etc.  In  other 
cases  the  patient  gradually  becomes  duller  and  weaker  from  the  distressing  pain, 
the  sleeplessness,  and  the  other  symptoms,  and  dies  with  the  signs  of  increasing 
general  weakness. 

Recovery  from  aneurism  of  the  aorta  scarcely  ever  occurs. 

Diagnosis, — The  diagnosis  of  aneurism  of  the  aorta  can  in  many  cases  be  made 
with  great  ease  and  certainty,  but  in  other  cases  it  is  very  difficult  and  even 
impossible.  If  the  direct  physical  signs  are  plain,  especially  if  we  feel  an  abnor- 
mal pvilsation,  we  shall  not  be  apt  to  commit  an  error;  but  the  diagnosis  presents 
great  difficulties  in  those  cases  in  which  the  aneurism  is  not  accessible  at  all,  or 
accessible  only  with  great  difficulty,  where  it  merely  causes  indefinite  symptoms, 
pain  in  the  chest,  occasional  oppression,  symptoms  of  pressure  on  neighboring  or- 
gans, etc.  A  very  stubborn  intercostal  neuralgia,  which  no  remedy  can  relieve, 
may  be  for  a  long  time  the  only  symptom,  often  misinterpreted,  of  a  latent  aneu- 
rism. The  disease  is  often  not  recognized,  however,  because  in  such  cases  we  do 
not  generally  think  of  the  possibility  of  an  aneurism,  and  hence  we  neglect  a  care- 
ful examination  of  the  heart  and  the  arteries,  and  also  the  search  for  other  symp- 
toms of  compression,  such  as  paralysis  of  the  vocal  cords;  but  sometimes,  even 
with  the  most  careful  examination,  the  diagnosis  can  not  amount  to  more  than 
a  suspicion. 

If  there  is  a  loud  systolic  murmur  in  the  second  intercostal  space  on  the  right 
without  other  decisive  signs,  it  may  be  difficult  to  make  a  differential  diagnosis  be- 
tween aneurism  and  aortic  stenosis. 

The  distinction  between  aneurism  and  other  tumors  in  and  about  the  thorax 
sometimes  presents  difficulties  in  diagnosis.  Mediastinal  sarcomata  and  abscesses, 
circumscribed  empyemas,  tumors  arising  from  the  sternum,  or  new  growths  in 
the  lungs  and  bronchial  glands,  may  all  give  rise  to  confusion.  We  can  scarcely 
lay  down  any  general  rules  for  diagnosis,  since  the  conditions  differ  in  almost 
every  case.  If  we  feel-  a  swelling,  its  pulsation  is  the  symptom  which  points  most 
to  an  aneurism,  but  we  must  be  certain  that  the  pulsation  is  not  merely  trans- 
mitted, but  that  it  really  takes  place  in  all  directions  within  the  swelling  itself. 
We  must  also  consider  the  auscultatory  symptoms,  the  condition  of  the  heart  and 
the  arteries,  and  any  symptoms  of  compression;  yet  in  such  cases  we  can  not 
always  make  a  definite  diagnosis. 

Treatment. — Many  attempts  have  been  made  to  bring  about  an  obliteration  of 
the  aneurism,  and  thus  a  recovery.  Although  the  methods  of  treatment  aiming 
at  this  have  obtained  decisive  results  in  the  aneurisms  of  peripheral  arteries,  their 
results  in  aneurism  of  the  aorta  are  still  of  a  very  doubtful  character;  yet  we  are 
always  justified  in  any  given  case  in  trying  one  of  the  methods  recommended. 

Persistent  compression  by  a  pad  can  of  course  be  employed  only  in  those  cases 
where  the  aneurism  projects  at  one  part  of  the  chest-wall.  The  pressure,  how- 
ever, usually  causes  great  pain,  and  hence  is  ill  borne. 

Tying  the  carotid,  the  subclavian,  or  both  vessels,  has  also  been  repeatedly 
performed  in  aneurism  of  the  arch  of  the  aorta,  sometimes  with  apparent  success, 
but  oftener  without  any  benefit. 

"  Acupuncture  "  of  the  aneurism  (Yelpeau)  consists  in  inserting  a  needle  or  an 
iron  wire  into  the  aneurismal  sac  in  order  to  excite  coagulation  in  it.  The 
results  obtained  by  it  in  aneurism  of  the  aorta  are  not  very  encouraging. 


ANEUEISMS    OF   THE   OTHEE   VESSELS  379 

Better  results  are  reported  from  galvano-piancture.  Two  needles  inserted  into 
the  aneurism  are  connected  with  the  poles  of  a  galvanic  battery,  by  which  a  weak 
current  is  passed  through  the  aneurism.  Here  we  must  regard  the  chemical  and 
electrolytic  action  of  the  current  as  well  as  the  mechanical  action  of  the  needles. 

Injections  of  chemical  substances  into  the  aneurismal  sac,  in  order  to  produce 
coagulation,  are  dangerous,  since  the  coagula  caused  by  thera  may  give  rise  to 
emboli.  Hence  we  have  abandoned  making  trial  of  liquor  ferri  sesquichloridi  and 
similar  substances.  We  can  better  recommend  injections  of  ergotine  into  the 
vicinity  of  the  sac,  two  to  five  grains  (gramme  0.1-0.3)  of  the  aqueous  extract  of 
ergot  dissolved  in  water  or  glycerine,  injected  every  day  or  two.  This  method 
was  first  employed  with  success  by  Langenbeck  in  peripheral  aneurisms.  Its  ac- 
tion depends  upon  a  contraction  of  the  smooth  muscles  in  the  wall  of  the  aneu- 
rism, caused  by  the  ergotine. 

We  can  expect  little  action  on  an  aneurism  from  the  use  of  internal  remedies, 
although  favorable  results  have  been  reported.  Especially  recommended  is  the 
long-continued  use  of  iodide  of  potassium  or  iodide  of  sodium,  drugs  which  have 
obtained  a  great  reputation  in  all  arterio-sclerotic  lesions  and,  in  particular,  in 
syphilitic  disease  of  the  arteries  (vide  supra,  aetiology  of  aneurism).  Yet  it  is 
easy  to  see  why  one  should  not  expect  too  much  from  the  iodides.  Acetate  of  lead, 
5  to  10  grains  (gramme  0.3-0.6)  daily  has  also  been  employed.  Its  value,  however, 
is  questionable. 

The  symptomatic  treatment  of  aneurism,  which  tries  to  relieve  the  patient's 
sufferings,  and  the  dietetic  measures  prescribed,  follow  the  generally  customary 
principles.  In  a  rupture  of  the  aneurism  externally  we  try  to  avert  the  fatal 
catastrophe  by  absolute  rest,  ice-bags,  styptic  cotton,  etc.  Treatment  is  powerless 
against  internal  perforations. 

[Tufnell's  method,  so-called,  which  has  given  good  results  in  abdominal  and 
peripheral  aneurisms,  proves  sometimes  useful  in  palliating  the  symptoms  and 
lengthening  the  course  of  aortic  aneurism.  The  aim  of  this  method  is  to  diminish 
the  force  and  rapidity  of  the  circulation,  and,  if  possible,  to  increase  the  fibrinous 
deposit.  It  is  carried  out  by  enforcing  absolute  rest  in  the  recumbent  position, 
and  by  limiting  the  amount  of  food,  especially  of  liquids.  About  ten  ounces  of 
solid  food  and  eight  of  liquid  are  allowed  daily,  divided  into  three  meals.] 


CHAPTEK  III 
ANEimiSMS  OF  THE   OTHER  VESSELS 

Aneurism  of  the  Abdominal  Aorta. — Its  favorite  seat  is  the  vicinity  of  the 
co?liac  axis.  In  many  cases  it  may  be  felt  through  the  abdominal  wall  as  a  pul- 
sating tumor,  over  which  a  systolic  sound  or  a  M'hirring  murmur  can  be  heard. 
The  possible  symptoms  of  compression  are  very  numerous.  The  stomach,  intestine, 
and  liver  (jaundice)  may  be  implicated.  Pressure  of  the  aneurism  upon  the  nerve 
trunks,  or  even  pressure  on  the  spinal  cord  after  gradual  erosion  of  the  vertebrae, 
with  consequent  severe  neuralgia,  paralysis,  etc.,  has  been  repeatedly  observed. 
Death  usually  ensues  from  rupture  of  the  aneurismal  sac  and  internal  hemor- 
rhage. 

Aneurism  of  the  trunk  of  the  innominate  is  rare.  Its  symptoms  are  very 
much  like  those  of  an  aneurism  of  the  arch  of  the  aorta.  If  we  feel  a  pulsating 
tumor,  it  is  usually  situated  somewhat  higher  up  than  the  aneurism  of  the  aorta, 
in  the  first  right  intercostal  space,  or  the  tumor  even  extends  into  the  supra- 


380  DISEASES   OF   THE   CIKCULATOEY   OEGAl^I^S 

clavicular  fossa.  In  rare  cases  aneurisms  of  the  subclavian  and  of  tlie  carotid 
have  been  observed.  We  have  ourselves  seen  an  aneurism  of  the  internal  carotid 
the  size  of  a  cherry  pressing  on  the  Gasserian  ganglion,  which  caused  an  extremely 
severe  trigeminal  neuralgia  lasting  for  years. 

Aneurism  of  the  pulmonary  artery  may  appear  as  a  pulsating  tumor  in  the 
second  left  intercostal  space.  It  is  usually  impossible  to  distinguish  it  with  cer- 
tainty from  an  aneurism  of  the  aorta. 

We  have  already  mentioned,  in  the  description  of  pulmonary  tuberculosis,  the 
great  importance  of  small  aneurisms  of  the  branches  of  the  pulmonary  artery  in 
pulmonary  cavities,  as  a  frequent  cause  of  haemorrhage. 

Aneurisms  of  the  arteries  of  the  brain,  which  are  relatively  most  frequent  in 
the  basilar  artery  and  the  artery  of  the  fissure  of  Sylvius  (the  middle  cerebral 
artery),  may  cause  severe  cerebral  and  bulbar  symptoms  (see  page  1052).  As  has 
already  been  mentioned,  miliary  aneurisms  of  the  cerebral  arteries  play  an  impor- 
tant part  in  the  aetiology  of  cerebral  haemorrhage  (q.  v.). 

The  symptomatology  and  treatment  of  aneurisms  of  the  peripheral  arteries 
belong  to  the  domain  of  surgery. 


CHAPTER  IV 
BUPTURE  OF  THE  AORTA 

A  RUPTURE  of  a  previously  healthy  aorta,  with  fatal  haemorrhage,  after  violent 
traumatic  influences,  has  been  seen  only  in  a  very  few  cases.  In  the  majority  of 
the  very  rare  cases  of  rupture  of  the  aorta  we  have  to  do  with  a  vessel  that  is 
already  atheromatous.  In  some  cases  a  special  exciting  cause  is  present,  and  in 
others  it  is  absent.  We  once  saw  sudden  death  caused  by  rupture  of  the  ascend- 
ing aorta  in  a  young  man  about  twenty-five,  who  before  that  seemed  perfectly 
healthy.  'No  trace  of  atheroma  was  found ;  but  at  the  point  of  rupture  there  was 
a  slight  protrusion  and  a  decided  thinning  of  the  wall,  which  was  probably  con- 
genital. The  formation  of  a  so-called  dissecting  aneurism,  which  has  often  been 
seen  in  the  aorta,  is  of  anatomical  interest.  Here  only  the  intima  and  media  are 
torn.  The  blood  burrows  between  them  and  the  adventitia  or  between  the  layers 
of  the  media.  Most  of  the  cases  of  dissecting  aneurism  of  the  aorta  also  result, 
like  rupture  of  the  aorta,  in  sudden  death.  In  many  cases  death  results  from  the 
secondary  perforation  of  the  aneurism  into  the  pericardium.  On  the  other  hand,  a 
sort  of  recovery  from  dissecting  aneurism  may  occur.  A  secondary  perforation 
takes  place  into  another  part  of  the  aorta  itself  (Bostrom).  Cases  of  this  sort  were 
formerly  more  than  once  mistaken  for  double  aorta.  If  the  capsule  containing  the 
blood  is  preserved  for  a  considerable  length  of  time,  the  symptoms  may  assume  the 
character  presented  in  ordinary  aortic  aneurism. 


CHAPTER  V 
NARROWING  OF  THE  AORTA 

Congenital  narrowness  of  the  aorta  and  its  branches  is  a  condition  to  which 
Eokitansky  first,  and  later  Virchow,  have  directed  attention.  We  find  this  anom- 
aly especially  in  those,  mostly  women,  who  during  life  have  shown  the  signs  of 


]^AEEOWING   OF    THE   AORTA  "       '  381 

persistent  chlorosis.  Sometimes  such  persons  are  backward  in  their  whole  devel- 
opment; they  retain  a  puerile  habit,  and  show  a  defective  development  of  the 
gtoitals..  They  often  suffer  from- palpitation,  faintness,  and  a  tendency  to  hsem- 
orrhages.  In  many  cases  the  heart  is  also  small,  but  in  others  it  is  dilated  and 
hypertrophied.  We  have  already  pointed  out  (page  350)  that  congenital  hypo- 
plasia of  the  aorta  may  be  regarded  as  the  cause  of  certain  cases  of  "  idiopathic 
hypertrophy  of  the  heart."  Valvular  disease  of  the  heart  has  been  repeatedly 
f o\ind  combined  with  general  narrowness  of  the  arterial  system.  During  life  this 
gynonialy  of  the  vascular  system  may  sometimes  be  suspected,  but  it  can  never 
be  recognized  with  certainty. 

-;  Harrowing  of  the  aorta  at  the  point  of  insertion  of  the  ductus  arteriosus  is  a 
lesian  observed  in  rare  cases,  whose  origin  probably  always  falls  in  the  period 
directly  after  birth,  and  is  associated  with  obliteration  of  the  foetal  ductus  arteri- 
osus. Other  congenital  anomalies  of  the  heart  are  usually  present  at  the  same  time. 
If  the  narrowing  of  the  aorta  is  not  very  marked,  it  may  be  properly  equalized  by 
a_  secondary  hypertrophy  of  the  left  ventricle  and  the  development  of  a  collateral 
circulation.  The  latter  is  brought  about  by  dilatation  of  the  anastomoses  between 
the  first  intercostal  artery,  the  dorsalis  scapulas,  the  subscapularis,  and  the  trans- 
versalis  colli  on  one  side,  and  the  lower  intercostal  arteries,  which  come  oif  from 
the  descending  aorta  below  the  narrowing,  on  the  other.  Anastomoses  are  also 
formed  between  the  mammary  and  the  superior  epigastric  on  one  side  and  the 
lumbar  and  femoral  arteries  on  the  other.  During  life  the  dilated  arteries  are 
prominent,  in  part  abnormally  tortuous,  and  perceptibly  pulsating,  especially  the 
dorsales  scapulse,  the  subscapulars,  the  mammaries,  and  the  epigastrics.  In  some 
cases  a  systolic  murmur  has  been  heard  over  some  of  these  vessels.  The  pulse 
in  the  arteries  of  the  lower  extremities,  the  femoral  and  popliteal,  is  very  weak 
and  scarcely  perceptible. 

In  many  cases  the  collateral  circulation  is  so  complete  that  the  person  affected 
may  feel  no  subjective  disturbance  at  all,  and  may  attain  an  advanced  age,  but  in 
other  cases  disturbances  of  the  circulation  appear  sooner  or  later,  and  the  patient 
finally  succumbs  to  dropsy.  Sudden  death  from  rupture  of  the  heart  or  of  the 
aorta  has  also  been  observed. 


10  BilV. 


DISEASES   OF   THE   DIGESTIVE   ORGANS 


SECTION  I 
Diseases  of  the  Mouth,  Toxgue,  axd  Salivary  Glands 

CHAPTEE  I 

CATARRHAL    STOMATITIS 

(CatarrJiol  Inflammation  of  the  Jloutii) 

Etiology. — Inflammation  of  the  buccal  mucous  membrane  is  not  infrequently 
the  direct  result  of  mechanical  or  chemical  causes.  As  mechanical  causes  we  may- 
mention  particularly  the  sharp  edges  of  broken  or  carious  teeth.  It  should  be 
said  that  often  infectious  organisms  {vide  infra)  are  active  at  the  same  time, 
because  they  gain  a  much  easier  foothold  on  account  of  the  presence  of  bad  teeth. 
Chemical  irritation  may  come  from  highly  spiced  food,  or  from  tobacco-chewing 
or  excessive  smoking.  Chemical  and  mechanical  irritation  provokes  stomatitis 
in  many  trades  which  expose  the  artisan  to  lime,  copper,  coal,  or  other  varieties 
of  dust.  In  drunkards  we  find  not  infrequently  a  chronic  stomatitis,  which  is 
characterized  by  a  thickly  coated,  moist,  and  shiny  tongue,  which  is  somewhat 
swollen  and  exhibits  indentations  on  its  side  due  to  its  pressure  against  the 
teeth.  Inflammation  of  the  mucous  membrane  of  the  mouth  from  poisoning 
with  corrosive  acids  or  alkalies  is  also  the  result  of  direct  chemical  irritation. 
It  may  take  the  form  of  severe  ulcerative  stomatitis  (see  the  following  chapter). 
The  mercurial  stomatitis,  which  results  from  acute  or  chronic  poisoning  with 
mercury,  is  caused  indirectly  by  the  particles  of  mercury  deposited  from  the 
blood  in  the  mucous  membrane.  This  mercurial  stomatitis  when  severe  always 
takes  the  form  of  ulceration  or  necrosis.  The  stomatitis  attendant  upon  the 
cutting  of  teeth  in  children  will  be  discussed  below. 

In  many  instances  stomatitis  comes  from  a  direct  propagation  of  inflammation 
from  neighboring  parts.  It  thus  forms  a  frequent  complication  of  pharyngeal 
catarrh,  and  less  often  of  rhinitis. 

Infection  plays  an  important  part  in  tbe  setiology  of  stomatitis.  The  local  in- 
flammation may  be  merely  part  of  a  constitutional  infectious  disease,  as  in  mea- 
sles, variola,  and  syphilis.  Stomatitis  is  still  more  frequently  a  comjjlication  of 
some  severe  and  protracted  illness,  when  the  mouth  is  not  properly  attended  to 
and  cleansed.  The  bits  of  food  and  the  mucus  quickly  begin  to  decay.  Great 
numbers  of  fungi  and  bacteria  invade  the  buccal  cavity,  and  excite  inflammation 
in  its  mucous  membrane.  Even  the  cases  of  i^rimary  stomatitis  which  sometimes 
occur  are  probably  all  of  an  infectious  character.  They  usually  soon  assume 
the  ulcerative  form.     Scorbutic  stomatitis  will  be  considered  under  scurvy. 

Clinical  History. — The  usual  sjTiiptoms  of  an  inflammation  of  mucous  mem- 

brane-^namely,    redness,    swelling,    and    increased    secretion — are    exhibited    in 

stomatitis.     The  redness  is  usually  most  intense  on  the  inside  of  the  cheeks  and 

on  the  gums.     Indeed,  we  have  the  special  name — gingivitis — for  inflammation 

383 


ULCERATIVE    STOMATITIS  383 

of  the  latter.  The  swelling  is  best  shown  by  the  indentations  made  by  the  teeth 
in  the  cheeks  and  the  edges  of  the  tongue.  The  tongue  and  gums  are  smeared 
with  mucus.  There  is  often  considerable  salivation.  If  the  inflammation  is 
more  active,  we  find  a  muco-purulent  coating  on  a  greater  or  less  portion  of  the 
membrane.  The  tongue  is  almost  always  thickly  coated.  If  we  scrape  off  a  little 
of  the  coating  and  put  it  under  the  microscope,  we  find  a  great  abundance  of 
pavement  epithelium,  in  part  fatty-degenerated,  pus,  micrococci,  and  remains  of 
food.  White  spots  made  up  of  epithelium  may  also  be  seen  on  various  parts  of  the 
oral  mucous  membrane.  Here  and  there  little  vesicles  appear  which  burst  and 
leave  superficial  ulcers. 

The  local  discomfort  of  severe  stomatitis  is  by  no  means  trifling.  There  is 
burning  pain,  which  interferes  with  taking  food,  and  usually  the  processes  of 
decomposition  occasion  a  constant  bitter  or  disgusting  taste  in  the  mouth,  as  well 
as  a  foul  and  offensive  breath. 

The  duration  of  the  disease  depends  on  the  nature  of  the  immediate  cause  or 
the  character  of  the  primary  disorder.  Usually  a  stomatitis  which  gets  well  in 
one  or  two  weeks  is  called  acute,  and  a  more  tedious  attack,  chronic.  The  chronic 
form  is  seen  in  topers,  inveterate  smokers,  and  persons  with  bad  teeth.  It  may 
last  for  years,  with  the  symptoms  described  above,  only  milder.  (For  lingual 
psoriasis,  vide  infra.') 

Treatment. — If  the  inflammation  is  considerable,  the  diet  must  be  liquid. 
Sometimes  cold  drinks  are  most  agreeable,  but  usually  lukewarm  are  pre- 
ferred. Often  the  pain  is  relieved  by  taking  from  time  to  time  a  sip  of  iced 
water  or  a  bit  of  ice ;  but  in  most  cases  the  patient  will  prefer  to  rinse  the  mouth 
with  lukewarm  water.  The  important  indication,  to  keep  the  mouth  as  clean  and 
pure  as  possible,  is  best  met  by  having  the  mouth  frequently  rinsed  out  with  a 
one-  or  two-per-cent.  solution  of  carbolic  acid,  a  two-per-cent.  solution  of  chlorate 
of  potash,  or  one  or  two  teaspoonfuls  of  a  one-per-cent.  solution  of  perman- 
ganate of  potash  in  a  glass  of  water.  It  is  also  advisable  to  rinse  the  mouth 
with  a  two-per-cent.  solution  of  peroxide  of  hydrogen,  and  with  thymol,  which  lat- 
ter is  the  chief  constituent  of  Miller's  mouth  wash,  the  ingredients  of  which  are : 
Thymol,  \  part ;  benzoic  acid,  30  parts ;  tincture  of  eucalyptus,  4  parts ;  distilled 
water,  Y50  parts.  In  children  who  can  not  do  this,  the  mouth  is  to  be  carefully 
washed  or  sprayed.  If  the  gums  are  spongy,  they  should  be  painted  with  a  mix- 
ture containing  equal  parts  of  tincture  of  myrrh  and  tincture  of  rhatany.  If 
there  are  superficial  ulcers  scattered  about,  it  is  sometimes  an  excellent  plan  to 
touch  them  lightly  with  lunar  caustic,  to  hasten  their  healing. 

Chronic  stomatitis  is  often  very  obstinate,  resisting  all  sorts  of  treatment  for  a 
long  time.  The  first  thing  is  to  remove  any  such  injurious  agencies  as  tobacco 
or  bad  teeth.  It  is  recommended,  besides  the  above-mentioned  remedies,  to  swab 
out  the  mouth  with  a  solution  of  corrosive  sublimate  (1  to  5,000)  or  of  lunar 
caustic  (1  to  30-50). 


CHAPTER   II 

ULCERATIVE    STOMATITIS 

{Stomacace) 

.^Itiology. — By  ulcerative  stomatitis  is  meant  a  severe  disease  of  the  buccal 
mucous  membrane,  with  superficial  necrosis  and  the  consequent  formation  of 
ulcers.  The  abnormal  processes  are  not  in  all  cases  identical,  and  their  cause 
may  vary.     Still  it  is  probable  that  infection  is  the  important  factor,  at  least  in 


384  DISEASES    OF   THE   DIGESTIVE   OEGANS 

the  primary  cases.  The  disease  has  repeatedly  been  epidemic,  chiefly  among  sol- 
diers in  barracks  or  on  a  campaign,  and  among  the  inmates  of  jails.  We  have 
repeatedly  seen  sporadic  cases  of  primary  ulcerative  stomatitis  with  fever.  In 
children  the  disease  is  especially  common  at  the  time  of  the  second  dentition. 
Here,  too,  endemic  and  contagious  influences  are  frequently  in  evidence. 

Mercurial  stomatitis  is,  from  a  practical  point  of  view,  the  most  important 
of  those  forms  of  ulcerative  stomatitis  which  are  referable  to  definite  chemical 
action.  It  is  due  to  the  inhalation  of  the  fumes  of  mercury  in  those  whose 
trade  or  scientific  occupation  exposes  them  to  this  danger,  and  very  frequently 
also  to  the  therapeutic  employment  of  mercury  in  the  form  of  calomel  or  mer- 
curial ointments,  and  the  like.     (For  the  scorbutic  form,  see  page  741.) 

Symptoms. — The  disease  usually  attacks  the  gums  of  the  lower  jaw  first,  gr?d- 
ually  spreading  thence  to  neighboring  portions  of  the  lips  and  cheeks.  The 
tongue  and  palate  are  generally  not  very  much  affected,  though  often  the  seat  of 
a  simple  catarrhal  inflammation.  In  severe  mercurial  stomatitis  the  gums  are 
especially  apt  to  be  affected.  The  ulcers  also  show  a  preference  for  the  angles 
of  the  lower  jaw,  and  those  portions  of  the  mucous  membrane  of  the  cheeks 
which  rest  upon  the  teeth. 

Inspection  shows  that  the  mucous  membrane  in  the  places  mentioned  has  a 
pasty,  purulent  coating.  The  gums  are  swollen,  spongy,  and  red,  and  bleed 
easily.  The  mucous  membrane  on  the  edges  of  the  gums  becomes  necrotic,  giving 
rise  to  ulcers.  The  incisor  teeth  are  so  loosened  by  gingivitis  that  they  may  even 
fall  out.  There  is  usually  profuse  salivation.  The  lymph-glands  at  the  angle 
of  the  lower  jaw  and  on  the  chin  are  generally  swollen.  The  breath  is  very 
offensive,  poisoning  the  air  of  the  whole  room. 

The  local  discomfort  of  the  patient  is  the  same  as  in  simple  stomatitis,  only 
much  worse.  It  is  very  difficult  to  take  nourishment.  In  many  cases  there  are 
marked  constitutional  symptoms.  The  patient  feels  very  weak  and  languid. 
The  primary,  and  sometimes  also  the  toxic,  cases  of  ulcerative  stomatitis  are 
associated  with  moderately  high  fever— 100.5°-102°  (38°-39°  C).  Wow  and 
then  severe  symptoms  of  constitutional  sepsis  have  followed  the  disease. 

The  course  of  ulcerative  stomatitis  is  favorable  in  the  great  majority  of  cases. 
With  good  treatment  and  nursing,  the  ulcers  gradually  clean  up,  and  at  the  end 
of  one  or  two  weeks  recovery  is  complete.  Exceptionally,  the  disease  may  be 
more  chronic.  The  most  frequent  way  in  which  recovery  is  delayed  is  that  the 
disease  extends  to  the  periosteum  of  the  lower  jaw,  causing  necrosis  of  small 
portions  of  the  bone,  which  must  be  expelled  before  the  patient  gets  well. 

The  treatment  does  not  differ  essentially  from  that  of  the  milder  forms  of 
stomatitis.  The  mouth  must  be  still  more  carefully  and  more  frequently  cleansed 
and  disinfected.  A  solution  of  potassic  chlorate  (1  to  30)  is  the  favorite  mouth- 
wash. Good  results  are  also  obtained  from  permanganate  of  potash,  boric  acid, 
peroxide  of  hydrogen,  and  similar  remedies.  Some  authors  strongly  recommend 
the  simultaneous  internal  administration  of  potassic  chlorate;  but  we  must 
employ  it  cautiously  in  children,  as  it  has  repeatedly  caused  poisoning.  For 
children  two  or  three  years  old  we  ought  not  to  give  over  fifteen  to  thirty  grains 
(grammes  1-2)  in  a  day. 

As  to  prophylaxis,  we  should  mention  that  all  patients  who  are  using  mercury 
should  employ  a  gargle  of  potassic  chlorate  faithfully  from  the  beginning  of 
treatment,  in  order  to  prevent  the  occurrence  of  mercurial  stomatitis.  If  saliva- 
tion occurs,  the  mercury  must  be  stopped. 


APHTHOUS    STOMATITIS  385 


CHAPTER  III 

APHTHOUS    STOMATITIS 

(AphthiV.     Disseminated  Fibrinous  Stomatitis) 

Aphthae  is  a  name  given  by  physicians  to  several  entirely  distinct  diseases. 
Many  doctors  call  every  disease  aphthse  in  which  there  are  white  spots  upon  the 
buccal  mucous  membrane.  It  is  thus  frequently  confounded  with  thrush.  The 
same  name  (Schwdmmchen,  or  fungus)  is  often  applied  indifferently  to  thrush 
and  to  aphthse. 

There  is  a  special  form,  known  as  Bednar's  aphthse.  In  new-born  children 
white  patches  are  not  infrequently  found  lying  symmetrically  on  both  halves  of 
the  hard  palate  near  the  alveolar  processes,  and  persisting  till  about  the  third 
month.  These  plaques  are  not  syphilitic,  although  often  thought  to  be.  They 
are  probably  due  merely  to  the  tongue  pressing  upon  the  thin  mucous  membrane 
during  nursing.  Generally  they  do  no  harm;  but  in  marantic,  neglected  chil- 
dren, they  may  develop  into  quite  deep  ulcers.  In  that  ease,  repeated  cauteriza- 
tion with  a  five-per-cent.  solution  of  argentic  nitrate  is  required. 

The  genuine  aphthse  are  roundish  spots  upon  the  mucous  membrane,  grayish 
white,  and  of  small  size,  unless  made  larger  by  the  confluence  of  several  into  one 
another.  They  usually  have  a  narrow,  red  areola.  They  are  most  numerous  on 
the  edges  and  dorsum  of  the  tongue  and  on  the  frsenum,  but  they  also  occur 
on  the  lips  and  cheeks.  The  attempt  to  remove  the  white  spot  with  forceps 
never  succeeds,  but  it  causes  bleeding.  In  addition  to  the  genuine  aphthae  there 
are  almost  always  the  signs  of  a  common  stomatitis,  which  may  be  mild  or  severe. 
The  white  spots  are  due  in  part  to  a  thickening  and  opacity  of  the  epithelium,  and 
in  part  are  said  to  be  caused  by  the  formation  of  a  fibrinous  exudation,  which 
penetrates  the  most  superficial  layers  of  the  mucous  membrane.  If  the  necrotic 
epithelium  is  cast  off,  the  aphthous  spot  develops  into  a  little  ulcer,  which  often 
heals  promptly,  but  which  may  be  very  obstinate. 

The  disease  occurs  chiefly  in  children,  and  at  the  time  of  the  first  dentition. 
The  child  is  usually  restless,  often  somewhat  feverish,  and  evidently  suffers  pain 
when  nursing.  Generally  there  is  considerable  salivation.  The  lymph-glands 
ma,y  be  a  little  enlarged.  On  the  outer  skin  in  the  neighborhood  of  the  mouth 
there  may  also  appear  a  few  blisters  and  pustules.  These,  as  a  rule,  have  no  con- 
nection with  herpes,  although  now  and  then  genuine  herpes  may  appear  in  asso- 
ciation with  aphthous  stomatitis.  The  disease  is  not  rare  in  adults.  Many  indi- 
viduals seem  especially  liable  to  it,  and  very  frequently  have  little,  white,  and 
often  very  painful  spots  here  and  there  on  the  tongue  or  elsewhere  in  the  mouth. 
These  have  a  tendency  to  develop  into  ulcers  which  are  usually  superficial,  but 
sometimes  deep.  They  may  prove  very  troublesome,  from  their  frequent  recur- 
rence and  the  hindrance  they  cause  to  speaking  and  mastication.  If  there  are 
fairly  deep  ulcerations  on  the  tongue  and  mucous  membrane,  the  patient's  coudi- 
tioftfora  time  is  very  painful  and  distressing. 

With  the  exception  of  the  form  just  described,  which  is  constantly  relaps- 
ing^-.aphthfe  almost  always  run  a  favorable  course.  There  is  usually  complete 
recovery 'in  a  week  or  two.  The  treatment  of  children  consists  in  carefully  wash- 
ing rojifc, the  mouth  with  cold  water,  and  in  administering  potassic  chlorate.  Of 
a  mixture  consisting  of  three  parts  of  potassic  chlorate,  twenty  of  syrup,  and  a 
hundred  of  water,  we  may  give  a  dessertspoonful  every  two  hours.  If  the  spots 
do  not  disappear,  we  can  paint  them  with  a  solution  of  permanganate  of  potash 
(1  to  150),  a  five-per-cent.  solution  of  sulphate  of  zinc,  or  a  solution  of  borax 
(1  to  30).  If  some  of  the  places  are  especially  painful,  particularly  in  adults, 
25 


386  DISEASES    OF   THE   DIGESTIVE    OEGAITS 

we  may  touch  them  with  lunar  caustic,  when  they  usually  are  soon  cured.  In  the 
constantly  recurring  form,  treatment  sometimes  proves  almost  unavailing.  Local 
cauterization,  which  unfortunately  in  such  cases  is  often  of  no  benefit  whatever, 
and  the  use  of  a  mouth-wash  containing  chlorate  of  potash  or  carbolic  acid  in 
weak  solution,  may  be  employed,  and,  furthermore,  some  physicians  strongly  rec- 
ommend the  internal  administration  of  iodide  of  potassium.  Calomel  also 
appears  sometimes  to  have  a  beneficial  influence. 

It  is  often  a  very  difficult  matter  to  treat  chronic,  recurrent,  aphthous  stoma- 
titis, and  the  ulcerations  which  are  occasioned  by  it  in  adults.  Cauterization 
with  lunar  caustic,  chromic  acid,  and  similar  agents  usually  does  more  harm 
than  good.  None  of  the  ordinary  mouth-washes  has  any  great  efi'ect.  A  much 
praised  remedy  is  the  chewing  of  bilberries,  either  fresh  or  boiled,  for  several . 
minutes  several  times  a  day,  and  we  have  ourselves  employed  it  in  some  cases 
with  good  results.  Some  physicians  also  recommend  the  internal  use  of  iodide 
of  potassium,  or  small  doses  of  calomel.  It  is  remarkable  that  habitual  aphthous 
stomatitis  sometimes  ceases  completely  for  months — for  example,  upon  change  of 
residence  or  during  a  visit  to  the  country — but  then  appears  afresh  without 
special  cause. 

In  conclusion,  as  to  setiology,  infection  is  a  not  unlikely  cause,  if  we  consider 
that  small  epidemics  or  endemics  have  repeatedly  occurred.  Lately  attention  has 
been  called  to  the  possibility  that  the  milk  of  cows  suffering  from  hoof-and- 
mouth  disease  may  be  a  source  of  infection.  That  infection  of  this  sort  may 
occur  seems  to  us  indubitable,  from  the  experience  of  others,  as  well  as  our  own. 
In  such  cases  there  is  not  only  a  severe  aphthous  stomatitis,  but  a  development 
of  vesicles,  pustules,  or  even  extensive  purvilent  inflammation  affecting  the 
fingers  and  nails,  and  occasionally  other  parts  of  the  body.  Most  cases  of  this 
kind  also  pursue  a  favorable  course,  but  a  few  epidemics  have  been  described  in 
which  the  disease  became  dangerous  to  life  because  of  constittitional  sepsis. 
Probably  the  various  forms  of  stomatitis  aphthosa  are  connected  with  various 
infectious  germs. 


CHAPTEE   IV 

THRUSH 

(Soo?:    Muguet) 

JEtiology. — Weak  and  artificially  nourished  children  are  particularly  liable  to 
this  disease ;  but  it  also  attacks  adults  who  are  suffering  from  phthisis,  carcinoma, 
and  severe  typhoid  or  typhus  fever.  In  it,  grayish-white  deposits  are  developed 
upon  the  buccal  and  pharyngeal  mucous  membrane.  The  microscope  shows  these 
collections  to  be  fungi;  there  are  a  multitude  of  oval  spores,  or  conidia,  and  a 
tangled  mass  of  long  mycelium  threads.  Until  lately  the  fungus  of  thrush  was 
called  o'idium  albicans,  and  was  held  to  be  identical  with  the  o'idium  lactis  found 
in  sour  milk.  This  view  is  now  abandoned,  although  no  other  has  as  yet  been 
established  with  regard  to  the  botanical  position  of  the  thrush  fungus.  Grawitz 
maintained  that  the  thrush  fungus  is  a  sprouting  fungus,  and  nearly  related  to 
the  mould  finigi  (mycoderma  vini,*  or  saccharomyees  albicans — Eees).  It  seems 
to  be  a  sort  of  transitional  form  between  the  sprouting  fungi  and  the  thread 
fungi,  inasmuch  as  it  appears  both  in  the  yeast  fonn  and  also  in  the  form  of 

*  Mycoderma  viui  is  that  fungus  which  is  found  in  the  development  of  vinegar  from  alcohol,  when 
alcoholic  bcverasres  sour. 


THRUSH  387 

threadlike  mycelia.  Plaut,  according  to  his  investigations,  makes  the  thrush 
fungus  identical  with  the  monilia  Candida,  which  belong  to  the  Torulacese.  At 
any  rate,  the  thrush  fungus  is  widely  distributed,  for  the  development  of  thrush 
upon  the  mucous  membrane  of  the  mouth  and  throat  is  a  frequent  phenomenon, 
especially  in  ill-nourished  children.  ISTursing-bottles  and  the  nipples  used  upon 
them  are  probably  not  infrequently  the  agents  by  which  the  disease  is  conveyed. 

Symptoms. — The  mucous  membrane  of  the  tongue,  cheeks,  and  soft  palate  is 
usually  somewhat  red  and  swollen.  Upon  it  we  see  at  first  small  white  spots, 
which  may  gradually  spread.  Microscopic  investigations  have  shown  that  the 
fungus  develops  first  in  the  middle  layers  of  the  epithelium.  From  this  starting- 
point  it  grows  not  only  upward,  but  also  downward  into  the  mucous  membrane. 
If  the  growth  is  abundant,  it  is  easy  to  scrape  ofF  the  upper  layers,  and  make  a 
diagnosis  by  aid  of  the  microscope.  In  exaggerated  cases  the  growth  may  even 
extend  from  the  pharynx  into  the  upper  part  of  the  oesophagus  and  the  entrance 
of  the  larynx;  but  we  never  find  thrush  in  the  larynx  itself,  or  the  nostrils,  or 
the  stomach — briefly,  in  no  place  where  there  is  cylindrical  epithelium.  Yet  in 
exceptional  cases  the  thrush  fungus  may  extend  its  growth  through  the  wall  of  a 
blood-vessel,  and  so  reach  the  circulation.  Usually  thrombosis  of  the  affected 
vessel  takes  place,  but  the  metastasis  of  thrush  to  the  brain  and  the  kidneys  has 
been  observed.  If  abscesses  are  associated  with  these  processes  they  depend  upon 
the  simultaneous  intrusion  of  pyogenic  cocci. 

As  a  rule,  thrush  is  accompanied  by  a  more  or  less  severe  stomatitis.  The 
fluids  of  the  mouth  have  an  acid  reaction.  IsTursing,  or  chewing,  and  swallowing, 
are  painful.  Still,  it  is  a  question  whether  the  stomatitis  is  due  to  the  fungus,  or 
whether  it  prepares  the  territory  for  the  fungus  to  settle  in.  jSTursing  infants, 
who  suffer  from  thrush,  often  have  diarrhoea  or  marasmus  at  the  same  time,  which 
latter  affections  are  more  probably  the  cause  than  the  result  of  the  thrush.  If 
vigorous  and  healthy  sucklings  are  attacked  by  thrush,  the  disease  is  usually 
quite  harmless,  quickly  vanishing  if  proper  cleanliness  is  maintained.  In  sickly 
children,  particularly  if  bottle-fed,  the  appearance  of  the  disease  is  very  ominous. 
If  there  is  a  large  amount  of  thrush  in  the  oesophagus,  the  ingestion  of  food 
may  be  seriously  interfered  with.  In  adults,  as  we  have  said,  thrush  is  with  few 
exceptions  confined  to  persons  greatly  prostrated  by  such  diseases  as  severe 
typhoid  fever  or  tuberculosis,  and  from  this  point  of  view  it  is  an  unfavorable 
symptom. 

Treatment. — To  prevent  the  development  of  thrush  in  children,  the  mouth 
must,  if  possible,  be  wiped  out,  each  time  they  drink,  with  a  cloth  wet  in  cold 
water ;  and  if  adults  are  very  ill,  they  require  equal  attention  in  this  regard.  As 
soon  as  we  see  the  first  traces  of  the  disease,  we  should  touch  the  parts  attacked 
with  a  brush  wet  in  an  aqueous  solution  of  borax  (1  to  20).  Honey  should  not 
be  added  to  the  borax  solution,  as  is  often  unwisely  done.  Another  good  solution 
is  permanganate  of  potash  (1  to  150).  If  the  thrush  extends  into  the  oesophagus 
the  most  efficient  remedy  (Baginsky)  is  said  to  be  the  internal  administration  of 
resorcin,  in  a  one-half-  to  one-per-cent.  solution,  the  dose  being  a  teaspoonful 
every  two  hours.  The  food  should  contain  as  little  sugar  as  possible,  as  this  fur- 
nishes a  favorable  culture  medium  for  the  thrush  fungus.  Mild  cases  can  usually 
be  cured  by  the  remedies  named.  If  the  thrush  has  once  got  a  vigorous  start  in 
the  mouth  of  marantic  children,  or  of  adults  suffering  from  an  incurable  disease, 
it  must  be  confessed  that  we  often  fail  to  check  its  growth. 


388  DISEASES    OF   THE   DIGESTIVE    OKGANS 


CHAPTER   Y 

GLOSSITIS 

{Parencliymatous  Inflammation  of  the  Tongue) 

Inflammation  of  tlie  true  lingual  parencliyma  is  rare,  although,  the  tongne's 
mucous  surface  is  frequently  involved  in  the  various  diseases  of  the  mouth. 

1.  Acute  parenchymatous  glossitis  is  the  name  given  to  an  inflammatory  in- 
filtration of  the  whole  or  a  part  of  the  tongue,  usually  ending  in  abscess.  The 
most  frequent  cause  is  the  sting  of  a  bee  or  wasp,  or  it  may  follow  burns  or  severe 
cauterization.  In  the  rare  instances  when  it  is  apparently  spontaneous,  it  is 
probable  that  some  little  wound  has  afforded  ingress  to  the  inflammatory  poison. 

The  symptoms  of  acute  glossitis  are  very  violent  in  the  severer  cases.  The 
tongue  is  enormously  swollen,  so  as  sometimes  to  protrude  from  the  mouth.  It 
has  a  thick,  soft,  purulent  coating,  and  often  presents  excoriations  and  ulcera- 
tions. The  subjective  symptoms  are  very  disagreeable.  The  patient  has  violent 
pain.  Talking  and  eating  are  almost  impossible.  There  is  usually  catarrhal 
inflammation  of  the  rest  of  the  mouth.  The  cervical  lymphatic  glands  are 
swollen.  The  salivation  is  profuse  and  very  annoying.  In  many  cases  the 
tongue  swells  so  much  as  to  cause  dyspnoea  and  more  or  less  suffocation.  There 
is  usually  fever. 

Treatment  consists  in  the  employment  of  ice,  which  the  patient  should  keep 
constantly  in  his  mouth,  if  possible.  Very  great  relief  follows  deep  scarification 
done  in  a  few  places  where  the  swelling  is  greatest.  As  soon  as  fluctuation  is 
obtained,  we  must  give  exit  to  the  pus.  This  is  usually  followed  by  a  rapid 
abatement  of  the  discomfort,  and  complete  recovery.  It  is  the  exception  that  the 
increasing  dyspnoea  necessitates  tracheotomy. 

2.  Glossitis  Dissecans. — This  is  a  chronic  disease,  of  comparatively  rare  occur- 
rence and  unknown  aetiology.  It  causes  the  gradual  development  upon  the  sur- 
face of  the  tongue  of  a  number  of  deep  flssures  and  indentations,  giving  the  organ 
an  uneven  and  ragged  look.  The  pain  is  due  to  the  frequent  presence  of  excoria- 
tions and  ulcers  in  these  fissures. 

The  trouble  is  not  intrinsically  dangerous,  nor  does  it  need  special  treatment. 
We  must  try  the  same  remedies  which  have  been  mentioned  above  in  connection 
with  the  various  forms  of  stomatitis,  such  as  antiseptic  mouth-washes,  the  chew- 
ing of  bilberries,  etc.  If  ulcers  are  present  they  sometimes  require  cauterization 
with  lunar  caustic. 

3.  Lingual  Psoriasis.  Leucoplacia.  (Tylosis;  Ichthyosis  linguce  ei  oris.) — 
This,  again,  is  a  superficial  disease,  the  astiology  of  which  is  unknown.  It  consists 
in  localized  circular  hyperplasiee  of  the  epithelium  of  the  tongue,  rarely  conjoined 
with  similar  spots  upon  the  cheeks  and  lips.  The  central  portion  of  mucous  mem- 
brane which  is  surrounded  by  this  whitish,  slightly  raised,  and  more  or  less 
circular,  wall  of  epithelium,  is  abnormally  smooth  and  of  a  reddish  color.  Usu- 
ally the  tongue  takes  on  a  resemblance  to  a  map  (lingua  geographica).  The  dis- 
ease generally  persists  for  years,  and  without  sjmiptoms  except  in  severe  cases. 
Often  it  is  found  by  chance  in  individuals  who  have  known  nothing  about  the 
unusual  appearance  of  their  tongues.  Still,  it  may  cause  a  hypochondriac  endless 
anxiety,  especially  if  he  takes  it  to  be  syphilitic. 

This  last  statement  applies  still  better  to  a  peculiar  disease  allied  to  psoriasis. 
It  is  called  leucoplacia,  and  affects  the  mucous  membrane  of  the  tongue  and 
mouth.  Usually  it  causes  the  appearance,  on  the  lateral  borders  of  the  tongue,  of 
dull-whitish  spots,  which  have  the  look  of  scars,  and  are  generally  somewhat 
notched.     As  a  rule,  the  lower  surface  of  the  tongue  and  the  cheeks  display  at  the 


NOMA  389 

same  time  similar  Tvliite  spots,  which  are  evidently  due  merely  to  thickening  of 
the  epithelium.  Certain  spots  may  disappear,  but  they  are  sure  to  be  replaced  by 
others,  so  that,  so  far  as  has  yet  been  observed,  the  disease  must  be  regarded  as 
incurable.  Still,  it  is  not  of  great  importance,  as  a  rule,  for  in  many  cases  the 
local  discomfort  is  very  slight.  If  the  indentations  along  the  sides  of  the  tongue 
become  cracked  or  ulcerated,  then  there  may  be  great  pain.  Leucoplacia  is  very 
often  associated  with  bodily  states  of  neurasthenia,  or  hypochondriasis,  particu- 
larly if  the  leucoplacia  appears  in  a  person  with  a  syphilitic  taint,  which  happens 
with  remarkable  frequency.  But  it  is  certainly  not  to  be  regarded  as  a  tertiary 
symptom,  rather  perhaps  as  a  sort  of  sequel  to  sj'philis,  although  many  cases  have 
no  connection  whatever  with  the  latter  disease.  Anti-syphilitic  treatment  is 
invariably  useless.  It  is  for  this  very  reason  important  that  the  physician  should 
be  well  acquainted  with  leucoplacia,  that  he  may  spare  his  patient  needless  anx- 
iety and  ineffectual,  or  perhaps  actually  harmful,  treatment  with  mercury.  The 
disease  has  no  relation  to  excessive  smoking,  one  proof  of  which  is  that  we  have 
seen  the  condition  in  women.  The  only  danger  of  leucoplacia  is  that  sometimes 
lingual  carcinoma  may  eventually  develop  on  the  spot  affected  with  it.  We  have 
in  this  case  to  deal  with  a  process  which  is  analogous  to  the  development  of  ven- 
tricular carcinoma  in  the  scars  of  old  ulcers,  or  of  cancer  of  the  gall-bladder  sub- 
sequently to  gall-stones.  Treatment  is,  as  we  have  said,  usually  unsuccessful. 
Still,  thorough  cleanliness  and  good  care  of  the  mouth  may  avert  any  great  dis- 
comfort. We  may  try  the  efPect  of  painting  the  spots  with  a  four-per-cent.  solu- 
tion of  borax,  or  a  five-per-cent.  solution  of  chromic  acid.  Lately  the  frequent 
chewing  of  boiled  bilberries  has  been  recommended  for  leucoplacia,  and  we  have 
had  good  results  from  this  procedure. 


CHAPTEK   YI 
NOMA 

(  Water-cancer.     Cancrum  oris) 

Noma  is  a  gangrene  of  the  cheek,  apparently  of  spontaneous  origin,  and  attack- 
ing chiefly  feeble  and  sickly  children.  The  disease  is  rare.  It  may  be  primary, 
but  it  is  usually  a  sequel  of  severe  diseases,  such  as  measles,  scarlet  fever,  typhus 
and  typhoid  fevers,  and  pneumonia.  Now  and  then  it  has  been  observed  in  adults. 
A  priori,  it  is  extremely  probable  that  noma  is  due  to  some  parasitic  micro-organ- 
ism ;  but  the  matter  has  not  yet  been  minutely  investigated.  It  deserves  mention 
that  noma  is  said  to  occur  with  miich  greater  relative  frequency  in  moist  regions 
along  the  coast — for  example,  in  Holland — than  in  Germany. 

The  disease  begins,  without  any  evident  occasion,  in  an  insignificant  spot  of 
gangrene  on  the  inner  surface  of  the  cheek — that  is,  in  the  mucous  membrane.  It 
is  usually  situated  near  the  corner  of  the  mouth.  Externally,  the  parts  are  soon 
swollen  by  collateral  oedema,  and  the  whole  cheek  gradually  becomes  hard  and 
infiltrated.  At  first,  all  we  see  upon  the  mucous  membrane  is  a  dirty-greenish 
spot  not  much  larger  than  a  silver  dime,  but  soon  the  whole  cheek  and  the  neigh- 
boring parts  are  one  mass  of  gangrene.  Bits  of  dead  tissue  come  away,  and  foul- 
smelling  ichor  flows  continuously  into  the  mouth.  The  collateral  oedema  may 
finally  pervade  that  entire  half  of  the  face.  The  neighboring  lymph-glands  are 
always  greatly  swollen. 

This  condition  is  as  a  rule  accompanied  by  fever,  often  reaching  or  ex- 
ceeding 104°  (40°  C).     The  general  health  may  indeed  for  a  time  be  astonish- 


390  DISEASES    OF   THE   DIGESTIVE   OEGANS 

ingly  little  affected;  but  gradually  prostration  comes  on,  or  even  general  sepsis 
develops,  with  fever,  stupor,  and  delirium.  Erequently  lobular  pneumonia,  which 
may  have  a  gangrenous  character,  is  produced  by  the  inhalation  of  sloughing  bits 
of  tissue ;  and  often  the  ichor,  being  swallowed,  excites  violent  and  offensive  diar- 
rhoea. The  local  discomfort  is  not  really  very  considerable  in  most  cases,  com- 
pared to  the  severity  of  the  disease.    There  may  even  be  no  pain  felt  whatever. 

The  prognosis  is  almost  always  fatal.  Death  sometimes  occurs  suddenly  from 
collapse.  Sometimes  it  comes  at  the  end  of  three  or  four  weeks,  from  a  gradual 
sinking  of  the  bodily  powers.  Recovery  has  been  seen  in  only  a  few  cases :  there 
is  a  line  of  demarkation  formed,  the  sloughs  come  away,  and  a  slow  convalescence 
follows,  leaving  extensive  and  usually  very  disfiguring  scars  behind. 

Treatment  must  have  for  its  chief  object  to  check  further  extension  of  the 
gangrene,  by  removing  all  parts  that  are  already  destroyed.  Local  cauterization 
with  concentrated  hydrochloric  acid,  or  fuming  nitric  acid,  or  lunar  caustic,  or 
chloride  of  iron,  is  usually  futile.  It  is  probably  the  best  way  to  remove  all  the 
gangrenous  portion  by  means  of  Paquelin's  thermo-cautery.  At  least  in  the  early 
stages  of  noma  we  may  hope  something  from  this  method  of  treatment ;  but  if  the 
case  is  far  advanced,  we  can  hardly  expect  to  accomplish  much. 

We  should  also  disinfect  the  mouth  as  thoroughly  as  possible.  The  most 
efficient  means  is  to  syringe  it  out  with  solutions  of  salicylic  or  carbolic  acids,  or 
permanganate  of  potash.  We  should  do  our  best  to  maintain  the  patient's 
strength. 


CHAPTER   VII 
PAROTITIS 


Parotitis,  or  inflammation  of  the  parotid  gland,  appears  not  only  as  a  pecul- 
iar, primary,  infectious  disease,  usually  epidemic,  but  also  as  a  secondary  compli- 
cation of  numerous  other  severe  diseases.  These  two  forms  should  be  considered 
separately. 

1.  Idiopathic,  Primary  Parotitis  (Epidemic  Mumps). — .Sltiology. — The  dis- 
ease occurs  in  epidemics  that,  although  not  very  frequent,  may  be  quite  extensive. 
Endemics  also  occur,  in  barracks  and  schools;  and  here  and  there  a  sporadic  case 
is  seen.  Children  and  young  adults  are  most  liable  to  it.  Nursing  infants  enjoy 
a  marked  immunity,  as  well  as  elderly  persons.  Males  are  much  oftener  attacked 
than  females. 

There  can  be  no  doubt  that  mumps  is  a  specific  infectious  disease,  and  claims 
have  already  been  made  of  the  discovery  of  its  specific  bacillus,  but  these  lack 
confirmation.  Still,  it  is  natural  to  suppose  that  the  infectious  matter  reaches 
the  gland  by  way  of  Steno's  duct.  Numerous  observations  support  the  view  that 
the  disease  is  directly  contagious;  but  the  degree  of  contagiousness  is  not  great. 
Perhaps  the  saliva  of  patients  has  something  to  do  with  the  extension  of  epidemic 
mumps.  The  period  of.  incubation  seems  to  vary.  On  the  average,  it  is  about 
fourteen  days. 

Clinical  History. — There  may  be  a  prodromal  stage  of  one  or  two  days,  with 
mild  feverish  symptoms.  The  disease  itself  begins  with  swelling  of  one  parotid 
gland.  The  swelling  is  directly  below  and  in  front  of  the  lobe  of  the  ear,  which 
is  gradually  pushed  upward.  In  the  next  few  days  the  swelling  rapidly  increases, 
and  it  and  the  collateral  oedema  of  the  cheek  and  floor  of  the  mouth  may  become 
very  considerable.     The  face  is  much  distorted,  but  often  makes  a  very  comical 


PAKOTITIS  391 

impression,  especially  as  everybody  knows  how  harmless  the  disease  is.     In  most 
cases  the  other  gland  also  swells  a  few  days  later. 

Suppuration  scarcely  ever  occurs  in  genuine  mumps.  If  it  is  seen  as  a  rare 
exception,  it  is  probably  due  to  secondary  infection.  The  swelling  often  becomes 
very  hard.  Generally  it  has  a  somewhat  doughy  consistency.  The  corresponding 
portion  of  skin  is  usually  pale  and  shiny.  The  submaxillary  gland  not  infre- 
quently swells  also  in  addition  to  the  parotid,  and  this  may  occur  upon  one  or 
both  sides  of  the  neck.  Penzoldt  has  observed  cases  in  which  the  submaxillary 
and  STiblingual  were  swollen,  but  not  the  parotid.  We  ourselves  have  seen  a 
swelling  of  the  submaxillary  precede  the  parotitis.  The  sublingual  gland  also 
seems  sometimes  to  be  involved  with  the  parotid. 

The  local  discomfort  is  moderate  in  most  cases.  There  are  local  pain  and 
difficulty  in  chewing,  but  less  in  swallowing  and  talking.  Often  quite  a  severe 
stomatitis  develops,  with  foul  breath. 

There  sometimes  seems  to  be  no  fever  whatever.  Usually  there  is  a  moderate 
elevation  of  temperature.  Often,  however,  it  reaches  102.5°-104°  (39°-40°  C). 
Only  occasionally  has  there  been  a  case  with  grave  typhoidal  symptoms. 

Complications. — It  is  not  rare  for  men  to  have  a  swollen  testicle  with  inflam- 
matory serous  exudation  into  the  tunica  vaginalis,  which  may  be  quite  painful, 
but  which  usually  subsides  in  a  few  days.  The  orchitis  is  usually  ushered  in  with 
a  fresh  rise  of  fever.  Resultant  suppuration  is  a  rare  occurrence.  Once  we  saw 
the  orchitis  appear  several  days  before  the  swelling  of  the  parotid  gland.  Double 
orchitis  is  rare.  In  boys  this  complication  is  much  more  exceptional  than  in 
adults.  Some  observers  have  mentioned  analogous  swellings  of  the  female  geni- 
tals (oophoritis)  and  mammae,  but  this  is  very  rare.  Sometimes  mumps  is  asso- 
ciated with  herpes  labialis. 

The  prognosis  of  epidemic  parotitis  is,  as  we  have  said,  almost  always  favor- 
able. The  trouble  seldom  lasts  more  than  a  week  or  ten  days,  when  the  swelling 
goes  down,  and  the  patient  completely  recovers.  Possible  but  exceptional  sequelae 
are :  ptyalism ;  cessation  of  the  salivary  secretion ;  chronic  swelling  of  the  paro- 
tid; deafness;  and  atrophy  of  the  testicle. 

The  diagnosis  is  easy.  The  only  thing  to  exclude  is  swelling  of  the  lymph- 
glands,  and  they  never  have  exactly  the  same  location  as  the  parotid. 

Special  treatment  is  hardly  necessary.  Children  should  be  kept  in  bed.  Usu- 
ally some  salve,  or  vaseline,  is  applied  to  lessen  the  feeling  of  tension.  If  reso- 
lution is  tedious,  we  may  paint  the  swelling  with  iodoform  collodion  (1-15)  or 
with  tincture  of  iodine;  or  we  may  prescribe  iodoform  ointment  (1-15).  If  there 
is  orchitis,  the  testicle  must  be  elevated,  as  by  a  suspensory  bandage.  If  the 
pain  and  swelling  are  marked,  an  ice-bag  should  be  applied. 

2.  Secondary  Suppurative  Parotitis. — This  secondary  form  may  be  a  compli- 
cation of  any  grave  disease.  In  most  cases  it  is  due  to  inflammatory  agents, 
probably  staphylococci  in  most  cases,  generated  by  decomposition  of  the  contents 
of  the  mouth,  which  agents  reach  the  gland  through  Steno's  duct.  It  was  formerly 
the  universal  belief  that  the  infection  was  metastatic,  being  conveyed  through 
the  blood-vessels;  but  it  is  not  certain  whether  this  occurs.  It  is  probable  that 
the  py^emic  form  is  in  many  instances  thus  produced.  Secondary  parotitis  is 
most  frequently  observed  in  typhus  and  typhoid  fevers.  It  is  also  seen  occasion- 
ally in  all  other  severe  acute  diseases,  and  in  phthisis  and  carcinoma. 

The  parotid  gland  swells,  just  as  in  the  primary  disease.  It  is,  however,  much 
oftener  of  excessive  size,  and  in  the  majority  of  cases  suppurates.  If  one  has  an 
opportunity  to  make  an  autopsy  on  such  a  case  of  secondary  parotitis  in  its  early 
stages,  the  cross-section  of  the  swollen  gland  presents  a  large  number  of  rather 
small  discrete  abscesseS.  These  finally  unite  to  form  one  larger  abscess,  which 
usually  discharges  outward  through  the  skin  or  into  the  external  auditory  meatus. 


392  DISEASES    OE   THE   DIGESTIVE   OEGAI^S 

Sometimes  tlie  parotid  suffers  from  gangrenous  inflammation,  and  there  is"  ex- 
tensive sloughing.  If  such  a  case  finally  gets  well,  still,  as  a  rule,  some  permanent 
injuries  have  been  inflicted:  there  is  facial  paralysis,  due  to  destruction  of  the 
facial  nerve,  or  deafness,  caused  by  an  extension  of  the  inflammation  to  the 
middle  ear. 

The  treatment  of  secondary  parotitis  is  that  of  any  suppurative  inflammation. 
We  may  at  first  try  to  scatter  the  swelling  by  ice  or  iodoform  ointment,  but  this 
usually  fails.  As  soon  as  fluctuation  is  detected,  the  spot  must  be  incised,  and  a 
drainage-tube  inserted.  The  prognosis  depends  chiefly  on  the  nature  and  course 
of  the  original  disease. 


CHAPTEE   Yin 
ANGINA    LTJDOVICI 

The  name  angina  Ludovici  is  applied  to  a  rather  rare  phlegmonous  inflam- 
mation of  the  floor  of  the  mouth.  Probably  this  is  not  occasioned  by  a  specific 
cause,  but  is  only  a  special  localization  of  the  ordinary  germs  which  occasion 
suppuration.  Its  starting  place  seems  to  be  the  submaxillary  gland,  at  least  in 
most  cases.    It  may  be  primary,  or  a  complication  of  other  severe  acute  diseases. 

Angina  Ludovici  usually  begins  with  swelling  in  the  neighborhood  of  the  sub- 
maxillary gland.  The  swelling  rapidly  increases,  and  comes  to  involve  the  whole 
floor  of  the  mouth  and  the  anterior  surface  of  the  throat.  It  causes  great  discom- 
fort. Talking,  chewing,  and  swallowing  are  almost  impossible.  There  is  usually 
fever,  and  in  many  cases  we  even  find  the  symptoms  of  general  sepsis.  There 
may  be  great  dyspncea,  due  either  to  compression  of  the  larynx  or  to  oedema  of 
the  glottis.  The  final  result  in  some  cases  is  an  extensive  sloughing  of  the  soft 
parts.  This  has  the  special  name  of  cynanche  gangrcenosa.  In  other  cases  an 
abscess  forms,  and  points  outward  or  into  the  oral  cavity.  The  swelling  is  some- 
times, though  seldom,  reabsorbed. 

The  prognosis  should  always  be  guarded,  for  severe  constitutional  symptoms 
and  a  fatal  ending  are  not  infrequently  seen,  particularly  if  the  patient  has  a 
weakly  constitution.     There  may  also  be  repeated  exacerbations  and  relapses. 

Treatment. — At  the  commencement  of  the  disease  we  may  make  the  attempt, 
in  suitable  cases,  to  check  the  process  by  local  depletion  and  by  ice ;  but,  as  soon 
as  suppuration  or  gangrene  begins,  the  case  becomes  a  surgical  one.  ISTow  and 
then  the  threatening  asphyxia  demands  tracheotomy. 


CHAPTER  IX 

ANOMALIES    OF    DENTITION 

{Difficult  Dentition) 

The  processes  of  dentition  play  so  important  a  role  in  the  disorders  of  child- 
hood that  we  feel  obliged  to  discuss  the  subject,  at  least  briefly. 

The  first  appearance  of  any  of  the  milk-teeth  usually  takes  place  when  the 
child  is  seven  to  nine  months  old;  it  may,  hoAvever,  occur  either  earlier  or  later 
than  this  period.  As  a  rule,  the  two  lower  central  incisoVs  are  cut  first ;  then  the 
upper  central  incisors  appear,  a  few  weeks  later,  and  next  the  lateral  incisors  of 


*S4aii34  a  * 


ANOMALIES    OF   DENTITION  393 

the  upper  jaw.  In  the  beginning  of  the  second  year  come  the  lower  lateral  inci- 
sors, and  almost  simultaneously  the  four  anterior  molars.  The  four  canine,  or 
"  eye  "  and  "  stomach"  teeth,  are  cut  in  the  second  half  of  the  second  year;  and 
last  of  all  comes  the  eruption  of  the  four  posterior  molars.  The  first  dentition  is 
therefore  completed  by  the  end  of  the  second  or  in  the  beginning  of,  the  third  year, 
with  the  development  of  all  the  twenty  milk-teeth.  The  accompanying  diagram 
(Fig.  44),  after  Vogel,  represents  the  order  in  which  the  separate  teeth  appear. 
In  the   fifth   or   sixth  year   the   milk-teeth 

begin  to  be  replaced  by  the  permanent  teeth  ^.JrrrTTrTrrrrAr^s 

of  the  second  dentition.  "  Trouble  with 
teething,"  however,  almost  invariably  refers 
to  anomalies  of  the  first  dentition. 

Noticeable  delay  in  teething  is  frequent 
in  weakly,  and  particularly  in  rachitic  chil-  ^**^^lCl£\£IDIlDJ 

dren,  in  whom  the  teeth  may  develop  not  in 
pairs    and    in    symmetrical    groups,    as    in  Fig.  44. 

healthy   children,    but    in    irregular   succes- 
sion.   In  such  cases,  sometimes,  all  the  teeth  are  not  cut  till  the  end  of  the  third 
year. 

On  the  other  hand,  it  sometimes  happens  that  certain  teeth  appear  very  early, 
or  even  are  present  at  birth.  If  an  abnormally  early  tooth  is  only  loosely  in- 
serted in  the  gums,  it  should  be  removed  with  the  forceps ;  for  it  interferes  with 
nursing,  and  injures  the  opposing  surface  of  the  mouth;  but  if  the  tooth  is  firm 
in  its  place,  we  let  it  be. 

During  the  eruption  of  the  teeth  there  is  in  every  child  considerable  redness  of 
the  mucous  membrane  and  an  increased  flow  of  saliva.  The  child  evidently  feels 
an  itching  in  the  mouth,  and  therefore  a  constant  desire  to  bite  something.  This 
simple  catarrh  is  sometimes  accompanied  by  a  slight  rise  in  temperature.  Occa- 
sionally there  is  a  severe  stomatitis,  with  which  fever  and  thrush  may  be  asso- 
ciated.    These  troubles  should  be  treated  as  already  described. 

In  consequence  of  the  salivation,  and  the  large  amount  of  saliva  which  is  swal- 
lowed, in  which  the  various  processes  of  decomposition  are  apt  to  develop,  we 
often  see  gastro-intestinal  diseases  in  teething  children.  In  most  children  a  tem- 
porary and  mild  diarrhoea  occurs.  We  should  be  particularly  careful  at  this 
period  about  the  child's  nourishment,  and  in  treating  any  marked  gastro-intes- 
tinal symptoms.  Experience  shows  also  that  teething  children  are  unusually 
liable  to  simple  or  even  capillary  bronchitis,  and  catarrhal  pneumonia. 

Nervous  disturbances  are  often  referred  to  dentition.  The  most  important 
symptom  of  this  kind  is  eclampsia.  The  attacks  are  sometimes  called  "  teething- 
convulsions."  Although  the  laity  go  too  far  in  ascribing  all  sorts  of  nervous  dis- 
orders to  teething,  still  experienced  specialists  do  recognize  the  possibility  of  such 
an  origin  for  many  cases.  Some  of  the  convulsions  may  in  fact  be  regarded  as 
reflex  (vide  infra  the  chapter  on  the  convulsions  of  children,  page  1151). 

When  the  upper  canines,  or  "  eye-teeth,"  are  being  cut,  there  is  sometimes  a 
unilateral  purulent  conjunctivitis,  which  is  perhaps  to  be  explained  as  an  exten- 
sion of  the  inflammation  by  way  of  the  antrum  of  Highmore  and  the  nostrils. 
Eczema  and  other  cutaneous  eruptions  have  been  often  ascribed  to  dentition, 
whether  justly  or  not  is  doubtful.  Yet  it  is  remarkable  that  little  children 
sometimes  have  an  eruption  of  facial  eczema  with  the  appearance  of  every  tooth. 

There  is,  of  course,  no  special  treatment  for  difficult  dentition;  and  the  vari- 
ous disturbances  which  it  may  indirectly  produce  are  to  be  treated  on  general 
principles. 


394  DISEASES    OF   THE   DIGESTIVE    ORGANS 


SECTIOISr  II 

Diseases  of  the  Soft  Palate,  Tonsils,  Pharynx,  and  Naso- 
pharynx 

CHAPTER   I 

SORE    THROAT 

{Inflammation  of  the  Soft  Palate  and  of  the  Tonsils) 

Etiology. — Acute  inflammation  of  the  soft  palate  and  tonsils,  in  its  various 
forms,  is  one  of  the  commonest  of  diseases.  Almost  everybody  has  had  personal 
experience  with  it.  It  is  chiefly  a  disease  of  early  life,  being  infrequent  after  the 
thirty-fifth  year.  Individual  predisposition  to  it  varies  greatly.  There  are  per- 
sons who  have  one  or  more  attacks  almost  every  year,  while  with  others  attacks 
are  rare  and  insignificant.  In  many  instances  exciting  causes  have  evidently 
been  potent.  Chief  among  these  is  catching  cold;  the  sufferer  has  had  wet  feet, 
or  has  been  talking  in  a  damp,  cold  atmosphere.  Most  cases,  therefore,  occur  in 
cool  weather,  although  now  and  then  attacks  may  occur  in  the  hottest  days  of 
summer.  Again,  direct  injuries  of  the  pharynx  may  produce  the  disease,  e.  g., 
the  smoky  atmosphere  of  inns,  combined  with  loud  talking  or  shouting;  the 
inspiration  of  poisonous  vapors;  cauterization  of  the  mucous  membrane  with 
concentrated  acids,  alkalies,  and  other  chemical  agents;  and  burns. 

Apart,  however,  from  these  last-named  external  irritants  we  have  many 
cases  of  primary  angina,  for  which  we  must  assume  an  infectious  origin.  This 
supposition  is  suggested  by  the  severity  of  the  constitutional  disturbance,  with 
fever,  the  nature  of  the  local  process  (giving  rise  to  suppuration),  and  the  occa- 
sional appearance  of  the  disease  in  an  epidemic  or  endemic  form.  At  the  same 
time,  exposure  to  cold  and  the  other  exciting  causes  above  mentioned,  may  often 
favor  its  development.  [Especially  when  tonsillitis  recLirs  in  an  individual,  or 
attacks  several  members  of  the  same  household  about  the  same  time,  it  is  well  to 
have  the  drainage  carefully  examined.  The  precise  connection  between  bad 
drainage  and  sore  throats  we  do  not  know,  but  that  they  are  often  connected  there 
seems  to  be  no  doubt.]  With  regard  to  the  nature  of  the  infectious  organism, 
there  is  as  yet  great  uncertainty.  When  the  tonsillitis  is  of  the  suppurative  par- 
enchymatous variety,  it  is  almost  certain  that  we  have  to  deal  not  with  specific 
germs,  but  with  staphylococci  and  other  ordinary  pus-organisms.  The  same  is 
probably  true  of  follicular  tonsillitis  also,  although  several  different  kinds  of 
pathogenic  organisms  may  be  concerned;  thus  we  may  find  not  only  staphylo- 
cocci, streptococci,  and  particularly  diplococci,  but  probably,  in  many  cases,  even 
the  genuine  diphtheria  bacillus. 

Frequently  the  inflammation  is  due  to  extension  from  neighboring  parts,  as 
in  coryza,  laryngitis,  and  stomatitis.  In  many  cases  both  affections  are  simulta- 
neous results  of  one  common  cause.  Finally,  sore  throat  may  be  a  symptom  of 
many  acute  infectious  diseases,  such  as  scarlet  fever,  measles,  small-pox,  and  ery- 
sipelas. 

To  distinguish  between  an  inflammation  of  the  soft  palate  by  itself  and  an 
affection  of  the  tonsils  is  not  practicable.  In  most  cases  the  tonsils  are  the 
stronghold  of  the  disease ;  less  often  we  find  the  inflammation  limited  to  the  soft 
palate. 

Clinical  History. — The  most  important  subjective  symptom  of  sore  throat, 
and  that  by  which  it  is  usually  first  recognized,  is  the  dilficult  and  painful  deglu- 
tition.    The  pain  is  sometimes  manifest  before  any  objective  changes  are  to  be 


SOKE   THROAT  395 

seen.  It  may  in  a  severe  case  be  very  violent  and  distressing.  The  pain  has  a 
"  darting  "  character,  or  sometimes  is  "  burning  " ;  and  it  is  most  acute  whenever 
the  patient  swallows,  although  in  well-marked  cases  it  seldom  entirely  intermits. 
Swallowing  is  not  only  painful,  but  it  is  laborious;  it  requires  more  than  usual 
effort  and  time.  The  patient  feels  constantly  as  if  he  had  to  swallow  a  big  lump. 
This  sensation  is  worse  if  the  tonsils  are  swollen.  It  is  a  matter  of  experience 
that  not  infrequently  an  "  empty "  swallowing  hurts  more  than  swallowing  a 
liquid  or  some  half -solid  substance. 

Talking  is  also  difficult.  Every  word  may  be  painful,  so  that  the  patient 
expresses  his  wishes  as  briefly  as  possible.  Even  in  a  mild  case,  speaking  for  any 
length  of  time  will  produce  a  burning  pain  in  the  throat.  The  impaired  mobility 
of  the  soft  palate  often  prevents  the  complete  cutting  off  of  the  nasal  passages  in 
talking,  so  that  the  voice  has  a  nasal  twang ;  and  often  it  sounds  as  if  the  patient 
were  talking  with  his  mouth  full :  he  has  the  "  voice  of  sore  throat." 

Further  local  discomfort  results  from  the  mucus  and  saliva  collecting  in  the 
mouth.  Salivation  is  not  infrequent,  probably  as  a  result  of  the  stomatitis  usu- 
ally present.  In  other  cases  the  patient  complains  that  his  mouth  feels  dry  and 
sticky.  Frequently  there  is  a  persistent  bad  taste  in  the  mouth,  and  the  breath 
is  disagreeable. 

With  these  local  disturbances,  more  or  less  severe  constitutional  symptoms  are 
almost  always  conjoined.  Indeed,  these  latter  may  begin  a  day  or  two  earlier 
than  the  local  symptoms.  The  patient  is  indisposed,  languid,  has  anorexia  and 
headache.  The  general  disturbance  may  be  surprisingly  great  in  comparison 
with  the  slight  objective  changes  in  the  tonsils. 

There  is  fever  in  most  of  the  well-marked  cases;  it  may  even  be  quite  high. 
Temperatures  of  103°  or  104°  (39.5°-40°  C),  or  even  higher,  are  not  rare.  Sore 
throat  can  not  be  said  to  have  one  particular  type  of  fever.  Usually  the  fever 
,appears  rather  abruptly,  remains  high  for  several  days,  with  an  occasional  slight 
interruption,  and  then  falls  with  equal  abruptness  to  normal  again. 

The  entire  attack  usually  lasts  only  a  few  days,  seldom  more  than  a  week. 
Even  when  a  person  is  quite  ill  for  several  days,  convalescence  is  almost  always 
rapid  and  complete — that  is,  if  the  patient  has  a  good  constitution. 

Special  complications  are  very  infrequent,  except  that  the  neighboring  parts — 
the  larynx,  mouth,  and  throat — are  not  seldom  involved.  Herpes  labialis  is  quite 
frequent.     Beyond  this  there  is  nothing  to  mention. 

Various  Forms  of  Sore  Throat 

The  symptoms  thus  far  mentioned  are  much  the  same  in  all  cases  of  sore 
throat,  varying  only  in  intensity  and  duration.  But  the  objective  changes  to  be 
observed  in  the  soft  palate  and  tonsils  are  noticeably  different  in  different  cases. 
Whether  the  aetiology  differs  also  we  have  no  certain  information.  In  some 
instances  it  seems  probable  that  it  does. 

We  shall  distinguish  five  chief  varieties  of  acute  sore  throat.  Transitional 
forms  are,  however,  by  no  means  rare.  Genuine  diphtheria,  which  is  a  specific, 
acute,  infectious  disease,  and  which  has  already  been  discussed,  does  not  need  to 
be  brought  up  again  here. 

1.  Catarrhal  Sore  Throat  (Simple  Catarrhal  Inflammation  of  the  Mucous 
Memhrane  of  the  Soft  Palate). — There  is  a  more  or  less  vivid  reddening  of  the 
mucous  membrane,  either  uniform  or  in  patches.  The  swelling  is  most  marked 
in  the  pillars  of  the  fauces  and  the  uvula.  The  surface  of  the  tonsils  is  likewise 
reddened;  their  size  may  be  somewhat  increased,  or  remain  unchanged.  The 
mucous  membrane  of  the  palate  and  uvula  may  be  covered  here  and  there  with  a 
thin  layer  of  muco-pus,  which  can  easily  be  wiped  off.  The  tonsils  may  present 
small,  superficial  erosions,  scattered  about.     These  little  ulcers  are  apt  to  lie  at 


396  DISEASES    OF   THE   DIGESTIVE   0EGA:N"S 

tlie  openings  of  the  follicles.  The  small  "  blisters  "  which  are  often  seen  on  the 
mucous  membrane  of  the  soft  palate  may  be  caused  in  various  ways.  Either  they 
are  mucous  glands  or  solitary  follicles,  swollen;  or,  rarely,  they  are  real  vesicles 
tilled  with  a  clear  fluid  and  produced  by  a  raising  up  of  the  epithelium.  The  cer- 
vical lymph-glands  are  usually  but  slightly  swollen,  if  at  all. 

This  is  the  common  and  mildest  form  of  sore  throat ;  and  it  may  be  over  in  a 
day  or  two.  In  some  instances,  however,  it  causes  considerable  local  and  gen- 
eral discomfort ;  but  the  disease  seldom  lasts  longer  than  five  to  eight  days. 

2.  Follicular  Tonsillitis. — ^In  this  form  there  is  not  only  more  or  less  catarrhal 
inflammation  of  the  soft  palate,  btit  a  decided  swelling  of  one  or  both  tonsils. 
On  the  reddened  surface  of  these  swollen  bodies  are  whitish-yellow  spots,  varying 
in  number  from  two  or  three  to  ten  or  more,  and  corresponding  to  the  follicles. 
These  spots  are  often  seen  to  be  plugs  projecting  from  the  openings  of  the  folli- 
cles. It  is  usually  easy  to  press  out  the  pasty  contents  of  the  follicle,  represented 
by  the  white  speck,  with  a  spatula.  The  microscope  shows  it  to  consist  of  numer- 
ous epithelial  cells  and  pus-corpuscles,  bacteria,  and  detritus,  and  sometimes  there 
are  also  crystals  of  the  fat  acids  and  cholesterine.  The  pus-corpuscles  may  so 
predominate  that  we  may  have  small  follicular  abscesses,  which,  on  being  opened, 
leave  superficial  ulcers  behind.  The  parenchyma  of  the  tonsil  is  swollen  with  a 
serous  and  cellular  infiltration,  increasing  the  bulk  of  the  part.  The  trouble  is 
usually  bilateral,  though  often  more  marked  and  extensive  on  one  side  than  on 
the  other.  In  the  severer  cases  the  cervical  lymph-glands  are  swollen.  The 
local  symptoms  and  still  more  the  constitutional  disturbance  in  follicular  ton- 
sillitis may  be  decided.  The  fever  not  infrequently  reaches  104°  (40°  C.)  or 
even  higher.  The  patient  feels  very  languid,  has  no  appetite,  and  complains  of 
headache;  but  there  are  mild  as  well  as  severe  cases.  The  disease  never  lasts 
longer  than  a  few  days,  even  when  the  fever  is  high  at  first.  The  yellow  spots 
vanish  from  the  tonsils,  and  there  is  rapid  recovery;  severe  complications  are 
hardly  ever  seen.  Often  there  is  a  herpes  labialis  and  there  may  be  slight  albu- 
minuria, but  this  very  rarely  amoimts  to  a  genuine  acute  nephritis.  It  should 
be  mentioned  that  sometimes  the  contents  of  a  few  of  the  follicles  remain  in 
them  for  a  considerable  length  of  time,  and  become  inspissated  and  calcified.  It 
is  not  a  rare  thing  to  find  such  plugs  in  the  tonsils  of  those  who  are  subject  to 
sore  throat.  Timid  and  hypochondriacal  individuals  are  sometimes  badly  fright- 
ened by  expectorating  these  old  chalky  plugs,  which  they  believe  to  be  "  tuber- 
cles"! 

From  an  etiological  standpoint,  follicular  tonsillitis  is  in  most  cases  entirely 
distinct  from  genuine  diphtheria,  and  so  far  the  search  for  the  Klebs-Lofiler 
bacillus  in  the  plugs  contained  in  the  follicles  has  almost  invariably  proved 
negative.  Still  it  is  noteworthy  that  precisely  at  the  time  of  diphtheria  epidem- 
ics follicular  tonsillitis  is  remarkably  frequent.  It  might,  after  all,  be  pos- 
sible that  the  mildest  degrees  of  diphtheria  present  themselves  in  the  garb  of  an 
apparently  simple  follicular  tonsillitis.  The  latter  is  very  probably  an  infec- 
tious disease;  but  this  matter  has  not  yet  been  settled  by  pathological  investi- 
gations. 

3.  Tonsillar  and  Peritonsillar  Abscess  (Parenchymatous  Sore  Throat; 
Quinsy). — In  this  form  the  swelling  of  the  tonsils  is  the  most  striking  sjnnptom. 
They  may  be  more  than  twice  their  natural  size.  The  anterior  pillars  of  the 
fauces  are  pushed  forward  and  become  convex.  The  swelling  extends  so  far 
toward  the  median  line  that  the  tonsil  touches  the  uvula;  or,  if  the  affection  is 
bilateral,  the  two  tonsils  press  against  each  other,  grasping  the  uvula  between 
them,  or  pushing  it  forward.  The  soft  palate  is  very  much  reddened,  particularly 
at  first.  Its  surface  is  usually  thickly  covered  with  mucus.  If  this  be  wiped  off, 
the  mucous  membrane  is  seen  to  have  a  moist,  oedematous  luster.     The  mucous 


SOKE   THEOAT  397 

membrane  of  the  tonsils  not  infrequently  suffers  a  superficial  necrosis.  Follicular 
and  parenchymatous  tonsillitis  are  often  combined. 

In  well-marked  cases  of  abscess  the  local  discomfort  is  usually  great.  With 
every  attempt  to  swallow  there  is  pain  which  shoots  into  the  ear.  The  patient 
is  in  a  pitiable  condition ;  he  can  neither  talk,  nor  swallow,  nor  gargle.  The  few 
words  which  he  painfully  utters  have  in  an  extreme  degree  the  nasal  quality  of 
the  "  voice  of  sore  throat." 

In  the  milder  cases  the  trouble  seldom  lasts  but  a  few  days  before  the  swell- 
ing goes  down,  and  the  discomfort  and  usually  rather  moderate  fever  gradually 
abate.  In  other  cases  an  abscess  of  the  tonsil  develops,  usually  on  one  side  only, 
but  it  would  be  more  correct  to  say  a  peritonsillar  abscess,  for  the  pus  usually 
collects  mainly  in  the  connective  tissue  between  the  tonsil  and  the  arch  of  the 
palate.  In  such  cases  the  mucous  m.embrane  bulges  out,  usually  at  a  point  in 
the  velum  of  the  palate,  and  on  palpation  there  is  a  sense  of  fluctuation,  and 
finally  the  abscess  ruptures.  In  other  cases,  however,  a  tonsillar  abscess  forms, 
as  a  rule,  on  only  one  side.  The  mucous  membrane  bulges  out  more  in  one  spot ; 
fluctuation  is  detected;  and,  finally,  the  abscess  breaks.  With  the  discharge  of 
the  pus  the  pain  is  relieved  very  rapidly,  or  it  may  vanish  at  once.  The  rest  of 
the  tonsil  soon  regains  its  former  size,  and  in  a  few  days  the  patient  is  well.  Re- 
lapses are  possible,  but  rare. 

Phlegmonous  sore  throat,  in  which  the  soft  palate  and  not  the  tonsil  is  chiefly 
affected,  is  infrequent.  Its  usual  cause  is  some  severe  external  injury,  such  as 
burns,  and  cauterization  with  concentrated  acids  or  alkalies.  The  swelling  ex- 
tends deep  down  into  the  submucous  tissue.  The  uvula  may  have  the  diameter  of 
one's  finger.  There  is  intense  hypersemia.  Sometimes  there  are  haemorrhages 
into  the  mucous  membrane :  this  is  called  haemorrhagic  sore  throat.* 

4.  Necrotic  Tonsillitis,  or  Necrotic  Sore  Throat. — This  name  is  applied  to  a 
disease  which  is  very  frequent  in  Leipsic,  but  seems  to  be  rather  rare  in  Erlangen, 
and  in  which  the  tonsils  are  the  main  seat  of  the  pathological  processes.  The 
pillars  of  the  fauces  and  the  uvula  are  but  slightly  affected  with  a  simple  ca- 
tarrhal inflammation.  The  tonsils  are,  as  a  rule,  moderately  swollen,  seldom  at- 
taining great  size.  The  mucous  membrane  covering  them  presents  a  whitish  or 
grayish-white  discoloration,  often  quite  extensive,  and  most  marked  on  the  side 
toward  the  uvula.  These  spots  are  often  erroneously  said  to  be  a  white  "  coat- 
ing " ;  but  a  more  careful  investigation  shows  that  there  is  in  reality  a  necrosis. 
The  process  may  be  superficial ;  sometimes  it  reaches  quite  deeply  into  the  struc- 
ture of  the  mucous  membrane.  It  is  not  possible  to  pull  off  this  white  matter, 
as  one  can  loosen  croupous  membranes,  although  little  bits  may  perhaps  be 
scratched  off  with  a  spatula  or  a  pair  of  forceps.  These  particles  are  found,  on 
microscopic  examination,  to  be  made  up  merely  of  detritus,  bacteria,  epithelium, 
and  pus-corpuscles.  The  necrosis  is  almost  invariably  confined  to  the  tonsils, 
and  a  sharp  boundary-line  separates  it  from  the  reddened  and  inflamed  pillars 
of  the  fauces.  After  a  few  days  the  slough  may  come  away,  leaving  behind  an 
ulcer,  which,  though  usually  shallow,  has  sometimes  a  considerable  depth.  This 
generally  cleans  up  rapidly.  In  severe  cases,  however,  the  floor  of  the  ulcer 
consists  for  a  number  of  days  of  a  dirty  necrotic  material,  which  comes 
away  only  gradually.  The  worst  cases  may  be  properly  called  "  gangrenous  ton- 
sillitis." 

Necrotic  tonsillitis  is  almost  always  attended  by  considerable  fever  and 
marked  constitutional  disturbance.     Children  particularly  seem  very  ill  in  the 

*  Another  form  with  the  same  name  occurs  where  there  is  violent  tonsillitis  with  necrosis  or  gan- 
grene. There  is  also  a  necrotic,  hsemorrliagic  sore  throat  accompanying  scurvy,  leukteraia,  and  analo- 
gous diseases. 


398  DISEASES    OF   THE   DIGESTIVE    OEGA^^S 

first  days  of  the  attack.  The  cervical  glands  are  usually  swollen,  but  seldom  as 
much  so  as  in  genuine  diphtheria. 

Despite  the  rather  ominous  commencement,  the  disease  does  not  last  a  great 
deal  longer  than  the  other  forms'  of  sore  throat.  It  seldom  continues  more  than 
five  to  eight  days  before  a  speedy  convalescence  begins. 

The  necrotic  tonsillitis  is  distinguished  from  the  follicular  form  by  the  greater 
area  of  the  white  or  grayish-white  spots.  Still  it  should  be  particularly  noted 
that  sometimes  combinations  of  these  two  varieties,  or  transitional  forms,  occur. 

Etiology. — In  our  opinion,  necrotic  tonsillitis  is  in  many  instances  an  en- 
tirely different  disease  from  genuine  diphtheria.  Perhaps  it  is  often  a  very 
intense  form  of  follicular  tonsillitis,  not  limited,  as  it  usually  is,  to  the  follicles. 
On  the  other  hand,  our  experience  in  sevei-al  epidemics  of  diphtheria  in  Leipsic 
and  Erlaugen  has  taught  us  that  in  all  probability  mild  cases  of  genuine  diph- 
theria of  the  tonsils  do  occur,  and  that  these  objectively  resemble  necrotic  ton- 
sillitis. This  is  the  only  way  to  explain  what  other  physicians  as  well  as  our- 
selves have  often  observed — namely,  that  necrotic  tonsillitis  appears  not  infre- 
quently in  families  at  the  same  time  with  severe  cases  of  genuine  diphtheria. 
Besides,  these  cases  of  necrotic  tonsillitis  are  sometimes  followed  by  the  char- 
acteristic "  diphtheritic  "  paralysis.  Still,  more  extensive  pathological  investiga- 
tion is  needed  to  settle  the  question  of  the  setiology  of  necrotic  tonsillitis. 

Diagnosis  and  Prognosis. — It  is  never  very  difficult  to  recognize  a  sore  throat, 
and  a  little  practice  makes  it  easy  in  m.ost  cases  to  decide  what  particular  vari- 
ety is  present,  if  we  examine  the  objective  changes  carefully.  It  is  very  important 
in  practice  to  distinguish  diphtheria  from  the  benign  forms  of  inflammation. 
Eollicular  and  necrotic  tonsillitis  are  very  frequently  mistaken  for  diphtheria — 
an  error  which  explains  the  success  of  a  large  number  of  remedies  said  to  cure 
diphtheria.  Many  physicians  call  every  case  of  sore  throat,  where  there  is  any- 
thing white  to  be  seen,  "  diphtheria."  Certainty  in  diagnosis  of  genuine  diphthe- 
ria can  be  gained  only  by  practice ;  no  description,  however  complete,  can  take  the 
place  of  personal  observation.  It  may  be  a  help  to  remember  that  in  both  follicu- 
lar and  necrotic  tonsillitis  the  white  spots  are  usually  limited  to  the  tonsils,  while 
in  croupous  sore  throat  the  deposits  are  generally  from  the  very  first  also  situated 
upon  the  pillars  of  the  fauces  and  the  uvula.  The  white  spots  of  the  follicular 
variety  can  generally  be  recognized  by  their  arrangement.  The  plugs  are  seen 
projecting  from  the  follicles.  In  necrotic  sore  throat  there  is  never  a  separable 
croupous  membrane  with  its  characteristic  histological  structure,  but  there  is  sim- 
ply a  superficial  necrosis  of  the  mucous  membrane  and  parenchyma.  In  doubtful 
eases  the  condition  of  the  cervical  lymph-glands  is  not  unimportant;  as  a  rule, 
they  are  much  more  affected  in  diphtheria  than  in  the  benign  cases.  Inasmuch 
as  we  have  seen  that  the  milder  forms  of  tonsillitis  may  be  setiologically  related 
to  diphtheria,  it  is  well  in  practice  to  make  a  guarded  prognosis,  even  in  cases  of 
follicular  and  necrotic  angina,  particularly  in  children;  and  we  should  always 
isolate  the  patient  from  other  children. 

Treatment. — These  troubles  iim  so  favorable  a  course  that  active  treatment  is 
very  seldom  needed.  The  gargle  usually  prescribed  generally  gives  the  patient 
more  discomfort  than  relief.  The  most  common  prescriptions  are:  Solutions  of 
potassic  chlorate  (5-10  :  300),  of  alum  (5-10  :  500),  or  of  boras  (10  :  300) ;  salt 
and  water;  and  weak  solutions  of  carbolic  acid  or  of  peiTuanganate  of  potash. 
To  paint  the  parts  is  a  useless  and  now  almost  obsolete  proceeding.  Inhalations 
of  spray  are  better,  with  alkaline  solutions,  diluted  lime-water,  alum,  or  tannin. 
It  is  beneficial  to  put  a  cold  wet  compress  around  the  throat.  Children  must  be 
kept  in  bed,  and  adults  are  generally  forced  to  go  to  bed,  if  the  constitutional 
symptoms  are  well  marked. 

In  parenchymatous  tonsillitis  with  a  tendency  to  suppuration  ice  will  some- 


CHEONIC   HYPEETEOPHY   OF   THE    TONSILS       '        399 

times  alleviate  the  pain.  Often,  however,  the  patient  can  not  bear  it.  If  there 
is  evident  fluctuation,  we  can  make  an  incision  Avith  a  spear-pointed  bistoury, 
after  guarding  a  portion  of  the  blade  with  sticking-plaster.  The  best  place  is 
almost  always  in  the  velum  palati,  corresponding  to  the  outer  boundary  of  the 
tonsil.  Great  relief  follows;  and  even  if  there  is  no  distinct  abscess  an  incision 
will  usually  give  relief,  if  there  is  excessive  swelling,  and  if  there  is  a  deeply- 
seated  abscess  will  facilitate  its  spontaneous  discharge.  Punctures  of  this  sort 
cause  scarcely  any  pain. 

We  may  add  that  if  a  person  is  subject  to  sore  throat,  he  can  lessen  his  liability 
to  attacks  by  hardening  his  skin  through  the  use  of  cold  baths.  [Hoffman  has 
pointed  out  that  in  some  cases  pennanent  recovery  can  be  attained  by  breaking 
do\vn  the  partitions  between  the  crypts  of  the  tonsils,  thus  establishing  thorough 
discharge  of  their  secretions. — V.] 


CHAPTEE   II 
CHRONIC    HYPERTROPHY    OF    THE    TONSILS 

Chkonic  hypertrophy  of  the  tonsils  occurs  not  only  in  those  who  have  had 
repeated  attacks  of  tonsillitis,  but  also  in  cases  in  which  no  occasion  for  it  can  be 
found.  Even  in  childhood  there  may  be  well-marked  hypertrophy,  which  must 
be  due  to  a  congenital  predisposition. 

The  condition  is  at  once  revealed  by  inspection.  There  may  be  no  signs  what- 
ever of  any  acute  or  chronic  inflammation,  or  there  may  be  an  accompanying 
chronic  pharyngitis.  The  tonsils  bulge  out  in  two  great  lumps.  They  may  be  so 
large  as  to  touch  the  uvula  on  each  side.  Histologically,  there  is  a  genuine  hyper- 
trophy of  the  organ — that  is,  an  increase  of  all  its  component  tissues. 

In  many  cases,  where  the  swelling  is  moderate,  there  is  no  discomfort.  The 
possessor  of  the  tonsils  is  not  aware  that  they  are  enlarged.  In  other  cases  the 
hypertrophy  proves  of  clinical  importance,  inasmuch  as  all  forms  of  sore  throat 
are  found  to  occur  more  frequently  if  the  tonsils  are  enlarged,  and  to  cause  more 
trouble  when  they  do  appear.  The  hypertrophied  organs  may  also  be  the  seat  of 
a  chronic  catarrh,  which  by  extension  gives  rise  to  chronic  nasal  catarrh,  catarrh 
of  the  Eustachian  tubes,  or  hoarseness. 

If  the  hypertrophy  is  considerable,  the  local  discomfort  may  be  quite  marked, 
.  Swallowing  is  rendered  difiicult,  if  not  painful.  Frequently  there  is  evident 
dyspnoea.  The  patient  has  to  breathe  through  his  mouth,  and  sometimes  when 
asleep  snores  and  snorts  in  a  way  to  frighten  one.  Children  are  particularly  apt 
to  suffer  in  this  manner.  Many  instances  of  pavor  nocturnus,  or  "  night  terrors," 
in  children  are  referable  to  this  cause.  We  have  already  mentioned  that  cases  of 
bronchial  asthma  sometimes  seem  to  be  connected  with  hypertrophy  of  the  tonsils 
(see  page  182). 

Treatment. — The  attempt  to  reduce  the  enlargement  by  applying  lunar  caus- 
tic, tincture  of  iodine,  etc.,  usually  fails.  If  there  is  much  distress,  if  the  patient 
is  subject  to  frequent  sore  throats,  or  if  the  hypertrophy  of  the  tonsils  keeps  up  a 
chronic  nasal  or  pharyngeal  catarrh,  then  the  simplest  remedy  is  to  remove  the 
tonsils.  The  operation  is  free  from  any  danger.  The  extirpation  of  hypertrophied 
tonsils  can  be  accomplished  either  with  the  tonsillotome,  the  galvano-cautery,  or 
with  scissors  and  forceps.  The  latter  way  is  the  simpler,  and  is  equally  easy. 
[In  adults,  excision  of  the  tonsils  sometimes  causes  troublesome  bleeding,  and  for 
them  the  galvano-caustic  snare  is  the  best  means  to  employ. — V.] 


400  DISEASES    OF   THE   DIGESTIVE    OKGAKS 

CHAPTEE   III 
CHRONIC    PHARYNGITIS 

iEtiology. — It  is  not  practicable  to  distinguish  between  chronic  catarrh  of  the 
soft  palate  and  of  the  pharynx,  for,  as  a  rule,  the  two  are  combined.  Sometimes 
the  condition  is  the  result  of  repeated  acute  attacks;  sometimes — and  probably 
oftener — it  is  due  to  persistent,  injurious,  local  influences.  A  large  number  of 
eases  originate  in  bad  habits,  or  in  abuse  incident  to  certain  vocations.  Exam- 
ples are  seen  in  smokers,  drunkards,  singers,  preachers,  teachers,  and  men  who 
work  out-doors.  In  talking  and  singing,  the  soft  palate  is  strained;  or  the  dis- 
ease is  excited  by  breathing  cold  or  impure  air,  or  by  such  chemical  irritants  as 
alcohol  or  tobacco.  In  many  cases,  chronic  pharyngitis  follows  chronic  rhinitis  or 
chronic  laryngitis.  The  general  passive  congestion  due  to  cardiac  disease  or  pul- 
monary emphysema  may  sometimes  promote  the  development,  or  prolong  the  ex- 
istence, of  a  chronic  pharyngitis. 

Symptoms. — The  local  discomfort  is  often  slight.  The  patient  gets  used  to  it, 
and  does  not  mind  it  except  when  there  is  some  exacerbation.  It  becomes  a  more 
important  matter  if  the  calling  of  the  patient  is  interfered  with,  as  in  a  preacher, 
singer,  or  teacher. 

I  Deglutition  is  seldom  impaired.  There  is  often,  however,  a  constant  feeling 
of  dryness,  burning,  or  scratching  in  the  throat.  The  patient  has  to  clear  his 
throat  frequently,  and  often  acquires  an  habitual,  short,  sudden  cough,  which  may 
or  may  not  be  dry.  The  expectoration,  if  there  is  any,  is  almost  pure  mucus. 
When  there  are  violent  efforts  to  clear  the  throat,  there  may  be  a  slight  haemor- 
rhage from  the  dilated  blood-vessels  of  the  posterior  wall  of  the  pharynx,  explain- 
ing the  presence  of  small  amounts  of  blood  in  the  expectoration.  This  blood 
often  has  a  dried-up  look,  as  if  not  fresh.  It  sometimes  leads  over-anxious  pa- 
tients and  physicians  to  suspect  pulmonary  hsemorrhage.  The  uvula  becomes  so 
long  that  its  tip  rests  on  the  tongue  or  the  posterior  wall  of  the  pharynx;  and 
this  gives  rise  to  a  peculiar  and  disagreeable  sensation  of  tickling.  All  these 
uncomfortable  feelings  are  temporarily  increased  if  anything  affects  the  throat 
unfavorably;  and  they  are  generally  at  their  worst  on  rising  in  the  morning, 
apparently  because  the  mucous  membrane  has  become  dry,  or  a  collection  of 
tough  mucus  has  formed  during  the  night.  Every  one  knows  how  drunkards  have 
to  hawk  and  cough  in  the  morning,  so  that  often  they  almost  strangle  or  vomit. 

On  inspection,  we  generally  find  the  mucous  membrane  reddened.  Very  often 
a  number  of  dilated  and  tortuous  veins  are  visible  both  on  the  soft  palate  and  in 
the  back  of  the  throat.  Of  equal  frequency  is  the  appearance  of  numerous  small 
gray  projections,  corresponding  usually  to  swollen  follicles  or  else  to  hyper- 
trophied  mucous  glands.  This  is  called  granular  pharyngitis.  Small  follicular 
ulcers  are  not  infrequent.  Exceptionally  there  are  more  extensive  catarrhal 
ulcers.  The  mucous  membrane  of  the  posterior  wall  of  the  pharynx  may  present 
patches  of  opaque  or  thickened  epithelium,  giving  the  surface  a  grayish-white 
appearance. 

Frequently  chronic  pharyngitis  is  combined  with  chronic  laryngitis,  evidenced 
by  hoarseness;  or  with  posterior  nasal  catarrh,  or  catarrh  of  the  Eustachian  tube, 
producing  deafness  and  ringing  in  the  ears. 

Varieties  of  Chronic  Pharyngitis 
1.  Chronic  Catarrh  of  the  Naso-pharynx,  or  Chronic  Posterior  Nasal  Ca- 
tarrh.— This  has  the  same  aetiology  as  the  ordinary  form.     It  is  practically  im- 
portant because  the  nose  and  ear  are  frequently  involved. 


CHRONIC   PHARYNGITIS  401 

The  anatomical  changes  are  essentially  those  already  depicted  under  chronic 
pharyngitis.  The  region  affected  can  not  be  seen  by  direct  inspection,  so  that 
accuracy  in  diagnosis  requires  the  use  of  a  nasal  speculum  (see  particulars  in  the 
works  mentioned  on  page  135).  The  ordinary-  examination  of  the  throat  may 
reveal  a  condition  which  is  quite  characteristic  of  posterior  nasal  catarrh :  a  col- 
lection of  mueo-pus,  or  of  firmly  adherent  dry  crusts,  rests  upon  the  posterior 
wall  of  the  pharynx,  and  can  be  seen  to  extend  upward  toward  the  naso-pharynx. 

The  local  discomfort  is  somewhat  similar  to  that  experienced  in  chronic 
pharyngitis.  There  is  a  scratchy  feeling,  or  a  feeling  as  if  there  were  a  foreign 
body  in  the  back  of  the  throat,  accompanied  by  a  constant  desire  to  blow  the  nose, 
hawk  or  cough.  Dried  and  decomposing  secretion  often  causes  extremely  foul 
breath.     There  is  often  also  vertigo,  and  occipital  headache. 

In  many  cases  the  nostrils  are  stopped  up.  The  posterior  opening  of  the  nos- 
trils is  closed  in  part  by  the  swelling  and  hypertrophy  of  the  mucous  membrane, 
and  in  part  by  the  accumulated  secretions.  The  patient,  therefore,  usually  has 
to  breathe  through  the  mouth.  The  ear  is  frequently  involved.  The  catarrh 
extends  into  the  Eustachian  tubes  and  the  tympanic  cavity,  or  the  opening  of  the 
tubes  is  occluded  with  the  secretions.  For  a  detailed  consideration  of  the  deaf- 
ness, tinnitus,  etc.,  thus  produced,  consult  works  on  otology. 

2.  Pharyngitis  Sicca,  or  ''Dry  Atrophic  Catarrh  of  the  Throat  and  Naso- 
pharynx."'— This  name  is  applied  to  an  atrophic  disease  of  the  mucous  membrane, 
which  sometimes  is  spontaneous  and  sometimes  is  a  sequel  of  chronic  pharyngitis. 
The  vv'hole  mucous  membrane  of  the  pharynx  and  the  naso-pharynx  (seen  with  the 
rhinoscope)  seems  pale,  smooth,  and  perfectly  dry,  and  has  a  peculiar  luster,  as  if 
varnished.  Here  and  there  tortuous  veins  project  from  the  general  anEemic 
surface. 

If  an  opportunity  is  afforded  to  examine  the  mucous  membrane  microscopic- 
ally, it  will  be  found  that  the  atrophy  involves  all  the  elements  of  the  tissue, 
though  the  follicles  and  mucous  glands  suffer  most. 

This  condition  may  not  cause  any  symptoms,  but,  in  many  cases,  the  patient 
suffers  constantly  and  considerably.  The  chief  trouble  is  a  feeling  of  dryness  in 
the  throat,  rendering  deglutition  difficult  or  even  painful.  There  is  also  a  con- 
stant desire  to  clear  the  throat.  The  secretion  hawked  up  may  be  scanty  and 
tough  or  more  abundant,  and  it  is  often  tinged  with  blood.  Actual  coughing 
may  also  be  due  to  pharyngeal  trouble  ("  throat-cough  ").  Talking  is  often  ren- 
dered difficult,  the  voice  grows  weak  and  it  becomes  easily  tired.  In  severe 
cases  there  is  considerable  general  debility.  Not  infrequently  pharyngitis  sicca 
is  associated  with  atrophic  rhinitis  {q.  v.),  but  it  occurs  also  where  there  is  no 
nasal  disease. 

The  disease  is  most  frequently  seen  in  the  elderly,  but  it  also  occurs  in  children 
and  young  persons.  It  is  especially  common  in  ill-nourished  individuals  or  in 
those  who  are  suffering  from  such  diseases  as  tuberculosis  or  chronic  nephritis. 

3.  Hypertrophic  Catarrh  in  the  Pharynx  and  Naso-pharynx. — An  opposite 
condition,  of  hypertrophy,  sometimes  results  from  chronic  catarrh.  The  changes 
consist  mainly  in  hyperplasia  of  the  lymphatic  tissue,  and  they  are  usually 
termed  "  adenoid  growths."  The  choanse  and  the  posterior  extremity  of  the  nasal 
septum  may  be  almost  completely  hidden  by  these  growths,  as  they  extend  down 
from  the  roof  of  the  pharj^nx  in  grayish-red,  uneven  masses.  In  many  cases  the 
hypertrophy  seems  to  originate  chiefly  in  KoUiker's  "  pharyngeal  tonsil." 

The  adenoid  growths  are  especially  common  in  childhood.  The  symptoms 
consist  in  a  change  of  the  voice  (which  loses  its  reverberating  quality  and  becomes 
nasal),  frequent  snuffling  and  hawking,  and  a  tough  mucous  secretion,  often 
tinged  with  blood.  Not  infrequently  there  is  headache.  Of  greater  importance 
is  ear-trouble,  which  is  often  occasioned  by  the  growths. 
20 


402  DISEASES    OF    THE   DIGESTIVE    OEGAXS 

An.  accurate  diagnosis  requires  rhinoscopy.  Positive  results  are  also  ofteu 
obtained  by  palpation.  The  index-finger,  being  pressed  backward  and  bent  up- 
ward, can  touch  the  protuberances  and  the  enhirged  pharyngeal  tonsil  in  the 
naso-pharynx. 

Prognosis.- — In  all  varieties  of  chronic  pharyngeal  catarrh,  the  prognosis  as- 
to  recovery  is  doubtful,  for  in  all  severe  cases  the  process  is  very  obstinate,  and 
permanent  restoration  to  health  exceptional.  It  is  essential  for  the  best  results 
that  all  injurious  influences  should  be  removed.  Even  if  decided  improvement 
occurs  there  is  a  tendency  for  the  trouble  to  grow  worse  again,  and  for  acute 
exacerbations  to  occur. 

Treatment. — Many  of  the  milder  cases  never  apply  to  a  physician.  The  pa- 
tient uses  some  domestic  remedy  or  gargle,  or  becomes  so  accustomed  to  the  dis- 
agreeable sensations  that  he  does  not  consider  it  necessary  to  do  anything  in 
particular  about  them. 

The  treatment  of  a  well-developed  case  requires  great  patience  and  persist- 
ence on  the  part  of  all  concerned.  If  there  is  some  underlying  disease,  such  as 
pulmonary  or  cardiac  disease,  that  must  be  treated.  All  exciting  causes  must  be 
avoided.  Energetic  local  treatment  is  also  indispensable.  This  has  been  greatly 
elaborated  by  specialists,  and  for  the  many  details  we  must  refer  to  their  writ- 
ings ;  but  the  following  remarks  will  meet  the  requirements  of  ordinary  practice : 

Gargles  are  seldom  satisfactory,  for  they  never  reach  farther  than  the  soft 
palate.  Inhalations  are  better;  we  may  use  solutions  of  alum  or  tannin,  or,  in 
mild  cases,  of  common  salt.  Still  more  efficient  is  the  painting  of  the  entire  sur- 
face of  the  pharynx  with  some  concentrated  solution.  The  physician  usually  has 
to  perform  this,  althoug'h  some  patients  learn  to  do  it  for  themselves.  Proper 
solutions  are :  Argentic  nitrate,  five  or  ten  per  cent. ;  tannin,  eight  to  twenty  per 
cent.;  tincture  of  iodine,  either  pure  or  diluted;  or  iodized  glycerine,  composed 
of  pure  iodine,  parts  0.5;  iodide  of  potassium,  2;  glycerine,  20,  with  the  addi- 
tion, if  desired,  of  two  drops  of  oil  of  peppermint.  These  applications  must  reach 
all  the  diseased  surface.  If  the  naso-pharynx  is  involved,  the  brush  must  accord- 
ingly be  bent  upward,  to  reach  that  region.  For  this  a  mirror  may  be  needed. 
It  is  very  important  to  make  the  applications  to  the  mucous  membrane  itself^ 
freed  from  any  interposing  secretions. 

In  the  treatment  of  chronic  posterior  nasal  catarrh  the  nasal  douche  (vide  dis- 
eases of  the  nose)  plays  an  important  part.  It  should  be  used  two  or  three  times 
a  day.  It  not  only  removes  the  collected  secretions,  but  it  is  a  means  of  making 
local  applications.  The  instrument  is  merely  a  fountain-syringe.  The  nozzle 
must  be  of  a  size  to  fill  the  nostril  completely.  The  force  of  the  current  should 
always  be  moderate,  and  the  patient's  head  should  be  sharply  flexed  forward. 
The  fluid  used — the  best  is  a  one-per-cent.  solution  of  sodic  chloride  or  bicarbonate 
— must  have  about  the  temperature  of  the  body.  Other  medicated  solutions  must 
be  very  weak,  such  as  sulphate  of  zinc,  1  to  1,000. 

The  insufflation  of  powders  into  the  throat  can  be  made  through  any  small 
glass  tube,  three  to  six  times  a  week.  Alum  or  tannin  may  be  used,  either  pure 
or  mixed  with  equal  parts  of  pulvis  giunmosus  [P.  G.,  made  of  gum-arabic,  three 
parts;  licorice-root,  two  parts;  and  sugar,  one  part],  or  3-5  parts  of  nitrate  of 
silver  to  100  of  starch.  For  the  naso-pharynx,  a  bent  tube  of  glass  or  hard 
rubber  is  to  be  introduced  through  the  mouth.  There  are  numerous  "  insuffla- 
tors "  to  be  had  at  the  instiiiment-makers. 

Many  baths  enjoy  a  great  reputation  for  the  cure  of  chronic  pharyngitis. 
Besides  Ems,  there  are  Reichenhall,  Kreuznach,  Salzungen,  the  cold  sulphur 
springs,  such  as  Weilbach.  and  many  others.  Good  results  are  also  achieved  in 
Kissingen  and  Marienbad,  if  these  places  are  favorable  to  the  patient's  general 
constitution. 


KETEOPHAKYNGEAL   ABSCESS  403 

In  pharyngitis  sicca,  the  nasal  douche  with  a  one-per-cent.  salt  solution  is  to 
be  recommended.  It  is  sometimes  also  beneficial  to  paint  the  parts  with  solution 
of  argentic  nitrate,  iodized  glycerine,  etc.  Many  irritating  influences  which  do 
harm  in  common  pharyngitis  seem  sometimes  actually  to  benefit  this  form — such 
as  smoking  and  taking  snufF. 

In  treating  the  hypertrophic  fonais  of  pharyngitis  and  the  adenoid  growths, 
cauterization  with  nitrate  of  silver  sufiices  for  the  milder  cases  alone.  A  thor- 
ough and  permanent  cure  can  be  achieved  only  by  removing  the  growths  with  the 
galvano-c  autery . 

[To  Hooper,  of  Boston,  belongs  the  credit  of  showing  that  a  radical  opera- 
tion for  the  removal  of  adenoid  growths  of  the  naso-pharynx  can  safely  be  done 
under  anaesthesia.  The  blood  does  not,  as  was  feared,  run  into  the  air-passages, 
but  either  into  the  stomach  or  outwardly.  Anaesthesia  thus  renders  it  possible 
to  scrape  away  with  the  finger  or  tear  away  with  forceps  the  hypertrophied  tissue 
at  one  sitting,  and  to  do  it  in  the  child  before  secondary  changes  have  taken  place 
in  the  facial  expression,  the  jaw,  the  ears,  or  the  form  of  the  chest.] 


CHAPTER   IV 
RETROPHARYNGEAL    ABSCESS 

Retropharyngeal  abscess  is  formed  by  a  suppurative  inflammation  of  the 
connective  tissue  lying  between  the  posterior  wall  of  the  pharynx  and  the  spinal 
column.  It  is  a  serious  disease,  although  a  rare  one.  If  unrecognized,  it  proves 
fatal  in  many  instances;  while,  if  a  correct  and  timely  diagnosis  is  made,  the 
patient  can  usually  be  easily  cured.  It  is  commonest  in  childhood,  and  before 
the  second  year.  It  almost  always  appears  as  a  primary,  acute  disease,  without 
any  special  cause  being  evident.  Probably  the  agents  which  excite  the  inflamma- 
tion penetrate  into  the  tissue  from  the  pharynx.  The  idea  that  the  inflammation 
originates  in  the  small  lymphatic  glands  which  lie  in  front  of  the  vertebrae  lacks 
proof  as  yet. 

The  disease  attacks  not  only  weakly  children,  but  those  who  have  been  per- 
fectly healthy  and  vigorous.  The  child  grows  restless  and  fretful,  and  does  not 
nurse  well.  Apparently,  deglutition  soon  becomes  painful,  but  one  can  not  be 
certain  about  this  except  in  older  children.  Generally,  the  respiration  quickly 
takes  on  a  peculiar  stertorous  character,  particularly  during  sleep.  Mucus  collects 
in  the  mouth  and  throat.  Upon  swallowing,  there  is  often  regurgitation  through 
the  mouth  or  nose,  or  some  of  the  food  gets  into  the  windpipe  and  causes  violent 
coughing.  The  lymph-glands  of  the  jaws  are  usually  somewhat  swollen,  and  the 
neighboring  parts  may  seem  slightly  oedematous.  After  a  week  or  two  the  dysp- 
ncea  gradually  increases.  Respiration  becomes  more  and  more  laborious,  with 
loud  rattling,  and  signs  of  stenosis.  The  jugular  veins  become  distended,  the 
lips  cyanotic,  and  portions  of  the  thorax  are  retracted  during  inspiration.  The 
voice  is  feeble,  and  may  be  hoarse  and  indistinct. 

The  correct  interpretation  of  these  symptoms,  which  are  common  to  various 
disorders,  requires  a  careful  examination  of  the  throat.  It  must  be  confessed 
that  this  has  its  difiiculties  in  an  infant.  Still,  we  can  sometimes  see  distinctly 
a  swelling  in  the  posterior  wall  of  the  pharynx.  This  may  be  either  in  the  median 
line  or  on  one  side.  All  doubt  is  removed  by  digital  examination,  in  making 
which,  however,  we  must  insert  a  wedge  between  the  teeth,  to  avoid  being  bitten. 
The  finger  detects  fluctuation. 


404  DISEASES    OF    THE   DIGESTIVE   OEGANS 

The  diagnosis  once  established,  the  abscess  must  be  opened  at  once.  We 
should  not  delay,  even  if  the  dyspnoea  has  not  yet  become  extreme.  To  use  the 
finger-nail  for  the  purpose,  as  has  been  recommended,  is  permissible  only  in  an 
emergency.  As  a  rule,  incision  is  made  with  a  bistoury,  of  which  all  but  the 
point  is  guarded  with  sticking-plaster.  The  left  index-finger  is  placed  upon  the 
abscess,  and  used  as  a  guide.  Meanwhile,  the  child's  head  is  kept  upright,  and,  as 
soon  as  the  cut  is  made,  bent  over  forward.  The  pus  pours  out  in  abundance.  It 
is  advisable  to  syringe  out  the  mouth  repeatedly  with  lukewarm  water.  The 
threatening  symptoms  vanish  almost  instantly  upon  the  escape  of  the  pus.  Ex- 
ceptionally, the  abscess  refills  and  requires  a  second  incision. 

If  the  trouble  is  not  correctly  diagnosticated,  or  if  the  abscess  is  not  opened 
promptly,  the  patient  may  suffocate.  The  abscess,  however,  may  burst  sponta- 
neously ;  then  there  is  either  speedy  recovery,  or  asphyxia  from  the  pus  filling  the 
larynx.  In  some  instances,  when  a  retropharyngeal  abscess  has  not  been  properly 
treated,  the  pus  has  gravitated  far  down  into  the  neck  and  posterior  mediastinTun. 
The  recognition  and  incision  of  the  abscess  may  prove  very  difficult  if  from  the 
start  it  is  situated  lower  down  in  the  throat  than  usual. 

Analogous  to  this  acute  idiopathic  abscess  of  which  we  have  been  speaking  is 
the  chronic  abscess  due  to  caries  of  the  cervical  vertebrae.  This  occurs  in  chil- 
dren as  well  as  adults.  Incision  of  such  abscesses  is  indicated  only  when  there 
is  danger  of  suffocation.  Because  of  their  tuberculous  character,  the  prognosis 
is,  of  course,  much  more  imfavorable  than  in  ordinary  suppurative  inflammation. 

Retropharyngeal  abscesses  sometimes  occur  in  pyaamia  or  other  severe  acute 
infectious  diseases,  but  they  have  hardly  any  interest  except  to  the  pathologist.* 


SECTION  III 
Diseases  of  the  CEsoPHAGUPi 

CHAPTER   I 

INFLAMMATION    AND    ITLCER    OF    THE    CESOPHAGUS 

etiology  and  Pathology. — The  various  forms  of  oesophageal  inflammation 
and  ulceration  are  not  of  very  great  clinical  importance.  The  processes  are  sel- 
dom of  a  severe  grade,  or,  if  so,  they  are  generally  a  part  of  some  complicated 
disease,  to  which  they  seldom  contribute  prominent  symptoms.  Very  likely  the 
milder  forms  of  inflammation  occur  frequently,  but  the  symptoms  are  hardly  ever 
characteristic. 

A  simple  catarrhal  inflammation  of  the  oesophageal  mucous  membrane  may 
be  caused  by  swallowing  substances  which  are  injurious  mechanically,  chem- 
ically, or  from  their  temperature.  It  may  also  occur  in  the  general  infectious 
diseases,  such  as  typhoid  and  typhus  fevers,  and  the  acute  exanthemata.  Any 
inflammation  of  neighboring  tissues  may  extend  into  the  oesophagus.  Chronic 
catarrh  is  seen  in  heart  disease,  from  the  passive  congestion.  It  is  also  found 
in  the  vicinity  of  other  chronic  oesophageal  diseases,  particularly  cancers  and 
diverticula  {vide  infra). 

*  Tuberculosis  of  the  pharynx  is  spoken  of  in  the  chapter  on  pulmonary  tuberculosis,  p.  248.  New 
growths  in  the  mouth  or  pharynx  belong  to  the  domain  of  surgery. 


INFLAMMATION   AND   ITLCEE   OF    THE   CESOPHAGUS        405 

The  acute  catarrh  is  distinguished  by  not  having  the  usual  increase_  of  secre- 
tion. The  epithelium  grows  spongy,  as  a  rule,  and  is  cast  off  more  rapidly  than 
usual,  so  as  to  suggest  the  name  of  a  desquamative  catarrh.  It  is  in  only  a  few 
cases  that  the  scanty  mucous  glands  become  swollen  and  look  like  papules  upon 
the  surface  of  the  membrane;  this  form  is  called  follicular  catarrh.  In  limited 
areas  the  desquamation  may  be  complete,  giving  rise  to  small  catarrhal  erosions. 
Likewise,  the  swollen  follicles  may  break  down  into  small  follicular  ulcers. 

In  chronic  catarrh  there  is  a  moderate  increase  in  the  secretion  of  mucus,  and 
a  marked  thickening  of  the  epithelium.  In  very  protracted  cases  actual  papillo- 
mata  may  finally  be  formed.     In  some  cases  ulcers  are  seen. 

Croupous  and  diphtheritic  inflammations  of  the  oesophagus  are  very  rare.  We 
have  already  said  that  the  specific  pharyngeal  diphtheria  frequently  extends  into 
the  larynx,  but  only  exceptionally  into  the  gullet.  Still,  we  have  ourselves  seen 
in  a  child  a  stricture  in  the  upper  third  of  the  oesophagus,  which  was  said  to  have 
been  a  result  of  a  severe  attack  of  diphtheria.  Isolated  cases  of  diphtheritic 
oesophagitis  have  also  been  seen  in  connection  with  severe  infectious  diseases, 
such  as  typhus,  typhoid,  small-pox,  cholera,  pysemia,  and  pulmonary  tuberculosis, 
as  well  as  in  the  course  of  Bright's  disease  and  cancer.  In  variola  it  is  not  un- 
usual for  pocks  to  appear  upon  the  oesophageal  mucous  membrane. 

A  purulent,  phlegmonous  oesophagitis  now  and  then  attacks  the  submucous 
layer.  It  may  be  either  diffuse  or  circumscribed.  The  mucous  membrane  is  dis- 
sected up  from  the  muscular  layer  by  the  pus,  and  pushed  inward,  so  as  to  dimin- 
ish the  lumen  of  the  oesophagus  more  or  less.  Most  of  the  cases  end  by  the  dis- 
charge of  matter  into  the  tube,  when  complete  recovery  may  ensue.  If  the  mu- 
cous membrane,  however,  has  been  extensively  undermined,  Zenker  states  that  a 
fissure-like  cavity  may  be  left,  even  after  healing  has  taken  place.  Its  walls  grow 
smooth,  and  finally  acquire  a  layer  of  fresh  epithelium. 

Purulent  oesophagitis  is  caused  either  by  the  presence  of  foreign  bodies  in  the 
oesophagus,  or  by  purulent  inflammation  in  neighboring  parts,  as  in  glandular 
abscess,  vertebral  abscess,  or  laryngeal  perichondritis.  It  has  now  and  then 
resulted  from  the  action  of  concentrated  acids  and  the  like  upon  the  mucous 
membrane. 

The  action  of  corrosive  poisons  (corrosive  oesophagitis)  is  to  cause  necrosis 
of  the  tissues,  which  in  its  turn  produces  inflammation.  The  inner  surface  of 
the  •  oesophagus  is  converted  into  a  rotten,  haemorrhagic,  sloughing  mass,  of  a 
dirty  gray  or  almost  black  color.  The  muscular  layer  itself  may  be  partly  de- 
stroyed. If  death  does  not  occur  speedily,  the  necrosed  portions  come  away,  leav- 
ing extensive  purulent  ulcers  behind.  These,  if  they  heal  at  all,  cause  large  cica- 
trices and  stenosis. 

Symptoms. — The  milder  cases,  as  we  have  stated,  produce  almost  no  distinc- 
tive symptoms.  Possibly  there  may  be  pain  along  the  oesophagus,  or  at  some  one 
point  in  it,  during  deglutition.  In  a  more  severe  case  the  pain  may  be  great; 
but  the  other  symptoms  are  usually  too  grave  for  this  to  excite  special  attention. 
Laborious  deglutition,  and  the  feeling  as  if  the  food  were  inclined  to  stick  in  the 
throat,  result  from  implication  of  the  muscular  layer.  A  diagnosis  of  the  par- 
ticular form  of  oesophagitis  is  attainable  only  when  the  aetiology  guides  us  to  it. 

Treatment  must  be  purely  symptomatic.  No  solid  food  should  be  taken.  The 
pain  is  to  be  allayed  by  bits  of  ice,  or  by  morphine. 


406  DISEASES    OF   THE   DIGESTIVE   OEGANS 

CHAPTEE   II 
DILATATION    OF    THE    CESOPHAGUS 

1.  Diffuse  Dilatation 

Diffuse,  spindle-shaped  dilatation  of  the  oesopliagus  is  observed  as  a  result  of 
stricture  of  the  cardiac  orifice.  At  first  the  muscular  coat  hypertrophies  as  the 
orifice  contracts,  and  is  able  to  overcome  the  obstruction,  so  that  there  is  no  dila- 
tation; but  as  soon  as  the  muscles  are  paralyzed,  and  food  collects  behind  the 
stricture,  the  dilatation  begins  and  keeps  on  increasing.  The  ectasis  is  greatest 
at  the  lower  end  of  the  tube,  as  is  natural  from  its  mode  of  origin,  and  gradually 
diminishes  upward. 

There  have  been  a  very  few  well-substantiated  instances  of  this  diffuse  spindle- 
shaped  dilatation,  without  any  demonstrable  stenosis  of  the  cardiac  orifice.  Their 
cause  is  unknown.  Sometimes  the  walls  of  the  oesophagus  may  have  been  ren- 
dered more  yielding  and  less  contractile  by  a  precedent  inflammation  or  other 
disorder.  In  other  cases,  some  chance  bend  or  distortion  of  the  lower  end  of  the 
oesophagus  may  have  produced  a  mechanical  obstruction.  In  some  cases  the  ex- 
citing cause  is  said  to  be  a  blow  on  the  chest,  or  the  lifting  of  a  heavy  weight. 
Perhaps  in  raany  cases  there  is  a  congenital  anomaly. 

The  symptom  of  this  condition,  when  well  developed,  is  a  chronic  difiiculty  in 
deglutition,  lasting  perhaps  for  years.  The  patient  himself  feels  that  most  of  the 
food  he  eats  does  not  reach  the  stomach,  but  lodges  higher  up.  Usually  the  food 
is  soon  afterward  vomited,  or  rather  gulped  up.  When  there  is  stenosis  of  the 
cardiac  orifice,  the  explanation  of  these  symptoms  is  easy.  It  is  much  harder 
to  explain  the  almost  equal  dysphagia  when  there  is  dilatation  without  stenosis. 
Sometimes  a  localized  bulging  of  the  wall  causes  the  food  to  collect  in  that  spot, 
and  thus  to  obstruct  the  lumen.  As  is  to  be  expected,  the  partial  or  complete 
hindrance  to  the  ingestion  of  food  results  in  marasmus. 

If  there  is  stenosis,  it  can  easily  be  detected  with  the  oesophageal  sound,  and 
all  the  symptoms  can  thus  be  explained.  In  the  rare  cases,  however,  of  diffuse 
dilatation  without  stenosis,  the  use  of  the  sound  does  not  give  us  so  much  infor- 
mation. If  the  instrument  passes  readily  into  the  stomach,  we  may  safely  exclude 
stricture;  but,  in  one  case  of  our  own,  we  made  an  erroneous  diagnosis  of  a 
diverticulum,  because  the  sound  sometimes  glided  readily  into  the  stomach,  and 
sometimes  could  not  be  passed.  A  pocket  must  have  been  formed  at  the  lower  end 
of  the  dilated  tube,  in  which  the  sound  caught. 

The  treatment  is  directed  chiefly  to  the  satisfactory  nourishment  of  the  pa- 
tient ;  for  the  oesophageal  trouble  itself  is  dangerous  only  as  it  prevents  the  taking 
of  food  and  leads  to  starvation.  We  do  not  speak  of  the  initial  lesion,  if  there  be 
one,  which  causes  the  dilatation.  If  nourishment  can  be  given  through  a  stom- 
ach-tube, the  patient  almost  invariably  shows  a  rapid  improvement,  which  lasts  as 
long  as  the  artificial  feeding  can  be  kept  up.  If,  however,  any  cause  prevents  the 
introduction  of  the  tube,  we  must  resort  either  to  nutrient  enemata  (vide  infra) — 
and  these  will  not  support  the  system  indefinitely — or  we  must  make  a  gastric 
fistula.  In  the  latter  case  the  prognosis  depends  on  the  success  of  the  operation 
and  the  nature  of  the  original  lesion. 

2.  Diverticula 

iEtiology  and  Pathology. — Circumsci-ibed  pouches  in  the  wall  of  the  oesopha- 
gus are  termed  diverticula.     They  are  divided  into  two  essentially  distinct  varie- 


DILATATIO^^   or    THE    (ESOPHAGUS  407 

ties  according  to  their  mode  of  origin.  Zenker  has  given  them  the  names  of 
pressure  and  traction  diverticula. 

The  diverticulum  due  to  pressure  is  extremely  rare.  It  is  caused  by  pressure 
upon  the  mucous  membrane  from  within,  by  which  some  abnormally  weak  spot 
is  forced  outward.  All  cases  that  have  been  carefully  examined  thus  far  have 
shown  that,  histologically,  the  wall  of  the  diverticulum  is  not  the  distended  but 
otherwise  unchanged  wall  of  the  oesophagus,  but  is  composed  exclusively  of  the 
mucous  membrane  and  the  thickened  submucous  coat.  We  are  therefore  obliged 
to  suppose  that  the  mucous  membrane  is  pushed  out  like  a  hernia  through  some 
gap  in  the  muscular  coat.  It  is  only  about  the  neck  of  the-  diverticulum  that  any 
muscular  fibers  are  found. 

The  original  factor,  therefore,  in  the  occurrence  of  a  pressure  diverticulum  is 
apparently  to  be  sought  in  some  circumscribed  lesion  of  the  muscular  coat.  As  a 
result  of  several  observations,  it  is  established  that  a  foreign  body,  sticking  in  the 
throat,  may  separate  some  of  the  muscular  fibers  and  push  the  mucous  membrane 
through  the  gap  thus  formed.  Or  a  severe  injury  leads  to  a  trifling  rupture  of 
the  muscular  coat,  and  then  the  food,  as  it  is  being  swallowed,  presses  out  the 
mucous  membrane  at  this  weakened  spot.  There  are  still  many  other  cases  in 
which  the  true  origin  of  the  diverticulum  remains  obscure. 

As  soon,  however,  as  the  formation  of  the  pouch  has  once  begun,  there  are 
many  influences  to  make  it  grow  larger.  Each  successive  bit  of  food,  as  it 
glides  by,  presses  upon  this  yielding  and  inelastic  spot.  Gradually  a  little  sac  is 
formed,  in  which  bits  of  food  lodge.  These  exercise  a  constant  pressure  upon  the 
walls  of  the  pouch,  and  by  their  weight  drag  it  bodily  downward.  The  larger  the 
pouch,  the  more  it  holds,  and  consequently  the  more  it  grows.  Thus  a  pressure 
diverticulum  of  the  smallest  size  originally  may  gradually  attain  to  a  diameter  of 
four  inches  or  more.  The  general  shape  of  the  diverticulum  may  approach  the 
Tiemi spherical,  or  it  may  be  more  cylindrical  or  pear-shaped. 

It  is  remarkable  that,  with  very  rare  exceptions,  these  pressure  diverticula  are 
always  situated  at  the  beginning  of  the  oesophagus,  or  rather  between  it  and 
the  pharynx,  and  almost  invariably  affect  the  posterior  wall.  The  pouch  hangs, 
therefore,  in  front  of  the  spinal  column.  It  pushes  out  through  the  lowest  fibers 
•of  the  inferior  constrictor  of  the  pharynx;  and  the  feebleness  of  this  muscle  is 
apparently  a  potent  factor  in  determining  the  precise  point  of  origin. 

The  cases  thus  far  seen  have  been  almost  all  in  men,  and  at  a  rather  advanced 
age.     A  few  cases  have  occurred  in  children. 

Traction  diverticula  are  much  more  common,  but  in  most  instances  have  little 
interest  except  for  the  pathologist.  They  are  not  infrequently  found  unexpected- 
ly at  the  autopsy.  Rokitansky,  and  later  Zenker,  have  given  explanations  of 
their  occurrence :  some  tissue,  which  has  formed  adhesions  to  the  oesophagus,  con- 
tracts and  gradually  pulls  out  the  oesophageal  wall  in  the  shape  of  a  funnel.  Bron- 
chial glands  are  apt  to  be  the  seat  of  the  contractile  change.  These  glands  are 
•situated  near  the  bifurcation  of  the  trachea,  and  accordingly  the  traction  diver- 
ticula occur  oftenest  at  this  level.  There  may  be  two  or  three  in  one  subject. 
'They  are  rarely  over  a  third  of  an  inch  in  depth.  From  within,  the  mucous 
membrane,  much  wrinkled  transversely,  is  seen  to  be  drawn  toward  the  apex  of  the 
•diverticulum.  The  wall  of  the  latter  consists  either  of  the  mucous  membrane 
alone,  bulging  out  like  a  hernia,  or  of  the  mucous  membrane  covered  by  the  mus- 
•cular  layer.  Inasmuch  as  children  quite  often  suffer  from  suppuration  and  case- 
ation of  bronchial  glands,  with  subsequent  shrinkage,  we  see  why  traction  diver- 
ticula are  frequent  in  children. 

Clinical  History. — The  large  pressure  diverticula  always  cause  grave  symp- 
toms, for  they  obstruct  more  and  more  each  day  the  passage  of  food.  At  first 
there  is  scarcely  any  disturbance.     Gradually,  however,  deglutition  is  impeded. 


408  DISEASES    OF   THE   DIGESTIVE    OEGANS 

A  portion  of  the  food  lodges  in  the  pouch,  and  is  either  wholly  or  in  part  regurgi- 
tated, though  perhaps  not  immediately.  Decomposition  is  apt  to  take  place  in 
the  contents  of  the  diverticulum,  giving  rise  to  foulness  of  the  breath  and  to 
nausea.  The  danger  reaches  its  climax  when  the  distended  sac  presses  sidewise 
upon  the  oesophagus  and  closes  its  lumen,  so  that  no  food  reaches  the  stomach. 
After  protracted  strangling  and  vomiting,  the  material  may  be  in  part  ejected, 
and  the  patient  enabled  once  more  to  swallow. 

Of  course  the  symptoms  in  individual  cases  depend  upon  the  mechanical  con- 
ditions present,  and  they  may  vary  greatly.  Patients  contrive  all  sorts  of  manip- 
ulations, by  which  they  manage  to  get  at  least  some  portion  of  their  food  down. 
Such  individuals  may  maintain  a  tolerable  degree  of  nutrition  for  years,  although 
they  scarcely  ever  are  in  a  normal  condition.  But  at  last  some  cause  or  other 
renders  the  amount  of  food  ingested  inadequate ;  whereupon  a  rapidly  progressive 
marasmus  sets  in,  and  the  patient  will  inevitably  starve  to  death  unless  some 
relief  is  afforded. 

The  most  valuable  objective  evidence  in  these  cases  is  gained  by  the  use  of  the 
oesophageal  sound.  If  the  sound  enters  the  sac,  its  passage  is  impeded.  If  it 
happens  to  slip  by  the  mouth"  of  the  diverticulum,  it  glides  readily  into  the 
stomach.  This  varying  result  may  sometimes  be  obtained  at  one  sitting  by 
repeated  trials,  and  is  of  the  greatest  importance  in  making  the  diagnosis. 

In  some  instances  where  the  sac  was  large,  a  tumor  in  the  neck  has  been 
observed  at  one  side  of  the  trachea,  appearing  after  eating  and  disappearing  when 
the  sac  emptied  itself.  Symptoms  due  to  compression  of  the  recurrent  and 
phrenic  nerves  and  of  the  blood-vessels  have  been  noticed  in  some  cases. 

Auscultation  of  the  cesophag-us  during  the  act  of  swallowing  has  been  prac- 
ticed, and,  of  late,  attempts  have  been  made  to  examine  it  with  a  speculum. 
Whether  these  methods  of  investigation  will  prove  valuable  for  diagnosticating 
diverticula,  experience  must  determine. 

The  traction  diverticula  are  usually  of  no  clinical  importance.  They  do  not 
affect  deglutition  at  all,  and  their  size  is  too  limited  to  permit  any  great  accumu- 
lation of  food  in  them.  There  is  but  one  way  in  which  they  are  dangerous :  the 
apex  of  the  funnel  may  undergo  ulceration  and  perforation.  A  foreign  body,  such 
as  some  bit  of  food,  produces  necrosis  of  the  wall,  by  what  is  probably  at  first  a 
purely  mechanical  irritation.  The  tissue  ulcerates ;  and  then  the  inflammation 
may  gradually  progress  till  it  causes  a  severe  and  usually  fatal  illness.  The  most 
frequent  event  is  perforation  into  a  bronchus,  followed  by  the  aspiration  of  food 
and  pulmonary  gangrene ;  or  the  perforation  may  take  place  into  the  pleiiral  cav- 
ity, exciting  an  ichorous  empyema.  In  other  cases  the  pericardium  or  a  large  vein 
has  been  perforated.  Many  a  case  of  apparently  spontaneous  pulmonary  gan- 
grene, or  purulent  inflammation  of  the  anterior  mediastinum,  or  empyema  has 
been  found  at  the  autopsy  to  have  been  brought  about  in  the  manner  above  indi- 
cated.    These  occurrences  are  fortunately,  however,  exceptional. 

Treatment. — The  only  possible  way  of  treating  the  large  pressure  diverticula 
successfully  would  be  by  operation.  Perhaps  surgery  will  some  day  win  victories 
in  this  domain.  In  the  meanwhile  our  efforts  are  confined  to  sustaining  the 
patient.  If  he  can  not  swallow,  we  must  try  to  feed  him  through  a  tube.  As 
long  as  this  is  possible,  starvation  is  averted.  It  is  well  to  have  the  patient 
pass  the  tube  himself.  He  will  find  out  how  best  to  avoid  the  sac  and  reach  the 
stomach.  If  food  can  no  longer  be  given  in  this  way,  there  remain  two  alterna- 
tives: rectal  feeding  (vide  infra),  or  making  a  gastric  fistula.  As  to  the  latter, 
there  has  been  thus  far  very  little  practical  experience,  because  cases  are  so  rare. 

The  traction  diverticula  admit  of  no  special  treatment.  If  the  events  above 
mentioned  occur,  we  must  endeavor  to  meet  the  indications  of  the  individual  case. 


STENOSIS    OF   THE   (ESOPHAGUS  409 

CHAPTER   III 
STENOSIS    OF    THE    (ESOPHAGUS 

etiology  and  Pathology. — Contractions  of  the  oesophagus  occur  with  such 
relatively  great  frequency  that  they  are  the  most  important  of  all  its  disorders. 
They  originate  in  various  ways.  By  far  the  commonest  cause  is  ring-shaped  car- 
cinoma of  the  tube.  The  new  growth  in  the  mucous  membrane  encroaches  more 
and  more  upon  the  lumen  of  the  oesophagus,  until  finally  it  fills  it.  Carcinoma 
will  be  discussed  at  length  in  the  next  chapter.  We  shall  here  confine  our  atten- 
tion to  its  purely  mechanical  action  in  causing  stenosis. 

OEsophageal  tumors  other  than  cancer  are  very  rare.  Fibrous  pedunculated 
polypi  have  been  observed  a  few  times.  They  usually  originate  in  the  lowest 
portion  of  the  anterior  wall  of  the  phaynx,  hanging  down  into  the  oesophagus, 
which  they  may  thus  obstruct. 

A  second  cause  of  stenosis  is  the  contraction  of  cicatrices  of  the  a3Sophageal 
wall.  The  most  frequent  occasion  for  this  is  the  extensive  ulceration  caused  by 
caustic  poisons,  such  as  concentrated  acids  or  alkalies.  If  the  victim  escapes  a 
speedy  death,  he  is  almost  certain  to  have  extensive  scars  formed  in  the  wall  of 
the  oesophagus.  These  scars  radiate  irregularly  in  all  directions,  and,  contract- 
ing, may  almost  completely  close  the  tube. 

Ulcers  from  other  causes,  resulting  in  stenosis  due  to  the  scars  they  leave,  are 
among  the  greatest  rarities.  Syphilis  has  been  the  well-established  cause  in  some 
instances,  and  Quincke  has  described  a  few  cases  in  which  there  were  ulcers  at  the 
lower  end  of  the  oesophagus  analogous  to  the  round  ulcer  of  the  stomach,  or 
"  ulcer  due  to  digestion  "  (vide  infra).  These  ulcers  also  may  eventually  produce 
cicatricial  stenosis. 

A  third  and  rare  cause  of  stenosis  of  the  oesophagus  is  compression  from 
tumors  external  to  it.  Such  swellings  may  originate  in  the  thyroid  gland,  or  in 
the  lymph-glands  of  the  neck  or  the  anterior  mediastinum;  or  the  swelling  may 
be  due  to  a  vertebral  abscess  or  an  aortic  aneurism.  This  form  of  stenosis  is  sel- 
dom extreme,  for  the  portion  of  the  tube  pressed  upon  is  usually  limited. 

ISText  on  the  list  after  stenosis  due  to  compression  is  usually  placed  what  is 
called  intermittent  dysphagia  {dysphagia  lusoria).  This  term  is  applied  to  the 
difiiculty  in  swallowing  which  is  said  to  be  caused  by  an  anomaly  in  the  course  of 
the  right  subclavian  artery.  The  artery  is  given  ofP  as  the  last  branch  from  the 
arch  of  the  aorta,  and  runs  toward  the  right  side  just  behind  or  just  in  front  of  the 
oesophagus.  It  seems,  however,  a  priori  improbable  that  the  feeble  pressure  of 
this  vessel  as  it  pulsates  should  impede  deglutition;  nor  has  it  yet  been  proved 
to  do  so.  It  would  be  more  natural  to  believe,  what  was  indeed  the  original  ex- 
planation of  the  phenomenon,  that  a  large  morsel  of  food  passing  down  the  oesoph- 
agus compresses  the  vessel  and  thus  excites  uneasiness  and  palpitation ;  but  so  far 
as  we  know  even  this  is  extremely  rare,  if  it  ever  occurs. 

Stenosis  due  to  foreign  bodies  belongs  to  surgery.  It  need  not  be  said  that 
the  clinical  symptoms  differ  greatly  in  different  cases.  Not  only  the  obstruction, 
but  also  a  possible  laceration  and  consequent  inflammation  are  to  be  considered. 
Occasionally  thrush  has  been  abundant  enough  to  cause  pronounced  symptoms  of 
stenosis. 

Above  the  point  of  stenosis,  no  matter  how  the  condition  arose,  if  only  it  is 
well  developed  and  has  lasted  a  certain  length  of  time,  the  circular  fibers  of  the 
muscular  coat  are  more  or  less  hypertrophied.  This  hypertrophy  is  due  to  the 
increased  force  required  to  propel  the  ingesta  downward.  In  many  cases  the  tube 
is  also  diffusely  dilated  above  the  stenosis. 


410  DISEASES    OF   THE   DIGESTIVE    ORGANS 

Symptoms. — The  effect  of  every  oesophageal  stenosis  is  to  render  deglutition 
difficult.  If  the  ease  is  a  mild  one,  the  patient  experiences  nothing  more  than  a 
moderate  pressure  in  the  oesophagus  upon  swallowing.  He  feels  that  the  morsel 
is  longer  than  usual  in  reaching  the  stomach.  Verj^  soon  he  notices  that  solid 
food  and  large  morsels  can  be  swallowed  only  with  difficulty.  Accordingly,  he 
is  gradually  led  to  confine  himself  to  a  liquid  diet,  takes  small  mouthfuls,  and 
always  washes  down  any  solid  food  with  a  swallow  or  two  of  liquid.  The  narrower 
the  stenosis,  the  more  he  is  ti'oubled.  Finally,  even  liquids  can  be  taken  only 
slowly  and  in  sips. 

It  must  not  be  thought  that  the  dysphagia  just  described  is  due  exclusively  to 
the  mechanical  obstruction  of  the  lumen.  Sometimes  a  patient  is  almost  entirely 
unable  to  take  nourishment,  and  yet  at  the  autopsy  no  adequate  mechanical 
obstruction  is  found.  The  dysphagia  must  therefore  be  due  to  some  lesion  of  the 
muscular  coat  of  the  oesophagus.  The  impaired  contractility  of  the  muscular 
coat  at  the  affected  spot  is  always  a  potent  factor  in  impeding  deglutition. 

As  soon  as  the  dysphagia  has  become  considerable  there  is  usually  regurgita- 
tion of  food.  At  first  only  a  portion  of  the  food  comes  up,  but  at  last  all  of  it.  If 
the  tube  has  become  dilated  above  the  stenosis,  food  may  collect  for  some  hours, 
and  then  be  regurgitated,  mixed  with  an  abundance  of  very  tenacious  mucus. 
We  saw  a  ease  of  this  kind  in  which  the  patient  could  fill  the  sac  above  the  stric- 
ture with  quite  a  large  amount  of  fluid  without  a  drop  reaching  the  stomach.  If 
he  bent  his  head  sharply  forward,  the  collected  fluid  would  run  out  again  through 
his  mouth.  It  was  not  until  the  pouch  was  completely  fllled  that  a  small  amount 
of  liquid  would  trickle  through  the  stenosis  into  the  stomach. 

Although  the  dysphagie  symptoms  above  described  generally  imply  oesophag- 
eal stenosis,  the  diagnosis  can  not  be  really  established  without  using  a  sound. 
Upon  introducing  this,  it  is  usually  easy  to  detect  the  obstacle,  which  may  either 
allow  the  instrument  to  pass,  with  a  noticeable  jerk,  or  else  prevent  its  further 
progress.  By  measuring  the  length  of  the  portion  introduced  before  the  stenosis 
is  reached  we  can  learn  its  position.  On  the  average,  the  entire  distance  from  the 
teeth  to  the  cardiac  sphincter  is  in  adults  sixteen  inches  (forty  centimetres) ; 
from  the  teeth  to  the  beginning  of  the  oesophagus,  six  inches  (fifteen  centime- 
tres) ;  and  consequently  the  length  of  the  latter  is  about  ten  inches  (twenty- 
five  centimetres).  If  we  succeed  in  passing  a  smaller  sound  through  the  stric- 
ture, the  feeling  as  we  move  it  back  and  forth  will  give  us  some  idea  of  the  length 
of  the  stenosis,  or  will  demonstrate  the  existence  of  several  lying  one  below  the 
other,  etc.  If  the  end  of  the  sound  can  be  moved  about  very  freely  above  the  ste- 
nosis, we  may  conclude  that  the  tube  is  dilated  there. 

Hamburger  has  employed  auscultation  of  the  oesophagus  for  diagnostic  pur- 
poses. If  we  listen  behind,  to  the  left  of  the  upper  dorsal  vertebrae  during  deglu- 
tition, we  hear  a  gurgling  sound,  due  to  the  act  of  swallowing,  extending  down 
the  tube  to  the  stenosis,  but  no  farther.  Then  come  all  sorts  of  sounds,  some  of 
them  caused  by  the  fluid  trickling  slowly  through  the  narrow  part,  and  some 
caused  by  regurgitation.  In  general,  the  results  obtained  by  auscultation  are 
rather  variable  and  uncertain. 

Having  established  the  fact  of  the  existence  of  a  stenosis,  we  have  next  to  de- 
termine its  nature,  which  is  our  chief  g-uide  to  prognosis  and  treatment.  In  cer- 
tain instances  the  history  of  the  case  gives  us  the  needed  information.  The  diag- 
nosis of  cicatricial  stricture  can  hardly  be  made  unless  the  patient  himself  tells  us 
of  being  burned  or  injured  by  caustic  poisons.  The  previous  history  is  likewise  of 
great  importance  if  the  stenosis  be  due  to  foreign  bodies  or  to  syphilis.  If  no  de- 
cisive setiological  factor  can  be  elicited,  we  must  carefully  examine  the  neck  and 
thorax,  with  regard  to  the  possible  existence  of  a  swelling  compressing  the 
oesophagus.     Wlien   an   aortic   aneurism  has   acted   in   this   way,   a   rhythmical 


STENOSIS    OF   THE   (ESOPHAGUS  411 

movement  has  sometimes  been  communicated  to  the  free  end  of  a  sound  intro- 
•duced  as  far  as  the  stenosis.  If  the  physical  examination  does  not  reveal  a  com- 
pressing tumor,  and  particularly  if  the  stenosis  has  developed  gradually  and  in  an 
elderly  person,  we  are  almost  compelled  to  assume  that  there  is  cancer  of  the 
■oesophagus.  This  is,  after  all,  by  far  the  most  frequent  cause  of  oesophageal  stric- 
ture. If  the  new  growth  has  ulcerated,  a  little  portion  of  it  may  adhere  to  the 
end  of  the  probe,  and,  on  microscopic  examination,  render  our  diagnosis  of  carci- 
noma certain. 

The  prevailing  characteristic  in  stenosis  of  the  oesophagus  is  inanition,  increas- 
ing as  the  dysphagia  increases.  The  patient  gets  to  be  very  much  emaciated,  and 
so  feeble  that  he  can  not  leave  his  bed.  The  temperature  is  subnormal ;  for  weeks 
it  keeps  at  95°  to  97°  (35°-36°  C).  The  pulse  grows  very  small  and  slow,  being 
40  to  60  per  minute.  The  heart-sounds  are  soft.  Respiration  is  superficial  and 
slow;  and  toward  the  close  of  life  short  pauses  occur  after  expiration,  before 
inspiration  begins.  The  stomach  and  intestines  are  so  empty  that  the  abdomen 
is  very  concave,  while  the  abdominal  walls  usually  feel  tense  and  resistant.  In 
all  cases  when  the  nature  of  the  stenosis  precludes  the  possibility  of  cure  or 
improvement,  death  results  from  increasing  exhaustion,  the  lamp  of  life  gradu- 
ally flickering  out. 

Prognosis  and  Treatment. — In  prognosis  the  main  factor  is  of  course  the 
nature  of  the  stenosis.  If  it  is  due  to  foreign  bodies  or  to  cicatrices,  it  may  be 
•completely  cured.  In  stenosis  from  other  causes  it  is  often  possible  to  produce 
-considerable  improvement,  at  least  temporarily.  The  final  result  must  be  con- 
fessed to  be  usually  unfavorable,  as  we  should  expect  from  the  nature  of  the  origi- 
nal trouble. 

The  treatment  is  chiefly  mechanical.  We  shall  not  speak  of  operations  for 
the  removal  of  new  growths,  etc.  What  we  do  refer  to  is  a  methodical  and  grad- 
ual dilatation  of  the  stricture.  Its  results  are  sometimes  brilliant,  particularly  in 
cicatricial  stenosis.  Other  varieties,  such  as  the  stenosis  from  cancer,  may  some- 
times undergo  considerable  though  but  temporary  improvement  with  this  treat- 
ment. 

The  best  instrument  to  employ  is  the  flexible,  so-called  English,  oesophageal 
hougie.  It  is  made  in  all  sizes.  If  the  stenosis  is  very  narrow  indeed,  we  may 
have  to  resort  to  catgut  at  first.  Whalebone  bougies,  with  olive-shaped  ivory  tips 
of  various  sizes  to  screw  on  the  end,  are  also  good,  except  that,  being  stifPer,  there 
is  more  danger  in  using  them.  For  introduction  of  the  bougie,  the  patient  should 
he  seated,  with  the  head  slightly  extended  backward.  The  first  two  fingers  of  the 
left  hand  are  introduced  into  the  throat  and  guide  the  instrument,  previously 
well  oiled,  over  the  back  of  the  tongue  and  the  epiglottis  into  the  oesophagus.  Of 
■course,  no  violence  must  be  used.  Otherwise  a  perforation  might  occur  if  there 
were  a  soft,  broken-down  cancer,  or  an  aortic  aneurism.  However,  such  a  mis- 
fortune is  very  exceptional. 

The  use  of  the  bougie  is  almost  invariably  beneficial  if  the  stricture  can  be 
passed.  The  patient  generally  finds  that  he  can  swallow  easier  than  before,  and 
will  himself  request  a  repetition  of  the  performance.  If  the  patient  is  an  intelli- 
gent person,  it  is  advisable  to  have  him  introduce  the  bougie  himself.  Patients 
■often  acquire  even  greater  skill  with  it  than  the  physician  has.  The  bougie 
should  be  passed  regularly  once  a  day,  or,  at  most,  twice  daily;  and  in  favorable 
cases  we  shall  be  able  gradually  to  increase  the  size.  If  so,  the  symptoms  speedily 
abate,  and,  with  the  increased  ingestion  of  food,  the  patient  gains  flesh  very  fast. 

If  the  stenosis  is  extreme,  and,  although  it  admits  the  bougie,  does  not  allow 
of  sufficient  nourishment,  we  must  pass  a  tube  into  the  stomach  through  which 
to  introduce  liquid  food.  Milk  is  the  best  food  to  choose.  Raw  eggs,  sugar,  wine, 
etc.,  may  be  mixed  with  it.     The  various  infant's  foods  and  Hartenstein's  "  legu- 


412  DISEASES    OF   THE   DIGESTIVE    0EGA:NS 

minose  "  are  also  excellent.  Their  consistence  is  favorable  for  the  purpose,  and 
they  supply  a  considerable  amount  of  nourishment  in  a  small  bulk.  Until  re- 
cently the  sounds  and  dilators  employed  in  stenosis  of  the  oesophagus  have  been 
usually  introduced  by  the  mouth,  but  of  late  the  practice  has  been  constantly 
growing  of  treating  stenosis  through  an  artificial  opening  in  the  (Desopliagus. 
Mechanical  dilatation  can  thus  be  accomplished  with  much  greater  rapidity  and 
completeness.  In  the  surgical  wards  here  in  Erlangen  admirable  results  have 
been  obtained  in  this  manner  in  cicatricial  stenosis;  whereas  in  carcinoma  of  the 
oesophagvis  the  improvement  is  of  course  merely  temporary,  although  the  symp- 
toms are  greatly  alleviated.  Further  particulars  with  regard  to  cesophagotomy 
are  to  be  sought  in  text-books  on  surg-ery,  where  a  description  of  some  other  modes 
of  treatment  of  oesophageal  stenosis  will  be  found,  including  the  insertion  of 
self -retaining  eanulse,  and  the  creation  of  an  artificial  gastric  fistula. 

We  desire  to  append  a  few  remarks  as  to  the  nourishment  of  patients  by  ene- 
mata,  to  which  we  are  particularly  apt  to  have  recourse  in  cases  of  oesophageal 
disease. 

Brilliant  results  are  never  to  be  expected  from  rectal  feeding.  It  is  indeed 
probable  that  life  may  be  by  this  means  somewhat  prolonged,  but  not  indefinitely. 
The  moral  effect,  however,  is  very  valuable,  when  the  patient  could  otherwise  re- 
ceive no  nourishment  whatever.  The  sufferer  feels  that  something  is  being  done 
to  avert  absolute  starvation. 

The  simplest  materials  for  the  nutrient  enemata  are  milk,  eggs,  and  wine ;  to 
which  we  may  add  pepsine  and  pancreatine  in  the  hope  of  promoting  absorption. 
Leube's  pancreatic  meat  emulsion  is  still  better,  although  more  troublesome  in  its 
preparation.  Leube's  directions  are  as  follows :  About  five  ounces  (grammes 
150)  of  meat,  cut  very  thin  and  then  minced  finely,  and  about  two  ounces 
(grammes  50)  of  minced  pancreas  (from  the  calf)  free  from  fat,  are  to  be  stirred 
with  about  three  ounces  (grammes  100)  of  lukewarm  water  until  the  mixture  has 
the  consistence  of  gruel.  Before  it  is  injected,  the  rectum  should  be  cleansed  by 
an  enema  of  plain  water.  One  such  enema  is  to  be  given  daily.  Also,  when  ene- 
mata of  milk  and  eggs  are  given,  the  rectum  must  invariably  be  first  rinsed  out 
with  plain  water.  Too  large  an  amount  ought  not  to  be  given  at  one  time,  say 
about  two  ounces  (grammes  50),  and  the  fluid  must  be  raised  to  about  the  tem- 
perature of  the  body.  [The  limit  in  quantity  set  by  the  author  is  smaller  than 
many  patients  can  retain.  If  the  fluid  is  injected  gently  and  slowly,  four  to 
eight  ounces  may  be  administered  every  six  hours,  and  cases  are  on  record  of 
patients  retaining  even  sixteen  ounces.  The  rectum  seems  capable  of  a  certain 
amount  of  training  in  this  regard,  so  that  the  amount  given  may  eventually  be 
greater  than  at  first.  Unusual  irritability  may  be  diminished  by  adding  to  the 
enema  about  five  minims  of  laudanum. — V.] 


CHAPTEE   IV 
CANCER    OF    THE    (ESOPHAGUS 

Etiology  and  Pathology. — Cancer  is  the  most  important  and  most  frequent 
affection  of  the  oesophagus.  We  have  already  mentioned  in  the  preceding  chap- 
ter that  often  stenosis  is  the  result  of  carcinoma  in  the  oesophageal  walls. 

Little  is  known  about  the  aetiology.  It  has  been  often  maintained  that  me- 
chanical, chemical,  or  thermic  irritation  of  the  mucous  membrane  may  result 
in  the  development  of  cancer;  but  this  is  not  certain.     It  receives  some  support 


CANCER   OF   THE    (ESOPHAGUS  413 

from  the  remarkably  frequent  occurrence  of  oesophageal  cancer  in  hard  drinkers. 
Now  and  then  the  patient  himself  will  allege  a  perfectly  definite  cause  for  his 
disease,  such  as  the  lodging  of  a  foreign  body,  or  the  swallowing  of  a  very  large 
or  very  hot  morsel.  Still  it  is  hardly  possible  in  any  particular  case  to  decide 
how  much  value  such  statements  have.  It  has  been  maintained  that  the  carci- 
noma sometimes  develops  in  the  sear  of  an  old  ulcer.  This  is  of  interest  when  we 
recall  the  similar  fact  in  regard  to  gastric  carcinoma  (vide  infra). 

(Esophageal  cancer  follows  the  general  rule  in  being  most  frequent  in  elderly 
people — somewhere  between  forty  and  sixty  years  of  age.  The  male  sex  is  de- 
•cidedly  more  often  attacked  than  the  female. 

As  we  might  expect  from  the  histological  character  of  the  epithelium  lining 
the  oesophagus,  primary  cancer  here  is  invariably  composed  of  pavement  cells. 
The  new  growth  may  be  either  hard,  firm,  and  fibrous,  or  it  may  be  soft,  succulent, 
and  but  scantily  supplied  with  connective  tissue.  The  first  variety  corresponds  to- 
the  "  scirrhus  "  of  older  writers,  and  the  second  to  "  medullary  "  cancer.  Usually 
the  new  formation  encircles  the  entire  tube  like  a  ring,  extending  three  to  ten 
centimetres  longitudinally.  Exceptionally  a  still  larger  portion  of  the  oesophagus 
is  involved,  sometimes  almost  all  the  mucous  membrane.  The  tumor  is  usually 
seated  in  the  lower  and  middle  thirds  of  the  oesophagus,  being  much  rarer  above. 

Symptoms  and  Complications. — In  the  great  majority  of  cases  the  symptoms 
are  those  of  a  gradually  increasing  stenosis,  with  its  results.  We  may  therefore 
refer  to  the  preceding  chapter  for  most  of  the  particulars.  There  are,  however, 
•exceptional  cases  in  which  the  carcinoma  is  fiat  and  entails  no  dysphagia,  or  so 
little  that  oesophageal  trouble  may  not  be  suspected.  We  have  repeatedly  seen 
•cases  of  extensive  secondary  hepatic  cancer,  or  of  pulmonary  gangrene  (vide 
■infra),  in  which  the  real  primary  disease  was  a  flat  cancer  of  the  oesophagus, 
which  gave  no  clinical  signs  of  its  existence,  and  was  therefore  not  diagnos- 
ticated. 

It  is  characteristic  of  the  stenotic  symptoms  produced  by  oesophageal  cancer 
that  sometimes  a  considerable  and  apparently  spontaneous  amelioration  occurs. 
This  is  because  of  an  ulceration  of  the  new  growth.  It  crumbles  away,  as  the 
result  of  superficial  disintegration.  The  tumor  is  transformed  into  an  ulcer,  and 
one  can  easily  understand  how  this  may  occasion  a  temporary  improvement  in 
deglutition. 

Important  clinical  symptoms  may  result  from  conditions  secondary  to  the  new 
growth.  The  cancer  may  extend  to  neighboring  organs.  Not  infrequently  the 
cardiac  extremity  of  the  stomach  is  thus  involved.  Sometimes  such  a  tumor  may 
he  felt  in  the  epigastrium ;  but  in  most  cases  there  is  nothing  to  indicate  that  the 
stomach  is  attacked. 

The  neighboring  parts  of  the  trachea  or  bronchi  are  sometimes  affected,  and 
important  symptoms  result  from  such  a  complication.  If  perforation  occurs,  an 
almost  certain  result  is  the  inhalation  of  food  or  of  decaying  bits  of  the  tumor, 
with  consequent  pulmonary  gangrene,  and,  as  a  rule,  speedy  death.  The  disease 
has  also  been  observed  to  attack  the  pleura,  and  end  in  perforation.  The  same 
is  true  of  the  pericardium  and  the  aorta.  A  few  instances  are  known  in  which  the 
vertebrae  have  been  involved,  the  spinal  cord  compressed,  and  paraplegia  thus  in- 
duced.    We  have  ourselves  seen  one  such  case. 

Quite  frequently  the  recurrent  nerve  is  affected,  and  a  paralysis  of  the  vocal 
cords  is  produced,  which  can  be  detected  by  the  laryngoscope.  This  nerve  lies 
so  close  to  the  oesophagus  that  it  is  peculiarly  exposed  to  injury  from  the  new 
growth  itself,  or  from  any  inflammatory  process  which  may  be  set  up  around  it. 

Metastatic  cancer  in  distant  organs  is  not  infrequent,  and  may  give  rise  to 
important  symptoms.  It  attacks  most  frequently  the  liver.  The  lungs,  kidneys, 
pancreas,  bones,  and  brain  are  also  liable  to  it. 


414  DISEASES    OF   THE   DIGESTIVE    OEGANS 

Pulmonary  gangrene  must  be  mentioned  as  a  relatively  frequent  complication^ 
and  one  which  has  serious  consequences.  We  have  already  stated  that  it  may 
result  from  perforation.  A  still  more  frequent  cause  is  the  inspiration  of  decay- 
ing masses  vomited  or  regurgitated  by  the  patient. 

Clinical  History,  Termination,  Prognosis,  and  Treatment.— The  disease  is. 
incurable.  Operative  removal  has  never  been  successful.  The  entire  duration  of 
the  disease  seldom  exceeds  a  year,  or  a  year  and  a  half.  At  the  end  of  this  period 
the  patient  dies  either  from  lack  of  nourishment  or  as  a  result  of  some  one  of  the- 
complications  above  enumerated.  Treatment  is  purely  symptomatic.  Temporary 
improvement  may  be  obtained  by  mechanical  treatment  of  the  stenosis.  The  par- 
ticulars about  this  may  be  found  in  the  preceding  chapter. 


CHAPTEE   Y 
ETTPTTJEE    OF    THE    (ESOPHAGUS 

Medical  literature  records  a  small  number  of  cases  which  prove  that  the  sud- 
den rupture  of  the  oesophagus  in  persons  previously  perfectly  well  is  possible^ 
although  of  course  very  rare.  The  first  and  most  famous  instance  was  described 
by  Boerhaave  in  1724. 

The  symptoms,  according  to  the  observations  thus  far  reported,  usually  com- 
mence with  sudden  nausea  and  vomiting,  during  or  shortly  after  a  hearty  meal. 
There  is  simultaneously  an  extreme,  general  collapse.  There  is  pallor  of  the  face 
and  extremities,  eold  perspiration,  and  an  extremely  feeble  pulse.  Sometimes  the 
patient  feels  a  sudden  darting  pain  in  the  chest.  Almost  invariably  an  extensive 
emphysema  overspreads  the  neck  and  thorax.  Death  results  in  a  few  hours,  or 
at  latest  in  a  few  days. 

The  autopsy  reveals  a  tear  in  the  oesophagus,  invariably  situated  in  its  lower 
half.  It  may  be  five  centimetres  long,  and  it  is  almost  always  longitudinal.  Food 
has  usually  escaped  into  the  surrounding  tissues,  in  which  case  a  secondary  puru- 
lent inflammation  exists,  if  death  was  not  immediate. 

Zenker  has  attempted  to  explain  this  remarkable  phenomenon  by  a  supposition 
which  is  really  very  plausible,  namely,  that  oesophagomalacia  always  precedes 
these  so-called  spontaneous  ruptures.  The  cause  of  this  softening  of  the  oesophag- 
eal walls  is  probably  the  action  of  gastric  juice  escaping  into  the  tube  and  attack- 
ing a  surface  which,  through  some  temporary  disturbance  in  the  circulation,  has- 
lost  its  normal  powers  of  resistance. 


CHAPTEE   VI 
NEUROSES    or    THE    (ESOPHAGUS 

1.  Spasm  of  the  CEsophagus. — In  rare  instances  oesophageal  disturbances  are- 
observed,  which  appear  to  result  from  spasmodic  contraction  of  its  muscular  coat. 
Nervous  and  hysterical  subjects  are  particularly  apt  to  present  temporarily  the 
symptoms  of  extreme  stenosis,  for  which  there  can  be  no  anatomical  basis.  Siach 
cases  are  termed  "  spastic  stenosis  "  of  the  oesophagus,  or  "  oesophagismus."  It  is, 
of  course,  possible  that  there  may  exceptionally  be  some  real  lesion  at  the  fotmda- 


EXAMINATION   OF    THE    GASTKIC    CONTENTS  415 

tion  of  the  trouble,  and  that  the  spasm  is  the  reflex  result  of  an  ulcer  or  inflamma- 
tion affecting  the  oesophagus.  It  is  even  affirmed  that  the  reflex  influence  may 
sometimes  originate  in  distant  organs,  such  as  the  uterus;  but  the  exact  nature 
of  these  reflex  spasms  is  at  present  exceedingly  obscure.  The  dysphagia  is  usually 
attended  by  a  painful  sense  of  constriction  in  the  throat  and  chest.  The  bougie 
comes  upon  an  obstruction,  which  usually  soon  yields.  This  circumstance,  that 
when  the  spasm  relaxes  it  is  possible  to  introduce  the  bougie  without  any  diffi- 
culty, confirms  the  diagnosis.  Other  important  factors  are,  the  character  of  the 
symptoms  as  a  whole  and  the  other  attendant  nervous  and  hysterical  disturbances. 
Some  authors  also  explain  the  "globus  hystericus  "—that  feeling  as  if  a  lump 
were  passing  tip  or  down  in  the  throat  and  chest — as  a  spasm  of  the  oesophagus. 

2.  Paralysis  of  the  CEsophagus. — Of  this  subject  we  have  little  accurate 
knowledge.  It  is  not  improbable  that  an  extensive  bulbar  paralysis,  affecting  the 
muscles  of  the  pharynx  and  larynx,  may  sometimes  involve  the  oesophagus;  al- 
though such  a  disturbance  hardly  ever  gives  rise  to  prominent  symptoms  in  this 
disease.  Ziemssen  asserts  that  sometimes  the  oesophagus  seems  to  participate  in 
post-diphtheritic  paralysis,  when  extensive. 


SECTION  IV 

Diseases  of  the  Stomach 

CHAPTEK   I 

BRIEF    PRELIMINARY    REMARKS    ON    THE     EXAMINATION    OF     THE 

GASTRIC    CONTENTS- 

When  a  disease  of  the  stomach  exists,  we  have  the  subjective  symptoms  to 
consider,  such  as  anorexia,  eructations,  vomiting,  and  gastric  pain,  together 
with  the  external  physical  signs  obtained  by  inspection  and  palpation,  such  as 
tenderness,  distention,  peristaltic  motion,  swelling,  and  tumors ;  and  we  also  have 
for  our  guidance  an  examination  of  the  stomach  and  the  stomach  contents.  The 
procedure  was  introduced  by  Leube,  followed  by  Ewald,  Boas,  Riegel,  and  many 
others.  It  is  carried  out  by  means  of  the  stomach-tube,  and  is  now  universally 
employed  among  physicians,  for  in  fact  its  results  are  so  important  and  decisive 
with  regard  to  diagnosis,  that  an  examination  of  this  sort  is  at  the  present  day 
indispensable  in  any  severe  case  of  persistent  gastric  trouble.  The  inconvenience 
of  the  investigation  for  the  patient  is  comparatively  slight,  especially  now  that 
a  soft  and  yielding  tube  (Nelaton)  is  employed.  This  should  have  free  aper- 
tures at  its  lower  extremity,  and  it  is  introduced  into  the  stomach  in  the  follow- 
ing manner:  The  tube  is  moistened  with  water,  put  into  the  patient's  mouth, 
and  passed  backward  over  the  base  of  the  tongue,  and  he  is  told  to  swallow  it,  as 
it  were;  the  physician  at  the  same  time  aids  by  pushing  the  tube,  but  he  does 
not  introduce  his  finger  into  the  patient's  mouth.  In  this  way  it  is  almost  always 
easy  to  introduce  the  instrument  into  the  oesophagus,  and  so  into  the  stomach. 
Most  patients,  if  the  tube  has  to  be  employed  frequently,  soon  learn  to  guide  it 

*  Complete  particulars  w'th  regard  to  the  methods  of  examining  the  gastric  contents  can  not  he  given 
here,  but  they  may  be  found  in  the  following  works:  Ewald,  Klinik  der  Verdauungskrankheiten ; 
Boas,  Diagnostik  und  Therapie  der  Magenkrankheiten :  Leo,  Diagnostik  der  Krankheiten  der  Ver- 
dauungsorgane ;  Kiegel.  Erkrankungen  des  Magens,  etc. 


416 


DISEASES    OF   THE   DIGESTIVE    OEGAl^S 


themselves.     Formerly  a  wire  was  placed  inside  the  tube  so  as  to  stiffen  it  for 
introduction,  but  this  is  ordinarily  useless,  if  not  a  hindrance. 

If  the  tube  has  been  introduced  into  the  stomach,  and  we  wish  to  obtain  a 
portion  of  the  contents  of  that  organ  for  examination,  it  can,  in  most  cases,  be 
got  by  simple  "  expression."  If  the  patient  makes  his  abdominal  muscles  tense 
("presses"),  or  if  he  makes  a  few  slight  efforts  to  vomit,  there  is  usually  a  suffi- 
cient amount  of  the  gastric  contents  expressed  through  the  tube  into  a  beaker 
held  to  receive  it.     This  portion  of  the  gastric  contents  is  filtered,  and  the  filtrate 


Fig.  45. — Method  of  washing  out  the  stomach.    (Erlangen  Medical  Cliiiique.) 


subjected  to  examination.  If  we  wish  to  empty  the  stomach  completely  ("  rinse 
it  out"),  the  upper  end  of  the  inserted  tube  is  connected  by  means  of  a  short 
piece  of  glass  tubing,  with  a  longer  rubber  tube  connected  at  its  other  end  with 
a  large  glass  funnel,  to  hold  about  a  litre  of  water.  If  warm  water  is  poured 
into  the  funnel  and  this  is  alternately  raised  and  lowered,  we  shall  eventually 
entirely  empty  the  stomach  (see  Fig.  45).  It  is  advisable  to  insert  a  short  bit  of 
glass  tubing  in  the  rubber  tube  (fenestra),  so  as  to  observe  whether  the  fluid 
runs  well  in  either  direction.     Kussmaul  originally  employed  a  "  stomach-pump  " 


EXAMI^TATIOX   OF   THE   GASTEIC    CONTENTS  41Y 

for  rinsing  out  the  stomach,  but  this  has  been  quite  universally  abandoned  for  the 
simple  siphon  apparatus  suggested  by  Hegar. 

By  use  of  the  stomach-tube  we  are  readily  enabled  to  settle  the  following 
important  points:  Eirst,  the  chemical  constituents  of  the  gastric  juice,  or  con- 
tents; second,  the  motor  activity  of  the  stomach;  and  third,  the  size  and  position 
of  the  organ. 

1.  Constituents  of  the  Gastric  Jnice,  particularly  Free  Hydrochloric  Acid, 
Pepsine,  and  Lactic  Acid. — In  a  healthy  person  the  stomach  is  almost  completely 
empty  in  the  morning  before  breakfast — i.  e.,  some  ten  or  twelve  hours  after  the 
preceding  evening  meal.  If  we  introduce  the  stomach-tube  we  obtain,  therefore, 
by  expression  either  nothing  at  all  or  a  very  small  amount  of  watery  mucus,  of 
neutral  reaction.  If  this  fluid  contains  a  little  hydrochloric  acid,  this  is  not  neces- 
sarily anything  abnormal,  but  if  there  is  a  large  amount  of  acid  fluid  in  the  fast- 
ing state  disease  is  indicated.  The  healthy  stomach  contains  in  the  morning  few 
vestiges  of  the  food  swallowed  the  day  before.  If  we  pour  in  some  water,  this  is 
returned  almost  perfectly  clear.  If  now  the  subject  of  examination  eats  a  so- 
called  test  breakfast,  consisting  of  an  ordinary  roll  and  a  large  cup  of  weak  tea, 
at  once  the  stomach  begins  to  secrete  its  peculiar  juice.  If  the  stomach-tube  is 
introduced  an  hour  after  a  test  breakfast  has  been  taken,  and  a  sufficient  amount 
of  the  stomach  contents  is  expressed  and  filtered,  we  shall  obtain  a  fluid  of  acid 
reaction,  and,  under  normal  conditions,  invariably  containing  free  hydrochloric 
acid  uncombined  with  albumen.  It  is  the  comparatively  small  amount  of  the 
test  breakfast  which  makes  it  most  suitable  for  the  determination  of  the  impor- 
tant question,  whether  the  stomach  secretes  hydrochloric  acid  in  a  satisfactory 
manner.  If  we  introduce  into  the  stomach  a  larger  amount  of  food  ("  test  meal," 
vide  infra)  there  will,  indeed,  in  most  cases,  be  free  hydrochloric  acid  after  one 
or  two  hours,  but  the  amount  of  albuminous  material  present  is  so  great  that  even 
under  normal  circumstances  all  the  hydrochloric  acid  secreted  is  taken  up  by  the 
albuminous  substances,  and  consequently  there  is  no  hydrochloric  acid  to  be 
discovered  by  our  ordinary  chemical  tests.  If,  on  the  other  hand,  we  do  not 
find  any  free  hydrochloric  acid  in  the  gastric  contents,  or,  at  any  rate,  merely 
doubtful  traces  of  it,  an  hour  after  the  test  breakfast,  this  condition  is  termed 
anacidity,  or  subacidity,  and  it  must  be  regarded  as  abnormal,  particularly  if  re- 
peated examination  leads  to  the  same  result.  The  term  acidity  in  this  connection 
relates  to  hydrochloric  acid.  Even  if  this  is  absent  it  is  perfectly  possible  that 
there  may  be  other  organic  acids  in  the  gastric  contents. 

The  test  for  the  presence  of  free  hydrochloric  acid  now  almost  universally 
employed  is  one  introduced  by  Giinzburg,  who  recommended  a  solution  of  2 
parts  of  phloroglucine  and  1  part  of  vanilline  in  30  parts  of  absolute  alcohol.  If 
we  mix  a  few  drops  of  this  phloroglucine-vanilline  in  a  saucer  with  a  few  drops 
of  the  filtered  gastric  contents  to  be  examined,  and  then  heat  the  mixture  cau- 
tiously so  as  to  avoid  charring,  there  will  immediately  develop  on  the  edge  of  the 
fluid  a  beautiful  red  border,  if  free  hydrochloric  acid  is  present.  Another  good 
reagent  for  free  hydrochloric  acid  is  methyl  violet.  This  requires  an  accurate 
comparison  of  colors,  so  that  the  weak  watery  solution  of  methyl  violet  is  divided 
into  two  portions  in  test-tubes.  If  now  we  add  to  one  test-tube  some  of  the 
gastric  contents  containing  free  hydrochloric  acid,  the  violet  is  immediately 
changed  into  a  distinct  blue  color,  which  is  evidently  different  from  the  original 
fluid  contained  in  the  other  test-tube.  Eor  a  third  test  what  is  called  Congo 
paper  is  employed — i.  e.,  strips  of  paper  colored  with  an  aqueous  solution  of 
Congo  red.  If  the  stomach  contents  contain  free  hydrochloric  acid,  the  red 
color  of  the  paper  is  changed  to  a  distinct  blue.  There  is  a  certain  inaccuracy 
in  this  last-mentioned  test  with  Congo  red,  as  the  red  is  colored  blue  by  concen- 
trated solutions  of  other  acids,  particularly  lactic  acid ;  but,  as  a  matter  of  fact, 
27 


418  DISEASES    OF   THE   DIGESTIVE   OEGANS 

the  otlier  acids  are  scarcely  ever  present  in  the  stomach  in  sufficient  amounts  to 
invalidate  the  test;  so  that  in  actual  practice,  if  the  Congo  paper  changes  to 
a  distinct  blue,  we  may  almost  always  infer  that  free  hydrochloric  acid  is  pres- 
ent. Still,  it  is  advisable  in  every  case  to  carry  out  the  two  other  tests  also, 
which  are  almost  as  simple  and  entirely  unambiguous.  There  is  a  reagent  often 
employed  which  indicates  the  presence  of  free  acids  in  general,  including  free 
lactic  acid.  It  consists  of  an  alcoholic  (or  aqueous)  solution  of  "  tropseoline  00." 
The  yellow  color  of  tropseoline  is  changed  to  a  beautiful  red  by  even  small  amounts 
of  acid,  but  still  more  readily  by  hydrochloric  acid  than  by  the  organic  acids. 
Blue  litmus  paper,  as  is  well  known,  is  colored  red  by  free  acids  as  well  as  by 
acid  salts.  If  the  examination  of  the  contents  of  the  stomach  an  hour  after  the 
test  breakfast  shows  the  presence  of  free  hydrochloric  acid,  an  experienced  ob- 
server will  often  be  able  to  estimate  from  the  degree  of  the  qualitative  reaction 
whether  he  is  dealing  with  a  small  or  considerable  amount  of  hydrochloric  acid. 
An  accurate  quantitative  estimation  is  possible  by  titration  of  the  stomach  con- 
tents with  a  decinormal  soda  solution,  for  which  a  few  drops  of  phenol-phthaleine 
solution  serve  as  index.*  The  amount  of  acid  determined  by  this  process  is  of 
course  the  sum  total  of  free  acids,  and  not  exclusively  the  free  hydrochloric  acid. 
Still,  provided  there  is  an  abundant  amount  of  hydrochloric  acid  in  the  gastric 
contents,  the  results  obtained  may  be  ascribed  without  great  error  to  hydro- 
chloric acid  alone;  for  experience  has  shown  that,  when  there  is  a  considerable 
amount  of  hydrochloric  acid  in  the  gastric  contents,  there  is  scarcely  ever  any 
considerable  amount  of  organic  acids  (vide  infra).  The  degree  of  acidity  of  the 
gastric  fluid  is  usually  expressed  in  the  number  of  cubic  centimetres  of  soda  solu- 
tion which  are  necessary,  as  shown  by  the  titration,  to  neutralize  100  cubic  centi- 
metres of  the  gastric  fluid ;  for  example,  if  we  have  required  6  cubic  centimetres  of 
soda  solution  to  neutralize  10  cubic  centimetres  of  the  gastric  contents,  the  acid- 
ity is  reckoned  at  60.  In  terms  of  hydrochloric  acid  we  would  have  60  multiplied 
by  3.65,  equal  to  19  milligrammes  of  hydrochloric  acid — that  is,  0.22  per  cent. 
The  degree  of  acidity  which  is  found  in  the  gastric  contents  of  healthy  persons 
after  the  test  breakfast  is  usually  55-65;  amounts  of  70-80  indicate  hyper- 
acidity. If  the  gastric  juice  contains  an  abundance  or  an  excess  of  hydrochloric 
acid,  the  further  question,  and  often  an  important  one,  arises  whether  there  is 
a  hypersecretion,  or,  more  correctly,  a  continuous  secretion  of  gastric  juice.  As 
we  have  already  mentioned,  the  normal  stomach  does  not  ordinarily  secrete  except 
when  its  mucous  membrane  is  affected  by  food  swallowed,  or  by  other  stimulating 
influences.  The  fasting  stomach  does  not,  as  a  i*ule,  contain  any  hydrochloric 
acid,  and  when  the  stomach  has  passed  the  food  on  into  the  duodenum,  its  secre- 
tion immediately  ceases.  In  order,  then,  to  determine  the  existence  of  hyper- 
secretion or  continuous  secretion,  we  must  examine  the  contents  of  the  fasting 
stomach  at  least  six  or  seven  hours  after  the  last  meal.  If  we  then  find  fluid  in 
the  stomach,  with  distinct  or  abundant  amounts  of  hydrochloric  acid  contained 
in  it,  we  are  justified  in  assuming  that  there  is  an  abnormal  hypersecretion  on 
the  part  of  the  stomach. 

Physiology  teaches  us  that  not  only  hydrochloric  acid  but  pepsine  in  associa- 
tion with  it,  is  necessary  for  the  peptonizing  of  albuminoids.  The  demonstra- 
tion of  pepsine  in  the  gastric  contents  is,  therefore,  essential  to  a  determination 
of  the  peptic  function  of  the  stomach.  Experience  has  shown,  however,  that 
pepsine  is  rarely  absent  from  the  gastric  juice,  and  if  there  is  a  distinct  secretion 
of  hydrochloric  acid  we  may  almost  always  assume  that  pepsine  is  secreted,  with- 
out making  any  special  examination.  Even  in  cases  of  anacidity  pepsine  often 
continues  to  be  secreted.     Still,  there  are  cases  when  the  direct  demonstration 

*  We  scarcely  need  to  describe  this  simple  process  more  fully. 


EXAMIXATIOiq'   OF   THE   GASTKIC   CONTENTS  419 

of  the  presence  or  absence  of  pepsine  in  the  gastric  juice  is  desirable.  The 
process  is  simple.  "We  obtain  some  gastric  contents  in  the  ordinary  way  after 
a  test  breakfast,  and  put  into  it  a-  square  shaving  of  the  white  of  a  hard-boiled 
egg.  Noraial  gastric  juice  containing  hydrochloric  acid  and  pepsine,  if  kept  at 
a  temperature  of  98.6°  (37°  C.)  in  an  incubator,  will  dissolve  the  flake  of  albu- 
men completely  in  from  thirty  to  sixty  minutes.  If  the  gastric  juice  contains  no 
hydrochloric  acid  but  only  pepsine,  the  albumen  will  be  dissolved  if  we  add  a  few 
drops  of  dilute  hydrochloric  acid.  If,  however,  pepsine  also  is  absent  from  the 
gastric  juice,  the  bit  of  albumen  will  swell  up  but  will  not  be  actually  dissolved, 
unless  we  add  artificial  pepsine. 

Besides  hydrochloric  acid  there  are  also  some  organic  acids  in  the  gastric 
juice ;  the  most  important  of  these  is  lactic  acid.  At  present  the  universal  belief 
is  that  the  lactic  acid  is  not  a  product  of  the  gastric  mucous  membrane,  but  the 
result  of  lactic-acid  fermentation  of  the  carbohydrates  in  the  gastric  contents, 
except  for  small  amounts  which  may  be  directly  introduced  with  the  food.  If 
we  test  the  gastric  contents  a  short  time  (fifteen  to  thirty  minutes)  after  a  test 
breakfast,  we  can  often  find  some  lactic  acid  present,  but  as  yet  no  hydrochloric 
acid.  This  corresponds  to  the  amylolytic  stage  of  gastric  digestion.  Later,  when 
the  secretion  of  hydrochloric  acid  has  begun,  the  lactic-acid  fermentation  prompt- 
ly ceases,  so  that  under  normal  conditions,  as  we  have  said,  we  find  hydrochloric 
acid  distinctly  present  an  hour  after  the  test  breakfast,  but  usually  no  lactic  acid. 
If  we  do  find  lactic  acid  it  is  always  an  indication  of  an  impaired  production  of 
hydrochloric  acid.  There  is  a  condition  which  is  especially  favorable  for  the 
formation  and  collection  of  large  amounts  of  lactic  acid  in  the  stomach.  This 
is  when  the  absence  of  hydrochloric  acid  is  associated  with  a  stagnation  of  the 
ingesta  in  the  stomach.  This  combination  is  especially  frequent  in  the  case  of 
carcinoma  of  the  pylorus  (q.  v).  Under  these  conditions  the  lactic-acid  fermenta- 
tion may  go  on  unchecked,  and  we  find  an  abundance  of  that  acid  in  the  stomach 
at  whatever  time  we  make  a  test. 

The  qualitative  test  for  lactic  acid  is  by  means  of  Ufifelmann's  reagent:  by 
adding  a  drop  of  ferric-chloride  solution  to  a  three-  or  four-per-cent.  solution  of 
carbolic  acid,  we  obtain  a  liquid  of  a  beautiful  steel-blue  color.  Upon  adding  to  a 
portion  of  this  blue  fluid,  contained  in  a  test-tube,  gastric  contents  in  which  there 
is  lactic  acid,  the  blue  color  changes  to  a  distinct  yellow,  or  yellowish-green. 
The  test  should  not  be  regarded  as  positive  unless  there  is  a  distinct  yellow  color. 
We  may  first  agitate  the  gastric  fluid  with  ether,  and  then  make  the  test  with  the 
ether  extract,  as  ether  takes  up  the  lactic  acid.  The  quantitative  estimation  of 
lactic  acid  is  tedious,  and  not  very  important  in  practice. 

The  fatty  acids  and  acetic  acid  are  not  found  in  the  gastric  contents  unless 
there  is  marked  fermentation,  and  their  presence  therefore  indicates  a  stagna- 
tion of  the  gastric  contents  (vide  infra),  and  the  absence  of  hydrochloric  acid, 
which  acts  as  an  antiseptic.  In  practice  we  form  an  opinion  as  to  the  presence 
of  these  acids  by  the  sense  of  smell,  since  their  demonstration  by  direct  chemical 
means  is  far  from  simple. 

2.  Determination  of  the  Motor  Activity  of  the  Stomach. — The  employment 
of  the  stomach-tube  also  enables  us  to  form  with  ease  a  satisfactory  estimate  of 
the  motor  function  of  the  stomach,  and  this  is  an  extremely  important  matter. 
As  physiology  teaches  us,  the  pylorus  remains  firmly  closed  during  the  first  part 
of  gastric  digestion.  It  does  not  open  until  the  food  is  sufiiciently  prepared, 
and  then  the  chyme  is  discharged  by  successive  jets  into  the  duodenum.  For 
practical  purposes  it  is  sufiicient  to  know  that  the  examination  of  healthy  per- 
sons has  shown  the  stomach  to  be  completely  empty  again  about  two  hours  after 
the  ingestion  of  a  small  amount  of  food — e.  g.,  after  the  test  breakfast  (vide 
supra).     If,  then,  we  rinse  out  the  stomach  two  hours  after  a  test  breakfast  we 


420  DISEASES    OF   THE   DIGESTIVE   OKGANS 

ought  not,  under  ordinary  circumstances,  to  find  any  large  amount  of  bread  in 
the  wash  water.  But  it  is  a  comparatively  easy  task  for  the  stomach  to  make 
away  with  the  test  breakfast ;  so  it  is  more  suitable,  if  we  desire  to  test  its  motor 
powers,  to  administer  what  is  called  a  test  meal,  consisting  of  a  plate  of  broth, 
150  grammes  (5  ounces)  of  underdone  broiled  steak  (minced),  50  grammes  (2 
ounces)  of  potato  puree,  and  a  roll.  A  meal  of  this  sort  disappears  from  the  stom- 
ach often  in  three  or  four  hours,  but  at  the  latest,  under  normal  conditions,  in 
seven  hours.  If  we  wash  out  the  stomach  seven  hours  after  a  test  meal  and  still 
find  any  considerable  amount  of  food,  it  is  sure  proof  of  an  unsatisfactory  dis- 
charge of  the  stomach  contents,  whether  as  a  result  of  impaired  motor  power  or, 
as  is  most  frequently  the  case,  of  a  mechanical  stenosis  of  the  pylorus.  If  we 
really  wish  to  know  how  long  portions  may  be  retained  in  the  stomach,  we  may 
add  to  the  meal  a  few  cranberries  or  green-colored  beans,  and  the  like.  Such 
easily  recognizable  things  may  sometimes  be  found  again  in  rinsing  out  the  stom- 
ach several  days  after  their  ingestion. 

It  is  of  course  understood  that  the  gastric  contents  which  we  obtain  a  shorter 
or  longer  time  after  a  test  meal  are  examined  with  regard  to  the  presence  of 
hydrochloric  and  lactic  acids,  and  also  with  regard  to  other  characteristics,  such 
as  the  presence  of  mucus  and  blood,  and  microscopic  appearances.  Many  impor- 
tant details  in  regard  to  these  matters  will  be  brought  up  in  later  chapters. 

In  this  connection,  however,  we  may  make  brief  mention  of  another  method 
originated  by  Ewald,  with  this  same  object  of  determining  the  motor  efficiency  of 
the  stomach.  The  patient  is  given,  early  in  the  morning,  a  gelatine  capsule 
containing  fifteen  grains  (gramme  1)  of  salol.  Salol  is  not  broken  up  until  it 
reaches  the  intestine,  when  it  separates  into  carbolic  and  salicylic  acids.  The 
salicylic  acid  is  then  immediately  excreted  in  the  urine,  and  readily  detected 
by  chloride  of  iron.  If  the  stomach  does  not  empty  itself  in  a  normal  manner, 
the  salicylic  reaction  is  often  to  be  detected  in  the  urine  even  after  twenty- 
four  or  thirty  hours,  at  which  time  it  would  have  vanished  under  normal  condi- 
tions. This  test  has  not  been  adopted  very  generally  in  practice,  because  it  is 
uncertain. 

3.  Estimation  of  the  Size  and  Position  of  the  Stomach. — The  position  and 
size  of  the  stomach  are  liable  to  great  variations,  and  with  regard  to  pathological 
conditions  it  is  important  to  determine  these  points  about  the  organ.  An  expe- 
rienced eye  may  sometimes  recognize  the  position  of  the  stomach  by  mere  observa- 
tion of  the  abdomen,  but  often  this  is  negative  or  misleading.  By  percussion  we 
may  distinguish  the  limits  of  the  deep  tympanitic  resonance  of  the  stomach  from 
the  usually  higher  tympanitic  resonance  of  the  surrounding  intestines ;  or  we  may 
mark  the  lower  limit  of  dullness  when  the  organ  is  full,  so  that  we  can  some- 
times form  a  tolerably  certain  opinion  as  to  the  lower  border  of  the  stomach. 
In  general,  these  results  are  deceptive  and  uncertain. 

With  the  aid  of  the  stomach-tube  the  matter  is  very  simple.  It  is  accom- 
plished by  blowing  up  the  stomach  with  air,  in  the  manner  first  elaborated  by 
Runeberg.  This  is  done  by  means  of  the  ordinary  double  rubber  bulb  [such  as  is 
employed  with  the  Paquelin  cautery;  or  with  a  simple  Davidson  syringe].  The 
method  used  by  us  in  our  wards  almost  every  day  is  as  follows:  The  patient  is 
either  fasting  or  has  had  his  stomach  thoroughly  rinsed  out,  and  lies  as  nearly 
horizontal  as  possible  upon  his  back.  The  stomach-tube,  being  introduced,  is  con- 
nected with  the  bulb  at  its  upper  end,  and  air  is  pumped  in.  As  the  pylorus  is 
almost  always  firmly  closed,  the  contours  of  the  stomach  become  visible  very 
shortly.  We  should  then  not  only  mark  the  position  of  the  greater  curvature  but 
also  that  of  the  lesser  curvature,  if  visible.  If  the  stomach  is  normal  in  position 
and  size,  the  protuberance  occupies  the  epigastrium  above  the  navel.  If  the  stom- 
ach is  dilated,  the  greater  curvature  reaches  below  the  navel ;  while  if  the  stomach 


examhstation  of  the  gasteic  contents  421 

as  a  whole  is  displaced  downward  (vide  infra,  gastroptosis),  the  smaller  curvature 
also  falls  to  the  neighborhood  of  the  navel  or  below  it. 

As  soon  as  we  disconnect  the  bulb  the  air  escapes,  and  the  distended  stomach 
collapses.  "We  can,  if  a  certain  degree  of  caution  is  used,  repeat  the  procedure 
more  than  once,  so  as  to  make  sure  of  our  results.  Of  course,  inflation  should 
be  interrupted  immediately  if  the  distention  of  the  stomach  becomes  painful; 
and  we  should  abstain  from  the  procedure  altogether  whenever  there  is  suspicion 
of  an  ulcer,  because  the  artificial  distention  of  the  stomach  in  this  case  might  do 
harm.  In  some  cases,  direct  inflation  does  not  render  the  contours  of  the  stomach 
distinctly  prominent,  probably  because  of  insufficiency  of  the  pylorus.  In  such 
cases,  and  in  such  only,  we  should  employ  a  rubber  bag  (condom)  fastened  on 
the  lower  end  of  the  tube,  having  previously  tested  its  distensibility.  When  this 
is  introduced  into  the  empty  stomach  and  blown  up,  we  can  usually  discern  it 
through  the  abdominal  walls  and  determine  the  position,  but  of  course  not  the 
size,  of  the  stomach.  For  ordinary  cases  the  first-described  method  is  not  only 
simpler  but  more  satisfactory,  and,  so  far  as  the  patient  is  concerned,  less  dis- 
agreeable. If  the  abdominal  walls  are  thick  with  fat  the  method  fails,  but  such 
a  condition  is  very  rare  when  there  is  severe  gastric  disease. 

The  simple  method  just  described  seems  to  us  to  have  rendered  entirely  super- 
fluous most  of  the  other  more  or  less  complicated  procedures  for  the  determina- 
tion of  the  size  and  position  of  the  stomach,  especially  as  no  better  results  are 
obtained  by  them.  This  last  statement  applies  especially  to  electric  transillumi- 
nation of  the  stomach  and  anterior  abdominal  walls  by  means  of  an  incandescent 
light  introduced  with  a  tube.  A  practiced  specialist  can  obtain  valuable  results 
in  this  way,  but  it  is  often  very  misleading. 

In  ordinary  practice  where  the  introduction  of  the  stomach-tube  is  not  always 
practicable,  the  old  method  recommended  by  Frerich  may  be  employed.  For  car- 
rying this  out  it  is  best  to  have  the  patient  fasting,  and  in  a  horizontal  position. 
Seventy-five  to  one  hundred  and  fifty  grains  (grammes  5-10)  of  tartaric  acid  are 
given,  and  immediately  after  an  equal  amount  of  bicarbonate  of  soda,  each  drug 
being  dissolved  in  half  a  glass  of  water.  At  once  there  is  an  abundant  production 
of  carbonic  dioxide.  The  stomach  is  blown  up  and  its  outlines  become  sometimes 
very  distinct,  both  for  observation  and  for  percussion.  The  great  advantage  of 
the  previously-described  method  of  pumping  in  air  consists,  however,  in  the  fact 
that  we  have  the  degree  of  distention  under  far  better  control,  and  that  we  can 
repeat  the  process  several  times  in  succession. 

To  sum  up  briefly  all  that  has  been  said,  a  careful  examination  of  the  stom- 
ach should  proceed  in  the  following  manner:  First,  rinsing  out  of  the  empty 
stomach  early  in  the  morning,  to  determine  whether  there  may  be  stagnation  (as 
indicated  by  lactic  acid)  or  hypersecretion.  We  should  also  notice  whether 
there  is  any  collection  of  mucus  in  the  stomach  when  fasting;  and  we  determine 
the  position  and  size  of  the  stomach  by  inflation.  Secondly,  the  stomach  being 
empty  we  administer  a  test  breakfast ;  an  hour  later  we  examine  the  contents  for 
hydrochloric  or  lactic  acid.  Thirdly,  at  noon  we  give  a  test  meal,  and  seven 
hours  later  wash  out  the  stomach,  to  determine  its  motor  efficiency.  If  there 
is  stagnation  of  the  gastric  contents,  we  test  again  for  hydrochloric  and  lactic 
acids. 

4.  Testing  the  Absorptive  Powers  of  the  Stomach. — Brief  mention  should  be 
made  of  Penzoldt's  method  of  determining  the  absorptive  powers  of  the  stomach. 
A  gelatine  capsule  filled  with  iodide  of  potassium,  if  swallowed  by  a  healthy  person 
fasting,  will  give  rise  at  the  end  of  ten  or  fifteen  minutes  to  a  reaction  for  iodine 
in  the  saliva  and  in  the  urine  (by  adding  sulphuric  acid  and  shaking  with  sul- 
phide of  carbon).  In  severe  diseases  of  the  stomach  the  time  required  is  often 
much  longer.     In  practice,  however,  the  method  has  not  been  highly  approved. 


422  DISEASES    OF   THE   DIGESTIVE   OEGAITS 

because  we  can  not  draw  any  certain  conclusions  from  it  as  to  the  absorption  of 
food — a  matter  about  which,  in  general,  we  possess  little  knowledge. 

5.  Demonstration  of  Blood  in  the  Gastric  Contents.— Any  admixture  of  blood 
with  the  contents  of  the  stomach  is  of  great  importance  in  the  diagnosis  of  cer- 
tain gastric  diseases,  particularly  ulcer  and  carcinoma.  If  there  is  fresh  blood 
mixed  with  the  vomitus  or  with  the  gastric  contents  obtained  by  washing  out 
the  stomach,  it  is  often  directly  recognizable  from  its  characteristic  appearance, 
but  if  the  blood  is  already  decomposed  or  intimately  mixed  with  the  food,  or 
present  in  very  small  amounts,  we  need  special  methods  for  its  certain  recogni- 
tion. Microscopic  examination  alone  is  insufficient,  for  the  red  corpuscles  are 
soon  destroyed  in  the  stomach.  The  method  of  spectrum  analysis  requires  a 
special  spectroscope.  We  search  for  the  characteristic  bands  of  hsematine  in  an 
ethereal  extract,  made  by  shaking  up  a  portion  of  the  gastric  contents,  to  which  a 
few  drops  of  glacial-acetic  acid  have  been  added,  with  ether.  For  medical  prac- 
tice the  most  useful  and  simple  method  is  Van  Deen's  test,  with  fresh  tincture 
of  guaiac  and  turpentine.  A  mixture  of  equal  portions  of  these  two  liquids  is 
poured  into  a  test-tube  upon  a  portion  of  the  gastric  contents.  If  blood  is  pres- 
ent there  at  once  appears  an  intense  blue  color,  but  certain  other  matters  con- 
tained in  the  food  may  cause  this  same  color  reaction,  so  that  it  is  more  satis- 
factory to  decompose  the  gastric  contents  with  a  few  drops  of  glacial-acetic  acid, 
then  extract  with  ether  and  perform  the  guaiac-turpentine  test  with  the  ether 
extract.  This  test  is  especially  distinct  if  there  are  organic  acids  present,  as  in 
case  of  carcinoma,  in  which  disease  the  stomach  contains  blood  in  association 
with  lactic  acid  but  no  hydrochloric  acid.  On  the  other 
^.      ^      ^  hand,  in  our  experience,  the  test  is  often  uncertain  in  the 

^^^  ^^       ^A'^       ^^^^  ^^  ulcer,  because  the  presence  of  hydrochloric  acid  is  a 
"^te      §        ^  ^^  hindrance.     Another  common  method  is  to  see  if  we  can 

-#'  M.  ^    lUl     produce  Teichmann's  hsemine  crystals  from  the  gastric 

^  ■^^  .^^         ^^        contents.    The  test  is  not  always  successful,  but  if  success- 
^  ^      .  r       ful  it  indicates  the  presence  of  blood.    We  put  a  small  por- 

^      ^m   ^  tion  of  the  suspected  gastric  contents  upon  an  object-glass 

M  g        ^  with  a  trace  of  common  salt,  and  a  few  drops  of  glacial- 

acetic  acid.  If  we  now  evaporate  slowly  to  drjoiess  there 
Fig.  46.— Hseraine  crystals,  are  formed  small,  brown,  rhombic  hsemine  crystals  (see 
Fig.  46),  which  can  be  seen  by  the  microscope.  Of  course, 
whenever  we  examine  the  contents  of  the  stomach  for  blood,  we  should  bear  in 
mind  that,  if  found,  the  blood  may  be  due  to  the  ingestion  of  underdone  meat, 
preparations  of  hsemoglobin,  or  similar  substances.  Finally,  we  scarcely  need  to 
repeat  that  in  all  important  cases  one  ought  not  to  be  satisfied  with  a  single  ex- 
amination of  the  stomach,  but  he  should  make  certain  of  his  results  by  repeated 
tests. 


CHAPTEE   II 


ACUTE    GASTRIC    CATARRH 

{Acute  Gastritis) 

.ffitiology  and  Pathological  Anatomy. — The  mucous  membrane  of  the  stom- 
ach not  being  open  to  direct  examination,*  as  is  that  of  the  mouth  and  throat, 
and  acute  gastric  disease  being  seldom  fatal  so  as  to  render  an  autopsy  possible, 

*  The  examination  of  the  mucous  membrane  of  the  stomach  by  means  of  the  stomach  mirror  and 
the  electric  light  involves  such  technical  cUihculties  that  it  has  not  as  yet  been  adopted  in  practice. 


ACUTE    GASTEIC    CATAKRH  423 

the  existence  of  acute  gastritis  is  mainly  a  matter  of  inference  from  our  observa- 
tions of  other  mucous  membranes.  When  some  harmful  agency  acts  in  a  direct 
manner  upon  the  mucous  membrane  of  the  stomach,  we  shall  usually  be  right  in 
supposing  that  there  is  a  greater  or  less  degree  of  genuine  inflammation  of  the 
lining  of  the  stomach,  unless  the  organ  in  a  simply  functional  way  at  once  rids 
itself  of  the  irritant — for  example,  by  vomiting  when  the  stomach  has  been 
"  overloaded."  If  some  noxious  material  acts  long  and  continuously  upon  the 
mucous  membrane,  there  will  be  abnormal  changes  not  only  in  the  blood-vessels 
and  the  interstitial  tissue,  but  also  in  the  cellular  elements  of  the  mucous  mem- 
brane and  its  glands.  As  yet,  we  know  little  about  the  miniite  degenerative 
changes  in  the  specific  secreting  cells.  The  microscopic  inflammatory  lesions, 
which  we  may  with  great  certainty  assume  to  be  present,  are  hypersemia  and 
swelling  of  the  mucous  membrane,  perhaps  associated  with  an  increase  in  the 
secretion  of  mucus,  and  with  small  hemorrhages  here  and  there.  If  the  irritant 
is  insignificant  the  lesions  will  be  mild  and  superficial  (mild  catarrhal  gastritis). 
If  the  noxious  agent  is  more  powerful  (for  example,  corrosive  poison)  it  will 
give  rise  to  a  deeper  parenchymatous  inflammation,  with  peeling  off  of  the 
mucous  membrane  and  similar  effects  (severe  toxic  gastritis). 

The  mild  catarrhal  forms  of  gastritis  are  caused  by  simple  chemical  and  me- 
chanical influences,  and  perhaps  by  thermic  irritation.  They  are  most  often  the 
result  of  errors  in  diet,  such  as  the  ingestion  of  too  large  an  amount  of  food,  or 
of  food  that  is  difficult  to  digest,  unsuitable,  highly  spiced,  or  very  acid.  In  the 
same  class  belong  the  acute  indigestion  following  excess  in  alcohol,  and  the  fre- 
quent derangement  of  the  stomach  from  taking  medicines;  and  also  cases  due 
to  the  accidental  or  willful  ingestion  of  all  sorts  of  injurious  and  poisonous  sub- 
stances. The  severe  cases  of  toxic  gastritis  are  most  often  caused  by  the  action 
of  concentrated  mineral  acids  and  alkalies.  In  this  class  comes  poisoning  from 
sulphuric  acid,  nitric  acid,  hydrochloric  acid,  caustic  potash,  and  caustic  soda. 

A  special  importance  attaches  to  the  ingestion  of  decaying  substances.  The 
incautious  use  of  tainted  meat  or  fish  may  be  followed  by  relatively  severe  forms 
of  acute  gastric  catarrh.  The  products  of  decomposition  act  as  chemical  irri- 
tants upon  the  mucous  membrane;  and  the  ferments  and  putrefactive  agents 
likewise  continue  in  activity  after  reaching  the  stomach,  and  thus  contribute  to 
produce  the  inflammation.  The  reason  that  this  sort  of  gastric  catarrh  is  not 
much  more  frequent  than  it  is,  is  undoubtedly  the  presence  of  hydrochloric  acid 
as  a  constituent  of  the  gastric  juice,  because  it  has  an  antiseptic  action. 

It  is  universally  assumed  that  a  chill  of  the  outer  surface  of  the  body  may 
excite  gastric  catarrh,  but  there  seems  to  be  actual  proof  of  this  in  but  few  cases. 
On  the  other  hand,  there  can  be  no  doubt  that  many  cases  of  acute  gastric  ca- 
tarrh, of  apparently  primary  origin,  are  referable  to  infection.  Infectious 
catarrh  of  the.  stomach  may  occur  at  times,  particularly  in  summer,  with  especial 
frequency.  As  to  the  precise  nature  of  the  pathogenic  germ  we  do  not  as  yet 
possess  any  certain  knowledge. 

The  predisposition  of  certain  individuals  to  gastric  catarrh  differs  greatly. 
Some  persons  always  have  a  "  weak  "  stomach,  and  the  disease  is  prone  to  attack 
feeble  children,  ansemic  persons,  fever  patients,  and  convalescents  from  severe 
diseases,  as  well  as  chronic  invalids  who  are  ill-nourished.  Enfeebled  persons  of 
this  sort  sometimes  fall  sick  when  vigorous  and  healthy  individuals  would  entirely 
escape.  In  many  of  these  cases  of  unusual  predisposition  to  gastric  disease,  we 
may  surmise  that  the  secretion  of  hydrochloric  acid  is  scanty,  and  that  there 
may  be  a  diminution  in  the  motor  power  of  the  stomach.  Each  of  these  factors 
would  of  course  render  ingested  irritants  more  hannful. 

Symptoms. — The  most  constant  subjective  symptom  is  anorexia.  In  many 
cases  the  very  thought  of  food  excites  disgust.     What  the  patient  does  eat  tastes 


424  DISEASES    OF   THE   DIGESTIVE    OKGANS 

flat,  and  lie  is  therefore  very  eager  for  piquant  dishes,  highly  spiced  or  sour. 
Thirst  is  often  present,  and  a  feeling  of  dryness  in  the  mouth. 

The  subjective  gastric  sensations  are  seldom  those  of  marked  pain;  but 
sometimes  there  are  attacks  of  pain  which  are  in  all  probability  due  to  cramplike 
contractions  of  the  muscular  coat.  The  usual  complaint  is  of  constant  pressure 
and  fullness.  Sometimes  the  patient  is  conscious  of  the  peristaltic  movements 
of  the  stomach.     He  has  "  rumbling  "  of  the  bowels. 

There  is  nausea,  and  often  vomiting.  In  severe  cases  everything  swallowed 
is  at  once  rejected.  The  vomitus  consists  for  the  most  part  of  undigested  food 
(often  ill-smelling),  with  which  mucus,  and  sometimes  bile,  is  mingled.  Eructa- 
tions of  gas  or  liquid  are  frequent. 

Physical  external  examination  reveals  little.  The  epigastrium  may  be  some- 
what prominent  as  a  whole,  and  may  be  tender  on  pressure.  The  tongue  is  almost 
always  thickly  coated  and  dry.  The  breath  is  usually  disagreeable,  and  there  is 
a  persistent  flat  or  bitter  taste  in  the  mouth.  In  ordinary  cases  of  acute  gastritis 
examination  of  the  gastric  contents  is  hardly  necessary,  but  in  severe  cases  we 
find  a  marked  diminution  in,  or  entire  absence  of,  the  hydrochloric-acid  reaction, 
and  distinct  delay  in  the  motor  activity  of  the  stomach.  Sometimes  lactic  acid 
and  the  fatty  acids  are  present  in  large  amounts. 

In  severe  cases  there  is  always  considerable  constitutional  disturbance.  The 
patient  feels  languid,  and  disinclined  for  any  exertion;  the  pulse  is  moderately 
rapid,  although  it  may  exceptionally  be  slower  than  normal;  the  urine  is  usually 
somewhat  concentrated,  often  it  gives  a  marked  indican  reaction.  There  may 
be  no  fever,  but  not  infrequently  there  is  a  moderate  elevation  of  temperature 
with  sensations  of  chilliness  or  heat.  In  rare  cases  we  may  observe  an  approach 
to  the  typhoid  condition,  with  such  nervous  symptoms  as  headache,  vertigo,  and 
dullness.  These  cases  were  formerly  termed  "  gastric  fever,"  and  they  are  prob- 
ably most  of  them  infectious,  but  yet  the  constitutional  symptoms  are  probably 
only  in  part  referable  to  coincident  constitutional  infection.  It  is  more  probable 
that  toxic  influences  are  exerted  by  the  abnormal  products  of  the  fermenta- 
tion which  takes  place  in  the  stomach.  For  example,  Senator  mentions  sulphur- 
etted hydrogen  as  thus  generated;  and  Litten  has  described  several  cases  in  which 
at  first  there  were  such  dyspeptic  symptoms  as  nausea,  vomiting,  flatulence,  and  a 
coated  tongue,  but  which  soon  gave  evidence,  by  restlessness,  headache,  great  mus- 
cular weakness,  and  a  gradual  lapse  into  somnolence,  of  rather  severe  nervous  dis- 
turbance in  addition.  The  breath  had  a  marked  "  fruity  "  odor ;  and,  on  adding 
chloride  of  iron  to  the  urine,  a  strong  reddish  color  was  developed,  as  in  the  so- 
called  acetone-reaction;  so  that  it  seems  probable  that  an  auto-intoxication  had 
occurred,  somewhat  resembling  diabetic  coma. 

Chief  among  complications  are  the  intestinal  symptoms,  which  are  frequently 
coincident  with  the  gastric  disorder.  Constipation  is  the  rule.  There  may  be 
diarrhoea.  The  gastric  catarrh  may  by  extension  involve  the  duodenum,  and  give 
rise  to  jaundice.  Sometimes  herpes  appears  upon  the  skin.  This  fact  argues  for 
the  infectious  nature  of  many  cases  of  gastric  catarrh. 

It  is  evident  from  what  has  been  said  that  acute  gastric  catarrh  is  by  no 
means  uniform  in  its  setiology,  and  the  general  course  of  the  disease  is  also  sub- 
ject to  great  variations.  Sometimes  there  are  mild  dyspeptic  symptoms  which 
vanish  in  the  brief  time  of  one  or  two  days,  while  in  other  cases  we  have  a  rather 
severe  disease  associated  with  considerable  constitutional  disturbance,  and  last- 
ing three  to  ten  days.  There  is  also  great  variation  in  the  intensity  of  the  vari- 
ous symptoms,  particularly  the  vomiting.  The  progress  of  the  case  may  be  irreg- 
tdar  and  there  may  be  relapses,  but  still,  the  prognosis  of  primary  acute  gastritis 
is  entirely  favorable.  The  diagnosis  is  usually  easy,  although  we  should  never 
omit  to  make  an  unprejudiced  and  careful  examination  into  the  general  condition. 


CHEONIC   GASTRITIS  425 

If  there  is  fever  we  should  bear  in  mind  the  possibility  of  a  mild  typhoid  (see 
typhoid  fever). 

Treatment. — If,  at  the  beginning  of  the  disease,  there  is  reason  to  suppose 
that  the  stomach  is  loaded  with  undigested  food,  an  emetic  is  indicated.  If  it  is 
desired  to  avoid  the  irritative  action  of  an  emetic  upon  the  gastric  mucous  mem- 
brane, a  subcutaneous  injection  of  one  sixth  of  a  grain  (gramme  0.01)  of  apo- 
morphine  may  be  given.  Still  more  efficient,  although  disagreeable  for  the  pa- 
tient, is  a  washing  out  of  the  stomach  by  means  of  the  stomach-tube,  particularly 
in  severe  cases  of  toxic  or  infectious  origin ;  but  of  course,  when  the  gastric  walls 
may  have  been  weakened  by  corrosive  poisons,  the  stomach-tube  is  contraindi- 
cated. 

In  most  cases,  however,  emetics  and  lavage  may  be  dispensed  with.  The 
treatment  in  such  cases  consists  mainly  in  a  strict  regulation  of  the  diet,  allow- 
ing for  a  time  nothing  whatever,  and  then  such  food  as  milk  porridge,  iced  milk, 
and  toast.  Of  internal  remedies,  ten  to  fifteen  drops  of  dilute  hydrochloric  acid 
in  half  a  wine-glass  of  water  sometimes  seems  beneficial;  while  in  other  cases, 
in  which  there  are  sour  eructations  and  vomiting,  alkalies  are  to  be  given.  We 
may  order  as  much  bicarbonate  of  soda  or  as  much  Carlsbad  salts  as  will  rest  on 
the  point  of  a  pen-knife,  or  Ems  water.  The  so-called  stomachics  and  bitters  are 
also  often  prescribed,  for  example,  compound  tincture  of  gentian  or  tincture  of 
rhubarb.  Another  favorite  remedy  is  resorcine,  of  which  four  grains  dissolved  in 
some  aromatic  water  may  be  given  every  two  hours.  If  the  vomiting  is  obstinate, 
relief  may  be  got  from  bits  of  ice  or  sips  of  cold  Seltzer  water.  In  severer  cases 
we  must  resort  to  narcotics,  such  as  opium,  cocaine,  and  chloroform,  administered 
internally. 

If  there  is  decided  constipation,  an  enema  must  be  employed,  or  such  laxatives 
as  calomel,  Epsom  salts,  or  rhubarb. 


CHAPTER  III 
CHRONIC   GASTRITIS— CHRONIC   CATARRH   OF   THE   STOMACH 

.Sltiology. — The  same  causes  which  excite  acute  gastric  catarrh,  if  often  re- 
peated, lead  at  last  to  chronic  catarrh  of  the  stomach;  but,  at  least  in  adults, 
infectious  influences  are  seldom  prominent  in  the  causation  of  the  disease.  In 
many  cases  it  is  due  chiefly  to  the  chemical  and  mechanical  irritation  of  an  un- 
suitable diet  long  continued.  By  far  the  most  frequent — indeed,  to  speak  more 
correctly,  the  only  frequent — form  of  chronic  gastric  catarrh  in  adults,  is  due  to 
hard  drinking.  The  habitual  use  of  distilled  liquors  is  more  influential  in  this  re- 
gard than  excess  in  wine  or  beer.  The  harm  done  by  alcohol  may  be  re-enforced 
by  other  dietetic  causes.  We  have  often  met  with  genuine  chronic  gastritis  in 
extremely  destitute  persons,  who  for  a  long  time  had  to  eat  food  that  was  insuf- 
ficient, bad,  or  even  decayed.  It  should  also  be  pointed  out  that  abnormal  condi- 
tions of  the  mouth,  and  particularly  dirty  or  carious  teeth,  may  occasion  dyspep- 
tic and  catarrhal  conditions.  Habitual  excess  in  smoking  is  also  said  sometimes 
to  occasion  chronic  gastritis;  and  finally,  it  is  probable  that  the  bad  habit  of 
rapid  eating  with  imperfect  mastication  leads  at  last  to  gastric  disturbance.  As 
is  the  case  with  all  external  irritants  of  this  sort,  the  results  are  influenced  by 
individual  differences  in  the  resisting  powers  of  the  affected  organ,  and  personal 
predisposition  to  disease  plays  a  certain  part  in  the  development  of  chronic  gas- 
tric catarrh.  Often,  as  we  have  already  noted,  this  predisposition  seems,  to  a 
certain  extent,  a  matter  of  family  and  heredity. 


426  DISEASES    OE   THE   DIGESTIVE    OEGANS 

Chronic  gastric  catarrh  is  not  always  a  primary  affection.  It  may  be  sec- 
ondary to  some  other  disease.  In  particular,  all  diseases  associated  with  portal 
congestion  are  apt  to  lead  to  secondary  catarrh  of  the  stomach.  This  includes 
hepatic  cirrhosis  and  hepatic  syphilis.  Again,  the  gastric  catarrh  associated  with 
chronic  cardiac,  pulmonary,  or  renal  disease  is  in  part  to  be  regarded  as  due  to 
congestion.  On  the  other  hand,  however,  we  should  always  consider  how  manifold 
are  the  other  conditions,  associated  with  all  sorts  of  chronic  diseases,  which  may 
lead  to  chronic  gastric  disturbance.  We  may  mention,  for  instance,  anaemia, 
muscular  insufficiency,  and  auto-intoxication. 

Pathology. — The  macroscopic  changes  in  the  gastric  mucous  membrane  are  in 
most  cases  very  moderate.  Usually  it  is  thickened  and  coated  with  a  layer  of 
tough,  grayish-white  mucus,  in  which  is  suspended  a  greater  or  less  amount  of 
detached  epithelium.  The  membrane  is  brownish  red,  unless  rendered  gray  by 
excessive  pigmentation.  Under  the  microscope  we  find  a  well-marked  infiltration 
of  the  interstitial  tissue  with  fine  cells,  and  well-marked  parenchymatous 
changes,  particularly  extensive  degeneration  of  the  glandular  cells.  All  these 
changes  are  especially  marked  in  the  pyloric  portion  of  the  stomach.  If  the 
catarrh  has  lasted  a  long  time  there  may  be  still  further  changes  in  the  mucous 
membrane.  In  many  cases  it  appears  smooth  and  atrophic.  The  glandular 
layer  of  the  stomach  may  at  last  be  almost  destroyed,  and  the  muscular  and  sub- 
mucous coats  share  in  the  atrophy,  while  the  organ  as  a  whole  is  usually  dilated. 
In  other  less  frequent  cases  there  is  a  marked  growth  of  interstitial  connective 
tissue,  with  resultant  contraction.  In  this  variety,  also,  the  glandular  layer  atro- 
phies, the  stomach  walls  grow  firmer,  and  the  whole  organ  shrivels  (cirrhosis  of 
the  stomach).  Contrasting  with  these  forms  which  lead  to  atrophy  or  sclerosis, 
there  are  others  which  occasion  a  hyperplasia  of  the  mucous  membrane.  Its 
inner  layer  is  thickened  and  mammillated  (Stat  mamelonne) ,  and  there  may  be 
actual  polypi  formed.  The  hyperplasia  in  these  cases  affects  mainly  the  gland- 
tubes  of  the  mucous  membrane,  but  there  is  also  a  considerable  thickening  of  the 
submucous  coat. 

Symptoms  on  the  Part  of  the  Stomach. — The  symptoms  of  chronic  gastric 
catarrh  are  the  same  dyspeptic  symptoms  which  we  meet  in  various  combination 
and  degree  in  all  diseases  of  the  stomach.  They  include  disturbance  of  the 
appetite;  pressure  or  pain  in  the  region  of  the  stomach;  a  bad  taste  in  the  mouth; 
abnormal  sensations  in  the  throat;  and  finally,  motor  phenomena,  including 
rumbling,  eructations,  and  vomiting. 

The  appetite  is  usually  impaired  in  chronic  gastric  catarrh.  There  is  some- 
times a  moderate  appetite,  but  it  is  soon  changed  to  a  feeling  of  repletion  upon 
the  ingestion  of  even  a  slight  amount  of  food.  In  other  cases  there  is  actual 
dislike  for  any  form  of  nourishment;  the  patient  eats  little,  and  prefers  highly 
spiced,  piquant  dishes.  There  is  often  a  persistent  bitter,  flat,  offensive,  or  other- 
wise abnormal  taste  in  the  mouth. 

Subjective  sensations  in  the  region  of  the  stomach  are  rarely  entirely  absent. 
As  a  rule,  there  is  a  feeling  of  fullness  or  pressure  and  of  dull  pain.  These  trou- 
bles may  either  be  constant,  or  occur  after  meals.  Sometimes,  especially  after 
errors  in  diet,  there  may  be  actual  pain.  This  is  termed  cardialgia  or  gastralgia, 
and  is  probably  due  in  most  cases  to  cramp-like  contractions  of  the  muscles ;  but 
in  general,  habitual  and  severe  pain  does  not  belong  to  the  clinical  picture  of 
simple  catarrh.  A  very  frequent  and  annoying  symptom,  which  is  particularly 
apt  to  come  on  after  eating,  is  the  eructation  of  gas,  usually  air,  but  sometimes 
gases  which  are  formed  in  the  stomach  by  the  processes  of  decomposition.  Such 
gases  have  a  disagreeable  odor.  The  eructations  may  bring  up,  also,  some  of  the 
fluid  contents  of  the  stomach.  If  there  is  a  bitter  taste  associated  with  it  this 
is  usually  occasioned  by  peptones,  but  sometimes  perhaps  by  bile  (vide  infra). 


CHEONIC   GASTEITIS  427 

Acid  eructations  indicate  excessive  acidity  of  the  gastric  contents,  ordinarily 
due  to  hydrochloric  acid  but  exceptionally  to  lactic  acid  (vide  infra),  or  to  the 
fatty  acids,  which  are  recognizable  by  their  odor.  The  burning  feeling  in  the 
pharynx  and  lower  down,  which  is  occasioned  by  acid  eructations  and  which  is 
usually  termed  heartburn,  is  almost  always  caused  by  an  excess  of  hydrochloric 
acid  in  the  gastric  contents,  and  consequently  is  not  a  frequent  symptom  of 
genuine  chronic  gastric  catarrh  (vide  infra). 

In  many  cases  the  feeling  of  nausea  increases,  especially  after  eating,  to 
actual  vomiting,  but  in  chronic  gastric  catarrh  vomiting  is  not  very  frequent, 
and  if  it  occurs  it  is  the  result  of  some  special  cause,  such  as  errors  in  diet.  There 
is  this  exception,  that  in  the  chronic  gastric  catarrh  of  drunkards  a  peculiar  fonn 
of  vomiting  is  very  common.  This  is  called  morning  vomiting.  By  this  is 
understood  a  fairly  regular  occurrence  of  vomiting  in  the  morning  before  break- 
fast, with  the  ejection  of  considerable  amounts'of  watery  mucus,  usually  alkaline. 
This  vomiting  is  due  not  only  to  the  chronic  catarrh  of  the  stomach,  but  also 
to  the  chronic  catarrh  of  the  pharynx,  which  latter  occasions  a  great  tendency 
to  gagging — e.  g.,  when  rinsing  out  the  mouth.  The  vomitus  consists  not  only  of 
mucus  from  the  stomach  but  in  large  part,  also,  of  a  mixture  of  saliva  and  mvicus 
from  the  mouth  and  throat.  In  the  other  forms  of  chronic  gastric  catarrh  the 
vomitus  consists  often  of  ill-digested  food  and  more  or  less  mucus.  If  there  are 
vigorous  efforts  at  vomiting  and  retching,  the  vomitus  may  contain  also  some  bile 
and  small  amounts  of  blood,  which  have  no  serious  significance. 

The  external  examination  of  a  patient  with  chronic  gastritis  shows  little 
unusual.  The  general  nutrition,  of  course,  is  often  impaired,  although  in  drunk- 
ards and  gourmands  an  abundant  fat  layer  persists  for  a  long  time.  The  tongue 
is  usually  coated,  especially  in  its  center,  while  its  sides  and  tip  are  red.  A 
thickly  coated  tongue  and  salivation  are  both  of  them  due  rather  to  accompany- 
ing stomatitis  and  pharyngitis — complications  which  are  present  in  the  case  of 
most  drunkards,  and  sometimes  also  in  excessive  smokers.  Examination  of  the 
epigastrium  shows  often  a  considerable  prominence  of  the  stomach  and  tender- 
ness on  pressure,  but  the  only  means  of  obtaining  an  actual  insight  into  the  abnor- 
mal process  is  a  careful  investigation,  by  means  of  the  stomach-tube.  This 
should  not  be  omitted  in  any  case  of  chronic  gastritis  of  any  severity,  especially  as 
the  results  of  it  furnish  the  only  true  guide  for  a  rational  treatment  of  the 
disease.  If  we  examine  the  gastric  juice  after  the  manner  already  described,  we 
shall  find  that  free  hydrochloric  acid  in  chronic  gastritis  is  scanty  (below  0.1  per 
cent.),  or  even  absent.  Its  complete  absence  is  particularly  common  in  chronic 
alcoholic  catarrh,  and  also  in  cases  of  chronic  gastritis  in  which  there  is  atrophy 
of  the  mucous  membrane.  In  the  latter  case  pepsine,  also,  is  often  absent.  With 
regard  to  abnormal  acids,  we  may  find  lactic  acid,  but  seldom  in  large  amounts, 
because  in  simple  chronic  catarrh  there  is  scarcely  ever  much  stagnation  of  the 
gastric  contents.  If  there  are  abnormal  processes  of  decomposition,  we  find 
acetic  acid,  butyric  acid,  and  volatile  fatty  acids,  but  these  are  very  rarely 
present. 

The  demonstration  of  an  excessive  production  of  mucus  in  the  stomach  is  of 
great  diagnostic  importance.  We  have  mentioned  that  sometimes  the  vomitus 
contains  a  distinct  admixture  of  mucus,  but  the  only  way  of  forming  an  accurate 
opinion  with  regard  to  the  amount  of  mucus  in  catarrh  of  the  stomach  is  by 
siphonage,  especially  in  cases  in  which  vomiting  is  absent  or  infrequent.  If  we 
examine  the  stomach  when  fasting  we  shall,  in  many  cases,  find  at  every  trial  an 
abundance  of  mucous  fluid  with  scarcely  any  other  ingredients.  In  other  cases 
there  is  more  apt  to  be  an  abundance  of  mucus  after  a  meal — either  in  a  viscid, 
ropy  fluid,  or  in  separate  transparent  masses  of  varying  size.  Excess  of  mucus 
in  the  stomach  is  usually  associated  with  anacidity,  but  there  are  a  few  excep- 


428  DISEASES    OF   THE   DIGESTIVE   OEGANS 

tional  cases  in  which  it  is  associated  with  increased  secretion  of  hydrochloric  acid 
(gastritis  acida;  acid  catarrh  of  the  stomach.  Boas,  Riegel,  and  others).  We 
must  avoid  confounding  secretion  from  the  mouth  and  pharynx  that  has  been 
swallowed  with  mucus  produced  in  the  stomach.  The  latter  is  intimately  mixed 
with  the  food,  if  there  be  any. 

The  motor  function  of  the  stomach  is  seldom  much  disturbed  in  chronic  gas- 
tritis. Often  it  is  surprising  how  rapidly  the  stomach  empties  itself ;  but  there 
may  be  delay,  partly  because  digestion  is  impaired  and  partly  because  there  is  a 
gradual  development  of  weakness  and  atrophy  of  the  muscular  coat  of  the  stom- 
ach, analogous  to  the  weakness  of  the  muscles  of  the  vocal  cords  in  chronic  laryn- 
gitis. If  food  is  long  retained  in  the  stomach,  there  is  probably  some  other  disease 
than  simple  catarrh.  The  size  of  the  stomach  in  chronic  catarrh  may  be  some- 
what increased,  but  this  has  no  special  importance. 

Symptoms  on  the  Part  of  other  Organs. — Course  of  the  Disease. — Of  the 
other  organs,  the  intestine  most  frequently  suffers  in  chronic  gastric  catarrh.  In 
almost  all  cases  of  chronic  gastric  catarrh  the  bowels  are  irregular.  Habitual 
constipation  is  the  rule,  but  sometimes  there  is  diarrhoea.  If  much  gas  is  gen- 
erated in  the  stomach,  the  intestinal  canal  often  becomes  implicated,  and  tym- 
panites and  flatulence  develop.  There  may  be  catarrh  of  the  duodenum  leading 
to  jaundice. 

The  urine  is  often  only  feebly  acid  in  reaction,  and  therefore  frequently  depos- 
its a  large  amount  of  phosphates.  We  miist  be  cautious,  however,  in  the  inter- 
pretation of  this  sign  and  the  value  we  lay  upon  it,  since  the  reaction  of  the 
urine  is  influenced  by  a  great  variety  of  conditions,  including  food,  drugs,  and 
the  loss  of  acid  by  vomiting. 

It  is  often  asserted  that  chronic  cutaneous  diseases  and,  in  particular,  certain 
forms  of  eczema,  are  due  to  catarrh  of  the  stomach,  but  this  is  not  certain,  though 
not  impossible. 

There  has  been  great  stress  laid,  particularly  in  recent  times,  upon  the  fre- 
quent occurrence  of  nervous  disturbance  in  association  with  chronic  catarrh  of 
the  stomach.  This  takes  the  form  of  hypochondriasis  and  depression  of  spirits 
in  association  with  all  sorts  of  other  nervous  symptoms,  including  pressure  in  the 
head,  headache,  dullness  of  mind,  and  dizziness  (vertigo  e  stomacho  laeso) ;  but, 
while  we  may  admit  that  the  disease  of  an  organ  which,  for  many  human  beings, 
is  the  main  source  of  happiness,  may  well  put  the  patient  out  of  sorts,  yet  there 
is  no  doubt  that  many  earlier  reports  about  nervous  disturbances  were  due  to  a 
confusion  of  chronic  gastric  catarrh  with  nervous  dyspepsia  (vide  infra).  Genu- 
ine chronic  catarrh  of  the  stomach,  as  such,  has  no  peculiar  relation  to  nervous 
disease,  except  in  the  rare  cases  in  which  certain  unusual  symptoms  develop,  not 
improbably  from  the  absorption  of  toxines. 

When  the  catarrh  is  of  any  duration  and  severity,  the  general  nutrition  is  apt 
to  be  seriously  impaired.  The  diminished  appetite  and  the  imperfect  digestion 
and  absorption  of  what  is  eaten  contribute  to  produce  a  gradual  and  considerable 
loss  of  weight.  The  fatty  and  muscular  tissues  atrophy.  The  skin  grows  dry  and 
harsh,  and  usually  has  a  dirty-pale  color.  In  rare  cases  of  extreme  atrophy  of  the 
mucous  membrane  (probably  almost  always  combined  with  atrophy  of  the  intes- 
tinal mucous  membrane)  there  are  developed  symptoms  like  those  of  progressive 
pernicious  anaemia  (q.v.). 

Individual  cases  differ  greatly  in  the  combination  of  symptoms  they  present 
and  in  their  course.  The  anorexia,  gastric  oppression,  eructations,  vomiting,  and 
other  important  disturbances  already  mentioned,  exhibit  the  greatest  diversity  in 
their  intensity  and  their  grouping.  In  the  milder  cases,  loss  of  appetite  and  mod- 
erate local  uneasiness  may  be  the  only  symptoms.  Frequent  vomiting  is  con- 
fined to  the  severer  cases.     The  disease  often  lasts  for  years,  especially  if  the 


CHEONIC   GASTEITIS  429 

patient  neg-lects  himself.     In  most  cases  there  are  frequent  remissions  and  exacer- 
bations, usually  dependent  upon  external  causes. 

The  disease  is  not  intrinsically  fatal  except  in  the  above-mentioned  rare  cases 
of  complete  atrophy  of  the  mucous  membrane,  but  the  general  debility  conse- 
quent upon  it  may  indirectly  shorten  life. 

Diagnosis. — If  we  except  the  self-evident  cases  of  chronic  alcoholic  catarrh, 
the  only  proper  way  of  making  a  diagnosis  of  chronic  gastritis  is  by  means  of  a 
careful  examination  with  the  stomach-tube,  along  with  a  consideration  of  the 
associated  conditions.  If  a  patient  has  for  some  time  been  suffering  from  the 
ordinary  gastric  symptoms  of  anorexia,  gastric  oppression,  eructations,  and 
vomiting,  we  must  first  determine  whether  we  have  to  deal  with  a  primary  dis- 
ease of  the  stomach,  or  with  a  secondary  disturbance  referable  to  such  condi- 
tions as  cardiac  disease,  renal  disease,  or  pulmonary  tuberculosis.  If  the  indi- 
gestion is  not  symptomatic  we  must  then  consider  in  order  each  of  the  primary 
diseases  of  the  stomach.  If  there  is  no  indication  of  ulcer  or  carcinoma,  we  have 
remaining  actual  gastritis,  nervous  dyspepsia  (q.v),  and  a  dislocation  of 
the  organ  (gastroptosis).  One  important  factor  is  the  general  condition  of  the 
patient — for  instance,  if  there  is  neurasthenia  or  the  like.  No  actual  conclusion 
can  be  reached,  however,  except  by  examining  the  contents  of  the  stomach.  We 
can  not  assume  that  there  is  a  chronic  gastritis  unless  there  are  direct  objective 
changes  to  be  demonstrated,  chief  among  which  is  an  abnormal  production  of 
mucus,  associated  with  a  change  in  the  amount  of  hydrochloric  acid  in  the  gas- 
tric juice.  This  change  is  in  most  cases  a  diminution,  but  exceptionally  an  in- 
crease of  the  amount  secreted.  We  wish,  in  this  connection,  to  emphasize  once 
more  the  statement  that  genuine  chronic  gastritis,  except  in  drunkards,  is  by  no 
means  a  common  disease  and  is  much  less  frequent  than  nervous  dyspepsia. 

Treatment. — If  the  disease  seems  to  be  merely  symptomatic — the  result,  for 
instance,  of  venous  stasis  due  to  chronic  cardiac,  pulmonary,  or  hepatic  dis- 
ease— our  efforts  must,  of  course,  be  directed  chiefly  to  the  relief  of  the  original 
trouble.  We  must  also  take  into  consideration  all  other  causative  influences, 
such  as  neglected  or  decayed  teeth,  improper  mode  of  life,  and  unhealthy  occu- 
pation. 

The  direct  treatment  of  chronic  gastric  catarrh  must  always  begin  with  a 
regulation  of  the  diet.  Such  vague  injunctions  as  "  to  be  cautious  "  or  "  to  avoid 
indigestible  articles  of  food "  are  useless.  The  patient  must  have  a  perfectly 
definite  bill  of  fare  prescribed  for  him;  nor  can  any  universal  one,  suitable  for 
all  cases,  be  drawn  up.  In  each  individual  instance  the  individual  circumstances 
must  be  considered.  The  personal  experiences  of  the  patient  himself  are  by  no 
means  to  be  disregarded.  One  man  may  be  quite  unable  to  digest  what  is  well 
borne  by  others,  and  vice  versa. 

In  the  first  place,  certain  foods  must  be  utterly  forbidden  to  such  patients  as 
do  not  themselves  avoid  whatever  disagrees  with  them.  All  articles  must  be 
prohibited  which  may  irritate  the  mucous  membrane,  either  mechanically  or 
chemically.  This  includes  all  the  coarser  sorts  of  vegetables  or  fruits,  containing 
a  large  proportion  of  indigestible  cellulose;  and  all  dishes  that  are  very  sour, 
strongly  salted,  or  highly  spiced.  Potatoes,  farinaceous  food,  and  all  substances 
composed  mainly  of  hydrocarbons,  must  also  be  interdicted;  because  almost  all 
the  abnormal  fermentative  processes,  the  evil  consequences  of  which  have  already 
been  considered,  are  promoted  by  the  hydrocarbons.  Fat  is  also  harmful.  It  im- 
pedes digestion  by  protecting  the  contents  of  the  stomach  from  the  action  of  the 
gastric  juice,  in  a  purely  mechanical  way;  and  then,  being  changed  into  the  fat 
acids,  it  causes  sour  eructations  and  pyrosis.  Yet  we  must  not  go  too  far  in 
forbidding  starches  and  fats.  Particularly  if  the  patient  is  emaciated  it  is 
advisable  to  give  such  fatty  substances  as  good  butter  and  cream  in  cautious 


4B0  DISEASES    OF   THE  DIGESTIVE   OEGANS 

amounts,  and  often  the  result  is  satisfactory.  In  general,  we  should  not  forget 
that  with  regard  to  diet  the  skill  of  the  physician  often  lies  more  in  what  he 
permits  than  in  what  he  forbids.  The  limitation  or  withholding  of  alcoholic 
beverages  is  an  important  point.  As  we  have  already  mentioned,  the  great 
majority  of  cases  of  chronic  catarrh  are  the  direct  result  of  excess  in  alcohol — 
the  most  important  factors  being  chemical  irritation  and  mechanical  distention 
of  the  mucous  membrane.  Moreover,  the  experiments  of  Fleischer  and  others 
have  shown  that  alcohol  prolongs  and  hinders  the  process  of  digestion.  In  every 
severe  case  it  is  better  to  forbid  alcoholic  beverages  entirely,  and  ordinarily  such 
an  injunction  is  much  better  obeyed  than  advice  to  use  them  sparingly.  In  mild 
cases  we  admit  that  small  portions  of  beer  and  wine  may  be  permitted  unhesi- 
tatingly, especially  if  the  patient  himself  experiences  no  feeling  of  discomfort 
from  them,  but  rather  an  improvement  in  his  appetite. 

In  determining  what  the  patient  may  be  allowed  to  eat,  we  are  to  consider,  as 
already  mentioned,  his  own  personal  experience  as  well  as  our  more  general 
knowledge.  An  intelligent  patient  will  often  be  himself  the  best  judge  of  what 
agrees  or  disagrees  with  him.  The  following  foods  are  very  easy  to  digest :  milk, 
soft-boiled  or  raw  eggs,  broths  (especially  veal  and  chicken  broths),  and  certain 
artificial  preparations,  chief  among  which  stand  the  Leube-Rosenthal  meat  solu- 
tion and  the  meat  juice  and  peptones  which  have  been  lately  put  upon  the 
market.  It  must  be  confessed  that  patients  soon  tire  of  these  last.  The  brain 
and  sweetbread  of  calves  are  easily  digestible;  also  birds,  such  as  pigeons,  chick- 
ens, and  partridges,  thin  shavings  of  raw  beef  or  raw  ham,  rice,  potato  puree,  etc. 
Gradually  we  may  proceed  to  somewhat  heartier  food — veal,  game,  roast  beef, 
trout,  and  light  farinaceous  dishes.  The  worse  the  symptoms  are  in  any  case, 
the  more  strict  must  we  be  in  regard  to  diet.  For  drink,  besides  water  or  Seltzer 
water,  very  weak  tea,  cocoa,  chocolate,  and  water  reddened  with  claret  are  allow- 
able.—Shall  we  permit  coffee  ?  This  is  often  a  question  of  great  interest  to  the 
patient:  it  must  be  answered  according  to  his  individual  experience.  Coarse 
bread  is  to  be  forbidden.  Ordinary  white  bread,  toasted,  if  it  seems  desirable, 
may  be  allowed  in  moderate  amount,  also  rusks. 

Solid  articles  of  diet  must  be  finely  cut  up  and  well  chewed  before  being 
swallowed.  The  food  mvist  not  be  very  hot  or  very  cold.  It  is  sometimes  advan- 
tageous to  take  more  than  three  meals  a  day,  each  one  being  proportionally 
smaller.  Other  patients  relish  their  food  better  if  the  intervals  between  eating 
are  prolonged.  It  should  be  added  that  excessive  smoking,  also,  is  harmful  in 
chronic  dyspepsia. 

There  are  other  special  indications  to  be  met.  In  all  severe  cases  by  far  the 
most  efficient  mode  of  treatment  consists  in  methodical  washing  out  of  the  stom- 
ach. This  is  especially  true  when  there  is  excessive  production  of  mucus,  or  a 
tendency  to  decomposition  of  food  in  the  stomach.  In  this  way  we  prevent  the 
accumulation  of  any  great  amount  of  undigested  food.  We  remove  the  excreted 
mucus  and  the  products  of  abnormal  fermentation  and  decomposition,  and  more- 
over, we  may  perhaps  exert  a  direct  and  favorable  influence  upon  the  mucous 
membrane.  In  such  cases,  we  ate  accustomed  to  rinse  out  the  stomach  daily,  and 
the  best  time  for  this  is  in  the  morning  before  the  patient  has  had  breakfast. 
Fresh  fluid  must  be  poured  in  and  emptied  out  rapidly,  until  the  stomach  is  freed 
from  all  foreign  material,  especially  mucus.  We  use  for  the  rinsing  fluid  a  weak 
solution  of  hydrochloric  acid  (one  to  two  per  mille),  or  a  one-per-cent.  solution  of 
either  common  salt  or  bicarbonate  of  soda ;  and,  if  there  is  much  mucus,  a  favor- 
ite remedy  is  very  dilute  lime-water,  two  to  four  tablespoonfuls  of  liquor  calcis  to 
a  litre  (quart)  of  water.  If  fermentation  is  going  on,  we  employ  weak  solutions 
of  hydrochloric,  boric,  or  salicylic  acids,  or  resorcine.  It  has  also  been  recom- 
mended to  spray  or  douche  the  mucous  membrane  of  the  stomach,  for  which  pur- 


CHEONIC    GASTKITIS  431 

pose  stomach-tubes  are  employed  with  niimerous  small  openings,  and  such  fluids 
are  chosen  as  weak  solutions  of  alum,  tannin,  and  condurango. 

If  we  now  turn  to  a  consideration  of  the  internal  remedies  used  in  chronic 
gastric  catarrh,  it  is  possible  to  decide  with  regard  to  their  employment  in  a  much 
more  intelligent  fashion  than  heretofore,  because  in  all  severer  cases  we  make  a 
more  accurate  investigation  of  the  digestive  process.  If  the  examination  of  the 
gastric  juice  shows  a  diminution  of  hydrochloric  acid,  this  may  be  artificially  sup- 
jjlied.  We  prescribe,  thirty  to  sixty  minutes  after  each  meal,  ten  to  fifteen  drops 
of  dilute  hydrochloric  acid  in  half  a  glass  of  water.  The  benefit  to  be  thus 
derived  must  not  be  overestimated.  In  appropriate  cases,  however,  its  influence 
is  favorable.  If  there  is  no  pepsine  in  the  gastric  juice  we  may  prescribe  pepsine 
as  well  as  hydrochloric  acid.  Pancreatine  and  papaine  are  also  recommended,  but 
their  usefulness  is  very  doubtful.  The  popular  wines  of  pepsine  are  not  to  be 
recommended,  because  of  the  alcohol  in  them. 

Alkalies  have  long  been  employed  as  well  as  hydrochloric  acid,  and  often  with 
good  results,  although  the  most  common  form  of  chronic  gastric  catarrh  has  a 
less  than  normal  secretion  of  hydrochloric  acid,  and  consequently  the  use  of 
alkalies  would  seem  to  be  contra-indicated;  yet  experience  shows  them  to  be 
useful.  Probably  their  beneficial  effect  is  that  they  neutralize  the  abnormal 
acids,  promote  the  emptying  of  the  stomach  into  the  duodenum,  dissolve  the 
mucus,  and  finally  stimulate  the  secretion  of  the  gastric  juice.  This  has  been 
experimentally  demonstrated  with  regard  to  carbonate  of  soda,  common  salt,  and 
carbonic  acid.  From  what  has  been  said  it  is  evident  that  in  chronic  gastric 
catarrh  alkalies  are  not  usually  given  during  digestion,  but  when  the  stomach  is 
empty  and  before  meals.  As  is  well  known,  the  alkalies  are  prescribed  more  espe- 
cially in  the  form  of  alkaline  mineral  waters,  which  the  patient  drinks  at  home, 
or  at  the  various  health-resorts.  The  springs  of  Carlsbad  possess  the  greatest 
reputation.  Those  at  Ems,  Kissingen,  Tarasp,  and  Vichy  also  deserve  to  be 
mentioned  as  health-resorts  for  patients  with  gastric  trouble.  A  good  portion 
of  the  benefit  at  these  places  is,  to  be  sure,  dependent  upon  the  fact  that  many 
patients  are  much  more  apt  to  follow  a  strict  regimen  when  they  make  use  of  a 
particular  "  cure  "  than  when  they  remain  at  home.  It  is  self-evident  that  large 
doses  of  bicarbonate  of  soda  are  indicated  in  that  form  of  chronic  gastritis  which 
is  associated  with  hypersecretion. 

If  the  character  of  the  vomitus,  or  gastric  contents  obtained  by  rinsing,  indi- 
cates abnormal  fermentation,  we  may  not  only  wash  out  the  stomach  (vide  supra), 
but  also  try  certain  antifermentative  remedies.  First  among  these  is  hydro- 
chloric acid  in  rather  large  doses,  and  we  also  give  salicylic  acid  (in  powders, 
containing  8  grains,  gramme  0.5) ;  creasote  (two  or  three  half-grain  pills  daily, 
gramme  0.03) ;  benzine  (20  drops  in  capsules  or  in  milk)  ;  and  similar  drugs.  As 
a  rule,  however,  the  last-named  remedies  are  seldom  employed. 

The  best  drugs  to  stimulate  the  secretion  of  gastric  juice  are  the  bitters.  It  is 
this  property  which  has  earned  them  the  name  of  stomachic  tonics.  Compound 
tincture  of  gentian,  tincture  of  nux  vomica,  tinctura  amara,  and  tinctura  calami, 
P.  G.,  quassia  and  columbo — these  are  much  employed.  In  general,  however, 
they  are  not  very  efficient.  An  excellent  tonic  in  many  of  these  cases  is  condu- 
rango  bark.  A  decoction  may  be  made  (15  parts  to  200  of  water)  ;  or  we  may 
employ  the  fluid  extract,  giving  a  teaspoonful  in  water  two  or  three  times  a  day. 

A  few  remedies  remain  to  be  mentioned,  which  are  said  to  exert  a  direct  bene- 
ficial influence  upon  the  catarrh,  and  which  many  physicians  extol  highly. 
Their  efficacy,  however,  is  somewhat  problematical.  We  refer  chiefly  to  subni- 
trate  of  bismuth,  sulphate  of  zinc,  and  nitrate  of  silver. 

Certain  symptoms  may  demand  especial  treatment,  such  as  vomiting.  It  will 
usually  yield  to  regular  and  persistent  washing  out  of  the  stomach.     Other  reme- 


432  DISEASES    OE   THE   DIGESTIVE    OEGAINtS 

dies  are  small  bits  of  ice,  and  minute  doses  of  opium  or  eliloral.     Potassic  bro- 
mide and  chloroform,  internally  administered,  may  also  be  tried. 

Violent  gastralgia  requires  narcotics,  such  as  morphine  and  opium.  The  best 
external  applications  are  poultices  or  wet  compresses.  "  Sour  stomach  "  may  be 
relieved  by  a  pinch  of  bicarbonate  of  soda,  or  of  calcined  magnesia.  Persistent 
anorexia  may  yield  to  the  bitters  mentioned  above,  or  to  sraall  doses  of  quinine 
or  compound  tincture  of  cinchona.  If  the  bad  taste  in  the  mouth  is  annoying, 
the  mouth  should  be  frequently  rinsed  out  with  Seltzer  water,  a  one-per-cent. 
solution  of  carbolic  acid,  or  five  drops  of  tincture  of  myrrh  to  a  glass  of  water. 
Eor  habitual  constipation,  enemata,  or  the  various  mineral  waters,  are  good; 
also  Carlsbad  salts.  In  obstinate  cases  pills  of  rhubarb  or  aloes  may  be  em- 
ployed. Still,  we  ought  never  to  forget  that  the  infrequency  of  the  stools  is  often 
merely  a  natural  consequence  of  the  scanty  diet,  and  that  it  is  therefore  possible 
to  do  harm  with  our  purgatives.  Iron  is  often  prescribed  for  the  concomitant 
ansemia ;  but  it  should  be  employed  cautiously,  for  it  is  often  ill  borne  in  gastric 
disease. 


CHAPTEE   IV 

PHLEGMONOUS    GASTRITIS 

{Furulent  Inflammation,  of  the  Stomach) 

Purulent  inflammation  of  the  stomach  is  very  rare,  and  little  is  yet  known 
about  it.  In  most  cases  no  special  caiises  for  it  have  been  ascertainable.  It  is 
occasionally  one  of  the  symptoms  of  grave  pyasmic  or  puerperal  inflammation. 
We  have  seen  one  case  in  which  suppuration  of  the  pharynx  led  to  an  acute 
phlegmonous  inflammation  of  the  submucous  coat  of  the  oesophagus,  also  involv- 
ing a  large  portion  of  the  stomach,  with  a  fatal  termination. 

Two  forms  are  distinguished — a  diffuse  and  a  limited  variety.  The  latter  is 
equivalent  to  gastric  abscess.  The  submucous  layer  is  almost  invariably  the 
chief  seat  of  suppuration.  Erom  this  starting-point  the  process  invades  the  mus- 
cular and  serous  coats  on  the  one  hand,  and  the  mucous  membrane  itself  on  the 
other — the  usual  result  being  multiple  sievelike  perforations  inward  or  outward. 

The  usual  symptoms  are  violent  gastric  derangement,  with  pain  and  vomiting, 
high  fever,  and  the  indications  of  constitutional  infection,  namely,  headache, 
delirium,  and  general  prostration.  Sometimes  the  disease  is  quickly  fatal,  some- 
times it  runs  a  more  chronic  course.  The  few  cases  in  which  recovery  has  been 
reported  are  somewhat  obscure. 

The  disease  can  never  be  diagnosticated  with  absolute  certainty.  Treatment 
must  be  purely  symptomatic.  Ice,  both  internally  and  externally,  and  the  nar- 
cotics, are  chiefly  employed. 


CHAPTER  V 


GASTRIC    ULCER 

{Simple  or  Round  Ulcer  of  the  Stomach) 

TEitiologJ. — Since  Cniveilhier  gave  the  first  accurate  description  of  gastric 
ulcer,  numerous  explanations  of  its  occurrence  have  been  propounded.  Even  yet 
there  is  no  universally  accepted  view.     "We  may,  in  general,  hold  to  the  assertion 


GASTKIC   ULCER  433 

tKat  the  development  of  an  ulcer  is  preceded  by  a  local  disturbance  of  nutrition, 
or  necrosis  of  the  gastric  mucous  membrane,  and  that  then  the  enfeebled  or 
necrotic  tissue  is  dissolved  by  the  gastric  juice — i.e.,  digested  ("peptic  ulcer"). 
But  it  is  not  known  what  are  the  special  causes  which  occasion  the  primary  dam- 
age to  the  tissue,  nor  why  the  loss  of  substance  when  it  occurs  is  not  at  once 
healed,  but  extends  in  width  and  depth.  There  is,  indeed,  no  lack  of  theories  to 
solve  these  questions,  and  pathologists  have  made  many  experiments  with  regard 
to  the  pathogenesis  of  gastric  ulcer. 

The  explanation  of  the  fact  that  the  normal  gastric  mucous  membrane  is  not 
attacked  by  gastric  juice  lies  probably  not  so  much  in  the  presence  of  the  alkaline 
blood  flowing  through  the  membrane  as  in  the  intrinsic  vital  resisting  powers  of 
the  normal  living  cells.  If  the  cells  are  in  any  way  damaged  there  occurs  at  once 
an  auto-digestion  at  that  spot.  Damage  of  this  sort  may  be  produced  experi- 
mentally in  different  ways;  for  example,  by  artificially  produced  embolism  of 
the  smaller  arteries  of  the  stomach,  and  by  wounds,  including  bruising,  burning, 
and  cauterization  of  limited  portions  of  the  mucous  membrane.  In  all  such  cases 
a  peptic  ulcer  is  formed,  but  almost  invariably  this  promptly  heals,  or,  at  any 
rate,  it  shows  no  tendency  at  all  to  extension.  If,  as  a  symptom  of  severe  gas- 
tritis or  portal  congestion,  there  are  small  haemorrhages  into  the  mucous  mem- 
brane, they  result  in  so-called  hsemorrhagic  erosions ;  but  these  again  are  limited 
to  the  small  spot  destroyed  by  the  haemorrhage. 

Virchow  assumed  that  ordinary  round  ulcer  of  the  stomach  in  man  is,  in  most 
cases,  the  result  of  the  plugging  of  the  small  vessels  with  a  thrombus  or  embolus, 
because  of  various  diseased  conditions  of  their  walls,  but  this  supposition  remains 
entirely  without  proof.  One  fact  that  tends  to  contradict  this  view  is  the  appear- 
ance of  ulcer  in  young  individuals  without  any  signs  of  cardiac  or  vascular  dis- 
ease. Other  investigators  thought  of  the  possibility  of  accidental  injuries,  and, 
perhaps  in  some  few  cases,  even,  of  external  trauma.  Such  suppositions  are  per- 
fectly possible,  although  they,  again,  in  most  cases  are  incapable  of  demonstra- 
tion. Then  we  have  still  to  meet  the  second  above-mentioned  question :  Why,  in 
all  such  cases,  the  little  erosions,  if  they  are  formed,  do  not  immediately  heal,  as 
the  experimentally  produced  ulcers  almost  invariably  do.  Lately  the  attempt  has 
been  made  to  settle  this  difficulty  by  pointing  out  that  in  ulcer  of  the  stomach 
the  acidity  of  the  gastric  juice  is  shown  to  be  abnormally  great.  This  hyper- 
acidity is  assinned  to  exist  even  before  the  development  of  the  ulcer,  and  in  a  cer- 
tain degree  to  cause  a  predisposition  for  its  development,  as  well  as  to  explain 
the  unwillingness  of  the  ulcer  to  heal  and  its  proneness  in  many  cases  to  extend 
farther,  to  spread.  If  a  gastric  ulcer  is  artificially  produced,  the  process  of  heal- 
ing may  be  considerably  delayed  by  introducing  solutions  of  hydrochloric  acid 
into  the  stomach.  It  is  very  possible  that  hyperacidity  of  the  gastric  juice  is  a 
factor  in  the  aetiology  of  ulcer,  but  the  whole  matter  is  by  no  means  easily  intel- 
ligible. We  remain  uncertain  as  to  what  is  the  primary  cause  of  the  ulcer,  and  it 
has  not  yet  been  proved  that  hypersecretion  and  hyperacidity  exist  before  the  for- 
mation of  the  ulcer.  We  might  also  believe  that  the  excessive  acidity  is  secondary 
to  the  sensory  irritation  occasioned  by  the  raw  spot.  In  a  word,  our  present 
knowledge  of  the  development  and  extension  of  gastric  ulcer  is  very  limited. 

Gastric  ulcer  occurs  but  seldom  in  childhood.  It  is  most  often  seen  between 
the  ages  of  eighteen  and  thirty.  The  cicatricial  stenosis  of  the  pylorus  and  other 
sequelae  are  often  seen  in  still  older  individuals,  between  thirty  and  forty-five 
years;  but  in  most  of  these  cases  the  disease  probably  originated  much  earlier. 
In  still  later  life  gastric  ulcer  is  rare.  In  general,  the  disease  seems  to  be  more 
frequent  in  the  female  sex  than  in  the  male ;  but  if  we  count  only  the  absolutely 
demonstrated  cases,  the  difference  is  not  a  very  great  one.  The  view  that  ulcer 
of  the  stomach  attacks  by  preference  anaemic  and  chlorotic  girls  is  very  general, 
28 


434  DISEASES    OF   THE   DIGESTIVE    ORGAlSrS 

but  to  the  author  seems  much  exaggerated.  The  probable  explanation  is  that 
gastric  disturbances  in  chlorotic  persons  are  often  ascribed  to  gastric  ulcer  with- 
out sufficient  reason.  Taking  into  consideration  only  the  absolutely  certain 
cases,  the  author's  experience  does  not  show  any  especially  close  connection 
between  chlorosis  and  gastric  ulcer.  Yet  it  must  of  course  be  confessed  that 
indubitable  cases  of  gastric  vlcer  occur  in  chlorotic  girls. 

Pathological  Anatomy. — The  ulcer  is  usually  approximately  round  or  oval. 
Its  borders  are  sharp ;  the  walls  often  slope  inward,  giving  the  ulcer  the  form  of  a 
shallow  funnel.  The  base  of  the  ulcer  is  almost  always  perfectly  clean,  so  that  in 
microscopic  sections  we  see  the  ends  of  the  gland  tubes  remaining  unchanged,  and 
reaching  out  into  the  surface  of  the  ulcer.  After  an  ulcer  has  lasted  some  time,  a 
reactive  inflammation  develops  around  the  necrotic  area,  leading  to  the  formation 
of  connective  tissue  and  cicatrization.  If  superficial,  it  does  not  extend  farther 
than  to  the  muscular  coat,  but  it  may  be  deep  enough  to  expose  the  serous  mem- 
brane, or  even  to  perforate  it  (vide  infra).  The  size  varies  greatly.  Some  are 
hardly  as  large  as  a  pea;  others  may  measure  ten  to  fifteen  centimetres  in  their 
greatest  diameter.  As  to  position,  most  of  them  are  found  near  the  pylorus.  They 
attack  the  posterior  wall  of  the  stomach,  particularly  the  neighborhood  of  the 
lesser  curvature,  far  more  frequently  than  the  anterior  wall,  but  the  greater 
curvature  is  not  infrequently  the  seat  of  an  ulcer.  As  a  rule,  we  find  but  a  single 
ulcer,  although  exceptions  to  this  statement  are  not  very  rare. 

If  an  ulcer  of  any  size  heals,  a  scar  is  formed,  with  radiating  lines  and  often  of 
considerable  size;  smaller  superficial  ulcers  heal  with  a  smooth  scar.  Cicatricial 
contraction  may  alter  the  shape  of  the  stomach  considerably.  If  a  deep  con- 
striction is  formed  around  the  middle  of  the  stomach,  we  have  what  is  called  the 
hour-glass  shape.  Scars  of  pyloric  ulcers  are  of  the  greatest  clinical  impor- 
tance, because  they  lead  to  cicatricial  stricture  of  the  pylorus,  with  resultant 
dilatation  of  the  stomach. 

If  the  gastric  ulcer  extends  to  the  serous  membrane,  the  final  result  may  be 
perforation  into  the  abdominal  cavity,  and  general  peritonitis,  unless  the  stom- 
ach previously  becomes  attached  at  the  point  threatened  to  some  neighboring 
organ,  because  of  adhesive  inflammation.  The  ulcers  being  usually  on  the  pos- 
terior wall  of  the  stomach,  it  is  oftenest  the  pancreas  to  which  the  stomach  be- 
comes adherent.  In  other  instances  it  is  the  liver,  transverse  colon,  diaphragm, 
or  spleen.  If  adhesions  are  formed  before  the  perforation  of  a  gastric  ulcer, 
there  may  be  circumscribed  peritoneal  abscesses.  These  are  situated  with  com- 
parative frequency  between  the  upper  surface  of  the  liver  and  the  diaphragm,  or 
between  the  stomach  and  the  diaphragm  (subphrenic  abscess).  Again,  after  such 
adhesions  there  may  be  perforation  into  the  pleural  cavity,  the  transverse  colon, 
the  pericardium,  or  the  lungs. 

The  ulcer  may  cause  erosion  of  a  blood-vessel,  and  thus  give  rise  to  one  of  the 
most  important  symptoms  of  the  disease,  namely,  gastric  hsemorrhage. 

Clinical  History. — There  may  be  absolutely  no  symptoms.  It  is  not  a  rare 
thing  to  find  at  autopsies  a  still  active  ulcer  of  the  stomach,  or  the  cicatrix  left  by 
one,  in  subjects  who  never  had  during  life  any  gastric  disturbances  whatever. 
"Nov  is  it  very  exceptional  for  a  person  suddenly  to  exhibit  grave  symptoms,  such  as 
gastric  hsemorrhage,  or  peritonitis  due  to  perforation,  when  there  has  been  no 
reason  previously  to  apprehend  the  existence  of  an  ulcer. 

In  other  instances  the  ulcer  does,  indeed,  give  rise  to  symptoms,  but  they  are 
not  sufficiently  characteristic  to  point  to  the  correct  diagnosis.  Usually  the  gas- 
tric symptoms  are  long  continued,  but  comparatively  slight.  They  consist,  for 
instance,  of  a  sense  of  oppression  or  slight  pain  in  the  epigastrium,  eructations, 
and  occasional  vomiting.  In  these  cases,  also,  grave  symptoms  consequent  upon 
the  ulceration  may  suddenly  arise. 


GASTRIC   ULCER  435 

In  a  third  class  of  cases  there  are  symptoms  which  are  to  a  certain  extent 
characteristic,  and  lead  with  more  or  less  definiteness  to  the  true  diagnosis. 
These  "  symptoms  of  ulcer  "  are  chiefly  a  peculiar  epigastric  pain,  which  is  usu- 
ally intermittent,  and  vomiting,  or,  what  is  yet  more  distinctive,  the  vomiting  of 
blood,  or  hsematemesis ;  also  the  signs  of  an  increased  secretion  of  hydrochloric 
acid  in  the  gastric  juice  (hyperchlorhydria  and  hypersecretion).  These  symp- 
toms and  their  diagnostic  value  we  must  now  consider  in  detail. 

Pain  in  the  stomach  is  one  of  the  most  frequent  symptoms  of  round  ulcer.  Its 
forms  are  very  diverse.  Often  the  patient  complains  only  of  a  diffuse,  painful 
sensation  of  pressure  referred  to  the  entire  region  of  the  stomach.  This  may  be 
uninterrupted,  or  it  may  occur  only  after  meals,  or  after  excessive  exertion,  or  as 
the  result  of  some  other  special  cause.  This  sort  of  pain  is  the  least  diagnostic  of 
any,  inasmuch  as  exactly  similar  sensations  may  be  caused  by  other  chronic  dis- 
orders of  the  stomach.  More  characteristic  of  ulcer  is  a  decided  cardialgia,  or, 
more  correctly,  gastralgia — that  is,  a  very  violent  pain,  coming  on  at  intervals 
like  neuralgia.  It  is  described  as  "  cutting,"  "  tearing,"  "  boring,"  and  the  like. 
These  attacks  of  pain  occur  at  various  times,  but  oftenest  after  eating,  and  par- 
ticularly after  the  ingestion  of  a  large  amount  of  food,  or  of  food  of  a  rather 
coarse  sort.  Often  they  occur  with  tolerable  regularity  a  definite  time  after 
eating,  say  half  an  hour  or  an  hour.  This  is  partly  to  be  explained  by  the  begin- 
ning of  the  expulsion  of  food  through  the  pylorus,  and  partly  by  the  acme  of  the 
secretion  of  acid  being  due  at  this  time.  The  pain  is  felt  chiefly  in  the  epigas- 
trium, but  not  infrequently  it  extends  toward  the  umbilicus,  backward  toward  the 
vertebrae,  into  the  thorax,  or  even  into  the  upper  extremities.  In  many  instances 
a  marked  sensation  of  thoracic  oppression  accompanies  it.  A  change  of  position 
may  sometimes  affect  the  severity  of  the  pain.  It  is  sometimes  observed  that 
the  patient,  when  lying  upon  his  right  side,  feels  violent  pain,  which  is  at  once 
relieved  by  changing  to  the  left  side,  probably  because  the  ulcer  is  located  near 
the  pylorus.  An  attack  of  cardialgia  may  last  for  a  few  minutes  or  for  several 
hours.  A  third  variety  of  pain  may  be  observed  in  gastric  ulcer.  The  suffering 
may  be  localized  in  a  very  limited  area.  Such  pain  is  thought  to  be  due  to  irrita- 
tion of  the  floor  of  the  ulcer  by  food,  or  to  its  edges  being  pulled  upon  during  the 
movements  of  the  organ.  It  generally  comes  on  after  eating,  and  ceases  if  the 
stomach  is  perfectly  quiet.  In  position,  this  pain  is  generally  epigastric,  but 
sometimes  it  is  umbilical,  or  even,  now  and  then,  more  toward  the  back.  In  many 
cases  of  gastric  ulcer  there  is  also  tenderness  on  pressure  in  a  quite  sharply  de- 
fined area  and  at  one  particular  spot.  Most  authors  regard  the  accurately  local- 
ized pain  as  the  most  nearly  pathognomonic ;  but  it  must  be  said  that  it  is  decid- 
edly the  least  frequently  exhibited  of  any.  Transitional  forms  and  combinations 
of  the  various  kinds  of  pain  are  often  observed.  Two  things  may  be  said  to  be 
characteristic  in  all  the  sorts  of  pain  connected  with  ulcer  of  the  stomach :  the 
localization  of  the  pain  each  time  in  the  same  spot;  and  the  relation  of  the  pain 
to  the  ingestion  of  food.  Complete  bodily  rest  is  beneficial;  external  pressure 
upon  the  epigastrium  usually  increases  the  pain. 

Vomiting  is  a  frequent  symptom  in  gastric  ulcer,  although  it  may  exception- 
ally be  absent  or  nearly  so.  Ordinarily,  vomiting  occurs,  like  the  cardialgic  at- 
tacks, after  eating,  and  particularly  after  partaking  of  indigestible  dishes.  The 
vomitus  in  such  cases  consists  mainly  of  partially  digested  food.  It  usually  has 
a  strongly  acid  reaction.  If  there  is  hypersecretion  there  may  sometimes  occur 
vomiting  of  a  strongly  acid  fluid,  not  containing  much  that  has  been  swallowed. 
If  the  ulcer  has  led  to  stenosis  of  the  pylorus,  the  way  in  which  the  vomiting 
occurs  is  very  characteristic.  We  shall  describe  this  form  of  vomiting  later,  in 
detail.  Vomiting  is  of  the  greatest  diagnostic  importance  when  blood  appears. 
This  may  be  intermixed  in  greater  or  less  amount  with  the  other  contents  of  the 


4:36  DISEASES    OE   THE   DIGESTIVE    OEGANS 

stomach,  or  it  may  be  vomited  as  pure  blood  (hsematemesis).  A  gastric  hsemor- 
rbage  demonstrated  by  the  vomiting  of  blood  is  the  most  valuable  diagnostic 
sign  of  gastric  ulcer.  If  there  is  no  hsemorrhage  at  all,  the  recognition  of  gastric 
ulcer  is  almost  always  rather  difficult  and  uncertain. 

Haematemesis  is  frequently  the  symptom  which  first  leads  the  patient  to  apply 
to  a  physician.  Up  to  this  time  he  may  have  felt  perfectly  well,  or,  although 
there  may  have  been  some  gastric  derangement,  he  has  not  thought  anything  of 
it.  The  patient  suddenly  becomes  faint,  perhaps  while  he  is  pursuing  his  regular 
occupation,  or  it  may  be  at  night.  He  feels  dizzy,  and  everything  looks  black. 
Then  he  has  nausea,  and  finally  is  obliged  to  vomit.  The  vomitus  is  either  pure 
blood,  or  a  mixture  of  blood  and  food.  It  is  partly  coagulated,  and  often  has 
a  rather  dark  or  blackish  color,  like  tar.  This  change  in  color,  as  well  as  the 
coagulation,  is  due  to  the  action  of  the  gastric  juice.  The  hsemoglobine  is  trans- 
formed by  the  action  of  the  hydrochloric  acid  into  hsematine.  If  the  blood,  before 
it  is  vomited,  has  remained  for  some  time  in  the  stomach,  the  vomitus  has  the 
appearance  of  "  coffee  grounds,"  and  no  longer  contains  unchanged  red  blood-cor- 
puscles (for  the  chemical  demonstration  of  blood,  vide  supra,  page  422).  The 
amount  varies  greatly  in  different  cases :  there  may  be  a  quart  or  more.  Some- 
times there  is  a  single  haemorrhage,  but  not  infrequently  blood  is  repeatedly  vom- 
ited either  at  short  intervals  or  on  successive  days.  Part  of  the  blood  escapes 
through  the  pylorus,  so  that,  after  a  profuse  gastric  haemorrhage,  blood  is  sure  to 
be  found  in  the  stools.  In  them  it  is  black  and  tarry.  Exceptionally  it  happens 
that  all  the  blood,  beyond  what  is  absorbed  from  the  intestinal  canal,  passes  off 
per  anum,  so  that  none  whatever  is  vomited.  In  such  cases  it  is  often  a  difficult 
matter  to  locate  the  haemorrhage.  If  there  is  a  sudden  f  aintness  with  pallor,  and 
without  vomiting,  but  followed  by  black  faecal  discharges,  we  should  always  think 
of  the  possibility  of  a  gastric  haemorrhage. 

The  consequences  of  gastric  haemorrhage  depend,  of  course,  chiefly  on  the 
amount  of  blood  lost.  Sometimes,  although  fortunately  rarely,  a  large  blood- 
vessel is  eroded  and  the  patient  dies.  This  event  may  be  sudden,  or  it  may  occur 
more  gradually  under  the  influence  of  repeated  haemorrhages  and  after  a  few 
days,  during  which  all  the  symptoms  of  acute  anaemia  are  exhibited.  On  the 
other  hand,  the  loss  of  blood  may  be  so  insignificant  as  to  produce  no  especial 
symptoms.  In  most  instances  life  is  not  actually  threatened,  but  yet  the  signs 
and  results  of  a  more  or  less  marked  general  anaemia  are  clearly  visible. 

In  such  cases  the  patient  feels  extremely  exhausted,  and  at  once  takes  to  his 
bed.  He  has  also  all  the  subjective  symptoms  of  cerebral  anaemia.  There  are 
vertigo,  tinnitus  aurium,  specks  before  the  eyes,  frequent  gaping,  and  sometimes 
headache.  To  assume  an  erect  posture  aggravates  the  disturbance.  There  is  usu- 
ally excessive  thirst.  Now  and  then  a  temporary  amaurosis  has  followed  an  ex- 
cessive haemorrhage. 

Objectively,  we  notice  at  once  the  excessive  pallor  of  the  skin,  particularly  of 
the  face.  The  lips  and  conjunctivte  are  also  blanched.  The  pulse  is  rapid,  and 
often  ill  sustained.  For  some  days  there  may  be  ansemic  murmurs  over  the  heart, 
and  there  is  a  distinct  sound  to  be  heard  in  the  femoral  arteries.  A  moderate  rise 
of  temperature  is  very  common,  probably  due  to  the  absorption  of  the  blood 
decomposing  in  the  intestines.  This  is  known  as  anaemic  fever.  The  urine 
is  pale,  and  usually  rather  abundant.  Its  specific  gravity  is  not  infrequently 
relatively  high,  namely,  1015  to  1020.  All  these  symptoms  are  directly  referable 
to  the  loss  of  blood,  and  they  will  be  discussed  with  greater  detail  in  the  section 
on  anaemia. 

If  the  haemorrhage  is  not  repeated,  the  patient  gradually  regains  his  strength. 
To  be  sure,  the  pallor  usually  persists  for  a  long  time,  but  the  disagreeable  symp- 
toms gradually  abate.     When  gastric  discomfort  has  existed  previously  to  the 


GASTRIC   ULCEE  437 

haemorrhage,  it  often  disappears  entirely  after  it — a  circumstance  which  is  prob- 
ably due  in  part  to  the  excessive  caution  of  the  patient  thereafter.  At  the  end  of 
a  few  weeks  the  patient  often  feels  perfectly  well  again ;  and,  indeed,  recovery  is 
not  infrequently  complete  and  permanent.  In  other  cases,  however,  the  symp- 
toms of  ulcer  return,  sooner  or  later. 

The  third  group  of  symptoms  in  ulcer  of  the  stomach  is  furnished  by  an  ex- 
amination of  the  gastric  contents,  with  the  aid  of  the  stomach-tube.  These  are 
of  extreme  importance.  Earlier,  when  the  soft  tube  now  universally  employed 
was  not  in  use,  we  feared  to  introduce  a  tube  into  the  stomach  in  case  of  ulcer, 
and  even  now  we  should  not  do  it,  in  case  of  h^matemesis,  if  it  can  be  avoided, 
until  some  weeks  have  elapsed;  but  with  this  exception  abundant  experience  has 
shown  that  we  do  not  need  to  be  at  all  timid  about  the  introduction  of  the  stom- 
ach-tube; and  particularly  if  there  is  doubt  about  diagnosis  we  should  never  fail 
to  avail  ourselves  of  it.  The  most  important  fact  which  the  investigations  of 
the  gastric  contents  in  patients  with  ulcer  has  taught  us  is  that  there  are  almost 
invariably  present  hyperacidity  and  hypersecretion  of  the  gastric  juice.  If  the 
stomach  is  examined  when  fasting,  we  shall  find  a  fluid  containing  a  large 
amount  of  hydrochloric  acid,  and  if  we  examine  it  an  hour  after  a  test  breakfast, 
we  shall  find  an  extreme  amount  of  acid  (vide  supra,  page  417).  This  fact  was 
discovered  by  Riegel,  and  we  have  found  it  true  in  all  uncomplicated  cases  of  ulcer 
of  the  stomach,  indeed  it  seems  to  be  so  much  the  rule  that  if  anacidity  were  found 
it  would  render  any  previous  suspicion  of  ulcer  extremely  improbable.  If,  how- 
ever, the  ulcer  has  led  to  stenosis  of  the  pylorus,  and  so  to  extreme  stagnation  of 
the  gastric  contents,  there  may  be  temporary  subacidity  or  anacidity  (vide 
infra).  Likewise — and  this  is  a  point  of  great  practical  importance — hydro- 
chloric acid  may  be  absent  if  a  gastric  carcinoma  has  developed  on  the  base  of  a 
former  gastric  ulcer  (vide  infra).  Lactic  acid  is  invariably  absent  when  there  is 
hyperacidity  from  hydrochloric  acid;  or,  at  most,  if  there  is  great  stagnation  of 
the  gastric  contents,  there  may  be  a  moderate  formation  of  lactic  acid.  It  is  also 
very  important  in  cases  in  which  there  is  no  vomiting  at  all,  to  examine  the  gastric 
contents  obtained  by  rinsing  out  the  stomach,  with  regard  to  the  possible  pres- 
ence of  blood.  Small  admixtures  of  blood  in  association  with  hyperacidity  are 
strong  evidence  of  gastric  ulcer. 

The  motor  efiiciency  of  the  stomach  in  ulcer  is  at  first  normal  or  even  some- 
what exaggerated,  because  the  digestion  of  albumen  is  very  energetic  owing  to 
the  excess  of  hydrochloric  acid  in  the  stomach.  But  if  the  ulcer  is  located  in  the 
pyloric  region  and  leads  to  a  cicatricial  stenosis,  the  emptying  of  the  stomach 
is  delayed  and  a  greater  or  less  amount  of  food  will  be  found  seven  or  eight  hours 
after  the  test  meal.  We  shall  later  describe  the  symptoms  of  well-marked  ob- 
struction of  the  pylorus.  If  there  is  suspicion  of  an  ulcer,  the  stomach  is  usually 
not  inflated  at  all,  or  if  so  only  by  means  of  the  condom  (see  page  421).  If,  how- 
ever, there  is  a  cicatricial  stenosis  of  the  pylorus,  or  an  hour-glass  contraction  of 
the  stomach,  our  best  means  of  determining  the  form  and  size  of  the  organ  are  by 
the  introduction  of  air. 

There  are  no  other  symptoms  in  gastric  ulcer  so  important  as  those  already 
described.  The  appetite  in  many  cases  is  well  maintained,  and  if  the  patient 
takes  little  food  it  is  only  because  he  dreads  the  ensuing  pain.  Eructations 
may  be  absent  or  there  may  be  sour  eructations  and  heartburn,  symptoms  refer- 
able to  the  existence  of  hypersecretion  and  hyperacidity.  The  tongue  is  seldom 
coated,  being  usually  smooth  and  red ;  the  bowels  are  apt  to  be  somewhat  consti- 
pated ;  the  urine  is  often  very  faintly  acid,  so  that  there  is  a  tendency  to  a  deposit 
of  phosphates. 

The  general  nutrition  of  the  patient  often  remains  good,  but  there  may  be 
marked  emaciation  if  there  is  a  long-continued  diininution  in  the  amount  of  food 


438  DISEASES    OF'  THE   DIGESTIVE    0EGA:NS 

taken,  or  if  there  is  obstinate  vomiting.  Sometimes,  but  by  no  means  invariably, 
the  patients  display  great  anaemia.  This  may  precede  the  nicer  (vide  supra, 
aetiology),  or  it  may  develop  in  association  with  the  symptoms  of  ulcer,  and  even 
without  any  severe  haemorrhage  to  explain  it ;  but  that  after  severe  hsematemesis 
there  should  be  a  severe  anaemia  is  a  matter  of  course,  and  has  already  been 
alluded  to. 

An  event  which  has  been  already  mentioned  under  pathology — namely,  perfo- 
ration due  to  the  ulcer — is  of  great  clinical  importance.  It  would  be  impossible  to 
particularize  here  all  the  possibilities  incident  to  it.  We  shall  confine  ourselves 
to  the  two  most  important  because  most  frequent  varieties  of  perforation:  (1) 
into  the  peritoneal  cavity,  causing  peritonitis,  and  (2)  into  the  left  pleura,  or 
left  lung. 

Perforation  into  the  peritoneal  cavity  leads  almost  invariably  to  a  quickly 
fatal  peritonitis.  When  the  ulcer  has  previously  caused  few  symptoms,  if  any, 
the  excruciating  abdominal  pain,  tympanites,  vomiting,  collapse,  and  sudden 
death  of  peritonitis  may  abruptly  supervene  upon  a  state  of  apparently  perfect 
health.  In  other  cases  in  which  there  has  been  a  previous  formation  of  adhe- 
sions, we  have  an  encapsulated  abscess,  either  subphrenic,  between  the  stomach 
and  the  diaphragm,  or  elsewhere  in  the  abdomen.  The  subphrenic  abscess  may 
contain  air  as  well  as  pus,  and  is  then  termed  pyo-pneumothorax  subphrenicus. 
In  making  a  diagnosis  of  any  subphrenic  abscess,  we  should  consider  the  direct 
and  constitutional  symptoms,  and  also  the  thoracic  signs,  for  the  respiration  and 
the  inspiratory  expansion  of  the  lungs  should  be  normal.  If  there  is  perforation 
outward  or  into  a  coil  of  intestine,  recovery  may  result.  More  often,  however,  the 
termination  is  fatal,  unless  surgical  intervention  is  successful. 

Perforation  into  the  left  pleural  cavity  we  have  observed  repeatedly.  It 
causes  a  purulent  or  septic  pleurisy  on  that  side,  and  pulmonary  gangrene  may 
develop  at  the  same  time  or  later,  as  a  result  of  perforation  into  the  lung.  When- 
ever we  meet  a  case  of  apparently  spontaneous,  left-sided  empyema,  we  should 
at  any  rate  always  think  of  the  possibility  of  gastric  ulcer. 

In  many  cases  of  ulcer  w6  observe  signs  of  threatening  perforation — that  is, 
localized  pain  due  to  peritonitis,  vomiting,  and  similar  symptoms,  and  yet  the 
case  finally  clears  up.  Probably  in  most  such  instances  there  is  a  limited  peri- 
tonitis resulting  in  adhesions. 

The  general  course  of  round  ulcer  of  the  stomach  varies  greatly,  as  we  can  see, 
in  different  cases.  Complete  recovery  is  by  no  means  rare.  In  other  cases  the 
symptoms  persist  for  years  with  varying  intensity.  We  have  already  spoken  of 
the  haemorrhage  and  perforation  which  may  suddenly  intervene,  and  of  their 
significance.  Eelapses  are  not  infrequent,  even  after  apparent  recovery.  If  the 
ulcer  cicatrizes,  the  scar  itself  may  give  rise  to  persistent  disturbances :  there  may 
be  obstinate  cardialgia,  or,  if  the  scar  is  at  the  pylorus,  dilatation  of  the  stomach 
(vide  infra)  may  gradually  be  developed.  This  extremely  important  sequel  of 
gastric  ulcer  deserves  special  consideration. 

The  cicatrization  and  contraction  of  a  gastric  u^lcer  which  result  in  stenosis 
of  the  pylorus  may  be  complete,  but  it  is  by  no  means  exceptional  for  the  ulcera- 
tive process  to  persist  in  other  places  while  there  is  a  scar  at  the  pylorus,  so  that 
we  may  have  the  symptoms  of  stenosis  combined  with  all  the  other  symptoms 
of  ulcer,  such  as  pain,  hyperacidity,  haemorrhage,  and  perforation.  When  there 
is  an  obstruction  of  the  pyloric  orifice  as  a  result  of  interstitial  thickening  and 
sear  formation  at  that  place,  a  group  of  extremely  characteristic  symptoms  is 
superimposed  upon  the  ordinary  symptoms  of  ulcer.  Perhaps  one  cause  of  the 
change  in  the  pylorus  is  the  destruction  of  the  muscular  coat  at  that  point. 

The  first  and  most  important  result  of  pyloric  stenosis  is  prolonged  retention 
of  the  gastric  contents.     So  long  as  the  muscular  coat  of  the  stomach  is  able  by 


GASTRIC   ULCER  439 

increased  effort  to  overcome  the  increased  resistance,  there  is  no  disturbance  to 
be  noticed.  It  is  proper  to  speak  of  a  compensated  pyloric  stenosis,  just  as  we 
speak  of  a  compensated  valvular  disease  of  the  heart ;  but  if  the  stenosis  becomes 
greater,  so  that  even  the  hypertrophied  muscular  coat  ceases  to  be  able  to  dis- 
charge the  chyme  into  the  intestine,  there  is  a  gradually  increasing  collection  of 
food  in  the  stomach,  and  the  only  way  for  the  organ  to  relieve  itself  is  by  vomit- 
ing. The  vomiting,  in  case  of  pyloric  stenosis,  is  somewhat  characteristic.  It 
occurs  from  time  to  time,  perhaps  at  intervals  of  two  or  three  days,  and  is  very 
profuse.  Then,  the  stomach  being  partially  emptied,  new  collections  may  form 
until  their  large  amount  leads  to  vomiting  again.  The  vomitus  in  cases  of 
stenosis  due  to  ulcer  is  usually  very  acid  and  contains  much  free  hydrochloric 
acid,  and  sometimes  blood.  The  stomach  itself  becomes  gradually  and  increas- 
ingly dilated,  because  of  the  stagnation  of  its  contents.  Usually  this  secondary 
dilatation  of  the  stomach  may  be  recognized  by  mere  external  examination.  We 
can  feel  the  stomach  as  a  great  limp,  flabby  bag ;  and  from  time  to  time  we  can  see 
its  walls  bulge  out  from  muscular  contraction.  We  can  often  distinctly  recog- 
nize the  peristaltic  waves  passing  from  the  fundus  to  the  pylorus.  In  the  region 
of  the  pylorus  we  may  sometimes,  though  by  no  means  invariably,  make  out  a 
distinct  resistance  on  palpation,  suggesting  a  tumor  and  corresponding  to  the 
thickening  of  the  gastric  walls  from  scar  formation.  In  such  cases  it  is  often 
especially  difiicult  to  distinguish  between  the  scar  of  an  ulcer  and  a  carcinoma. 
Even  if  we  can  feel  no  tumor,  visible  contractions  of  the  stomach  with  distinct 
peristalsis  are  almost  invariably  pathognomonic  of  pyloric  stenosis.  In  such 
cases  there  is  usually  a  cramplike,  painful  sensation,  associated  with  every  marked 
contraction  of  the  muscular  coat.  During  these  contractions  of  the  stomach 
its  contour  is  often  so  evident  that  we  can  obtain  a  perfectly  distinct  idea 
of  its  size,  extent  (often  reaching  below  the  navel),  and  position.  But  we  must 
especially  emphasize  the  fact  that  the  size  of  the  stomach,  its  dilatation,  is  not 
the  essential  point.  The  main  thing  is  the  stenosis  of  the  pylorus,  and,  above  all, 
the  degree  of  consequent  motor  inefficiency.  With  regard  to  the  latter,  we  can 
reach  no  complete  conclusions  without  using  the  stomach-tube.  With  its  aid 
M^e  can  determine  the  amount  the  stomach  contains,  and  recover  ingesta,  such  as 
cranberries  and  green-colored  vegetables,  which  have  been  eaten  many  days  before. 
If  we  empty  the  stomach  completely  and  give  a  test  meal,  we  can  gauge  more 
accurately  the  degree  of  motor  insufficiency.  We  may  also  determine  precisely 
the  position,  form,  and  size  of  the  stomach  when  emptied,  by  means  of  inflation. 
In  exceptional  cases  there  is  a  large  amount  of  bile  mingled  with  the  gastric 
contents.  The  author  surmises  that  in  such  cases  the  cicatricial  process  has 
changed  the  pylorus  into  a  rigid,  though  narrow,  tube,  which  can  neither  be 
opened  nor  closed.  Thus  we  have  an  "  insufficiency  "  associated  with  the  steno- 
sis of  the  pylorus,  so  that  no  obstacle  is  opposed  to  the  entrance  of  bile  into  the 
stomach. 

When  there  is  a  well-marked  uncompensated  stenosis  of  the  pylorus,  there  is 
always  a  decided  impairment  of  the  general  health.  Nutrition  grows  more  and 
more  imperfect  because  of  the  persistent  vomiting,  and  there  may  be  extreme 
emaciation.  Still,  many  patients  with  stenosis  due  to  ulcer  may  maintain  a 
tolerable  condition  of  health  for  many  years,  if  they  take  proper  care  of  them- 
selves by  regular  washing  of  the  stomach  and  by  eating  proper  food  (vide  infra) ; 
but  finally,  even  in  such  individuals,  the  symptoms  grow  worse,  or  a  new  trouble 
develops,  one  of  which  there  is  always  danger  in  any  case  of  stenosis  due  to  ulcer. 
We  refer  to  the  secondary  development  of  carcinoma  at  the  seat  of  the  former 
ulcer.  This  happens  not  infrequently,  and  is  to  be  considered  at  length  in  the 
next  chapter.  There  remain  to  be  mentioned  some  special  symptoms,  associated 
with  ulcers  of  the  pylorus  when  they  lead  to  stenosis.     There  is  usually  a  de- 


440  DISEASES    OF   THE   DIGESTIVE    OEGANS 

cided  tendency  to  constipation ;  the  urine  is  faintly  acid  and  often  lias  an  abun- 
dant deposit  of  phosphates ;  the  pulse  is  often  remarkably  infrequent ;  and  final- 
ly, there  are  sometimes  attacks  of  tetany. 

Diagnosis. — The  diagnosis  can  be  made  only  when  the  above-mentioned  char- 
acteristic symptoms  are  present.  Of  these,  hsematemesis  is  by  far  the  most  sig- 
nificant, for  it  is  with  very  few  exceptions  the  result  of  gastric  ulcer.  Particu- 
larly is  this  true  of  individuals  under  middle  age. — But  how  shall  we  determine 
whether  the  blood  ejected  did  not  come  from  the  nose  or  the  lungs,  rather  than 
the  stomach?  The  answer  is  not  ahvays  easy.  If  an  epistasis  occurs  at  night, 
a  part  of  the  blood  often  flows  back  into  the  naso-pharynx,  and,  being  swallowed, 
excites  vomiting,  so  that  a  gastric  haemorrhage  is  suggested. 

In  doubtful  cases  we  must,  therefore,  make  an  accurate  examination  of  the 
nose.  It  is  also  very  important  for  the  physician  to  remember  that  blood  may 
be  "  vomited  "  in  hysterical  cases.  If  there  is  also  nervous  cardialgia,  one  might 
easily  be  misled  to  assume  the  existence  of  a  gastric  ulcer.  Usxially,  however,  we 
can  make  sure  of  the  diagnosis  by  means  of  the  other  symptoms  of  hysteria  (see 
the  chapter  on  hysteria),  and  by  examining  the  "vomited"  blood.  The  latter 
does  not  come  from  the  stomach  at  all,  but  from  the  gums,  the  pharynx,  or  the 
naso-pharynx,  and  consequently  it  is  almost  always  comparatively  bright  red, 
rather  fluid,  and  mixed  with  mucus  and  saliva ;  and  on  microscopic  examination 
it  shows  pavement  epithelium  and  micro-organisms  from  the  mouth. 

The  diagnosis  between  gastric  and  pulmonary  haemorrhage  in  doubtful  cases 
depends  on  the  following  factors :  1.  The  previous  condition  of  the  patient — 
whether  he  has  had  cough,  expectoration,  and  other  pulmonary  symptoms,  or,  on 
the  other  hand,  gastric  pain  and  vomiting.  2.  On  the  character  of  the  haemor- 
rhage, whether  accompanied  by  vomiting  or  by  cough.  But  there  may  have  been 
both.  Violent  vomiting  may  excite  a  coLigh;  and,  on  the  other  hand,  blood 
which  has  been  coughed  up  may  be  in  part  swallowed  and  induce  vomiting.  3. 
On  the  character  of  the  blood:  if  from  the  lungs,  it  is  usually  bright-red  and 
frothy,  containing  bubbles  of  air,  with  few  clots,  and  of  alkaline  reaction.  In 
gastric  haemorrhage  it  is  usually  dark,  mixed  with  food,  partly  clotted,  and  acid 
in  reaction  from  admixture  with  the  gastric  juice.  4.  On  the  results  of  physical 
examination.  In  this,  of  course,  we  must  be  extremely  cautious  after  a  haemor- 
rhage, lest  the  movements  of  the  patient  excite  fresh  bleeding;  and  yet  we  may 
be  able  to  perceive  from  the  general  condition  of  the  patient,  or  from  dullness  at 
the  apices,  or  moist  rales,  that  pulmonary  disease  is  probable.  If  the  blood  came 
from  the  stomach,  we  usually  detect  nothing  but  the  signs  of  anasmia.  6.  The 
subsequent  symptoms.  In  cases  of  pulmonary  haemorrhage  there  is  almost  sure 
to  be  an  expectoration,  for  the  next  few  days,  either  of  pure  blood  or  of  matter 
stained  with  blood;  and,  in  gastric  haemorrhage,  the  next  dejection  will  almost 
certainly  be  black,  from  the  presence  of  decomposed  blood.  In  doubtful  cases, 
the  appearance  of  blood  in  the  stools  almost  invariably  settles  the  question  in 
favor  of  gastric  haemorrhage.  The  best  way  of  testing  for  blood  in  the  fteces  is 
by  means  of  guaiac  and  turpentine  (vide  supra). 

If  no  gastric  haemorrhage  has  ever  occurred  in  the  course  of  the  disease,  vio- 
lent and  persistent  gastralgia  of  the  peculiar  character  above  described  is  that 
symptom  which  would  first  arouse  suspicion  of  an  ulcer,  particularly  if  the  pain 
is  from  time  to  time  associated  with  vomiting.  If  hyperacidity  or  hypersecretion 
has  been  demonstrated,  this  condition  in  association  with  other  symptoms  may 
greatly  strengthen  the  diagnosis.  Severe  gastric  pain,  combined  with  hyper- 
secretion, makes  the  diagnosis  of  gastric  ulcer  very  probable.  To  make  an  abso- 
lutely certain  distinction  between  ulcer  and  nervous  hj-perseeretion  (q.  v.)  is 
impossible,  if  there  is  no  haematemesis.  In  general,  we  must  remember  that  it 
is  often  possible  to  observe  more  or  less  distinct  "  symptoms  of  ulcer,"  without 


GASTEIC   ULCER  Ul 

being  absolutely  certain  that  an  ulcer  exists.  Often  we  are  obliged  to  await  the 
further  course  of  the  disease,  and  particularly  the  results  of  treatment,  in  order 
to  settle  our  doubts. 

The  two  diseases  which  it  is  most  difficult  to  distinguish  from  ulcer  are  nerv- 
ous dyspepsia  with  nervous  gastralgia,  and  carcinoma.  When  we  consider  these 
diseases  we  shall  discuss  at  greater  length  the  differential  diagnosis  between  them 
and  ulcer  of  the  stomach.  Chlorotic  patients,  also,  often  have  gastric  symptoms 
(see  the  chapter  on  chlorosis)  which  excite  suspicion  of  an  ulcer,  especially  as 
hypersecretion  of  the  gastric  juice  is  often  associated  with  chlorosis.  Frequently 
it  is  impossible  to  make  an  absolute  diagnosis  in  these  cases,  but  the  results  of 
treatment  may  be  decisive.  Preparations  of  iron,  particularly  Blaud's  pills,  are 
ill  borne  in  ulcer,  while  in  case  of  genuine  chlorosis  they  usually  cause  rapid  im- 
provement in  the  gastric  symptoms,  as  well  as  in  the  general  condition. 

Prognosis. — The  chief  dangers  in  ulcer  of  the  stomach,  hsemorrh^ge  and  per- 
foration, have  already  been  spoken  of.  Whether  these  complications  will  actually 
occur  in  any  individual  case,  and  when,  we  can  not  determine. 

There  can  be  no  doubt  that  a  large  number  of  ulcers  heal  perfectly ;  but,  as  we 
have  already  said,  even  the  resulting  scar  may  cause  trouble.  We  must  remem- 
ber the  possibility  of  persistent  gastric  disturbance,  particularly  cardialgia,  and 
also  the  development  of  a  cicatricial  stenosis  with  its  consequences.  Finally,  we 
have  the  danger,  already  mentioned,  of  the  eventual  development  of  carcinoma 
in  the  scar  of  an  old  ulcer. 

Treatment. — If  the  diagnosis  of  gastric  ulcer  is  evident,  or  if  the  symptoms 
are  of  such  a  nature  that  there  is  a  justifiable  suspicion  of  an  ulcer,  the  patient 
should  be  urgently  advised  to  submit  himself  to  careful  and  methodical  treat- 
ment ;  for  it  is  only  by  means  of  a  sufficiently  persistent  and  properly  conducted 
treatment  that  we  can  hope  for  good  therapeutic  results  in  ulcer  of  the  stomach. 

One  essential  condition  is,  that  the  patient  should  keep  his  bed  for  the  first 
part  of  the  treatment,  at  least  for  three  or  four  weeks.  Complete  bodily  rest  is 
certainly  important  in  promoting  healing  of  the  ulcer.  The  patient  should  also 
have  moist  compresses,  or,  still  better,  as  Leube  has  advised,  warm  poultices 
applied  all  day  long  to  the  epigastrium.  These  applications  are  very  good  for 
the  pain,  and  they  also  have  a  certain  psychological  importance,  for  they  reconcile 
the  patient  to  keeping  quiet  in  bed.  Thirdly,  and  this  is  probably  the  most  impor- 
tant point,  the  patient  must  keep  strictly  to  a  prescribed  diet.  This  diet  we 
are  about  to  describe  at  length.  The  main  consideration  in  determining  the  pa- 
tient's diet  is  that  all  mechanical  and  chemical  irritation  of  the  floor  of  the 
ulcer  must  be  avoided.  Fourthly,  we  should  have  regard  to  the  almost  in- 
variable existence  of  hyperacidity  of  the  gastric  juice.  We,  therefore,  give  to 
patients  alkaline  carbonates,  either  in  the  form  of  Carlsbad  water  (on  waking 
a  large  glassful  of  the  Miihlbrunnen  warmed  to  about  98.6°  F.,  37°  C. ;  then,  in 
the  forenoon,  between  ten  and  eleven,  as  much  more),  or,  what  we  consider  in 
many  ways  still  better,  bicarbonate  of  soda  (either  alone  or  combined  with  sub- 
nitrate  of  bismuth).  Of  the  soda  we  should  give  as  much  as  is  held  upon  the 
point  of  a  knife,  every  hour,  so  as  to  keep  the  gastric  juice  constantly  neutralized. 
With  regard  to  the  dietetic  treatment  of  gastric  ulcer,  the  best  way  is  to  follow 
Leube's  example,  and  have  four  diet  lists.  Beginning  with  the  first,  we  gradually 
go  on  at  definite  intervals  of  time  to  the  second,  third,  and  fourth.  For  the 
first  ten  days  of  treatment  the  patient  follows  the  first  diet  list.  This  contains 
boiled  milk;  broth;  unsweetened  rusks,  softened  by  soaking;  to  this  we  may  add 
the  artificial  solutions  of  meat,  particularly  that  of  Leube-Rosenthal.  Then, 
during  the  next  week,  we  have  the  second  diet  list,  comprising  gruel,  soft-boiled 
rice  and  oatmeal,  eggs,  boiled  calf's  brain  and  sweetbread,  boiled  pigeon  and 
chicken.    From  the  eighteenth  to  the  twenty-fourth  day  of  treatment  we  have,  in 


442  DISEASES    OF   THE   DIGESTIVE    OEGANS 

addition,  the  third  diet,  with  shavings  of  raw  beef  and  beefsteak,  potato  puree, 
boiled  calf's  feet,  and  for  beverage  some  tea  or  weak  coffee.  From  the  twenty- 
fourth  to  the  thirtieth  day  the  patient  has  the  fourth  diet  list — that  is,  broiled 
fowl  or  pigeon,  partridge,  venison,  roast  beef,  tenderloin,  finely  chopped  maca- 
roni, and  bread.  It  is  understood  that  with  each  advance  in  diet  the  previous 
diet  lists  are  also  permitted.  In  general,  the  patient  has  about  five  meals  a 
day,  the  amount  of  each  being  determined  by  the  appetite  and  symptoms  of  the 
patient.  If  everything  goes  favorably,  the  gastric  pain  will  wholly  cease  after 
a  few  days  of  this  diet,  under  the  other  regulations  above  enumerated.  The  pa- 
tient then  proceeds  toward  recovery  without  any  discomfort,  except  possibly 
hunger.  If  the  transition  to  a  more  advanced  diet  causes  pain,  we  must  resort 
for  a  few  days  to  the  simpler  foods.  In  general,  the  above  suggestions  must  be 
regarded  as  an  outline  from  which  certain  variations  may  be  made  to  suit  the 
individual  case,  yet  we  may  be  well  assured  that  the  results  are  better  and  more 
certain  the  more  strict  and  methodical  the  treatment  is.  If  the  patient  has  borne 
the  articles  of  the  fourth  diet  list  for  about  a  week  without  any  discomfort  he  may 
go  on  by  slow  degrees  to  other  simple  dishes,  such  as  veal,  pike,  trout,  porridge, 
vegetables,  and  other  similar  articles,  and  so  to  an  ordinary  diet.  Of  course,  cau- 
tion in  eating  and  drinking  is  necessary  for  a  long  time. 

With  the  mode  of  treatment  just  described,  we  shall  in  most  cases  accomplish 
as  much  as  possible;  but  if,  despite  this  regimen,  the  symptoms  do  not  cease, 
there  are  two  other  remedies  which  deserve  to  be  tried — viz.,  subnitrate  of  bis- 
muth and  nitrate  of  silver.  These  are  specially  employed,  also,  in  treating  poor 
persons  whose  circumstances  often  render  it  impossible  to  carry  out  strict  dietary 
rules.  The  subnitrate  of  bismuth  is  almost  always  given  in  combination  with 
bicarbonate  of  soda :  of  a  mixture  containing  3  to  5  parts  of  bismuth  and  30 
parts  of  soda  we  give  several  times  a  day  a  generous  "  knife-point  full "  before 
meals.  In  severe  and  obstinate  cases  of  ulcer,  we  can  from  our  own  experience 
recommend  also  "injections"  of  bismuth  (Eleiner).  The  patient's  stomach  is 
washed  out  in  the  morning  before  breakfast,  and  then  5  iv-v  (grm.  15-20)  of 
the  subnitrate  of  bismuth  suspended  in  a  glass  of  warm  water  is  poured  slowly 
into  the  stomach-tube;  the  patient  should  at  the  same  time  lie  on  his  right  side, 
and  so  remain  for  at  least  half  an  hour.  The  heavy  bismuth  powder  is  expected 
to  deposit  itself  upon  the  surface  of  the  ulcer  (which  is  probably  in  the  pyloric 
portion  of  the  stomach),  and  th^^s  in  a  mechanical  way  protect  it  from  irritation 
and  promote  its  healing.  The  symptomatic  results  of  this  method  are  sometimes 
excellent.  Often,  also,  favorable  results  are  obtained  from  nitrate  of  silver.  This 
may  be  partly  explained  by  its  neutralization  of  the  hydrochloric  acid,  and  the 
formation  of  chloride  of  silver.  The  drug  is  prescribed  in  a  solution  of  six  grains 
to  four  ounces  of  water  (gram.  0.3-120),  to  be  kept  in  opaque  glass,  and  of  this  a 
teaspoonful  should  be  given  three  or  four  times  a  day  before  meals. 

Sometimes  the  violent  pain  does  not  abate  under  the  ordinary  treatment,  and 
demands  symptomatic  remedies.  Of  course,  morphine  is  the  most  efficient,  given 
internally  or  subcutaneously.  Chloroform  may  also  be  tried:  we  give  a  table- 
spoonful  of  a  mixture  containing  1  part  to  120  of  water.  Gerhardt  recommends 
for  the  gastric  pain  3  or  4  drops  of  the  solution  of  perchloride  of  iron  in  a  wine- 
glass of  water. 

Excessive  vomiting  and  persistent  nausea  are  likewise  to  be  combated  by  the 
narcotics.  Opium  is  the  best;  morphine,  cocaine,  chloral,  and  bromide  of  potas- 
sium may  also  be  tried.  At  the  first  appearance  of  blood  in  the  vomitus  the  great- 
est bodily  quiet  and  most  careful  dieting  is  absolutely  indispensable.  For  the  first 
day  or  two  it  is  best  to  allow  nothing  except  ice-cold  milk  and  bits  of  ice  in  the 
mouth  to  appease  the  burning  thirst.  In  severe  cases  we  may  try  giving  water 
and  milk  by  the  rectum,  so  as  to  afford  the  stomach  complete  rest.     The  patient 


GASTRIC   ULCEE  443 

must  lie  as  quietly  as  he  can.  A  flat  ice-bag,  not  too  heavy,  should  be  placed  on 
the  epigastrium.  In  case  of  persistent  nausea  or  eructations,  small  doses  of 
opium  or  morphine  are  to  be  prescribed.  If  the  heemorrhage  is  obstinate  we  may 
try  the  subcutaneous  injection  of  ergotine,  or,  by  mouth,  acetate  of  lead  or  chlo- 
ride of  iron.  •  We  must  wait  four  or  five  days  after  a  haemorrhage  before  Tve  can 
give  a  little  more  food  by  the  mouth,  and  this  must  be  allowed  cautiously  and  in  a 
liquid  form. 

If  peritonitis  appears  as  the  result  of  perforation,  the  best  means  to  try  are 
the  outward  application  of  ice  to  the  epigastrium  and  the  internal  use  of  opiuna 
in  large  amounts — that  is,  half  a  grain  to  a  grain  (grm.  0.03-0.05)  every  two  or 
three  hours,  or  twenty  to  thirty  drops  of  laudanum.  Unfortunately,  however, 
the  cases  are  exceptional  in  which  the  peritonitis  does  not  become  general.  The 
only  remaining  hope  lies  in  surgical  interference,  although  the  results  even  of 
laparotomy  are  dubious. 

If  the  symiJtoms  of  pyloric  stenosis  are  growing  more  and  more  distinct — 
that  is,  if  the  hypertrophied  muscular  coat  of  the  stomach  is  no  longer  vigorous 
enough  to  prevent  the  stagnation  of  food,  with  consequent  dilatation  of  the  stom- 
ach and  vomiting,  we  can  perhaps  restore  the  patient  to  a  comfortable  condi- 
tion by  means  of  regular  washing  out  of  the  stomach,  combined  with  a  suitable 
diet.  This  irrigation  prevents  any  great  and  burdensome  accumulation  of  food 
in  the  stomach.  Moreover,  it  rids  the  patient,  for  a  time  at  least,  of  the  large 
amount  of  strongly  acid  gastric  juice  which  is  usually  present.  These  beneficial 
and  agreeable  effects  are  soon  so  noticeable  that  often  the  patient  learns  to  rinse 
out  his  stomach  himself,  or  even,  by  bending  over  and  pressing,  to  empty  out  the 
gastric  contents  through  the  tube.  As  a  rule,  in  cases  of  gastrectasia  resulting 
from  pyloric  stenosis,  we  wash  out  the  stomach  every  morning  before  breakfast. 
Ordinary  lukewarm  water  suffices,  but  if  there  is  an  excessive  secretion  of  hydro- 
chloric acid  it  is  satisfactory  to  employ  1-  or  2-per-cent.  solutions  of  bicarbonate 
or  borate  of  sodium.  In  severe  cases  the  operation  may  be  repeated  in  the  even- 
ing before  supper. 

V^  The  diet  in  stenosis  following  ulcer  should  consist  of  such  articles  of  food 
only  as  can  pass  with  comparative  ease  through  the  narrow  pylorus,  being  at  the 
same  time  highly  nutritious.  Most  suitable  are  milk,  eggs,  soups  with  the  addi- 
tion of  meat-juice,  somatose,  oatmeal,  rice,  or  flour;  gruel  made  from  rice,  oat- 
m.eal,  or  preparations  like  Mellin's  food;  and  finally,  finely  chopped  meat  of  all 
sorts.  The  meals  should  not  be  too  large,  but  should  rather  be  frequently  re- 
peated— a  little  food  often. 

In  this  way  it  is  often  possible  to  give  the  patient  considerable  relief  for 
many  years,  and  even  to  make  him  gain  weight.  Other  methods  of  treatment 
— by  applying  electricity  to  the  stomach,  by  cautious  massage  of  the  organ,  or  by 
the  administration  of  strychnine — may  be  employed  now  and  then  in  practice,  but 
they  have  no  special  value  in  actual  stenosis. 

It  may  well  be  questioned  whether  the  existence  of  such  patients,  who  are 
preserved  from  excessive  discomfort  only  by  means  of  daily  lavage  and  a  monot- 
onous and  limited  diet,  is  really  bearable;  and,  still  further,  what  are  we  to  do 
when,  in  spite  of  the  most  skillful  treatment  by  the  method  described,  the  symp- 
toms persist  and  the  nutrition  and  strength  of  the  patient  grow  gradually  more 
and  more  impaired?  For  such  there  is  still  the  possibility  of  actual  and  com- 
plete recovery.  We  refer  to  surgical  intervention.  In  no  other  severe  disease 
of  the  stomach  do  operative  procedures  offer  so  great  a  prospect  of  favorable 
result  as  in  stenosis  of  the  pylorus  following  ulcer,  and  therefore  it  has  been  our 
rule  for  a  series  of  years,  in  every  severe  case  of  this  sort,  to  urge  the  patient 
strongly  to  an  operation.  Moreover,  we  should  not  delay  too  long,  if  the  patient 
is  already  enfeebled,  or  if  there  is  reason  to  suspect  that  carcinoma  is  developing. 


U4c  DISEASES    OF   THE   DIGESTIVE    OEGAIN^S 

The  operation  is  usually  gastro-enterostomy,  or  sometimes  pyloroplasty;  but  we 
can  not  enter  here  into  particulars.  Certainly  we  ought  not  to  conceal  from 
the  patient  that  we  have  to  do  with  a  serious  operation,  which  is  not  absolutely 
without  danger;  yet  in  the  great  majority  of  cases  the  results  of  treatment  are 
excellent.  After  a  successful  operation  the  patient  is  freed  from  all  discomfort, 
he  regains  the  appearance  of  health,  and  sometimes  even  the  dilatation  of  the 
stomach  completely  disappears.  It  is  true  that  later,  perhaps  years  later,  re- 
lapses may  occur,  whether  because  of  special  mechanical  conditions  or  from  the 
development  of  secondary  carcinoma;  but  even  then  perhaps  assistance  will  be 
given  by  a  second  operation. 

[In  cases  of  recent  hsemorrhage  or  markedly  painful  digestion,  the  editor  has 
pursued  the  following  plan  of  treatment  with  apparently  good  results :  The  most 
powerful  agent  in  the  promotion  of  cicatrization  is  rest.  Absolute  rest  in  bed  is 
therefore  enjoined,  with  the  secondary  end  in  view  of  reducing  the  demands  of 
the  system.  The  patient  is  then  fed  exclusively  by  the  rectum  for  at  least  one 
week,  generally  for  two  weeks,  nothing  but  a  little  water  being  given  by  the 
mouth.  A  simple  cleansing  enema  is  given  once  daily;  and  at  six-hour  intervals 
a  nutrient  enema,  six  to  eight  ounces  in  bulk,,  and  composed  of  one  or  two  raw 
eggs,  an  ounce  of  expressed  beef  juice,  and  fully  peptonized  milk,  is  administered. 
Tolerance  by  the  rectum  is  promoted  by  the  addition  to  the  enema  of  a  few  drops 
of  laudanum.  After  one  or  two  weeks  small  quantities  of  milk  at  frequent  inter- 
vals are  given  by  the  mouth,  and  the  rectal  alimentation  is  gradually  diminished 
as  that  of  the  stomach  is  increased.  Pain  usually  ceases  immediately  on  the 
cessation  of  gastric  ingestion,  and  the  loss  of  weight  during  a  fortnight  of  rectal 
feeding  is  surprisingly  small.] 


CHAPTER   VI 
CANCER    OF    THE    STOMACH 

.ffitiology. — We  can  not  here  discuss  the  aetiology  of  carcinoma  in  general, 
and  we  shall  therefore  merely  enumerate  the  factors  which  experience  has  shown 
to  favor  the  development  of  cancer  in  the  stomach. 

Age  has  a  remarkable  influence.  Gastric  cancer  is  decidedly  most  frequent 
late  in  life,  between  the  fortieth  and  sixtieth  year.  Still  it  is  occasionally  seen 
in  younger  persons.  We  have  ourselves  seen  several  cases  in  persons  between 
twenty-two  and  twenty-five  years  of  age. 

Sex  is  of  no  importance. 

Heredity  has  a  slight  but  undeniable  influence.  The  most  famous  example  of 
the  transmission  of  cancer  is  presented  by  the  family  of  ITapoleon. 

The  relations  of  gastric  cancer  to  previous  disease  of  the  stomach  is  very 
important.  It  is  not  probable  that  the  tendency  to  cancer  is  increased  by  fre- 
quent errors  in  diet,  indulgence  in  alcohol,  or  similar  causes.  Most  of  those  who 
are  attacked  by  gastric  cancer  have  previously  lived  in  a  perfectly  temperate  man- 
ner, and  report  that  they  have  thus  far  always  enjoyed  a  good  digestion.  The 
exception  is  to  discover  that  there  has  been  any  special  injury  or  trauma,  such  as 
scalding  or  corrosive  poisoning,  and  if  there  is  a  history  of  them  they  are  to  be 
regarded  as  merely  contributory  causes.  Far  more  important,  however,  is  the  fact 
which  the  investigations  of  Hauser  have  lately  confirmed,  that  gastric  carcinoma 
is  not  infrequently  developed  in  the  cicatrized  edges  of  a  previous  gastric  ulcer. 
We  have  ourselves  had  a  considerable  number  of  cases  in  which  both  the  clinical 
course  of  the  disease  and  the  results  of  the  autopsy  illustrated  this  mode  of  devel- 
opment. 


CANCER   OF   THE    STOMACH  445 

Pathology. — The  stomach  is  a  favorite  seat  for  cancer.     About  a  third  of  all 

cases  of  cancer  are  gastric.  The  parts  of  the  organ  most  often  attacked  are  the 
pyloric  end  and  the  lesser  curvature.  Less  frequently  the  cardiac  end  and  the 
fundus  suffer. 

The  new  growth  takes  the  form  either  of  a  circumscribed  tumor  or  of  a  diffuse 
infiltration,  thickening  the  walls.  The  disease  invariably  originates  in  the  mu- 
cous layer,  extending  thence  into  the  submucous,  muscular,  and  serous  coats. 
Often  the  cancer  extends  by  way  of  the  lymph-channels,  or  sometimes  the  veins. 
The  lymph-glands  and  the  omentum  are  frequently  attacked  by  the  new  growth. 
Moreover,  we  find  metastases  in  the  peritoneum,  and  also  with  particular  fre- 
quency and  abundance  in  the  liver,  whither  cancerous  cells  are  carried  by  the 
branches  of  the  portal  vein.  The  connective  and  muscular  tissues  in  the  neigh- 
borhood of  the  cancer  are  quite  often  considerably  hypertrophied. 

Histologically,  gastric  cancer  is  of  the  cylindrical-cell  variety,  starting  from 
the  glandular  epithelium.  The  soft  tumors  are  termed  medullary;  the  firm  and 
hard,  scirrhous  or  fibroid.  The  medullary  cancers  are  particularly  apt  to  be 
quite  extensively  broken  down  on  their  exposed  internal  surface,  thus  forming 
what  are  known  as  cancerous  ulcers.  This  seems  to  be  mainly  the  result  of  the 
gastric  juice  acting  on  the  superficial  and  insufficiently  vascularized  portion  of 
the  tumor.  The  base  of  these  ulcers  is  usually  clean,  as  we  should  expect  from 
the  mode  of  their  production.  In  many  cases  of  rather  young  subjects,  and  some- 
times in  others,  we  find  colloid  cancer.  This  form  also  may  appear  either  in  nod- 
ules or  as  a  diffuse  growth,  infiltrating  the  tissues.  It  is  peculiarly  apt  to  involve 
the  peritoneum  extensively,  with  consequent  ascites. 

Clinical  History. — Most  cases  of  gastric  cancer  exhibit  a  combination  of 
grave  digestive  disturbances  with  a  relatively  rapid  loss  of  flesh  and  strength. 
Now  and  then  the  gastric  symptoms  assume  less  prominence.  The  chief  sign  of 
disease  is  a  constantly  progressive  marasmus  or  anaemia,  the  true  cause  of  which 
is  either  entirely  latent  or  not  unmistakably  recognizable  till  late  in  the  illness. 

Some  of  the  gastric  symptoms  are  not  very  characteristic.  They  merely  show 
that  digestion  is  disordered.  The  tongue  is  usually  thickly  coated  and  dry. 
There  is  loss  of  appetite  and  distress  after  meals.  The  patient  complains  of  a 
disagreeable  sensation  of  pressure  in  the  epigastrium,  increased  by  food.  Some- 
times this  amounts  to  actual  eardialgia.  Many  patients  are  annoyed  by  eructa- 
tions. Occasionally  vomiting  is  troublesome ;  in  other  instances  there  is  scarcely 
any.  The  constant  recurrence  of  vomiting  is  an  almost  sure  sign  that  the  cancer 
is  situated  in  the  pyloric  region  and  obstructs  the  orifice.  The  vomitus  may  con- 
tain nothing  but  mucus  and  ingesta;  or  it  may  assume,  from  the  admixture  of 
blood,  a  very  characteristic  and  somewhat  pathognomonic  appearance. 

Free  gastric  haemorrhage  and  consequent  hsematemesis  is  exceptional,  or  at 
least  it  is  much  less  frequent  than  in  ulcer  of  the  stomach ;  but  the  vomitus  often 
contains  decomposed  blood,  and  in  many  cases  this  will  be  for  a  time  almost  a 
constant  appearance.  Most  of  the  ulcerated  cancers  bleed  frequently,  a  little  at 
a  time.  When  it  reaches  the  stomach  the  blood  is  decomposed  and  gives  that 
well-known  "  coffee-grounds,"  or  "  chocolate-colored  "  appearance  to  the  vomitus, 
or  to  the  gastric  contents  obtained  by  means  of  a  stomach-tube,  which  is  so  im- 
portant a  symptom  for  the  diagnosis  of  cancer  of  the  stomach.  In  such  cases 
the  best  means  for  demonstrating  the  presence  of  blood,  in  the  brownish  or  black- 
ish fluid,  is  the  guaiac-turpentine  test  (vide  supra,  page  422).  This  gives  an 
extremely  distinct  reaction  in  the  case  of  carcinoma  of  the  stomach,  because 
lactic  acid  also  is  usually  present.  We  should  mention  that  in  the  case  of  ulcer- 
ating carcinoma  ventriculi  the  vomitus  may  have  so  foul  an  odor  that  it  may 
even  be  regarded  as  stercoraceous. 

Immediate  microscopic  examination  of  the  vomitus  may  reveal  red  blood- 


446  DISEASES    OF   THE   DIGESTIVE    OEGAXS 

globules.  Further,  the  vomitus  consists  of  partially  digested  food,  and  also  con- 
tains an  abundance  of  micro-organisms.  Sarcinas  are  found  much  less  often  in 
carcinoma  than'  in  ulcer  of  the  stomach,  but  we  frequently  see  under  the  micro- 
scope an  abundance  of  yeast  cells,  and  of  long  threadlike  bacilli  -which  perhaps 
have  a  relation  to  lactic-acid  fermentation.  It  is  extremely  rare  to  find  in  the 
vomitus  characteristic  particles  of  cancer.  It  is  somewhat  less  unusual  to  find 
little  pieces  of  the  growth  attached  to  the  stomach-tube,  when  the  carcinoma  is  at 
the  cardiac  end  or  in  the  fundus  of  the  stomach.  These,  if  obtained,  are  of 
course  to  be  submitted  to  microscopic  examination. 

The  external  examination  of  the  stomach  should  always  be  made  when  the 
patient  is  lying  flat  on  his  back.  Sometimes  we  can  clearly  recognize  by  mere 
inspection  the  position  and  size  of  the  organ,  any  peristaltic  motions  (vide 
infra)  that  there  may  be,  and  even  in  some  cases  the  presence  of  a  tumor.  Pal- 
pation is,  however,  more  important.  In  a  great  many  cases  the  new  growth  can 
be  felt  with  distinctness  through  the  abdominal  wall  as  a  hard  irregular  tumor. 
Its  situation  is,  in  a  majority  of  cases,  the  epigastrium.  Carcinoma  of  the 
pylorus,  which  is  the  most  common,  is  usually  felt  in  the  right  half  of  the  epi- 
gastrium; carcinoma  of  the  greater  curvature  somewhere  in  the  level  of  the 
navel.  But  it  should  be  considered  that  the  position  of  the  stomach  may  be  con- 
siderably altered  by  the  presence  of  a  growth — for  example,  we  have  seen  a  case 
of  pyloric  cancer  with  secondary  dilatation  of  the  stomach,  in  which  the  pylorus 
had  sunk  so  low  that  the  tumor  could  be  felt  about  a  hand's  breadth  above  the 
symphysis.  In  some  cases  the  tumor  varies  its  position  (vide  infra)  according 
to  the  degree  of  distention  of  the  stomach.  The  influence  of  respiration  upon  the 
tumor  is  various.  As  a  rule,  cancer  of  the  pylorus  does  not  change  its  place 
much  with  respiration,  unless  it  is  adherent  to  the  liver.  Carcinomata  of  the 
lesser  and  greater  curvatures  usually  do  move  with  respiration;  and  when  dis- 
placed downward  they  may  be  held  in  that  position  with  the  hand,  returning  to 
their  ordinary  location  when  the  hand  is  removed.  Tumors  of  the  liver  and 
cancers  of  the  stomach  which  are  adherent  to  the  liver  can  not  be  thus  held  down. 
When  the  carcinoma  is  situated  high  up,  in  the  lesser  curvature  or  near  the 
oesophagus,  it  may  not  be  felt  at  all  except  during  inspiration. 

In  a  minority  of  the  cases  no  tumor  can  be  felt  at  any  time.  This  is  true  in 
most  instances  of  diffuse  cancerous  infiltration  of  the  walls  of  the  stomach.  Under 
such  circumstances  the  diagnosis  can  not  often  be  definitely  established.  The 
tumor  is  undiscoverable,  first,  in  most  cases  of  diffuse  cancerous  infiltration  of 
the  stomach-walls.  We  may,  indeed,  notice  an  increased  sense  of  resistance  and 
hardness  in  the  epigastrium,  but  we  can  not  refer  this  condition  with  certainty  to 
a  new  growth.  Secondly,  the  new  growth  may  extend  chiefly  inward,  toward  the 
cavity  of  the  organ,  and  may  thus  escape  detection.  And,  finally,  the  tumor 
may  be  so  concealed  by  the  liver  or  the  edge  of  the  ribs  that  it  is  inaccessible  to 
the  touch.  Such  cancers  as  attack  the  cardiac  extremity,  the  posterior  wall,  or 
the  lesser  curvature  of  the  stomach,  are  particularly  apt  to  be  out  of  reach  of 
palpation. 

PerciTSsion  of  the  cancer  rarely  gives  flatness,  but  instead  a  muffled  tym- 
panitic resonance.  This  is  sometimes  an  influential  factor  in  the  differential 
diagnosis  from  cancer  of  the  liver.  In  a  few  cases,  upon  auscultation  in  the 
neighborhood  of  the  tumor,  we  may  hear  a  soft  systolic  murmur,  probably  due 
to  compression  of  a  rather  large  artery. 

The  examination  of  the  gastric  contents  is  of  the  greatest  diagnostic  impor- 
tance. While  introducing  the  stomach-tube,  or  perhaps,  if  need  be,  a  less  flex- 
ible instrument,  we  should  notice  whether  the  tube  enters  the  stomach  with 
ease.  Carcinoma  at  the  cardia  is  not  infrequently  the  cause  of  a  sensible  resist- 
ance to  the  tube  when  it  passes  the  lower  end  of  the  oesophagus.    With  regard 


CAl^CEK    OF    THE    STOMACH  4^7 

to  the  examination  of  the  gastric  contents,  the  chief  point  is  about  free  hydro- 
chloric acid.  Von  der  Yelden  first  pointed  out  what  numerous  investigations 
have  since  confirmed,  that  in  almost  all  cases  of  gastric  carcinoma  there  is  no 
free  hydrochloric  acid,  so  that  the  phloroglucine-vanilline  reaction  an  hour  after 
the  test  breakfast  is  negative.  Associated  with  other  symptoms  this  is  an  ex- 
tremely important  diagnostic  sign  (vide  infra).  The  cause  of  this  almost  invari- 
able absence  of  free  hydrochloric  acid  in  carcinoma  of  the  stomach  has  not  yet 
been  determined,  especially  as  this  symptom  has  often  been  observed  very  early  in 
the  course  of  the  disease.  The  associated  catarrh  of  the  gastric  mucous  mem- 
brane and  its  secondary  atrophy  may  have  some  influence,  but  probably  there 
are  also  other  unknown  causes  at  work.  An  examination  for  pepsine  may  be 
omitted  in  practice:  it  also  often  turns  out  negative.  Far  greater  importance 
attaches  to  the  fact  that  the  gastric  contents  in  carcinoma  are  very  apt  to  show 
a  surprising  amount  of  lactic  acid.  This  is  almost  invariably  so  when  the  car- 
cinoma obstructs  the  pylorus.  The  explanation  of  this  is  very  simple.  There  is 
no  hydrochloric  acid  to  exert  an  antiseptic  action,  and  the  food  is  stagnant  in 
the  stomach,  so  that  there  is  an  especially  favorable  opportunity  for  the  develop- 
ment of  a  vigorous  lactic-acid  fermentation.  There  is,  then,  nothing  specific 
about  the  presence  of  lactic  acid  in  the  gastric  contents  in  cases  of  carcinoma, 
only  it  is  a  very  frequent  and  therefore  not  unimportant  symptom. 

The  motor  efficiency  of  the  stomach  is  impaired  in  most  cases  of  carcinoma, 
except  in  cancer  afi^ecting  the  cardia,  or  in  small  cancers  on  the  fundus.  When- 
ever there  is  an  extensive  development  of  carcinoma  of  the  stomach,  the  muscu- 
lar coat  of  the  organ  is  sufiiciently  damaged  to  embarrass  its  motor  activity; 
but  of  course  the  hindrance  to  the  discharge  of  its  contents  is  greatest  when  the 
new  growth  is  at  the  pylorus.  In  this  case,  besides  the  direct  destruction  of  the 
muscular  tissue,  we  have  the  purely  mechanical  stenosis,  and  this  may  at  last 
become  extreme.  For  this  reason,  if  we  find  a  marked  stagnation  of  the  ingesta 
we  can  usually  infer  that  the  seat  of  the  carcinoma  is  the  pylorus  (vide  infra). 
We  should  not  omit  to  inflate  the  stomach  when  it  is  possible.  We  can  thus 
determine  not  only  the  size  and  position  of  the  stomach,  but  also  its  relations  to 
any  tumor  that  may  be  felt;  and  finally,  it  should  be  added  that  a  test  for  blood 
(vide  infra)  should  be  made  with  the  fluid  obtained  by  washing  out  the  stomach. 

Certain  peculiarities  in  the  clinical  picture  of  gastric  carcinoma  are  occa- 
sioned by  its  special  location ;  if  at  the  cardia,  the  symptoms  are  similar  to  those 
of  cancer  of  the  oesophagus.  As  soon  as  the  cardia  is  narrowed,  the  patient 
himself  feels  that  it  is  difficult  for  food  to  enter  the  stomach,  and  speedily  there 
appears  vomiting,  or,  more  accurately,  regurgitation  of  food,  so  that  the  patient 
can  take  nothing  but  liquid  nourishment.  The  diagnosis  of  carcinoma  at  the 
cardia  is  usually  easy.  We  feel  the  resistance  at  the  cardia  with  the  stomach- 
tube  some  16  to  18  inches  (40-45  centimetres)  from  the  front  teeth.  Externally 
the  growth  can  not  be  felt  until  it  invades  the  lesser  curvature  of  the  stomach. 
Then  we  often  feel  the  tumor  in  the  epigastric  angle,  especially  on  deep  inspira- 
tion. In  carcinoma  of  the  fundus  the  symptoms  may  be  indefinite  for  a  long 
time.  The  pylorus  remaining  permeable,  there  may  be  no  vomiting  at  all.  In 
late  stages  the  tumor  which  may  be  felt  is  often  very  large,  particularly  if  there  is 
involvement  of  the  omentum,  which  changes  it  into  a  great  cancerous  mass. 

When  cancer  at  the  pylorus  leads  to  stenosis,  the  clinical  picture  is  especially 
important  as  well  as  very  common  and  very  characteristic.  As  soon  as  there  is 
a  hindrance  to  the  emptying  of  the  stomach,  whether  because  the  muscular  coat 
is  impaired  by  infiltration  with  carcinoma  or  because  there  is  the  direct  mechan- 
ical obstacle  of  stenosis,  there  result  retention  and  accumulation  of  food  in  the 
stomach,  with  exaggerated  peristalsis,  and  finally  gastric  dilatation.  The  cir- 
cumstances are  precisely  similar  to  those  depicted  in  the  preceding  chapter  when 


448  DISEASES    OE   THE   DIGESTIVE   OEGANS 

speaking  of  cicatricial  stenosis  (cf.  page  438).  In  advanced  cases  the  contours 
of  the  dilated  organ  are  clearly  seen  through  the  emaciated  and  collapsed  abdom- 
inal walls.  Erom  time  to  time  a  contraction  occurs,  and  we  see  the  peristaltic 
wave  slowly  travel  toward  the  pylorus.  Very  often  the  carcinomatous  growth 
near  the  pylorus  is  distinctly  palpable,  and  even  visible.  Often  it  moves  with 
respiration.  Washing  out  the  stomach  will  demonstrate  the  stagnation  of  its 
contents,  and  by  inflation  we  determine  its  size  and  position.  If  the  stomach 
is  not  emptied  artificially,  from  time  to  time  very  large  amounts  are  vomited,  the 
vomitus  being  invariably  devoid  of  hydrochloric  acid  but  containing  much  lactic 
acid,  and  sometimes  also  showing  fermentation.  If  we  let  some  of  the  gastric 
contents,  obtained  by  vomiting  or  through  the  tube,  stand  in  a  glass  vessel,  it 
divides  into  layers.    If  fermentation  has  set  in,  a  foamy  layer  is  formed  on  top. 

We  have  now  enumerated  the  symptoms  of  gastric  cancer,  referable  to  the 
stomach  itself.  The  greatest  attention  should  also  be  paid  to  the  general  dis- 
turbance of  nutrition  occasioned  by  this  gastric  disease.  Loss  of  flesh  is.  not 
rarely  the  very  first  symptom  which  calls  the  patient's  attention  to  his  disease. 
This  wasting  is  observed  earliest  in  eases  which  are  attended  with  anorexia  and 
vomiting.  The  patient  also  gradually  takes  on  that  familiar  sallow  cachectic 
look  which  is  characteristic  of  most  cases  of  cancer.  Some  patients  become  ex- 
cessively anasmic.  The  skin  acquires  a  waxy  pallor,  and  there  are  all  the  symp- 
toms which  result  from  great  anasmia,  such  as  cerebral  disturbances  and  func- 
tional cardiac  murmurs.  Sometimes  the  blood  itself  presents  decided  peculiar- 
ities in  such  cases.  Thus  we  may  find  microcytes  and  poikilocytes  in  it.  Gas- 
tric cancer  and  pernicious  anaemia  (q.  v.)  have  been  repeatedly  confounded. 
In  one  such  case  we  made  the  interesting  discovery  of  extremely  abundant  meta- 
static cancer  in  the  bones.  As  the  bone  marrow  is  known  to  have  something  to 
do  with  the  production  of  the  blood,  it  may  be  that  the  ansemia  was  due  to  this 
abnormal  condition.  At  any  rate,  the  grave  ansemia  which  results  from  cancer 
can  not  be  regarded  in  just  the  same  light  as  the  loss  of  flesh  and  the  cachexia. 
We  often  find  extreme  ansemia  in  patients  who  are  tolerably  well  nourished, 
while,  on  the  other  hand,  many  patients  with  carcinoma,  though  emaciated 
to  a  skeleton,  do  not  display  this  peculiar  ansemic  pallor.  The  ansemia 
must,  therefore,  depend  upon  some  special  circumstances.  Probably  it  is  most 
frequently  caused  by  continued  though  small  haemorrhages,  due  to  ulceration  of 
the  new  growth. 

Special  derangements  of  other  organs  are  relatively  infrequent.  Metastatic 
cancer  is  of  importance.  It  attacks  the  liver  chiefly.  If  the  hepatic  new  growth 
is  considerable,  it  may  quite  overshadow  the  primary  cancer — there  being  jaun- 
dice and  a  greatly  enlarged,  nodular,  and  tender  liver.  Secondary  carcinosis 
of  the  peritonseum  is  also  apt  to  cause  marked  symptoms,  such  as  ascites  and 
abdominal  pain.  Secondary  cancer  may  also  involve  the  mesenteric  and  retro- 
peritoneal lymph-glands,  the  lungs,  and  other  organs,  but  it  does  not  usually  give 
rise  to  striking  symptoms  when  so  situated,  although  the  discovery  of  even  small 
metastases  by  palpation  may  have  great  diagnostic  significance.  Older  physi- 
cians frequently  mention  the  occurrence  of  swollen  lymph-glands  above  the  left 
clavicle,  but  we  have  scarcely  ever  found  them  there,  although  we  have  paid 
special  attention  to  this  point.  Swelling  of  the  inguinal  glands  is  more  impor- 
tant. We  have  seen  small  metastases  in  them  several  times.  Finally,  we  would 
like  to  call  special  attention  to  the  appearance  of  small  secondary  nodules  at  the 
navel,  a  fact  which  we  have  repeatedly  noticed.  The  discovery  of  such  a  growth 
is  of  great  diagnostic  value  when  no  primary  tumor  can  be  made  out  by  palpation. 

Direct  extension  of  the  new  growth  into  neighboring  organs  is  not  very  fre- 
quent. We  will  venture  to  mention  one  case  which  we  saw,  on  account  of  its 
great  rarity.     The  new  growth  caused  adhesion  of  the  anterior  wall  of  the  stom- 


CAlSrCEE   OF   THE    STOMACH  449 

o( 
aeh  to  the  abdominal  w^lls,  and  then,  penetrating  through  them  and  the  skin  of 
the  epigastrium,  finally  appeared  as  a  tumor,  of  about  the  size  of  one's  fist,  pro- 
jecting outward.  If  a  cancer  ulcerates,  it  may  destroy  all  the  layers  of  the 
stomach,  and  result  in  perforation  and  secondary  peritonitis;  or,  if  previous 
adhesions  have  been  formed,  the  perforation  may  open  up  an  abnormal  communi- 
cation between  the  stomach  and  some  neighboring  part  of  the  intestine.  The 
transverse  colon  is  the  part  usually  perforated;  less  often  the  small  intestine. 

As  to  the  bowels,  constipation  is  the  rule.  Diarrhoea  is  rare.  The  urine  is 
usually  pale  and  but  slightly  acid.  Its  amount  is  diminished,  as  we  should  expect 
from  the  slight  amount  of  nourishment  taken,  and  from  the  vomiting.  Over  the 
heart  we  may  sometimes  hear  soft  anaemic  murmurs.  The  pulse  is  usually  accel- 
erated, although,  if  there  be  extreme  marasmus,  it  may  be  slow. 

The  temperature  is  often  normal.  If  the  patient  is  greatly  emaciated  it  is 
not  infrequently  subnormal,  but,  on  the  other  hand,  if  the  thermometer  is  care- 
fully used  we  shall  very  often  find  occasional  irregular  elevations  of  temperature, 
100.5°-102°  (38°-39°  C),  or  even  a  persistent  or  intermittent  fever.  The  cause 
of  these  elevations,  exclusive  of  complications,  is  probably,  in  most  cases,  the 
absorption  of  septic  material  from  the  ulcerated  surface  of  the  carcinoma.  If 
there  are  haemorrhages,  another  factor  may  be  the  absorption  of  the  decomposed 
blood  (fibrine  ferment).  Not  infrequently,  in  advanced  stages  of  the  disease 
there  is  more  or  less  oedema  of  the  ankles,  hands,  and  other  parts.  The  explana- 
tion of  this  is  the  same  as  in  most  cases  of  oedema  in  cachectic  and  anaemic 
patients — viz.,  the  impaired  nutrition  of  the  vascular  walls,  the  hydrsemia,  and 
the  associated  cardiac  weakness.  Sometimes  there  also  occur  marked  pains  in 
the  arms  and  legs.  The  temperature  is  normal,  or  even  subnormal.  If  there  is 
some  inflammatory  complication,  or  if  the  anaemia  is  extreme,  fever  may  occur. 

The  entire  duration  of  the  disease  may  be  one  or  two  years.  It  is  excep- 
tional for  it  to  last  longer,  except  when  the  cancer  develops  in  the  floor  of  a  pre- 
existing ulcer.  In  this  case  the  symptoms  of  gastric  ulcer  pass  into  those  of 
carcinoma.  The  change  may  be  gradual,  but  there  may  be  an  intervening  period 
of  apparent  health.  We  have  by  careful  questioning  repeatedly  been  able  to 
make  the  diagnosis  of  this  transformation  during  the  life  of  the  patient,  in  cases 
later  confirmed  by  autopsy.  In  individual  instances  the  disease,  of  course,  exhib- 
its many  variations  and  departures  from  the  typical  course.  Sometimes  the  con- 
stitutional symptoms  of  weakness  and  emaciation  are  more  prominent,  and  some- 
times the  distinctively  gastric  disturbances. 

The  fatal  termination  is  usually  preceded  by  the  symptoms  of  constantly  in- 
creasing weakness.  It  may  be  hastened  by  complications,  such  as  perforative 
peritonitis.  Now  and  then  grave  nervous  symptoms  appear,  often  quite  sud- 
denly. The  patient  falls  into  a  condition  resembling  that  of  diabetic  coma 
(q.  v.),  he  is  somnolent,  and  has  a  peculiar  dyspnoea,  with  deep  and  labored  res- 
pirations. Such  an  attack  is  probably  due  to  auto-intoxication,  and  almost 
always  ends  fatally.    Recovery  from  cancer  of  the  stomach  is  unknown. 

Diagnosis. — Gastric  cancer  is  a  comparatively  frequent  disease,  and  in  every 
case  in  which  there  are  well-marked  gastric  symptoms,  particularly  in  an  elderly 
person,  the  physician  should  think  of  the  possibility  of  this  grave  disease.  The 
suspicion  is  all  the  more  justified  when  the  symptoms  occur  in  a  previously 
healthy  individual  without  known  cause,  and  if  they  are  associated  from  the 
start  with  a  cachectic  look  and  a  feeling  of  weakness  and  languor,  as  well  as 
with  marked  emaciation.  If  now,  having  such  suspicions,  we  wish  to  reach  a 
diagnosis,  the  first  requirement  is  a  thorough  investigation  of  the  stomach. 
External  examination  should  be  particularly  directed  to  the  discovery  of  a  pal- 
pable tumor,  if  any  exists.  We  should  examine  while  the  patient  is  lying  on  his 
back  or  on  his  side.  If  possible,  the  stomach  should  be  empty  and  we  should 
29 


450  DISEASES    OF   THE  DIGESTIVE   ORGANS 

palpate  while  the  patient  is  breathing  quietly,  and  also  while  he  is  taking  deep 
inspirations.  If  a  tumor  can  be  felt,  the  next  question  is  whether  it  actually 
arises  from  the  stomach,  or  from  some  other  organ.  In  most  cases  the  other 
clinical  symptoms,  such  as  vomiting,  have  already  indicated  the  stomach  as  the 
seat  of  the  disease,  and  thus  we  know  the  origin  of  the  tumor.  On  the  other 
hand,  however,  there  may  be  great  obscurity,  and  many  cases  of  gastric  tumor 
have  been  confounded  with  carcinoma  of  the  left  lobe  of  the  liver,  the  pancreas, 
the  omentum,  the  transverse  colon,  and  other  parts.  It  is  difficult  to  lay  down 
special  rules  for  diagnosis,  because  the  difficult  cases  almost  invariably  have  their 
own  special  peculiarities.  Of  importance  in  every  case  are  an  accurate  local 
examination,  a  mapping  out  of  the  neighboring  organs,  inflation  of  the  stomach 
and  perhaps  also  of  the  colon,  determining  whether  the  mass  moves  with  respira- 
tion, and  a  consideration  of  all  the  other  factors.  Among  these  last  the  most 
important  is  the  result  of  an  examination  with  the  stomach-tube.  The  main 
question  in  every  case  is  the  presence  or  absence  of  free  hydrochloric  acid  in  the 
gastric  juice.  If  it  is  absent  on  repeated  examination  our  suspicion  of  carcinoma 
is  confirmed,  provided  the  other  symptoms  point  in  the  same  direction ;  but  if  they 
do  not,  the  absence  of  free  hydrochloric  acid  is  by  no  means  so  grave  a  matter,  for 
it  is  absent  often  enough  under  other  circumstances.  It  is,  however,  a  fact  of 
great  practical  importance  that  when  free  hydrochloric  acid  has  been  distinctly 
and  repeatedly  demonstrated  in  the  gastric  juice,  we  can  usually  absolutely 
exclude  gastric  cancer,  even  if  other  symptoms  point  to  it.  If  there  is  no  free 
hydrochloric  acid,  but  lactic  acid,  and  also  impaired  motor  efficiency,  the  cir- 
cumstances are  different.  In  such  a  case,  even  if  no  tumor  can  be  felt,  there 
is  great  probability  of  a  gastric  carcinoma,  probably  involving  the  pylorus.  An- 
other very  important  point  is  the  demonstration  of  blood  in  the  gastric  con- 
tents (vide  supra,  page  422).  If  we  have  distinct  "coffee-ground"  vomitus,  and 
at  the  same  time  achlorhydria,  these  factors  alone  almost  establish  the  diagno- 
sis, but  even  smaller  amounts  of  blood  obtained  by  lavage  are  important.  Final- 
ly, we  should  bear  in  mind  that  when  no  gastric  tumor  is  made  out  there  may 
be  metastatic  growths  which  can  be  felt — for  example,  in  the  lymph-glands — and 
thus  a  diagnosis  of  cancer  confirmed. 

In  case  of  symptoms  which  indicate  stenosis  of  the  pylorus,  with  subsequent 
gastrectasia,  it  is  of  great  practical  importance  to  determine  whether  they  are 
due  to  cancer  or  to  the  scar  of  an  ulcer.  In  this  instance,  even  if  we  feel  a 
tumor,  that  fact  is  not  decisive,  for  the  cicatricial  hyperplasia  of  gastric  ulcer 
may  cause  a  distinct  tumor;  but,  as  a  rule,  it  is  not  difficult  to  reach  a  decision. 
Suggesting  a  scar  from  ulcer  would  be :  long  duration  of  the  disease  (two  years, 
sometimes  four  or  five  years,  and  longer) ;  youth  of  the  patient ;  comparatively 
healthy  appearance ;  distinct  history  of  ulcer ;  cardialgia ;  profuse  hsematemesis ; 
and  finally,  as  a  decisive  factor,  the  demonstration  of  an  abundance  of  hydro- 
chloric acid  and  hypersecretion  in  the  stomach.  Under  these  circumstances  the 
differentiation  of  stenosis  from  ulcer  is  absolutely  certain.  On  the  other  hand, 
there  is  complete  certainty  of  a  cancerous  stenosis  if  the  disease  has  developed  in  a 
comparatively  brief  time — in  one  or  two  years ;  if  it  has  attacked  an  elderly  per- 
son; if  there  is  distinct  cachexia;  and,  most  important  of  all,  if  hydrochloric 
acid  is  never  demonstrable  in  the  gastric  contents,  while  there  is  an  abundance 
of  lactic  acid.  Other  cases  occur  which  are  not  typical  and  of  easy  diagnosis. 
Age,  duration  of  the  disease,  and  previous  symptoms  may  suggest  a  stenosis  due 
to  ulcer,  and  yet  on  washing  out  the  stomach  we  find  no  hydrochloric  acid  at  all, 
or,  at  most  a  faint  trace.  In  these  cases  we  are  usually  justified  in  assuming 
that  carcinoma  has  developed  secondarily  on  the  floor  of  a  former  ulcer.  It 
must  be  confessed  that  in  simple  stenosis  following  ulcer,  when  there  is  an 
excessive  stagnation  of  the  gastric  contents,  there  may  be  temporarily  a  com- 


CANCER  OF  THE  STOMACH  451 

plete  combination  of  all  the  hydrochloric  acid  with  albumen,  and  consequently 
no  reaction  for  free  hydrochloric  acid;  but  if  the  stomach  is  washed  out  a  few 
times  we  soon  find  an  abundance  of  free  hydrochloric  acid.  On  the  other  hand, 
when  a  stenosis  due  to  ulcer  has  lasted  for  a  long  time,  our  suspicions  should  be 
aroused  if  the  reaction  for  hydrochloric  acid  is  persistently  feeble  or  at  times 
absent,  and  in  its  place  or  along  with  it  lactic  acid  appears  in  the  gastric  con- 
tents. We  have  ourselves  repeatedly  seen  this  gradual  transition  of  simple 
stenosis,  due  to  ulcer  with  hypersecretion,  into  carcinomatous  stenosis  with 
aehlorhydria.  Finally,  it  should  be  remarked  that  there  is  also  a  stenosis  of  the 
pylorus  due  to  simple  hypertrophy  of  its  walls,  without  any  ulcer  or  carcinoma. 
We  have  ourselves  seen  a  few  cases  of  this  sort,  which  presented  the  ordinary 
symptoms  of  pyloric  stenosis  with  great  dilatation,  and  ended  fatally.  The 
pathogenesis  of  this  rare  condition  has  not  yet  been  explained.  We  venture  to 
suggest  that  perhaps  it  may  be  due  to  congenital  anomalies.  As  yet,  unfortu- 
nately, no  particulars  are  known  as  to  the  constituents  of  the  gastric  juice  in 
these  cases,  and  for  the  present  it  is  scarcely  possible  to  make  a  diagnosis  of 
them  with  certainty. 

Treatment. — If  once  the  diagnosis  of  gastric  carcinoma  has  been  settled,  the 
question  arises  whether  there  is  any  definite  prospect  of  success  from  surgical 
treatment.  If  not,  our  treatment  can  be  merely  symptomatic  with  the  object 
of  alleviating  the  patient's  suffering,  and  preserving  his  strength  as  long  as 
possible. 

The  first  point  in  symptomatic  treatment  is  a  regulation  of  the  diet.  In  gen- 
eral, we  advise  mainly  liquids  and  soft  foods,  including  milk,  gruel,  rice,  sago,, 
delicate  vegetables,  potato  puree,  softened  zwieback,  toast,  or  water-crackers, 
and  delicate  puddings.  We  may  also  permit  finely  chopped  or  scraped  meat,  or,, 
still  better,  fowl;  and  fish,  such  as  trout,  pike,  and  perch-pike.  Such  artificial 
foods  as  somatose,  neutrose,  beef  peptone  and  beef  juice,  and  infants'  foods,  do^ 
good  service  for  a  time.  If  the  appetite  fails  we  order  stomachics — for  exam- 
ple, compound  tincture  of  cinchona.  The  fluid  extract  of  condurango  deserves  a 
special  mention,  and  has  been  a  favorite  prescription  in  gastric  carcinoma  since 
condurango  bark  was  recommended  by  Friedreich.  We  usually  prescribe  hydro- 
chloric acid  after  meals  (15  to  20  drops  of  the  dilute  acid  in  water)  in  the  hope 
of  making  up  for  the  aehlorhydria.  Pain  is  alleviated  by  narcotics,  such  as  mor- 
phine, opium,  codeine,  belladonna,  and  chloroform,  and  by  moist  warm  or  cold 
applications.  Warm  poultices  on  the  epigastrium  for  several  hours  a  day  are 
usually  beneficial.  To  combat  obstinate  vomiting  we  may  give  the  narcotics 
just  named  or  bits  of  ice,  but  the  best  remedy  is  rinsing  out  the  stomach,  pro- 
vided the  patient  is  not  too  feeble.  If  there  are  sour  or  offensive  eructations, 
we  prescribe  bicarbonate  of  soda,  magnesia,  or  powdered  charcoal.  If  the  pyloric 
cancer  is  leading  to  stenosis  with  stagnation  of  food  in  the  stomach,  the  daily 
washing  out  of  that  organ  is  an  excellent  means  of  relieving  the  patient  for  a 
time,  at  least,  of  a  great  part  of  his  discomfort.  If  this  is  practiced  regularly 
with  either  pure  water  or  a  1-  or  2-per-cent.  solution  of  hydrochloric  acid,  and 
if  the  diet  is  suitable,  there  may  be  a  great  temporary  improvement  in  the  condi- 
tion and  even  a  not  inconsiderable  gain  in  weight.  But,  despite  all  our  efforts, 
the  symptoms  may  become  worse  and  worse  till,  finally,  the  subcutaneous  injec- 
tion of  morphine  may  be  indispensable.  Then  our  whole  object  is  to  alleviate 
the  patient's  sufferings,  and  to  give  him  moral  support  and  encouragement. 

When  the  vigor  of  the  patient  is  such  as  to  permit  the  consideration  of  surgi- 
cal interference,  the  more  promptly  the  operation  is  undertaken  the  more  chance 
is  there  of  eradicating  the  disease  and  obtaining  permanent  recovery.  It  is, 
therefore,  permissible  when  there  is  incipient  disease  and  the  diagnosis  is  not 
yet  fully  established,  although  somewhat  probable,  to  propose  to  the  patient  an 


452  DISEASES    OF   THE   DIGESTIVE    OKGAJSTS 

exploratory  laparotomy,  to  be  immediately  followed  by  a  regular  operation,  pro- 
vided the  case  turns  out  to  be  a  suitable  one.  The  results  of  operations  on  car- 
cinoma of  the  stomach  have  not  been  very  brilliant.  Still,  in  many  cases  the 
surgeon  is  fully  justified  in  endeavoring  to  combat  an  otherwise  absolutely  hope- 
less disease,  since  there  is  some  prospect  of  recovery.  Although  there  have  been 
many  failures,  surgeons  have  obtained  a  number  of  extremely  satisfactory  recov- 
eries under  these  circumstances.  If  there  is  a  stenosis  of  the  pylorus  and  yet 
it  is  no  longer  possible,  or  at  least  no  longer  wise,  to  extirpate  the  tumor,  gastro- 
enterostomy may  give  very  great  relief.  If  the  patient  survives  the  operation, 
the  suffering  is  much  diminished  and  nutrition  may  decidedly  improve.  For  the 
particulars  we  refer  to  surgical  treatises. 


CHAPTEE   VII 

ANOMALIES    OF    THE    SECRETION    OF    GASTRIC    JUICE 

{Achylia  Gastrica  and  Hypersecretion  of  the  Gastric  Juice) 

In  the  present  chapter  are  to  be  considered  those  dyspeptic  conditions  which 
are  associated  with  a  change — that  is,  either  a  diminution  or  an  increase — in  the 
secretion  of  the  gastric  juice,  independently,  at  least  in  most  cases,  of  any  defi- 
nite anatomical  lesion.  We  have  here  to  consider,  therefore,  no  marked  catar- 
rhal condition  or  new  growth  of  the  stomach,  nor  gastric  ulcer  with  hypersecre- 
tion. The  cause  of  the  change  in  secretion  in  the  cases  here  considered  must 
rather  be  sought  in  the  disturbances  of  the  activity  of  the  cells,  the  special  occa- 
sion of  which  is  as  yet  almost  entirely  unknown.  Many  clinical  observations,  it 
is  true,  indicate  that  abnormal  nervous  influences  are  important  in  this  con- 
nection, but,  on  the  other  hand,  it  is  possible  that  the  explanation  lies  in  primary 
changes  in  the  minute  structure  and  chemistry  of  the  secreting  cells  themselves. 
Besides  this  uncertainty  of  aetiology,  there  is  also  an  absolute  lack  of  thorough 
anatomical  investigations  in  this  regard,  so  that  it  is  at  present  a  very  difficult 
matter  to  map  out  and  depict  accurately  these  abnormal  conditions.  We  must, 
therefore,  limit  ourselves  preliminarily  to  a  simple  statement  of  the  clinical  facts 
thus  far  known,  and  present,  as  well  as  we  can,  the  leading  points  of  view  for 
the  interpretation  and  treatment  of  these  groups  of  symptoms. 

1.  Anacidity  of  the  Stomach  (Achlorhydria). — Achylia  Gastrica. — Fen- 
wick  was  the  first  to  observe  that  there  are  eases  of  chronic  and  complete  ab- 
sence of  any  demonstrable  secretion  of  gastric  juice,  independently  of  chronic 
gastritis  or  gastric  carcinoma,  but  associated  with  an  almost  complete  atrophy 
of  the  glandular  apparatus  of  the  gastric  mucous  membrane.  The  clinical  pic- 
ture in  these  cases  displayed  scarcely  any  marked  gastric  symptoms.  Anorexia 
and  moderate  oppression  after  eating  were  almost  the  only  indications  of  dys- 
pepsia; but  there  were  observed  gradually  progressive  antemia  and  emaciation, 
so  that  finally  the  general  weakness,  independent  of  any  other  local  symptoms, 
resulted  in  death.  Since  then  we  have  learned,  particularly  from  the  investiga- 
tions of  Martins,  that  the  grave  symptoms  of  these  cases  can  not  possibly  be 
caused  by  an  atrophy  and  cessation  of  function  of  the  gastric  glands  alone,  but 
occur  only  when  there  is  also  present  an  atrophy  of  the  intestinal  mucous  mem- 
brane. 

It  has  been  shown,  and  we  have  ourselves  repeatedly  found,  that  it  is  possible 
to  have  an  achylia  gastrica — that  is,  persistent  absence  of  hydrochloric  acid 
(and  pepsine,  vide  infra),  without  any  noticeable  disturbance  of  nutrition,  and 


AlsrOMALIES    OF   THE    SECEETION   OF   GASTEIC   JUICE     453 

with  only  slight  and  fugitive  dyspeptic  symptoms,  or  even  with  no  gastric  symp- 
toms whatever.  In  all  these  cases  it  is  wholly  probable  that  the  digestion  and 
absorption  by  the  intestines  are  perfectly  normal,  and  completely  replace  the 
digestive  function  of  the  stomach.  It  is  only  requisite  that  the  intestines  should 
preserve  their  normal  function,  and  that  the  motor  power  of  the  stomach  should 
be  unimpaired.  In  such  cases  the  stomach  serves  to  a  certain  degree  merely  as  a 
reservoir  for  the  ingested  food,  which  it  duly  passes  on  to  the  intestines;  in 
them  are  present  in  abundance  all  the  reagents,  bile,  pancreatic  juice,  and  intes- 
tinal juice,  requisite  for  the  further  absorption  of  the  ingesta.  There  is  only 
one  defect  in  these  persons  with  achylia  gastrica :  there  is  no  disinfection  of  the 
gastric  contents  by  means  of  the  hydrochloric  acid  of  the  gastric  juice.  Ordi- 
narily this  lack  is  unimportant,  but  if  any  hurtful  material  reaches  the  stomach 
it  is  more  likely  to  lead  to  disturbance  than  under  normal  conditions.  This 
explains  why  those  persons  with  achylia  gastrica  have  a  "  sensitive  "  stomach  and 
are  prone  to  suffer  from  temporary  dyspepsia.  They  very  often  also  have  a 
striking  tendency  to  diarrhoea.  But  if  such  individuals  live  cautiously  and  are 
not  exposed  to  any  especial  injurious  influences,  they  feel  perfectly  well  and  may 
be  extremely  well  nourished. 

Is  there  an  atrophy  of  the  gastric  mucous  membrane  as  a  foundation  for 
these  benign  cases  of  achylia  gastrica?  It  is  possible,  and  in  many  cases  even 
probable,  that  there  is;  but  it  is  not  certain.  This  is  certain:  that  sometimes 
a  long  persistent  absence  of  hydrochloric  acid  has  been  observed  clinically,  and 
later  an  autopsy  has  shown  no  anatomical  explanation  of  the  condition.  Thus, 
for  example,  a  short  time  ago  the  author  had  a  patient  under  observation  in 
his  wards  for  a  considerable  time  with  diabetes  mellitus,  in  whose  gastric  juice 
no  trace  of  hydrochloric  acid  could  be  demonstrated,  although  repeated  examina- 
tions were  made.  The  patient  died,  comatose,  and  the  stomach  seemed  to  be 
perfectly  normal,  even  upon  microscopic  examination.  Here  there  may  perhaps 
have  been  some  toxic  inhibition  of  the  secretion.  At  any  rate,  observations  like 
this  prove  that  when  there  is  no  gastric  juice  secreted,  we  can  not  assert  that  any 
marked  anatomical  change  will  be  found  in  the  gastric  mucous  membrane. 

From  what  has  been  said  it  follows  that,  according  to  the  present  state  of 
our  knowledge,  we  must  distinguish  several  forms  of  achylia  gastrica  (or  of  long 
persistent  gastric  anacidity).  We  should  mention  incidentally  that  in  a  strict 
sense  the  name  achylia  should  be  employed  only  for  that  condition  in  which  there 
is  a  constant  absence  not  only  of  hydrochloric  acid,  but  also  of  pepsine,  indicat- 
ing a  complete  drying  up  of  the  secretion  of  gastric  juice.  Those  cases,  in  which 
free  hydrochloric  acid  is  never  demonstrable  but  pepsine  is  found,  should,  in 
strictness,  be  termed  anacidity,  or,  better,  achlorhydria.  In  practice  it  is  true 
that  we  can  not  always  make  these  fine  distinctions,  and  that  even  such  cases 
as  present  not  an  absolute  absence  but  a  slight  or  occasional  trace  of  hydro- 
chloric acid  are  put  in  this  latter  category.  We  distinguish  the  three  follow- 
ing forms  of  achylia : 

1.  Achylia  or  achlorhydria  may  appear  as  a  symptom  in  certain  other  diseases 
of  the  stomach,  particularly,  as  we  have  already  seen,  in  severe  acute  and  chronic 
gastritis  (when  there  is  genuine  catarrh  of  the  stomach),  and  also  in  cancer  of 
the  stomach.     These  cases  are  to  be  termed  "  symptomatic  achylia." 

2.  Achylia  or  achlorhydria  may  appear  as  a  necessary  result  of  marked 
atrophy  ("  anadenia  ")  of  the  gastric  mucous  membrane.  Here  the  further  point 
is  to  determine  the  causes  of  this  distinctly  characterized  anatomical  change  in 
the  gastric  mucous  membrane.  Sometimes  it  seems  to  be  the  result  of  a  previous 
catarrhal  inflammation  (atrophic  catarrh,  analogous  to  similar  conditions  of 
other  mucous  membranes — vide  supra,  page  426).  How  far  this  assumption 
agrees  with  the   facts  must  be   determined   by  further  careful   investigation. 


454  DISEASES    OF   THE   DIGESTIVE   OEGANS 

Apart  from  this  secondary  or  inflammatory  atrophy  there  is  also  a  simple  pri- 
mary atrophy  of  the  mucous  membrane.  The  cause  of  this  condition  is  most 
likely  to  be  found  in  congenital  peculiarities,  of  which  we  as  yet  possess  no  in- 
timate knowledge.  We  might  see  a  certain  analogy  in  progressive  muscular 
atrophy.  In  these  cases  of  atrophy  of  the  gastric  mucous  membrane  there  is  no 
demonstrable  secretion  of  hydrochloric  acid,  nor  of  pepsine.  The  gastric  contents 
obtained  in  the  ordinary  way  are  absolutely  devoid  of  peptic  activity,  but  at  the 
same  time  the  muscular  efficiency  of  the  stomach  is  in  many  cases  perfectly  nor- 
mal, and  this  explains  why,  although  there  is  no  secretion  of  gastric  juice,  there 
are  no  marked  symptoms  of  gastric  discomfort.  In  many  cases,  however,  the 
atrophy  of  the  gastric  mucous  membrane  is  coincident  with  an  atrophy,  or  at 
least  with  marked  changes  of  the  intestinal  mucous  membrane.  Then  it  is 
inevitable  that  severe  disturbances  of  nutrition  should  gradually  develop,  for  the 
food  can  not  be  sufficiently  digested  and  absorbed.  Such  patients  grow  progres- 
sively thin  and  feeble.  Often  they  suffer  from  marked  intestinal  symptoms, 
having  persistent  diarrhoea,  alternating  with  constipation.  By  suitable  treat- 
ment and  nursing  such  patients  may  improve,  or  at  least  their  symptoms  may  be 
checked.  In  a  few  rare  cases  death  finally  occurs.  The  clinical  picture  of  per- 
nicious anaemia  (g.  v.)  has  been  repeatedly  presented  in  association  with  this 
sort  of  atrophy  of  the  stomach  and  intestines.  In  our  opinion,  however,  the 
nature  of  these  cases  is  still  unsettled,  since  the  atrophy  of  the  intestinal  mucous 
membrane  of  itself  might  well  lead  to  extreme  inanition,  but  not  to  a  specific 
anaemia.  Eor  this  there  must  be  present  some  special  circumstances  with  which 
we  are  as  yet  unacquainted. 

3.  The  third  form  is  simple  functional  achylia.  Here  belong  the  not  infre- 
quent cases  in  which  the  symptoms  are  not  usually  particularly  severe,  consist- 
ing of  anorexia,  gastric  oppression,  nausea,  and  rarely  vomiting.  The  complaint 
may  have  been  of  recent  origin.  On  careful  examination  of  the  gastric  contents, 
we  find  complete  absence  of  hydrochloric  acid,  while  pepsine  may  be  present,  or, 
again,  in  other  cases  entirely  absent.  The  motility  of  the  stomach  is  normal,  as 
a  rule,  but  it  may  be  somewhat  impaired,  probably  because  of  a  coincident  weak- 
ness of  the  muscular  coat  (see  the  following  chapter).  With  suitable  treatment 
the  symptoms  diminish  or  vanish,  but  there  is  no  change  with  regard  to  the  ab- 
sence, or  approach  to  absence,  of  hydrochloric  acid  and  pepsine.  It  can  not  be 
determined  how  long  this  condition  has  existed.  Sometimes  such  patients  say, 
as  we  have  already  mentioned,  that  they  have  been  rather  subject  to  mild  dys- 
pepsia or  to  temporary  attacks  of  diarrhoea.  Often,  however,  their  previous 
health  has  been  good.  Whether  we  should  invariably  assume  that  there  is  a 
marked  atrophy  of  the  gastric  mucous  membrane  in  all  such  cases  is  very  ques- 
tionable. Probably  we  have  rather  to  do  with  an  impairment  of  the  secretory 
capacity  of  the  individual  stomach  from  causes  not  at  present  accurately  deter- 
minable. Apparently  there  are  not  a  few  persons  with  achylia  of  this  sort.  In- 
asmuch as  the  condition  runs  along  without  any  special  sjrmptoms,  it  is  not 
diagnosticated  by  the  physician,  and  the  patient  is  not  subjected  to  an  accu- 
rate examination  until  digestive  disturbance  arises  because  of  some  special  cause 
(vide  supra),  and  then  the  anomaly  is  detected.  If  such  patients  do  suffer  from 
persistent  dyspepsia  there  will  usually  be  found  some  special  reason  for  it,  such 
as  motor  incapacity,  possibly  dislocation  of  the  stomach,  or  genuine  "  nervous  " 
dyspepsia,  meaning  by  that  term  dyspepsia  of  psychical  origin.  It  would  be  an 
interesting  question  to  investigate  whether  individuals  with  persistent  achylia  do 
not  perhaps  have  a  predisposition  to  the  development  of  carcinoma. 

The  diagnosis  of  achylia,  whether  essential  or  secondary,  can  alwaj^s  be  easily 
made  by  means  of  a  careful  examination  of  the  gastric  contents  (see  the  first 
chapter  of  this  section).     Of  course,  the  diagnosis  is  not  established  until  re- 


Al^OMALIES    OF   THE    SECRETION   OF   GASTRIC    JUICE     455 

peated  and  painstaking  examinations  have  been  made  at  various  times  and 
under  various  circumstances,  and  have  invariably  given  the  same  negative  result. 
If  achylia  is  demonstrated,  the  next  question  is  whether  it  is  merely  symptomatic 
or  essential.  The  presence  of  chronic  gastritis  is  excluded  by  the  absence  of 
all  etiological  factors  and  of  excessive  mucous  secretion,  and  by  the  general 
course  of  the  disease.  The  suspicion  of  cancer  will  often  likewise  be  rendered 
untenable  by  the  general  course  of  the  disease,  and  the  absence  of  a  tumor.  In 
cases  of  atrophy  of  the  gastric  and  intestinal  mucous  membrane,  with  conse- 
quent emaciation,  there  may  be  very  great  difficulty  in  excluding  cancer.  On 
the  whole,  however,  the  course  of  gastro-intestinal  atrophy  is  much  slower  than 
that  of  carcinoma.  Accompanying  signs  of  pyloric  stenosis  invariably  indicate 
the  presence  of  carcinoma;  and  if  we  are  enabled  by  the  absence  of  any  severe 
disturbance  of  nutrition  to  exclude  any  marked  atrophy  of  the  gastric  and  intes- 
tinal mucous  membrane,  we  reach  at  last  a  diagnosis  of  simple  functional  achylia 
by  exclusion.  Whether  in  such  cases  there  is  a  demonstrable  anatomical  change 
in  the  gastric  mucous  membrane,  the  present  state  of  our  knowledge  does  not 
enable  us  to  determine. 

We  do  not  need  to  enter  upon  a  special  discussion  of  the  treatment  of  symp- 
tomatic achylia.  The  severe  cases  of  achylia  which  occasion  extreme  disturb- 
ance of  nutrition  need  the  most  careful  dietetic  management.  They  should  have 
such  food  as  milk,  soups,  eggs,  and  meat-peptones.  Practical  experience  will 
usually  be  a  better  guide  than  any  theoretical  considerations.  Internally  we 
may  try  hydrochloric  acid  and  preparations  of  pepsine  and  pancreatine,  also  all 
sorts  of  stomachics,  including  nux  vomica  and  condurango.  The  stomach  may 
be  rinsed  out  with  a  2-per-mille  solution  of  hydrochloric  acid,  and  galvanic  elec- 
tricity may  be  employed.  It  is  self-evident  that  when  there  is  actual  atrophy  of 
the  mucous  membrane,  the  results  of  treatment  must  be  very  limited.  The 
milder  cases  of  achylia  do  not  need  treatment  except  when  special  dyspeptic 
symptoms  appear,  or  when  there  is  intestinal  disturbance,  such  as  diarrhoea ;  then 
the  treatment  is  the  same  as  in  ordinary  disturbances  of  the  stomach  or  bowels, 
including  a  suitable  diet,  hydrochloric  acid,  perhaps  rinsing  out  the  stomach  a 
few  times,  and,  in  case  of  diarrhoea,  opium.  If  the  symptoms  subside,  and  we 
now  find  there  is  a  persistent  achylia,  of  course  we  must  earnestly  recommend 
such  individuals  to  exercise  a  certain  caution  with  regard  to  diet.  They  should 
not  take  too  great  a  quantity  of  food  at  one  time,  and  in  general  should  choose 
a  largely  vegetable  diet — i.  e.,  one  containing  an  abundance  of  starches.  There 
is  this  exception,  that  if  the  achylia  is  associated  with  a  dread  of  eating  and  a 
tendency  to  hypochondriasis,  we  must  encourage  the  patient  to  take  a  rather 
abundant  amount  of  nourishment  and  employ  hydrotherapy  and  other  general 
tonics. 

2.  Hypersecretion  and  Hyperacidity  of  the  Gastric  Juice  (Acid  Dyspepsia). 
—We  have  seen  in  the  first  chapter  of  this  section  that  it  may  be  regarded  as  a 
rule,  that  when  fasting  the  stomach  is  almost  completely  empty,  and  that  an  hour 
after  a  test  breakfast  (vide  supra,  page  418)  the  acidity  of  the  gastric  contents 
is  about  55  to  65.  The  investigations  of  late  years  have  shown,  however,  that 
this  rule  has  numerous  individual  exceptions  not  necessarily  pathological.  There 
are  many  persons  who  secrete  scarcely  any  hydrochloric  acid  (vide  supra),  and 
also  there  are  apparently  still  more  who  always  have  hydrochloric  acid  in  the 
stomach  even  when  fasting,  and  whose  hydrochloric-acid  index  after  a  test  break- 
fast is  as  high  as  80  to  100,  or  even  higher.  Many  such  individuals  have  no 
dyspeptic  disturbances  whatever,  so  that  the  unusual  abundance  of  hydrochloric 
acid  can  be  regarded  only  as  an  individual  peculiarity  of  secretion,  and  not  due 
to  disease.  In  other  such  cases,  however,  there  are  decided  gastric  symptoms, 
and  these  symptoms  are  such  as  to  indicate  very  strongly  their  direct  dependence 


456  DISEASES    OF   THE   DIGESTIVE    OEGANS 

upon  the  increased  production  of  acid.  This  state  is  termed  acid  dyspepsia,  by 
which  we  mean  the  abnormal  excess  of  hydrochloric  acid  at  the  time  of  diges- 
tion— that  is,  hyperacidity  as  distinguished  from  hypersecretion,  which  latter 
term  is  applied  to  the  continuous  secretion  of  gastric  juice  even  when  digestion 
is  not  taking  place,  the  stomach  having  received  no  food,  or  having  discharged 
its  contents  into  the  pylorus.  Hypersecretion  is  probably  almost  always  associ- 
ated with  hyperacidity,  but  not  vice  versa.  However,  we  can  not  maintain  a 
strict  clinical  distinction  between  the  two  in  practice. 

Essential,  acid  dyspepsia  should  be  sharply  distinguished  from  symptomatic 
hyperacidity  and  hypersecretion,  such  as  occur  perhaps  in  certain  forms  of  gas- 
tritis (page  428),  and  almost  invariably  in  ulcer  of  the  stomach.  This  distinc- 
tion is  very  important,  even  from  a  practical  point  of  view.  It  must  be  con- 
fessed that  it  may  be  scarcely  possible  to  make  a  differential  diagnosis,  as  we 
shall  soon  see,  between  ulcer  and  hypersecretion;  but  we  can,  at  any  rate,  hold 
fast  to  the  important  theoretical  distinction  between  the  two  conditions.  The 
term  "  essential "  hypersecretion  ought  to  be  applied  only  to  cases  in  which  there 
is  an  increase  in  the  secretion  of  hydrochloric  acid,  without  any  ulcer  forma- 
tion. If  we  regard  hypersecretion  as  a  possible  cause  of  ulcer  (vide  supra,  page 
433),  then  ulcer  can  be  termed  merely  a  complication  of  hypersecretion. 

As  to  the  causes  of  simple  hyperacidity  and  hypersecretion  we  have  as  yet, 
unfortunately,  scarcely  any  knowledge.  Very  few  histological  examinations 
of  the  mucous  membrane  in  characteristic  cases  have  thus  far  been  made.  It  is, 
therefore,  at  present  customary  to  assume  that  hypersecretion  is  a  "  neurosis," 
and  this  view  is  apparently  confirmed  by  the  frequent  combination  of  hypersecre- 
tion with  other  nervous  conditions.  We  must  later  discuss  this  point  more  fully. 
On  the  other  hand,  however,  it  is  not  impossible  that  functional  disturbances  of 
cellular  activity  may  lead  to  increase  in  the  secretion.  We  are  ourselves  in- 
clined to  class  many  cases  of  hypersecretion  along  with  the  well-known  cases  of 
increase  in  the  secretion  of  sweat  (hyperidrosis  of  the  hands  and  feet),  of  saliva, 
and  of  similar  products.  Eor  such  it  is  not  at  all  essential  that  there  should  be 
abnormal  nervous  conditions. 

Having  such  imperfect  insight  into  the  true  nature  of  these  processes,  we 
must  provisionally  take  a  purely  clinical  standpoint,  and  describe  the  phenomena 
seen  in  practice.  It  should  be  added  that  some  of  the  conditions  are  by  no  means 
infrequent,  but  it  is  often  difficult  to  interpret  accurately  what  we  observe.  One 
important  question  is  how  far  the  symptoms  which  are  present  are  actually  refer- 
able to  the  hypersecretion  as  such,  and  how  far  they  are  due  to  the  other  anoma- 
lies which  often  accompany  the  hypersecretion,  such  as  general  nervousness,  gas- 
troptosis,  and  chlorosis.  In  order  to  get  a  better  comprehension  of  the  subject 
we  shall  distinguish  in  what  follows  several  forms  of  acid  dyspepsia,  but  we  wish 
to  repeat  that  a  perfect  differentiation  is  impossible,  particularly  between  hyper- 
acidity and  hypersecretion. 

1.  Dyspepsia  with  Hyperacidity  (Hyperchlorhydria) . — The  conditions  which 
belong  in  this  category  are  most  often  found  in  young  females.  They  are 
very  often  conjoined  with  symptoms  of  chlorosis,  general  nervousness,  etc.  Cer- 
tain errors  in  diet  may  also  excite  hyperchlorhydria,  such  as  hot  or  highly  spiced 
food,  and  particularly  too  strong  coffee;  and  dyspeptic  conditions  with  hyper- 
chlorhydria are  frequently  observed  in  excessive  smokers. 

The  symptoms  are  tolerably  characteristic.  They  occur  especially  after  eat- 
ing, and  sometimes  only  after  certain  kinds  of  food,  and  consist  first  of  a  sense 
of  oppression  in  the  stomach,  often  increasing  into  genuine  cardialgia.  Usually 
the  pain  does  not  appear  until  two  or  three  hours  after  eating — i.  e.,  at  a  time 
when  the  stomach  is  already  empty,  although  the  excessive  secretion  of  acid  is 
still  going  on.     Many  patients  have  noticed  that  if  they  then  take  some  more 


ANOMALIES    OF   THE    SECEETION   OF   GASTEIC   JUICE     457 

food  or  drink  their  pain  will  abate.  This  is  easy  to  understand.  Often  there 
will  be  acid  eructations  at  the  time  of  the  excessive  formation  of  acid,  and  a 
distinct  feeling  of  heartburn.  The  acid  gastric  contents  may  be  vomited,  but 
this  is  not  especially  frequent.  When  the  stomach  is  completely  empty,  the  pa- 
tient feels  perfectly  well  again.  Inasmuch  as  the  appetite  is  usually  unimpaired, 
nutrition  remains  fairly  good.  The  general  course  of  the  disease  is  chronic,  with 
marked  variations.  At  many  times  the  symptoms  are  aggravated,  particularly 
under  the  influence  of  psychical  disturbances,  such  as  anger  or  excitement,  or  be- 
cause of  an  unsuitable  mode  of  life.  At  other  times  the  symptoms  may  entirely 
vanish. 

The  diagnosis  of  hyperchlorhydria  may  be  suggested  by  the  symptoms  just 
described,  but  it  can  not  be  established  except  by  means  of  the  stomach-tube. 
External  examination  of  the  stomach  shows  nothing  special  except  that  there 
may  be  a  moderate  diffuse  tenderness  on  pressure.  It  is  not  surprising  that 
often  there  is  gastroptosis.  If  we  examine  the  stomach  when  fasting,  it  is  empty 
or  almost  empty,  provided  the  case  is  one  of  pure  hyperchlorhydria.  The  acid 
index  after  a  test  breakfast  is  very  high,  70  to  100  or  over.  The  digestive  power 
of  the  gastric  juice  is  greater  than  normal.  It  is  therefore  natural  to  find,  as 
we  do  find,  that  the  stomach  is  entirely  empty  as  a  rule  as  soon  as  three  or  four 
hours  after  a  test  meal;  which  indicates  also  a  good  degree  of  motor  power.  At 
that  time  hydrochloric  acid  is  still  present.  On  the  other  hand,  digestion  of 
starch  in  the  stomach  is  impeded  by  the  abundance  of  hydrochloric  acid. 

If  we  find  things  as  above  depicted,  the  diagnosis  of  hyperchlorhydria  as  such 
is  established.  But  a  difficult  question  remains  to  be  answered — ^whether  the 
case  is  one  of  simple  functional  increase  of  the  secretion,  or  whether  the  hyper- 
acidity is  symptomatic  of  an  ulcer.  If  there  are  no  characteristic  symptoms  of 
ulcer,  such  as  gastric  haemorrhage  and  localized  tenderness,  it  is  often  impossible 
to  answer  this  question  with  more  than  a  certain  degree  of  probability.  It  is 
characteristic  of  simple  hyperchlorhydria  that  the  pain  is  often  improved  upon 
taking  food,  while  in  ulcer  the  pain  is  aggravated.  If  there  are  well-marked 
symptoms  present  of  general  nervousness,  this  is  usually  decidedly  in  favor  of 
"  nervous  hyperacidity."  Finally,  the  results  of  treatment  may  aid  us  in  diag- 
nosis (vide  infra). 

The  mode  of  treatment  will  be  considered  with  that  of  hypersecretion. 

2.  Dyspepsia  with  Hypersecretion  of  the  Gastric  Juice  ("  Continuous  Floiv 
of  Gastric  Juice  "). — Here  belong  those  cases  of  dyspepsia  in  which  the  examina- 
tion of  the  stomach  shows  the  presence,  even  when  fasting,  of  considerable 
amounts  of  fluid  containing  an  excess  of  hydrochloric  acid,  and  in  which  this 
hypersecretion  can  not  be  regarded  as  the  result  of  an  ulcer. 

The  disease  is  much  more  exceptional  than  simple  hyperchlorhydria.  It  ap- 
pears in  men  somewhat  oftener  than  in  women.  No  special  setiological  factors 
can  be  named,  except  long-continued  mental  strain  and  excitement;  often  no 
cause  can  be  made  out. 

The  symptoms,  as  in  hyperchlorhydria,  consist  of  cardialgia,  sour  eructations, 
heartburn,  and  not  infrequently  vomiting.  Pain  often  appears  when  no  food  has 
been  taken.  When  vomiting  occurs  there  may  be  little  or  no  food  in  the 
vomitus,  but  merely  a  cloudy,  often  bile-stained  fluid,  strongly  acid,  with  a  very 
sharp  taste  and  so  irritating  that  it  causes  burning  pain  in  the  pharynx.  The 
appetite  is  generally  good,  and  the  patients  have  usually  found  out  by  experi- 
ence that  if  they  drink  some  tea  so  as  to  dilute  the  gastric  juice,  or  take  some 
sort  of  food,  they  get  relief.  Often  there  is  abnormal  thirst ;  the  bowels  are  usu- 
ally constipated;  the  urine  faintly  acid  and  turbid  with  deposits  of  phosphates; 
the  pulse  is  often  slow;  in  many  cases  there  is  a  distinct  general  neurasthenic 
condition,  associated  with  the  dyspepsia.    Here,  again,  the  only  method  of  arriv- 


458  DISEASES    OF   THE   DIGESTIVE   OEGAl^'S 

ing  at  a  certain  diag-nosis  is  by  examining  tlie  gastric  contents.  The  decisive 
point  is  that  in  the  morning  before  breakfast  we  should  invariably  find  a  consid- 
erable amount  of  fluid,  containing  practically  no  portions  of  food  but  a  large 
percentage  of  hydrochloric  acid.  At  the  same  time  it  should  be  particularly 
pointed  out  that  it  is  not  abnormal,  now  and  then,  to  find  a  teaspoonful  or  two  of 
fluid  in  the  stomach,  containing  hydrochloric  acid,  while  fasting.  It  is  not 
proper  to  speak  of  the  case  as  one  of  hypersecretion  unless  we  can  obtain  from 
the  fasting  stomach,  without  special  effort,  some  two  or  three  ounces  (50-100 
cubic  centimetres)  of  strongly  acid  fluid.  Along  with  the  hypersecretion  there 
is  usually  hyperchlorhydria,  so  that  we  find  a  high  acid  index  an  hour  after  the 
test  breakfast.  If  we  give  a  test  meal,  and  examine  three  hours  later,  we  shall 
find  that  the  meat  has  vanished,  while  the  digestion  of  starches  has  been  decid- 
edly delayed  by  the  hyperacidity.  Some  seven  hours  after  the  test  meal  the 
stomach  is  empty  of  food,  but  probably  contains  an  abundance  of  acid  secretion. 

If  we  inflate  the  stomach,  we  may  flnd  the  organ  dislocated  downward  (gas- 
troptosis).  This,  however,  is  merely  a  chance  complication.  There  is  never 
great  dilatation.  If  we  find  the  stomach  much  enlarged,  our  suspicions  are  at 
once  directed  to  pyloric  stenosis,  and  this  condition  is  usually  easily  diagnosti- 
cated, one  important  indication  being  delay  in  the  emptying  of  the  stomach. 
Whenever  the  stomach  in  a  fasting  condition,  or  seven  or  eight  hours  after  a  test 
meal,  is  found  to  contain  not  only  an  abundance  of  hydrochloric  acid,  but  in 
addition  considerable  amounts  of  partially  digested  food,  the  condition  is  not 
one  of  simple  hypersecretion,  but  of  hypersecretion  combined  with  stenosis  of 
the  pylorus  due  to  ulcer.    This  puts  an  entirely  different  aspect  on  the  case. 

It  is  a  much  more  difiicult  matter  to  distinguish  hypersecretion  from  a  gastric 
ulcer  without  stenosis.  Indeed,  sometimes  an  absolute  decision  is  almost  impos- 
sible. In  such  instances  we  may  be  enabled  to  form  an  opinion  by  considering 
the  general  course  of  the  disease,  the  associated  neiwous  symptoms,  and  all  the 
special  sjmiptoms  (vide  supra). 

In  general,  the  course  of  acid  dyspepsia  with  hypersecretion  is  chronic,  but 
variable.  The  prognosis  is  not  unfavorable,  and  correct  management,  based,  as 
it  must  be,  upon  an  accurate  examination,  may  bring  about  very  satisfactory 
results. 

In  the  treatment  of  acid  dyspepsia,  including  hypersecretion  as  well  as  sim- 
ple hyperchlorhydria,  we  meet  with  one  difficulty  in  the  fact  that  we  can  seldom 
absolutely  exclude  ulcer  of  the  stomach.  The  physician  must,  therefore,  deter- 
mine whether  he  shall  begin  with  a  course  of  treatment  for  ulcer  or  not.  We 
believe  that  in  all  cases  in  which  the  symptoms  have  existed  for  a  considerable 
time  and  are  sev(5re,  and  in  which  there  has  been  no  systematic  treatment  as  yet, 
it  is  wise  to  treat  the  patient  as  if  there  were  an  ulcer.  If  the  case  is  one  of 
simple  acid  dyspepsia  this  can  do  no  harm,  and  if  it  is  one  of  ulcer  it  is  the  only 
method  that  can  do  good.  In  either  case,  the  quiet,  the  unirritating  diet,  and 
the  administration  of  alkalies  are  certainly  appropriate.  Moreover,  cases  are 
not  infrequent  in  which  the  patients  are  anxious  and  hypochondriacal,  and  upon 
them  a  methodically  conducted  "  cure  "  for  ulcer  often  has  a  favorable  subjective 
influence.  Still,  this  just-mentioned  combination  of  acid  dyspepsia  with  de- 
cided nervous  and  hypochondriacal  disturbances  may,  on  the  other  hand,  render 
the  effect  of  a  strict  ulcer  treatment  quite  unfavorable.  This  applies  to  patients 
who  have  long  been  tortured  by  a  dread  of  gastric  ulcer,  have  consequently  gone 
through  the  appropriate  treatment  many  times  already,  and  have  grown  thin  and 
feeble  as  the  result  of  an  excessively  cautious  dietary.  For  such  unfortunates 
there  may  be  no  use  whatever  in  repeating  a  strict  course  of  treatment  suitable  to 
ulcer.  Such  a  procedure  confirms  the  patient  in  his  apprehensions,  and  merely 
makes  him  more  wretched. 


A:N0MALIES    of   the    SECEETION   of   gastric   juice     459 

We  see,  then,  how  carefully  we  should  consider  the  individual  in  the  treat- 
ment of  acid  dyspepsia,  and,  above  all,  how  much  weight  we  should  assign  to  the 
general  condition  as  well  as  to  thedyspeptic  symptoms.  It  is  often  advisable  to 
begin  with  a  course  of  treatment  for  ulcer  in  the  ordinary  manner,  but  upon  the 
prompt  cessation  of  symptoms  to  make  a  more  rapid  transition  than  usual  to 
nourishing  food  and  other  therapeutic  methods.  The  more  convinced  the  physi- 
cian becomes  that  he  has  to  do  with  simple  "  nervous  "  hypersecretion  and  not 
with  an  ulcer,  the  less  need  has  he  to  pursue  a  strict  dietetic  treatment.  In 
such  cases  it  is  best  to  prescribe  for  the  patient  a  diet  list,  containing  an  abun- 
dance of  albuminoids,  including  meat,  fish,  eggs,  and  milk;  and  with  this,  rye 
bread  and  butter,  and  easily  digested  vegetables.  There  should  be  as  great  a 
limitation  as  possible  of  alcoholic  beverages,  spices,  strong  coffee,  and  sour  arti- 
cles, as  well  as  of  puddings  and  starchy  vegetables.  Yet  in  such  cases,  also,  one 
must  be  guided  by  the  individual  experiences  of  the  patient  as  well  as  by  merely 
theoretical  considerations.  As  to  drugs,  of  course  alkalies  come  first.  We 
should  be  guided  by  the  circumstances  of  the  particular  case  in  prescribing,  sev- 
eral times  a  day,  particularly  after  meals,  a  knife-point  full  of  bicarbonate  of 
soda,  or  some  similar  powder,  such  as  bicarbonate  of  soda  and  calcined  magnesia, 
equal  parts;  or  bicarbonate  of  soda,  30  parts;  subnitrate  of  bismuth,  5  parts;  and 
similar  drugs.  If  there  is  hypersecretion  we  like  to  give  the  patient  in  the  morn- 
ing, before  breakfast,  a  half  litre  (pint)  of  warm  Carlsbad  water,  or  the  artificial 
Carlsbad  salt,  dissolved  in  water.  In  severe  cases  of  hypersecretion  regular  wash- 
ing out  of  the  stomach  is  advantageous.  The  best  time  to  do  this  is  in  the  early 
morning.    We  may  employ  a  one-per-cent.  solution  of  bicarbonate  of  soda. 

Atropine  and  the  narcotics,  such  as  morphine  and  codeine,  have  been  recom- 
mended for  the  purpose  of  diminishing  the  secretion  of  the  gastric  glands.  We 
have  ceased  to  expect  any  benefit  from  their  use,  and  we  would  warn  the  physician 
against  their  unnecessary  employment. 

The  simultaneous  constitutional  treatment  is  very  important,  particularly 
in  all  cases  associated  with  neurasthenic  symptoms  (vide  infra,  the  chapter  on 
nervous  dyspepsia).  From  this  point  of  view  there  is  much  benefit  in  drinking 
the  waters  at  Carlsbad,  Tarasp,  and  similar  watering  places,  in  connection  with 
the  hope  of  constitutional  improvement  from  the  outdoor  life,  the  baths,  cold 
sponging  and  rubbing,  and  similar  agencies.  In  treatment  at  home  these  last 
factors  must  always  be  duly  considered, 

3.  Periodical  (Intermittent)  Hypersecretion  (Gastroxynsis). — In  the  con- 
dition here  to  be  described,  persons  who  at  other  times  feel  perfectly  well,  with- 
out any  digestive  disturbance,  are  rather  suddenly  attacked  by  violent  gastric 
pain,  sour  eructations,  and  vomiting.  The  intervals  between  attacks  may  be 
longer  or  shorter,  and  there  may  be  either  some  exciting  cause  or  no  apparent 
reason  for  the  disturbance.  The  vomitus  consists  of  large  amounts  of  watery 
fluid  containing  an  excess  of  hydrochloric  acid.  During  these  attacks  the  gen- 
eral condition  of  the  patient  is  wretched;'  he  looks  pale,  his  pulse  is  small  and 
frequent.  Often  there  is  extremely  violent  headache  at  the  same  time.  An 
attack  of  this  sort  lasts  a  few  hours,  or  even  two  or  three  days.  Often  it  ends 
with  considerable  suddenness,  to  be  followed  by  a  period  of  good  health  which 
may  last  a  week  or  even  months,  or  longer. 

The  causes  of  this  strange  disease  are  entirely  unknown,  but  it  certainly  seems 
as  if  there  were  conditions  of  irritation,  originating  in  the  nervous  system.  It 
seems  to  us  indubitable  that  there  is  a  close  relation  between  gastroxynsis  and 
migraine  (see  the  chapter  on  migraine).  It  is  a  very  important  fact  that  almost 
precisely  the  same  group  of  symptoms  occurs  in  tabes  dorsalis  (q.v),  under 
the  name  of  gastric  crisis.  In  every  case,  therefore,  the  physician  should  exam- 
ine the  tendon  reflexes  and  the  pupils ;  but  attacks  of  this  sort  undoubtedly  occur 


460  DISEASES    OF   THE   DIGESTIVE    OEGANS 

when  tabes  is  absent.     It  may  be  added  that  in  its  well-marked  form  the  condi- 
tion is  quite  rare. 

If  possible  we  should  examine  the  gastric  secretion  in  the  time  between  at- 
tacks, as  well  as  during  the  attack.  It  appears  that  many  cases  of  periodical 
gastroxynsis  are  merely  acute  exacerbations  of  a  constant  hypersecretion.  In 
such  cases  there  are  likely  to  be  mild  dyspeptic  symptoms  in  the  intervals,  and  a 
careful  treatment  of  these  by  lavage,  alkalies,  and  Carlsbad  water  has  an  excel- 
lent effect  upon  the  paroxysms.  If  there  are  coincident  neurasthenic  symptoms, 
of  course  the  greatest  stress  must  be  laid  upon  constitutional  treatment.  The 
treatment  of  the  paroxysm  itself  is  seldom  very  successful.  The  best  remedy 
is  bromide  of  sodium  in  large  doses.  We  may  also  try  chloral,  chloroform, 
belladonna,  codeine,  and  also  antipyrine.  Externally,  warm  compresses  or  hot 
poultices  may  be  applied  over  the  stomach.  If  the  pain  is  very  violent  a  subcu- 
taneous injection  of  morphine  may  be  almost  indispensable,  although  we  should 
avoid  it  if  possible. 


CHAPTEE   VIII 

ABNORMALITIES    IN    THE    SIZE    AND    POSITION    OF    THE    STOMACH— 
MOTOB    DISTURBANCES    OF    THE    STOMACH 

1.  Abnormalities  in  the  Size  of  the  Stomach. — Atony  of  the  Stomach. — 

Like  any  other  organ,  the  stomach  may  present  considerable  difTerences  in  its 
size  without  being  pathological.  These  differences  partly  depend  upon  con- 
genital conditions,  and  partly  are  associated  with  the  mode  of  life.  It  has  long 
been  known  that  certain  classes  of  people  who  eat  very  bulky  articles  of  diet 
(e.  g.,  a  great  proportion  of  potatoes),  and  other  large  eaters,  including  many  dia- 
betics, have  noticeably  large  stomachs;  but  a  change  in  size  of  this  sort  can 
not  be  reg'arded  as  pathological,  provided  the  function  of  the  stomach  is  not  im- 
paired. The  excessive  distention  of  the  organ,  or  the  excessive  demands  upon  the 
functional  activity  of  the  muscular  coat  of  the  stomach,  may  finally  render  it 
unequal  to  its  task.  Then  we  reach  a  pathological  disturbance,  a  sort  of  over- 
strain of  the  stomach,  a  muscular  insufficiency  analogous  to  the  myopathic  dis- 
eases of  the  heart,  which  have  been  so  much  studied.  Obviously  one  important 
factor  here  would  be  the  original  quality  of  the  muscular  fiber:  if  the  muscles 
of  the  stomach  are  weak  from  the  start,  they  will  become  insufficient  all  the 
sooner. 

We  must  state  that  in  our  experience  well-marked  cases  of  primary  idiopathic 
dilatation  of  the  stomach,  as  an  expression  of  pure  muscular  insufficiency,  seem 
to  be  far  from  frequent,  although  slight  degrees  of  muscular  weakness  occur 
quite  often. 

From  what  has  been  said,  it  is  evident  that  the  physician  should  lay  little 
stress  upon  the  mere  estimation  of  the  size  of  the  stomach.  And,  indeed,  its  size 
varies  greatly  according  to  the  amount  ingested.  We  can  form  an  opinion  of  the 
size  of  the  organ  by  percussion  of  the  empty  stomach,  or  by  percussing  it  alter- 
nately empty  and  filled  with  water  by  means  of  the  stomach-tube,  or,  what  is 
much  simpler  and  more  certain,  by  distending  it  with  air,  as  above  mentioned 
(page  420).  In  general,  we  can  say  there  is  dilatation  of  the  stomach  if  the 
lower  border  of  the  fundus  extends  below  the  level  of  the  navel  while  the  lesser 
curvature  is  in  a  normal  position;  but,  as  we  have  said,  the  important  question 
is  not  the  size,  but  the  motor  ability  of  the  organ,  and  it  is  far  more  important 
to  determine  the  functional  activity  by  means  of  a  test  meal,  in  the  manner 


THE   SIZE   AND   POSITIOI^   OF   THE    STOMACH  461 

already  explained  (page  420),  Ihan  to  find  out  the  mere  size  of  the  stomach.  If 
the  organ  empties  itself  in  a  normal  way,  any  dilatation  that  there  may  be  has 
no  significance.  If  there  is  some  tendency  to  stagnation  of  the  gastric  contents 
because  of  muscular  insufiiciencj^  we  may  have  mild  dyspeptic  symptoms,  such 
as  gastric  oppression,  eructations,  or  even  occasional  vomiting. 

If,  however,  we  find  that  the  stomach  is  dilated  and  that  the  motor  efficiency 
is  decidedly  impaired,  with  actual  stagnation  and  accumulation  of  ingesta  in 
the  stomach,  we  ourselves  think  it  is  always  justifiable  to  assume  that  there 
is  a  pyloric  stenosis.  In  such  case  the  disease  with  which  we  have  to  deal  is  not 
a  dilatation  of  the  stomach,  but  an  ulcer  or  cancer  of  the  pylorus,  which  leads 
to  stenosis  and  its  results,  as  we  have  already  described  at  length  (pages  438  and 
447).  It  has  often  been  maintained  that  in  cases  of  primary  muscular  dilata- 
tion there  may  occur  mechanical  kinks  in  the  pylorus  and  sacculations  in  the 
stomach,  so  as  to  cause  a  considerable  hindrance  to  the  emptying  of  the  viscus. 
This  may  be  possible,  but  we  have  never  seen  such  a  case,  nor  read  a  conclusive 
report  of  one. 

In  this  place  a  symptom  may  be  mentioned  which  is  often  regarded  as  a  sign 
of  dilatation.  We  refer  to  splashing  in  the  stomach  when  palpation  is  practiced 
by  a  sort  of  pushing  or  thrusting  motion.  Marked  splashing  is  indeed  very  often 
audible  in  cases  of  actual  dilatation  due  to  stenosis  of  the  pylorus,  but  it  is  very 
frequently  heard  in  persons  who  have  dyspepsia,  and  even  in  persons  who  are 
perfectly  well.  Children  sometimes  play  at  producing  splashing  sounds  in  their 
own  stomachs,  and  by  practice  acquire  great  technical  dexterity!  And  in  pre- 
cisely the  same  way  the  sound  is  produced  by  nervous  and  hypochondriacal  pa- 
tients, to  whom  the  splashing  is  a  source  of  anxiety.  Splashing  occurs  when  air 
and  fluid  are  both  present  in  the  stomach,  provided  the  abdominal  walls  as  well 
as  the  gastric  walls  are  not  too  tense.  In  this  sense  it  is,  therefore,  correct  to 
associate  so-called  atony  of  the  stomach  with  the  splashing,  because  it  may  often 
be  due  to  a  certain  laxity  of  the  muscular  coat  of  the  stomach,  but  we  should 
never  lay  any  special  stress  upon  the  sound,  unless  upon  examination  we  find  at 
the  same  time  a  distinct  disturbance  of  the  motor  efficiency  of  the  stomach. 

It  follows,  therefore,  that  mere  dilatation  of  the  stomach  is  not  an  independ- 
ent disease.  For  example,  in  practice  we  may  unhesitatingly  refer  every  case  of 
well-marked  dilatation  with  decided  stagnation  of  the  gastric  contents  to  steno- 
sis of  the  pylorus,  and  of  course  this  latter  is  to  be  regarded  as  the  true  disease. 
At  the  same  time,  however,  there  are  slight  degrees  of  gastric  dilatation,  or  per- 
haps a  better  expression  would  be  idiopathic  motor  insufficiency  of  the  stomach 
(muscular  atony  of  the  stomach),  which  occur  when  there  is  no  reason  for  be- 
lieving that  there  is  any  anatomical  change  at  the  pylorus.  We  may  assume 
that  such  motor  insufficiency  exists  when  there  is  a  slight  but  distinct  tendency 
for  food  to  accumulate  in  the  stomach. 

In  treating  this  simple  muscular  atony,  we  should  first  regulate  the  diet.  The 
separate  meals  must  not  be  too  large,  but  they  should  be  nutritious,  and  per- 
haps even  somewhat  stimulating.  Eye  bread,  small  portions  of  vegetables,  and 
nourishing  meat  dishes  are  by  no  means  interdicted.  Large  amounts  of  liquid 
are  to  be  avoided,  as  they  needlessly  dilate  the  stomach.  In  simple  atony,  lavage 
is  seldom  necessary.  At  the  most,  we  might  at  the  beginning  of  treatment  com- 
pletely empty  the  stomach  a  few  times.  Other  suitable  measures  are  cold  spon- 
ging and  rubbing  of  the  epigastrium,  the  application  of  electricity  (particularly 
the  galvanic  current)  to  the  stomach,  and  cautious  massage  of  that  region. 
Among  internal  remedies,  nux  vomica  deserves  to  be  employed. 

Whether  there  is  such  a  thing  as  abnormal  smallness  of  the  stomach,  giving 
rise  to  symptoms,  is  not  yet  known.  Perhaps  there  may  be  such  a  condition  in 
cases  in  which  feeble  and  ill-nourished  individuals,  usually  of  the  female  sex. 


462  DISEASES    OF   THE   DIGESTIVE   0EGA:N'S 

can  take  but  a  few  morsels  before  they  have  a  feeling  of  fullness  and  satiety,  and 
so  never  become  well  nourished  despite  every  effort.  We  may  find  the  stomach 
very  small  as  a  secondary  result  in  many  forms  of  inanition,  particularly  in  as- 
sociation with  stenosis  of  the  oesophagus  and  of  the  cardia. 

2.  Abnormal  Position  of  the  Stomach. — Gastroptosis. — ^Kussmaul  was  the 
first  to  call  attention  to  the  great  frequency  of  the  downward  dislocation  of  the 
stomach.  Glenard  has  written  much  about  it.  Either  the  entire  organ  may 
sink  down,  or,  what  is  more  common,  the  right  half  alone,  so  that  the  organ 
takes  a  vertical  position.  The  cause  of  this  anomaly  may  lie  partly  in  congenital 
conditions,  but  in  the  main  it  is  certainly  the  purely  mechanical  result  of  the 
pressure  of  clothing.  Gastroptosis  is  an  extremely  common  phenomenon  in  grown- 
up girls  and  women  who  wear  tightly-laced  corsets,  and  fasten  the  bands  of  their 
clothing  snugly  about  them.  It  also  occurs  in  men,  but  far  less  often.  Usually, 
with  the  gastroptosis  is  associated  a  change  in  the  position  of  other  organs,  occur- 
ring in  the  same  way.  In  particular,  the  right  kidney  becomes  abnormally  mov- 
able, and  consequently  readily  palpable  (see  the  chapter  on  movable  kidney),  and 
the  transverse  colon  sinks  down  either  in  its  right  half  or  in  its  middle  portion. 
Glenard  has  termed  this  condition  enteroptosis,  and  ascribed  to  it  an  important 
role  in  the  aetiology  of  nervous  dyspepsia  and  neurasthenia.  Well-marked  cases  of 
enteroptosis  are  most  frequent  in  women  who  have  lax  abdominal  walls  because  of 
repeated  confinements. 

The  experienced  eye  may  often  recognize,  or  at  least  surmise,  gastroptosis 
upon  external  inspection  of  the  abdomen.  One  is  struck  by  the  collapsed  appear- 
ance of  the  epigastrium,  where  one  often  feels  marked  pulsation  of  the  abdom- 
inal aorta.  Below  the  navel,  on  the  other  hand,  is  seen  a  protuberance,  the  shape 
of  which  may  quite  distinctly  suggest  the  contours  of  the  stomach.  At  this 
spot,  below  the  navel,  distinct  splashing  may  not  infrequently  be  obtained  by 
proper  palpation.  An  absolute  diagnosis  of  gastroptosis,  however,  requires  the 
artificial  inflation  of  the  stomach  (vide  supra,  page  420).  When  this  is  done  the 
abnormal  position  of  the  stomach  is  immediately  recognized.  Of  course,  the 
most  important  point  is  the  demonstration  of  a  downward  displacement  of  the 
lesser  curvature.  This  is  found  halfway  between  the  navel  and  the  epigastric 
angle,  or  often  even  at  the  level  of  the  navel.  The  downward  displacement  of 
the  greater  curvature  alone  does  not  establish  gastroptosis,  because  it  may  be 
due  to  dilatation  of  the  stomach. 

Inflation  of  the  stomach  is  such  a  simple  and  reliable  method  of  examina- 
tion that  there  scarcely  seems  any  real  necessity  for  other  methods.  Eor  this 
reason  Einhorn's  recommendation  of  electric  transillumination  of  the  stomach, 
by  means  of  an  incandescent  light  introduced  into  the  organ  ("  gastro-diaphanos- 
copy"),  is  scarcely  likely  to  become  generally  adopted  by  physicians.  It  gives 
some  indications  of  the  position  of  the  stomach,  but  the  conclusions  drawn  from 
its  use  are  by  no  means  infallible.  The  displacement  of  the  kidney,  which  is 
often  associated  with  gastroptosis,  can  be  easily  recognized  by  means  of  palpa- 
tion. The  position  of  the  colon  (coloptosis)  can  be  demonstrated  by  distending 
the  large  intestine  with  air  or  water. 

The  question  of  the  clinical  significance  of  gastroptosis  is  not  very  easy  to 
answer.  In  the  first  place,  it  should  be  remarked  that,  if  we  pay  attention  to 
the  subject,  we  shall  find  that  well-developed  gastroptosis  is  very  frequent  in  per- 
sons who  have  not  the  slightest  symptoms.  On  the  other  hand,  there  are  many 
patients,  especially  women,  who  complain  of  such  annoyances  as  pressure  and  a 
sense  of  fullness,  attacks  of  gastric  pain,  eructations,  and  occasional  vomiting, 
and  who  are  found  to  have  a  distinct  gastroptosis.  In  such  a  case  we  should 
invariably  proceed  to  test  the  secretory  and  motor  functions  of  the  stomach. 
Very  often  these  are  perfectly  normal,  and  such  a  condition  scarcely  justifies  us 


NERVOUS   DYSPEPSIA  4^ 

in  assuming'  offhand  that  there  is  a  causative  relation  between  the  gastroptosis 
and  the  patient's  symptoms.  Gastroptosis  is  so  common  that  the  relation  is  more 
likely  one  of  simple  coincidence.  If  we  make  a  searching  examination  into  the 
patient's  condition  we  shall  usually  discover  that  the  gastric  symptoms  are  asso- 
ciated with  many  other  symptoms  of  a  neurasthenic  kind,  and  hence  are  very 
likely,  for  the  most  part,  of  purely  psychical  origin  (see  the  following  chapter). 

Still,  it  can  not  be  absolutely  denied  that  certain  disagreeable  sensations  in 
the  abdomen  and  along  the  digestive  tract  may  be  directly  dependent  upon  gas- 
troptosis; and,  furthermore,  gastroptosis  in  some  few  cases  seems  to  occasion  a 
mechanical  hindrance  to  the  discharge  of  the  stomach  contents,  especially  be- 
cause of  the  vertical  position  of  the  organ,  so  that  we  have  a  sense  of  oppression 
in  the  stomach,  eructations,  and  other  symptoms;  but  this  motor  insufficiency 
should  be  proved,  not  assumed.  As  a  rule,  even  well-marked  gastroptosis  is  not 
associated  with  any  disturbance  of  the  motor  function  of  the  stomach.  There  is 
more  likelihood  that  the  habitual  constipation,  which  often  accompanies  the 
dyspeptic  symptoms  of  gastroptosis,  is  at  least  in  part  the  result  of  an  associated 
coloptosis. 

Eor  the  treatment  of  the  dyspeptic  symptoms  which  may  be  present  in  a 
ease  of  gastroptosis,  we  have  a  most  desirable  basis  in  the  gastroptosis  itself, 
although  the  author  at  least  is  convinced  that  its  main  efficacy  is  subjective. 
If  gastroptosis  has  been  made  out,  we  must  absolutely  forbid  the  wearing  of 
tightly-laced  corsets,  or  too  snugly  fitting  gowns.  It  is  often  useful  to  apply  a 
wide  abdominal  band  above  the  symphysis.  This  in  many  cases  fully  replaces 
the  more  complicated  "  abdominal  corsets  "  and  similar  apparatus.  With  regard 
to  diet,  we  forbid  the  taking  of  large  amounts  of  liquid,  and  prescribe  nourishing 
food  that  is  not  bulky.  Particularly  when  patients  are  emaciated  and  appre- 
hensive, we  often  do  the  greatest  good  by  ordering  a  highly  nutritious  diet.  The 
region  of  the  stomach  should  be  rubbed  briskly  once  or  twice  a  day  with  cold 
water  or  brandy.  The  employment  of  faradic  and  galvanic  electricity  or  mas- 
sage is  particularly  indicated  when  constipation  is  present. 

Of  course  we  must  pay  attention,  as  we  have  said,  to  the  general  neurasthenic 
condition,  which  is  usually  also  present.  In  this  regard  great  importance  at- 
taches to  a  suitable  mental  treatment,  in  order  to  free  the  patient  from  her  exag- 
gerated anxiety  and  apprehension. 


CHAPTER  IX 

^TERVOUS    DYSPEPSIA 

{Gastric  Neurasthenia) 

We  have  repeatedly  indicated  in  the  preceding  chapter  that  many  disturb- 
ances of  the  gastric  functions  may  be  due  to  changes  in  the  innervation  of  the 
stomach,  or  to  actual  disease  of  its  nerves;  thus  some  have  been  inclined  to 
refer  the  disturbances  of  the  secretion  of  the  gastric  juice,  such  as  hyperacidity 
and  hypersecretion,  to  abnormal  conditions  of  the  secretory  nerves.  Many  cases 
of  "  cardialgia  "  have  been  regarded  as  pure  "  neuralgia  "  of  the  sensory  nerves 
of  the  stomach;  and  also  in  the  domain  of  the  muscular  activity  of  the  stom- 
ach, authors  have  distinguished  conditions  of  nervous  weakness  (nervous  atony 
of  the  stomach)  and  of  nervous  irritability  of  the  muscular  coat  (so-called 
"  peristaltic  unrest "  of  the  stomach ;  constant  rumbling  in  the  stomach  and 
similar  symptoms).     There  is  no  doubt  that  in  cases  of  severe  organic  disease  of 


464:  DISEASES    OF   THE   DIGESTIVE    OEGANS 

the  nervous  system  there  may  be  'well-marked  gastric  symptoms  as  direct  conse- 
quences of  nervous  irritation — for  example,  we  have  nervous  vomiting  in  cerebral 
tumor  and  meningitis,  and  gastric  crises  in  tabes.  It  is,  therefore,  not  impos- 
sible that  there  may  also  be  primary  diseases  of  the  sensory,  motor,  and  secre- 
tory nerves  of  the  stomach  with  corresponding  symptoms,  but  this  is  by  no  means 
proved,  and  it  is  certain  that  such  actually  "  nervous  "  gastric  diseases  are  very 
rare,  if  they  occur  at  all.  At  present,  clinical  experience  does  not  justify  us  in 
putting  in  this  category,  with  any  degree  of  certainty,  any  disorder  except  the 
state  above  described  (page  459),  in  which  there  is  periodical  vomiting  with  gas- 
tric pain  and  hypersecretion. 

There  are  numerous  cases  which  are  at  present  habitually  termed  nervous 
dyspepsia,  but  in  our  opinion  the  overwhelming  majority  of  these  have  an  origin 
different  from  the  one  implied.  Such  patients  assert  that  after  every  meal 
they  have  pressure  and  pain  in  the  stomach,  that  after  a  few  mouthfuls  the 
stomach  feels  full  and  distended,  and  consequently  they  often  have  palpitation 
and  a  troublesome  feeling  of  constraint  in  the  chest.  The  patients  frequently 
complain  of  eructations  also,  and  occasionally  of  vomiting.  These  symptoms 
are  all  such  as  occur  in  the  same  way  in  actual  diseases  of  the  stomach,  but  in 
these  patients  there  are  usually  certain  other  symptoms  present,  which  indicate 
the  nervous  character  of  the  disease.  In  the  first  place,  it  is  noticeable  that  the 
above  symptoms  display  striking  variations  in  their  severity.  The  same  patient 
who  to-day  complains  of  great  distress  in  his  stomach  after  a  few  spoonfuls  of 
soup,  at  another  time,  when  he  is  in  a  happy  and  lively  frame  of  mind,  will  eat  a 
large  dinner  without  being  reminded  that  he  has  a  stomach;  but  as  soon  as  he 
gets  angry  or  irritated,  or,  in  brief,  in  a  "  sensitive  "  condition,  the  gastric  symp- 
toms appear  at  once  in  an  exaggerated  form.  On  all  such  occasions,  therefore, 
we  see  most  clearly  the  influence  of  the  imagination  and  of  general  psychical 
irritation  on  the  behavior  of  the  stomach.  Every  one  knows  that  a  violent  rage 
or  any  experience  arousing  anxiety  or  hope — any  excitement,  sad  or  joyful — ^may 
imraediately  destroy  the  appetite;  and  very  great  mental  disturbance  not  infre- 
quently also  causes  vomiting  or  similar  symptoms.  In  the  same  way  in  sensitive 
individuals  even  the  mildest  psychical  influences  produce  similar  results;  but 
in  this  regard  there  is  nothing  which  has  so  unfavorable  an  influence  as  that 
state  of  psychical  disturbance  which  is  associated  with  great  concern  for  one's 
own  health — that  is,  a  condition  of  hypochondriacal  anxiety — anxiety  lest 
something  which  has  been  eaten  may  do  damage;  constant  dread  that  a  grave 
disorder  of  the  stomach  may  be  developing.  These  mental  disturbances  are  es- 
pecially influential  in  maintaining  and  progressively  aggravating  the  abnor- 
mal condition.  This  is  the  explanation  of  that  peculiar  psychical  hypersesthesia 
which  feels  the  acutest  "  pain "  in  the  stomach,  when  there  is  really  nothing 
but  a  perfectly  normal  general  sensation.  And  the  same  explanation  applies 
to  certain  muscular  contractions — half  unconscious,  half  voluntary — ^which 
occasion  eructations,  vomiting,  and  similar  phenomena.  The  patient  has  some 
symptoms  which  he  feels  subjectively,  and  some  which  seem  to  him  to  be  actually 
objective,  and  they  are  in  part  the  result  of  pure  imagination  (or  "  auto-sug- 
gestion") and  in  part  the  physiologically  necessary  consequence  of  the  great 
psychical  disturbance. 

What  we  wish  to  emphasize  is  our  conviction  that  in  the  great  majority  of 
cases  of  nervous  dyspepsia  we  are  not  dealing  with  any  functional  disturbance  of 
the  gastric  nerves,  but  with  abnormal  "  psychogenic  "  irritations  of  the  central 
nervous  system,  the  results  of  which  are  apparent  mainly  in  the  domain  of  the 
gastric  functions.  iN'ervous  dyspepsia  is  merely  one  example  of  that  great  group 
of  nervous  diseases  which  owe  their  origin  mainly  to  hypochondriacal  disturb- 
ances of  mind,  and  which  may  appear  in  the  most  diverse  organs.     It  is  properly 


NEEVOUS   DYSPEPSIA  465 

notliing  but  a  symptom  of  the  constitutional  "  nervousness  "  or  neurasthenia,  and 
is  therefore  termed  by  many  physicians,  with  absolute  correctness,  gastric  neu- 
rasthenia. By  careful  clinical  observation  it  is  easy  to  demonstrate  that  almost 
all  the  ordinary  gastric  symptoms  may,  under  favorable  circumstances,  be 
excited  by  purely  psychical  influences.  It  is  evident  that  anorexia  is  often  the 
result  of  simple  mental  disturbance,  especially  when  of  a  hypochondriacal  char- 
acter; but  excessive  craving  for  food  (bulimia)  is  certainly  in  most  cases  also 
of  purely  psychical  origin,  arising  from  special  imperative  conceptions.  There 
is  no  doubt  that  the  most  varied  abnormal  sensations,  ranging  from  simple 
oppression  to  a  most  acute  pain  in  the  stomach,  may  have  a  purely  subjective 
origin.  The  best  proof  of  this  lies  in  the  often  apparently  miraculous  efl'ect  of 
remedies  which  have  a  purely  suggestive  and  psychical  influence  (simple  reassur- 
ance of  the  patient,  hypnotism,  and  various  external  and  internal  remedies).  It 
is  very  important  to  know  that  in  many  cases  also  eructations  and  vomiting  have 
a  merely  psychical  and  central  origin.  They  are  due  to  the  influence  of  certain 
ideas  which  make  the  eructations  or  vomiting  appear  unavoidable,  and  the 
action  at  first  is  due  to  unconscious  volition,  and  finally  becomes  a  sort  of  dis- 
eased habit.  Many  nervous  and  hypochondriacal  patients  who  regard  them- 
selves as  dyspeptics  become  true  virtuosi  in  eructations  and  vomiting,  the  reflex 
process  becoming  easier  and  easier  because  of  repetition,  and  being  excited  by 
unconscious  volition.  General  psychical  disturbance  may  also  cause  eructations 
and  vomiting  by  direct  stimulation.  We  know  persons  who  are  attacked  with 
nausea  and  vomiting  upon  any  great  excitement.  Even  in  children  it  is  by  no 
means  rare  to  observe  persistent  vomiting  after  almost  every  meal,  and  that  this 
is  of  a  purely  "  nervous  "  character  appears  from  the  rapid  beneficial  effect  of 
exclusively  psychical  treatment — e.  g.,  if  the  child  is  strictly  forbidden  to  vomit. 
"We  often  see  just  the  same  condition  in  adolescent  girls,  frequently  associated 
with  other  hysterical  symptoms.  In  this  connection  it  should  be  briefly  men- 
tioned that  there  may  be  a  "  nervous  " — that  is,  hysterical — hsematemesis.  (For 
particulars  in  regard  to  this,  the  reader  is  referred  to  the  chapter  on  hysteria; 
and,  in  general,  the  chapters  on  hysteria  and  neurasthenia  should  be  referred  to 
as  supplementing  what  has  been  said  here.) 

Very  often  other  nervous  symptoms  are  observed  besides  those  referred  to 
the  stomach.  There  are  signs  of  excessive  mental  irritability,  symptoms  ref- 
erable to  the  head,  such  as  headache,  pressure  in  the  head,  vertigo;  abnormal 
sensations  in  the  extremities,  of  pain,  coldness,  numbness,  and  the  like.  There 
are  almost  invariably,  also,  certain  attendant  intestinal  symptoms.  The  patient 
complains  of  bloating  of  the  abdomen,  and  of  irregular  and  sluggish  bowels. 

ISTervous  dyspepsia  becomes  a  more  serious  matter  when  the  patient  is  pre- 
vented from  taking  sufficient  nourishment,  by  fear  of  committing  errors  in  diet, 
and  because  of  the  loss  of  appetite  which  his  mental  uneasiness  occasions.  There 
are  sometimes  complete  nervous  anorexia,  a  constant  dread  of  eating  or  an  actual 
aversion  toward  any  food,  and  a  considerable  or  excessive  emaciation,  usually 
associated  with  great  bodily  weakness.  Such  patients  finally  take  to  their  beds 
and  give  the  impression  of  severe  illness. 

Diagnosis. — In  many  cases  the  experienced  physician  can  make  an  extremely 
probable  diagnosis  of  nervous  dyspepsia  merely  from  the  symptoms  which  the 
patient  enumerates.  The  true  condition  is  suggested  by  the  general  nervous- 
ness, by  the  prominence  of  anxiety  and  of  hypochondriacal  notions,  the  variabil- 
ity of  the  symptoms  and  their  relation  to  psychical  irritation,  and  the  other 
attendant  symptoms  of  a  nervous  character,  such  as  headache,  vertigo,  palpita- 
tion, and  a  sense  of  oppression.  Still,  it  is  easy  to  be  deceived,  because  the  symp- 
toms seem  to  be  so  objective  that  the  physician  feels  constrained  to  believe  thnt 
there  is  some  organic  disease  of  the  stomach,  although  none  exists,  and  because, 
30 


466  DISEASES    OF    THE   DIGESTIVE   OEGANS 

on  the  other  hand,  an  actual  disease  of  the  stomach  may  he  present  in  a  yery 
nervous  individual  and  fail  to  be  recognized,  being  wholly  obscured  by  the  gen- 
eral nervous  phenomena.  Eor  this  reason,  even  in  cases  which  seem  to  be  the 
most  simple,  we  would  do  well  to  make  a  careful  objective  examination,  and  this 
is  of  course  an  absolute  necessity  in  all  cases  which  are  obstinate  and  severe. 

Often  the  objective  examination  shows  clearly  normal  conditions  in  every 
respect :  the  external  examination  is  normal,  and  the  position,  secretion,  and 
motility  of  the  stomach  are  normal.  In  such  a  case  the  diagnosis  is  established, 
and  the  mere  result  of  examination  will  often  have  a  most  beneficial  effect  upon 
the  patient.  For  this  reason  a  painstaking  examination  is  often  the  best  rem- 
edy for  many  patients  with  nervous  dyspepsia.  It  is  more  difficult  to  reach  a 
conclusion  when  certain  abnormalities  are  found,  although  there  are  no  signs 
of  indubitable  organic  disease — that  is,  there  is  no  tumor  nor  evidence  of  steno- 
sis of  the  pylorus  nor  genuine  haemorrhage — but  we  do  find,  for  example, 
distinct  hyperacidity  or  hypersecretion;  less  often  achlorhydria ;  very  frequently 
gastroptosis ;  and  often,  it  is  said  (although,  according  to  the  author's  experi- 
ence, this  is  rare),  some  slight  disturbance  of  motility,  so-called  atony  of  the 
muscular  coat  of  the  stomach.  How  shall  such  cases  be  interpreted?  Shall  we 
always  lay  stress  exclusively  upon  the  objective  anomalies  which  are  discovered, 
and  refer  to  them  every  one  of  the  many  symptoms  the  patient  enumerates  ?  In 
the  author's  opinion,  this  would  often  be  erroneous.  It  has  been  especially 
emphasized  in  the  preceding  chapters  that  the  conditions  mentioned  are  frequent 
and  are  apt  to  cause  no  symptoms  at  all,  so  that  if  we  find  associated  with  well- 
marked  nervous  dyspepsia  a  gastroptosis,  or  a  moderate  hypersecretion,  or  achlor- 
hydria, in  many  cases  the  association  is  a  mere  chance  coincidence  without  sig- 
nificance. We  think  that  such  conditions  should  not  be  wholly  disregarded,  but 
yet  their  clinical  importance  should  not  be  overestimated;  and  from  a  therapeu- 
tic point  of  view,  also,  they  should  be  borne  in  mind,  but  never  to  the  neglect 
of  that  general  psychical  treatment  which  is  usually  much  more  important. 
Such  conditions  also  are  very  useful  as  a  handle  for  mental  therapeutics  (as  we 
have  already  pointed  out),  because  of  the  favorable  effect  which  treatment  of 
them  has  upon  the  mind  of  the  patient. 

A  most  difficult  question  in  diagnosis,  in  our  opinion,  is  to  distinguish  be- 
tween ulcer  and  nervous  dyspepsia  when  there  is  distinct  hypersecretion  without 
evident  signs  of  ulcer  (see  page  458).  In  such  a  case  all  the  separate  symp- 
toms must  be  duly  considered,  and  yet  we  may  be  obliged  to  await  the  further 
development  of  the  disease  and  the  results  of  treatment  before  arriving  at  a 
conclusion.  Patients  with  nervous  dyspepsia  are  apt  to  grow  worse  and  worse 
under  strict  treatment  for  ulcer,  while  an  opposite  mode  of  treatment  (vide 
infra)  often  has  the  most  brilliant  results. 

Prognosis. — The  prognosis  depends  mainly  on  the  outward  circumstances  of 
the  patient.  If  the  harmful  mental  influences  or  other  setiological  factors  are 
persistently  active,  actual  and  permanent  recovery  is  hardly  to  be  expected ;  but  if 
the  cause  can  be  removed,  complete  recovery  is  not  rare,  even  in  what  seem  to  be 
grave  cases.  A  liability  to  relapses  is,  of  course,  almost  always  left  behind,  as 
most  patients  are  constitutionally  nervous. 

Treatment. — If  nervous  dyspepsia  has  once  been  diagnosticated,  the  proper 
aim  of  our  therapeutic  efforts  becomes  perfectly  definite.  We  must,  in  the  first 
place,  convince  the  patient  that  he  has  no  incurable  or  even  dangerous  gastric 
disease,  but  that,  on  the  contrary,  his  stomach  is  perfectly  capable  of  performing 
its  functions  in  a  normal  manner.  !N"othing  could  be  more  harmful  to  a  sufferer 
from  nervous  dyspepsia  than  to  have  his  physician  manifest  great  anxiety  about 
treatment,  and  prescribe  a  very  strict  diet.  The  patient  must  rather  be  grad- 
ually led  to  use  an  abundance  of  nutritious  food.     It  is  in  this  way  alone  that 


NEEVOUS   DYSPEPSIA  467 

he  regains  a  confidence  in  himself,  when  he  sees  that  the  hearty  food  does  him  no 
harm,  that  he  is  gaining  flesh,  and  that  the  bowels  are  becoming  regular. 

Internal  remedies  are  best  omitted  altogether  if  the  patient  has  already  taken 
a  good  deal  of  medicine.  If  they  are  successful,  it  is  usually  because  of  their 
influence  on  the  mind.  It  is  very  important  to  make  sure  that  there  is  no  abuse 
of  purgatives.  If  we  must  prescribe  some  medicine,  the  bitter  tonics  are  most 
suitable,  particularly  the  tincture  of  nux  vomica.  For  anaemic  patients,  we  may 
order  iron,  quinine,  or  arsenic.  For  nervous  vomiting  and  eructations,  bro- 
mide of  potassium  is  to  be  given,  or  antipyrine  and  similar  remedies.  Treatment 
with  cold  water  and  with  electricity  are  often  extremely  beneficial,  although 
probably  their  effect  is  mainly  subjective,  for  in  cases  of  this  sort  psychical  treat- 
m.ent  is  of  the  greatest  importance.  Even  if  we  gravely  command  the  patient 
not  to  yield  to  the  impulse  to  vomit,  but  to  resist  it  as  much  as  possible,  siich  an  in- 
junction will  often  do  away  with  the  symptom,  and  it  is  not  rare  to  find  in  cases 
of  nei^ous  vomiting  that  it  will  cease  as  soon  as  nourishing  diet  is  allowed, 
although  previously  it  has  occurred  invariably  after  the  most  delicate  kinds  of 
food.  It  is  often  very  advantageous  in  nervous  vomiting  to  limit,  as  far  as  pos- 
sible, the  amount  of  liquids,  such  as  soup  and  milk,  and  to  prescribe  a  dry  sub- 
stantial diet.     In  many  cases  the  vomiting  will  then  cease  very  promptly. 

If  there  are  certain  objective  abnormalities  present  as  well  as  the  purely  nerv- 
ous symptoms,  we  must  pay  a  certain  amount  of  attention  to  these  (vide  supra). 
If  there  is  gastroptosis,  we  should  forbid  constriction  of  the  waist  by  the  cloth- 
ing, and  should  order  a  suitable  abdominal  bandage.  If  there  is  hypersecretion, 
we  should  employ  alkalies,  or  possibly  lavage ;  if  achlorhydria,  hydrochloric  acid. 

Those  methods  of  treatment  are  of  great  value  which  are  directed  to  the  ton- 
ing up  of  the  body  in  general  and  the  nervous  system  in  particular.  The  patient 
m.ay  go  into  the  country  or  to  the  mountains  or  the  seashore.  Methodical  treat- 
ment with  cold  water  is  good;  in  particular,  sponging  combined  with  rubbing  of 
the  trunk  and  the  whole  body  almost  always  gives  good  results.  On  the  other 
hand,  those  health-resorts  which  often  do  good  in  the  case  of  organic  gastric  dis- 
ease are  but  seldom  beneficial  in  nervous  dyspepsia.  Thus,  we  have  frequently 
seen  such  patients,  who  had  been  sent  by  their  physicians  to  Carlsbad,  return 
worse  rather  than  better.  We  have  repeatedly  found  electricity  valuable,  al- 
though we  surmise  that  its  subjective  effect  may  be  of  chief  importance.  Gal- 
vanism is  applied  along  the  spinal  column,  and  also  through  the  stomach  horizon- 
tally, one  large  electrode  being  placed  upon  the  epigastrium  and  the  other  on  the 
back.  It  is  well  to  reverse  the  current  frequently.  Faradization  and  massage 
of  the  abdominal  walls  are  indicated,  especially  when  there  is  constipation. 

We  need  hardly  add  that  the  aetiological  factors  must  not  be  overlooked.  The 
patient  must  be  warned  against  mental  or  bodily  overexertion,  emotional  excite- 
ment, etc.  The  main  point  is  to  aim  at  a  methodical  moral  training  of  the 
patient.  He  should  learn  to  feel  and  to  behave  like  a  healthy  person.  He  should 
regain  his  self-control,  and  not  allow  himself  to  be  upset  by  every  slight  psychical 
shock,  whether  subjective  or  coming  from  without.  It  is  self-evident  that  this 
goal  is  to  be  attained  not  by  baths  and  prescriptions,  but  by  correct  moral  guid- 
ance. The  best  proof  of  the  correctness  of  our  views,  with  regard  to  the  true 
nature  of  this  disease,  lies  in  the  therapeutic  successes  which  can  be  obtained  in 
this  manner  alone,  although  it  is  a  pity  that  they  are  more  often  achieved  by 
empirics  and  quacks  than  by  scientifically  educated  physicians.  It  is  therefore 
true  of  nervous  dyspepsia,  as  of  all  other  similar  neurasthenic  conditions,  that 
it  is  to  be  cured  not  by  physic  but  by  the  physician. 


468  DISEASES    OE   THE   DIGESTIVE    OEGAl^S 

SECTION  V 

Diseases  of  the  Intestines 

CHAPTEE   I 

INTESTINAL    CATARRH 

( Catarrhal  Enteritis) 

etiology. — The  majority  of  cases  of  intestinal  catarrh,  like  gastric  catarrh, 
are  due  to  an  abnormal  irritation  of  the  mucous  membrane  of  the  intestine  by 
its  contents.  In  many  cases  the  irritants  are  of  a  mechanical  or  a  chemical 
nature,  and  depend  upon  the  quantity  and  quality  of  the  food  taken,  which  ex- 
plains why  catarrh  of  the  stomach  and  catarrh  of  the  intestine  are  so  often  com- 
bined with  each  other.  iNToxious  substances,  taken  into  the  system  by  the  inges- 
tion of  spoiled  food,  such  as  spoiled  meat,  fish,  beer,  etc.,  very  often  play  a  part  in 
the  origin  of  intestinal  catarrh. 

To  the  intestinal  catarrhs  caused  by  improper  food  we  may  add  the  toxic 
catarrhs  which  are  produced  by  the  direct  ingestion  of  poisonous  substances  into 
the  digestive  tract.  Severe  inflammations  of  the  intestinal  mucous  membrane 
arise  from  poisoning  by  mineral  acids  and  corrosive  alkalies,  arsenic,  corrosive 
sublimate,  etc.  Intestinal  catarrh  may  also  arise  from  the  imprudent  use  of 
certain  drugs,  especially  active  cathartics. 

A  great  many  cases  of  intestinal  catarrh  are  due  to  infectious  influences; 
these  include  most  of  the  apparently  spontaneous  catarrhs,  and  also  many,  if  not 
all,  of  the  catarrhs  attributed  to  taking  cold  or  getting  wet,  and,  finally,  those 
affections  which  often  develop  epidemically  or  endemically  in  hot  weather,  and 
which  we  term  summer  complaint,  cholera  morbus,  etc.  Cholera  morbus  is  an 
especially  severe  form,  and  it  will  be  described  more  fully  later  on.  We  must  also 
mention  here  that  intestinal  catarrh  is  very  often  one  symptom  of  other  general 
infectious  diseases,  such  as  typhoid,  dysentery,  septic  diseases,  or  severe  malaria. 

In  a  final  class  of  cases  intestinal  catarrh  develops  from  disturbances  of  the 
circulation,  which  cause  a  passive  hypersemia  of  the  intestinal  mucous  membrane. 
Diseases  of  the  liver  and  portal  vein,  aiid  also  chronic  diseases  of  the  heart,  kid- 
neys, and  lungs,  are  the  chief  affections  which  produce  a  stasis  in  the  portal  sys- 
tem, and  thus  an  intestinal  catarrh;  but  here  the  stasis  is  probably,  in  most  cases, 
only  a  predisposing  factor  in  the  development  of  the  catarrh,  since  the  action  of 
all  other  irritants  is  made  easier  by  the  disturbance  of  the  circulation. 

The  great  frequency  of  intestinal  catarrh  in  both  sexes,  and  at  every  age,  is 
well  known.  Children,  above  all,  have  a  pronounced  tendency  to  diseases  of 
the  intestine,  so  that,  by  a  probable  estimate,  almost  one  third  of  the  illnesses 
of  children  are  to  be  referred  to  the  intestinal  canal.  We  will  give  a  special 
description  of  intestinal  catarrh  in  children  on  account  of  this  fact. 

Pathological  Anatomy. — The  pathological  changes  in  catarrhal  inflammation 
of  the  intestines  are  essentially  the  same  as  are  met  with  in  the  inflammation 
of  any  other  mucous  membrane.  Redness  and  swelling  of  the  mucous  coat, 
increased  secretion  of  mucus,  and  in  severe  cases  purulent  products  on  the  sur- 
face of  the  membrane,  and  a  cellular  infiltration  of  the  tissue  itself,  are  the  well- 
known  processes  characteristic  of  all  catarrhal  inflammations.  The  solitary  and 
agminated  follicles  often  swell  in  follicular  catarrh,  and  they  may  finally  become 
the  seat  of  superficial  follicular  ulcers.  We  often  find  superficial  erosions  on 
the  rest  of  the  mucous  membrane,  and  in  severe  cases  the  so-called  catarrhal 
ulcers. 


INTESTINAL   CATAEEH  469 

If  the  catarrh  has  lasted  a  long  time,  we  sometimes  find  a  considerable  thick- 
ening of  the  mucous  membrane,  which  is  due  to  hyperplasia  of  the  connective 
tissue,  and  gives  an  uneven,  puffy  appearance  to  the  internal  surface  of  the 
intestine.  Circumscribed  hyperplasia  of  the  connective  tissvie  may  actually  lead 
to  the  formation  of  polypi.  If  the  orifices  of  Lieberklilin's  follicles  are  stopped, 
we  have  a  cystic  degeneration  of  the  follicles  from  the  retention  of  the  intestinal 
juice. 

We  very  often  find,  however,  a  considerable  atrophy  of  the  mucous  membrane, 
especially  in  the  chronic  intestinal  catarrh  of  children.  This  atrophy,  which  has 
lately  been  carefully  investigated,  especially  by  JSTothnagel,  affects  chiefly  the 
glandular  layer  of  the  mucous  coat.  In  place  of  the  glands,  which  in  many  parts 
may  wholly  disappear,  we  find  connective  tissue  more  or  less  rich  in  cells.  The 
atrophy  is  usually  most  pronounced  in  the  colon  and  the  lower  part  of  the  ileum. 
The  muscular  coat  may  also  take  part  in  the  atrophy. 

Certain  peculiarities  of  catarrh  affecting  single  portions  of  the  intestine  will 
be  mentioned  later  on. 

Symptomatology. — The  symptom  by  which  chiefly  we  determine  an  affection 
of  the  intestinal  canal,  and  which  in  the  milder  cases  is  often  almost  the  only 
sign  of  an  intestinal  catarrh,  is  diarrhoea — that  is,  abnormally  frequent  stools  of  a 
looser  consistency  than  usual;  yet,  strictly  speaking,  we  should  not  attribute 
every  diarrhoea  to  a  catarrh  of  the  intestinal  mucous  membrane,  since  a  large 
number  of  influences  may  directly  produce  an  increased  peristalsis  and  a  conse- 
quent diarrha3a.  Thus,  for  instance,  it  is  a  well-known  fact  that  sudden  terror  or 
great  anxiety  may  sometimes  cause  an  obstinate  diarrhoea  in  a  very  short  time. 
In  general  nervous  and  neurasthenic  conditions,  we  sometimes  have  a  chronic 
diarrhoea  which  can  be  due  only  to  abnormal  processes  of  innervation — "  nervous 
diarrhoea."  The  diarrhoea  which  may  arise  immediately  after  taking  cold  is  also 
merely  the  result  of  abnormally  great  peristaltic  movements  excited  in  a  reflex 
manner.  Probably  a  number  of  chemical  and  infectious  irritants  may  also  stimu- 
late the  movements  of  the  intestines,  and  thus  set  up  a  diarrhoea,  without  causing 
at  the  same  time  a  catarrh  of  the  mucous  membrane.  Practically,  however,  we 
can  not  make  a  sharp  distinction  between  diarrhoea  and  intestinal  catarrh;  and, 
in  most  of  the  diarrhoeas  which  have  lasted  for  some  time,  we  are  certainly  right 
in  supposing  that  there  are  actual  anatomical  lesions  of  the  intestine,  as  well  as 
functional  disturbances. 

There  are  two  chief  factors  which  cause  diarrhoea  in  intestinal  catarrh.  In  the 
first  place,  as  has  already  been  intimated,  the  same  injurious  substances  which 
cause  the  catarrh  also  excite  peristalsis.  The  many  products  of  the  abnormal 
processes  of  decomposition  in  the  intestine  also  exert  a  like  influence.  Besides  the 
abnormal  irritants,  however,  we  ought  also  to  consider  an  abnormally  great  irri- 
tability of  the  intestinal  walls  in  catarrh.  Thus  it  happens  that  the  fluid  contents 
of  the  intestine  are  expelled  by  the  vigorous  peristaltic  movements  (which  the 
liatient  himself  often  feels  as  a  "rumbling  in  the  abdomen"),  before  the  normal 
consolidation  of  the  faeces  is  completed  by  the  absoi-ption  of  water.  The  food, 
under  normal  conditions,  passes  through  the  small  intestine  in  two  or  three  hours, 
and  thus  the  consolidation  of  the  fasces  takes  place,  as  is  well  known,  almost  ex- 
clusively in  the  colon.  We  see,  therefore,  why  the  diarrhoea  owes  its  origin 
chiefly  to  the  increased  peristalsis  of  the  large  intestine ;  although  in  many  cases 
the  peristaltic  action  of  the  small  intestine  is  also  increased. 

Besides  increased  peristalsis,  another  circumstance  may  perhaps  contribute  to 
the  diarrhoea,  viz.,  the  greater  fluidity  of  the  contents  of  the  intestine  due  to  the 
increased  secretion  of  mucus  and  the  exudation  caused  by  the  catarrhal  inflam- 
mation. 

In  the  intestinal  catarrh  due  to  passive  congestion  we  must  consider  still  an- 


470  DISEASES    OF   THE   DIGESTIVE   OEGANS 

other  factor,  to  explain  the  thin  and  watery  stools — namely,  the  diminished  ab- 
sorption of  water  by  the  intestine  from  disturbance  of  the  circulation.  In  other 
catarrhs  this  factor  is  quite  subordinate  to  increased  peristalsis. 

The  diarrhoeal  dejections  show  a  considerable  difference  in  regard  to  their 
minor  characteristics.  Their  number  varies  very  much.  There  are  sometimes 
two  or  three,  and  sometimes  ten  or  more,  evacuations  in  the  twenty-four  hours. 
The  consistency  of  the  stools  is  pap-like,  or  almost  wholly  watery.  This  is  due 
to  the  abnormal  amount  of  water  in  them,  amounting  to  ninety  or  ninety-five  per 
cent.,  while  the  amount  in  normal  stools  is  about  seventy-five  per  cent.  The 
color  of  the  thin  stools  in  intestinal  catarrh  is  usually  bright  yellow,  but  they  are 
sometimes  greenish  from  the  admixture  of  bile  pigment,  and  sometimes  slimy 
(vide  infra). 

In  only  a  part  of  the  cases  does  microscopic  examination  give  us  information 
as  to  the  extent  and  intensity  of  the  catarrh.  We  usually  find  the  remains  of  the 
food,  muscular  fibers,  starch-granules,  and  fat,  and  also  countless  bacteria,  and 
often  triple  phosphates,  occasional  pus-corpuscles,  and  cylindrical  epithelium — 
chiefly  the  constituents  which  are  found  in  normal  stools.  Further  peculiarities 
will  be  mentioned  below. 

Besides  the  diarrhoea,  there  is  often,  but  by  no  means  always,  abdominal  pain 
in  intestinal  catarrh,  either  continuous,  or  having  the  character  of  paroxysmal, 
so-called  colicky  pains.  In  catarrh  of  the  rectum  there  is  that  constant  painful 
desire  to  go  to  stool  which  we  term  tenesmus. 

Physical  examination  of  the  abdomen  gives,  on  the  whole,  few  important 
results.  Sometimes  the  abdomen  is  flat,  and  sometimes  there  is  meteorism. 
Marked  peristaltic  action  of  the  intestines  often  causes  gurgling  and  rumbling 
noises — horhorygmi.  On  palpation,  the  abdomen  is  often  somewhat  sensitive. 
The  peculiar  colicky  pains,  however,  are,  as  a  rule,  alleviated  by  external  pressure. 
In  rare  cases  we  may  detect  a  fluctuation  on  palpation,  if  the  intestine  contains 
much  fluid.  The  results  of  percussion  depend  largely  upon  the  contents  of  the 
intestines.  There  is  dullness  on  percussion  if  the  intestines  are  full,  and  also  if 
they  are  contracted  and  devoid  of  air. 

In  many  cases  of  simple  diarrhoea  the  general  health  is  practically  unaffected, 
but  in  other  cases  of  acute  intestinal  catarrh,  especially  in  the  severe  infectious 
forms,  the  disturbance  of  the  general  health  may  be  considerable.  The  patient 
feels  so  dull  and  weak  that  he  stays  in  bed.  We  often  see  a  moderate  rise  of  tem- 
perature, between  100°  and  102°  (38°-39°  C).  There  are  very  often  gastric 
symptoms  also,  especially  loss  of  appetite  and  vomiting.  Other  organs  are  quite 
rarely  affected,  except  in  duodenal  catarrh,  when  the  liver  is  involved  (vide  infra). 
In  acute  infectious  intestinal  catarrhs,  there  is  sometimes  an  eruption  of  herpes 
on  the  lips.  We  have  repeatedly  seen,  in  severe  cases  of  acute  enteritis,  marked 
muscular  and  articular  pains,  and  even  slight  but  manifest  swelling  of  the  joints. 
There  may  also  be  albuminuria,  casts,  and  even  the  signs  of  acute  nephritis,  as 
a  sequel  of  enteritis. 

Different  Forins  of  Intestinal  Catarrh. — Since  the  intestine  is  an  organ 
which  is  only  slightly  accessible  to  physical  examination  during  life,  and  since 
we  can  only  rarely  make  a  post-mortem  examination  in  the  mild  diseases  of  the 
intestine,  our  knowledge  as  to  the  different  forms  of  enteritis  is  defective  in  many 
respects.  In  practice  we  content  ourselves  in  most  cases  with  diagnosticating  an 
intestinal  catarrh  simply  from  the  existence  of  diarrhoea,  without  laying  much 
stress  upon  the  special  variety;  but  in  many  cases  some  points  can  be  obtained 
which  give  more  accurate  information  as  to  the  seat  of  the  catarrh.  The  distinc- 
tion between  acute  and  chronic  intestinal  catarrh  is  also  of  practical  significance. 

Duodenal  catarrh  can  be  diagnosticated  only  if  it  is  combined  with  jaundice. 
The  details  regarding  it  may  be  found  in  the  chapter  on  catarrhal  jaundice. 


INTESTINAL   CATAERH  4:Y1 

Isolated  catarrh  of  the  small  intestines,  of  the  jejunum  and  ileum,  is  probably 
only  of  rare  occurrence,  except  when  the  upper  portions  of  the  colon  are  involved. 
We  can  very  rarely  diagnosticate  it  with  certainty,  but  there  are  a  number  of  fac- 
tors which  permit  us  to  decide  that  the  small  intestine  is  chiefly  affected,  or  at 
least  that  it  is  involved  in  the  disease.  In  the  first  place,  we  may  assume  an  affec- 
tion of  the  small  intestine,  from  obvious  reasons,  in  all  those  cases  in  which  there 
are  also  gastric  disturbances.  It  is  evident  that,  in  the  frequent  combination  of 
gastric  and  intestinal  catarrh,  the  portions  of  the  intestine  nearest  the  stomach 
will  be  chiefly  affected.  Physical  examination  of  the  abdomen  also  gives  some 
indications,  since  the  slight  sensitiveness  and  swelling  of  the  abdomen,  as  well  as 
the  visible  abnormal  peristaltic  action,  affect  chiefly  the  middle  and  lower  por- 
tions of  the  abdomen  in  catarrh  of  the  small  intestines,  while  the  analogous 
symptoms  in  catarrh  of  the  large  intestine  affect  the  lateral  and  upper  por- 
tions of  the  abdomen,  corresponding  to  the  anatomical  course  of  the  colon.  We 
can  not  make  a  sharp  distinction,  however,  in  this  respect.  The  results  which 
auscultation  and  percussion  over  the  abdomen  give  in  regard  to  the  point  of  origin 
of  the  gurgling  sounds  and  the  fullness  of  the  loops  of  intestine  are  very  rarely 
unequivocal,  and  hence  are  of  little  value  in  diagnosis. 

Careful  examination  of  the  stools  gives  us  more  information.  As  has  already 
been  said,  we  need  not  have  diarrhoea  in  a  catarrh  confined  to  the  small  intestines, 
since  diarrhoea  is  due  only  to  the  increased  peristalsis  of  the  large  intestine ;  hence 
diarrhoea  is  absent,  for  example,  in  most  cases  of  duodenal  catarrh  (catarrhal 
jaundice).  In  more  extensive  catarrh  of  the  small  intestines  the  firm  stools 
passed  may,  however,  be  regarded  as  pathological,  because,  on  microscopic  exami- 
nation, they  appear  intimately  mixed  with  little  lumps  of  hyaline  mucus  (Noth- 
nagel).  As  a  rule,  of  course,  catarrh  of  the  small  intestines  is  combined  with  a 
catarrh  of  the  upper  portion  of  the  large  intestine.  Then  we  have  a  diarrhoea, 
but  the  thin  stools  show  some  peculiarities  which  point  to  an  implication  of  the 
small  intestines.  As  a  result  of  the  increased  peristalsis  of  the  small  intestines, 
we  find  certain  constituents  in  the  stools  which  are  normally  contained  in  the 
small  intestines,  but  which  under  normal  conditions  are  no  longer  to  be  met  with 
in  the  faeces  in  the  large  intestine.  We  find  here,  in  the  first  place,  undigested 
constituents  of  the  food,  large  masses  of  muscular  fiber,  or  even  fragments  of  meat 
which  may  be  recognized  by  the  naked  eye,  and  also  starch  and  fat.  Of  course 
the  opposite  hypothesis  does  not  hold  good,  that,  if  we  find  a  large  amount  of  the 
undigested  portions  of  the  food  in  the  stools,  it  must  necessarily  always  point  to  a 
catarrh  of  the  small  intestines,  since  the  digestion  may  be  impaired  by  other  cir- 
cumstances, and  increased  peristalsis  of  the  intestines,  from  any  cause,  must  re- 
sult in  the  same  symptoms.  A  diarrhoea,  in  which  the  thin  stools  contain  a  very 
large  amount  of  undigested  particles  of  food  which  can  be  recognized  by  the 
naked  eye,  was  formerly  called  lientery,  and  the  term  is  still  occasionally  used. 

If  the  stools  contain  bile  in  addition  to  some  portions  of  the  food,  it  is  to  a  cer- 
tain degree  characteristic  of  catarrh  of  the  small  intestines.  Under  normal  con- 
ditions the  contents  of  the  small  intestines  alone  show  Gmelin's  test  for  bile-pig- 
ment, while  the  contents  of  the  large  intestine,  and  also  the  normal  stools,  do 
not.  In  intestinal  catarrh,  with  increased  peristalsis  of  the  small  and  large  intes- 
tines, there  is,  however,  often  quite  a  large  admixture  of  still  undecomposed  bile- 
pigment.  The  green  stools  which  are  so  often  seen  in  the  diarrhoea  of  children, 
and  more  rarely  in  that  of  adults,  are  also  well  known.  Such  stools  usually  show 
a  marked  color  reaction  with  nitric  acid.  In  other  cases  we  find  only  certain  con- 
stituents of  the  stools  stained  with  bile — a  fact  to  which  jSTothnagol  has  called 
special  attention.  Yellow  pigmented  bits  of  mucus,  and  cylindrical  epithelium 
and  roimd  cells  stained  with  bile,  are  especially  characteristic  of  the  diarrhoea  of 
catarrh  of  the  small  intestines. 


472  DISEASES    OF   THE   DIGESTIVE   OEGAKS 

Catarrh  of  the  large  intestine  is  probably  present  in  every  diarrhoea,  as  has 
been  repeatedly  stated,  inasmuch  as  the  thin  stools  can  be  explained  only  by  an 
increased  peristalsis  of  the  large  intestine;  but  in  a  number  of  cases  -we  have 
symptoms  which  point  especially  to  a  disease  of  the  large  intestine,  particularly  of 
its  lower  portion. 

Physical  examination  of  the  abdomen  should  show  changes,  such  as  swelling, 
sensitiveness  to  pressure,  etc.,  chiefly  in  the  lateral  portions,  corresponding  to 
the  course  of  the  colon;  but  this  is  rather  a  theoretical  hypothesis  than  a  sign  of 
practical  value.  We  can  not  definitely  affirm,  either,  that  "  colicky  pains "  are 
characteristic  of  catarrh  of  the  large  intestine  alone.  The  condition  of  the  stools, 
however,  is  of  importance.  In  the  first  place,  we  may  note  that,  if  the  stools  con- 
tain many  masses  of  mucus  which  may  be  recognized  by  the  naked  eye,  it  is  of 
diagnostic  significance.  As  we  have  seen  above,  the  stools  in  catarrh  of  the  small 
intestines  also  contain  mucus,  but  it  is  intimately  mixed  with  the  other  constitu- 
ents of  the  faeces,  and  hence  it  can  usually  be  recognized  only  by  the  microscope. 
In  catarrh  of  the  large  intestine,  however,  the  mucus  rather  adheres  to  the  out- 
side of  the  other  constituents,  and  is  often  present  in  large  masses  visible  to  the 
naked  eye.  If  the  catarrh  affects  the  lower  part  of  the  large  intestine  chiefly,  it 
may  be  that  the  intestinal  contents  are  already  formed  into  firm  lumps,  which 
may  sometimes  be  wholly  or  partly  inclosed  in  a  layer  of  mucus.  In  acute  catarrh 
of  the  lowest  part  of  the  large  intestine  the  evacuations  are  sometimes  composed 
chiefly  of  pure  mucus,  with  a  greater  or  less  admixture  of  pus,  as  is  seen  especially 
in  the  "catarrhal  flux"  (see  the  chapter  on  dysentery).  The  more  the  rectum  is 
involved  in  the  inflammation,  the  worse  is  that  painful  feeling  of  tension  and 
pressure  at  the  anus  during  and  after  the  evacuation,  which  we  term  tenesmus. 

Isolated  inflammation  of  the  rectum  (proctitis)  is,  at  least  in  part,  directly 
accessible  to  examination  by  the  finger  or  by  the  speculima.  Painful  tenesmus 
and  an  admixture  of  mucus,  and  especially  of  pus  in  the  stools,  are  the  chief 
symptoms  of  the  disease.  In  most  cases,  however,  we  have  to  do,  not  with  a  pri- 
mary disease,  but  with  a  secondary  catarrh  of  the  rectal  mucous  membrane,  as  a 
result  of  different  morbid  conditions  in  the  vicinity  of  the  rectum,  or  of  new 
growths,  syphilitic  processes,  etc.,  in  the  rectum  itself.  Periproctitis  (ischio- 
rectal abscess)  belongs  to  the  domain  of  surgery,  and  can  not  be  described  here. 

Intestinal  catarrh  is  divided  into  an  acute  and  a  chronic  form. 

In  the  acute  intestinal  catarrhs,  excluding  the  toxic  inflammations,  we  class 
simple  diarrhoea,  which  usually  passes  off  in  a  few  days,  and  the  severe  enteritis, 
which  is  probably  usually  infectious,  and  is  attended  by  a  marked  disturbance  of 
the  general  health,  by  fever,  and  sometimes  by  gastric  symptoms  also,  as  well  as 
by  herpes,  by  occasional  slight  albuminuria,  by  articular  pains,  etc.  It  lasts  from 
three  to  ten  days.  Cholera  morbus  (vide  infra)  is  to  be  regarded  as  a  special  form 
of  acute  infectious  inflammation  of  the  gastric  and  intestinal  mucous  membranes. 

Chronic  intestinal  catarrh  either  comes  from  an  acute  disease  of  the  intestinal 
mucous  membrane,  or  gradually  develoiDS  independently.  In  adults  it  is  by  no 
means  a  frequent  disease,  at  least  as  reg'ards  pronounced  cases,  and  is  much  rarer, 
for  example,  than  chronic  gastric  catarrh;  but  we  have  already  mentioned  that  it 
is  very  common  in  practice  among  children. 

In  regard  to  the  setiologj'^  and  symptomatology,  much  the  same  may  be  said  of 
chronic  catarrh  which  we  have  learned  to  recognize  in  considering  acute  catarrh. 
In  regard  to  aetiology  we  must  note,  in  adults,  chiefly  the  intestinal  affections 
remaining  after  an  attack  of  some  acute  disease — e.  g.,  dysentery,  severe  malaria, 
or  tyi)hoid.  Among  the  most  prominent  symptoms  are  the  abnormal  evacuations, 
usually  alternating  between  diarrhoea  and  constipation,  due  chiefly  to  the  atrophy 
of  the  muscular  coat  and  the  disturbance  of  the  nervous  apparatus.  'SVe  must  also 
mention,  as  a  prominent  symptom,  the  secondary  disturbances  of  the  general 


rs:TESTIXAL   CATAEEH  473 

nutrition,  sucli  as  emaciation  and  anaemia.  In  regard  to  peculiarities  in  the  char- 
acter of  the  stools,  we  must  refer  to  what  has  been  said  above.  As  chronic  catarrh 
of  the  large  intestine  is  far  commoner  than  chronic  catarrh  of  the  small  intes- 
tines, we  very  often  find  large  amounts  of  mucus  in  the  stools. 

Treatment. — Most  of  the  milder  cases  of  acute  intestinal  catarrh  need  only  a 
dietetic  treatment.  If  the  patient  avoids  all  injurious  substances  for  a  few  days, 
he  recovers  completely.  The  different  gruels,  such  as  barley  and  oatmeal  gruel,  and 
also  weak  broths,  milk,  and  thoroughly  toasted  bread,  or  the  German  zwiehach, 
are  generally  regarded  as  the  most  suitable  food.  The  coarser  vegetables  and 
fruits,  fat  meat  and  brown  bread,  are  to  be  avoided  as  much  as  possible.  The 
best  beverage  is  tea,  or  claret  diluted  with  water.  In  other  respects  we  may 
refer  to  the  dietetic  rules  laid  down  under  the  treatment  of  chronic  gastric 
catarrh. 

It  is  also  an  important  rule,  confirmed  by  much  experience,  to  keep  the  abdo- 
men warm.  Children  should  always  stay  in  bed,  and  adults  should  do  so,  at  least 
in  all  severe  cases.  It  is  a  good  plan,  particularly  in  children,  to  protect  the  abdo- 
men from  cold  by  a  flannel  band. 

In  many  of  the  mild  cases  it  is  scarcely  necessary  to  use  internal  remedies. 
Gum  mixture  (P.  G.)  or  almond  mixture  is  a  good  prescription  if  there  is  no  other 
special  indication,  but  in  severe  cases  further  medication  may  be  proper.  If 
we  have  reason  to  suspect  some  irritating  ingesta  or  a  collection  of  fseces  as  a 
cause  of  the  intestinal  catarrh,  a  cathartic  acts  favorably  at  the  beginning  of  the 
treatment,  in  spite  of  the  existence  of  diarrhoea.  Our  best  cathartic  in  such  cases 
is  castor-oil  or  calomel.  In  all  those  cases  in  which  many  thin  dejections  point  to 
a  greatly  increased  peristalsis  of  the  intestine,  we  use  astringents,  especially 
opium,  which  we  give  in  the  form  of  the  simple  tincture  or  the  wine  in  doses  of 
ten  or  fifteen  drops,  one  to  three  times  a  day;  or  as  a  powder,  half  a  grain  to  a 
grain  (gramme  0.03  to  0.05)  of  opium  with  a  grain  (gramme  0.05)  of  sugar,  two 
or  three  times  a  day.  It  is  also  well  to  combine  the  opium  with  some  mucilagi- 
nous vehicle,  as  2  parts  of  laudanum  to  150  of  gum  mixture  or  decoction  of  salep 
(P.  G.),  a  tablespoonfid  every  two  or  three  hours.  Tannic  acid  and  the  like  are 
seldom  employed  in  acute  enteritis. 

If  there  is  severe  colic,  opium,  or,  under  some  circumstances,  an  injection  of 
morphine  is  the  best  remedy.  In  milder  cases  it  is  sufficient  to  apply  warmth  to 
the  abdomen,  by  warm  poultices  or  hot  towels.  The  colic,  however,  often  depends 
upon  the  presence  of  old  faecal  masses  in  the  intestine,  when  it  is  necessary  to 
prescribe  a  cathartic,  such  as  castor-oil. 

In  all  eases  in  which  the  symptoms  point  to  a  more  intense  disease  of  the  large 
intestine,  local  treatment  may  be  employed.  This  is  chiefly  of  importance  in  the 
treatment  of  chronic  intestinal  catarrh  situated  mainly  in  the  large  intestine. 
We  irrigate  the  large  intestine  daily  with  weak  astringents,  and  sometimes  with 
disinfectants.  The  necessary  apparatus  is  very  simple.  It  consists  of  an  ordi- 
nary irrigator,  to  which  a  rubber  tube,  about  half  a  metre  long  and  with  a  proper 
tip,  is  attached.  Instead  of  the  irrigator  we  can  use  a  large  glass  funnel,  a  "  He- 
gar's  funnel."  "We  may  very  well  use,  for  an  end-piece  to  be  introduced  into 
the  rectum,  a  long,  soft,  elastic  oesophageal  tube,  which  can  easily  be  pushed 
quite  high  up.  The  fluids  used  for  irrigation  must  always  be  warmed  to  about 
85°  (30°  C.),  and  should  be  allowed  to  run  in  gradually  and  slowly.  The  amount 
of  fluid  used  for  one  irrigation  should  be  two  or  three  pints  (l-lj  litre),  or  some- 
times more.  The  patient  keeps  on  his  back  during  the  irrigation.  The  knee- 
elbow  position,  which  is  much  more  uncomfortable  than  the  dorsal,  is  only  occa- 
sionally necessary.  The  fluids  most  used  are  a  one-  or  two-per-cent.  solution  of 
salicylic  acid,  solutions  of  salicylic  and  boracic  acids  combined,  a  one-per-cent. 
tannin  solution,  or  a  solution  of  acetate  of  lead  (1  to  1,000). 


474  DISEASES    OF   THE   DIGESTIVE   OEGANS 

If  there  is  painful  tenesmus,  it  is  usually  relieved  by  suppositories  of  cacao 
butter  containing-  extract  of  opium. 

In  chronic  intestinal  catarrh  a  careful  regulation  of  the  diet  is  of  the  greatest 
importance.  To  be  avoided  are  fruits  and  sour  or  greasy  dishes,  indigestible  vege- 
tables and  pudding-s,  coarse  bread,  and  above  all,  beer;  and  to  be  recommended 
are  tender  lean  meat  (sirloin),  sweetbread,  fish  that  are  not  oily  (such  as  trout 
and  pike),  potato  puree,  and  particularly  soft-boiled  rice  and  sago.  In  regard  to 
eggs  and  milk,  individual  experience  must  decide.  Beyond  this  the  main  point  is 
overcoming  the  chronic  diarrhcea.  Besides  the  cautious  use  of  opium,  the  as- 
tringents are  to  be  particularly  borne  in  mind,  either  alone  or  combined  with 
opium.  Those  most  often  prescribed  are  tannic  acid,  acetate  of  lead,  columbo, 
and  logwood.  We  have  also  seen  excellent  results  in  mild  cases  from  the  steady 
use  of  bilberry  wine.  The  preparations  of  bismuth  also  deserve  to  be  recom- 
mended, particularly  the  salicylate  (8  to  15  grains  several  times  a  day,  gramme 
0.5-1),  and  the  newly  introduced  tannigen  (acetyl-tannin)  and  tannalbine  (albu- 
minate of  tannin)  in  doses  of  eight  grains  or  more  (gramme  0.5)  several  times  a 
day.  In  case  the  offensive  odor  of  the  discharges  indicates  abnormal  decomposi- 
tion in  the  intestinal  canal,  we  employ  naphthaline  in  doses  of  li  to  5  grains 
(gramme  0.1-0.3)  several  times  a  day.  We  often  have  to  try  various  remedies  in 
a  particular  case  before  we  find  one  that  is  efficient.  Great  care  should  be  exer- 
cised that  there  be  no  long  periods  of  constipation;  if  necessary,  we  may  use  in- 
jections, saline  laxatives,  or  castor-oil. 

Good  results  are  often  obtained  in  chronic  intestinal  catarrh  by  drinking  the 
waters  at  Carlsbad,  Tarasp,  Kissingen,  Marienbad,  or  Homburg,  particularly  in 
cases  with  occasional  constipation. 

It  is  of  practical  importance  to  distinguish  the  genuine  eases  of  chronic  in- 
testinal catarrh  with  an  anatomical  basis,  from  the  common  nervous  disturbances 
of  the  digestive  tract.  ISTot  infrequently  the  most  diverse  symptoms  on  the  part 
of  the  intestine,  including  colic  and  irregularity  of  the  bowels,  appear  as  part  of  a 
general  neurasthenia  or  nervousness  (see  page  1193).  In  such  cases  there  is  little 
benefit  from  internal  remedies  and  strict  diet,  while  appropriate  general  treat- 
ment with  cold  water,  electricity,  and  massage  is  often  attended  with  the  best 
results.  With  regard  to  this  compare  also  the  chapters  on  nervous  dyspepsia  and 
on  habitual  constipation. 

APPEE^DIX 

Membranous  Enteritis  and  Mucous  Colic. — The  name  of  membranous  enter- 
itis or  mucous  colic  is  applied  to  a  condition  which  is  not  very  common,  but  yet 
of  great  practical  importance.  It  is  characterized  chiefly  by  the  habitual  dis- 
charge with  the  faeces  of  a  great  abundance  of  mucus,  in  the  form  of  membranes. 
The  disease  is  observed  especially  in  women,  but,  in  rare  cases,  also  in  men.  It  is 
noticeable  that  the  patient  is  almost  always  a  nervous,  hysterical,  or  hypochon- 
driacal individual. 

In  many  cases  a  discharge  of  the  membranes  takes  place  in  separate"  attacks, 
which  occur  either  daily  or  at  longer  intervals,  and  are  associated  with  severe 
colic  ("mucous  colic").  The  membranes  are  gray  or  reddish  gray,  and  often  cy- 
lindrical or  rolled  up  in  a  ball.  They  consist  mainly  of  mucine — sometimes,  it  is 
said,  of  albuminoid  matters  also — and  examined  under  a  microscope  they  are 
usually  found  to  contain  an  unusual  amount  of  desquamated  cylindrical  epithe- 
lium, with  a  very  small  number  of  leucocytes,  and  perhaps  also  a  few  crystals  of 
triple  phosphate  and  cholesterine.  In  other  cases  there  are  scarcely  any  attacks 
of  colic,  but  merely  a  persistent  discharge  of  the  above-described  membranes  and 
bits  of  mucus.  The  true  discharges  of  the  bowels  are  almost  always  very  sluggish 
and  very  hard. 


CHOLEEA  MOKBUS  4T5 

There  is  still  much  uncertainty  as  to  the  true  nature  of  this  diseased  condi- 
tion. Whether  there  is  a  genuine  "  enteritis  "  is  doubtful,  at  least  with  regard 
to  many  cases.  The  noticeably  frequent  association  of  the  disease  with  hys- 
teria and  neurasthenia  seems  to  indicate  nervous  causes  for  the  exaggerated  pro- 
duction of  mucus.  The  formation  of  the  membranes  probably  takes  place  through 
the  rolling  up  of  the  mucus  in  the  depths  of  the  longitudinal  folds  of  the  colon 
during  its  cramp-like  contractions. 

The  course  of  the  disease  is  usually  tedious,  but  complete  recovery  may  occur ; 
there  is  no  danger.  The  nutrition  of  the  patient  may  remain  perfectly  normal, 
but  in  some  cases  it  is  greatly  impaired.  This  depends  chiefly  upon  the  character 
of  the  other  nervous  symptoms  present. 

The  treatment  is  partly  local,  by  means  of  irrigations  with  alkaline  solutions, 
or  diluted  lime-water,  and  the  injection  of  oil  and  similar  measures;  and  partly, 
or  rather  chiefly,  general,  for  the  cure  of  the  associated  neurasthenia.  The  most 
common  modes  of  treatment  are  by  means  of  hydrotherapy,  electricity,  and  mas- 
sage. In  addition,  we  should  combat  the  habitual  constipation  in  the  ordinary 
ways  (vide  infra). 


CHAPTER  II 

CHOLERA    MORBUS 

t       {Cholera  Nostras.     Cholera  Infantum) 

By  the  name  "  cholera  morbus  "  we  mean  an  acute  disease  of  the  stomach  and 
intestinal  canal  of  a  definite  form,  whose  symptoms  in  severe  cases  greatly  resem- 
ble those  of  genuine  Asiatic  cholera.  It  is  in  the  highest  degree  probable,,  from 
the  whole  course  of  the  disease,  that  cholera  morbus  also  depends  upon  an  acute 
infection  of  the  body  by  a  specific  germ;  but  this  germ  has  not  yet  been  iden- 
tified. 

Cholera  morbus  comes  on  usually  as  an  epidemic,  and  almost  exclusively  in 
the  hot  summer  months — June  to  August.     Hence  it  is  often  tei-med  summer 
cholera.     Children  in  the  first  two  years  of  life  are  chiefly  attacked,  especially 
those  who  are  artificially  fed  or  who  have  recently  been  weaned.     The  disease ' 
also  attacks  older  children  and  adults,  but  much  more  rarely. 

[Special  opportunities  are  afforded  in  this  country  for  the  study  of  cholera 
infantum.  The  causative  conditions  are,  briefly,  unsuitable  food,  a  high  tempera- 
ture, and  bad  hygiene — conditions  which  are  all  combined  and  attain  their  maxi- 
mum intensity  in  large  cities.  That  a  high  thermometric  range  alone  is  not  sufii- 
cient  is  shown  by  the  comparative  immunity  of  all  country  districts.  Those  who 
live  in  the  country,  or  who  have  never  been  busied  among  the  city  poor,  have  no 
idea  of  the  atmosphere  breathed  by  the  children  of  the  poorer  classes,  especially 
during  the  heated  term,  nor  of  the  extreme  difficulty — impossibility  we  can  almost 
say — of  getting  really  good  milk.  Even  if  the  milk  was  good  at  the  start  and  it  has 
not  been  tampered  with,  the  time  which  necessarily  elapses  after  it  is  drawn  from 
the  cow  and  before  it  reaches  the  consumer  permits  marked  fermentative  changes 
during  hot  weather.  And  milk  is  and  must  remain  the  main  article  of  diet  for 
children  under  two  years  of  age.] 

The  symptoms  of  cholera  morbus  are  those  of  a  severe  acute  gastro-enteritis. 
The  disease  begins  suddenly,  or  after  some  slight  warning,  with  violent  vomiting 
and  severe  diarrhoea.  In  some  cases  one  of  these  symptoms  predominates,  and  in 
others  the  other.  The  vomitus  consists  partly  of  the  food' taken,  and  partly  of  a 
slimy,  watery  substance.    The  stools  at  first  retain  their  faecal  character,  but  they 


476  DISEASES    OE   THE   DIGESTIVE   OEGANS 

soon  become  more  colorless  and  more  watery,  so  tliat  they  sometimes  approach, 
the  well-known  rice-water  appearance  of  the  stools  in  genuine  cholera.  Abdomi- 
nal pain  is  usually  absent,  but  a  feeling  of  pressure  and  constraint  in  the  epigas- 
trium is  often  present.  The  diminished  secretion  of  urine  and  the  frequent  mus- 
cular pains  cause  the  whole  type  of  the  disease  to  resemble  genuine  cholera  still 
more  closely.     There  is  sometimes  a  cutaneous  eruption  resembling  roseola. 

The  severe  constitutional  disturbance  is  especially  characteristic.  The  pa- 
tient becomes  extremely  dull  and  has  a  wasted  look,  the  voice  is  weak  and  hoarse, 
an  unquenchable  thirst  sets  in,  the  pulse  is  very  small,  the  skin  of  the  face  and 
the  extremities  is  cool  and  livid;  in  short,  we  have  the  pronounced  picture  of  a 
general  collapse.  The  body  heat  also  falls,  although  at  the  first  stage  of  the  dis- 
ease there  is  often  a  rise  of  temperature. 

[The  temperature  is  always  high,  even  during  the  stage  of  collapse,  when  the 
skin  and  extremities  are  cool  to  the  touch;  if  the  thermometer  is  introduced  into 
the  rectum — generally  the  best  place,  by  the  way,  to  take  the  temperature  in 
young  children— it  will  rise  to  101°  to  102°,  and  is  more  apt  to  reach  104°  to  107°. 
This  shows  that  inflammation  plays  a  large  part  in  the  pathology  of  the  disease.] 

The  picture  of  a  severe  general  disease  is  especially  prominent  in  cholera  infan- 
tum. In  severe  cases  of  this  form  of  the  disease  the  general  restlessness,  which  at 
first  exists,  rapidly  passes  into  somnolence.  The  child  lies  with  sunken,  half- 
closed  eyes,  the  conjunctivae  are  slightly  injected,  the  cornese  are  cloudy,  the  face 
is  pale  and  cyanotic,  the  fontanelles  are  depressed,  the  skin  is  cool,  and  the  pulse 
is  small  and  frequent  and  it  can  scarcely  be  counted.  Amid  these  symptoms, 
which  are  usually  termed  "  hydrocephaloid  "  by  specialists  in  children's  diseases 
[Marshall  Hall],  death  comes  on  in  coma  or  with  slight  convulsions.  There  can 
scarcely  remain  room  for  doubt  that  these  severe  cases  of  gastro-enteritis  are  of 
infectious  origin,  and  that  the  constitutional  symptoms  are  the  result  of  toxic 
matters  generated  in  the  intestine  under  the  influence  of  the  micro-organisms 
(vide  supra,  the  chapter  on  acute  gastritis).  Another  peculiar  symptom  which 
occurs  in  severe  cholera  infantum  is  the  so-called  sclerema  adiposum.  While  the 
temperature  keeps  sinking  the  extremities  become  peculiarly  stiff  and  rigid,  and 
the  skin  grows  pale  and  firm.  This  phenomenon  is  caused  by  the  fat  in  the  fat 
cells  of  the  subcutaneous  connective  tissue  stiffening  as  a  result  of  the  low 
[superficial]  temperature. 

The  mortality  of  children  with  cholera  infantum  is  very  marked,  especially  in 
large  cities,  and  among  the  poorer  classes  of  society.  Severe  cases  usually  end 
fatally  in  a  few  days,  but,  on  the  other  hand,  many  cases  recover,  either  because 
the  course  of  the  disease  from  the  first  is  not  so  severe,  or  because  eases  appar- 
ently hopeless  take  a  favorable  turn.  In  adults  it  is  extremely  rare  to  see  cholera 
morbus  terminate  unfavorably.  Patients  also  recover  quite  rapidly  from  appar- 
ently severe  conditions,  although  the  stomach  and  intestines  often  remain  rather 
sensitive  for  a  long  time. 

The  anatomical  appearances  in  children  who  die  of  cholera  infantum  usually 
contrast,  from  their  insignificance,  with  the  severe  symptoms  observed  during  life. 
The  catarrhal  affection  of  the  gastric  and  intestinal  mucous  membranes  is  not 
at  all  prominent  in  the  cadaver,  and  the  solitary  follicles  and  Peyer's  patches 
show  only  a  slight  swelling.  A  careful  microscopic  examination  of  the  intestinal 
mucous  membrane  shows,  however,  quite  severe  inflammation.  The  other  lesions 
which  are  most  frequently  seen  are  lobular  atelectases  in  the  lungs,  venous  hyper- 
semia  and  oedema  of  the  pia  mater,  and  slight  lesions  of  the  kidneys. 

The  diagnosis  of  cholera  morbus  presents  no  difficulty  if  the  characteristic 
symptoms  of  the  disease  are  present.  The  distinction  between  it  and  genuine 
Asiatic  cholera  used  to  be  occasionally  quite  difficult,  and  it  was  rendered  possible 
only  by  considering  the  setiological  factors,  and  the  evident  connection  between 


liTTESTmAL   CATAKKH   OF   CHILDEEN"  4YY 

the  individual  case  and  other  eases  of  undoubted  cholera.  By  Koch's  discovery  of 
the  comma-bacillus  in  Asiatic  cholera  the  distinction  between  the  two  diseases 
has  now  become  absolutely  certain.  ^  In  all  suspicious  cases,  therefore,  we  must 
examine  the  dejections  for  comma-bacilli,  and  upon  the  result  of  this  examina- 
tion depends  the  determination  of  the  proper  means  of  prophylaxis. 

The  treatment  of  cholera  morbus  in  adults  must  be  first  to  take  special  care  to 
limit  the  diet.  The  food  should  be  only  gruels,  or  at  most  broth,  soft-boiled  eggs, 
and  milk.  It  is  a  good  plan  to  give  the  milk  iced,  and  in  small  amounts.  The 
distressing  thirst  is  best  relieved  by  cracked  ice.  Wine  (iced  champagne)  is  to  be 
given  if  the  general  weakness  becomes  marked. 

Among  drugs,  opium  is  the  most  effective  remedy,  and,  whether  in  powder,  as 
the  extract,  or  in  liquid  form,  as  laudanum,  it  is  the  first  thing  to  use  to  relieve 
the  diarrhoea  and  vomiting.  All  other  remedies  which  are  recommended  in  chol- 
era morbus  in  adults,  such  as  nitrate  of  silver,  are  quite  subordinate  to  opium. 
We  may  combine  small  doses  of  calomel  with  the  opium.  If  there  is  a  severe  col- 
lapse which  threatens  life,  it  is  advisable  to  make  a  subcutaneous  injection  of 
water,  containing  0.6  per  cent,  of  salt,  or  5  per  cent,  of  grape  sugar. 

We  are  more  cautious  in  prescribing  opiates  for  children,  although  here  small 
doses  of  opium,  one  or  two  drops  of  laudanum  according  to  the  age  of  the  child, 
may  often  be  indispensable.  In  fresh  cases  calomel  has  obtained  a  great  reputa- 
tion, a  sixth  of  a  grain  (gramme  0.01)  two  or  three  times  a  day.  Ice-cold  cow's 
milk,  given  in  teaspoonfuls,  serves  best  as  food,  if  the  child  can  not  be  fed  natu- 
rally by  breast-milk. 

Many  specialists  recommend  that  no  food  at  all  should  be  given  for  a  few  days, 
but  merely  a  sufiicient  amount  of  cold  water  or  chamomile  tea.  If  nothing  will 
stay  on  the  stomach,  we  may  try  a  subcutaneous  injection  of  0.6  per  cent,  saline 
solution.  If  there  are  symptoms  of  severe  collapse,  we  should  immediately  em- 
ploy hot  baths  at  100°  F.  (30°  E.),  with  the  addition  of  10  to  15  ounces  of  mus- 
tard (300-500  grammes)  and  hot  packs,  as  well  as  such  stimulants  as  camphor 
or  alcohol  subcutaneously.  To  guard  against  desiccation  of  the  sclera  and  cor- 
nea, the  eyes  should  be  covered  with  compresses  moistened  with  solutions  of  ace- 
tate of  lead,  corrosive  sublimate,  etc. 


CHAPTER  III 

INTESTINAL    CATARRH    OF    CHILDREN 

{Chronic  Dy»pepda  of  Children.    Pedatrojphy) 

The  great  frequency  and  the  practical  importance  of  the  "  dyspeptic  condi- 
tions "  in  children  in  the  first  years  of  life,  which  conditions  are  associated  with 
severe  disturbances  of  nutrition,  justify  a  short  description  of  them,  but  we  must 
refer  to  the  special  manuals  on  children's  diseases  for  a  detailed  account. 

That  diseases  of  the  digestive  organs  play  so  large  a  part  in  children's  troubles 
is  owing,  on  the  one  hand,  to  the  great  sensitiveness  which  the  digestive  apparatus 
in  children  shows  to  the  irritants  which  are  brought  in  contact  with  it,  and,  on 
the  other,  to  the  too  common  foolishness  and  carelessness  which  the  child's  parents 
and  nurses  show  in  its  feeding.  Of  course  it  is  not  always  ignorance  and  neglect, 
but  often,  Tinfortunately,  poverty  and  want  which  cause  children  to  suffer,  and 
explain  the  terrible  mortality  in  the  first  years  of  life. 

The  simple  fact  that  by  far  the  larger  number  of  children  who  suffer  from 
dyspeptic  and  atrophic  conditions  are  fed  artificially,  leads  us  to  the  belief  that 


478  DISEASES    OF   THE   DIGESTIVE   OEGANS 

the  cause  of  most  of  the  intestinal  diseases  in  children  is  to  be  found  in  faulty  and 
injudicious  feeding.  The  food,  which  is  not  suited  to  the  child's  digestive  powers, 
is  only  imperfectly  absorbed;  it  undergoes  many  processes  of  decomposition, 
whose  products  irritate  the  intestinal  mucous  membrane  and  give  rise  to  increased 
peristaltic  action.  Thus  the  imperfect  digestion,  or  "  dyspepsia,"  excites  a  ca- 
tarrh of  the  gastric  and  intestinal  mucous  membrane,  by  which  again,  in  a  vicious 
circle,  the  digestive  power  is  still  further  reduced.  Hence  the  boundary  between 
"  dyspepsia  "  and  catarrh  can  be  drawn  only  artificially.  It  is  certain  that  infec- 
tious influences  also  play  an  important  part  in  the  intestinal  diseases  of  children. 
One  proof  of  this  is  that  indigestion  is  much  more  frequent  during  the  hot 
weather  than  during  the  winter  months,  but  although  numerous  bacteriological 
investigations  have  been  made,  observers  have  not  yet  been  successful  in  deter- 
mining special  pathogenic  organisms  for  the  several  varieties  of  intestinal  catarrh. 

The  anatomical  changes  of  the  intestinal  mucous  membrane  in  children  who 
die  of  "  chronic  intestinal  catarrh "  are,  as  a  rule,  only  slightly  marked,  and 
contrast,  in  their  apparent  insignificance,  with  the  severe  intestinal  symptoms 
observed  during  life.  Probably  here  also  the  toxic  influences  of  the  matters 
abnormally  generated  in  the  intestine,  play  a  more  important  part  than  do  the 
anatomical  changes.  We  must  remember,  however,  that  most  catarrhal  condi- 
tions are  hard  to  recognize  in  the  cadaver  because  of  the  disappearance  of  the 
hyperaemia.  The  changes  present  are  quite  important,  but  they  require  micro- 
scopic examination  for  their  detection.  Sometimes  the  swelling  of  the  follicles  is 
especially  marked — follicular  catarrh.  Follicular  ulcers  are  also  seen.  In  other 
cases  the  atrophy  of  the  mucous  membrane,  which  is  often  seen  after  chronic 
catarrhs,  is  the  chief  lesion.  Chronic  thickening  and  swelling  of  the  mucous 
membrane  is  of  rarer  occurrence.  In  most  of  the  severe  cases  the  large  intestine, 
and  also  the  lower  portion  of  the  ileum,  are  the  chief  seat  of  the  changes.  "We 
often  find  a  swelling  of  the  mesenteric  lymph-glands,  and  also  a  fatty  liver.  In 
the  lungs  extensive  atelectases  or  nodules  of  catarrhal  pneumonia  often  develop 
as  a  result  of  the  imperfect  respiration. 

The  symptoms  of  chronic  intestinal  catarrh  are,  in  the  first  place,  those  due 
directly  to  the  intestinal  trouble,  and,  secondly,  the  quite  rapid  disturbance  of  the 
child's  general  nutrition. 

The  condition  of  the  stools  is  the  most  important  intestinal  symptom.  The 
normal  dejection  in  children  until  they  are  weaned  is  of  the  color  of  the  yolk  of 
an  egg,  of  a  rather  pasty  consistency,  and  of  a  faintly  sour  smell.  In  intestinal 
catarrh  the  stools  are  more  frequent,  six  or  seven,  and  even  more,  a  day.  They  are 
thinner,  more  watery,  contain  large  flakes  and  lumps  of  undigested  bits  of  case- 
ine  and  other  remains  of  food,  and  smell  badly.  They  very  often  have  a  green 
color,*  or  acquire  it  on  standing.  We  may  find  admixtures  of  mucus,  sometimes 
in  the  form  of  the  so-called  "  sago  grains,"  especially  in  catarrh  of  the  large 
intestine.  With  the  microscope  we  find  in  severe  cases,  besides  particles  of  food, 
leucocytes  and  epithelial  cells,  threads  and  clumps  of  mucus,  and  innumerable 
bacteria  of  all  shapes.  There  are  also  crystals  of  triple  phosphate,  when  the  stools 
have  an  alkaline  reaction,  and  needle-shaped  crystals  of  the  fatty  acids,  as  well  as 
plates  of  cholesterine,  when  the  discharges  are  acid. 

There  is  no  definite  distinction  in  regard  to  the  dejections  in  catarrh  of  the 
large  and  of  the  small  intestines.  On  the  whole,  the  rule  holds  that,  in  catarrh 
of  the  small  intestines  chiefly,  the  stools  are  larger,  they  are  passed  with  more 
wind  or  gas,  and  show  a  more  uniform  consistency;  while  in  catarrh  of  the  large 
intestine  they  are  smaller  but  more  frequent,  ten  or  twenty  a  day,  are  passed 
noiselessly,  are  associated  with  tenesmus,  and  show  a  different  consistency  in 


•  The  statement  that  this  green  eolor  is  due  to  a  special  variety  of  bacillus  lacks  confirmation. 


INTESTIlSrAL   CATAEEH   OF   CHILDEEl^  479 

their  various  parts,  partly  normal,  partly  thin,  partly  slimy,  etc.  Examination 
of  the  abdomen  has  some  importance,  for,  as  a  rule,  in  catarrh  of  the  small  intes- 
tines the  abdomen  is  much  swollen,  while  in  catarrh  of  the  large  intestine  it 
is  often  deeply  sunken.  The  liver  is  often  enlarged  and  distinctly  palpable,  and 
sometimes  the  spleen  also. 

We  often  find  disturbances  in  the  stomach,  vomiting,  eructations,  etc.,  as  well 
as  trouble  in  the  intestines.  There  may  be  thrush  in  the  mouth,  or  the  develop- 
ment of  aphthous  ulcers. 

Among  other  complications,  we  see  diseases  of  the  respiratory  tract,  includ- 
ing bronchitis,  atelectasis,  and  catarrhal  pneumonia;  also  albuminuria,  eczema, 
furunculosis,  and  nervous  disturbances. 

In  almost  all  long-continued  cases,  however,  the  general  disturbance  of  nutri- 
tion, the  atrophy  (athrepsia)  of  the  child,  takes  the  first  place  in  the  picture  of 
the  disease.  The  muscles  become  shriveled  and  flabby,  and  the  whole  body  finally 
becomes  so  much  emaciated  that  the  pale,  dry  skin  hangs  in  broad  folds  and  wrin- 
kles about  the  bones,  whose  prominences  are  everywhere  visible.  The  face  is 
sharp,  and  has  an  aged  expression  ("  Voltaire-face  ")  from  the  many  little  folds 
of  the  skin.  The  eyes  are  dull,  lusterless,  and  wide  open;  the  voice  is  merely  a 
low,  hoarse  whimper.  The  abdomen  is  deeply  sunken,  or  in  some  cases  it  is 
swollen  by  meteorism,  in  peculiar  contrast  to  the  emaciation  elsewhere;  and  its 
surface  is  traversed  by  bluish  veins. 

From  this  sad  picture,  unfortunately  so  frequently  seen  in  practice  among 
children,  we  can  usually  recognize  the  condition  of  things  at  the  first  glance,  for 
by  far  the  larger  part  of  the  cases  called  "  pedatrophy  "  are  due  to  chronic  digest- 
ive disturbances.  Very  often  it  is  combined  with  rachitic  changes  in  the  bones, 
of  whose  occurrence  we  shall  speak  further  in  the  description  of  rachitis.  Tuber- 
cular changes,  too,  are  often  found  in  the  cadaver,  especially  in  the  lungs  and  the 
bronchial  and  mesenteric  lymph-glands.  In  such  cases,  of  course,  the  tuberculosis 
is  usually  to  be  regarded  as  the  main  disease,  upon  which  the  intestinal  affection, 
which  may  be  simple  or  even  tubercular,  has  developed  secondarily.  During  life 
tuberculosis  in  little  atrophic  children  may  very  easily  be  overlooked. 

If  we  would  give  a  full  account  of  the  treatment  of  the  atrophic  conditions  in 
children  due  to  digestive  disturbances,  we  must  include  in  our  consideration  the 
entire  hygiene  and  care  of  children  in  health  and  disease,  for  all  children's  physi- 
cians are  united  in  the  opinion  that,  as  the  cause  of  most  intestinal  diseases  in 
children  is  to  be  found  in  improper  feeding,  so  recovery  from  existing  digestive 
disturbances  can  take  place  primarily  only  by  a  corresponding  proper  and  judi- 
cious feeding.  In  what  follows  we  can  refer  only  to  the  most  important  principles 
and  general  points  which  are  here  to  be  considered. 

The  only  proper  and  natural  food  for  a  child  in  its  first  year  is  breast-milk. 
All  dyspeptic  conditions  are  much  rarer  in  children  who  are  nursed  than  in  bot- 
tle-fed children,  and,  when  they  do  occur  in  children  at  the  breast,  they  often 
are  only  of  brief  duration.  They  are  then  to  be  referred  usually  to  certain  dis- 
turbances in  the  mother,  such  as  disease,  improper  food,  or  severe  mental  excite- 
ment. The  return  of  menstruation  or  a  new  pregnancy  has  sometimes  an  unfa- 
vorable influence  on  the  character  of  the  milk.  Finally,  we  may  mention  that 
in  spite  of  the  best  of  milk,  if  the  breast  is  given  irregularly  and  too  frequently,  it 
may  cause  anomalies  of  digestion  in  nursing  children. 

Most  of  these  slight  disturbances  are  easily  quieted.  Sometimes  the  fault 
lies  in  the  unsuitable  diet  of  the  wet  nurse.  If  this  is  too  rich  in  fat  or  in  albu- 
men, the  breast-milk  may  not  be  well  borne.  Exceptionally  it  happens  that,  with- 
out any  discoverable  reason,  the  milk  of  a  wet-nurse  "  does  not  agree  "  with  the 
child.  Then  we  must  change  the  nurse.  The  atrophic  conditions  which  develop 
and  progress  in  children,  in  spite  of  plenty  of  normal  food,  are  usually  due,  not  to 


480  DISEASES    OF   THE   DIGESTIVE   OEGAITS 

simple  digestive  disturbances,  but  to  deep-seated,  general,  constitutional  diseases 
like  tuberculosis,  or  syphilis. 

The  great  majority  of  cases  of  chronic  intestinal  catarrh  and  chronic  atrophy 
are  found,  as  we  have  said,  in  bottle-fed  children.  The  first  question  which  every 
physician  should  ask  a  mother  who  brings  him  such  a  child  for  treatment,  must 
therefore  refer  to  the  sort  of  feeding  which  the  child  has.  If  the  mother,  for  any 
reason,  can  not  nurse  it  herself,  and  if  the  bottle-fed  child  has  digestive  disturb- 
ances, we  must  invariably  consider,  in  the  first  place,  the  possibility  of  i^rocuring  a 
wet-nurse.  Feeding  by  the  milk  of  a  wet-nurse  is  a  remedy  which,  at  least  in 
many  cases,  by  saving  the  child's  life,  repays  the  many  annoyances  and  quite 
large  expense  which  a  wet-nurse  causes.  We  must  tell  the  parents  this,  and  repre- 
sent to  them,  without  reserve,  the  great  dangers  which  threaten  the  life  of  every 
bottle-fed  baby.  Complete,  and  sometimes  even  quite  rapid,  recov'eiy  may  be  ob- 
tained through  a  wet-nurse,  even  in  cases  of  severe  chronic  intestinal  catarrh, 
when  atrophy  and  weakness  are  already  very  far  advanced. 

Often,  however,  it  is  impossible  to  hire  a  wet-nurse,  especially  in  the  poorer 
classes  of  society.  We  must  continue  bottle-feeding,  and  these  are  the  cases 
among  which  chronic  intestinal  catarrh  demands  the  greatest  number  of  victims ; 
yet  even  here  the  physician  can  always  do  much  good  by  instructing  the  parents. 

The  best  substitute  for  mother's  milk  is  cow's  milk.  This  must  be  as  fresh  as 
possible,  and  is  given  boiled.  A  grejit  and  most  beneficial  advance  in  the  arti- 
ficial nourishment  of  infants  was  made  by  the  introduction  of  Soxhlet's  apparatus 
for  boiling  milk.  This  accomplishes  an  almost  complete  sterilization  of  the  milk 
and  the  vessels  which  contain  it.  One  part  of  the  milk  must  be  diluted,  accord- 
ing to  its  quality,  with  two  or  three  parts  of  boiled  water  in  the  first  months,  in 
children  from  four  to  six  months  old  with  equal  parts  of  water,  and  in  older 
children  with  abovit  half  as  much  water.  At  the  age  of  about  nine  to  twelve 
months,  the  child  may  have  undiluted  milk.  In  general  we  give  the  milk  warmed 
to  about  85°  (28°  C.),  but  children  with  gastro-intestinal  catarrh  often  bear 
cold  milk,  given  in  small  amounts,  better  than  warm.  There  are  special  addi- 
tions made  to  the  milk,  with  the  intent  of  rendering  the  cow's  milk  a  better  sub- 
stitute for  mother's  milk.  Of  these,  the  first  to  be  mentioned  is  milk  sugar.  In 
feeble  children  experience  shows  that  it  is  often  very  advantageous  to  dilute  the 
milk  with  oatmeal  water  or  rice  water.  Sometimes,  also,  the  addition  of  veal 
broth  is  most  satisfactory. 

Cow's  milk,  properly  diluted,  is  better  for  children  with  chronic  intestinal 
catarrh,  in  many  cases,  than  any  other  food.  In  severe  acute  digestive  disturb- 
ances, however,  it  is  sometimes  advisable  to  omit  the  milk  entirely  for  a  few  days, 
and  give  instead  of  it  only  a  little  chamomile  tea  or  some  mucilaginous  drink 
such  as  oatmeal  gruel  made  with  water  and  strained,  or  decoction  of  salep.  In 
chronic  dyspepsia  we  must  first  try  good  cow's  milk.  If  the  milk  is  not  well  borne, 
if  the  diarrhoea  increases,  and  if  the  child  becomes  still  more  emaciated,  we  may 
try  to  get  milk  from  another  and  better  soiirce ;  but  it  often  happens  either  that 
we  can  not  procure  good  milk,  or  that  the  child  can  not  bear  even  the  best  cow's 
milk.  We  are  then  obliged  to  have  recourse  to  one  of  the  many  "  artificial  foods  " 
and  "  substitutes  for  mothers'  milk  "  in  the  market.  We  can  not  here  go  into  par- 
ticulars concerning  these.  Each  of  these  preparations  has  occasional  good  results 
to  show,  but  none  of  them  has  an  uncontested  pre-eminence  over  the  rest.  We 
will  mention  the  preparations  most  in  use  at  present,  of  whose  value  in  individual 
cases  we  have  convinced  ourselves:  Swiss  condensed  milk  and  the  infants'  foods 
of  ISTestle,  Kufeke,  Loffkmd,  and  Theinhardt,  as  well  as  many  others.  Gartner's 
cream-milk  (Fettmilch)  is  sometimes  advantageous.  It  is  artificially  prepared 
and  contains  little  caseine  but  much  fat. 

If  we  keep  fast  to  the  principle  that  every  intestinal  catarrh  in  children  is  to 


mTESTINAL   CATAEEH   OF   CHILDEEl^  481 

be  treated  in  the  first  place  by  a  judicious  regulation  of  the  diet,  in  many  cases  we 
shall  not  have  to  use  any  drugs.  These  may  be  of  service  only  when  we  have  also 
carried  out  the  dietetic  measures  which  are  specially  necessary. 

Calomel  has  obtained  the  greatest  reputation  in  the  treatment  of  intestinal 
catarrh  in  children.  It  deserves  to  be  tried,  particularly  in  rather  early  cases,  in 
doses  of  tV  to  i  of  a  grain  (gramme  0.005-0.01)  in  powder.  If  the  diarrhoea  lasts 
a  long  time,  we  may  very  well  use  opiates,  although  with  great  caution.  The  com- 
bination of  calomel  and  opium  often  does  good  service. 

1^  Calomel gr.  J  (grm.  0.01) ; 

Extracti  opii  •'  gr.  bV  (    "      0.002)  ; 

Pulv.  acacise   gr.  ss  (    "     0.03). 

M.  et  ft.  pulv. 

Sig. :  One  such  powder,  three  or  four  times  a  day. 

With  little  children  we  may  put  two  to  four  drops  of  laudanum  in  three 
ounces  (grammes  100)  of  liquid,  such  as  gum  mixture,  salep  decoction,  muriatic- 
acid  mixture,  etc.,  and  give  a  dessertspoonful  of  this  every  two  or  three  hours. 

Many  attempts  have  been  made  to  check  the  abnormal  processes  of  decomposi- 
tion in  the  intestine  by  prescribing  remedies  which  possess  antiseptic  and  anti- 
zymotic  properties.  Creasote  has  been  warmly  recommended  by  many,  four  to 
six  drops  in  two  ounces  (grammes  50)  of  water  with  half  an  ounce  (grammes  15) 
of  syrup,  a  teaspoonful  every  two  hours.  Other  drugs  used  for  the  same  purpose 
are  naphthaline,  one-half-  to  one-per-cent.  solution  of  dilute  muriatic  acid  in 
water,  and  one-per-cent.  solution  of  chloral  in  water.  A  prescription  for  naph- 
thaline is  as  follows : 

]^  Naphthaline   0.5  to     1.0; 

Mucilag.  acacise, 

Aquse  destillat aa  40.0 ; 

01.  menth^  piperitse gt.  j. 

M.  Sig. :  Shake.     Teaspoonful  every  two  hours. 

If  the  stools  have  a  green  color,  it  is  said  that  lactic  acid  is  especially  beneficial. 
A  teaspoonful  of  a  two-per-cent.  solution  may  be  given  fifteen  minutes  after  every 
m.eal. 

A  number  of  other  remedies,  "  astringents,"  are  given  to  act  directly  on  the 
diseased  mucous  membrane.  Those  most  to  be  recommended  in  chronic  diarrhoea 
are  subnitrate  of  bismuth,  one  or  two  grains  (gramme  0.05-0.1)  four  to  six  times 
a  day,  which  may  be  combined  with  opium,  nitrate  of  silver  (1  to  2,000  solution), 
alum  (1  to  200  solution),  guarana,  five  to  fifteen  grains  (gramme  0.3-1.0),  three 
times  a  day,  and  many  others.  Of  late,  tannalbine  has  been  much  recommended 
for  diarrhoea  in  children;  smaller  children  should  receive  four  grains  (gramme 
0.25)  several  times  a  day,  and  larger  children  twice  as  much,  in  milk  or  water. 

If  a  large  amount  of  mucus  in  the  stools  points  to  a  catarrh  of  the  large  intes- 
tine, we  may  sometimes  employ  irrigation  of  the  colon  with  excellent  results.  We 
inject  the  fluid,  one-per-cent.  solution  of  tannin  or  alum,  or  solution  of  acetate  of 
lead  (1  to  3  to  1,000),  once  or  twice  a  day.  The  amount  of  fluid  to  be  introduced 
at  once,  by  a  TIegar's  funnel,  with  a  gum-elastic  catheter,  may  reach  one  or  two 
pints  (half  a  litre  to  a  litre). 

In  many  cases  of  chronic  diarrhoea  it  is  said  that  the  continued  use  of  the 
water  of  the  Carlsbad  Miihlbrunnen  proves  wonderfully  beneficial  even  for  little 
children.  If  there  are  at  the  same  time  marked  gastric  symptoms,  such  as  fre- 
quent vomiting,  we  may  advantageously  employ  lavage.  This  is  performed  by 
means  of  a  soft-rubber  catheter,  about  six  millimetres  in  diameter,  connected 
31  * 


482  DISEASES    OE   THE   DIGESTIVE    OEGANS      , 

with  a  rubber  tube  attached  to  a  small  glass  funnel.  Eor  liquid  we  take  a  weak 
solution  of  hydrochloric  acid,  1  or  2  parts  per  mille,  or  a  0.5-per-cent.  solution  of 
boracic  acid. 

[In  view  of  the  great  importance  of  this  malady,  it  seems  desirable  to  remark 
on  one  or  two  points. 

In  the  first  place,  prophylactic  measures  are  deducible  directly  from  the  seti- 
ology.  'No  child  should  be  kept  in  a  large  city  in  summer,  if  it  can  be  provided 
for  at  the  sea-shore  or  in  the  country.  The  vast  number  who  must  perforce  re- 
main are  to  be  kept  under  the  best  general  hygienic  conditions  possible.  Mothers 
should  be  encouraged  to  take  their  children  to  the  relatively  pure  air  of  the  public 
parks  as  much  as  they  can.  The  relation  between  diet  and  the  diarrhoea  of  chil- 
dren should  be  dwelt  upon  whenever  there  is  opportunity. 

The  establishment  of  boards  of  health  has  done  much,  and  will  do  more,  to 
check  the  ravages  of  summer  diarrhoea. 

Great  advances  have  been  made  in  the  artificial  digestion  of  cow's  milk  within 
a  few  years.  By  the  aid  of  the  preparations  of  Fairchild  Bros.  &  Foster  the 
caseine  is  digested  in  part,  and  the  remaining  portions  coagulate  in  light  flocculi ; 
at  the  same  time  no  appreciable  taste  is  imparted  to  the  milk,  provided  that  a 
moderate  amount  of  care  is  exercised.  The  importance  of  preventing  the  forma- 
tion of  large,  firm  curds  has  long  been  recognized,  and  an  older  means  of  attain- 
ing this  end  was  mechanically  to  separate  the  curd  by  adding  to  the  milk  a  barley 
or  other  similar  water-gruel.  Mellin's,  Horlick's,  and  Ridge's  foods  also  deserve 
mention  in  this  connection.] 


CHAPTER   IV 

TYPHLITIS    AND    PEBITYPHLITIS 

{Appendicitis.     TypMitis  Stercoralis.     Inflammation  of  tJte  Ccecum) 

.ffitiology  and  Pathological  Anatomy. — Inflammation  of  the  caecum  and  its 
vicinity  has  a  special  place  among  the  diseases  of  single  portions  of  the  intes- 
tines. The  reason  why  circumscribed  inflammation  so  often  develops  here  is  to 
be  found  in  the  peculiar  anatomical  arrangement  of  the  csecum  and  its  appendix, 
fhe  vermiform  process.  It  is  evident  that  the  conformation  of  the  parts  makes 
it  particularly  easy  for  inflammatorj'  germs  to  settle  in  this  place. 

Formerly  it  was  believed  that  the  inflammation  might  often  be  limited  to  the 
csecum  itself.  It  was  asserted  that  impacted  ffecal  matter  occasioned  mechanical 
irritation  of  the  intestinal  wall,  and  thus  facilitated  the  attack  of  chemical  and 
infectious  agents.  In  this  way  arose  the  doctrine  of  "  typhlitis  stercoralis,"  but 
no  such  simple  typhlitis  has  ever  been  demonstrated  post-mortem,  and  although  it 
can  not  be  absolutely  denied  that  under  certain  circumstances  there  may  occur  a 
genuine  typhlitis,  as  a  result  of  the  accumulation  of  ffeces,  yet  its  frequency  has 
certainly  been  much  overestimated  (Sahli).  It  is  years  since  the  author  has 
made  a  diagnosis  of  "  typhlitis  stercoralis." 

By  far  the  greatest  number  of  cases  of  acute  inflammation  in  the  ileo-csecal 
region  are  perityphlitis;  that  is,  inflammation  of  the  peritoneum  and  the  con- 
nective tissue  surrounding  the  caecum.  From  the  point  of  view  of  pathological 
anatomy,  we  might  term  the  inflammation  of  the  retro-csecal  tissue  paratyph- 
litis, inasmuch  as  it  is  extra-peritoneal,  in  distinction  from  the  true  intra-peri- 
toneal  peritj^hlitis ;  but  clinically  we  can  not  maintain  this  distinction,  or  at 
most,  imperfectly.  The  starting  point  for  perityphlitis  is  the  vermiform  appen- 
dix.    To  this  there  are  rare  exceptions  in  which  the  inflammation  arises  from' 


TYPHLITIS   AND  PERITYPHLITIS  483 

perforation  of  the  csecum  itself.  The  appendix,  although  of  so  little  physiolog- 
ical importance  and  a  merely  rudimentary  portion  of  the  intestine,  plays  an  im- 
portant part  in  pathology.  Small  fsecal  masses  from  the  caecum  often  enter  the 
vermiform  appendix,  and,  under  some  circumstances,  they  may  remain  there.  The 
fluid  in  them  is  absorbed,  they  are  very  often  incrusted  with  lime-salts,  and  thus 
the  little  so-called  "  faecal  calculi "  are  formed.  In  many  cases  the  return  of 
faecal  masses  into  the  caecum  is  probably  hindered  by  the  valve  at  the  orifice  of  the 
vermiform  appendix,  Gerlach's  valve.  Foreign  bodies,  such  as  little  seeds  of 
fruit,  often  enter  the  vermiform  appendix  and  perhaps  give  rise  to  the  formation 
of  a  faecal  calculus;  but  one  must  be  cautious  in  assuming  that  any  small  hard 
mass  is  a  foreign  body,  for  these  calculi  often  have  such  a  rounded  shape  that 
they  were  formerly  considered,  very  erroneously,  to  be  retained  cherry-stones. 

In  many  cases  faecal  calculi  may  remain  in  the  vermiform  appendix  for  a  long 
time  without  producing  any  further  injurious  results,  but  as  a  rule  they  cause  a 
mechanical  irritation  of  the  mucous  membrane  which  leads  to  inflammation,  and 
often,  in  some  circumscribed  spots,  to  a  pressure  necrosis,  and  later  to  ulceration 
of  the  vermiform  appendix.  If  the  ulcer  does  not  cicatrize — it  always  may — the 
ulceration  gradually  deepens.  The  pressure  necrosis  of  the  wall  allows  ingress 
to  the  ordinary  pathogenic  agents  of  inflammation  and  suppuration,  among  which 
the  colon  bacillus  probably  plays  the  chief  role.  The  inflammation,  once  started, 
rapidly  spreads  to  the  surrounding  tissues.  In  rare  cases  a  diffuse  general  peri- 
tonitis is  immediately  developed.  In  by  far  the  greatest  number  of  cases  there 
are  timely  adhesions  around  the  appendix,  so  that  the  inflammation  is  limited 
and  encapsulated. 

It  is  improbable  that  faecal  calculi  occasion  the  development  of  all  cases  of 
perityphlitis,  but  they  certainly  do  of  the  majority.  It  may  be  that  the  inflam- 
matory germs  sometimes  reach  and  attack  the  appendix  unaided.  One  circum- 
stance that  would  favor  such  an  occurrence  is  the  abundance  of  adenoid  tissue 
in  the  appendix,  which  has  suggested  a  comparison  with  the  follicles  of  the  ton- 
sils. Sonnenburg  has  insisted  that  in  many  cases  the  inflammation  may  be  en- 
tirely limited  to  the  vermiform  appendix.  This  is  possible,  but  in  our  opinion  it 
is  out  of  the  question  to  make  at  the  bedside  an  absolute  diagnosis  of  "  appen- 
dicitis simplex." 

With  regard  to  the  nature  of  the  inflammation  in  perityphlitis,  there  can  be 
no  doubt  that  it  is  almost  always  purulent,  but  this  does  not  mean  that  there  is 
always  a  marked  destruction  of  tissue  with  the  formation  of  an  extensive  abscess. 
Such  results  are  found  only  in  the  severe  and  long-continued  cases.  In  the  ordi- 
nary milder  cases  there  are  usually  merely  an  infiltration  of  the  tissue  with  pus 
cells,  and  an  inflammatory  oedema  of  the  tissue,  or  perhaps  also  a  limited  fibrinous 
exudation.  There  is  an  inflammatory  tumor  which  consists  essentially  of  the 
thickened  intestinal  walls  and  the  coils  of  intestine  glued  together,  and  perhaps 
sometimes  also  of  impacted  faecal  matter;  and  inside  of  this  there  is  an  actual 
abscess,  small  and  localized,  and  lying  usually  in  the  immediate  neighborhood  of 
the  appendix. 

Perityphlitic  inflammation  can  very  well  be  compared  with  the  exudate  of 
parametritis,  for  in  this  also  the  cellular  infiltration  predominates  over  the  forma- 
tion of  pus.  In  rare  cases  there  may  be  an  encapsulated  exudation  of  a  more  sero- 
purulent  character. 

The  further  pathological  changes  in  perityphlitis  will  be  best  considered  in 
connection  with  the  clinical  symptoms. 

Symptoms  and  Clinical  Course. — We  have  already  said  that  there  is  great 
doubt  whether  simple  "  typhlitis  stercoralis  "  ever  occurs,  and  therefore  we  shall 
refrain  from  giving  a  description  of  its  symptoms,  which  we  should  have  to  invent, 
and  turn  at  once  to  those  clinical  phenomena  which  we  observe  in  acute  inflam- 


484  DISEASES    OF   THE   DIGESTIVE   OEGANS 

mation  of  tlie  ileo-csecal  region,  and  wliicli  are  now  almost  "universally  termed 
"  perityphlitis  "  [appendicitis] .  This  disease  has  great  clinical  importance,  for 
it  is  very  frequent  both  in  children  and  adults,  and  involves  great  danger  to  life, 
especially  if  there  is  not  prompt  surgical  interference. 

The  symptoms  of  perityphlitis  have  usually  a  rather  acute  development.  The 
patient  has  felt  perfectly  well,  and,  as  a  rule,  has  not  even  suffered  from  consti- 
pation, when  he  has  a  rather  sudden  pain  in  the  ileo-csecal  region.  There  may  be 
no  occasion  for  this,  or  there  may  be  some  such  cause  as  stooping,  lifting,  or  a 
long  walk.  ISTot  infrequently  there  is  slight  vomiting,  and  the  patient  feels 
languid  and  feverish.  The  bowels  may  be  constipated,  but  sometimes  they  con- 
tinue regular.  Many  patients  are  obliged  to  go  to  bed  at  once,  but  others  keep 
about  for  some  days  till  they  are  forced  to  give  up  because  of  the  aggravation  of 
their  symptoms,  particularly  the  pain.  It  is  a  point  of  some  practical  importance 
that  the  pain  is  by  no  means  invariably  referred  to  the  region  of  the  c^cum  at 
first,  particularly  as  the  position  of  the  appendix  is  veiy  variable,  l^ot  infre- 
quently the  pain  is  localized  more  in  the  middle  of  the  abdomen  or  toward  the 
left,  or  upward.  It  is  not  until  subsequent  days  of  the  attack  that  the  pain  grad- 
ually settles  in  the  true  ileo-csecal  region. 

Upon  objective  examination  we  usually  find  distinct  local  changes  in  the  ileo- 
csecal  region,  even  in  the  first  days  of  the  disease.  Our  manipulations  should  be 
extremely  cautious.  It  may  be  possible  by  careful  inspection  alone  to  recognize 
a  limited  swelling.  In  that  case  it  is  very  important  to  determine  whether  ten- 
derness is  present.  This  may  be  very  considerable,  or  comparatively  slight.  The 
typical  painful  spot  (McBurney's  point)  is  said  to  be  an  inch  to  an  inch  and  a  half 
(three  or  four  centimetres)  inward  from  the  anterior  superior  spinous  process, 
on  the  line  joining  this  process  with  the  navel.  This  localization  does  not  pos- 
sess great  importance,  because  the  painful  spot  varies  in  different  cases.  Some- 
times the  greatest  pain  is  felt  posteriorly,  in  the  lumbar  region,  suggesting  a 
retro-csecal  paratyphlitic  abscess  (vide  supra).  Lastly,  there  is  decisive  impor- 
tance in  the  discovery  of  abnormal  resistance,  or  of  a  more  or  less  sharply-defined 
tumor  due  to  the  inflammatory  exudation  (vide  supra).  This  tumor  can  usually 
be  made  out.  For  this  purpose  we  recommend  particularly  the  employment  of  the 
palm  of  the  hand  in  gentle  pushing  movements,  beginning  on  the  left  side  and 
gradually  proceeding  toward  the  ileo-c^cal  region.  This  is  the  best  way  of 
determining  the  size  of  the  inflammatory  mass.  In  milder  cases  it  is  also  per- 
missible to  make  deeper  palpation,  if  we  are  cautious.  The  examination  per 
anum  may  be  very  important :  we  have  seen  a  number  of  cases  in  which  no  exu- 
dation could  be  demonstrated  by  external  palpation,  while  a  large  inflammatory 
tumor  could  be  distinctly  felt  through  the  rectum.  The  results  of  palpation  are 
confirmed  by  percussion,  which  gives  either  a  muffled  tympanitic  resonance,  or 
m.arked  dullness  over  the  seat  of  the  disease.  In  general,  however,  the  results  of 
percussion  should  not  be  interpreted  too  strictly,  for  they  are  ambiguous,  because 
of  the  variations  in  the  degree  of  intestinal  distention. 

There  are  other  symptoms  to  be  considered  besides  the  local  ones.  Of  great 
importance  are  the  aspect  and  general  condition  of  the  patient.  If  the  patient 
has  no  suggestion  of  the  "  abdominal  facies  "  (vide  infra,  chapter  on  peritonitis), 
it  is  very  probable  that  the  inflammation  remains  circumscribed.  It  is  also  im- 
portant to  study  the  chart  of  the  temperature  and  pulse.  Elevation  of  the  bod-  ■ 
ily  temperature  invariably  suggests  aggravation  of  the  local  process.  Marked 
acceleration  of  the  pulse  almost  invariably  indicates  active  suppuration,  and  the 
advent  of  sepsis.  In  most  cases  the  fever  at  first  varies  from  101°  to  103°  (38.5°- 
39.5°  C),  and  if  the  patient  keeps  quiet  it  falls  in  the  next  few  days.  The  pulse 
varies  from  80  to  100.  ISTot  infrequently  there  is  a  decided  remission  in  all  the 
symptoms  after  the  first  two  or  three  days.     In  the  most  favorable  cases,  con- 


TYPHLITIS   AND   PEEITYPHLITIS  485 

valescence  may  ensue  upon  this  change,  but  very  often  the  fever  rises  again,  and 
in  such  cases  there  is  great  need  of  caution.  The  bowels  are  almost  always  con- 
stipated from  the  start.  Vomiting  occurs  only  temporarily,  if  at  all.  Frequent 
eructations  and  a  return  of  vomiting  later  on  in  the  attack  are  unfavorable  symp- 
toms. In  many  cases  there  is  temporary  difficulty  in  micturition,  so  that  a  cath- 
eter must  be  employed.  There  is  apt  to  be  a  distinct  increase  in  the  amount  of 
indican  in  the  urine  early  in  the  attack. 

A  question  of  the  greatest  clinical  importance  is  whether  the  perityphlitis  will 
lead  to  the  formation  of  a  large  abscess  or  not.  We  have  already  said  that  in  a 
pathological  sense  almost  all  cases  of  perityphlitis  are  suppurative,  but  the  forma- 
tion of  a  large  collection  of  pus  is  of  practical  importance.  This  is  recognized 
by  an  increase  in  the  fever,  or  by  the  mere  persistence  of  the  fever.  If  the  fever 
lasts  more  than  a  week  or  a  week  and  a  half,  suppuration  is  highly  probable.  If 
there  is  a  temperature  of  104°  to  105°  (40°-40.5°)  we  may  suspect  suppuration, 
even  at  an  early  period,  particularly  if  the  rate  of  the  pulse  corresponds  to  the 
height  of  the  fever.  Rigors  are  not  frequent  at  all,  but,  if  they  do  occur,  they  in- 
dicate abscess  formation.  The  local  signs  are  not  very  valuable  in  the  diagnosis 
of  an  abscess.  Early  in  the  attack  it  is  scarcely  ever  possible  to  detect  fluctua- 
tion, for  the  abscess  is  deeply  situated  and  surrounded  by  infiltrated  tissue.  For 
an  absolute  decision  it  is  usually  necessary  to  resort  to  exploratory  puncture. 
This  should  be  done  with  a  long,  slender  needle,  carefully  disinfected,  and  it  need 
cause  no  apprehension;  but  still  it  should  never  be  employed  unless  there  is  an 
important  reason  for  it. 

The  further  course  of  perityphlitis  is  favorable  in  the  overwhelming  majority 
of  cases.  After  a  few  days,  or  a  week  or  so,  if  the  treatment  is  appropriate,  the 
symptoms  abate  and  the  fever  disappears;  it  may  fall  gradually  or  defervescence 
may  be  quite  rapid,  almost  like  a  crisis.  The  inflammatory  tumor  shrinks,  the 
pain  abates,  the  bowels  become  regular,  and  the  patient  gradually  regains  com- 
plete health.  Often  there  are  manifold  variations  in  the  disease,  which  lengthen 
its  duration.  With  regard  to  the  pathological  changes  in  these  eases  that  re- 
cover, of  course  we  have  no  accurate  knowledge.  Sometimes  it  is  probable  that 
there  never  is  a  well-marked  abscess  formation,  but  only  an  inflammatory  infiltra- 
tion of  the  tissue,  which  subsides  again.  It  is  probable  that,  in  many  cases,  there 
is  a  small  abscess  which  discharges  spontaneously  into  the  intestine,  usually  into 
the  csecum,  but  exceptionally  into  other  portions  of  the  intestine.  One  thing 
which  seems  to  us  to  suggest  such  a  spontaneous  discharge  of  an  abscess  is  the 
not  infrequent  occurrence  of  a  crisis,  with  rapid  fall  of  temperature  and  simul- 
taneous cessation  of  all  the  other  symptoms.  Still,  we  scarcely  ever  detect  pus  in 
the  stools,  for  the  pus-corpuscles  are  changed  during  their  passage  from  the  colon 
to  the  rectum.    Perhaps  in  some  cases  small  localized  abscesses  are  reabsorbed. 

If  there  is  a  larger  abscess,  and  it  does  not  discharge  into  the  intestine  or 
receive  surgical  attention,  the  pus  seeks  other  paths.  The  worst  occurrence  is 
perforation  into  the  general  abdominal  cavity,  with  consequent  diffuse  perito- 
nitis and  speedy  death.  Or  the  abscess  may  continue  to  grow,  and  finally  break 
through  the  abdominal  wall;  or  it  may  extend  downward  into  the  iliac  fossa  or 
the  groins,  or  perforate  into  the  rectum,  bladder,  or  other  parts.  It  has  also 
happened  that  the  suppuration  has  involved  the  ileo-c£ecal  vein,  with  consequent 
pylephlebitis  and  the  formation  of  abscesses  in  the  liver.  In  most  of  these  chronic 
cases  the  symptoms  are  those  of  a  tedious  septico-pysemia  such  as  is  nowadays, 
thanks  to  the  progress  of  surgery,  very  rarely  seen.  As  the  inflammation  origi- 
nates from  perforation  of  the  intestine,  the  pus  is  apt  to  be  extremely  offensive, 
whenever  there  is  any  extensive  abscess  formation. 

The  greatest  caution  is  demanded  even  in  cases  in  which  the  course  of  the  dis- 
ease seems  at  first  favorable.     The  improvement  of  the  second  or  third  day  after 


486  DISEASES    OE   THE   DIGESTIVE   OEGANS 

the  sudden  onset  of  tlie  illness  is  often  deceptive,  as  we  have  already  mentioned, 
but  later  on  there  may  be  manifold  vicissitudes  in  its  course,  so  that  it  is  neces- 
sary to  watch  the  patient  constantly  and  closely.  Often  there  will  be  a  fresh 
elevation  of  temperature  and  the  formation  of  an  abscess  late  in  the  attack.  If 
the  bowels  are  obstinately  constipated  the  symptoms  of  obstruction  may  appear, 
such  as  tympanites,  frequent  eructations,  or  even  faecal  vomiting.  Complications 
in  other  organs  are  exceptional. 

Diagnosis. — In  general,  there  is  no  difficulty  in  the  diagnosis  of  perityphlitis, 
but  it  is  difficult  and  to  a  certain  degree  impossible  to  determine  accurately  about 
the  anatomical  changes,  the  exact  location  and  size  of  the  inflammatory  tumor, 
or  the  formation  of  an  abscess.  Here  a  careful  examination,  including  palpa- 
tion per  anum,  is  indispensable.  In  so  far  as  this  relates  to  the  extremely  impor- 
tant question  of  surgical  interference,  we  shall  revert  to  the  matter  when  consid- 
ering treatment. 

In  those  rare  cases  of  perityphlitis  which  have  a  chronic  course,  the  disease 
may  be  confounded  with  new  growths,  particularly  carcinoma  originating  in  the 
caecum  or  the  appendix.  Mistakes  in  diagnosis  have  also  been  occasioned  by 
tumors  of  the  right  kidney  and  the  right  ovary,  and  by  psoas  abscess  due  to  Pott's 
disease.  In  this  connection  it  may  be  mentioned  that  in  rare  cases  the  lumen  of 
the  appendix  may  become  occluded.  The  portion  of  the  appendix  thus  cut  off  is 
then  gradually  distended  by  the  secretion  of  its  mucous  membrane,  giving  rise  to 
so-called  dropsy  of  the  vermiform  appendix.  This  may  occasion  a  tumor  which 
can  be  felt  in  the  ileo-csecal  region. 

Prognosis. — If  we  take  all  the  cases  of  acute  inflammation  of  the  ileo-csecal 
region,  we  shall  find  that  some  80  or  90  per  cent,  get  well  without  operation,  but 
still  it  should  be  emphatically  stated  that  perityphlitis  is  a  dangerous  disease, 
and  every  year  brings  no  small  number  of  individuals,  both  children  and  adults,  to 
sudden  death.  The  main  danger  lies  in  the  rapid  onset  of  general  peritonitis,  or 
of  severe  sepsis.  Even  after  the  patient  has  survived  the  attack  he  may  be  trou- 
bled in  various  ways.  Eor  instance,  the  resultant  adhesions  and  chronic  exu- 
dates may  impede  the  action  of  the  bowels  for  a  long  while.  The  frequency  of 
recurrent  attacks  is  also  to  be  considered.  Many  persons  have  repeated  attacks 
of  perityphlitis  to  the  number  of  four  or  six,  or  even  more  during  their  lives. 
This  is  probably  the  result  of  peculiar  anatomical  conditions. 

Treatment. — Formerly,  when  the  opinion  was  still  held  that  many  of  the  cases 
of  acute  inflammation  of  the  ileo-csecal  region  were  to  be  regarded  as  simple 
typhlitis  stereoralis  due  to  constipation,  the  first  question  in  treatment  was 
whether  to  give  laxatives  or  opium.  If  there  was  typhlitis,  laxatives  ought  to  be 
given;  if  perityphlitis,  opium.  The  aim  of  diagnosis,  therefore,  was  to  distin- 
guish between  these  two  conditions.  To-day  the  conception  of  simple  typhlitis 
has  been  almost  completely  abandoned,  or,  at  any  rate,  it  has  become  very  limited, 
and  consequently  the  question  of  treatment  has  become  simpler,  for  now  laxa- 
tives are  scarcely  ever  given  at  the  onset  of  the  disease.  Perhaps  we  have  gone 
too  far  in  this  direction,  for  most  of  the  older  physicians  will  certainly,  like 
the  author,  recall  many  cases  of  what  was  supposed  to  be  typhlitis  stereoralis  in 
which  rapid  recovery  followed  the  immediate  use  of  castor-oil.  Still,  it  can  not 
be  disputed  that  the  premature  employment  of  laxatives  may  do  harm,  while  the 
administration  of  opium  in  a  proper  dose  probably  never  leads  to  unfavorable  con- 
sequences. Eor  this  reason  we  now  make  it  a  rule  in  any  case  of  inflammation 
in  the  ileo-c^cal  region,  with  acute  onset,  to  begin  with  opium ;  but  it  is  impor- 
tant, above  all,  that  upon  the  first  appearance  of  pain  the  patient  should  remain 
perfectly  quiet  in  bed,  and  should  have  for  nourishment  merely  milk  or  soup,  but 
no  solids.  An  ice-bag  should  be  applied  at  first  over  the  seat  of  the  disease,  and 
this  may  be  replaced  later,  or  at  once,  in  case  cold  is  not  well  borne,  by  wet  com- 


TYPHLITIS   AND   PEEITYPHLITIS  487 

presses  or  poultices.  Opium  is  administered  in  the  form  of  laudanum,  giving  fif- 
teen to  twenty  drops  several  times  a  day,  or  one  half  grain  to  a  grain  of  the  ex- 
tract (gramme  0.3-0.5).  The  amount  of  opium  to  be  administered  is  determined 
by  the  pain.  In  severe  cases  one  must  not  hesitate  to  use  large  doses,  but,  on  the 
other  hand,  the  dangerousness  of  the  remedy,  particularly  in  children,  should 
never  be  forgotten.  The  local  application  of  eight  to  ten  leeches  has  become  en- 
tirely out  of  fashion  and  may  be  dispensed  with,  but,  nevertheless,  it  is  unde- 
niable that  leeches  sometimes  give  the  patient  decided  relief.  With  this  treat- 
ment of  rest,  diet,  opium,  and  ice,  the  pains  are  usually  soon  relieved.  There  is 
no  necessity  at  first  to  be  anxious  about  opening  the  bowels.  Usually  there  is  no 
harm  if  the  patient  goes  without  a  movement  for  five  to  eight  days,  providing  that 
his  condition  is  satisfactory  as  regards  his  general  health,  pulse,  and  temperature. 
It  is  indeed  not  unusual  to  have  a  natural  operation  of  the  bowels  while  rather 
large  doses  of  opium  are  being  administered,  but  if  the  abdomen  becomes  more 
and  more  distended  and  there  is  rather  long-continued  constipation,  we  need  not 
hesitate  to  make  a  cautious  use  of  injections.  For  this  we  usually  choose  cool 
soapsuds,  and  let  it  run  through  an  ordinary  fountain  syringe  into  the  colon, 
while  the  patient  is  lying  on  his  back.  If  necessary,  the  injections  must  be  re- 
peated, and  of  their  beneficial  effect  we  have  often  been  convinced. 

We  have  already  insisted  that  every  patient  with  perityphlitis  should  be  most 
carefully  watched,  however  favorable  the  course  of  the  disease  seems  to  be.  The 
physician  must  ask  himself  every  minute  whether  further  symptomatic  treat- 
ment is  permissible,  or  whether  it  may  not  be  necessary  to  have  the  abscess  opened 
by  surgical  interference;  for,  although  we  are  by  no  means  of  the  opinion  that 
every  ease  of  perityphlitis  without  exception  demands  surgical  treatment,  yet 
there  is  no  doubt  that  prompt  surgical  interference  can  save  many  lives.  The 
question  when  operation  is  required  is  consequently  prominent  at  present  in  all 
discussions  of  this  disease.  Our  answer  can  only  be,  in  general,  that  immediate 
operation  is  invariably  indicated  as  soon  as  we  infer  that  perityphlitic  suppura- 
tion is  present.  We  dare  not  wait  for  its  absorption  or  its  spontaneous  discharge 
into  the  intestine,  because  of  the  possibility  of  its  breaking  through  into  the  peri- 
toneal cavity,  or  arousing  a  constitutional  sepsis,  or  some  chronic  suppurating 
process.  The  most  important  signs  of  the  imminence  of  these  dangers  may  be 
again  summed  up  as  follows :  persistence  or  fresh  exacerbation  of  the  fever,  after 
the  first  three  to  five  days;  increase  in  the  frequency  of  the  pulse  beyond  100  to 
120,  and  diminution  in  the  tension  of  the  pulse  (both  pulse  signs  are  important, 
because  they  almost  invariably  suggest  a  large  abscess)  ;  increase  in  the  local 
phenomena;  and,  finally,  above  all,  unfavorable  appearance  of  the  patient,  a  be- 
ginning "  abdominal  f  acies."  If  these  symptoms  appear  there  must  be  no  hesi- 
tation about  the  operation.  If  we  are  still  in  doubt,  we  may  first  make  an  ex- 
ploratory puncture.  If  even  a  drop  of  pus  is  obtained,  operation  is  absolutely 
demanded. 

It  is  impossible  to  give  more  detailed  rules,  of  general  application,  with  re- 
gard to  the  question  of  operating.  The  individual  circumstances  of  each  partic- 
ular case  and  the  personal  experience  of  the  physician  must  always  be  controlling 
factors.  ISTo  physician  can  avoid  unfortunate  occurrences  in  perityphlitis,  and 
the  most  experienced  practitioner  will  never  escape  a  certain  feeling  of  uneasiness 
in  any  case  of  the  disease;  still,  it  would  certainly  be  better  to  operate  too  early 
than  too  late.  It  is  true  that  when  the  general  condition  of  the  patient  is  favor- 
able, waiting  is  advisable,  but,  as  Sahli  has  well  said,  it  must  always  be  an 
"  armed  peace."  For  particulars  as  to  laparotomy  and  further  treatment,  as  well 
as  concerning  the  question  of  the  necessity  of  removing  the  appendix,  the  reader 
is  refei-red  to  text-books  on  surgery. 


488  DISEASES    OF    THE   DIGESTIVE    ORGANS 

CHAPTER   V 
PERFORATING    ULCER    OF    THE    DUODENUM 

There  is  a  form  of  ulcer  of  tlie  duodenum,  especially  of  its  upper,  horizontal 
portion,  whicli  is  precisely  analogous  to  the  round  gastric  ulcer  in  regard  to  aeti- 
ology, pathological  anatomy,  and,  very  largely,  symptomatology.  The  ulcer  is 
probably  also  due  in  most  cases  to  the  action  of  the  acid  gastric  juice  on  the  duo- 
denal mucous  membrane,  under  conditions  which  have  been  detailed  more  fully 
in  the  setiology  of  gastric  ulcer.  We  must  mention  here  the  noteworthy  fact  that, 
after  extensive  burns  of  the  external  skin,  ulceration  of  the  duodenum,  rarely  of 
the  stomach  also,  has  been  repeatedly  observed.  This  is  probably  due  to  the 
thrombosis  of  a  duodenal  vessel,  occasioned  by  the  setting  free  of  fibrine  ferment. 

Ulcer  of  the  duodenum  is  much  rarer  than  the  round  gastric  ulcer,  and,  in  dis- 
tinction from  the  latter,  it  has  been  found  decidedly  oftener  in  men  than  in 
women. 

Many  cases  of  ulcer  of  the  duodenum  run  their  course  entirely  without  symp- 
toms, or  they  cause  no  symptoms  until  sudden  haemorrhage  appears  (from  erosion 
of  the  pancreatico-duodenalis,  gastro-duodenalis,  etc.)  with  hsBmatemesis  and 
bloody  stools  (quite  often  bloody  stools  alone  without  hsematemesis),  or  until 
there  are  suddenly  signs  of  peritonitis  from  perforation.  In  many  cases  a  type 
of  disease  exists  for  a  long  time  whose  symptoms,  as  we  have  said,  are  so  like  the 
clinical  symptoms  of  gastrie  ulcer  that  we  can  very  rarely  distinguish  the  two 
forms  with  certainty  during  life.  We  notice  especially  continuous  or  neuralgic 
pain,  which,  in  ulcer  of  the  duodenum,  has  its  chief  seat  in  the  right  hypochon- 
drium.  Severe  gastric  symptoms,  especially  vomiting-,  are  not  as  common  as  in 
gastric  ulcer.  The  general  health  and  general  nutrition  may  remain  quite  undis- 
turbed for  a  long  time. 

Ulcer  of  the  duodenum  ends  by  cicatrization  and  recovery,  or  by  cicatrization 
and  the  formation  of  stenosis,  with  secondary  dilatation  of  the  upper  portion  of 
the  duodenum  and  of  the  stomach.  In  regard  to  the  different  adhesions  and  per- 
forations of  the  ulcer  into  neighboring  organs,  we  may  refer  to  what  has  been 
said  of  gastric  ulcer. 

The  treatment  must  be  governed  by  the  same  principles  which  were  laid  down 
in  the  treatment  of  gastric  ulcer,  especially  as  the  diagnosis  is  usually  doubtful. 


CHAPTER   YI 
TUBERCULOSIS    OF    THE    INTESTINES 

TuBEECULOSis  of  the  intestines  is  in  most  cases  a  secondary  disease,  and  is  one 
symptom  of  a  more  extensive  general  tuberculosis.  It  develops  most  frequently 
in  the  course  of  chronic  pulmonary  tuberculosis,  and  depends  here,  as  we  have 
seen  (compare  page  249),  upon  an  infection  of  the  intestines  by  the  tubercular 
sputum  that  has  been  swallowed. 

Intestinal  tuberculosis,  however,  may  also  be  a  primary  disease,  and  the  source 
of  further  extension  of  tuberculosis  over  the  body.  "  Tuberculosis  of  the  abdomi- 
nal organs,"  which  usually  comes  from  the  intestines,  has  a  clinical  significance, 
especially  in  children.     It  is  not  improbable  that  in  such  cases  the  first  infection 


TUBERCULOSIS    OF   THE   IXTESTINES  489 

of  the  intestine  comes  from  without,  and  that  the  tubercular  poison  is  taken  into 
the  body  with  the  food.  Here  we  must  suspect  especially  the  milk  from  cows 
with  pearly  distemper — that  is,  with  tubercular  disease. 

The  anatomical  changes  in  intestinal  tuberculosis  are  precisely  analogous  to 
the  tubercular  changes  in  other  mucous  membranes.  The  tubercular  new  growth 
has  its  origin  usually  in  the  lymph-apparatus  of  the  intestine,  in  the  solitary  folli- 
cles, and  in  Peyer's  patches.  The  first  miliary  tubercles  form  beneath  the  epi- 
thelium, and  soon  fuse  with  one  another  into  a  diffuse  infiltration.  In  its  further 
course  the  infiltration  on  one  side  extends  deeper  into  the  surrounding  tissue,  so 
that  it  attacks  the  submucous  and  muscular  coats  and  even  extends  to  the  serous 
coat,  and  on  the  other  side,  by  the  destruction  of  the  new  gTOwth  which  begins  at 
the  surface  and  constantly  spreads,  tubercular  ulcers  are  formed.  We  can  often 
make  out  with  the  naked  eye  single  miliary  tubercles  or  groups  of  them  at  the 
base  or  in  the  infiltrated  edges  of  the  ulcer.  This  is  especially  i)lain  in  deep- 
seated  ulcers  on  the  corresponding  jDortion  of  the  serous  coat.  The  form  of  the 
larger  tubercular  ulcers  is  often  irregular.  In  many  cases  the  long  diameter  of 
the  ulcer  is  parallel  to  the  circumference  of  the  intestine,  so  that  the  girdle-like 
ulcers,  which  are  especially  characteristic  of  tuberculosis,  are  formed. 

Tubercular  ulcers  are  situated  both  in  the  large  and  in  the  small  intestines. 
They  are  usually  most  marked  in  the  vicinity  of  the  ileo-csecal  valve.  Tubercular 
ulcers  in  the  stomach  are  extremely  rare.  Besides  the  intestinal  tuberculosis 
there  is  veiy  often  tuberculosis  of  the  mesenteric  lymph-glands,  and  also  fre- 
quently tuberculosis  of  the  peritoneum. 

The  symptoms  of  intestinal  tuberculosis  are  usually  quite  subordinate  to  the 
symptoms  caused  by  other  co-existing  tubercular  affections.  There  may  often  be 
quite  extensive  tubercular  ulcers  without  any  marked  symptoms,  but,  as  a  rule, 
the  onset  of  diarrhcea  turns  the  attention  to  the  intestinal  complication  (see  the 
chapter  on  pulmonary  tuberculosis). 

Tubercle  bacilli  have  been  repeatedly  demonstrated  in  the  fsecal  discharges, 
but  it  is  not  very  easy  to  find  them,  and,  moreover,  their  diagnostic  significance 
is  impaired  by  the  fact  that  they  may  be  referable  to  sputum  which  has  been 
swallowed. 

Primary  tuberculosis  of  the  abdominal  organs  sometimes  presents  quite  a  char- 
acteristic type  of  disease,  especially  in  children.  This  was  termed  by  the  older 
physicians  tahes  mesenterica.  The  chief  feature  of  this  type  of  disease  consists  in 
a  progressive  general  emaciation  and  anaemia,  which  are  usually  associated  with  a 
persistent  hectic  fever,  which  obstinately  resists  all  the  remedies  employed.  The 
abdomen  is  usually  swollen  by  meteorism,  but  it  is  sometimes  flat  and  sunken.  In 
some  cases,  but  less  frequently  than  was  formerly  believed,  we  can  feel  the  swollen 
mesenteric  lymph-glands  through  the  abdominal  wall  during  life.  The  involve- 
ment of  the  mesenteric  IjTnph-glands  obstructs  the  lymph-channels  which  serve 
for  the  absorption  of  fat,  a  circumstance  which  undoubtedly  contributes,  along 
with  others,  to  the  excessive  emaciation  frequently  seen.  The  liver  may  be  en- 
larged and  its  lower  border  can  often  be  felt.  The  bowels  are  irregular,  and  there 
is  usually  a  moderate  diarrhoea,  persisting  in  spite  of  all  remedies.  The  invari- 
ably fatal  termination  is  due  to  an  increase  of  the  general  marasmus,  or  to  a  final 
acute  tubercular  affection,  such  as  miliary  tuberculosis  or  tubercular  meningitis. 
The  autopsy  shows  tuberculosis  of  the  intestines,  peritoneum,  lymph-glands,  liver, 
etc.,  to  a  greater  or  less  extent.  The  lungs  may  be  quite  free  from  tuberculosis. 
We  will  return  to  this  affection  in  the  description  of  tuberculosis  of  the  peri- 
toneum. 

The  treatment  of  intestinal  tuberculosis  can  be  only  symptomatic.  Besides  the 
general  dietetic  treatment  which  seeks  to  keep  up  the  patient's  strength  as  far  as 
possible,  medical  interference  is  demanded  by  the  abdominal  pain  and  diarrhcea. 


490  DISEASES    OF   THE   DIGESTIVE   OEGANS 

The  chief  remedy  is  opium,  either  alone  or  combined  with  tannin,  tannigen,  ace- 
tate of  lead,  or  subnitrate  of  bismuth.  Sometimes  a  decoction  of  logwood  is 
beneficial.  Talc  also  has  lately  been  recommended ;  about  six  or  seven  ounces  (200 
grammes)  are  given  daily,  suspended  in  milk.  We  have  seen  some  good  results 
from  it.  The  most  serviceable  local  applications  are  poultices  or  cold  compresses. 
In  other  respects  the  treatment  coincides  with  the  general  treatment  of  tuber- 
culosis (vide  supra). 


CHAPTEE   VII 
SYPHILIS    OF    THE    RECTUM 

In  not  very  rare  cases  we  see  in  the  rectum,  especially  in  its  lower  portions, 
extensive  syphilitic  ulcerations,  which  produce  a  severe  and  practically  important 
tjTpe  of  disease.  The  more  intimate  relation  between  syphilis  of  the  rectum  and 
the  general  syphilitic  process  is  not  perfectly  clear.  According  to  quite  a  wide- 
spread opinion,  the  infection  of  the  rectum  comes  from  the  secretion  trickling 
down  from  the  ulcers  of  the  genitals.  The  facts  seem  to  support  this  view,  since 
syphilis  of  the  rectum  is  seen  much  more  frequently  in  women  than  in  men. 
Some  authors  have  even  asserted  that  all  the  so-called  "  syphilitic  "  ulcers  in  the 
rectum  have  no  connection  at  all  with  genuine  syphilis,  but  are  chancroids.  It  is 
in  fact  striking,  even  if  it  by  no  means  proves  such  a  hypothesis,  that,  at  the 
autopsy  of  persons  who  have  died  of  "  syphilis  of  the  rectum,"  we  rarely  find  defi- 
nite syphilitic  changes  in  other  internal  organs — a  fact  which  we  also  can  confirm. 

The  most  characteristic  mark  of  syphilitic  ulcers  in  the  rectum  is  their  tend- 
ency to  form  cicatrices  and  stenoses.  This  result  of  the  ulcer  is  also  important 
in  its  clinical  relations,  since  the  chief  symptoms  of  the  disease  usually  begin  with 
the  development  of  the  stenosis.  The  seat  of  the  stenosis  is  usually  so  low  down 
that  we  can  conveniently  reach  it  with  the  finger,  on  a  digital  examination  of  the 
rectum  during  the  patient's  life.  The  rectum  narrows  like  a  funnel  upward,  and 
we  can  feel  the  quite  sharp  edge  of  the  ring-like  cicatrix  with  the  point  of  the 
finger.  This  funnel-shaped  stenosis  of  the  rectum  is  so  characteristic  of  syphilis 
of  that  organ  that,  in  almost  all  cases,  we  can  make  the  diagnosis  with  perfect 
certainty  from  this  alone. 

The  rectum  and  the  descending  colon  are  usually  dilated  above  the  stenosis, 
and  here  extensive,  irregular  ulcerations,  with  undennined  edges,  are  usually 
found  in  the  mucous  membrane.  These  are  partly  of  a  specific  nature,  and  partly 
diphtheritic  ulcers  caused  by  the  pressure  of  the  accumulated  fsecal  masses. 

The  symptoms  of  syphilis  of  the  rectum  usually  develop  quite  gradually.  At 
first  the  bowels  are  irregular,  and  there  are  disturbances  of  defsecation  which  stub- 
bornly resist  the  ordinary  remedies  employed.  There  are  sometimes,  in  the  first 
stage  of  the  disease,  frequent  and  severe  haemorrhages  with  the  dejections,  as  we 
have  seen,  and  for  a  long  time  these  may  falsely  be  considered  to  be  "  bleeding 
from  htemorrhoids."  The  symptoms  become  more  marked  as  cicatrization  of  the 
ulcer  increases  and  as  stenosis  of  the  rectum  develops.  There  is  usually  a  decided 
catarrh  of  the  rectum,  so  that  the  thin  stools  contain  a  large  admixture  of  mucus 
and  pus.  The  patient's  condition  is  extremely  distressing,  from  the  pains  with  the 
frequent  but  always  scanty  dejections,  and  from  the  severe  tenesmus.  Nodular 
thickenings  and  prolapse  of  the  mucous  membrane,  and  sometimes  true  hasmor- 
rhoids,  form  about  the  anus.  The  patient's  strength  constantly  diminishes  from 
the  pain  and  the  continual  diarrhoea.  He  finally  becomes  emaciated,  looks  very 
pale  and  wretched,  and  has  fever  toward  night.     Death  ensues  from  increasing 


CANCER   OF   THE   INTESTINES  491 

general  weakness,  or  rarely  from  a  terminal  peritonitis  due  to  perforation,  after 
the  whole  disease  has  lasted  one  and  a  half  to  two  and  a  half  years. 

This  unfavorable  tennination  -unfortunately  seems  to  be  the  rule  in  all  the 
cases  described;  hence  the  prognosis  is  to  be  regarded  as  very  serious  in  all  cases 
of  syphilis  of  the  rectum.  Improvement  worthy  of  mention,  or  even  perhaps 
recovery,  is  possible  only  when  the  disease  is  recognized  at  the  outset  and  properly 
treated. 

At  the  outset  of  the  disease  the  treatment,  of  course,  must  consist  chiefly  of  an 
energetic  general  attack  upon  the  syphilis  by  mercurial  inunction  and  iodide  of 
potassium ;  but,  when  once  the  characteristic  funnel-shaped  stenosis  of  the  rectum 
has  formed,  we  can  not  expect  much  from  anti-syphilitic  medication,  since  this 
can  no  longer  exert  any  influence  on  the  cicatrices  and  their  results.  Improve- 
ment is  now  to  be  obtained  only  by  mechanical  dilatation  of  the  stenosis  by 
bougies,  or,  if  this  is  not  enough,  by  a  surgical  operation.  A  suitable  local  treat- 
ment by  irrigation  is  also  of  benefit  to  the  catarrh  and  to  the  ulcers  that  still  exist 
in  the  rectum.    Internally,  we  may  continue  to  use  iodide  of  potassium. 


CHAPTER   VIII 
CANCER    OF    THE    INTESTINES 

The  development  of  cancer  is  far  more  rare  in  the  intestine  than  in  the 
stomach.  Carcinoma  is  seen  with  any  frequency  only  at  the  lower  end  of  the 
intestine,  in  the  rectum.  Next  in  frequency  is  carcinoma  of  the  colon,  particu- 
larly the  caecum,  the  sigmoid  flexure,  and  the  hepatic  and  splenic  flexures.  Car- 
cinoma is  very  much  less  common  in  the  small  intestine,  in  which  its  favorite  seat 
is  the  duodenum,  particularly  the  neighborhood  of  the  common  duct. 

Most  cancers  of  the  intestine  appear  in  the  form  of  ring-like  swellings  that 
take  in  the  whole  circumference  of  the  intestine.  More  rarely  we  find  a  more 
diffuse  papillary  proliferation,  extending  over  a  larger  surface  of  the  intestine. 
There  is  often  quite  an  extensive  destruction  of  the  new  growth  on  the  surface 
of  the  cancer,  from  which  deep  ulcerations  arise.  Often  metastases  are  found  in 
the  lymph-glands,  liver,  and  other  organs.  Above  a  cancerous  obstruction  the 
intestine  is  usually  dilated,  with  thickening  of  its  muscular  coat,  and  inflamma- 
tion or  ulceration  of  its  mucous  membrane  due  to  the  impacted  ffecal  matter. 
In  its  histological  structure,  cancer  of  the  intestine  is  to  be  regarded  as  invariably 
a  cylindrical-celled  carcinoma,  which  sometimes  shows  a  plainly  glandular  struc- 
ture— adeno-carcinoma — and  sometimes  that  of  the  other  forms  of  cancer — seir- 
rhus,  medullary,  or  colloid. 

Cancer  of  the  intestines,  like  all  cancers,  occurs  chiefly,  if  not  invariably,  in 
advanced  life. 

The  clinical  symptoms  of  cancer  of  the  intestines  are  only  in  a  part  of  the 
cases  so  pronounced  that  we  can  make  a  positive  diagnosis  of  the  disease.  The 
symptoms  vary  with  the  location  of  the  growth. 

Cancer  of  the  rectum  begins  usually  with  distress  at  stool  (tenesmus)  and  pain 
in  the  rectum,  which  at  first  comes  only  with  defsecation,  but  later  becomes  almost 
continuous.  The  pain  often  shoots  into  the  neighboring  parts — the  sacrum,  the 
thighs,  the  genitals,  etc.  The  local  symptoms  gradually  increase,  the  stools  often 
contain  some  mucus  and  blood,  and  diarrhoea  alternates  with  obstinate  constipa- 
tion. The  patient  also  becomes  emaciated,  and  constantly  grows  weaker  and 
more  miserable.     Finally,  we  often  find  a  complete  paralysis  of  the  sphincter  ani, 


492  DISEASES    OF   THE   DIGESTIVE    OEGANS 

so  that  a  mucous,  bloody  fluid  constantly  oozes  from  the  half-open  anus.  An 
absolute  diagnosis  can  usually  be  made  with  ease  by  digital  examination  of  the 
rectum.  This  examination  should  never  be  omitted  in  any  suspicious  case,  for 
otherwise  it  is  only  too  easy  to  make  a  mistake.  Many  a  fatal  case  might  perhaps 
have  been  saved  by  a  timely  diagnosis.  External  piles  are  particularly  common 
in  cancer  of  the  rectum,  and  their  presence  should  by  no  means  prevent  the  physi- 
cian from  an  internal  examination.  If  there  is  cancer  of  the  rectum,  the  finger 
upon  being  introduced  detects  an  irregular,  firm  growth,  and  we  can  usually  make 
out  with  approximate  accuracy  its  extent  and  its  invasion  of  neighboring  organs, 
such  as  the  vagina  and  bladder.  Examination  with  the  rectal  speculum  some- 
times makes  the  diagnosis  more  accurate.  In  some  cases  the  destruction  of  the 
new  growth  may  cause  perforation  into  the  organs  mentioned,  and  we  can  easily 
understand  the  results  of  this,  such  as  cystitis,  purulent  discharges  from  the 
vagina,  etc.  We  may  also  have  peritonitis  from  perforation.  Secondary  cancer 
appears  with  especial  frequency  in  the  liver,  also  in  the  peritoneum  and  elsewhere. 

Carcinoma  of  the  colon  causes,  as  a  rule,  only  very  indefinite  symptoms,  which 
for  a  long  time  are  hard  to  interpret.  These  symptoms  consist  chiefly  of  distress 
at  stool,  obstinate  constipation,  dull  pains  in  the  abdomen,  and  the  signs  of  slowly 
increasing  general  weakness  and  emaciation.  If  the  stenosis  of  the  intestine 
increases  there  are  usually  attacks  of  colic,  with  the  gradual  or  perhaps  rapid 
development  of  all  the  symptoms  of  obstruction  of  the  bowels  (vide  infra,  Chapter 
XI).  In  many  cases  the  shape  of  the  faeces  is  peculiar.  They  are  ribbon-shaped, 
or  consist  of  queer  flattened  nodules  which  have  a  certain  resemblance  to  sheep's 
dung  (scybala).  JSTot  infrequently  we  find  in  the  dejections  an  admixture  of 
mucus,  pus,  and,  what  is  still  more  important,  blood ;  if  blood  is  persistently  pres- 
ent in  the  movements  (to  be  determined  by  the  guaiac-turpentine  test,  vide  supra, 
page  422),  or  if  there  are  bloody  or  muco-purulent  masses  in  the  discharges, 
cancer  is  suggested.  Exceptionally  there  may  be  found  in  the  stools  small  de- 
tached portions  of  the  new  growth.  The  examination  of  the  abdomen  is  often 
negative,  but  sometimes  it  is  possible  to  feel  the  new  growth  through  the  abdom- 
inal walls  as  a  distinct  tumor.  One  characteristic  of  the  tumor  occasioned  by 
intestinal  carcinoma  is  that  it  may  be  very  movable,  and  change  its  position 
because  of  its  own  M^eight  or  of  the  collections  of  faecal  matter.  As  a  rule,  the 
growth  does  not  move  with  respiration,  except  possibly  in  carcinoma  of  the  trans- 
verse colon.  It  is  easy  to  confound  intestinal  carcinoma  with  carcinoma  of  the 
stomach,  the  mesentery,  or  the  mesenteric  lymph-glands.  It  is  very  important  to 
know  that  in  case  of  intestinal  carcinoma  the  tumor  which  is  felt  may  be  not  the 
new  growth  at  all,  but  the  hardened  fsecal  masses  collected  above  it.  Such  fsecal 
accumulations  may  cause  all  sorts  of  errors  as  to  the  situation  and  dimensions  of 
the  new  growth.  In  such  cases  a  correct  conclusion  may  not  be  obtained  until 
after  continued  observation  and  the  use  of  laxatives  and  enemata.  It  is  also 
true  that  ordinary  fsecal  masses  may  be  mistaken  for  cancer  of  the  intestine  when 
there  is  no  intestinal  disease  of  any  sort.  In  exceptional  cases  there  may  be 
perforation  of  cancer  of  the  colon  into  the  stomach,  with  the  formation  of  a 
gastro-colic  fistula;  or  perforation  of  cancer  of  the  sigmoid  flexure  into  the 
bladder  or  into  the  peritoneum,  with  a  secondary  peritonitis,  which  may  be  local- 
ized or  dift'use.  Carcinoma  of  the  caecum  is  often  indistinguishable  for  a  long 
while  from  tumors  due  to  chronic  typhlitis,  or  perityphlitis.  Cancer  is  suggested 
by  the  age  of  the  patient,  the  tedious  course,  and  the  progressive  aggravation  of 
the  illness,  and  sometimes  also  by  swelling  of  the  inguinal  lymph-glands.  In  the 
surgical  wards  in  Leipsic  we  observed  a  case  of  cancer  originating  in  the  vermi- 
form appendix,  which  penetrated  through  the  skin. 

Cancer  of  the  small  intestine  is  very  rare.  It  is  distinguished  by  the  very 
great  movability  of  the  tumor,  if  one  is  found.     The  symptoms  are  those  of  grad- 


H^MOEEHOIDS  493 

ually  increasing  stenosis  (vide  infra).  Cancer  of  the  duodenum  is  similar  in 
many  respects  to  cancer  of  the  stomach,  particularly  of  the  pylorus.  It  leads  to 
stenosis  of  the  duodenum,  and  consequently  to  dilatation  of  that  portion  of  the 
duodenum  which  is  above  the  new  growth,  and  of  the  stomach,  and  so  occasions 
the  well-known  symptoms  of  gastrectasia  (vide  supra,  page  438).  Cancer  which 
is  seated  in  the  neighborhood  of  the  common  duct  usually  causes  excessive  and 
persistent  jaundice. 

The  course  of  all  cases  of  intestinal  cancer  is  absolutely  unfavorable.  The 
disease  may  last  for  a  considerable  time,  about  two  or  three  years.  On  the  other 
hand,  the  duration  of  the  special  symptoms  may  be  brief — that  is,  a  few  months 
or  weeks ;  undoubtedly  because  the  condition  existed  long  before  it  caused  symp- 
toms. The  final  result  in  intestinal  carcinoma  takes  the  form  either  of  increas- 
ing general  weakness,  or  of  perforation  with  fatal  suppurative  peritonitis.  Death 
may  also  be  occasioned  by  extensive  and  foul  suppuration  in  the  surrounding  con- 
nective tissue,  or  by  phlebitis  and  pyaemia.  Most  cases  run  their  course  as  a 
more  or  less  rapid  obstruction  of  the  intestine,  which  may  become  almost  com- 
plete. Sometimes,  however,  ulceration  of  the  cancer  occurs,  and  there  is  a  tem- 
porary abatement  of  the  symptoms  of  stenosis. 

The  only  possibility  of  successful  treatment  in  intestinal  carcinoma  is  by 
surgical  methods.  The  results  of  operation  are  very  favorable  in  cases  of  cancer 
of  the  rectum  if  the  disease  is  not  situated  too  high,  and  has  not  extended  too  far. 
Cancer  of  the  other  parts  of  the  intestine  has  a  much  less  promising  outlook. 
If  surgical  interference  is  impracticable,  treatment  must  be  merely  symptomatic, 
with  a  view  of  alleviating  suffering. 

We  will  append  a  few  remarks  about  sarcoma  of  the  intestine.  This  is  a  very 
rare  disease,  which  originates  from  the  submucous  layer  or  else,  in  the  form  of 
lympho-sarcoma,  from  the  lymph-follicles  of  the  intestine,  particularly  of  the 
small  intestine.  Both  varieties  exhibit  a  tendency  to  extend  cylindrically  over 
considerable  areas  along  an  intestinal  coil.  They  usually  do  not  lead  to  stenosis, 
but  they  may  even  cause  dilatation  of  the  affected  portion  of  the  intestine.  The 
tumors  which  are  formed  may  attain  to  very  considerable  size.  The  most  promi- 
nent symptoms  are  general  weakness  and  ansemia,  associated  with  slight  fever. 
These  constitutional  symptom.s  are  more  prominent  than  the  local  ones.  The 
course  is  usually  rapid  and  ends,  after  six  to  twelve  months,  in  death. 


CHAPTER   IX 
HJEMORRHOIDS 

By  the  name  "  haBmorrhoids  "  we  mean  diffuse  or  varicose  dilatations  of  the 
hfemorrhoidal  veins,  especially  of  the  venous  plexuses  at  the  lower  end  of  the 
rectum,.  Ha3morrhoids  are  single  large  varices,  which  usually  rise  from  the  sub- 
mucous layer,  and  push  the  mucous  membrane  out  before  them.  If  they  are  situ- 
ated outside  of  the  sphincter  ani  we  speak  of  external  haemorrhoids,  in  distinction 
from  internal  hfemorrhoids,  which  lie  above  the  sphincter.  The  size  of  the  nod- 
ules varies  with  the  fullness  of  the  dilated  veins ;  but  haemorrhoids,  as  a  rule,  do 
not  consist  exclusively  of  dilated  vessels,  for  we  often  find,  at  the  same  time, 
considerable  thickening  of  the  surrounding  connective  tissue,  so  that  the  whole 
mucous  membrane  has  a  swollen  appearance,  with  a  polypoid  proliferation  in 
parts.     The  hasmorrhoids  usually  present  themselves  as  bluish  tumors,  from  the 


494  DISEASES    OF   THE   DIGESTIVE   OEGAls^S 

size  of  a  pealo  that  of  a  walnut,  which,  surround  the  anus  like  a  garland.  Most 
of  them  have  a  broad  base,  while  others  are  apparently  pedunculated. 

The  chief  cause  of  haemorrhoids  is  frequently-repeated  stasis  in  the  veins 
affected.  The  position  of  the  hsemorrhoidal  veins  is  such  that  their  contents  are 
constantly  pressing  downward  by  the  action  of  gravity,  and  the  development  of 
varices  is  further  promoted  by  their  complete  lack  of  valves.  Special  local  con- 
ditions often  contribute  also  to  render  the  escape  of  blood  difficult;  thus  hasmor- 
rhoids  are  particularly  frequent  during  pregnancy,  also  in  persons  with  habitual 
constipation,  and  consequently  in  individuals  who  follow  sedentary  pursuits. 
Haemorrhoids  are  sometimes  found  as  a  result  of  portal  congestion  (in  hepatic 
cirrhosis  and  similar  conditions),  and  finally  in  general  circulatory  disturbances 
due  either  to  pulmonary  or  cardiac  disease ;  but  these  cases  are  not  so  frequent  as 
was  formerly  supposed.  Quite  often,  however,  we  can  discover  no  sufficient  cause 
for  the  development  of  the  disease,  and  we  are  then  forced  to  the  hypothesis  of  a 
local  disease  of  the  affected  venous  plexus,  which  is  probably  often  connected  with 
an  individual,  and  apparently  sometimes  hereditary,  predisposition.  We  most 
frequently  see  haemorrhoids  in  men  in  middle  life. 

Haemorrhoids  sometimes  cause  only  slight  symptoms,  or  none  at  all,  but  in 
other  cases  they  are  a  tedious,  burdensome,  and  even  distressing  evil.  The  chief 
symptom  is  pain,  which  is  felt  as  a  constant  burning  at  the  anus,  but  which  in- 
creases to  great  severity  at  each  dejection.  There  is  much  pain  when  the  haemor- 
rhoids and  the  surrounding*  tissue  gradually  get  into  an  inflamed  condition.  In 
the  skin  about  the  anus,  erythema,  excoriations,  and  sometimes  small  but  very 
painful  fissures  are  formed.  The  mucous  membrane  at  the  lower  end  of  the 
rectum  is  often  found  in  a  catarrhal  state,  which  gives  rise  to  the  presence  of  pus 
and  mucus  in  the  dejections — "  mucous  haemorrhoids."  The  worst  symptoms  are 
caused  when  by  pressing  and  straining  at  stool  an  internal  pile  is  forced  outward, 
and  constricted  by  the  sphincter.  If  the  constriction  is  not  speedily  relieved  the 
extruded  varix  becomes  much  swollen  and  inflamed.  This  change  is  favored  by 
a  cramp-like  contraction  of  the  sphincter.  Under  such  circumstances  there  may 
result  a  purulent  phlebitis  associated  with  very  great  pain,  high  fever,  and  severe 
constitutional  disturbance.  Sometimes  we  find  a  thrombus,  thrombo-phlebitis, 
or  suppurative  periproctitis,  even  if  there  is  no  previous  constriction. 

Haemorrhoidal  bleeding  is  a  frequent  and  familiar  symptom,  which  rises  from 
a  rupture  of  the  dilated  veins,  and  usually  comes  on  at  stool.  The  haemorrhage  is 
seldom  very  large,  so  that  the  loss  of  blood  is  in  itself  very  rarely  dangerous. 
Still,  the  rectal  haemorrhage  may  be  repeated  so  often  as  to  cause  severe  and  per- 
sistent anaemia.  The  swelling  of  the  varices  after  the  haemorrhages  have  ceased 
explains  why  the  haemorrhoidal  symptoms  are  apt  to  be  less  marked  as  long  as 
there  are  haemorrhages  than  when  there  are  none.  Hence  the  old  term  of  the 
"  golden  vein  "  for  haemorrhoidal  bleeding. 

Besides  the  local  symptoms  mentioned,  in  the  anus,  there  are  sometimes  other 
symptoms  which  are  due  to  an  implication  of  the  neighboring  venous  plexuses, 
the  vesical,  prostatic,  and  sacral  plexuses.  There  is  often  pain  in  the  sacral 
region,  difficulty  in  micturition,  and  in  women  vaginal  catarrh,  anomalies  of  men- 
struation, etc.  Since  the  symptoms  of  some  co-existing  morbid  conditions,  such 
as  abnormal  corpulency,  or  chronic  gastro-intestinal  catarrh,  may  be  added  to  the 
general  picture,  we  can  comprehend  why  medical  superstition  has  found  in  haem- 
orrhoids an  excuse  for  the  strangest  ideas,  like  that  of  "  transposed  haemor- 
rhoids " !  The  scientific  physician  should  be  careful  not  to  refer  such  manifold 
sjrmptoms  to  haemorrhoids  without  due  consideration,  for  otherwise  important  dis- 
eases may  be  readily  overlooked. 

Treatment. — The  treatment  of  chronic  piles  consists  mainly  in  caring  for  a 
regular  and  easy  evacuation  of  the  bowels.     This  is  the  best  means  to  diminish 


HABITUAL   COl^STIPATIOX  495 

the  local  diseomlort  (.see  the  next  chapter).  The  diet  to  be  prescribed  should  be 
determined  by  the  constitution  of  the  patient.  It  is  usually  advisable  to  limit 
the  ingestion  of  milk  and  to  recommend  in  its  stead  a  larger  proportion  of  vege- 
tables, in  a  broad  sense,  including  finait,  such  vegetables  as  grow  below  the  surface 
of  the  ground,  simple  puddings,  and  rice.  It  is  usually  advantageous  to  pre- 
scribe a  sufficient  amount  of  physical  exercise,  also  warm  or  cool  sitz-baths,  and 
cool  sponging  with  rubbing.  Moreover,  laxatives  are  to  be  considered,  particu- 
larly waters  containing  Epsom  salts,  also  the  regular  use  of  injections  of  cold 
water  or  oil;  compound  licorice  powder,  or  other  laxative  powders  or  pills;  and 
perhaps  a  course  of  the  waters  at  Carlsbad,  Marienbad,  Kissingen,  or  Tarasp.  A 
laxative  used  with  special  frequency  in  the  treatment  of  piles  is  sulphur.  This 
is  the  chief  constituent  of  most  "  pile  powders,"  e.  g. : 

R   Sulphuris  loti,            )  __  r^       /  ^-n 

Potassii  bitartratis,  [ ""3^^-  fe™-  15) ; 

rosLlhari'eitri,*      \ ^\  --=•  (^-  !»)•    ^- 

The  local  treatment  consists  chiefly  in  protecting  the  piles  from  irritation. 
The  parts  are  best  cleaned  after  every  movement  of  the  bowels  with  cotton  or  soft 
linen,  and  the  region  of  the  anus  is  to  be  touched  with  oil,  vaseline,  or  borated 
vaseline.  If  there  are  slight  inflammatory  symptoms  we  apply  compresses  wet 
with  a  solution  of  acetate  of  lead,  or  ice-water,  or  inject  olive-oil  into  the  rectum, 
or  try  suppositories  containing  morphine  or  cocaine.  If  the  inflammation  is 
more  severe  a  few  leeches  are  often  beneficial.  Constricted  piles  we  should  en- 
deavor as  soon  as  possible  cautiously  to  replace  with  the  finger.  The  pain  attend- 
ing this  operation  is  often  so  severe  that  chloroform  narcosis,  or  at  least  the  local 
application  of  cocaine,  is  required.  If  there  is  suppurative  phlebitis  an  incision 
is  necessary.  In  some  cases  a  radical  operation  for  the  piles  may  be  performed  at 
the  same  time. 

The  bleeding,  from  piles  is,  as  we  have  said,  seldom  severe  enough  to  demand 
special  treatment,  such  as  the  use  of  ice,  chloride  of  iron,  or  packing  the  rectum. 
If  the  haemorrhage  is  repeated  and  serious,  or  if  the  inflammation  causes  persist- 
ent and  extreme  discomfort,  we  should  urgently  recommend  operative  removal  of 
the  piles.  Particulars  as  to  the  methods  employed  for  this  purpose,  such  as  the 
use  of  the  thermo-cautery  or  the  knife,  will  be  found  in  the  text-books  on 
surgery. 

[Persistent  and  intelligent  treatment  will  often  bring  about  very  great  relief, 
or  even  complete  cure,  in  chronic  cases.  There  are  many  local  applications,  each 
of  which  has  its  warm  advocates — so  many  that  it  is  not  possible  here  to  go  into 
details.  Suffice  it  to  say  that  an  astringent  with  or  without  an  anodyne  may  be 
used  as  an  enema,  in  suppository  or  in  ointment.  The  fluid  extract  of  hamamelis, 
glycerine,  and  some  other  remedies  given  by  the  mouth,  are  reported  to  have 
afforded  good  results.] 


CHAPTER   X 
HABITUAL    CONSTIPATION 

Persistent  tendency  to  constipation  is  a  frequent  symptom  in  many  different 
acute  and  chronic  cases.     We  often  see  persistent  sluggishness  of  the  bowels  in  all 

*  Powdered  sugar,  3  j ;  volatile  oil,  gtt.  ij.    M. 


496  DISEASES    OF   THE   DIGESTIVE   OEGA^tS 

sorts  of  conditions  of  weakness,  in  general  ansemia,  in  diseases  of  the  stomacli, 
intestines,  liver,  lungs,  heart,  and  nervous  system,  and  it  is  caused  by  a  great 
variety  of  circumstances.  Often  the  weakness  of  the  peristalsis  of  the  intestine, 
and  particularly  of  the  colon,  is  merely  one  manifestation  of  a  general  debility; 
in  other  cases  the  activity  of  the  intestine  is  subnormal  because  of  the  insuffi- 
cient and  unstimulating  diet,  or  because  of  the  lack  of  physical  exercise.  In  a 
third  class  of  cases  there  is  disease  of  the  intestinal  wall  itself,  such  as  catarrhal 
conditions,  circulatory  disturbance,  atrophy  of  the  muscular  coat,  or  constriction 
of  the  lumen  of  the  intestine.  And  finally,  a  fourth  cause  is  disturbance  of  the 
innervation  of  the  intestine,  because  of  disease  of  the  brain  or  spinal  cord. 

The  above  are  examples  of  symptomatic  constipation,  but  in  this  chapter  we 
shall  not  discuss  these,  but  rather  eases  of  habitual  constipation  occurring  as  an 
apparently  independent  disease.  This  may  appear  alone  or  associated  with  other 
disturbances  likewise  purely  functional.  The  causes  of  this  frequent  and  impor- 
tant condition  are  by  no  means  invariable,  and  we  are  still  far  from  a  clear  under- 
standing of  the  nature  of  all  the  disturbances  that  belong  in  this  category.  Some- 
times habitual  costiveness  seems  to  be  associated  with  a  congenital  functional 
weakness  of  the  muscular  coat,  or  perhaps  of  the  nervous  apparatus  of  the  intes- 
tines. At  any  rate,  it  is  often  possible  to  trace  the  symptoms  back  to  the  earliest 
childhood.  In  other  cases  it  is  apparently  an  improper  mode  of  life  which  exer- 
cises a  disturbing  effect  upon  the  intestinal  activity ;  lack  of  bodily  exercise  often 
leads  to  disorders  of  the  bowels,  and,  still  more,  irregularity  in  eating  and  an  im- 
proper choice  of  food.  Sometimes  external  mechanical  influences  promote  con- 
stipation. In  women  unsuitable  apparel,  tight  bands  around  the  waist,  tightly- 
laced  corsets,  and  the  like,  certainly  produce  in  many  cases  a  permanent  malposi- 
tion of  the  intestinal  organs  ("  enteroptosis,"  compare  above  the  chapter  on  gas- 
troptosis,  page  460),  and  particularly  of  the  large  intestine.  It  is  not  improbable 
that  these  conditions  are  in  part  the  cause  of  the  chronic  constipation  which  is 
so  frequent  in  women  and  girls.  In  women  frequent  pregnancies  may  also  exert 
a  causative  influence  by  inducing  laxness  of  the  abdominal  walls  and  a  tendency 
to  enteroptosis. 

Habitual  constipation  is  associated  still  more  frequently  with  general  neuras- 
thenia than  with  any  of  the  conditions  thus  far  enumerated  (compare  the  chapter 
on  neurasthenia,  page  1193).  The  nature  of  this  association  is  probably  not  the 
same  in  every  case.  Often  neurasthenia  and  constipation  seem  to  be  co-ordinate 
symptoms;  sometimes  the  existing  constipation  has  an  unfavorable  effect  upon 
the  psychical  condition  of  the  patient,  rendering  him  feeble,  fretful,  out  of  sorts, 
and  nervous.  As  a  rule,  however,  neurasthenia  is  the  primary  disease,  and  then 
the  irregularity  of  the  bowels  appears  as  a  result  of  abnormal  nervous  influences, 
or  of  secondary  conditions  (vide  infra).  Often  the  two  states  act  in  a  vicious 
circle,  each  sustaining  and  aggravating  the  other.  The  most  essential  factor  is 
often  the  hypochondriacal  tendency  of  the  patient.  He  ascribes  an  excessive 
importance  to  irregularity  of  the  bowels,  and  regards  every  slight  disturbance  as 
of  extreme  gravity.  Even  when  the  movements  are  sufficient  he  can  not  free 
himself  frora  a  disordered  apprehension  that  they  are  not  really  adequate.  Such 
patients  come  at  last  to  devote  almost  all  their  thoughts  to  their  illness  and  make 
the  most  painstaking  observations  and  investigations  of  their  dejections,  having 
energy  for  nothing  else  and  no  joy  in  life.  They  seek  aid  from  all  sorts  of  physi- 
cians and  quacks,  and  yet  they  have  no  actual  confidence  in  any  one  and  do  not 
follow  the  practitioner's  directions  with  the  requisite  persistence.  In  many  of 
these  cases  the  constipation  is  only  apparent,  or  imaginary.  The  patient  fears  to 
eat  any  hearty  food  and  takes  little  nourishment,  and  consequently  the  excreta 
are  scanty.  In  other  instances,  however,  the  abnormal  psychical  conditions  have 
a  direct  inhibitory  influence  upon  the  intestinal  activity.    The  intestine  gets  out 


HABITUAL   CONSTIPATION"  40Y 

of  the  habit  of  regular  action.  Moreover,  the  unwise  use  of  internal  laxatives 
may  entail  actual  disease  of  the  intestine. 

Consequently,  if  the  physician  wishes  to  form  a  reliable  opinion  with  regard 
to  the  intestinal  function  in  a  case  of  chronic  constipation  from  actual  observa- 
tion, the  first  requisite  is  that  he  should  himself  see  the  dejections  of  the  patient 
for  some  time,  while  the  diet  is  normal  and  all  laxatives  are  omitted.  This  is 
much  easier  in  a  hospital  or  sanitarium  than  in  ordinary  private  practice.  When 
a  patient  is  under  observation  in  this  way  it  should  be  noticed  whether  the  abdo- 
men becomes  much  distended,  and  whether  hardened  faecal  matter  can  be  felt  in 
the  colon  or  the  sigmoid  flexure.  Furthermore,  the  dejections  should  be  examined 
as  to  their  amount  and  character.  They  may  seem  nubby,  hard,  or  as  if  they 
were  "  burned,"  or  of  abnormally  small  diameter,  or  flattened,  or  covered  with 
mucus.  If  we  find  that  the  evacuations  are  distinctly  abnormal  we  infer  that 
there  is  actual  disturbance  of  the  intestinal  functions;  while,  on  the  other  hand, 
our  examinations  often  show  that  the  complaints  are  exaggerated  or  imaginary. 

The  treatment  of  habitual  constipation  is  a  difficult  and  often  a  thankless 
task,  and  it  demands  patience  and  professional  tact.  It  goes  without  saying  that 
we  must  first  of  all  look  for  the  causal  factors.  If  we  succeed  in  improving  the 
underlying  disease — as,  for  instance,  the  chronic  gastro-intestinal  catarrh,  the 
chronic  affections  of  the  heart  or  lungs,  the  anasmic  conditions,  or  certain  nervous 
troubles — a  regulation  of  the  bowels  often  follows  of  itself.  In  ordinary  habitual 
constipation  we  must  first  attend  to  the  patient's  diet.  Since  most  of  these 
patients  also  suffer  from  symptoms  of  nervous  dyspepsia,  they  are  usually  very 
careful  in  their  diet,  and  take  only  a  little,  easily  digestible,  and  chiefly  liquid 
food.  It  is  no  wonder  that  no  good  dejections  follow  such  food.  Improvement 
can  be  obtained,'  in  such  cases,  only  by  eating  plenty  of  food  which  can  mechan- 
ically stimulate  the  intestine.  Hence  we  must  try  to  bring  the  patient  back  to 
ordinary  "  household  fare  " — to  take,  besides  plenty  of  meat,  a  sufficient  amount 
of  bread,  vegetables,  etc.  It  is  a  very  good  thing  to  recommend  especially  certain 
kinds  of  bread,  such  as  Graham-bread  or  rye-bread,  and  also  larger  amounts  of 
butter,  besides  fruit,  prunes,  grapes,  apples,  pears,  dates,  and  figs  either  raw  or 
boiled,  almonds,  nuts,  and  honey.  It  is  often  efficacious  to  have  the  patient  drink 
a  glass  of  cold  water  in  the  morning  before  breakfast.  Of  true  laxatives  we  should 
be  very  sparing,  for  the  patient  readily  becomes  accustomed  to  them,  and  the  dose 
has  to  be  constantly  increased.  Among  the  milder  laxatives  the  various  waters 
which  contain  Epsom  salts,  siich  as  Friedrichshall,  usually  one  or  two  wineglass- 
fuls,  are  prescribed.  For  more  continued  use  we  may  also  recommend  tamarinds, 
rhubarb,  aloes,  jalap,  cascara  sagrada,  and  extract  of  frangula.  It  is  not  possible 
in  this  connection  to  give  a  minute  description  of  all  these  remedies.  They  are 
prescribed  in  the  most  varied  combinations  in  the  shape  of  pills  and  powders.  It 
is  often  necessary  to  make  repeated  changes  in  the  medicine  and  its  dose  before 
the  most  effectual  prescription  is  hit  upon,  for  there  are  many  individual  pecul- 
iarities in  this  regard.  There  are  patients  with  simple  habitual  constipation  who 
for  years  take,  every  evening,  some  powdered  rhubarb,  or  one  or  two  laxative  pills, 
with  a  good  result  and  feel  perfectly  well.  In  most  cases,  however,  the  efficiency 
of  the  internal  laxatives  gradually  fails,  the  patient  is  obliged  to  take  more  and 
more  powerful  remedies,  or  increasing  doses,  in  order  to  get  any  effect.  In  such 
instances  it  is  always  best  to  abandon  internal  laxatives  altogether,  and  in  their 
stead  to  employ  external  physical  agencies,  or  to  stimulate  the  rectum  by  means 
of  injections,  irrigations,  and  the  like. 

The  regular  use  of  injections,  if  carried  oi;t  in  a  proper  manner,  may  be  con- 
tinued for  a  long  time  without  harm.  The  practice  may  indeed  be  carried  to  an 
injurious  excess,  and  occasion  at  last  a  catarrh  of  the  rectal  mucous  membrane, 
because  of  the  constant  local  irritation,  or,  at  any  rate,  a  needless  dependence 
32 


498  DISEASES    OF   THE   DIGESTIVE    OEGAXS 

upon  local  stimulation.  The  simplest  way  of  making  an  injection  is  by  means  of 
the  fountain  syringe.  There  are  also  various  shapes  of  injection  syringes  used  by 
many.  For  a  fluid  we  choose  simple  warm  water,  or,  what  is  often  more  efficient, 
cold  water.  We  can  strongly  recommend  the  employment  of  soapsuds  (a  tea- 
spoonful  of  powdered  soap  to  a  pint  or  two  of  water).  Lately,  again,  injections 
of  oil  have  been  in  great  vogue.  The  patient  is  placed  on  his  left  side,  and  by  the 
means  of  a  fountain  syringe,  eight  to  sixteen  ounces  (250  to  500  grammes)  of 
fresh  poppy  oil  [or  fresh  cotton-seed  oil]  (olive-oil  is  much  dearer)  is  slowly  intro- 
duced into  the  rectum.  Small  injections  of  glycerine,  one  to  two  drachms 
(grammes  5-10)  are  also  effectual.  Still  more  convenient  and  often  satisfactory 
is  the  employment  of  glycerine  suppositories,  which  are  dissolved  in  the  rectum 
by  the  heat  of  the  body. 

The  external  physical  remedies  employed  in  habitual  constipation  are  mas- 
sage, electricity,  and  hydrotherapy.  Regular  massage  is  often  attended  with 
good  results.  The  patient  is  stroked  with  the  flat  of  the  hands  Avith  moderate 
or  even  with  considerable  pressure,  beginning  at  the  caecal  region,  and  proceeding 
along  the  colon  to  the  sigmoid  flexure.  There  may  also  be  cautious  kneading 
of  the  abdomen.  A  ball  may  be  used  for  massage.  This  is  very  convenient,  and 
can  be  carried  out  by  the  patient  himself.  An  iron  ball,  weighing  about  five 
pounds  and  sewed  up  in  flannel,  is  rolled  for  several  minutes  in  a  spiral  course 
over  the  abdomen,  its  general  direction  being  that  of  the  hands  of  a  watch.  The 
electrical  treatment  consists  of  faradization  of  the  abdominal  walls,  or  galvaniza- 
tion of  the  intestine,  one  electrode  being  placed  upon  the  back.  In  the  way  of 
hydrotherapy,  cold  rubbing  and  sponging  are  employed,  and  are  often  associated 
with  massage.  In  addition  to  these  methods  medical  gymnastics  may  be  simul- 
taneously practiced,  with  a  view  to  regular  bodily  exercise,  and  the  invigoration 
of  the  abdominal  muscles. 

In  the  treatment  of  habitual  constipation  associated  with  hypochondriasis,  the 
flrst  rule  is  to  treat  the  patient's  mental  condition.  We  should  not  make  merry 
over  his  trouble,  nor  should  we  rudely  let  him  feel  that  we  do  not  consider  his 
complaints  so  important  as  he  himself  imagines.  The  patient  does  not  deserve 
to  be  scoffed  at,  since  his  subjective  symptoms  are  to  him  of  the  most  urgent 
nature;  but  it  is  extremely  important  to  divert  his  thoughts  from  his  trouble. 
As  in  many  other  reflex  processes,  so  in  defsecation,  the  voluntary  attention 
abnormally  directed  to  it  has  an  inhibitory  action.  Hence  we  admonish  the 
patient  to  think  of  his  trouble  as  little  as  possible  and  to  begin  his  regular  activ- 
ities again,  and  we  try  to  convince  him  of  the  groundlessness  of  his  fears.  The 
cathartics,  which  most  patients  have  already  taken  freely  without  the  desired 
action,  are  usually  of  no  advantage  at  all.  On  the  contrary,  it  is  almost  always 
necessary  to  forbid  the  patient  to  use  cathartics  at  all. 

We  should  not  only  employ  a  suitable  dietary  (vide  supra),  but  we  should  seek 
to  stimulate  the  intestinal  peristalsis  by  such  external  means  as  massage  and 
electricity  {vide  supra).  It  is  true  that  a  considerable  part  of  the  success  of  these 
methods  is  due  to  their  psychical  effect  upon  the  patient,  but  there  is  no  doubt, 
also,  of  their  direct  invigorating  influence  upon  the  muscular  coat  of  the  intes- 
tine. We  must  not  omit  a  proper  general  treatment :  cold  sponging,  baths,  a 
country  residence,  and  sufficient  physical  exercise.  Finally,  it  is  often  very  useful 
to  cause  the  patient  to  go  to  the  closet  at  a  fixed  hour  daily,  even  if  there  be  no 
special  desire  for  a  stool,  and  to  try  to  have  a  movement  of  the  bowels.  Thus  a 
sort  of  training  and  education  of  the  bowels  is  achieved,  even  when  the  patient 
at  first  believes  it  impossible. 

By  these  means  only  do  we  succeed  in  giving  the  patient  renewed  courage,  and 
sometimes  finally  in  attaining  recovery  even  in  severe  and  persistent  cases. 
In  all  cases  of  habitual  constipation  we  should,  however,  not  only  endeavor  to  hit 


STEICTUEE   AXD    OBSTEUCTIOX   OF   THE   INTESTrN:ES    499 

upon  the  proper  means  for  making  the  bowels  act,  but  if  it  is  in  any  wise  possible 
we  should  also  strive  to  arrange  the  patient's  life  so  sensibly  and  suitably  that  he 
will  have  regular  and  satisfactory  evacuations  without  any  special  means.  To  ac- 
complish this,  it  is  often  requisite  that  we  should  persuade  the  patient  to  give  up 
all  laxatives,  no  matter  how  constipated  he  may  be.  Such  a  course  is  naturally 
much  more  practicable  in  an  institution  than  in  a  private  house.  The  author  has 
himself  repeatedly  treated  patients  with  habitual  constipation  simply  by  regimen 
— i.  e.,  by  proper  diet,  cold  sponging,  and  sufficient  exercise  or  gymnastics,  with- 
out any  other  remedies.  In  such  patients  the  stool  would  often  be  delayed  for 
five,  eight,  or  ten  days,  and  yet,  what  is  remarkable,  without  any  special  incon- 
venience. Then  at  last  the  bowels  would  move  spontaneously,  or  with  the  aid  of 
a  small  injection  of  cold  water,  and  would  gradually  assume  complete  normal 
regularity. 


CHAPTER  XI 
STRICTURE    AND    OBSTRUCTION    OF    THE    INTESTINES 

.aitiology  and  Pathological  Anatomy. — Different  pathological  processes  may 
lead  to  stricture  or  complete  obstruction  of  the  intestinal  tube  in  different  parts. 
Since  in  this  affection  the  purely  mechanical  effect  of  the  intestinal  stenosis  is  the 
chief  cause  of  the  clinical  symptoms,  the  type  of  the  disease  is  very  similar  in  all 
the  cases  of  this  class,  in  spite  of  the  manifold  anatomical  causes.  Hence,  after 
enumerating  the  individual  affections  which  may  lead  to  stricture  of  the  intes- 
tines, we  shall  describe  their  symptoms  in  common. 

The  anatomical  causes  of  stricture  or  obstruction  of  the  intestines  are  as  fol- 
lows: 

1.  Congenital  closure  of  the  intestines  is  found  at  the  anus,  atresia  ani,  and 
much  less  frequently  in  the  colon  or  small  intestines.  The  form  first  mentioned 
is  the  only  one  of  clinical  interest,  since  it  may  be  relieved,  at  least  in  some  cases, 
by  operation.  All  the  other  forms  of  congenital  closure  of  the  intestines  are 
incompatible  with  a  long  duration  of  life. 

2.  Tumors  and  Cicatricial  Strictures. — Cancer  of  the  intestine  is  the  only 
tumor  that  has  any  clinical  significance.  "We  have  already  described  its  most 
important  anatomical  relations  and  the  possibility  of  intestinal  stenosis  as  a  re- 
sult of  it. 

We  see  cicatricial  strictures  most  frequently  in  the  large  intestine  after  recov- 
ery from  dysenteric  ulcers.  The  syphilitic  stenosis  of  the  rectum,  which  we  have 
already  described,  is  also  of  practical  importance.  Syphilitic  ulcerations  with 
cicatricial  stenosis  also  occur  in  higher  portions  of  the  colon,  perhaps  even  excep- 
tionally in  the  small  intestine.  Typhoid  ulcers  scarcely  ever  lead  to  cicatricial 
stenosis.  Strictures  consequent  upon  tuberculous  ulcers  of  the  intestine  are 
somewhat  more  frequent  than  typhoid  strictures,  but  still  they  are  very  rare. 
Cases  have  been  observed  in  which  there  were  several  tuberculous  strictures  of 
the  intestine,  while  no  sign  of  tuberculosis  could  be  found  elsewhere  in  the  body. 
Stenosis  of  the  duodenum  after  the  healing  of  a  duodenal  ulcer  (vide  supra)  re- 
sembles, in  its  clinical  symptoms,  stenosis  of  the  pylorus,  and  not  stenosis  of  the 
intestines. 

3.  Intestinal  Obstruction. — The  most  frequent  form  of  intestinal  obstruction 
comes  from  the  impaction  of  faeces.     From  the  different  conditions  which  cause 


500  DISEASES    OF   THE   DIGESTIVE    OEGAiTS 

enfeeblement  of  the  peristaltic  movements,  an  accumulation  of  faeces  (copro- 
stasis)  may  arise,  especially  in  the  colon.  This  accumulation  gradually  but  con- 
stantly increases  until  it  leads  to  well-marked  symptoms  of  intestinal  obstruction, 
and  in  cases  of  obstruction  from  other  anatomical  causes,  faecal  impaction  not 
infrequently  aggravates  the  condition. 

We  see  obstruction  of  the  intestines  from  other  causes  much  less  frequently 
than  from  impaction  of  faeces.  In  some  cases  impacted  gall-stones  have  been 
found,  especially  in  the  lower  part  of  the  ileum  and  in  the  neighborhood  of  the 
ileo-caecal  valve,  almost  completely  stopping  up  the  lumen  of  the  intestine.  Gen- 
uine intestinal  calculi  (composed  of  phosphates)  may  exceptionally  lead  to  ob- 
struction. Likewise,  occasionally  conglomerations  have  been  found,  composed  of 
indigestible  portions  of  food,  vegetable  fibers,  the  seeds  of  fruit,  potato  skins, 
grape  skins,  and  also  clumps  of  round-worms.  We  must  also  mention  here  the 
very  rare  cases  in  which  a  large  foreign  body  has  been  swallowed  and  wedged  itself 
into  some  part  of  the  intestine.  Such  a  thing  has  been  seen,  especially  in  chil- 
dren and  among  the  insane. 

4.  Intestinal  Constriction. — Although  the  mechanism  of  intestinal  constric- 
tion in  external  herniae  lies  in  the  domain  of  surgery,  we  must  mention  here  the 
chief  causes  of  the  so-called  internal  intestinal  constriction,  internal  incarcera- 
tion, or  strangulation.  In  the  abdominal  cavity  itself  pouches  and  diverticula 
are  found,  as  either  normal  or  abnormal  formations,  in  which  single  loops  of  in- 
testine may  be  caught  and  constricted.  The  duodeno-jejunal  hernia — the  so-called 
Treitz's  retro-peritoneal  hernia — is  worthy  of  special  mention,  and  comes  from  the 
entrance  of  a  loop  of  intestine  into  the  duodeno-jejunal  fossa.  This  hernia  may 
become  very  large.  It  is  sometimes  found  by  accident  in  the  cadaver,  not  having 
caused  any  symptoms  during  life,  but  in  rare  cases  it  may  be  the  cause  of  acute 
internal  constriction.  We  must  also  mention  the  hernia  of  the  omental  bursa — 
where  a  loop  of  intestine  passes  through  the  foramen  of  Winslow — the  intersig- 
moid  hernia,  the  subcaecal  hernia,  etc.  Diaphragmatic  hernia  is  of  greater  prac- 
tical significance  because  it  is  somewhat  commoner.  By  this  name  we  designate 
both  genuine  protrusions  into  the  diaphragm,  and  also  the  passage  of  abdominal 
viscera  through  congenital  or  acquired  (traumatic)  defects  in  the  diaphragm. 
These  herniae  may  exist  without  symptoms,  or  at  least  without  causing  any  signs 
of  severe  disease,  but  in  some  cases  they  cause  obstruction  by  constricting  or 
twisting  a  dislocated  loop  of  intestine. 

Those  cases  in  which  abnormal  slits  and  holes  in  the  omentum  or  mesentery 
give  rise  to  internal  constriction  are  to  be  added  to  the  list  of  the  internal  hernias. 
Finally,  abnormal  cords,  membranes,  and  false  ligaments  in  the  abdominal  cav- 
ity are  a  comparatively  frequent  cause  of  internal  constriction.  Such  cords 
and  bands  are  sometimes  left  as  the  results  of  a  former  peritonitis,  and  may  cause 
constriction  or  kinks  of  single  loops  of  intestine.  Small  diverticula  of  the  colon 
sometimes  form  adhesions  due  to  localized  peritonitis,  as  we  have  ourselves  seen, 
and  thus  occasion  dangerous  intestinal  stenosis.  One  such  false  ligament,  which 
must  be  specially  mentioned,  is  found  as  a  prolongation  of  Meckel's  diverticulum. 
By  this  we  mean  that  diverticulum  which  must  be  regarded  as  the  remains  of  the 
omphalo-mesenteric  duct,  still  persisting,  which  has  its  seat,  corresponding  to  the 
duct,  from  half  a  metre  to  a  metre  above  the  ileo-caecal  valve.  A  firm  cord  some- 
times arises  from  the  free  end  of  this  diverticulum,  the  obliterated  omphalo- 
mesenteric vein,  which  adheres  to  some  part  of  the  internal  abdominal  wall  and 
may  cause  constriction  of  the  intestine.  Adhesion  of  the  free  end  of  the  vermi- 
form appendix  has  been  the  cause  of  internal  constriction  in  some  cases. 
'  5.  Twists  (volvulus)  and  Knots  of  the  Intestine. — Twists  about  the  mesenteric 
axis,  and  complete  constriction  of  a  portion  of  intestine  from  this  cause,  are  seen 
most  frequently  in  the  sigmoid  flexure,  especially  if  the  mesentery  of  the  flexure 


STRICTURE   AND    OBSTRUCTION   OF   THE   INTESTINES     501 

is  unusually  narrow  congenitally.  The  spontaneous  correction  of  this  abnormal 
condition  is  hindered  by  the  weight  of  the  loops  of  intestine  filled  with  gas  and 
masses  of  fseces,  and  by  other  portions  of  intestine  lying  on  the  place  of  twisting. 
Sometimes  other  poi*tions  of  intestine  wind  themselves  several  times  about  the 
pedicle  of  the  twisted  loop  so  as  to  form  a  regular  knot.  Such  twistings 
have  been  seen  especially  between  the  sigmoid  flexure  and  a  portion  of  the  ileum. 
External  injury  sometimes  gives  rise  to  the  formation  of  a  knot.  In  some  cases 
abnormally  great  peristalsis,  severe  diarrhoea,  precedes  the  appearance  of  obstruc- 
tion. We  have  observed  a  fatal  case  of  volvulus  in  the  highest  part  of  the  small 
intestine,  consequent  upon  violent  vomiting,  excited  by  a  remedy  administered  by 
a  quack,  for  tapeworm.  A  most  important  factor  in  the  development  of  the 
symptoms  of  twist  is  the  mechanical  strangulation  of  the  blood-vessels  of  the  in- 
testine. This  causes  a  great  disturbance  of  the  circulation,  leading  to  paralysis, 
tympanitic  distention,  and  final  gangrene  of  the  intestinal  coils  which  are  in- 
volved. 

6.  Invagination  of  the  Intestine  (Intussusception) . — If  a  portion  of  intestine 
is  pushed  into  the  lumen  of  the  portion  that  lies  next  below,  we  term  the  process 
invagination.  The  cause  of  this  is  usually  assumed  to  be  a  diminution  or  a  com- 
plete absence  of  peristalsis  in  a  circumscribed  portion  of  intestine.  If  now  there 
are  energetic  movements  in  the  portion  immediately  above,  they  push  this  into  the 
paralyzed  portion.  According  to  Nothnagel,  the  beginning  of  the  invagination 
is  a  spastic  contraction  of  a  limited  portion  of  the  intestine,  in  the  shape  of  a  ring. 
This  furnishes  a  fixed  point,  and  the  contractions  of  the  longitudinal  muscles  of 
the  intestine  below  the  constricted  area  are  said  to  draw  the  lower  portion  of  the 
intestine  upward  over  this  ring. 

In  the  post-mortem  examinations  of  children  we  frequently  find  intussuscep- 
tion of  the  ileum,  which  has  occurred  shortly  before  death  and  so  is  of  no  clinical 
importance.  Sometimes  intussusception  has  occasioned  the  most  severe  symp- 
toms of  intestinal  obstruction.  It  occurs  particularly  in  children  up  to  the  tenth 
year,  and  it  may  be  of  sudden  onset  without  any  apparent  cause.  Intussusception 
of  this  sort,  which  often  involves  a  considerable  extent  of  the  intestine,  may  have 
its  seat  at  almost  any  part  of  the  bowels.  The  intussusception  most  frequently 
involves  the  csecum  and  the  lowest  part  of  the  ileum,  pushing  thence  into  the 
colon  (invaginatio  ileoccecalis) ;  intussusception  of  this  sort  may  be  so  extensive 
in  children  that  the  invaginated  ileum  reaches  into  the  rectum,  or  even  projects 
from  the  anus.  There  are  cases  in  which  the  ileum  alone  is  involved,  and  less 
frequently  the  colon  alone.  The  invaginated  portion  of  intestine  usually  suffers 
compression  of  its  blood-vessels,  particularly  the  veins.  This  is  followed  by  in- 
flammation of  the  constricted  portion,  and  the  inflammation  often  extends  to  the 
peritoneum.  Not  infrequently  there  is  gangrene  of  the  inner  portion  of  the  intes- 
tine, as  a  result  of  strangulation  of  the  afferent  vessels.  The  necrotic  portions 
may  slough  off,  and  be  discharged  at  stool.  Such  an  occurrence  has,  in  a  few  re- 
corded cases,  led  to  spontaneous  recovery  from  the  intussusception,  and  from  the 
obstruction  which  it  had  caused. 

We  must  mention  intestinal  polypi  as  a  special  cause  of  intussusception,  as 
they  gradually  pull  that  portion  of  the  intestine  in  which  they  are  situated  into 
the  neighboring  portion  next  below  by  their  weight.  This  has  been  repeatedly 
observed. 

7.  Compression  of  the  Intestine  from  without,  by  tumors  of  the  uterus,  ovarian 
cysts,  pelvic  abscesses,  omental  tumors,  etc.,  has  been  met  with  in  rare  cases  as  a 
cause  of  intestinal  stenosis.  The  symptoms  of  stricture  in  such  cases  develop 
either  very  gradually  or  sometimes  rather  suddenly. 

We  must  now  mention  certain  pathological  changes  which  may  follow  every 
obstruction,  from  whatever  causes  it  may  arise. 


502  DISEASES    OE   THE   DIGESTIVE   OEGAITS 

The  further  changes  in  the  intestine  deserve  the  chief  attention.  Above  the 
constricted  point  it  is  usually  greatly  swollen  from  gas  and  the  accumulation  of 
fgeces.  But  it  should  be  noted  that  the  abundant  fluid  found  above  the  narrow 
part  of  the  intestine  is  by  no  means  due  exclusively  to  the  ingesta,  but  probably  is 
largely  the  result  of  transudation,  and  the  secretion  of  intestinal  juices.  The 
intestinal  contents  are  very  apt  to  undergo  putrid  decomposition.  This  gives  rise 
to  a  large  amount  of  gas  which  may  not  be  reabsorbed,  so  that  above  the  obstruc- 
tion there  is  apt  to  be  a  very  marked  tympanites.  This  may  distend  almost  "the 
entire  intestine  above  the  constriction,  or  the  distention  may  be  limited  to  the 
constricted  coils  in  which  circulation  has  been  impaired,  and  in  which  conse- 
quently there  is  a  greater  tendency  to  decomposition  and  the  formation  of  gas. 
The  intestinal  coils  thus  distended,  being  irritated  by  their  decomposing  contents, 
usually  soon  become  inflamed;  their  walls  become  permeable  for  bacteria,  and 
thus  all  forms  of  intestinal  obstruction  lead  to  enteritis,  and  usually  promptly  to 
peritonitis.  A  severe  diphtheritic  process  often  develops  in  the  intestine,  with 
ulceration  above  the  stenosis.  In  the  inflamed,  softened  intestinal  wall,  thin 
from  its  abnormal  distention,  a  little  tear  easily  occurs  in  some  spot,  or  more 
rarely  a  genuine  perforation  following  an  ulcer.  Some  of  the  putrefying  contents 
of  the  intestine  thus  enter  the  abdominal  cavity,  and  an  intense  purulent  or  ichor- 
ous peritonitis  is  unavoidable.  This  is  why  acute  peritonitis  is  so  frequent  a  le- 
sion in  persons  who  die  of  intestinal  obstruction.  If  the  intestinal  stenosis  has 
lasted  a  long  time,  we  usually  find  in  the  upper  portion  of  the  intestine,  besides 
the  signs  of  inflammation,  a  manifest  hypertrophy  of  the  muscular  coat,  the  re- 
sult of  the  abnormally  active  peristalsis  by  which  the  muscle  has  tried  to  over- 
come the  obstacle.  The  intestine  below  the  constriction,  in  contrast  to  the  part 
just  described,  appears  narrow,  contracted,  and  empty. 

The  changes  in  the  other  organs  correspond  to  the  general  inanition.  The 
frequent  development  of  inhalation-pneumonia  is  easily  explained,  if  severe  vom- 
iting has  preceded  (vide  infra). 

Clinical  History. — In  regard  to  the  clinical  symptoms  we  must  distinguish  the 
cases  with  a  rapid,  complete  obstruction  of  the  intestine  from  those  in  which  the 
condition  develops  gradually,  and  where  there  is,  therefore,  at  least  for  a  time, 
merely  a  constriction  of  the  intestine. 

1.  Intestinal  Constriction. — The  first  symptom  of  the  partial  intestinal  con- 
strictions, which  arise  from  cicatricial  strictures  and  new  growths,  from  partial 
blocking  up  of  the  lumen,  from  intussusceptions,  etc.,  is  usually  a  disturbance  in 
defsBcation.  The  bowels  are  costive,  they  move  only  at  long  intervals,  and  their 
motion  is  often  associated  with  pain  and  tenesmus.  In  the  description  of  cancer 
of  the  intestines  we  have  already  mentioned  that  the  fseces  passed  sometimes 
have  a  peculiar,  flat,  compressed,  or  scybalous  form.  Blood  and  mucus  are  often 
mixed  with  the  dejections  and  are  due  to  the  character  of  the  primary  disease. 
In  some  cases  there  is  no  constipation,  and  there  may  be  even  constant  diar- 
rhoea. We  can  easily  understand  from  the  physiological  conditions  that  in  ste- 
nosis of  the  small  intestines,  whose  contents  have  an  approximately  fluid  con- 
sistency, disturbances  of  defecation  are  less  apt  to  take  place  than  in  stenosis 
of  the  large  intestine,  where  the  faecal  masses  have  already  assumed  a  more  firm 
consistency. 

Physical  examination  of  the  abdomen  often  gives  important  and  valuable 
information.  The  abdomen  is  usually  swollen  by  meteorism  (vide  supra).  The 
intensity  of  the  meteorism  varies  very  much  in  different  cases  and  at  different  times 
in  the  same  patient.  Meteorism  is  sometimes  absent,  especially  in  stenosis  at  the 
beginning  of  the  intestine.  There  may  then  be  gastrectasis.  The  marked  peristal- 
tic movements,  plainly  visible  through  the  abdominal  walls,  are  very  character- 
istic of  most  intestinal  contractions.     The  contour  of  single  loops  of  intestine  is 


STEICTUKE   AND    OBSTRUCTION   OF   THE   INTESTINES     503 

often  marked,  at  times  quite  sharply,  and-  then  we  can  semetimes  feel  the  thick- 
ened intestinal  walls  through  the  lax  abdominal  wall.  As  a  rule,  these  vigorous 
contractions  are  associated  with  severe  colic.  We  may  often  decide  upon  the  seat 
of  the  stenosis  from  the  location  and  course  of  the  visible  peristaltic  movements. 
In  general,  it  is  true  that  peristalsis  is  much  more  noticeable  when  the  stenosis 
is  in  the  small  intestine  than  when  it  is  in  the  colon.  We  must  finally  state 
that  we  have  been  repeatedly  struck  by  the  great  extent  and  strength  with 
which  we  could  feel  the  pulsation  of  the  aorta  through  the  swollen  loops  of  in- 
testine. If  we  put  our  ear  to  the  anterior  abdominal  wall  we  can  often  hear 
many  gurgling  and  splashing  noises,  which  sometimes  have  a  distinct  metallic 
quality.  Eructations  are  frequent,  and  in  some  cases  there  is  occasional 
vomiting. 

The  duration  of  all  these  symptoms  varies  with  the  nature  of  the  primary 
lesion.  Of  course  the  greatest  importance  attaches  to  the  condition  of  the  mus- 
cular layer  of  the  intestine  above  the  constricted  spot.  For  a  time  the  muscle 
may  overcome  the  obstruction  because  of  its  gradual  hypertrophy,  but  at  last  the 
muscular  coat  becomes  insufficient,  and  consequently  the  symptoms  become  more 
severe.  This  explains  why  the  symptoms  of  intestinal  stenosis  change  gradually 
or  suddenly  into  those  of  complete  intestinal  obstruction.  With  this  change  we 
have  grave  symptoms.  Sometimes,  in  cases  of  chronic  stenosis  of  the  intestine, 
some  temporary  causes  may  occasion  repeated  attacks  of  intestinal  obstruction, 
which,  however,  are  relieved  and  give  place  again  to  the  milder  symptoms  of  mere 
stenosis. 

The  duration  of  all  these  symptoms  differs  with  the  form  of  the  primary  dis- 
ease. Either  gradually  or  sometimes  quite  suddenly  the  symptoms  of  intestinal 
constriction  pass  into  those  of  obstruction.  Then  the  same  type  of  disease  devel- 
ops as  is  seen  in  all  acute  internal  strangulations. 

2.  Intestinal  Obstruction. — The  symptoms  of  intestinal  obstruction  (ileus) 
form  one  of  the  severest  and  most  frightful  conditions  known  to  pathology.  The 
patient  undergoes  a  rapid  change  for  the  worse.  The  signs  of  collapse  quickly 
develop;  the  face  sinks  in  and  assumes  a  wasted  and  sharp  expression,  the  ex- 
tremities become  cool  and  livid,  the  pulse  is  frequent  and  can  scarcely  be  felt, 
the  voice  is  weak  and  lifeless.  Respiration  is  impeded  by  the  upward  dislocation 
of  the  diaphragm.  The  temperature  usually  falls,  but  it  occasionally  rises.  As  a 
rule,  there  is  profuse  perspiration.  The  abdomen  is  much  swollen  from  meteor- 
ism,  and  is  usually  very  tender  on  pressure  from  beginning  peritonitis.  The 
passage  of  faeces  and  the  escape  of  flatus  cease  entirely.  We  often  see  the  peristal- 
tic motions  of  the  intestines  above  the  obstruction  through  the  abdominal  walls, 
but  in  some  cases  the  muscular  coat  is  so  paretic  that  it  is  no  longer  capable  of 
marked  peristalsis. 

The  most  characteristic  symptom  of  intestinal  obstruction  is  the  vomiting  of 
feculent-smelling  masses,  the  so-called  stercoraceous  vomiting.  There  is  often 
frequent  eructation  at  the  beginning  of  the  attack.  The  vomitus  at  first  is  of  the 
iisual  character,  but  it  soon  acquires  a  manifestly  putrid,  faecal  odor,  and  becomes 
finally  precisely  like  the  stools  in  diarrhoea.  The  old  opinion  is  false  that  in 
this  vomiting  real  fsecal  masses  were  forced  backward  from  the  large  intestine 
into  the  stomach  by  an  antiperistaltic  action  of  the  intestine.  Stercoraceous 
vomiting  occurs,  not  only  when  the  obstruction  is  in  the  large  intestine,  but  also 
(and  oftener)  in  obstruction  of  the  small  intestines.  In  this  case  we  have  to  do 
with  a  putrid  decomposition  of  the  contents  of  the  intestine  stagnating  above  the 
obstruction  (vide  supra).  Part  of  this  putrid  mass  reaches  the  stomach  because 
of  accumulation  and  regurgitation,  since  the  pylorus  gradually  yields  to  the  in- 
creasing swelling  of  the  small  intestines.  It  is  very  likely  that  retrograde  "  anti- 
peristaltic "  movements  of  the  intestinal  muscles  contribute  to  the  passage  upward 


504:  DISEASES    OF   THE   DIGESTIVE    OKGAiNrS 

of  the  intestinal  contents.  The  vomiting-  itself  is  probably  caused  in  large  part 
by  the  irritation  of  the  peritoneum,  and  perhaps  by  the  stimulation  of  the  abnor- 
mal matter  which  has  entered  the  stomach.  If  death  does  not  occur  in  a  short 
time,  the  clinical  picture  exhibits  distinct  indications  of  secondary  peritonitis; 
the  temperature  rises  a  little,  the  skin  grows  dry  and  hot,  and  the  abdomen  is 
very  tender  upon  pressure. 

We  must  mention,  finally,  the  important  changes  in  the  urine  which  occur  in 
the  various  forms  of  constriction.  In  the  contents  of  the  intestine,  stagnating 
above  the  stenosis,  large  amounts  of  indol  and  phenol  are  formed  from  the  decay 
of  the  albuminous  substances,  along  with  other  products  of  decomposition;  they 
are  in  part  absorbed  and  excreted  with  the  urine.  Hence,  in  stenosis  of  the  small 
intestines  we  often  find  that  the  urine  contains  an  increased  amount  of  indican  * 
(Jaffe)  and  phenol  (Brieger),  but  in  stenosis  of  the  large  intestine  the  amount  of 
indican  in  the  urine  is  not  increased,  because  the  albuminous  substances  capable 
of  decomposition  are  no  longer  present  in  the  contents  of  the  large  intestine  to 
cause  it. 

The  course  of  intestinal  obstruction  differs  according  to  the  anatomical  causes 
which  exist  in  different  cases.  In  many  cases  of  acute  internal  strangulation  the 
severe  type  of  general  disease  above  described  develops  in  a  very  short  time,  and 
may  lead  to  death  in  a  day  or  two.  In  such  cases  death  is  caused  by  the  poisonous 
action  of  the  absorbed  gases,  generated  by  decomposition,  or  it  may  be  due  to 
reflex  paralysis  of  the  cardiac  nerves.  Usually,  however,  the  course  is  somewhat 
longer,  and  occupies  about  a  week.  In  intestinal  obstruction  which  develops 
gradually  from  intestinal  constriction,  the  disease  may  go  on  longer  and  show 
many  variations  in  its  intensity.  In  mere  intestinal  constriction  we  can  make 
fewer  definite  statements  as  to  the  duration  and  course  of  the  affection,  since 
the  symptoms  of  the  disease  depend  entirely  upon  the  form  of  the  primary 
disorder. 

In  a  great  majority  of  cases  intestinal  obstruction  terminates  unfavorably. 
Death  results  either  from  increasing"  collapse  or  from  secondary  peritonitis  (vide 
supra),  or  in  rare  cases  from  further  complications,  such  as  pysemic  conditions  or 
pneumonia.  Eecovery  (independent  of  operation)  may  occur  even  after  the 
severest  symptoms,  but  it  is  very  rare.  The  obstructions  from  impaction  are  most 
hopeful  for  recovery.  Impacted  gall-stones,  fsecal  accumulations,  etc.,  may  be 
evacuated,  after  which  the  severe  symptoms  disappear.  The  possibility  of  recov- 
ery in  intussusception,  by  throwing  off  the  gangrenous  internal  portion  of  intes- 
tine, has  been  mentioned  above.  We  can  not  wholly  deny  that  internal  strangu- 
lations are  capable  of  restoration,  although  the  prognosis  must  almost  always  re- 
main doubtful  on  account  of  the  uncertainty  of  the  diagnosis  in  any  indi- 
vidual case. 

In  the  partial  intestinal  constrictions,  too,  the  nature  of  the  trouble  causes  an 
unfavorable  termination  in  most  cases,  either  from  the  primary  disease  itself  or 
from  the  complete  obstruction  that  finally  follows,  but  the  possibility  of  recovery 
can  not  be  wholly  excluded  in  certain  conditions,  such  as  impaction  or  external 
compression. 

Varieties  of  Intestinal  Obstruction. — Diagnosis. — To  go  into  details  as  to  the 
clinical  symptoms  of  all  the  separate  forms  of  intestinal  constriction  and  obstruc- 
tion would  lead  merely  to  repetitions.  In  most  of  the  acute  and  many  chronic 
cases  the  diagnosis  can  generally  be  made  only  as  to  the  presence  of  a  mechanical 

*  The  indican  test  is  performed  in  the  foUowinpr  ■"ay  :  We  mix  equal  volume?  of  urine  and  oflBeinal 
hydrochloric  acid  (P.  G.),  and  then  add,  drop  by  drop,  a  concentrated  solution  of  chloride  of  lime 
shaking  it  after  each  drop.  If  now  chloroform  is  added,  upon  shaking  again,  the  chloroform  will  take 
on  a  striking  blue  color,  if  the  urine  contains  any  considerable  amount  of  indican. 


STEICTURE   AXD   OBSTRUCTIOIT   OF   THE   INTESTINES     505 

obstacle  in  the  intestine,  but  the  nature  of  the  obstruction  can  at  best  be  merely 
surmised.  Yet  in  many  cases  we  may  reach  a  more  exact  diagnosis  by  careful 
questioning  and  examination.  Above  all,  we  should  accurately  examine  all  the 
known  localities  for  external  rupture,  including  the  inguinal  canal,  the  thighs, 
and  the  navel,  and  we  should  never  omit  to  make  rectal  and  vaginal  examinations. 
Often  valuable  conclusions  can  be  reached  by  inflation  of  the  colon  by  means  of  a 
rectal  tube  attached  to  an  ordinary  Davidson's  syringe,  for  in  this  way  stenosis  of 
the  colon  is  sometimes  rendered  distinctly  palpable.  It  is  also  very  important  to 
ii.->ake  a  careful  examination  of  the  abdomen  as  early  as  possible,  employing  sight, 
touch,  and  percussion.  We  can  often  recognize  the  place  of  obstruction  because 
of  the  localized  protuberance,  and  the  tenderness  of  certain  intestinal  coils.  It 
is  of  the  greatest  importance  to  detect  intestinal  peristalsis,  if  present.  With 
regard  to  distinguishing  between  stenosis  of  the  colon  and  of  the  small  intestine, 
stenosis  of  the  small  intestine  is  indicated  by  a  special  prominence  of  the  central 
portion  of  the  abdomen,  by  the  visible  and  active  peristaltic  motion  of  many  coils 
of  intestine,  by  the  occurrence  of  feecal  vomiting,  and  by  the  presence  of  a  strong 
reaction  of  indican  in  the  urine;  while  stenosis  of  the  large  intestine  is  char- 
acterized by  a  distention  which  corresponds  more  with  the  course  of  the  colon, 
without  much  visible  peristalsis,  and  a  slow  development  of  severe  constitutional 
symptoms.  We  shall  recur  later  to  the  differential  diagnosis  between  intestinal 
obstruction  and  diffuse  peritonitis,  when  considering  the  latter. 

Of  the  special  varieties  of  intestinal  obstruction,  we  will  call  attention  to  two 
as  of  practical  importance.  Intussusception  appears,  as  we  have  indicated, 
mainly  in  children.  Its  symptoms  usually  begin  rather  suddenly  with  violent 
abdominal  pain.  There  soon  appear,  also,  liquid  dejections  of  bloody  mucus  or 
almost  clear  blood,  originating  from  the  constricted  portion  of  the  intestine. 
O-fff^n  there  is  great  tenesmus  and  protrusion  of  the  anus.  We  have  already  men- 
tioned that  sometimes  the  invaginated  portion  of  intestine  may  be  felt  in  the 
rectum.  The  further  course  corresponds  with  the  ordinary  symptoms  of  intes- 
tinal obstruction,  except  that  it  should  be  said  that  faecal  vomiting  does  not 
occur  in  the  ordinairy  ileo-csecal  intussusception,  until  comparatively  late  in  the 
attack.  The  other  form  of  intestinal  obstruction  which  we  wish  to  mention  here 
is  due  to  the  accumulation  of  large  amounts  of  fsecal  matter  in  the  rectum.  We 
sometimes  find  monstrous  accumulations  of  faeces  in  the  rectum,  especially  in  old 
women  who  have  previously  suffered  from  habitual  constipation,  or  in  whom 
constipation  is  due  to  some  other  affection.  Severe  symptoms  usually  come  on 
quite  suddenly,  after  long-continued  mild  prodromal  symptoms,  and  these  severe 
symptoms  are  much  like  the  picture  of  internal  strangulation — severe,  sometimes 
colicky,  abdominal  pain,'  great  tenderness  of  the  abdomen,  which  is  usually 
swollen,  marked  general  collapse,  loss  of  strength,  a  small  pulse,  an  outbreak  of 
cold  sweat,  vomiting,  etc.  If  we  try  to  give  an  enema  in  such  cases,  very  little 
fluid  runs  into  the  rectum.  On  introducing  the  finger,  it  usually  strikes  solidly 
on  old.  hard,  faecal  masses  above  the  sphincter,  and  there  is  often  nothing  left  but 
to  undertake  the  dirty  task  of  removing  at  least  a  part  of  the  scybala  with  our 
own  hands.  We  may  then  succeed,  by  repeated  enemata  and  by  giving  cathartics 
internally,  in  removing  sometimes  quite  an  incredible  amount  of  accumulated 
faeces,  and  in  obtaining  thus  a  rapid  recovery  from  the  condition. 

[The  diagnosis  of  the  nature  of  an  intestinal  obstruction  is  so  difiicult  in  many 
cases,  and  yet  so  important  with  reference  to  treatment,  that  the  editor  ventures 
to  introduce  tables  of  differential  diagnosis  of  the  more  common  forms  of  the 
condition.  These  tables  are  based  upon  the  masterly  prize-essay  of  Treves,  of 
London. 


506 


DISEASES    OF   THE   DIGESTIVE   OEGANS 


ACUTE  INTESTINAL  OBSTRUCTION 

Chief  Common  Symptoms. — Sudden  pain,  intermittent  or  constant,  with  exacerbations  ;  tends  to  become 
constant  with  time.  Vomiting,  early,  severe,  becoming  feculent.  Constipation,  more  or  less  abso- 
lute.   Abdominal  distention.    Shock. 


Age  and  Sex. 
History 

Onset 

Pain 

Local  Ten- 
derness . . 

Vomiting 

Constipation  . 


Prostration 

Tenesmus.  . . . 
Abdominal 

Wall  . . . . 
Tumor 

Meteorism  . . 


Strangulation  by  Bands  or 
THROtJGH  Apertures  (25 
per  cent,  of  all  cases  of 
acute  obstruction). 


Young  adults ;  rare  after  40. 

Previous  peritonitis  in  68  per 
cent. ;  previous  attacks  of 
obstruction  in  13  per  cent. 

Sudden  in  70  per  cent. 

Early,  severe,  continuous, 
with  exacerbations. 

Absent  at  first,  appears  later. 

Early,  marked ;  in  60  per  cent. 

becomes  feculent ;  affords 

no  relief. 
Continuous  and  absolute  ;  no 

blood. 

Marked. 

Absent. 

Flaccid  unless  peritonitis. 
Very  rare. 

Slight,  appears  about  third 
day. 


Volvulus  op  Colon. 


Males  as  4  :  1  ;  40  to  60. 
Previous  constipation. 


Sudden. 

Early,  less  severe,  intermit- 
tent at  first,  becoming  con- 
stant with  exacerbations. 

Early  over  distended  coil, 
and  constant. 

Less  early,  severe  and  con- 
stant ;  often  affords  relief. 

Early  and  absolute  ;  no 
blood. 

Rather  less  marked  ;  may  be 

dyspnoea. 
In  15  per  cent. 

Rigid  from  early  peritonitis. 
Absent. 

Early,  rapid,  increases,  and 
is  extreme. 


Acute  Intussusception. 


More  than  50  per  cent,  under 

10  years. 
Usually  negative. 


Sudden  in  75  per  cent. 
Early  and  severe  :  increasing 

and  later  subsiding;  at  first 

paroxysmal. 
Common  about  a  tumor. 

Still  less  early  and  severe :  in 
25  per  cent,  becomes  fecu- 
lent. 

Seldom  absolute  ;  diarrhoea 
not  uncommon ;  blood  in  80 
per  cent. 

Marked. 

In  55  per  cent.,  and  often 
early. 

Flaccid  unless  peritonitis. 

In  50  per  cent. ;  invagination 
sometimes  felt  in  rectum. 

Rare,  unless  jiiarked  consti- 
pation. 


N.  B.— No  trustworthy  conclusions  can  be  drawn  from  the  seat  of  the  pain  as  to  the  seat  of  the  ob- 
struction unless  local  peritonitis  comes  on.  The  pain  is  usually  referred  in  all  forms  to  the  region  of  the 
navel.  In  complete  obstruction  the  pain  is  constant,  though  with  exacerbations  ;  intermittent  pain  shows 
that  the  obstruction  is  partial.    Coils  of  intestine  are  not  visible  through  the  abdominal  wall  in  acute  cases. 

CHRONIC  INTESTINAL  OBSTRUCTION 


Stricture  of  the  Small 
Gut. 

Stricture  of  the  Large 
Gut. 

E^CAL  Accumulation. 

Age  and  Sex.. 

Adults. 

Adults. 

Adults  ;  more  common  in  fe- 
males, the  hysterical,  the 
insane,  hypochondriacs. 

History 

Cancer,   trauma,  tuberculo- 

Cancer, trauma,    tuberculo- 

Previous constipation. 

sis  ;  disordered,  imperfect. 

sis,  dysentery ;  disordered. 

irregular  action  of  bowels 

imperfect,  irregular  action 

from    time    to  time,   with 

of    bowels   from    time   to 

intervals    of    comparative 

time,     with     intervals    of 

ease. 

comparative  ease. 

Gradual. 

Intermittent. 

Late,  scanty,  feculent  only  to- 

Gradual. 

Intermittent. 

Less  prominent,  rarely  fecu- 

Gradual. 

Pain 

Less  prominent. 

Vomiting 

Late,  scanty,  rarely  feculent, 

ward  end  of  acute  attack  ; 

lent  or  provoked  by  food. 

often  absent. 

may  be  provoked  by  food. 

Constipation.  . 

May    alternate    with    diar- 

Form of  faeces  may  be  al- 

Gradually  increasing :    may 

rhoea  ;  blood  points  to  can- 

tered ;  blood  points  to  can- 

be spurious  diarrhcea  ;    no 

cer. 

cer. 

blood. 

Tenesmus 

Absent. 

Often  present. 

Absent. 

Meteorism 

Not  marked,  unless  acute  at- 

Often marked. 

Late:  generally  increases  with 

tack. 

obstruction. 

Tumor 

Only  in  cancer,  and  then  in 
30  per  cent. 

Only  in  cancer,  and  then  in 
40  per  cent.  ;  may  be  felt 

Common     and     distinctive ; 

most  easily  felt  in  caecum  ; 

in  rectum. 

little  or  no  tenderness ; 
sometimes  movable,  and 
can  be  changed  in  shape. 

Coils  of  In- 

Marked    in    proportion     to 

Marked     in    proportion    to 

Rarely  seen. 

testine..  . . 

emaciation. 

emaciation. 

N.  B.— In  any  form  of  chronic  obstruction,  the  symptoms  of  acute  occlusion  may  suddenly  supervene.] 


Treatment. — As  soon  as  tlie  dangerous  signs  of  intestinal  obstruction  are  rec- 
ognized by  the  physician,  his  first  duty  is  to  make  as  careful  an  examination  (vicZe 
supra)  as  possible,  so  as  to  determine  whether  the  obstruction  may  not  be  within 
the  reach  of  direct  treatment.     If  there  is  an  incarcerated  external  hernia,  it 


STEICTUEE   AND   OBSTRUCTION   OF    THE   INTESTINES    507 

demands  such  operative  treatment  as  is  taught  by  surgery.  If  there  is  an  impac- 
tion of  gall-stones,  or  intestinal  calculi,  or  foreign  bodies,  we  may  in  some  cases 
furnish  appropriate  assistance  by  the  cautious  use  of  laxatives.  The  treatment 
of  faecal  impaction  is  of  special  importance.  We  have  described  the  most  fre- 
quent form  of  this  in  detail  above.  As  has  already  been  said,  it  is  usually  neces- 
sary to  remove  at  least  a  part  of  the  faeces  with  the  fingers,  or  some  instrument 
like  a  dressing-forceps  or  a  spoon.  In  the  second  place,  we  may  use  large  enemata 
of  pure  water,  or  preferably  soap-suds,  which  must  often  be  repeated  four  or  five 
times  a  day,  until  they  have  a  satisfactory  result.  These  are  best  given  by  a  fun- 
nel and  an  oesophageal  tube  ("  intestinal  tube  ")  introduced  as  high  as  possible 
into  the  intestine.  Cathartics  administered  internally  serve  as  aids,  especially 
castor-oil  and  rhubarb. 

In  stenosis  of  the  rectum  from  cicatrices  and  new  growths  we  can  also  some- 
times employ  local  surgical  treatment.  The  treatment  of  fsecal  accumulations 
usually  plays  an  important  part  here.  Finally,  the  cases  of  ileo-csecal  invagina- 
tion, in  which  the  lower  end  of  the  invaginated  ileum  reaches  the  rectum,  may 
receive  local  treatment.  We  may  try  a  partial  replacement  by  a  "  sponge-sound  " 
(an  elastic  oesophageal  tube  to  the  end  of  which  a  sponge  is  fastened).  Blowing 
in  air  by  the  bellows  was  also  recommended  for  this  purpose  by  the  old  physicians. 
As  a  rule,  however,  we  use  here  large  enemata  of  warm  water,  which  sometimes 
seem  to  exert  a  favorable  mechanical  action.  Very  often  it  is  impossible  to  apply 
direct  treatment  to  the  cause  of  the  obstruction,  or  even  to  determine  with  any 
approach  to  correctness,  the  anatomical  cause  and  the  seat  of  the  obstruction.  In 
these  difficult  cases  the  physician  must  resort  at  first  to  merely  symptomatic  treat- 
ment. It  goes  without  saying  that  the  patient  should  have  complete  physical  rest. 
All  food  should,  if  possible,  be  entirely  forbidden.  The  torturing  thirst  may  be 
relieved  by  bits  of  ice  or  sips  of  cold  bitter  tea.  Formerly  when  there  was  obstruc- 
tion of  the  bowels  it  was  the  custom  to  make  trial  of  laxatives,  first  employing 
milder  remedies,  then  more  vigorous  drugs,  and  finally,  as  a  "  last  resort,"  metallic 
mercury  in  single  doses  of  from  5  to  10  ounces  (150  to  300  grammes),  which  is 
sometimes  claimed  to  act  mechanically  in  "  desperate  cases  "  by  its  weight.  Ex- 
cept among  some  champions  of  mercury,  the  present  opinion  among  physicians 
tends  far  more  to  the  belief  that  cathartics  are  usually  of  no  service,  but  are  often 
directly  injurious  by  increasing  the  resistance.  Hence  we  have  at  present  gone 
over  to  the  treatment  of  severe  internal  incarcerations  with  large  doses  of  opium 
(20  drops  of  laudanum  or  2  to  3  grains  [gramme  0.1-0.2]  of  opium,  several 
times  a  day) .  Opium  acts  favorably  on  the  patient's  pain,  the  vomiting  is  dimin- 
ished, and,  by  quieting  the  peristalsis,  the  danger  of  increasing  the  stenosis  and 
tearing  the  intestine  is  also  lessened.  In  fact,  the  opium  treatment  has  many 
favorable  results  on  record.  Sometimes  the  first  dejection  appears  during  the 
administration  of  opium.  Morphine  subcutaneously  injected  has  much  less  effect 
upon  the  intestine  than  opium;  its  employment  is  therefore  limited  to  cases  in 
which  pain  is  so  violent  as  to  demand  relief. 

Since,  therefore,  there  are  many  objections  to  the  internal  use  of  cathar- 
tics, we  may  try  large  enemata  in  those  cases  in  which  the  seat  of  the  stenosis  is 
not  known  to  be  in  the  large  intestine.  They  must  be  given  with  caution,  but 
persistently,  and  they  must  often  be  repeated;  then  they  sometimes  give  good 
results,  even  in  severe  cases.  Unpleasant  effects  have  been  reported  by  other 
observers,  but  we  ourselves  have  never  seen  any.  The  introduction  of  air  into 
the  rectum,  instead  of  water,  has  been  recommended  and  has  been  useful,  particu- 
larly when  the  obstruction  was  situated  low  down  and  was  the  result  of  a  kink  or 
some  similar  trouble.  The  employment  of  regular  lavage  (Kussmaul,  Cahn,  and 
others)  is  very  beneficial  in  manj;-  cases  of  faecal  vomiting;  if  this  is  a  prominent 
symptom,  the  stomach  should  be  washed  out,  in  every  case  of  intestinal  obstruc- 


508  DISEASES    OF   THE   DIGESTIVE   OEGANS 

tion.  Large  amounts  of  feculent  liquid  are  frequently  removed  through  the 
stomach-tube;  and  it  is  easy  to  see  that  freeing  the  stomach  of  its  accumulations 
may  favor  a  more  vigorous  peristalsis.  Even  when  the  nature  of  the  intestinal 
obstruction  precludes  definitive  recovery,  lavage  usually  gives  no  inconsider- 
able relief. 

We  need  not  enter  into  details  as  to  the  general  treatment.  It  goes  without 
saying  that  the  patient's  strength  must  be  kept  up  as  much  as  possible,  and  that 
in  severe  states  of  collapse  all  possible  stimulants  must  be  used,  such  as  stro- 
phanthus,  camphor,  and  ether.  Local  applications  to  the  abdomen  are  usually  ill 
borne  on  account  of  the  tenderness,  but  still  we  may  try  ice  poultices  or  wet  com- 
presses. Opium  is  the  best  remedy  for  pain  and  vomiting,  as  already  stated,  but 
it  must  often  be  replaced  by  subcutaneous  injections  of  morphine.  In  cases  of 
extreme  gaseous  distention  the  intestinal  coils  may  be  punctured  with  the  needle 
of  a  subcutaneous  syringe  and  the  gas  in  part  evacuated.  This  sometimes  proves 
very  beneficial. 

Finally,  the  surgical  treatment  of  intestinal  obstruction  is  most  important. 
It  is  true  that  we  should  not,  as  a  rule,  proceed  immediately  to  laparotomy  at  the 
beginning  of  the  characteristic  symptoms,  but  if  we  produce  no  effect  by  means 
of  opium,  injections,  lavage,  and  similar  measures,  and  if  the  general  condition 
and  the  pulse  grow  decidedly  worse,  then  in  many  cases  laparotomy  is  the  only 
means  of  possible  salvation.  Sometimes  the  existing  obstruction  may  be  thus 
detected  and  removed.     (For  particulars,  see  text-books  on  surgery.) 

[The  safety  with  which  laparotomy  is  now  performed  has  stimulated  the  study 
of  all  affections  on  which  the  operation  has  any  bearing.  Internal  strangula- 
tions and  invaginations  may  be  relieved,  and  the  portion  of  intestine  containing 
a  non-cancerous  stricture  can  be  excised.  An  early  operation  offers  much  better 
chances,  of  course.  In  these  days  persons  should  not  be  allowed  to  die  directly 
from  intestinal  occlusion  without  an  attempt  being  made  to  restore  the  permea- 
bility of  the  canal  by  surgical  means.] 


CHAPTEE   XII 

INTESTINAL    PARASITES 

(HelmintJdasis) 

1.  Tape-worms 

Natural  History  of  the  Tape-worm. — Three  of  the  tape-worms  (cestodes) 
which  are  found  in  the  intestines  have  a  clinical  significance:  the  taenia  solium, 
the  taenia  mediocanellata,  and  the  hothriocephahts  latus. 

1.  The  taenia  solium  is,  when  fully  developed,  two  or  three  metres  long.  Its 
head  (Figs.  47  and  48)  is  about  the  size  of  that  of  a  pin,  and  has  four  projecting 
cup-like  suckers,  and  in  front  a  beak  with  about  twenty-six  hooks.  The  top  of  the 
head  is,  as  a  rule,  plainly  pigmented.  A  small  neck,  about  an  inch  long,  is 
attached  to  the  head,  and  then  follow  the  single  "  joints  "  {proglottides)  of  the 
tape-worm,  of  which  the  youngest,  lying  near  the  head,  are  still  very  small  and 
short.  They  gradually  increase  in  length  and  breadth,  and  at  about  a  metre  from 
the  head  they  have  an  approximately  quadrilateral  shape.  The  segments  which 
lie  farther  down,  and  which  have  already  reached  puberty,  have  the  form  of  pump- 
kin seeds,  and  are  nine  or  ten  millimetres  long  and  six  or  seven  wide.  The  matrix 
or  uterus  runs  through  the  middle  of  each  mature  segment  (see  Fig.  49),  and  from 
it,  on  each  side,  go  seven  or  eight  side  branches,  which  ramify  like  a  tree.     On 


INTESTINAL   PAEASITES 


509 


one  side,  a  little  below  tlie  middle,  lies  the  sexual  orifice  (Fig'.  49,  a).  The  male 
sexual  organs  consist  of  a  number  of  little  clear  vesicles  in  the  anterior  portion  of 
the  segments.  The  thick-shelled  eggs  (Fig.  50,  3)  develop  in  the  uterus,  and  con- 
tain an  embryo  with  six  booklets. 

The  taenia  solium  inhabits  the  small  intestines  of  man.     Its  head  clings  to  the 
mucous  membrane  so  tightly,  usually  at  some  point  in  the  upper  third  of  the  small 


Fm.  47.— (.l<rLiiii  Heller.) 
Heau  of  taenia  solium. 


Fig.  48.— (From  Heller.  )    Head  of  cysticercus  of 
the  brain. 


intestine,  that  the  neck  is  often  torn  off  in  trying  to  loosen  the  worm  from  the 
intestinal  wall.  The  rest  of  the  worm,  which  is  in  part  in  many  coils,  extends 
to  the  lower  part  of  the  ileum,  but  only  exceptionally  into  the  csecum.  From  the 
lower  end  long  chains,  or  single  mature  segments,  are  often  detached,  mix  with 
the  contents  of  the  intestine,  and  are  passed  with  the  faeces,  together  with  some 
of  the  eggs  from  the  uterus. 

The  further  development  of  the  eggs  of  the  taenia  solium  takes  place  in  another 
"host,"  almost  always  in  the  hog.  Hogs  are  infected  by  eating  faeces,  offal, 
etc.,  containing  taenia  eggs.  The  thick  shell  of  the  eggs 
is  dissolved  in  the  hog's  stomach,  and  the  free  embryos 
pierce  the  walls  of  the  stomach  and  intestines  and  travel 
with  the  blood-current,  or  through  the  tissues,  into  the 
different  organs,  especially  into  the  muscles.  Here  they 
develop,  in  two  or  three  months,  into  cysts  something 
larger  than  a  pea,  from  whose  walls  a  newly  developed 
taenia-head  arises,  a  so-called  scolex  (nurse).  These 
cysts  are  termed  worm-cysts,  measles,  or  cysticerci  cellu- 
losce.  They  live  from  three  to  six  years;  then  they  die 
and  become  calcified.  If  a  cysticercus  gets  into  a  man's 
stomach  from  his  eating  raw  or  imperfectly  cooked  ham 
or  pork,  a  new  and  complete  taenia  sprouts  from  the 
scolex,  which  forms  mature  segments  in  throe  or  four 
months. 

"We  usually  find  only  one  tape-worm  in  a  man,  but  sev- 
eral specimens  have  been  seen  at  the  same  time  in  the  same  intestine.     The 
length  of  a  tape-worm's  life  is  not  certainly  known,  but  it  has  happened  that 
some  persons  have- lodged  the  same  tape-worm  for  ten  or  fifteen  years. 

Although  the  fully  developed  taenia  solium  is  seen  only  in  man,  as  we  have 
said,  the  cysticercus  cellulosae  has  been  found,  in  rare  cases,  in  dogs,  rats,  and  mon- 
keys, etc.,  as  well  as  in  hogs.  It  is  a  particularly  important  fact  that  the  cysti- 
cercus cellulosae  itself  may  also  occur,  as  such,  in  man.     If  tape-worms  or  mature 


Fig.  40. —(From  Heller.) 
Tsenia  solium.  Mature 
segment. 


510 


DISEASES    OF   THE   DIGESTIVE    OEGANS 


segments  get  into  a  man's  stomach  in  any  way,  probably  by  auto-infection  by  the 
finger,  etc.,  the  embryos  travel  into  other  organs.     Cysticerci  are  often  found  in 


Fig.  50.— Comparative  view  of  the  eggs  of  some  of  the  commoner  intestinal  parasites.  1.  Egg  of  distoma 
hepaticum.  2.  Distoma  lanceolatum.  3.  Taenia  sohum.  4.  Taenia  mediocanellata.  5.  Bothriocephalus 
latus.    6.  Oxyuris  vermicularis.    7.  Triehocephalus  dispar.    8.   Ascaris  lumbricoides. 

men,  singly  or  in  groups,  especially  in  the  skin,  the  brain,  the  eye,  and  the  mus- 
cles. There  is  a  special  form  of  cysticercus  of  the  brain,  in  which  we  find  a  whole 
chain  of  cysts,  like  a  cluster  of  grapes,  but  sterile,  the  so-called  cysticercus  race- 
mosus. 

2.  The  iwnia  mediocanellata,  or  taenia  saginata  (from  saginare,  to  fatten),  is 
far  more  common  than  the  taenia  solium  in  many  parts  of  Germany.  It  is  longer 
than  the  taenia  solium,  being  about  three  or  four  metres 
long,  and  its  individual  joints  are,  on  the  whole,  broader 
and  thicker.  The  head  (Fig.  51)  has  also  four  prominent 
cup-like  suckers,  but  it  has  no 
crown  of  hooklets.  The  mature 
segments  differ  from  the  proglot- 
tides of  taenia  solium,  in  that  the 
central  uterus  sends  off  many  more 
(twenty  to  thirty)  side  branches, 
which  divide  dichotomously,  and 
not  like  a  tree.  The  sexual  open- 
ing is  also  on  the  side  (Fig.  52,  a). 
The  life-history  of  the  taenia 
mediocanellata  is,  on  the  whole, 
like  that  of  the  taenia  solium.  The 
taenia  mediocanellata,  however, 
throws  off  single  mature  segments 
much  more  frequently  than  the 
taenia  solium.  These  segments  are 
found  in  the  faeces,  and  here  they  often  exhibit  a  crawling  motion.  A  kindred  fact 
is  that  it  is  always  easy  to  find  large  numbers  of  tape-worm  eggs  in  the  faeces 
of  individuals  who  harbor  the  taenia  mediocanellata.  This  is  usually  difiicult 
in  the  case  of  taenia  solium.  The  cysticercus  of  taenia  mediocanellata  does  not 
inhabit  pork,  but  beef,  so  that  the  infection  of  man  by  this  tape-worm  comes 
from    eating    raw    beef.      In    man    the    cysticercus    of    taenia    mediocanellata. 


Fig.  51.— (From  Heller.) 
Head  of  taenia  medio- 
canellata. 


Fig.  52. — (From  Heller.) 
Taenia  mediocanellata. 
Mature  segment. 


INTESTINAL   PAEASITES 


511 


Figs.  53  and  54.— (From  Heller.) 
Fig.  53.— Head  of  bothriocephalus  latus.    a. 

Lateral  view,  enlarged,     b.  Natural  size. 
Fig.    54.  —  Bothriocephalus    latus.       Mature 

segment. 


which  is  somewhat  smaller  than  the  cysticercus  cellulosae,  has  never  yet  been 
observed. 

3.  The  hoihriocephalus  latus  occurs  in  Holland,  Switzerland  (Geneva),  Pome- 
rania,  East  Prussia,  Hamburg,  and  Eussia  (the  German  Baltic  provinces).  It  has 
not  yet  been  observed  in  middle  Germany.     It  is  the  largest  tape- worm ;  it  may  be 

six  or  eight  metres  long,  and  sometimes  has  over  four  thousand 
"  joints.     The  head  of  the  bothriocephalus   (Fig.  53)   consists  of  a 

little  club-shaped  swelling,  with  two  slit-like  depressed  suckers  on 
the  sides.  A  long,  thread-like  neck  joins  the  head  to  the  youngest 
segments.  The  full-grown  segments  (Fig.  54)  are  short,  but  are 
distinguished  by  their  great  breadth.  The  largest  segments  meas- 
ure in  length  about  three  or  four  millimetres,  and  in  breadth  ten 
or  twelve,  but  the  last  joints  are  longer  and 
are  not  so  broad,  so  that  they  have  an  ap- 
proximately quadrilateral  form.  The  uterus 
consists  of  a  very  tortuous  canal  in  the  cen- 
ter. The  sexual  orifice  does  not  lie  on  one 
side,  as  in  the  taenia,  but  in  the  middle  of 
the  abdominal  surface,  nearer  the  anterior 
border  of  the  segment  than  the  posterior. 
The  eggs  (vide  supra.  Fig.  50,  5)  are  of  an 
oval  form,  and  have  a  hood-shaped  lid  at 
one  end.  They  are  to  be  found  in  almost  every  dejection  of  persons  affected  with 
a  bothriocephalus.  Single  joints  of  the  tape-worm  are  not  passed  with  the  stools, 
but  portions  of  the  worm,  several  feet  long,  come  away  from  time  to  time,  espe- 
cially in  the  spring  and  autumn. 

The  eggs  develop  only  in  fresh  water.  The  embryo  (Fig.  55),  which  is  formed 
in  them  in  a  few  months,  and  is  provided  with  six  booklets  and  with  vibrating 
cilia,  is  swallowed  by  fishes  (chiefly  pike  and  eel-pouts  according  to  Braun,  salmon 
according  to  Kiichenmeister),  and  develops  in 
their  muscles  and  internal  organs  into  cysticerci. 
The  infection  of  man  with  bothriocephalus  comes 
from  eating  such  fish  containing  cysticerci. 

4.  These  three  kinds  of  tape-worms  that  have 
been  enumerated  are  the  most  important,  but  we 
will  briefly  mention  the  taenia  nana  and  the  tania 
cucumerina  {taenia  elliptica).  The  first  of  these, 
the  taenia  nana  [dwarf],  is  the  smallest  tape-worm, 
being  only  1.0  to  1.5  centimetre  long.  The  long- 
head is  provided  with  four  suckers  and  a  circlet 
of  hooks  which  can  be  extended  far  o.ut.  The 
anterior  joints  are  very  narrow  and  short,  those 
farther  back  broadening  not  inconsiderably.  The 
taenia  nana  is  very  frequent  in  Italy  and  also  in 
Sicily.  In  Germany  it  has  been  seen  only  excep- 
tionally. Its  cysticercus  is  said  to  inhabit  snails. 
dren,  and  in  them  sometimes  in  very  great  numbers.  Single  joints  are  difficult 
to  find  in  the  dejecta,  but  the  discovery  of  its  eggs  with  the  microscope  is  very 
easy.  The  expulsion  of  the  worm  by  means  of  santonine  and  thymol  (vide  infra) 
is  usually  a  simple  matter. 

The  taenia  cucumerina  is  twenty  to  twenty-five  centimetres  long.  Its  poste- 
rior joints  are  six  to  eight  millimetres  long,  but  have  a  width  of  only  one  milli- 
metre. The  head  is  provided  with  many  booklets ;  the  beak  can  be  extended  and 
retracted.  The  taenia  cucumerina  occurs  especially  in  children.  Its  cysticercus 
is  found  in  the  dog. 


Fig.  55.— Embryo  of  bothriocephalus 
latus,  with  its  ciliated  coat. 
(Leuckart.) 


It  is  seen  especially  in  chil- 


512  DISEASES    OF   THE   DIGESTIVE    OEGAXS 

Symptoms  and  Diagnosis. — In  many  cases  tape-worms  are  lodged  in  the  intes- 
tines without  causing  any  morbid  symptoms.  We  can  recognize  their  presence 
only  by  occasionally  finding  the  joints  in  the  dejections. 

In  other  cases,  however,  tape-worms  cause  a  list  of  disturbances  which  are 
often  exaggerated  by  anxious,  hypochondriacal,  and  nervous  persons,  but  which 
ought  not  to  be  too  little  regarded.  The  symptoms  are  referred  chiefly  to  the 
intestinal  canal.  Sometimes  there  is  quite  severe  abdominal  pain,  which  may 
assimie  a  colicky  character.  The  patient  also  frequently  complains  of  irregularity 
of  the  bowels,  and  of  occasional  diarrhoea,  which  alternates  with  constipation. 
Many  general  symptoms  are  also  added  to  those  mentioned — loss  of  appetite,  or  at 
times  marked  voracity,  general  languor,  disinclination  to  work,  mental  disturb- 
ance, depression,  etc.     Often  the  general  nutrition  is  considerably  impaired. 

There  are  also  certain  symptoms  to  be  mentioned  which  were  formerly  ex- 
plained as  "  reflex."  Still,  it  is  very  possible  that  poisonous  matter  may  be  pro- 
duced by  the  tape-worms  under  certain  circumstances,  about  which  we  do  not  yet 
have  accurate  knowledge,  and  that  these  poisons  occasion  some  of  the  symptoms 
of  tape-worm  (vide  infra).  Among  these  we  sometimes  see  marked  salivation, 
tickling  in  the  nose,  dilatation  of  the  pupils,  palpitation,  vomiting,  headache  (mi- 
graine), etc.  In  some  cases  even  severe  spasms  -and  choreic  conditions  have  been 
referred  to  the  presence  of  tape-worms  (particularly  the  taenia  nana)  in  the  intes- 
tinal canal,  but  it  is  hard  to  decide  how  far  such  a  supposed  connection  can  really 
be  regarded  as  justified. 

Thus  in  most  cases  tape-worms  cause  comparatively  little  disturbance,  but  they 
may  occasion  severe  illness.  Of  late  years  it  has  been  observed  that  when  the 
bothriocephalus  latus,  or  exceptionally  a  taenia,  is  present  in  the  intestines 
there  will  often  be  an  extremely  severe  ansemia,  quite  like  pernicious  anaemia 
(g.  v.).  The  patient  becomes  excessively  pale  and  feeble,  the  blood  shows  marked 
oligocythemia  and  poikilocytosis ;  there  are  ansemic  cardiac  murmurs  and  simi- 
lar symptoms.  This  condition  also  is  probably  referable  to  poisonous  matter 
produced  by  the  bothriocephalus  latus,  absorbed  by  the  intestines,  and  fatal  to 
the  red  blood-corpuscles.  If  the  tape-wornl  is  promptly  expelled  there  is  rapid 
and  complete  recovery. 

Although  many  of  the  symptoms  mentioned  may  arouse  suspicion  as  to  the 
presence  of  a  tape-worm,  the  diagnosis  can  be  made  only  by  finding  the  joints 
or  eggs  of  the  tape- worm  in  the  dejections.  In  many  cases  the  patient  himself 
brings  some  of  the  segments  found  by  him  in  the  dejections  to  the  physician,  but 
in  judging  of  them  a  certain  caution  is  always  necessary,  since  shreds  of  mucus, 
remains  of  food,  etc.,  are  quite  frequently  presented  to  the  physician,  under  the 
idea  that  they  are  segments  of  tape-worm.  But,  on  the  other  hand,  it  is  also  very 
important  that  the  physician  himself  should  not  forget  the  possibility  of  a  tape- 
*vorm  and  should  himself  direct  attention  in  suspicious  cases  to  the  dejections  of 
the  patient.  If  there  is  a  taenia  mediocanellata  or  a- bothriocephalus  latus,  it  is 
usually  easy  to  find  the  eggs  in  the  faeces,  but  in  the  case  of  taenia  solium  this  is 
more  difficult.  With  taenia  solium  we  usually  have  to  search  for  segments  of  the 
tape-worm  in  the  stools.  Many  patients  with  all  sorts  of  indefinite,  mild,  gas- 
tric and  intestinal  symptoms,  or  such  general  symptoms  as  headache  or  languor, 
or  even  graver  disturbances,  such  as  apparent  pernicious  antemia,  are  finally 
cured  when  the  true  cause  of  the  disease  is  found  to  be  a  tape-worm. 

If  we  obtain  a  few  joints  of  the  tape-worm  we  should  endeavor  to  determine 
from  them  the  species.  If  we  spread  out  the  pieces  of  tape-worm  between  two 
microscopic  slides,  the  thicker,  fatter  segments  of  the  ta3nia  mediocanellata,  with 
its  many-branched  uterus,  may  usually  be  distinguished  without  difficulty  from 
the  more  tender  and  more  translucent  segments  of  the  taenia  solium,  with  a 
smaller  number  of  lateral  branches  to  its  sexual  apparatus.     The  statement  of 


INTESTINAL  PAEASITES  513 

many  patients  tliat  single  segments  of  tape-worm  come  from  tliem  at  other  times 
than  when  at  stool,  and  that  they  find  them  on  their  underclothing,  almost  always 
points  to  the  presence  of  a  taenia  mediocanellata  in  the  intestine.  The  eggs  of 
taenia  solium  and  taenia  saginata  can  be  distinguished  from  one  another  with 
extreme  difficulty  in  the  faeces,  while  it  is  easy  to  diagnosticate  the  bothrioceph- 
alus  latus  by  its  eggs,  as  they  are  so  characteristic  (vide  supra.  Fig.  50). 

If  we  suspect  a  tape-worm,  without  having  secured  the  certain  evidence  of  seg- 
ments or  eggs  in  the  dejections,  it  is  a  good  plan  to  give  the  patient  a  mild  cathar- 
tic, such  as  castor-oil,  or  a  dose  of  boiled  pumpkin-seeds,  since  after  this,  if  the 
intestine  harbors  a  tape-worm,  single  portions  of  it  often  come  away. 

Treatment. — The  "  tape-worm  cures,"  which  are  recommended  in  so  great  a 
number  that  we  can  by  no  means  mention  all  of  them  here,  but  only  the  most 
important  and  the  most  serviceable,  aim  at  killing  or  benumbing  the  worm,  and 
then  at  removing  it  from  the  intestine  in  toto  by  cathartics. 

We  usually  begin  with  a  so-called  "  preparatory  treatment."  This  is  to  cleanse 
the  intestine,  especially  the  large  intestine,  from  old  fsecal  masses,  in  order  to  pre- 
pare as  free  a  passage  as  possible  for  the  worm.  For  this  purpose  we  give  the 
patient  a  mild  laxative,  or,  better  still,  a  large  enema  of  cold  water.  Many  physi- 
cians recommend  that  there  should  first  be  given  some  active  purge,  such  as  calo- 
mel or  castor-oil,  but  this  is  exhausting  to  the  patient,  and  we  believe  it  is  not 
usually  necessary.  We  also  forbid  for  a  day  or  two  the  use  of  vegetables,  black 
bread,  etc.,  and  prescribe  instead  a  limited  diet  of  white  bread,  some  meat,  milk, 
and  coffee.  It  is  a  wide-spread  practice  to  take  during  the  preparatory  treatment 
certain  articles  of  food  to  "  make  the  worm  ill."  Among  these  a  salad  of  finely 
chopped  and  very  salt  herring  with  onions  and  garlic  is  especially  recommended. 
A  similar  action  is  also  ascribed  to  strawberries,  cranberries,  and  bilberries.  Hence, 
on  the  day,  and  especially  on  the  afternoon,  before  treatment,  we  have  the  patient 
take  a  large  amount  of  the  articles  of  food  mentioned,  such  as  herring  salad. 

On  the  next  morning,  after  everything  has  been  prepared,  after  the  bowels 
have  moved  the  night  before,  etc.,  the  patient  takes  no  breakfast,  or  only  some 
strong  sweet  cafe  noir.  Then  he  takes  the  special  anthelmintic,  and  in  one  or 
two  hours,  if  he  feels  a  great  pressure  in  the  abdomen,  he  also  takes  a  few  spoon- 
fuls of  castor-oil  or  rhubarb. 

The  number  of  taenicides  recommended  is,  as  we  have  said,  very  great.  At 
present  the  following  are  most  in  use : 

Many  experienced  physicians  and  we  ourselves  nov/  employ  almost  exclusively 
the  ethereal  extract  of  male  fern  (oleoresina  aspidii).  It  is  true  that  the  reliabil- 
ity of  this  drug  as  dispensed  by  different  apothecaries  varies,  but  in  most  cases,  if 
we  can  obtain  a  good  fresh  preparation,  the  result  is  perfectly  satisfactory.  It 
should  be  said,  however,  that  the  drug  is  not  entirely  free  from  danger ;  in  excep- 
tional cases  larg^  doses  have  caused  symptoms  of  poisoning,  particularly  amauro- 
sis, also  jaundice;  and  even  death  has  occurred.  We  should,  therefore,  hold 
firmly  to  the  rule  of  never  exceeding  a  dose  of  two  and  a  half  to  three  drachms 
(grammes  10-] 2).  We  have  never  seen  unfortunate  results  from  this  amount. 
The  best  way  of  administering  the  drug  is  in  the  gelatine  capsules  which  are  for 
sale,  of  which  each  contains  thirty  grains  (two  grammes)  of  the  extract. 

The  bark  of  pomegranate-root  {cortex  radicis  Punicce  granati)  is  one  of  the 
most  efficient  remedies.  We  formerly  prescribed  it  in  combination  with  the 
ethereal  extract  of  male  fern,  in  the  following  prescription: 

I>   Granati  radicis  corticis ^iv-v  (grm.  120-150) ; 

Aquae   O  ij   (grm.  1,000). 

Macerate  for  twenty-four  hours,  and  boil  until  it  is  reduced  to  ^v  (grm.  150). 

Add:  Oleoresinse  filicis gr.  Ixxv  (grm.  5). 

33 


514  DISEASES    OF   THE   DIGESTIVE    OEGANS 

The  whole  amount  is  to  be  taken  in  three  or  four  doses  as  near  together  as  pos- 
sible. In  order  to  obviate  the  bad  taste  of  the  remedy  and  to  increase  the  action 
by  administering  a  larger  amount  at  once,  it  has  been  recommended  to  introduce 
the  whole  amount  of  a  still  stronger  decoction  of  pomegranate-root  directly  into 
the  stomach  by  means  of  an  oesophageal  tube.  As  a  rule,  it  is  well  to  avoid  this 
procedure. — The  tannate  of  pelletierine,  prepared  from  the  pomegranate-root,  is 
also  to  be  recommended.  It  is  almost  tasteless,  and  in  doses  of  eight  to  twenty- 
five  grains  (gramme  0.5-1.5)  is  said  to  be  a  very  certain  tsenicide. 

Another  remedy,  which  has  often  proved  successful,  is  kousso-flowers.  We 
give  three  or  four  powders,  each  containing  seventy-five  grains  (grammes  5)  of 
powdered  kousso-flowers,  in  white  wine,  giving  a  glass  of  wine  containing  one  pow- 
der about  every  half-hour.  Rosenthal's  "  kousso  tablets  "  are  more  agreeable  to 
take  and  are  very  good,  but  they  are  more  expensive.  Twenty  of  these,  of  fifteen 
grains  each  (gramme  1),  may  be  taken  without  danger  within  an  hour  with  cafe 
noir  or  lemonade.  During  the  period  of  treatment  the  patient  must  lie  as  quiet 
as  possible  in  order  to  avoid  vomiting.  Up  to  the  present  time  we  have  not  had 
sufiicient  experience  of  the  koussine  or  kosseine,  prepared  from  the  alcoholic  ex- 
tract of  kousso-leaves,  which  is  said  to  be  very  efficient  in  doses  of  thirty  to  forty- 
five  grains  (grammes  2-3). 

Of  the  other  remedies  we  may  mention  kamala.  We  give  the  powder  or 
tablets,  in  doses  of  75-150  grains  (grammes  5-10).  This  is  a  mild  remedy  and  used 
chiefly  for  children.  We  may  also  give  oil  of  turpentine,  one  or  two  ounces 
(grammes  40-60)  in  two  doses  in  milk — an  efficient  but  rather  dangerous  remedy 
in  these  doses ;  and  finally  chloroform.  Lately,  physicians  have  recommended 
pumpkin-seeds,  which  have  long  been  known  as  a  popular  remedy.  One  advan- 
tage is  that  they  do  not  have  the  bad  taste  of  almost  all  the  other  remedies  for 
tape-worm.  About  one  hundred  and  twenty  seeds,  or  for  children  half  as  many, 
are  peeled,  pounded  up,  and  mixed  with  sugar,  or  else  made  into  an  emulsion,  and 
administered. 

The  treatment  is  to  be  regarded  as  absolutely  successful  only  when  we  find  the 
head  of  the  tape-worm,  as  well  as  its  joints,  in  the  patient's  dejections.  We  may 
best  search  for  the  head  in  the  faeces  by  diluting  the  dejection  repeatedly  with 
water,  and  pouring  off  the  water.  The  tape-worm  then  remains  at  the  bottom  of 
the  vessel.  As  it  may  be  that  the  head  has  been  dislodged  even  if  it  has  not  been 
found,  we  should  not  repeat  the  treatment  for  tape-worm  until,  some  months  later, 
there  are  indubitable  signs  that  the  tape-worm  still  exists. 

Every  tape-worm  treatment  is  rather  drastic,  and  hence  it  is  well,  after  the 
treatment  is  over,  to  recommend  the  patient  to  be  prudent  in  his  diet,  and  to 
be  careful  about  his  digestive  tract  for  some  time.  In  persons  who  are  very  weak, 
or  who  have  some  other  disease,  we  do  not  willingly  undertake  to  remove  a  tape- 
worm without  urgent  reasons;  but  in  people  who  are  otherwise  healthy  it  is 
always  well  to  get  rid  of  a  tape-worm,  even  if  it  causes  no  severe  symptoms.  The 
chief  reason  for  this  is  that  taenia  solium  might  occasion  cysticerci  in  the  brain. 
The  best  time  for  undertaking  a  treatment  is  when  joints  or  large  pieces  of  the 
worm  come  away  quite  frequently  of  their  own  accord.  We  should  never  pre- 
scribe a  treatment  on  the  mere  statements  or  suspicions  of  the  patient.  We  must 
always  convince  ourselves  with  complete  certainty  of  the  presence  of  a  tape-worm 
in  the  intestine. 

We  must  finally  mention  that  the  only  efficient  prophylaxis  against  acquiring 
a  tape- worm  lies  in  entirely  avoiding  the  use  of  raw  or  half -cooked  beef  or  pork. 
The  more  widely  spread  the  taking  of  raw  meat  is,  as  in  Abyssinia,  the  more  com- 
mon are  tape-worms  in  man.  Certain  callings,  like  those  of  the  cook  or  the 
butcher,  are  also  especially  exposed  to  infection. 


INTESTINAL  PAEASITES 


515 


2.  Round-worms 

(Ascaris  lumbricoides) 

Natural  History. — Ascarides  are  pale-reddish,  cylindrical  worms,  pointed  at 
both  ends,  with  the  sexes  in  different  individuals.  The  females  are  thirty  or 
forty  centimetres  long,  the  males  about  twenty-five. 
At  the  cephalic  end  of  the  worm  are  found  three  lips 
furnished  with  fine  teeth.  The  tail  is  straight  in  the 
females  and  curved  in  the  males.  In  the  female  sex- 
ual organs  (Fig.  56)  sixty  millions  of  eggs  may  de- 
velop, at  a  rough  estimate.  These  eggs  are  often 
found  in  the  faaces  of  persons  who  have  round-worms 
in  their  intestines  (see  Fig.  50,  8).  They  have  a  great 
capacity  of  resisting  external  influences,  and  a  worm- 
like embryo  develops  in  them  in  about  nine  weeks. 
The  further  dissemination  of  round-worms  takes 
place  without  any  intermediate  host  in  this  manner: 
the  eggs  containing  the  embryo  worms  are,  through 
some  chance,  swallowed  and  then  grow  in  the  intes- 
tines into  sexually-mature  worms.  Experimental  in- 
fection with  the  eggs  of  round-worms  gives  distinctly 
positive  results  (Lutz,  Epstein). 

The  round-worms  inhabit  chiefly  the  small  intes- 
tine. In  severe  vomiting  they  often  reach  the  stom- 
ach and  are  vomited  up.  In  individual  cases  they 
have  been  found  in  the  bile-ducts,  in  the  air-passages, 
and,  after  perforation  of  the  intestine,  in  the  abdom- 
inal cavity.  The  number  of  round-worms  existing 
at  the  same  time  in  the  intestine  may  be  very  con- 
siderable. We  find  them  most  commonly  in  chil- 
dren and  in  adults  from  the  lower  classes.  Round- 
worms have  been  repeatedly  observed  to  crawl  out 
of  the  anus,  the  mouth,  or  the  nose  of  children  during 
sleep. 

The  round-worm  is  also  common  in  hogs  and  cat- 
tle as  well  as  in  man. 

Symptoms. — In  general,  round-worms  are  innocent 
parasites,  which  may  exist  in  large  numbers  in  the 
intestines  without  any  bad  results.  In  other  cases 
they  cause  symptoms  similar  to  those  ascribed  to 
teniae — abdominal  pain,  languor,  itching  of  the  nose 
and  skin,  urticaria,  burning  in  the  eyes,  salivation, 
etc. — symptoms  which  are  all  ambiguous,  and  whose 
definite  connection  with  the  presence  of  round-worms 
it  is  hard  to  make  out.  Occasionally  they  excite  long- 
continued  and  persistent  vomiting,  or  violent  diar- 
rhcea,  these  symptoms  persisting  until  the  worms  are 
expelled,  when  they  promptly  cease.  Leichtenstern 
found  that  it  was  not  very  exceptional  for  children  to 
be  noticeably  ansemic  when  harboring  ascarides,  and 
to  improve  remarkably  when  the  worms  were  expelled. 

The  cases  recorded  in  literature  are  quite  numerous  in  which  severe  nervous 
symptoms  have  been  caused  by  round-worms  and  have  disappeared  after  the  re- 
moval of  the  parasites.    However  cautious  we  may  be  in  accepting  such  state- 


FiG.  56.— (From  Heller.)  Asca- 
ris lumbricoides.  Female,  143 
millimetres  lonp.  a.  Vagina. 
b.  Intestine,  c.  Boundary  be- 
tween the  uterus  and  oviducts. 
d.  Longitudinal  bands.  e. 
Coil  of  oviducts  and  ovaries. 


516  DISEASES    OF   THE   DIGESTIVE    OEGA^-S 

ments,  neTertheless  their  credibility  can  not  be  ■wliolly  denied.  We  ■would  men- 
tion especially  conynlsions,  epileptiform  seizures,  choreic  and  cataleptic  conditions, 
contractures,  and  temporary  mental  disturbances,  which  are  claimed  to  be  excited 
by  ascarides.  It  is  said  that  children  with  ascarides  not  infrequently  exhibit 
mild  nerrous  disturbances,  such  as  headache,  vertigo,  mydriasis,  and  chills.  All 
these  symptoms,  and  also  those  above  enumerated,  are  perhaps  not  so  immediately 
dependent  upon  the  presence  of  the  worms  in  the  intestinal  canal,  but  are  due 
rather  to  toxines  developed  under  certain  circumstances. 

In  some  cases  the  presence  of  ascarides  may  excite  much  more  severe  symp- 
toms by  unfortunate  accidents,  as,  for  example,  sudden  suffocation  from  the 
entrance  of  a  round-worm  into  the  larynx.  When  a  very  large  number  of  round- 
worms have  been  present  in  the  intestine,  severe  symptoms  of  intestinal  stenosis 
have  been  observed  from  their  rolling  together  into  a  ball.  If  a  round-worra 
crawls  into  the  bile-ducts,  it  may  give  rise  to  jaundice,  and  even  to  the  develop- 
ment of  an  abscess  of  the  liver.  In  the  abscesses  of  the  anterior  abdominal  wall, 
usually  termed  "  worm  abscesses,"  the  round-worms  probably  play  a  purely  acci- 
dental part.  We  have  to  do  in  such  cases  with  peritis-phlitic  abscesses  or  with 
inflamed  hernige,  which  have  perforated  externally,  by  which  the  round-worms 
which  are  accidentally  found  in  the  intestines  pass  out,  without  having  any  causal 
relation  to  the  abscess. 

The  diagnosis  of  round-worms  is  not  usually  difficult.  Often  a  few  worms 
appear  of  themselves,  or  as  the  result  of  a  simple  laxative.  If  not,  search  must  be 
made  in  the  dejections  for  the  eggs  of  the  ascarides.  These  are  always  easily 
found.  It  is  advisable  to  obtain  a  particle  of  the  contents  of  the  rectum  for  the 
purpose  of  microscopic  examination  by  introducing  an  elastic  catheter. 

Treatment. — The  oldest  remedy  for  ascarides  is  worm-seed  —  santonica. 
This  is  best  given  in  the  form  of  an  electuary — santonica,  a  drachm  (grammes  5)  ; 
jalap,  fifteen  grains  (gramme  1)  ;  and  syrup,  an  ounce  (grammes  30),  to  be  taken 
in  three  doses — in  combination  with  a  cathartic.  Of  late,  worm-seed,  on  account 
of  its  bad  taste,  has  been  almost  wholly  replaced  by  santonine,  which  is  derived 
from  it.  This  is  prescribed  in  one-  or  two-grain  (gramme  0.05-0.10)  powders,  or 
still  more  frequently  in  the  form  of  santonine  troches  ("  worm-tablets  "),  which 
may  be  had  of  any  apothecary.  It  is  well  to  give  santonine  also  in  connection  with 
a  cathartic,  such  as  calomel.  We  give  the  patient  one  or  two  doses  of  santonine 
in  the  morning  for  three  days,  and  on  the  fourth  we  give  a  cathartic.  Severe 
symptoms  of  poisoning — spasms — ^have  been  seen  only  occasionally  from  the  care- 
less use  of  it.  Milder  symptoms,  such  as  a  yellowness  of  the  urine  and  conjune- 
tivEB,  and  xanthopsia,  or  seeing  everything  yellow,  are  somewhat  more  frequent. 

In  exceptional  cases  santonine  fails  to  expel  the  ascarides.  We  may  then  try 
male  fern  or  thymol  (grains  8-24,  gramme  0.5-1.50)  in  two  or  three  doses  given 
in  the  course  of  the  day. 

3.  Oxyuris  vermicularis 

(Seat-womis.     Pin-u-oi-Tns) 

Natural  History. — The  oxyures  are  little  round  worms,  the  females  ten  or 
twelve  millimetres  long,  the  males  only  three  or  four  (see  Figs.  57  and  58).  The 
eggs,  when  they  reach  the  human  stomach,  develop  very  rapidly.  The  embryos, 
set  free,  collect  in  the  small  intestine  and  later  mainly  in  the  ctecum.  As  soon 
as  they  become  sexually  mature  they  pair,  and  then  wander  gradually  down 
into  the  rectum,  where  they  collect  in  great  numbers.  When  the  eggs  inside 
the  female  become  ripe,  the  female  leaves  the  rectum  and  lays  its  eggs  outside, 
where  they  are  soon  destroyed  (Leichtenstern).  The  eggs  may  easily,  however, 
be  conveyed  by  fingers  or  by  articles  of  diet,  or  by  similar  means,  to  the  stomach 
of  the  same  host  or  of  some  other  person,  whereupon  the  development  of  the  worm 


INTESTIJS^AL   PAEASITES 


oil 


begins  afresh.  As  will  be  readily  understood,  children,  with,  their  untidy  habits, 
are  much  more  exposed  to  infection  with  the  oxyuris  than  adults.  The  fact  that 
the  female  oxyuris  never  lays  its  eggs  in  the  intestine  explains  why  the  eggs  of  the 
oxyuris  are  rarely  if  ever  found  in  the  stools.  The  female  crawls  out  of  the  anus 
to  deposit  its  eggs.  Male  as  well  as  female  worms 
are  discharged  with  the  stools.  The  entire  cycle  of 
development  of  the  oxyuris  occupies  about  fourteen 
days.  The  number  of  these  worms  which  may  be 
present  at  the  same  time  in  the  intestine  is  very 
considerable,  so  that  "  the  entire  mucous  mem- 
brane of  the  colon  is  covered  with  them  like 
a  fur." 

Symptoms  and  Treatment. — The  oxyures  found 
in  the  upper  portions  of  the  intestine  and  in  the 
cfficum  cause  no  symptoms  whatever,  but  in  the 
lower  part  of  the  rectum  their  presence  causes  local 
symptoms,  especially  a  very  severe  feeling  of  itching 
and  burning  in  the  anus,  which  makes  the  child  con- 
stantly scratch  and  dig  with  his  fingers.  This 
itching  of  the  anus  is  most  severe  at  night  in  bed. 
In  girls  the  oxyures  frequently  travel  into  the  va- 
gina, by  which  an  intense  itching  is  also  set  up 
there,  which  sometimes  leads  to  masturbation.  In 
some  cases  in  boys  and  men,  oxyures  have  been 
found  to  be  the  cause  of  abnormal  sexual  irritation. 
Other  clinical  symptoms  are  rare,  but  sometimes 
there  may  be  anaemia  or  nervous  disturbances,  and 
in  rare  cases  marked  intestinal  catarrh,  or  inflamma- 
tion of  the  vulva. 

The  diagnosis  of  oxyures  is  not  difficult.  Our 
attention  is  called  to  the  itching  of  the  anus,  etc., 
and  we  look  for  worms.  Single  worms  are  easily 
found  in  the  dejections,  and  often  on  the  skin  about 
the  anus. 

Treatment  is  directed  first  to  the  expulsion  of  the 
thread-worms  from  the  rectum,  and  the  prevention 
of  any  fresh  self-infection.  For  this  purpose  the 
chief  means  are  large  injections,  which  must  be  em- 
ployed persistently,  once  or  twice  a  day,  for  weeks; 
for  fluid  we  may  choose  simple  warm  water,  or  water 
containing  vinegar,  salt,  or  glycerine.  Injections 
containing  corrosive  sublimate  or  carbolic  acid  are 
effective,  but  they  should  never  be  employed  because 
of  the  danger  of  poisoning.  It  is  difficult  to  remove 
completely  the  oxyuris  from  the  upper  part  of  the 
intestine,  particularly  from  the  caecum.  For  this 
purpose  the  most  efficient  remedy  seems  to  be  san- 
tonine,  perhaps  combined  with  calomel  or  castor- 
oil.  The  itching  at  the  anus  is  alleviated  by  cold 
compresses  or  by  the  inunction  of  small  amounts  of  unguentum  hydrargyri. 

Extreme  cleanliness  is  very  important.  The  anus  should  be  frequently  washed, 
and  also  the  fingers,  particularly  the  finger  nails,  to  prevent  the  spread  of  the 
parasites. 

[Enemas  containing  infusion  of  quassia,  alum,  eucalyptol,  tannin,  etc.,  are 


Fig.  58. 

Fig.  .57.  —  Oxj-uris  ■cermicularis. 
Natural  size.  1.  Female.  2. 
Two  males. 

Fig.  .58.— (From  Heller.)  Oxyuris 
vermicularis,  enlarged,  a.  31a- 
ture  female,  not  yet  impreg- 
nated, b.  Male.  c.  Female 
containing  eggs. 


518 


DISEASES    OF   THE   DIGESTIVE    OEGANS 


Fig.  59. 


much,  in  use.  A  plain  enema  should  be  given  first,  to  unload  the  rectum  and  clean 
the  membrane  as  far  as  possible,  so  that  the  anthelmintic  may  reach  the  worms 
when  introduced.] 

4.  Anchylostoma  duodenale 

{Dochmius  seu  St?'OvgyLus  duodenalis) 

The  anchylostoma  duodenale  is  a  worm  first  observed  in  upper  Italy  and  in 
Egypt  in  large  numbers,  of  which  many  inhabit  the  upper  portion  of  the  small 
intestine,  especially  the  duodenum,  but  also  the  jejunum  and  ileum.     The  male 
is  six  to  ten  millimetres  long,  the  female  ten  to  eighteen.    At  the  cephalic  end 
(Figs.  59,  60)  is  found  a  bell-shaped  mouth-capsule,  which  is 
provided  with  two  small  teeth  on  its  dorsal  edge,  and  four 
larger  curved  teeth  on  its  ventral  edge.    With  this  sucking 
and  biting  apparatus  the  worm  fixes  itself  firmly,  like  a  wet 
cup,    on   the    intestinal   mucous    membrane,    and    is    nour- 
ished by  the  blood  which  it  sucks  out.    The  place  in  the  in- 
testine to  which  an  anchylostoma  has  fastened  may  be  rec- 
ognized in  the  cadaver  as  a  little  ecchymosis.     The  worms 
sometimes  bore  completely  into  the  inner  part  of  the  mucous 
coat. 

The  eggs  of  the  anchylostoma  are  discharged  in  great 
numbers  with  the  faeces  {vide  infra).  From  these  the  larvae 
develop  and  thrive,  particularly  in  the  dirty  water  of  mud 
puddles  and  ditches;  and  by  means  of  water  that  is  spat- 
tered, or  more  often  by  dirty  hands,  they  reach  the  mouth 
and  the  intestinal  canal  of  man  again,  and  then  rapidly 
develop  to  sexual  maturity. 

If  the  intestine  harbors  many  anchylostomata,  the  small 
but  constant  loss  of  blood  caused  by  them  is  not  without  in- 
fluence on  the  organism.  In  addition  there  are  probably  spe- 
cific toxic  influences  which  have  an  injurious  effect  upon  the 
red  blood-corpuscles.  The  symptoms  of  a  severe  anaemia 
gradually  develop.  Griesinger  first  made  the  discovery,  in 
the  year  1854,  that  the  disease  long  known  by  the  name  of 
"  Egyptian  chlorosis "  was  caused  by  the  anchylostoma 
duodenale.  Since  then  confirmatory  observations  have  been 
made  in  many  parts  of  the  tropics. 

The  disease  caused  by  the  anchylostoma  has  become  par- 
ticularly known  in  Europe  because  of  the  great  frequency 
with  which  it  occurred  among  the  Italian  laborers  who  were  employed  in  building 
the  Saint  Gothard  Tunnel.  Since  then  many  well-established  cases  have  been 
found  in  other  lands;  e.  g.,  Hungary;  Germany,  particularly  in  the  brickmakers 
of  the  Rhine ;  also  repeatedly  in  miners  and  laborers  in  tunnels. 

The  symptoms  of  the  disease  consist,  as  we  have  said,  of  a  gradually  increas- 
ing general  anaemia,  for  which  no  special  organic  lesion  can  be  made  out  objec- 
tively as  a  cause.  The  patient  also  suffers  from  very  great  general  weakness  and 
languor,  dyspnoea,  palpitation,  headache,  a?dema,  etc.  The  changes  in  the  blood 
(oligocythaemia,  poikilocytosis)  are  precisely  similar  to  those  seen  in  pernicious 
anaemia.  The  disease  may  last  for  months,  or  even  years,  and  it  often  ends 
fatally,  if  it  be  not  recognized  and  treated  in  time. 

Leichtenstern  has  made  numerous  and  accurate  observations  with  regard  to 
the  brickmakers  of  Cologne.  He  states  that  no  symptoms  are  observed  for  three 
or  four  weeks  after  infection  with  the  embryos  of  the  anchylostoma.  Some  five 
or  six  weeks  after  infection,  when  the  parasites  become  sexually  mature  and  breed. 


Fig.  60. 

Fig.  59.  —  Anchylostoma 
duodenale.  Natural 
size.  a.  Male.  b. 
Female. 

Fig.  60.— (From  Heller.) 
Anchylostoma  du- 
odenale, enlarged. 
Head  with  bell-like 
mouth. 


INTESTINAL  PAKASITES 


510 


there  appear  bloody  diarrhoea,  intestinal  colic,  and  accompanying  progressive 
anaemia.  At  this  time  there  is  probably  more  shifting  about  of  the  parasites  in 
the  intestine,  while  they  later  become  more  fixed.  This  explains  why  the  dis- 
ease evinces  a  more  acute  and  severe  character  at  first,  and  then  takes  on  the 

form  of  a  chronic  anaemia,  with  great 
diminution  or  cessation  of  the  bloody 
stools. 

The  diagnosis  is  easy  if  we  only  think 
of  the  possibility  of  anchylostoma.  It  is 
not  very  difiicult  to  find  an  abundance  of 
eggs  in  the  faeces.  They  are  of  oval  shape 
and  characterized  by  the  frequent  pres- 
ence in  them  of  two  or  more  spherules  due 
to  subdivision  (see  Fig.  61).  The  worms 
themselves  are  not  usually  found  in  the 
stools  unless  anthelmintics  have  been  ad- 
ministered. Charcot's  crystals  are  often 
found  in  the  dejections  previous  to  the  ap- 
pearance of  the  anchylostoma  eggs  (Leich- 
tenstem). 
If  the  disease  is  recognized,  treatment  is  usually  satisfactory.  We  prescribe 
the  same  anthelmintics  as  for  the  other  intestinal  parasites,  particularly  extract 
of  male  fern  in  suitable  doses  (2-3  drachms,  10-12  grammes),  besides  laxatives 
and  injections.  In  this  way  it  is  often  possible  to  banish  the  parasites  entirely 
from  the  intestinal  canal,  and  thus  to  induce,  even  in  severe  cases,  a  complete  and 
often  surprisingly  rapid  recovery.  Besides  extract  of  male  fern,  thymol  has  been 
found  an  effectual  remedy.  Of  this,  about  two  and  a  half  to  three  and  a  half 
drachms  (10-14  grammes)  are  given  daily  in  doses  of  thirty  grains  (two  grammes) 
each.  Eor  children  the  dose  is  proportionally  less.  Leichtenstern  recommends 
that  a  few  doses  of  calomel  and  one  or  two  injections  should  be  administered  oh 
the  day  preceding  the  specific  treatment  with  male  fern  or  thymol. 

The  prophylaxis  from  infection  with  anchylostoma  is  an  important  matter  in 
industrial  hygiene.  The  points  chiefly  to  be  considered  are  to  enjoin  the  greatest 
cleanliness  upon  the  workmen,  to  arrange  properly  for  the  reception  and  removal 
of  the  excreta,  and  to  provide  good  drinking  water. 


Fig.  61.— Egg  of  anchylostoma  duodenale.  a 
to  d,  various  stages  of  segmentation  ;  e, 
egg  with  embryo.    (From  Perroncito  and 

SCHULTHESS.) 


5.  Trichoceplialus  dispar 

(  W hip-worm) 

The  trichocephalus  dispar  is  a  worm  four  or  five  centimetres  long,  whose  ante- 
rior part  is  very  thin,  but  whose  posterior  part  is  decidedly  thick  (Fig.  62).  It 
resides  chiefly  in  the  caecum,  but  also  in  the 
colon,  where  it  is  often  found  in  small  num- 
bers, and  sometimes  in  abundance.  The  yellow 
or  reddish-brown  eggs  of  the  parasite  are 
characteristic,  and  they  may  be  easily  found 
in  the  f  seces  upon  microscopic  examination,  but 
the  parasites  themselves  scarcely  ever  come 
away  spontaneously  with  the  dejections.  As 
a  rule,  the  trichocephalus  has  no  clinical  sig- 
nificance, but  lately  Mossbrugger  has  reported  a  few  cases  of  severe  trouble  in 
children,  due  to  this  parasite.  The  infection  was  supposed  to  be  due  to  eating 
earth.  The  symptoms  consisted  in  great  anaemia  and  in  long-continued  and  vio- 
lent diarrhoea,  with  watery  movements  containing  mucus  and  blood.     The  dejec- 


l?i«.  \)Z.- 


irium  HEi.LKH.;   'Iricliocepnaius 
dispar. 


520  DISEASES    OF   THE   DIGESTIVE    OEGAiq-S 

tions  also  showed  many  eggs  of  the  trichocephalus,  and  Charcot's  crystals.  Treat- 
ment was  very  difficult  and  tedious,  for  the  ordinary  anthelmintics  seemed  to 
have  slight  effect.  The  most  promising  remedies  in  such  cases  would  probably  be 
extract  of  male  fern  and  thymol. 


SECTIOX  VI 

Diseases  of  the  Peritoneum 

CHAPTEE   I 

ACUTE    PERITONITIS 

{Inflammation  of  the  Bowels) 

Etiology. — There  are  two  ways  by  which  inflammatory  agents  most  fre- 
quently reach  the  peritoneum:  one  is  from  the  gastro-intestinal  tract,  and  the 
other — in  women — is  from  the  genitals. 

All  the  diverse  forms  of  ulceration  which  attack  the  digestive  canal  may  in- 
volve the  serous  layer.  In  such  a  case  an  inflammation  arises  which  is  at  first 
limited,  but  which  may  under  certain  circumstances  become  more  extensive. 
This  inflammation  may  be  regarded  as  analogous  to  that  of  the  pleura  in  pneu- 
monia ;  but  the  anatomy  of  the  stomach  and  intestine  is  such  that  very  often  an 
ulcer  in  their  walls  ends  in  a  complete  perforation.  If  this  occurs,  the  inflamma- 
tory germs  contained  in  the  primas  vias  at  once  escape  into  the  peritoneal  cavity 
and  there  excite  an  inflammation ;  which,  from  the  specific  character  of  its  cause, 
is  invariably  purulent,  and  very  frequently  is  at  the  same  time  septic  or  ichorous. 
The  possibility  of  a  peritonitis  due  to  perforation,  as  a  result  of  the  various  ulcera- 
tive processes  of  the  stomach  and  intestines,  has  been  frequently  referred  to  in  the 
previous  sections  of  this  work.  Thus,  it  may  occur  in  simple  ulcer  and  in  ulcerat- 
ing cancer  of  the  stomach ;  in  typhoid,  tubercular,  or  dysenteric  ulceration  of  the 
intestine ;  in  ulceration  of  the  intestine  above  intestinal  stenoses  of  many  varie- 
ties; and  in  the  small  ulcers  of  the  vermiform  appendix  due  to  the  pressure  of 
hard  substances. 

The  female  organs  of  generation  are  the  other  frequent  source  of  peritonitis. 
In  labor  and  premature  delivery  the  genital  tract  is  often  directly  infected.  The 
infection  may  also  occur,  although  much  less  frequently,  at  other  times;  for  ex- 
ample, during  menstruation.  The  various  forms  of  inflammation  which  are  thus 
set  up,  including  endometritis,  metritis,  and  parametritis,  may  in  several  differ- 
ent ways  reach  the  peritoneum  and  excite  peritonitis.  A  septic  inflammation  of 
the  endometrium  may  involve  the  peritoneum  by  direct  extension  up  the  Fallo- 
pian tubes.  In  other  cases  it  is  through  the  lymph-vessels  that  a  purulent  metritis 
or  parametritis  spreads  to  the  peritoneum.  The  larger  parametritic  abscesses  may 
break  into  the  peritoneal  cavity.  It  is  to  be  particularly  noticed,  however,  that  in 
many  cases  of  septic  puerperal  peritonitis  the  uterus  and  its  appendages  are  in  a 
perfectly  normal  condition,  having  served  merely  as  a  gateway  to  the  inflamma- 
tory agents  without  suffering  any  harm  themselves. 

Besides  these  two  chief  sources  of  peritonitis,  numerous  others  are  possible, 
although  much  less  frequent. 

Sometimes  peritonitis  is  due  to  an  extension  of  inflammation  from  other 
abdominal  viscera.    Hepatic  abscess,  suppurating  hydatid  cysts  of  the  liver,  ulcer 


ACUTE   PERITONITIS  521 

of  the  biliary  ducts,  splenic  abscess  or  infarction,  purulent  nephritis  or  pyelitis, 
abscess  near  the  bladder  or  in  the  prostate,  suppurating  ovarian  cysts,  tubal  preg- 
nancy, psoas  abscess,  and  Pott's  disease — all  these  may  produce  peritonitis,  either 
by  direct  extension  or  by  perforation. 

It  is  worthy  of  note  that  peritonitis  may  occur  as  a  sequel  of  pleurisy.  The 
pleural  and  peritoneal  cavities  are  directly  connected  by  the  lymph-vessels  of  the 
diaphragm;  and  empyema  as  well  as  tubercular  pleurisy  (see  next  chapter)  may 
spread  to  the  peritoneum. 

Penetrating  wounds  of  the  abdomen  are  a  fruitful  source  of  acute  peritonitis. 
Surgical  operations  upon  abdominal  organs  come  under  the  same  head.  A  large 
number  of  laparotomies  proved  fatal  before  antisepsis  was  introduced,  because  the 
inflammatory  germs  thus  admitted  excited  a  diffuse  septic  peritonitis.  Even  tap- 
ping the  abdomen  for  ascites  may  cause  acute  peritonitis  if  the  trocar  is  not  asep- 
tic. Abdominal  injuries,  in  which  the  walls  are  not  penetrated,  very  rarely,  if 
ever,  give  rise  to  peritonitis.  One  way  in  which  they  have  been  said  to  produce 
it  is  by  exciting  internal  haemorrhage.  In  the  new-born,  peritonitis  exceptionally 
results  from  infection  through  the  navel. 

Far  less  frequent  are  those  cases  of  acute  peritonitis  which  occur  as  a  part  of 
certain  general  diseases.  In  this  class  belong  first  the  peritonitis  associated  with 
acute  articular  rheumatism  (q.v.).  This  is  usually  benign.  It  must  be  re- 
garded as  analogous  to  the  "  rheumatic "  inflammation  which  occurs  in  other 
serous  membranes,  including  the  endocardium,  pericardium,  and  pleura.  It  is 
possible  that  rheumatic  peritonitis  of  this  sort  may  exceptionally  occur  as  an 
apparently  primary  disease.  It  is  a  well-established  fact  that  peritonitis  may 
also  develop  in  the  course  of  acute  or  chronic  nephritis.  This  we  have  ourselves 
observed.  It  is  of  course  comparable  with  the  inflammation  which  not  infre- 
quently attacks  the  pericardium  and  pleura  in  the  course  of  nephritis.  The  exact 
cause  of  it  has  not  yet  been  settled.  Perhaps  one  factor  is  the  retention  in  the 
blood  of  the  solids  which  ought  to  be  excreted  with  the  urine.  We  must  also 
mention  that  in  very  rare  instances  a  specific  gonorrhoeal  peritonitis  occurs,  either 
in  connection  with  a  constitutional  infection  from  gonorrhoea,  perhaps  associated 
with  gonorrhceal  synovitis  or  endocarditis,  or  from  the  direct  extension  of  gonor- 
rhoeal inflammation  from  other  parts  to  the  peritoneum. 

From  all  that  has  been  said,  it  is  evident  that,  from  a  purely  setiological  stand- 
point, peritonitis  is  by  no  means  a  stereotyped  and  uniform  disease.  The  actual 
pathogenic  agents,  exclusive  of  the  rare  cases  of  mere  intoxication,  are  always 
bacteria,  but  bacteria  of  diverse  kinds.  In  the  cases  of  peritonitis  due  to  per- 
foration, the  bacterium  coli  seems  to  play  an  important  part,  and  often  also 
streptococci  are  influential.  The  cases  of  septic  or  puerperal  peritonitis  are 
mostly  occasioned  by  streptococci;  rarely  the  peritonitic  exudation  has  been 
found  to  contain  pneumococci,  gonococci,  proteus  forms,  and  other  germs.  Not 
infrequently  there  seems  to  be  a  mixed  infection  from  the  start.  Actinomycosis 
of  the  peritoneal  cavity  has  been  already  briefly  mentioned  (see  diseases  of  the 
pleura,  page  303). 

Pathology. — Like  the  analogous  inflammations  of  the  pleura  and  pericardium, 
peritonitis  is  divided  into  different  varieties  according  to  the  character  of  the 
inflammatory  exudation.  The  nature  of  the  exciting  cause  of  most  cases  of  peri- 
tonitis is  such  that  by  far  the  most  frequent  variety  is  the  fibrino-purulent.  If  the 
process  involves  the  entire  peritoneum — that  is,  if  there  is  a  "  diffuse  general  peri- 
tonitis " — ^we  generally  find  upon  opening  the  abdomen  that  the  parietal  layer  of 
the  peritoneum  and  the  outer  surface  of  the  intestinal  coils  are  distinctly  red- 
dened, from  marked  vascular  injection.  There  may  even  be  small  ecchymoses 
here  and  there.  The  serous  membrane  is  clouded,  a  result  partly  of  desquamation 
of  its  endothelium,  and  partly  of  the  more  or  less  abundant  fibrinous  exudation 


522  DISEASES    OF   THE   DIGESTIVE   OEGANS 

which  covers  the  peritoneum  with  a  sheet  of  coagulated  fibrine.  Very  often  the 
coils  of  intestine  have  formed  numerous  adhesions  with  one  another  (compare 
pleuritic  adhesions).  In  cases  of  brief  duration  these  can  still  be  easily  broken 
up,  but  after  a  prolonged  illness  they  are  extremely  firm.  There  is  usually  also 
some  free,  fluid,  fibrino-purulent  exudation  in  the  abdominal  cavity.  Its  amount 
varies  greatly.  Sometimes  there  is  only  a  small  quantity  of  opaque  fluid  in  the 
dependent  portions  of  the  cavity;  sometimes  there  are  many  quarts,  causing  great 
distention  of  the  abdomen.  The  exudation  seldom  inclines  to  a  sero-purulent 
character.  It  is  usually  predominantly  purulent.  Very  often  the  purulent 
exudation  undergoes  decomposition  into  the  offensive  sanious  fluid  of  septic 
peritonitis.  This  is  particularly  apt  to  occur  when  the  disease  originates  from  an 
intestinal  perforation  or  from  puerperal  poisoning.  The  perforation  through  the 
walls  of  the  intestine  is  sometimes  so  large  as  to  admit  considerable  amounts  of 
intestinal  gases  and  faeces  into  the  peritoneal  cavity.  It  is  also  possible  that  the 
putrefaction  of  peritoneal  exudations  may  generate  offensive  gases.  In  rare  in- 
stances the  exudation  is  hsemorrhagic ;  but  most  cases  of  hsemorrhagic  peritonitis 
do  not  belong  here,  but  come  rather  under  the  tubercular  or  cancerous  forms  (vide 
infra). 

In  severe  and  protracted  cases  of  peritonitis  the  intestine  is  involved  to  a  cer- 
tain extent.  There  is  a  collateral  inflammatory  oedema  of  its  walls,  causing  some- 
times a  considerable  increase  in  thickness,  while  at  the  same  time  they  may  be 
non-resistant  and  easily  torn.  The  weakness  of  the  muscular  layer  of  the  intes- 
tine may  amount  to  complete  paralysis,  and  thus  permit  excessive  intestinal  tym- 
panites, either  diffuse  or  local. 

Milder  forms  of  general  peritonitis  with  sero-fibrinous,  or  chiefly  serous,  exuda- 
tion are  relatively  infrequent.  Under  this  head  would  come  certain  apparently 
primary  and  usually  chronic  cases  with  favorable  issue,  and  also  the  peritonitis 
which  sometimes  occurs  as  a  sequel  of  an  ascites  which  has  existed  for  some  time 
(see  next  chapter).  Probably  also  in  these  rare  cases  of  peritonitis  arising  in  the 
course  of  acute  rheumatism  and  ending  in  recovery,  the  exudation  has  been 
sero-fibrinous. 

We  have  spoken  thus  far  of  diffuse  general  peritonitis,  but  cases  are  not 
rarely  seen  of  circumscribed  or  "  encapsulated  "  peritonitis.  Here,  also,  we  have 
mild  varieties  with  fibrinous  exudations  on  the  one  hand,  and  on  the  other  puru- 
lent inflammation.  The  milder  inflammation  is  a  result  of  the  extension  of  the 
most  varied  forms  of  inflammation  from  neighboring  organs.  Thus,  deep  intesti- 
nal ulcers,  for  example,  give  rise  to  a  mild  circumscribed  inflammation  of  the  cor- 
responding portion  of  the  serous  layer.  A  similar  condition  results  from  super- 
ficial splenic  infarctions ;  from  various  hepatic  diseases,  when  they  reach  the  sur- 
face of  the  liver;  and  from  numerous  pathological  conditions  of  the  female 
genitals.  In  many  of  these  cases  the  peritonitis  takes  a  chronic  course  and  leads 
to  adhesions,  and  hence  is  called  adhesive  peritonitis. 

CircTxmscribed  purulent  peritonitis  has  precisely  the  same  aetiology  as  the 
general  form,  with  this  single  difference,  that  firm  adhesions  are  quickly  formed 
around  the  spot  whence  the  inflammation  proceeds,  limiting  it  and  preventing  it 
from  involving  the  entire  peritoneum.  It  occurs  most  frequently  as  a  purulent 
perityphlitis  (q.  v.)  consequent  upon  perforation  of  the  vermiform  appendix;  and 
also  as  pelvic  peritonitis,  which  is  a  possible  sequel  of  most  of  the  forms  of  puer- 
peral inflammation  to  which  the  uterus  and  its  appendages  are  liable.  But  we 
may  also  have  encapsulated  purvilent  peritonitis  after  the  perforation  of  gastric 
and  intestinal  ulcers,  or  of  suppurative  processes  in  the  biliary  passages,  and  from 
similar  causes.  If  the  abscess  is  situated  directly  below  the  diaphragm  it  is 
termed  subphrenic. 

Histologically  considered,  acute  peritonitis  is  perfectly  analogous  to  the  in- 


ACUTE   PERITONITIS  523 

flammatory  processes  which  attack  other  serous  membranes.  The  endothelium 
becomes  degenerated,  and,  for  the  most  part,  is  cast  off.  There  is  an  exudation 
from  the  blood-vessels  of  a  fibrinous  fluid,  which  is  partly  coagulable,  and  with 
this  exudation  round  cells  escape  in  greater  or  less  abundance.  In  the  further 
progress  of  the  disease  there  is  an  inflammatory  new  growth  of  vascular  connect- 
ive tissue,  which  probably  originates  chiefly  from  the  endothelium  and  the  perma- 
nent tissue-cells,  but,  according  to  some,  starts  in  part  also  from  the  wandering 
cells.  The  new  formation  of  blood-vessels  certainly  seems  to  be  due  chiefly  to 
budding  from  the  capillaries  of  the  serosa.  Thus  arise  the  adhesions  of  connective 
tissue  and  the  false  membranes  found  in  chronic  cases  between  the  different  coils 
of  intestine.  They  lead  in  process  of  time  to  marked  thickening  and  retraction 
of  the  omentum  and  mesentery  (peritonitis  deformans).  Most  cases  of  purulent 
peritonitis  prove  fatal  in  the  early  acute  stage.  If  a  case  recovers,  the  exudation 
undergoes  fatty  degeneration,  and  its  cellular  constituents  are  thus  disintegrated 
and  then  are  absorbed. 

The  results  of  circumscribed  purulent  peritonitis  are  detailed  in  connection 
with  the  clinical  history. 

Clinical  History. — 1.  Acute  General  Peritonitis. — The  following  description 
applies  chiefly  to  the  severe  purulent  form,  the  one  by  far  most  frequently  met 
with.  It  occurs  in  most  instances  after  perforation,  in  puerperal  cases,  and  after 
external  injuries,  such  as  surgical  operations.  In  most  of  these  cases  the  perito- 
nitis is  a  secondary  disease,  so  that  it  must  obviously  be  greatly  modified  in  its 
general  characteristics  and  behavior  by  the  original  trouble.  In  the  first  place,  the 
onset  is  modified.  Many  cases  of  peritonitis  due  to  perforation  begin  abruptly, 
the  patient  having  been  previously  in  perfect  health.  Thus,  as  already  men- 
tioned, the  first  indication  of  a  gastric  or  duodenal  ulcer  may  be  given  by  perfora- 
tion. Most  cases  of  perforation  of  the  vermiform  appendix  present  equally  sud- 
den and  unexpected  symptoms. 

There  are  many  other  cases  in  which  the  symptoms  of  peritonitis  supervene 
upon  those  of  some  grave  disease  already  existing.  For  example,  typhoid  fever, 
intestinal  tuberculosis  or  intestinal  stenosis,  may,  by  causing  perforation,  excite 
a  peritonitis.  Here  the  symptoms  of  this  secondary  disease  may  be  more  or  less 
completely  veiled  by  the  other  grave  local  and  constitutional  disturbances. 

Again,  an  acute  general  peritonitis  may,  as  we  have  already  said,  be  the  sequel 
to  a  local  and  circumscribed  inflammation  of  the  peritoneum.  Thus,  a  purulent 
perityphlitis,  or  a  purulent  puerperal  pelvic  peritonitis,  may  finally  become  uni- 
versal. In  such  unfortunate  cases  the  change  in  symptoms  is  often  gradual,  and 
is  not  clearly  pronounced. 

We  have  now  indicated  certain  variations  from  the  general  course  of  the  dis- 
ease; but,  with  these  exceptions,  almost  every  case  of  acute  general  peritonitis, 
whatever  its  aetiology,  presents  clinical  symptoms  which  are  so  characteristic  and 
typical  that  a  general  description  of  the  disease  will  be  both  easy  and  advanta- 
geous. 

The  symptoms  of  acute  peritonitis  form  two  groups,  the  local  and  the  constitu- 
tional. The  latter  are  the  result  of  the  local  disturbance  acting  upon  the  general 
condition  of  the  patient. 

Of  the  local  symptoms,  pain  deserves  to  be  named  first.  It  is  usually  the 
earliest  symptom;  and,  as  the  disease  progresses,  it  is  generally  the  excruciating 
abdominal  pain  which  attracts  most  attention.  The  localization  of  the  pain  in 
the  beginning  of  the  illness  may  be  of  diagnostic  value  in  doubtful  cases,  if  such 
as  to  indicate  the  possible  starting-point  of  the  inflammation,  for  example,  the 
vermiform  appendix  or  a  gastric  ulcer.  Later  the  pain  extends  over  the  whole 
abdomen.  As  a  rule,  there  are  brief  remissions  followed  by  fresh  exacerbations. 
The  pain  is  aggravated  by  voluntary  movements,  by  deep  inspirations,  and  prob- 


524:  DISEASES    OF   THE   DIGESTIVE    OEGANS 

ably  by  intestinal  peristalsis.  The  abdominal  tenderness  is  often  extreme  in 
peritonitis,  and  is  very  characteristic.  The  gentlest  palpation  is  torture,  and  often 
the  slightest  pressure  of  the  bed-clothes  is  almost  unbearable.  Frequently  the 
greatest  tenderness  is  in  the  umbilical  region. 

Acute  peritonitis  seldom  exists  without  pain.  The  exceptions  to  this  rule  are 
seen  chiefly  in  patients  who  are  extremely  prostrated,  and  whose  sensibility  and 
intelligence  are  much  impaired.  Here  the  peritonitis  itself  may  escape  notice — 
as  in  severe  typhoid  or  in  the  last  stage  of  tuberculosis. 

Physical  examination  of  the  abdomen  greatly  aids  the  diagnosis  in  many 
ways. 

As  a  rule,  the  abdomen  is  distended.  This  is  an  early  symptom,  and  gradually 
becomes  more  and  more  pronounced.  It  is  due  mainly  to  the  intestinal  tympa- 
nites, which  we  have  already  mentioned,  which  sometimes  becomes  very  great 
if  the  muscular  fibers  of  the  intestine  are  paralyzed.  In  the  later  stages  the 
liquid  effusion  into  the  peritoneal  cavity  of  course  contributes  to  the  prominence 
of  the  abdomen,  but  even  then  the  distention  is  seldom  so  uniform  or  so  broad  as 
in  ascites.  In  peritonitis,  coils  of  distended  intestine  can  often  be  recognized  by 
their  characteristic  contour  through  the  abdominal  wall.  Palpation  also  often 
shows  a  very  characteristic  diversity  in  the  sense  of  resistance  in  different  por- 
tions of  the  abdomen,  occasioned  by  variations  in  the  amount  of  exudation,  by 
adhesions,  or  by  the  dilatation  of  some  of  the  intestinal  coils,  and  similar  causes. 

In  general,  if  the  abdominal  wall  is  yielding  and  thin,  the  peritonitic  disten- 
tion will  be  greater,  so  that  it  is  most  marked  in  puerperal  cases,  where  the  preced- 
ing pregnancy  has  rendered  the  walls  lax.  In  a  person  with  powerful  muscles  and 
tense  abdominal  walls  the  convexity  of  the  abdomen  is  seldom  great.  In  some 
cases  there  is  no  convexity  whatever.  The  walls  may  be  as  hard  as  a  board,  and 
the  abdomen  flat  or  slightly  concave.  In  such  cases  the  diagnosis  may  be  difficult. 
Sometimes,  again,  the  original  retraction  of  the  abdominal  walls  is  succeeded  by 
more  or  less  distention  of  the  abdomen. 

Percussion  over  the  distended  intestinal  coils  yields  a  resonant  and  usually 
tympanitic  sound.  It  is  not  till  a  considerable  amount  of  liquid  effusion  has 
collected  that  there  is  dullness,  most  marked  in  the  dependent  portions  of  the 
abdomen.  If  there  is  much  tympanites,  however,  quite  a  large  effusion  may  exist 
without  being  detected  on  percussion.  Percussion  also  gives  results  analogous  to 
those  of  palpation,  in  that  there  is  often  a  diversity  in  the  quality  of  the  reso- 
nance of  different  portions  of  the  abdomen  in  peritonitis. 

Usually  there  is  too  much  pain  to  permit  a  careful  examination  of  the  change 
of  dullness  consequent  upon  change  of  decubitus.  In  general,  the  numerous  adhe- 
sions between  the  separate  coils  of  intestine  also  not  infrequently  interfere  with 
the  free  motion  of  the  peritonitic  exudations. 

Percussion  not  only  gives  information  about  the  existence  of  a  liquid,  puru- 
lent effusion,  but  is  also  of  value  in  determining  the  level  of  the  diaphragm,  as 
affected  by  abnormal  abdominal  distention.  The  upper  limit  of  hepatic  dullness  is 
raised  to  the  fifth  or  even  the  fourth  rib.  The  heart  is  also  pushed  up.  There  is 
a  tympanitic  resonance  above  the  margin  of  the  ribs  on  the  right  side.  The  area 
of  hepatic  dullness  is  not  only  displaced  upward,  but  is  also  evidently  diminished. 
This  is  due  in  part  to  coils  of  distended  intestine  overlapping  the  anterior  edge  of 
the  liver,  and  in  part  to  the  organ  being  tilted  upward  in  such  a  way  that  its 
area  of  contact  with  the  anterior  wall  of  the  body  is  less  than  normal.  Various 
authors  formerly  laid  great  stress  upon  the  total  disappearance  of  hepatic  dull- 
ness, regarding  it  as  a  sure  sign  that  gas  has  escaped  from  the  intestine  into  the 
abdominal  cavity.  The  inference  is  not  always  correct.  The  liver  may  be  dis- 
placed backward  by  coils  of  intestine,  and  hepatic  dullness  be  thus  abolished, 
although  there  is  no  air  free  in  the  peritoneal  cavity. 


ACUTE   PEEITONITIS  525 

If  there  Is  a  considerable  effixsion,  it  is  possible,  as  in  ascites  (g.  v.),  to  get  a 
sensation  of  fluctuation  by  gentle,  quick  palpation. 

As  a  rule,  auscultation  of  the  abdomen  does  not  throw  much  light  on  a  case 
of  peritonitis.  In  the  distended  coils  of  intestine  "we  not  infrequently  hear  all 
sorts  of  gurgling  and  splashing  sounds.  Sometimes  we  hear  a  peritonitic  friction- 
sound,  due  to  the  movements  of  respiration,  causing  two  rough  surfaces  to  rub 
against  each  other.  In  particular,  perihepatic  friction  is  heard  not  very  infre- 
quently. 

If  the  results  of  physical  examination  leave  us  still  in  doubt  as  to  the  pres- 
ence of  a  peritonitic  exudation,  we  may  attain  certainty  by  an  exploratory 
puncture,  and  at  the  same  time,  if  there  be  any  exudation,  determine  its 
character. 

Almost  always  the  stomach  and  intestinal  canal  are  disturbed  by  any  severe 
case  of  peritonitis. 

As  to  the  stomach,  vomiting  is  the  most  frequent  and  important  symptom. 
Vomiting  is  often  seen  early  in  the  disease,  and  recurs  frequently  as  the  illness 
progresses.  It  sometimes  is  spontaneous,  and  sometimes  follows  the  ingestion  of 
food.  If  spontaneous,  the  vomitus  consists  of  watery  mucus,  usually  of  a  green- 
ish tinge.  We  do  not  know  absolutely  the  cause  of  the  vomiting  in  peritonitis. 
Apparently  it  is  in  part  a  reflex  action,  excited  by  the  inflammation  of  the  serous 
membrane.  Possibly  the  external  pressure  of  the  exudation  also  affects  the  stom- 
ach; and  it  may  be  that  absorbed  toxines  also  excite  vomiting.  It  must  be  added 
that  vomiting  may  be  absent  in  acute  peritonitis.  This  is  seen  when  the  patient 
is  comatose,  and  sometimes  also  when  the  peritonitis  has  developed  upon  perfora- 
tion of  a  gastric  ulcer,  because  the  contents  of  the  stomach  are  thus  emptied  out 
through  the  hole  in  its  walls.  The  vomiting  is  usually  accompanied  by  frequent 
eructations. 

Of  the  intestinal  symptoms,  the  reader  has  already  become  acquainted  with 
the  tympanites,  and  also  with  the  fact  that  it  is  due  mainly  to  a  paresis  of  the 
muscular  fibers  of  the  intestine.  This  same  muscular  weakness  furnishes  an 
obvious  reason  for  the  persistent  constipation  usually  observed  in  peritonitis ;  but 
we  may  have  diarrhoea  instead,  from  increased  peristalsis  and  secondary  intes- 
tinal catarrh. 

The  pushing  up  of  the  diaphragm  has  a  noteworthy  effect  upon  the  thoracic 
organs.  The  lower  lobes  of  the  lungs  are  compressed,  so  that  considerable  dysp- 
noea results.  The  heart  is  likewise  crowded  upward,  so  that  the  apex-beat  is  usu- 
ally to  be  felt  in  the  fourth  intercostal  space. 

Every  case  of  acute  peritonitis  that  is  at  all  extensive  has  marked  constitu- 
tional effects.  These  are  in  part  the  result  of  the  wakefulness  due  to  pain,  and 
the  restlessness  and  fever.  But  perhaps  there  are  also  definite  reflex  inhibitory 
influences,  originating  in  the  irritation  of  the  peritoneal  nerves  and  affecting 
chiefly  the  heart,  just  as  Goltz  in  his  well-known  experiment  killed  a  frog  by 
blows  upon  the  abdomen.  The  chief  factor,  however,  is  in  all  probability  the  tox- 
ines which  are  very  readily  absorbed  from  the  peritonitic  exudation  by  the  peri- 
toneum, and  thus  enter  the  circulation. 

There  is  no  other  disease,  except  internal  strangulated  hernia — and  the  effect 
of  that  is  perfectly  analogous — which  produces  general  collapse  so  quickly  as 
does  peritonitis.  The  countenance  ("  fades  abdominalis  ")  is  rapidly  altered,  the 
cheeks  fall  in,  and  the  eyes  become  hollow.  The  nose  grows  sharp  and  cool,  the 
lips  and  tongue  dry.  The  skin  of  the  extremities  is  also  cool  and  bluish,  as  a  re- 
sult of  impaired  circulation.  The  patient  is  extremely  feeble.  The  chief  cause  of 
all  these  symptoms  is  the  excessive  weakness  of  the  heart.  The  peritonitis  has 
hardly  begun  before  we  find  the  pulse  small  and  soft.  In  many  severe  cases  the 
pulse  finally  becomes  almost  imperceptible.    At  the  same  time  the  pulse-rate  in- 


526  '        DISEASES    OF   THE   DIGESTIVE    ORGAl^S 

creases,  as  is  usual  in  collapse  from  any  cause,  so  that  120  to  140  beats  per  minute 
is  not  an  exceptional  rapidity. 

The  temperature  varies  greatly  in  different  cases.  It  may  be  high  in  the 
rectum,  although  the  skin  feels  cool.  Still,  very  high  fever  is  not  usual;  and 
there  are  often  considerable  remissions.  We  even  frequently  observe  the  subnor- 
mal temperature  of  collapse.  The  number  of  respirations  per  minute  is  usually 
30  to  40.  This  increased  rate  is  due  not  only  to  the  compression  of  the  lower 
lobes  of  the  lungs,  but  also  to  the  pain  caused  by  full  inspirations  and  to  the  im- 
peded circulation. 

The  intellect  remains  in  most  cases  almost  unimpaired  to  the  end.  There  may 
exceptionally  be  mild  delirium,  or  an  approach  to  stupor,  toward  the  close. 

The  course  of  acute  general  peritonitis  in  the  great  majority  of  cases  is  unfa- 
vorable. With  the  appearance  of  the  grave  symptoms  just  depicted  the  prognosis 
becomes  almost  hopeless.  The  course  of  the  disease  is  also  comparatively  rapid. 
Marked  variations  in  the  intensity  of  the  symptoms  are  infrequent.  The  grave 
local  and  constitutional  symptoms  persist,  and,  as  a  rule,  the  patient  dies  at  the 
end  of  a  few  (two  to  six)  days.  Still,  it  is  not  well  to  make  general  dogmatic 
statements  as  to  the  clinical  history,  for  the  aetiology  of  each  individual  case  im- 
presses upon  it  individual  characteristics.  A  peritonitis  resulting  from  gastric 
•  or  intestinal  perforation  is  usually  quickly  fatal.  The  same  is  true  of  almost  all 
cases  of  puerperal  septic  peritonitis.  In  a  few  cases,  however,  the  inflammation 
is  limited,  by  the  encapsulation  of  the  exudation.  These  may  finally  end  in 
recovery  through  perforation  of  the  abdominal  walls  or  perforation  into  the  in- 
testinal canal.  ISTow  and  then  an  acute  general  peritonitis  may  assume  a  chronic 
form.  The  effusion  is  mostly  reabsorbed,  and  the  newly-formed  adhesions  and 
false  membranes  contract  into  firm  bands  of  connective  tissue.  The  liver,  spleen, 
and  other  abdominal  viscera  acquire  a  tough  coating  of  connective  tissue.  The 
omentum  and  mesentery  are  shortened  and  thickened.  Indeed,  the  omentum 
may  roll  itself  almost  completely  up.  Although  the  clinical  symptoms  become  less 
severe,  weakness  usually  persists,  with  gradual  exhaustion  and  death.  Often  the 
intestine  is  so  bent  or  pinched  as  to  give  rise  to  grave  symptoms  from  stenosis. 

Recovery  from  acute  general  peritonitis  is  very  exceptional.  If  seen,  it  is  usu- 
ally in  mild  cases,  such  as  sometimes  occur  after  menstruation,  abortion,  or  labor. 
Peritonitis  as  a  complication  of  acute  articular  rheumatism  is  a  very  rare  event. 
Its  termination  is  generally  favorable.  In  all  eases  of  this  kind  the  inflammation 
is  probably  not  purulent,  but  sero-fibrinous. 

2.  Acute  Circumscribed  Peritonitis. — The  local  symptoms  of  this  are  essen- 
tially the  same  as  we  have  just  ascribed  to  the  general  form ;  except  that,  a  smaller 
extent  of  tissue  being  involved,  they  are  correspondingly  limited.  The  pain  and 
tenderness  are  confined  mainly  to  one  region,  but  its  boundaries  are  never  sharply 
defined.  On  palpation  of  this  region,  we  find  an  increased  resistance  which  is 
sometimes  almost  like  that  produced  by  a  tumor.  If  there  is  an  encapsulated 
effusion,  we  may  detect  fluctuation,  particularly  if  the  abscess  is  going  to  point 
outward.  On  percussion  over  the  affected  spot,  there  is  either  dullness  or  a  mufiled 
tympanitic  resonance. 

The  constitutional  symptoms  are  likewise  those  of  general  peritonitis,  only 
usually  less  severe.  Reflex  vomiting  does  occur,  but  is  seldom  so  persistent  as  in 
the  diffuse  inflammation.  The  physical  weakness  and  symptoms  of  collapse  are 
decided,  but  do  not  usually  become  extreme.  There  is  generally  an  irregular  fever, 
which  may  now  and  then  assume  an  intermittent,  pysemic  character.  Most 
cases  run  a  chronic  course.  If  the  illness  be  very  much  prolonged,  death  may 
finally  ensue  from  general  debility.  Recovery  is  possible  if  the  pus  can  be  let  out. 
This  may  be  accomplished  either  by  the  surgeon  or  by  ISTature.  Spontaneous  dis- 
charge of  the  abscess  may  take  place  through  the  abdominal  walls,  into  the  in- 


ACUTE   PEKITONITIS  527 

testine,  or  even,  in  rare  instances,  through  the  pleura  into  the  lungs.  But  if  the 
pus  finds  its  way  into  the  general  peritoneal  cavity,  the  peritonitis  becomes  diffuse 
and  causes  death. 

To  describe  in  detail  each  separate  variety  of  circumscribed  peritonitis  would 
occupy  too  much  space,  and  would  also  lead  to  useless  repetitions.  We  have 
already  spoken  at  some  length  of  one  especially  imi3ortant  form — namely,  peri- 
typhlitis. Perimetritis  and  pelvic  peritonitis  are  chiefly  puerperal  affections,  and 
are  fully  discussed  by  writers  on  gynaecology. 

Abscesses  which  are  very  deeply  situated — as,  for  instance,  behind  the  stomach 
or  in  front  of  the  spinal  column,  or  perinephritic — ^may  prove  very  difficult  to  diag- 
nosticate, being  so  far  out  of  reach.  Sub-diaphragmatic  abscesses  containing  air 
deserve  a  brief  mention  (pyo-pneumothorax  subphrenicus) .  They  are  sometimes 
observed  as  a  result  of  perforation  of  the  stomach  or  transverse  colon.  Lying 
between  the  liver  and  the  diaphragm,  they  crowd  the  latter  upward  and  the  liver 
downward,  and  are  liable  to  be  mistaken  for  pyo-pneumothorax.  It  is  to  be  noted 
that  in  subphrenic  abscess  the  lower  limit  of  the  lungs  moves  up  and  down  with 
respiration  (see  above,  page  438).  Sub-diaphragmatic  abscesses  containing  no 
air  also  occur,  originating  in  the  liver  or  spleen.  Finally,  there  is  a  rare  form  of 
circumscribed  purulent  peritonitis  to  be  noted,  to  which  children  seem  especially 
exposed.  It  declares  its  presence  by  a  painful  fluctuating  tumor  above  the  left 
groin,  which  usually  points  into  the  rectum  and  ends  in  recovery. 

Diagnosis. — The  diag-nosis  of  peritonitis  is  in  many  cases  an  easy  matter,  when 
we  have  the  characteristic  symptoms  of  tenderness  and  tympanites,  vomiting,  and 
collapse.  Often  the  starting-point  of  the  inflammation  is  equally  obvious,  in 
cases  of  secondary  peritonitis  supervening  upon  some  disease  which  we  have 
already  clearly  recognized,  such  as  typhoid  fever,  gastric  ulcer,  or  puerperal  dis- 
eases. But  where  the  peritonitis  is  apparently  primary,  we  must  inquire  care- 
fully into  the  previous  history  and  the  earliest  symptoms  of  the  attack,  in  order 
to  form  even  a  surmise  as  to  aetiology. 

The  diagnosis  is  sometimes  greatly  obscured  by  the  fact  that  under  certain  cir- 
cumstances very  similar  symptoms  may  be  excited  by  other  disorders  affecting 
the  intestines.  Thus,  in  typhoid  fever  there  may  be  great  tympanites  and  grave 
constitutional  symptoms,  with  abdominal  pain,  so  that  peritonitis  may  be  diagnos- 
ticated, while  the  autopsy,  if  there  be  one,  discloses  no  signs  of  it.  Deep  ulcers  of 
the  intestine,  however  produced,  may  give  rise  to  such  great  abdominal  tender- 
ness as  likewise  to  simulate  peritonitis.  The  differential  diagnosis  between  peri- 
tonitis due  to  perforation  and  acute  intestinal  obstruction  (q.  v.)  is  often  very 
difficult.  In  both,  when  there  is  severe  constitutional  infection,  the  symptoms 
are  almost  the  same,  and,  furthermore,  diffuse  peritonitis  may  occasion  such  a 
paralysis  of  the  intestine  or  such  excessive  tympanites  as  to  prevent  any  motion 
of  the  bowels,  and  even  to  cause  faecal  vomiting.  On  the  other  hand,  intestinal 
obstruction  is  not  infrequently  complicated  by  general  peritonitis,  so  that  the 
two  conditions  may  both  exist  simultaneously.  The  following  are  the  chief  points 
of  distinction  between  them,  although  even  these  are  not  infallible : 

Peritonitis  Intestinal  Obstruction 

1.  Begins  with  fever  and  with  abdominal  1.  Bepins  without  fever  and  without 
pain,  often  localized.  mai'ked  alxlominal  pain. 

2.  Abdomen  very  sensitive  to  pressure,  2.  Abdomen  at  first  soft  and  not  espe- 
hard,  and  tense.  eially  tender  upon  pressure. 

3.  Pain  tends  to  abate  as  the  disease  3.  Abdominal  i)ain  gradually  and  con- 
goes  on.  stantly  inoi-oasins;. 

4.  No  visible  peristalsis  of  the  intestines.  4.  Visible  peristalsis;  intestinal  coils  can 

be  felt  like  rolls. 

5.  Seldom  faecal  vomiting,  frequently  hie-  5.  Distinct  faecal  vomiting,  hiccough  rare, 
cough  and  simple  vomiting. 

6.  Exudation  demonstrable  in  the  perito-  6.  No  free  exudation  in  the  peritoneal 
neal  cavity.                                                               cavity. 


528  DISEASES    OF   THE   DIGESTIVE   OEGANS 

Another  diagnostic  error,  which  we  have  already  mentioned,  is  not  infrequent 
— that  is,  the  occurrence  of  peritonitis  may  be  entirely  overlooked.  This  is  espe- 
cially likely  to  happen  when  the  localized  symptoms,  such  as  pain  and  tympanites, 
are  very  slight.  Sometimes  the  only  things  which  call  attention  to  the  onset  of 
peritonitis  are  the  rapid  change  in  the  general  condition  of  the  patient,  and  in 
his  pulse  and  temperature. 

It  is  not  always  easy  to  diagnosticate  circumscribed  peritonitis,  even  when  the 
trouble  is  not  deep-seated  and  therefore  inaccessible.  It  is  not  infrequently  mis- 
taken for  a  new  growth.  In  doubtful  cases,  a  careful  use  of  the  aspirating  needle 
is  the  more  necessary,  because  the  presence  of  an  encapsulated  peritonitic  exuda- 
tion in  almost  all  cases  demands  operative  interference. 

It  is  well  to  remember  that  a  pregnant  uterus  and  a  distended  and  therefore 
painful  bladder  have  each  repeatedly  been  mistaken  for  peritonitis !  Hysterical 
meteorism  (see  the  chapter  on  hysteria)  may  also  be  erroneously  ascribed  to  peri- 
tonitis. 

Treatment. — Although  severe  cases  are  generally  almost  hopeless,  yet  we  must 
try  to  meet  the  symptomatic  indications,  and  must  do  all  in  our  power  to  promote 
a  limitation  of  the  process,  if  it  be  possible. 

External  counter-irritants  or  "  revulsants  "  are  seldom  of  much  use.  Painting 
with  tincture  of  iodine  and  mercurial  inunctions  seem  so  utterly  purposeless  that 
they  should  be  discarded.  The  local  abstraction  of  blood  can  not  be  employed  in 
an  extensive  peritonitis  with  constitutional  prostration.  It  is  only  in  a  circum- 
scribed peritonitis  which  is  very  painful,  and  when  the  general  condition  of  the 
patient  remains  comparatively  favorable,  that  bleeding  is  to  be  considered. 
Under  these  circumstances,  the  application  of  eight  to  fifteen  leeches  sometimes 
causes  decided  abatement  of  the  pain.  The  local  application  of  ice  to  the  abdomen 
is  universally  in  vogue.  It  usually  moderates  the  pain,  and  it  may  also  have  a 
beneficial  influence  in  quieting  peristalsis.  Still,  some  patients  can  not  bear  ice, 
and  sometimes  hot  cloths  and  poultices  give  great  relief. 

Of  all  internal  remedies,  there  is  but  one  of  great  value,  namely,  opium.  This 
in  large  doses  (15  to  20  drops  of  laudanum  or  a  grain — gramme  0.05 — of  extract  of 
opium  every  one  or  two  hours)  almost  always  proves  beneficial.  It  moderates 
both  the  pain  and  the  vomiting  or  eructations;  and  also,  by  diminishing  the 
peristaltic  movements  of  the  intestine,  opium  contributes  in  another  way  to 
assuage  the  suffering  and  possibly  to  limit  the  spread  of  the  inflammation.  Ex- 
perience shows  that  almost  all  patients  bear  even  very  large  doses  of  opium  re- 
markably well  in  peritonitis.  Perhaps  this  is  because  the  drug  is  only  slowly 
absorbed.  To  substitute  injections  of  morphine  for  opium  is  wise  only  in  cases 
where  we  wish  to  produce  narcosis  as  rapidly  as  possible,  or  when  the  vomiting 
or  pain  does  not  prove  amenable  to  the  ordinary  treatment.  In  such  cases  we 
may  also  prescribe  laudanum  by  enema. 

Sometimes  particular  symptoms  demand  special  attention.  For  vomiting  we 
may  employ,  besides  opium,  bits  of  ice,  small  quantities  of  sherbet,  and  perhaps 
chloroform  or  cocaine.  If  tympanites  is  excessive,  we  may  try  to  remove  some  of 
the  gas  through  a  rectal  tube  passed  as  high  up  as  possible.  Many  physicians  also 
puncture  the  distended  intestinal  coils  with  a  fine  trocar.  Collapse  and  cardiac 
failure  require  the  exhibition  of  stimulants,  such  as  champagne  or  other  alcoholic 
liquors,  or  doses  of  ether  or  camphor  given  subcutaneously.  It  is  generally  very 
difiicult  to  nourish  the  patient.  As  a  rule,  small  quantities  of  ice-cold  milk  are  the 
best  of  anything,  as  food. 

The  surgical  treatment  of  acute  peritonitis  is  constantly  growing  in  impor- 
tance. It  is  self-evident  that  in  the  case  of  a  circumscribed  abscess  in  the  abdom- 
inal cavity  the  only  way  of  giving  prompt  relief  is  by  operative  interference;  but 
even  in  acute  diffuse  peritonitis  the  results  obtained  by  laparotomy,  while  not 


CHEONIC   AND    TUBEECULAR   PERITONITIS  529 

brilliant,  are  encouraging,  and  further  trials  are  the  more  imperative,  because 
otherwise  the  prognosis  of  such  cases  is  almost  absolutely  hopeless.  The  more 
promptly  the  inflammatory  germs  and  septic  matter  are  removed  from  the  ab- 
dominal cavity,  the  greater  is  the  possibility  of  permanent  cure.  The  details 
of  the  surgical  treatment  of  peritonitis  must  be  sought  elsewhere. 


CHAPTEE   II 
CHRONIC    AND    TUBERCULAR    PERITONITIS 

.ffitiology. — Chronic  non-tubercular  peritonitis  is  a  rather  rare  disease.  It  is 
found  most  frequently  in  post-mortem  examinations  of  patients  who  have  had  for 
a  long  time  ascites  due  to  venous  stasis — for  example,  in  chronic  cardiac  or 
hepatic  cases.  The  chronic  peritonitis,  however,  is  not  the  direct  result  of  the 
passive  hyperemia  in  such  cases,  but  is,  as  already  hinted,  due  in  most  instances 
to  the  puncturing  of  the  abdomen  during  life  for  the  removal  of  the  ascitic  fluid. 
Exceptionally,  a  chronic  peritonitis  occurs  as  a  sequel  to  some  severe  intestinal 
disorder,  such  as  ulceration.  Thus,  chronic  peritonitis  is  sometimes  observed  to 
follow  typhoid  fever. 

Chronic  peritonitis  may  furthermore  be  the  result  of  an  acute  peritonitis. 
The  latter  seldom  terminates  in  this  way,  but  still  it  may,  when  rather  mild  and 
not  quickly  fatal.  The  encapsulated  exudations  of  peritonitis  usually  persist  a 
long  while,  as  was  implied  in  the  preceding  chapter. 

There  is  still  great  imcertainty  about  the  aetiology  of  those  cases  which  start 
in  a  subacute  or  chronic  manner,  without  special  cause.  Sometimes  they  seem  to 
be  due  to  an  injury  of  the  abdomen;  in  other  cases  there  are  special  constitu- 
tional influences,  si;ch  as  alcoholism,  which  may  occasion  the  disease.  In  chil- 
dren, and  less  often  in  adults,  we  sometimes  see  cases  of  "  simple  exudative  peri- 
tonitis," with  a  serous  exudation,  which  we  are  inclined  to  regard  as  analogous  tO' 
the  ordinary  cases  of  pleurisy  with  elfusion.  It  is  possible  that  in  such  instances 
pathogenic  organisms  of  various  kinds  occasion  the  inflammation;  but  in  order 
of  frequency  there  is  scarcely  a  doubt  that  tuberculosis  should  be  named  first. 
Just  as  in  pleurisy,  many  cases  of  what  is  apparently  primary  "  simple  "  perito- 
nitis turn  out  eventually  to  be  tuberculous. 

The  tubercular  is  the  most  frequent  form  of  chronic  peritonitis.  It  is  often 
merely  a  part  of  the  tuberculosis  of  serous  membranes  in  general  (vide  pages  289 
and  365),  of  which  mention  has  been  already  repeatedly  made.  In  these  cases  it  is 
usually  due  to  a  conveyance  of  the  process  from  the  pleura  through  the  diaphragm. 
Another  way  in  which  tubercular  peritonitis  may  arise  is  by  infection  from  neigh- 
boring tubercular  organs.  Tubercular  intestinal  ulcers  are  among  the  chief 
causes  of  this  kind,  the  ulcer  extending  to  the  peritoneum;  or  the  peritonitis  may 
be  excited  by  tubercular  retroperitoneal  or  mesenteric  lymph-glands.  In  women 
tubercular  peritonitis  may  be  developed  in  consequence  of  tuberciilosis  of  the 
genital  organs.  Tuberculosis  of  the  uterus  sometimes  affects  the  Fallopian 
tubes  by  direct  extension,  and  thence  the  virus  enters  the  abdominal  cavity  and 
excites  its  specific  inflammation.  In  conclusion,  we  have  to  mention  that,  in  gen- 
eral miliary  tuberculosis,  the  peritoneum  also  may  be  the  seat  of  numerous  tuber- 
cles, although  these  do  not  as  a  rule  give  rise  to  important  symptoms. 

Pathology. — In  severe  cases  of  chronic  peritonitis — and  scarcely  any  others 
have  come  to  autopsy — the  peritoneum  is  usually  found  to  be  considerably  thick- 
ened. The  intestinal  coils  are  joined  to  one  another  and  to  the  neighboring 
34 


530  DISEASES    OF   THE   DIGESTIVE    OEGANS 

organs  by  numerous  and  'extensive  adhesions.  The  false  membranes  are  often 
delicate  and  easily  separable,  but  in  some  cases  it  is  a  hard  matter  to  disenta~ngle 
the  confused  mass  into  which  the  intestines  have  been  rolled.  Sometimes  the  liver 
and  spleen  are  covered  by  firm,  tough  capsules.  The  omentum  and  mesentery  are 
much  shrunken;  hence  the  name  peritonitis  deformans.  The  omentum  may  in- 
deed be  transformed  into  a  single  thick  cord.  As  a  rule,  there  is  little  liquid  effu- 
sion, and  perhaps  none.  In  simple  chronic  peritonitis,  such  fluid  as  may  be  pres- 
ent is  usually  a  cloudy  serum,  sero-pus  being  seldom  seen. 

There  are  sometimes  many  clots  of  fibrine  suspended  in  the  fluid.  If  the  abdo- 
men has  been  repeatedly  punctured  during  the  life  of  the  patient,  we  often  may 
recognize  the  separate  punctures,  on  the  inner  surface  of  the  peritoneum,  from 
the  haemorrhages,  adhesions,  or  similar  changes  which  have  occurred.  In  rare  in- 
stances a  peculiar  form  of  chronic  peritonitis  has  been  observed  as  a  sequel  to 
punctures  for  ascites,  called  by  Friedreich  "  chronic  hasmorrhagic  peritonitis  with 
hcematoma."  In  it  almost  the  entire  peritoneum  is  covered  by  a  newly  formed 
membrane  permeated  with  large  ecchymoses. 

We  will  also  mention  briefly  a  peculiar  form  of  chronic  peritonitis,  which 
has  not  yet  been  sufficiently  investigated.  This  leads  to  the  formation  of 
numerous  small  nodules  in  the  peritoneum,  which  are  usually  at  first  regarded 
as  tubercles,  but  upon  microscopic  examination  are  found  to  be  nodules  of  con- 
nective tissue. 

Tubercular  disease  of  the  peritoneum  may  be  divided  into  two  forms :  tuber- 
culosis of  the  peritoneum,  which  may  be  acute  or  chronic ;  and  tubercular  peri- 
tonitis, which  is  usually  chronic.  In  tuberculosis  the  iDcritoneum  is  covered 
with  numerous  tubercular  nodules,  varying  in  size  from  a  millet-seed  up  to  a  pea ; 
but  there  is  not  much  coincident  inflammatory  change.  In  genuine  tubercular 
peritonitis,  on  the  other  hand,  the  inflammatory  changes  above  described  are  well 
marked,  while  sometimes  it  requires  a  microscopic  examination  to  demonstrate  the 
tubercular  nature  of  the  inflammation,  by  the  detection  of  tubercles  and  cheesy 
degeneration  in  the  newly  formed  tissue.  Tubercular  peritonitis  is  usually  rather 
chronic,  so  that  the  adhesions  are  numerous  and  strong.  The  amount  of  liquid 
effusion  varies,  being  sometimes  considerable  and  sometimes  scanty.  Just  as  in 
tubercular  pleurisy,  it  is  not  rare  for  the  exudation  to  be  bloody.  In  long-con- 
tinued peritoneal  tuberculosis  the  omentum  is  found  irregularly  thickened,  and 
the  whole  intestinal  cavity  filled  with  tumor-like  masses  (lymph-glands,  etc.). 
Among  the  more  important  associated  conditions  we  have  tuberculosis  of  other 
organs,  and  also  the  comparatively  frequent  combination  of  tubercular  perito- 
nitis with  hepatic  cirrhosis  (q.  v.). 

Clinical  History. — Diagnosis. — If  an  acute  peritonitis  becomes  chronic,  the 
violent  symptoms  gradually  abate,  while  another  group  of  symptoms  takes  their 
place.     In  other  cases  the  chronic  disease  develops  gradually  and  insidiously. 

The  sensitiveness  of  the  abdomen  is  never  so  extreme  as  in  the  acute  inflamma- 
tion. Sometimes,  to  be  sure,  the  patient  complains  of  dull  pains  and  a  sense  of 
abdominal  oppression,  but  quite  often  the  pain  is  either  constantly  or  at  times 
insignificant.  On  physical  examination,  we  usually  find  moderate  distention  of 
the  abdomen.  Frequently  this  is  not  perfectly  uniform,  certain  coils  of  intestine 
being  especially  prominent.  Occasionally  there  is  no  abdominal  distention  what- 
ever, the  belly  is  flat  or  concave,  and  the  walls  are  tense  and  unyielding.  The 
abdomen  is  more  distended  if  there  is  a  large  amount  of  liquid  exudation  or  if 
there  is  extensive  tuberculous  new  growth. 

In  many  instances  palpation  furnishes  very  characteristic  signs ;  for  sometimes 
the  thickening  of  the  omentum  and  the  numerous  fibrous  inter-intestinal  bands 
above  described  can  be  felt  through  the  abdominal  walls  as  peculiarly  resistant 
masses  or  uneven  prominences.     Indeed,  if  the  omentum  is  rolled  up,  it  may 


CHEONIC   AND    TUBEKCULAE   PEEITOISriTIS  531 

closely  simulate  a  new  growth.  The  same  is  true  of  enlarged  lymph-glands.  Not 
infrequently,  particularly  in  tubercular  peritonitis,  the  liver  is  enlarged  so  that 
its  lower  edge  can  be  felt.  But  in  other  cases  of  chronic  peritonitis  there  are  no 
changes  discoverable  by  palpation;  or  they  may  be  concealed  by  an  effusion  or 
by  the  tenseness  of  the  abdominal  walls.  A  large  exudation  can  be  demonstrated 
by  the  great  distention,  or  by  its  causing  fluctuation,  or  by  the  signs  yielded  on 
percussion.  As  a  result  of  the  adhesions  of  the  intestines  to  one  another,  the  fluid 
does  not  change  its  position  very  readily  upon  change  of  position  of  the  patient. 
This  circumstance  is  indeed  one  means  of  differentiating  between  peritonitic  ex- 
udation and  ordinary  ascites.  Not  infrequently  the  resonance  upon  percussion  is 
very  greatly  impaired,  even  when  there  is  no  large  amount  of  fluid  exudation. 
This  is  probably  due  to  thickening  of  the  peritoneum,  fibrinous  deposits,  and  sim- 
ilar changes.  Peritouitic  friction-sounds  are  sometimes  audible,  particularly  in 
the  hepatic  region.  It  has  been  already  stated  that  the  distortions  and  flexions 
which  the  intestines  may  undergo  in  chronic  peritonitis  may  result  in  obstruction. 
In  the  same  way  the  duodenum  or  the  ductus  choledochus  may  be  so  occluded  as 
to  occasion  persistent  jaundice^, 

The  objective  signs  of  both  the  simple  and  tubercular  forms  of  chronic  peri- 
tonitis have  been  embraced  in  one  description,  because  the  abdominal  signs  of  the 
two  are  identical.  To  differentiate  between  them,  other  factors  must  be  consid- 
ered. We  regard  the  patient's  constitution  and  general  appearance,  and  inquire 
into  his  family  history,  or  discover  if  there  are  other  ^etiological  factors,  such  as 
previous  tubercular  disease.  A  careful  thoracic  examination  is  extremely  impor- 
tant. If  we  find  the  signs  of  coincident  pulmonary  tuberculosis,  or  of  pleurisy, 
then  it  is  almost  indubitable  that  the  peritonitis  is  tubercular.  The  course  of 
the  fever  is  very  important.  Persistent  hectic  fever  must  always  arouse  strong 
suspicions  of  tuberculosis.  The  character  of  the  exudation  obtained  by  aspira- 
tion may  be  significant,  for  the  admixture  of  blood,  as  we  have  already  said, 
occurs  mainly  in  tubercular  peritonitis ;  but  we  may  also  have  serous  exudation 
in  tubercular  peritonitis,  just  as  in  the  ordinary  tubercular  pleurisy.  Tubercle 
bacilli  are  not  usually  present  in  the  exudation  of  tubercular  peritonitis. 

To  diagnosticate  simple  tuberculosis  of  the  peritoneum,  when  not  attended  by 
marked  inflammatory  changes,  is  generally  a  difficult  matter.  Often  it  is  abso- 
lutely impossible.  Frequently  there  is  no  abdominal  pain  or  tenderness  whatever. 
The  abdomen  is  usually  but  moderately  distended,  as  a  result  of  the  effusion 
present.  If  we  find  such  a  condition  in  a  patient  who  is  known  to  have  some  other 
tubercular  affection,  we  are  justified  in  suspecting  that  there  is  a  simple  tubercu- 
losis of  the  peritoneum. 

It  is  not  unusual  to  observe  the  combination  of  hepatic  cirrhosis  with 
peritonitis,  which  we  have  already  briefly  mentioned.  We  have  then  splenic 
tumor  and  the  other  signs  of  portal  congestion,  in  addition  to  the  symptoms 
of  chronic  peritonitis,  such  as  pain  and  fever.  The  amount  of  fluid  in  the  abdo- 
men is  usually  considerable.  As  a  rule,  the  patients  are  hard  drinkers.  The 
hepatic  cirrhosis  may  be  the  primary  disease,  and  if  so,  it  joins  with  the  con- 
stitutional results  of  alcoholic  excess  in  promoting  the  liability  to  tuberculous 
infection. 

Particular  notice  should  be  given  to  the  chronic  peritonitis  of  children,  already 
mentioned.  The  occurrence  of  ascites  in  children  between  the  ages  of  two  and 
ten  years  has  been  observed  repeatedly,  both  by  other  authors  and  by  ourselves. 
The  ascites,  which  may  be  considerable,  can  not  be  traced  to  any  cause,  and  after 
a  few  months  completely  disappears.  The  child  during  this  time  is  usually  rather 
pale  and  languid,  but  not  much  emaciated,  nor  does  he  suffer  great  local  discom- 
fort. There  may  be  no  fever.  Since  the  cases  often  recover,  their  pathological 
anatomy  remains  obscure.     Probably  they  are   a  mild  form  of  simple  chronic 


532  DISEASES    OF   THE   DIGESTIVE   ORGANS 

peritonitis.     Still,  of  course,  there  may  be  other  causes  for  the  ascites,  such  as 
hereditary  syphilitic  disease  of  the  liver. 

In  children,  tubercular  peritonitis  plays  an  important  part  in  general  tubercu- 
losis of  the  abdominal  organs,  a  condition  known  as  tabes  mesenterica.  In  these 
cases  the  tuberculosis  probably  originates,  as  we  have  already  said,  in  the  intes- 
tine, so  that  usually  we  find  the  intestine,  peritoneum,  liver,  and  abdominal  lymph- 
glands  all  simultaneously  involved.  The  clinical  symptoms  are  often  due  mainly 
to  the  peritonitis.  The  abdomen  is  distended  and  painful,  and  there  is  an  eiiusion. 
Often  there  is  also  obstinate  diarrhoea,  as  a  result  of  tubercular  intestinal  ulcers, 
with  persistent  fever  of  an  intermittent  character,  emaciation,  and  anaemia.  The 
tubercular  process  may  eventually  involve  the  lungs,  pleura,  meninges,  and  other 
organs,  or  it  may  never  extend  beyond  the  abdomen. 

As  to  the  course  of  chronic  peritonitis  we  have  little  to  say.  The  simple 
chronic  peritonitis  may  terminate  in  recovery,  although  on  account  of  other 
co-existing  lesions  this  event  is  rare,  except  in  the  special  form  which  children 
present.  Many  cases  of  tubercular  peritonitis  prove  fatal  in  a  few  months  or. 
weeks.  The  fatal  termination  of  peritoneal  tuberculosis  may  be  occasioned  by  a 
septic  peritonitis,  due  to  perforation.  We  have  seen  two  cases  of  this  sort  in 
which  the  tubercular  focus  perforated  the  intestinal  wall  from  its  outer  side. 
In  many  instances,  however,  chronic  tubercular  peritonitis  has  a  favorable  issue, 
or  at  least  there  is  very  great  abatement  of  all  symptoms.  This  is  particularly 
apt  to  be  the  case  in  what  is  called  primary  tuberculosis  of  the  serous  mem- 
branes in  general  (vide  supra).  If,  in  this  disease,  there  is  no  simultaneous 
tuberculosis  of  the  lungs,  intestines,  or  other  organs,  then  the  final  reabsorption 
of  the  exudation  is  possible,  just  as  in  tubercular  pleurisy.  It  must  be  confessed 
that  often  the  recovery  is  not  permanent,  for  the  tubercles  may  appear  later  in 
some  other  part  of  the  body. 

Treatment. — The  means  by  which  we  can  exercise  a  favorable  influence  upon 
the  course  of  chronic  peritonitis  are  scanty.  Attention  to  nourishment,  absolute 
Test  in  bed,  and  hygienic  surroundings  are  very  important;  but,  beyond  this, 
treatment  is  mainly  symptomatic.  The  chief  local  applications  are  poultices  or 
fomentations,  perseveringly  employed.  There  is  seldom  such  persistent  and  severe 
pain  as  to  demand  opiates,  but  they  may  be  required  for  the  diarrhoea  which  is 
apt  to  occur.    On  the  other  hand,  enemata  and  mild  laxatives  may  be  indicated. 

Of  special  drugs,  the  preparations  of  iodine  should  be  mentioned,  including 
iodide  of  potassium  and  syrup  of  the  iodide  of  iron,  although  the  use  of  these  is 
seldom  attended  with  obvious  improvement.  The  persistent  daily  inunction  of 
fifteen  to  thirty  grains  (one  or  two  grammes)  of  mercurial  ointment  or  oleate  of 
mercury  into  the  abdomen  seems  often  to  be  beneficial.  If  there  is  considerable 
exudation,  diuretine,  acetate  of  potash,  and  similar  diuretic  remedies  are  indi- 
cated. Whether  curative  results  are  to  be  expected  from  tuberculine,  further 
experience  must  determine. 

Of  late,  the  surgical  treatment  of  peritoneal  tuberculosis  has  had  very  favor- 
able results.  It  has  been  observed  that  in  many  cases  of  tuberculous  peritonitis, 
laparotomy,  with  as  complete  an  evacuation  of  the  exudation  as  possible  (better 
than  can  be  accomplished  by  mere  puncture  of  the  abdomen),  exercises  a  won- 
derfully beneficial  influence  upon  the  course  of  the  disease,  and  even  seems  in 
many  cases  to  occasion  complete  recovery.  This  fact  is  interesting,  although  not 
yet  wholly  explained.  Further  observations  must  be  collected  with  regard  to  this 
procedure,  but  our  own  experience  justifies  us  in  strongly  recommending  it.  Par- 
ticulars with  regard  to  its  employment  (leaving  the  abdominal  wound  open  and 
packing  with  iodoform  gauze)  are  taught  in  works  on  surgery. 

[In  the  opinion  of  the  editor,  what  surgery  has  done  for  us  in  this  affection  is 
rather  to  demonstrate  the  curability  of  many  cases  than  to  work  their  cure.    For- 


ASCITES  533 

merly,  if  the  diagnosis  of  tubercular  peritonitis  was  made  and  the  patient  recov- 
ered, the  very  fact  of  recovery  was  held  to  invalidate  the  diagnosis.  But  the 
surgeon's  knife  has  laid  bare  the  miliary  tubercles  to  the  eye,  given  an  exit  to  the 
serous  exudation,  and  recovery  has  ensued.  But  we  see  other  cases  get  well  after 
simple  tapping,  and  we  see  still  others  which  present  just  as  good  a  clinical  picture 
of  the  affection  and  recover  without  interference  of  any  kind.  Such  recovery 
may  be  temporary,  tuberculosis  breaking  out  afresh  in  the  peritoneum  or  else- 
where, or  it  may  be  permanent.  If,  in  spite  of  rest  and  appropriate  general  treat- 
ment, considerable  effusion  persists,  aspiration  or  siphonage  should  be  practiced. 
Laparotomy  should  probably  be  reserved  for  those  rather  rare  cases  which  seem 
to  be  rapidly  getting  worse,  and  those  in  which  the  fluid  reaccumulates  after  one 
or  more  tappings. 

In  expressing  the  belief  that  tubercular  peritonitis  recovers,  the  editor  does  not 
lose  sight  of  the  fact  that  multiple  fibrous  nodules  occur  disseminated  over  the 
peritoneum,  indistinguishable  by  the  unaided  eye  from  tubercles.] 


CHAPTER   III 

ASCITES 

( Hydroperitoneuin) 

The  name  ascites  is  given  to  a  collection  of  transuded  serum  in  the  abdominal 
cavity,  due  to  venous  stasis.  The  peritoneal  veins  belong  to  the  portal  system,  so 
that  among  the  diseases  which  lead  to  ascites  those  which  impede  the  portal  cir- 
coilation  are  chief.  As  we  shall  see  in  the  next  section,  ascites  is,  therefore,  of  fre- 
quent occurrence  in  cirrhosis  of  the  liver,  syphilitic  disease  of  the  liver,  compres- 
sion of  the  portal  vein  by  tumors,  thrombosis  of  the  portal  vein,  and  similar 
disorders.  Ascites  is  also  frequently  present  as  one  of  the  dropsical  symptoms  in 
general  circulatory  disturbances,  such  as  cardiac  disease  or  pulmonary  emphy- 
sema, and  in  the  course  of  various  acute  and  chronic  renal  affections. 

The  clinical  significance  of  ascites  is  due  partly  to  the  local  discomfort  occa- 
sioned by  the  presence  of  any  considerable  amount  of  fluid  within  the  abdominal 
cavity.  Small  quantities  of  serum  are  often  unnoticed  by  the  patient ;  but,  where 
many  quarts  (fifteen  to  twenty,  or  even  more)  of  transudation  exist,  the  abdomi- 
nal walls  become  greatly  distended,  and  the  patient  has  a  very  troublesome  feeling 
of  pressure,  weight,  and  tension.  What  is  of  still  greater  importance  is  the  crowd- 
ing upward  of  the  diaphragm.  Respiration  is  thereby  not  a  little  impeded.  If 
the  ascites  is  great,  the  lower  lobes  of  the  lungs  are  so  compressed  that  a  consider- 
able degree  of  atelectasis  is  produced. 

To  demonstrate  ascites  by  physical  examination  is  possible  only  Avhen  a  con- 
siderable accumulation  exists.  Then  the  belly  is  prominent,  its  walls  are  tense 
and  shining,  and,  the  base  of  the  thorax  being  gradually  distended  by  the  pressure 
of  the  liquid,  the  lower  part  of  the  thorax  seems  much  broader  than  the  upper. 
Distended  veins  are  usually  visible  through  the  skin  of  the  abdomen,  like  blue 
lines,  here  and  there.  As  soon  as  the  abdominal  tension  has  attained  a  certain 
degree,  fluctuation  can  be  perceived,  by  laying  both  hands  upon  the  abdomen  and 
imparting  gentle  but  quick  impulses  to  the  fluid  through  the  walls.  Percussion 
gives  a  dull  sound  everywhere  that  the  fluid  is  in  contact  with  the  abdominal 
walls.  Gravity,  of  course,  leads  the  liquid  to  occupy  the  dependent  part?.  In  the 
dorsal  decubitus,  and  when  the  transudation  is  of  medium  amount,  the  dullness  is 
bounded  in  the  central  and  upper  parts  of  the  abdomen  from  a  region  of  tympa- 


534:  DISEASES    OE   THE   DIGESTIVE    OEGAITS 

nitic  resonance  by  a  line  concave  toward  the  head  of  the  patient.  The  surface  of 
the  liquid  being  horizontal,  of  course  the  dullness  reaches  nearer  to  the  thorax 
along  the  sides  of  the  abdomen  than  in  the  central  line.  We  would  add,  that 
where  the  layer  of  ascitic  fluid  is  thin  we  can  obtain  dullness  only  by  light,  super- 
ficial percussion.  If  the  pleximeter  or  finger  is  pressed  deeply  in,  the  fluid  is 
crowded  to  one  side,  and  we  get  a  tympanitic  sound  from  the  underlying  coils  of 
intestine.  A  factor  of  great  diagnostic  value  is  the  change  of  dullness  on  change 
of  position  of  the  patient.  If  he  lies  upon  one  side,  the  fluid  seeks  the  dependent 
portions  of  the  cavity,  and  gives  rise  to  extensive  dullness  there,  while  the  oppo- 
site side  now  yields  a  tympanitic  resonance.  Or,  if  he  changes  to  the  other  side, 
it  in  turn  becomes  dull,  and  the  side  previously  dull  becomes  tympanitic.  Similar 
differences  are  found  between  the  results  of  percussion  in  a  horizontal  and  in  a 
sitting  posture.  It  is  only  when  the  accumulation  is  very  abundant  that  there  is 
dullness  over  the  entire  abdomen. 

The  signs  mentioned  enable  us  in  most  cases  to  make  a  diagnosis  of  ascites 
with  ease  and  certainty.  It  is,  indeed,  not  always  easy  to  distinguish  a  transuda- 
tion of  serum  from  the  exudation  of  chronic  peritonitis,  for,  of  course,  either  sort 
of  fluid  would  yield  the  same  physical  signs.  Only,  the  change  in  the  area  of 
dullness  consequent  upon  a 'change  of  position  is  less  pronounced  in  case  of  an 
exudation,  because  the  peritonitic  adhesions  impede  the  movements  of  the  fluid; 
and  we  have,  besides,  all  the  other  symptoms  to  guide  us :  there  may  be  pain, 
fever,  or  thickening  of  the  peritoneum  discoverable  on  palpation,  or  sigiis  of  tuber- 
culosis; or,  on  the  other  hand,  there  may  be  some  cardiac  or  hepatic  disease, 
which  would  render  ascites  probable.  If  the  fluid  is  drawn  off,  its  character  will 
sometimes  aid  us  in  diagnosis.  Ascites  yields  pure  serum,  containing  almost  no 
morphological  constituents.  Its  specific  gravity  is  usu-ally  less  than  that  of  a 
peritonitic  exudation,  because  it  contains  less  albumen.  We  may  say  that  the 
specific  gravity  of  the  fluid  found  in  peritonitis  is  generally  above  1018,  and  that 
of  ascites  about  1012,  or  even  lower.  Hasmorrhagic  ascites  sometimes  occurs  in 
aneemic  patients  who  are  suffering  from  marked  portal  obstruction,  as  we  have 
ourselves  seen,  for  example,  in  hepatic  syphilis. 

Chylous  ascites  due  to  an  abundance  of  fat  in  the  fluid  may  appear  as  a  result 
of  occlusion  of  the  thoracic  duct,  but  it  should  be  pointed  out  that  ascitic  fluid 
has  sometimes  a  chylous  opacity,  even  when  it  contains  no  fat  (emulsion  of  albu- 
minous substances  ?). 

There  may  be  equal  difficulty  in  the  exclusion  of  ovarian  cysts,  particularly 
since  the  cysts  are  sometimes  so  large  as  to  fill  the  whole  abdominal  cavity.  We 
must  first  map  out  accurately  the  dullness  on  percussion,  and  also  see  if  it  varies 
with  changes  of  position.  In  cases  of  ovarian  tumor,  change  of  position  does  not 
make  much  difference.  The  resonance  on  percussion  of  the  deepest  and  most 
dependent  portions  of  the  abdomen  may  be  misleading,  in  this  wa3%  that  even  in 
ascites  a  narrow  zone  here  may  be  tympanitic.  This  should  be  remembered. 
Thus,  just  above  the  symphysis,  there  is  sometimes  a  tympanitic  resonance  in 
ascites  which  might  readily  be  mistaken  for  a  proof  of  the  existence  of  an  ovarian 
tumor.  The  explanation  is  that  in  the  places  indicated  a  coil  of  intestine  with  a 
short  mesenteric  attachment  may  remain  in  contact  with  the  abdominal  wall  in 
spite  of  ascitic  accumulations.  Eurther  aid  in  the  differential  diagnosis  is  to 
be  obtained  from  the  history  of  the  case  (place  where  the  swelling  began),  from  a 
consideration  of  possible  causative  diseases,  and  from  a  vaginal  examination,  in- 
cluding direct  palpation  of  the  ovaries.  In  ascites  the  uterus  is  freely  movable, 
while  in  case  of  ovarian  tumors  it  is  often  bound  down  by  adhesions.  Further 
particulars  may  be  sought  in  books  on  gynaecology. 

The  treatment  of  ascites,  of  course,  depends  largely  upon  the  disease  of  which 
it  is  a  symptom.     As  to  the  symptomatic  treatment  of  ascites  itself,  we  will  con- 


CANCEE   OF    THE   PEEITOATEUM  535 

fine  ourselves  to  a  few  words  about  tapping.  This  operation  is  indicated  when 
the  local  disturbances  caused  by  the  ascites  are  great;  that  is,  if  there  is  an 
unbearable  sensation  of  pressure  and  tension,  and,  above  all,  if  the  crowding  up  of 
the  diaphragin  causes  much  dyspnoea.  The  instrument  to  be  used  is  a  common 
trocar  of  medium  size.  If  strength  permits,  the  puncture  can  be  most  conven- 
iently done  with  the  patient  sitting  in  a  chair,  or  crosswise  on  the  edge  of  the 
bed.  We  then  choose  for  the  best  place  for  the  puncture  the  linea  alba,  about 
halfway  between  the  navel  and  the  symphysis.  Of  course  we  should  first  see  that 
the  bladder  has  been  emptied.  If  the  patient  is  very  ill,  we  are  often  obliged  to 
make  the  puncture  while  he  is  in  bed ;  we  then  insert  the  instrument  in  the  lower 
and  left  side  of  the  abdomen,  about  halfway  between  the  navel  and  the  anterior 
superior  spine.  As  a  rule,  the  removal  of  ascitic  fluid  is  easy  and  free  from 
danger.  The  exudation  should  never  be  allowed  to  escape  too  rapidly.  We  may 
permit  large  amounts  of  liquid  (five  or  ten  quarts,  or  more)  to  flow  slowly  away  at 
one  tapping.  We  close  the  puncture  with  a  piece  of  sticking  plaster,  or  with  iodo- 
form-collodion.  Often  the  fluid  trickles  out  through  the  opening,  because  the 
abdominal  walls  have  lost  their  elasticity  on  account  of  the  persistent  distention. 
We  may  then  employ  a  suture  to  close  it.  After  tapping,  the  laxness  of  the  walls 
is  favorable  to  palpation  of  the  abdominal  organs. 

Inasmuch  as  tapping  does  not  remove  the  cause,  there  is  in  most  cases  a  very 
rapid  reaccumulation  of  fluid.  Thus  the  system  is  deprived  of  much  albumen, 
and  nutrition  is  impaired,  so  that  tiot  infrequently  the  operation  is  followed  by 
decided  loss  of  strength.  Therefore,  we  should  not  tap  in  ascites,  as  a  rule,  unless 
the  indications  for  the  operation  are  urgent. 

[If,  as  is  very  frequently  the  case,  the  fluid  continues  to  drain  away  through  the 
puncture  after  the  trocar  is  withdrawn,  good  rather  than  harm  results,  provided 
the  danger  of  irritation  of  the  skin  and  of  bed-sores  is  kept  in  mind  and  guarded 
against,  and  an  instrument  of  moderate  size  is  used. 

Flint  advocates  early  and  repeated  tappings  if  the  fluid  causes  discomfort  and 
does  not  yield  to  diuretics  or  cathartics.  The  pressure  is  removed  in  a  measure 
from  the  abdominal  and  thoracic  organs,  and  nutrition  is  thus  promoted.  The 
fluid  is  likely  to  return,  but  it  does  not  always  do  so,  or  it  may  do  so  only  slowly. 
He  reports  cases  in  which,  after  repeated  removal,  the  fluid  ceased  to  return  and 
the  patient  remained  apparently  well.  The  result  must  depend,  of  course,  chiefly 
on  the  underlying  cause,  which  is  sometimes  very  obscure. 

In  cases  of  cirrhosis  the  same  principles  govern  Flint's  treatment.] 


CHAPTEE   IV 
CANCER    OF    THE    PERITONEUM 

Carcinoma  is  the  only  new  growth  of  any  practical  importance  to  which  the 
peritoneum  is  liable.  Primary  endothelial  cancer,  analogous  to  the  growth  which 
attacks  the  pleura,  is  very  rare.  Cancerous  growths  here  arc  usually  secondary 
to  cancer  of  the  stomach,  intestine,  pancreas,  liver,  or  some  other  organ.  Often 
the  secondary  nodules  are  numerous,  and  almost  as  small  as  peas,  presenting  Avhat 
is  called  miliary  carcinosis  of  the  peritoneum.  They  cover  the  omentum,  mesen- 
tery, and  parietal  peritoneum.  Separate  nodules  of  larger  size  are  less  frequent. 
These  may  be  found  in  the  omentum,  in  Douglas's  pouch,  around  the  navel,  or  in 
other  situations.  Colloid  cancer  attains  the  most  diffuse  and  extensive  develop- 
ment of  any  variety.     The  retroperitoneal  lymph-glands  may  also  present  at  the 


536  DISEASES    OF   THE   DIGESTIVE    OKGANS 

same  time  large  cancerous  growths.  Often  the  development  of  cancer  in  the  peri- 
toneum is  attended  with  pronounced  inflammatory  disturbances — that  is,  we  have 
a  cancerous  peritonitis. 

The  symptoms  of  peritoneal  cancer  resemble  in  many  points  those  of  chronic 
tubercular  peritonitis.  Simple  miliary  carcinosis  may  be  very  insidious  and  give 
rise  to  no  special  symptoms,  so  that  it  often  is  unsuspected.  In  many  cases  a 
moderate  amount  of  fluid  collects  in  the  abdomen,  and  this,  if  we  are  aware  of  the 
existence  of  a  primary  cancerous  growth,  may  lead  us  to  surmise  a  secondary  peri- 
toneal carcinosis.  The  symptoms  are  much  more  pronounced  if  there  is  cancer- 
ous peritonitis.  In  that  case  there  is  usually  very  severe  pain,  marked  abdominal 
distention,  and  constipation.  We  may  sometimes  feel  the  larger  nodules  in  the 
omentum  or  upon  the  inner  surface  of  the  anterior  wall  of  the  abdomen,  or  even 
those  in  the  lowest  part  of  the  abdomen,  by  palpation  through  the  vagina.  We 
have  repeatedly  observed  the  development  of  palpable  nodules  in  the  navel  in  car- 
cinosis of  the  peritoneum.  If  the  exuded  fluid  be  drawn  off,  it  is  sometimes 
merely  serous,  but  it  may  be  hsemorrhagic.  When  the  new  growth  has  been  dif- 
fuse, and  particularly  in  case  of  colloid  cancer,  the  exudation  has  repeatedly  been 
found  to  present  a  milky  opacity.  Sometimes  this  fluid  also  has  been  tinged  with 
blood.  The  opacity  is  due  to  fat,  from  fatty-degenerated  and  disintegrated  can- 
cer cells.  Occasionally  the  microscope  reveals  characteristic  cancerous  elements 
in  the  fluid.  [Diagnosis  based  upon  the  microscope  alone  has  repeatedly  proved 
to  be  erroneous. — V.] 

The  diagnosis  can  not  be  made  with  any  positiveness  unless,  as  a  sequel  to  a 
primary  cancerous  growth  already  demonstrated,  we  observe  the  evident  tokens 
of  peritoneal  disturbance,  such  as  free  fluid,  pain,  points  of  resistance  on  palpa- 
tion, and  distention  of  the  abdomen.  Other  factors  are  the  patient's  age,  cancer- 
ous cachexia,  and  secondary  glandular  enlargements,  particularly  in  the  groins. 

Treatment  must  be  confined  to  efforts  at  mitigation  of  the  suffering.  Warm 
applications,  morphine,  and  supporting  measures  are  chiefly  employed. 


SECTION  vir 

Diseases  of  the  Liver,  Bile-ducts,  and  Portal  Vein 
CHAPTEE   I  I 

CATARRHAL    JAUNDICE 

(Icterus  catarrhalis.     Gastro-d/uodenal  Catarrh  with  Jaundice) 

.ffitiology  and  Pathological  Anatomy. — Catarrhal  jaundice  is  still  the  almost 
universal  term  applied  to  the  most  common  form  of  jaundice.  It  develops  in 
previously  healthy  individuals,  usually  in  a  rather  acute  manner,  and  sooner  or 
later  (as  a  rule,  after  some  weeks)  terminates  in  complete  recovery.  The  names 
"catarrhal"  or  "  gastro-duodenal "  jaundice  rest  upon  the  supposition  that  the 
entire  process  is  due  to  a  catarrhal  inflammation  of  the  duodenal  mucous  mem- 
brane. This  catarrh  is  said  often  to  spread  from  the  stomach  to  the  duodenum, 
and  in  the  duodenum  to  invade  the  region  of  the  duodenal  papilla  and  extend  up 
the  common  duct.  The  common  duct,  it  was  claimed,  became  obstructed  by  the 
swollen  mucous  membrane  or  by  the  tough  mucus  which  was  secreted,  and  thus 
blocked  up  the  bile  secreted  in  the  liver.  This  mechanical  obstruction  was  re- 
garded as  the  cause  of  the  jaundice. 


CATAERHAL   JAUXDICE  53 T 

Of  late  it  has  been  objected  to  this  old  doctrine  of  catarrhal  jaundice  that  the 
supposed  catarrh  of  the  duodenum  and  larger  bile  ducts  has  never  yet  been  abso- 
lutely demonstrated.  In  a  few  cases  of  jaundice,  in  which  at  autopsy  a  plug  of 
mucus  has  been  found  in  the  lower  portion  of  the  common  duct  or  the  duodenal 
papilla,  it  is  said  that  the  explanation  of  the  mucous  plug  is  simply  that  the  mucus 
has  collected  because  the  bile  has  not  been  secreted,  and  has  not  flowed  through  the 
duct.  The  jaundice  should  not  be  regarded  at  all  as  due  to  the  obstruction,  but 
rather  as  a  result  of  a  disturbance  of  the  function  of  the  liver  cells  (paracholia), 
such  that  the  bile  is  not  secreted  into  the  minute  bile-ducts,  but  directly  into  the 
capillaries  and  smallest  lymph-channels. 

In  our  opinion,  this  latter  theory  seems  to  be  somewhat  artificial  and  certainly 
not  absolutely  established,  although  it  seems  to  offer  a  simple  explanation  of 
many  other  forms  of  jaundice,  particularly  of  that  following  certain  poisons. 
There  is  only  one  respect  in  which  we  think  that  there  is  an  urgent  necessity  for 
change  in  the  old  doctrine  of  catarrhal  jaundice.  We  do  not  associate  the  essen- 
tial process  with  ordinary  gastric  and  intestinal  catarrh  consequent  upon  such 
causes  as  errors  in  diet,  but  we  regard  the  disease  as  in  most  cases  an  independent 
one  due  to  a  special  cause.  This  cause  is  in  all  probability  a  definite  infection, 
the  particulars  with  regard  to  which  are  as  yet  entirely  unknown ;  but  meanwhile 
we  can  scarcely  imagine  that  its  anatomical  effect  is  anything  other  than  the 
development  of  an  inflammatory  catarrh  of  the  bile-ducts,  with  a  probably  vary- 
ing involvement  of  the  stomach  and  duodenum.  It  is,  of  course,  very  possible 
that  there  may  also  be  toxic  influences  at  work,  but  at  present  their  thorough 
study  seems  impracticable. 

The  main  reason  for  assuming  that  there  is  an  infectious  factor  in  the  devel- 
opment of  catarrhal  jaundice  is,  that  not  at  all  infrequently  the  disease  appears 
in  epidemics  and  endemics.  Rather  extensive  epidemics  of  jaundice  have  been 
repeatedly  observed  in  barracks,  prisons,  and  communities  in  a  manner  to  be  ex- 
plained only  by  the  supposition  of  some  local  source  of  infection.  In  some  in- 
stances the  epidemics  of  jaundice  have  followed  revaccination,  obliging  one  to 
think  of  the  transfer  of  the  pathogenic  organism  by  means  of  inoculation.  In 
the  frequent  sporadic  cases  it  is  not  usually  possible  to  demonstrate  any  special 
cause  for  the  disease,  except  that  there  is  often  a  connection  with  some  marked 
error  in  diet,  with  catching  cold,  or  some  mental  excitement,  such  as  anger.  In 
most  instances  there  is  nothing  of  this  sort  to  be  discovered,  and  this  again  sug- 
gests an  infectious  origin  for  the  disease.  Catarrhal  jaundice  is  observed  chiefly 
in  youthful  individuals ;  sex  has  no  marked  influence. 

Symptoms  and  Clinical  Course. — Very  frequently,  though  not  invariably, 
there  are,  for  some  days  before  the  appearance  of  the  jaundice,  definite  signs  of 
gastro-intestinal  disturbance,  as  well  as  certain  constitutional  symptoms.  Obsti- 
nate vomiting,  marked  pain  in  the  stomach,  and  similar  symptoms  are  not  infre- 
quent. Very  often  the  trouble  begins  with  loss  of  appetite,  a  bad  taste  in  the 
mouth,  nausea,  a  sense  of  pressure  in  the  epigastrium,  eructations,  and  constipa- 
tion, accompanied  by  languor.  Soon  after,  the  patient  himself  notices  the  yellow 
color  of  the  skin,  or  his  attention  is  called  to  it  by  those  about  him. 

We  still  hold  provisionally  to  the  view  that  the  cause  of  catarrhal  jaundice  is 
mechanical;  and  we  desire,  with  a  view  to  preventing  repetition,  to  describe  here 
with  some  minuteness  those  symptoms  which  occur  in  varying  severity  in  all  cases 
of  obstructive  jaundice. 

The  bile  is  secreted  in  the  liver  under  an  extremely  low  pressure,  and  conse- 
quentlj'  a  comparatively  slight  obstruction  in  the  bile-ducts  suffices  to  prevent  the 
discharge  of  bile  into  the  intestine.  In  ordinary  catarrhal  jaundice,  and  also 
in  other  varieties  of  jaundice,  the  obstruction  to  the  flow  of  bile  is  seldom  com- 
plete, and  if  so,  only  for  a  time.    Still  a  considerable  amount  of  bile  collects,  and 


538  DISEASES    OF   THE   DIGESTIVE   OEGAIvTS 

distends  even  the  intrahepatic  ducts.  As  soon  as  this  stasis  has  reached  a  cer- 
tain point,  the  stag-nant  bile  is  absorbed  by  the  hepatic  lymph-vessels.  Thus  the 
bile  and  all  its  constituents  are  poured  into  the  blood  by  way  of  the  thoracic  duct 
and  carried  to  all  parts  of  the  body.  No  more  than  a  few  days  need  elapse  before 
the  bile-pigments  are  absorbed  into  the  tissues,  and  give  rise  to  the  evident  yellow 
color  of  the  skin  and  visible  mucous  membranes  which  we  call  jaundice.  Usu- 
ally the  yellowness  of  the  conjunctiva  is  the  first  thing  to  attract  attention.  Later 
the  entire  skin  becomes  yellow,  and  the  same  color  is  plainly  visible  in  the 
mucous  membrane  of  the  mouth  and  throat,  especially  after  we  have  produced 
temporary  anaemia  by  pressure,  as  in  the  lips.  Of  course,  the  internal  organs, 
which  we  can  not  see,  are  likewise  stained.  Any  abnormal  collection  of  liquid 
will  also  have  a  marked  yellow  color.  The  cornea,  the  peripheral  nerves,  and 
the  cartilages  alone  escape  unstained.  In  other  parts  we  may  not  only  find 
this  diffuse  impregnation  with  the  biliary  pigments,  but  even  solid  granules  of 
the  latter. 

A  jaundiced  patient  often  presents  other  indications  of  the  presence  of  biliary 
coloring  matter  than  the  color  of  his  skin.  There  is  often  an  itching  of  the  skin, 
which  may  be  very  troublesome.  It  may  be  so  bad  at  night  as  to  disturb  sleep. 
The  scratching  thus  induced  often  causes  numerous  excoriations  and  fissures, 
which  may  even  occasion  quite  large  furuncles.  Urticaria  is  also  sometimes  ob- 
served. A  peculiar  disease  of  the  skin,  which  has  been  described  in  connection 
with  jaundice,  is  called  xanthelasma.  It  presents  bright-yellow  spots,  usually 
somewhat  elevated,  which  are  found  mainly  on  the  eyelids,  though  also  on  other 
parts  of  the  body. 

The  remaining  symptoms  of  hepatogenous  jaundice  may  be  divided  into  two 
groups.  The  first  group  comprises  the  symptoms  excited  by  the  presence  of  the 
biliary  constituents,  and  particularly  of  the  biliary  acids,  in  the  blood,  while  the 
second  group  is  due  to  the  lack  of  bile  in  the  intestinal  canal. 

We  have  seen  that,  when  the  biliary  outlets  are  occluded  or  narrowed,  the  con- 
stituents of  the  bile  are  absorbed  by  the  lymphatics.  We  have  already  learned  in 
part  what  becomes  of  the  bile-pigment  thus  conveyed  into  the  blood-vessels.  That 
it  also  displays  poisonous  properties  has  been  maintained  by  some  investigators, 
but  has  not  yet  been  absolutely  proved.  The  presence  of  the  bile-acids  in  the 
blood  at  any  rate  is  of  considerable  clinical  importance.  Physiology  has  shown 
that  these  acids  possess  certain  injurious  qualities,  and,  among  others,  the  power 
to  destroy  red  blood-corpuscles.  But  in  reality  few  if  any  blood-corpuscles  are 
destroyed  by  the  bile-acids  in  the  blood,  because  they  are  too  much  diluted,  and, 
besides,  seem  in  large  part  to  be  quickly  decomposed  after  absorption.  These  acids 
do  really,  however,  excite  certain  nervous  centers  in  a  way  to  give  rise  to  decided 
clinical  symptoms.  The  most  frequent  effect  is  that  produced  by  the  cholate  of 
sodium  upon  the  cardiac  ganglia,  or  possibly  also  upon  the  center  for  the  vagus, 
and  it  is  evinced  by  a  slowing  of  the  pulse.  This  is  an  almost  invariable  phenom- 
enon, provided  there  be  no  fever  or  other  complication,  and  is  seen  not  only  in 
simple  catarrhal  jaundice  but  in  all  cases  of  hepatogenous  icterus.  The  pulse-rate 
is  from  64  to  50,  or  even  less.  Slight  irregularity  in  the  heart's  action  is  not 
infrequent.  There  are  certain  other  nervous  disturbances  often  seen  in  jaundice, 
referable  to  the  presence  in  the  blood  of  biliary  constituents,  and  in  particular 
of  biliary  acids.  Sometimes  there  is  a  striking  languor  and  muscular  weakness, 
or  headache,  or  the  patient  is  "  out  of  sorts."  Grave  nervous  symptoms,  sometimes 
seen  in  jaundice  and  grouped  tinder  the  name  of  cholcemia,  are  discussed  in 
another  chapter.  It  also  deserves  a  brief  mention  here  that  many  cases  with 
marked  jaundice  have  a  noticeable  tendency  to  bleeding — that  is,  a  sort  of  "  hsem- 
orrhagic  diathesis."  Haemorrhages  into  the  skin  and  in  the  viscera  are  quite 
often  seen,  and  also  epistaxis  and  analogous  occurrences. 


CATAERHAL   JAUNDICE  539 

We  come  now  to  a  consideration  of  those  symptoms  which  arise  because  the 
bile  does  not  reach  the  intestine.  In  this  regard  the  standpoint  of  modern  physi- 
ology is  essentially  different  from  the  old  views.  Formerly  the  bile  was  valued  as 
an  important  digestive  secretion ;  now  it  is  regarded  by  many  merely  as  an  excre- 
tion, containing  certain  end-products  of  metabolism;  but  perhaps  this  view  is 
extreme,  for  the  very  fact  that  the  bile  is  discharged  into  the  upper  part  of  the 
intestine  suggests  that  it  has  a  certain  significance  in  the  processes  to  which  the 
intestinal  contents  are  subjected,  and  there  is  certainly  one  function  of  the  bile 
which  is  indisputable — viz.,  that  it  promotes  the  absorption  of  fat.  The  bile  both 
contributes  to  the  emulsifying  of  fat,  and  also  promotes  the  passage  of  the  fat- 
drops  through  the  intestinal  walls  into  the  lacteals.  Now,  in  hepatogenous  icterus 
this  work  remains  undone,  as  is  shown  by  the  fatty  stools.  From  time  imme- 
morial the  white  clay-colored  stools  of  jaundice  have  been  well  known,  and  are 
employed  as  the  best  measure  of  the  completeness  of  biliary  retention.  The  light 
color  of  the  stools  is  due  partly  to  the  lack  of  biliary  pigment,  for  it  is  that  chiefly 
which  imparts  to  normal  fseces  their  dark-brown  color;  but  the  characteristic 
white  clay  color  is  due  exclusively  to  the  presence  of  undigested  fat  in  large 
amounts.  We  have  ourselves  performed  the  experiment  of  putting  a  patient  with 
extreme  hepatogenous  icterus  upon  a  diet  containing  as  little  fat  as  possible,  and 
have  found  that  the  stools  then  became  light  brown,  and  not  at  all  like  clay. 
Upon  microscopic  examination  of  the  f  feces  in  jaundice,  sheaf -like  aggregations 
of  crystals  are  almost  invariably  observed.  These  were  formerly  supposed  to  be 
tyrosine,  but  Oesterlein  has  shown  them  to  be  in  reality  lime  or  magnesia  soap. 

Besides  this  influence  upon  the  absorption  of  fat,  there  have  been  two  other 
properties  ascribed  to  the  bile,  having  apparent  significance  for  the  pathology  of 
jaundice.  In  the  first  place,  there  is  the  antiseptic  power  of  the  bile;  this  was  said 
to  explain  the  fact  that  in  patients  with  biliary  obstruction  the  fasces  usually 
have  a  particularly  bad  odor,  and  also  that  there  are  often  excessive  tympanites 
and  flatulence.  Secondly,  the  bile  was  reputed  to  exert  an  influence  upon  intesti- 
nal peristalsis — hence,  the  constipation  frequently  seen  in  jaundice.  Of  late,  how- 
ever, authorities  have  felt  doubts  about  ascribing  either  of  these  properties  to  the 
bile.  The  foul  odor  of  the  faeces  may  be  associated  with  the  imperfect  digestion 
of  fat,  and  the  constipation  with  the  change  in  the  diet  and  with  other  circum- 
stances. 

We  must  mention  one  other  point :  If  the  obstrviction  to  the  discharge  of  bile 
is  actually  situated  at  the  papilla  duodenalis — and  this  was  formerly  regarded 
as  certain  in  catarrhal  jaundice — then  the  discharge  of  pancreatic  juice  must  also 
be  affected,  and  we  must  also  consider  the  results  of  the  exclusion  of  this  secretion 
from  the  intestinal  contents;  but  we  do  not  possess  definite  knowledge  as  to  the 
actual  effects  of  such  an  exclusion. 

We  must  now  inquire  what  becomes  of  the  absorbed  bile.  As  to  the  biliaiy 
acids,  we  have  already  said  that  they  probably  undergo  decomposition.  Of  the 
other  constituents,  including  the  taurine  and  cholesterine  and  the  pigmentary 
matter,  we  know  the  fate  of  the  last-named  only — that  is,  we  have  learned  how 
Nature  seeks  to  rid  herself  of  this  foreign  substance.  As  soon  as  the  amount  of 
bile-pigment  in  the  blood  and  tissues  becomes  considerable,  excretory  efforts  are 
made,  in  which  the  kidneys  take  the  chief  share.  Certain  changes  take  place  in 
the  urine  almost  simultaneously  with  the  first  appearance  of  a  jaundiced  hue  in 
the  skin ;  and  these  changes  are  due  to  the  urine  containing  excreted  biliary  color- 
ing matter. 

The  urine  of  jaundice  is  generally  recognizable  from  its  color,  which  is  dark 
brown,  like  beer.  The  foam  caused  by  shaking  it  is  not  Avhite,  but  decidedly 
yellow.  A  bit  of  white  filter-paper  dipped  in  the  urine  is  stained  yellow.  If  the 
urine  is  shaken  with  chloroform  in  a  test-tvabe,  the  chloroform  dissolves  the  pig- 


540  DISEASES    OF    THE   DIGESTIVE    OEGANS 

ment,  and,  on  being  allowed  to  collect  at  the  bottom  of  the  tube,  displays  a  decided 
yellow  color.  This  is  known  as  the  "  chloroform  test."  Another  reaction  which 
usually  gives  a  satisfactory  result,  but  not  always,  is  Gmelin's.  If  urine  contain- 
ing bile-pigment  is  slowly  poured  down  the  sides  of  a  test-tube  containing  a  few 
cubic  centimetres  of  nitric  acid,  the  zone  between  these  two  liquids  exhibits  a  fine 
play  of  colors.  The  oxidizing  effect  of  the  acid  upon  the  biliary  pigment  produces 
a  number  of  colored  rings,  the  hig-hest  and  most  characteristic  of  which  is  green ; 
next  comes  blue,  then  violet  and  red.  Gmelin's  test  often  shows  very  prettily  if 
one  filters  the  urine  and  then  adds  a  drop  of  nitric  acid  to  what  remains  upon  the 
moist  filter-paper.  The  characteristic  colored  rings  form  around  this  drop.  In- 
stead of  nitric  acid,  we  may  use  tincture  of  iodine,  diluted  with  nine  parts  of 
water.  If  a  small  amount  of  this  solution  is  poured  upon  urine  containing  bile, 
in  a  test-tube,  there  is  usually  developed  a  ring  of  a  beautiful  green  color  between 
the  two  fluids. 

The  biliary  acids  also  may  be  detected  in  the  urine  of  jaundice;  but  the  pro- 
cess is  somewhat  tedious,  and  the  knowledge  gained  is  of  no  great  practical  im- 
portance. 

The  urine  very  often  contains  morphological  elements  which  are  characteristic. 
ISTothnagel  was  the  first  to  describe  minutely  the  icteric  casts — that  is,  hyaline 
casts  which  usually  have  a  yellow  tinge  and  quite  often  are  completely  covered 
with  dark-yellow  granules  or  with  epithelium.  The  urine  may  contain  a  little 
■  albumen  also,  but  this  is  not  constant.  If  we  add  acetic  acid,  there  may  be  an 
opacity  developed  which  is  said  to  be  due  to  nucleine.  All  these  changes  in  the 
urine  point  to  a  slight  degree  of  damage  done  the  renal  parenchyma  by  the  biliary 
pigment  excreted. 

[The  presence  or  absence  of  albumen  depends  largely  on  the  amount  of  the 
biliary  constituents  and  on  the  length  of  time  they  continue  in  action  on  the  kid- 
neys ;  their  effect  on  these  organs  is  more  or  less  that  of  an  irritant.] 

The  sweat-glands  also  take  part  in  the  excretion  of  bile-pigment.  The  latter 
can  be  demonstrated  in  the  perspiration  of  jaundiced  persons,  as  well  as  in  their 
urine,  l^ot  infrequently  the  patient's  linen  is  colored  yellow  by  the  sweat.  On 
the  other  hand,  no  bile-pigment  is  found  in  the  tears,  saliva,  gastric  juice,  or  secre- 
tions other  than  those  mentioned. 

Having  now  considered  the  phenomena  common  to  all  cases  of  hepatogenous 
icterus,  we  revert  to  the  subject  of  simple  catarrhal  jaundice.  The  prodromal 
gastric  symptoms  usually  last  a  few  days,  more  rarely  a  week  or  two,  when  the 
skin  becomes  evidently  jaundiced  and  the  other  results  of  the  icterus  are  also 
seen.  The  urine  grows  dark  with  biliary  pigment,  the  stools  become  light-colored 
and  more  or  less  clay-colored.  The  nervous  system  is  not  usually  seriously  de- 
ranged, but  still  most  patients  feel  very  languid,  and  have  anorexia  and  a  tend- 
ency to  constipation.  The  pulse  often  becomes  somewhat  slower  than  normal,  and 
sometimes  the  temperature  also  is  subnormal,  97°  or  98°  (36°-36.5°  C),  but 
there  may  be  slight  fever. 

In  most  cases  the  physical  examination  of  the  liver  is  of  interest,  the  organ 
being,  as  already  mentioned,  enlarged  from  the  retained  bile.  Accordingly,  the 
lower  boundary  of  hepatic  dullness  usually  extends  the  breadth  of  two  or  three 
fingers  below  the  edge  of  the  ribs,  and  not  infrequently  the  lower  margin  of 
the  organ  can  be  plainly  felt.  Often  the  gall-bladder  is  so  distended,  both  by  bile 
and  possibly  by  the  mucus  which  the  bladder  itself  secretes,  that  it  projects  from 
under  the  edge  of  the  liver.  In  such  cases,  as  Gerhardt  tells  us,  we  may  some- 
times make  out  by  percussion  a  convexity  in  the  lower  line  of  hepatic  dullness, 
which  corresponds  to  the  gall-bladder.  If  the  abdominal  walls  are  lax,  we  may  even 
feel  the  distended  viscus.  As  a  rule,  there  is  not  much  distress  in  the  hepatic  re- 
gion, although  now  and  then  there  is  a  certain  sensation  of  pressure  or  tension. 


CATAREHAL   JAUNDICE  541 

The  symptoms  depicted  seldom  last  longer  than  a  few  weeks.  Usually  a 
patient  who  takes  proper  care  of  himself  begins  to  feel  better  in  even  less  time. 
The  urine  grows  lighter  colored,  the  stools  darker,  and  the  pulse  more  rapid.  The 
yellow  color  of  the  skin  often  remains  visible  for  quite  a  while,  although  gradu- 
ally diminishing,  even  after  the  patient  feels  perfectly  well;  but  at  last  the  jaun- 
dice disappears  also  and  recovery  is  complete.  Eelapses  are  indeed  possible,  par- 
ticularly after  errors  in  diet ;  but  they  are  rare. 

The  termination  of  catarrhal  jaundice  is,  therefore,  almost  invariably  favor- 
able. The  entire  course  of  the  disease  occupies  about  three  to  six  weeks,  rarely  a 
longer  period.  It  is  a  very  exceptional  occurrence,  but  one  which  we  must  always 
think  of  as  possible,  for  this  apparently  mild  and  secure  condition  to  be  suddenly 
merged  into  the  grave,  pernicious  variety  of  jaundice.  (See  the  chapter  on  acute 
yellow  atrophy  of  the  liver  and  pernicious  jaundice.) 

Diagnosis. — Catarrhal  jaundice  is  usually  easily  diagnosticated.  The  diag- 
nosis is  made  chiefly  from  the  course  of  the  disease — the  development  of  jaundice, 
preceded  by  gastric  symptoms,  in  a  previously  healthy  person,  and  generally  in  a 
youthful  individual.  It  is  very  important  to  exclude  other  conditions  which 
might  occasion  jaundice.  We  must  consider,  therefore,  whether  the  history  of 
the  case  suggests  the  presence  of  gall-stones  (pain,  hepatic  colic),  and  be  vigilant 
in  our  physical  examination  to  detect  a  possible  cirrhosis  or  new  growth.  In  the 
case  of  elderly  patients,  particularly,  it  is  not  rare  for  what  was  at  first  regarded 
as  an  attack  of  ordinary  catarrhal  jaundice  eventually  to  disclose  itself  as  a 
grave  chronic  disease,  such  as  cancer  of  the  gall-bladder.  We  should  not  make  a 
diagnosis  of  catarrhal  jaundice  until  we  have  carefully  weighed  all  the  rational 
and  objective  signs. 

Treatment. — Most  cases  of  catarrhal  jaundice  terminate  favorably  and  require 
no  active  treatment.  Rest  and  prudence  are  indicated,  and  the  diet  should  be 
carefully  regulated,  that  the  gastro-duodenal  catarrh  may  not  be  aggravated.  Fat 
must  not  be  eaten,  for,  as  we  have  seen,  it  is  not  assimilated,  and  only  excites 
abnormal  processes  of  decomposition  in  the  intestinal  canal.  Lean  meat,  bread, 
soups,  if  not  too  rich,  vegetables,  cooked  fruit,  and  lemonade  or  tamarind-water 
are  allowable.  Milk  is  to  be  avoided  as  a  rule,  because  of  the  fat  it  contains,  but 
yet  it  is  often  well  borne.     Alcohol  is  to  be  allowed  very  sparingly  if  at  all. 

We  should  also  employ  internal  remedies  to  mitigate  the  assumed  gastric  ca- 
tarrh. The  various  stomachic  tonics  are  frequently  prescribed.  Rhubarb  is  a 
favorite  drug.  A  very  good  medicine  is  Carlsbad  water,  or  the  artificial  Carlsbad 
salts,  of  which  latter  the  dose  is  half  a  tablespoonful  to  a  tablespoonful,  in  a  tum- 
bler of  warm  water,  before  breakfast,  or  twice  a  day.  The  alkalies  are  said  to 
have  a  favorable  influence  upon  the  gastro-intestinal  mucous  membrane,  and 
they  are  also  laxative ;  that  they  furthermore  promote  the  secretion  of  bile,  as 
many  assume,  is  doubtful ;  but  there  is  no  doubt  that  the  flushing  of  the  kidneys 
by  an  abundance  of  liquid  is  beneficial.  If  there  is  obstinate  constipation  we 
are  obliged  sometimes  to  resort  to  more  powerful  remedies,  such  as  castor-oil, 
calomel,  or  rhubarb. 

Lately  much  enthusiasm  has  been  displayed  about  the  treatment  of  catarrhal 
jaundice  by  large  enemata  of  cold  water.  The  injections  are  said  to  overcome  the 
biliary  retention  by  exciting  peristalsis,  and  possibly  by  also  promoting  the  secre- 
tion of  bile.  Once  a  day  a  quart  or  two  of  water,  at  60°  to  70°  (12°-18°  R.),  is 
injected,  and  is  retained  as  long  as  possible.  The  good  efPect  is  said  to  be  observ- 
able in  a  few  days,  both  in  the  general  condition  of  the  patient  and  in  the  dimin- 
ished amount  of  bile-pigment  in  the  urine,  as  well  as  the  darker  color  of  the 
stools.  Other  physicians  recommend  injections  of  a  pint  to  a  quart  (J  to  1 
litre)  of  lukewarm  water  several  times  a  day.  We  have  tried  both  methods  re- 
peatedly without  being  able  to  convince  ourselves  that  the  course  of  the  disease 


542  DISEASES    OF   THE   DIGESTIVE    OEGANS 

is  thus  rendered  much  different  from  that  under  simple  dietetic  management; 
still,  one  may  try  irrigations,  especially  if  the  case  is  obstinate.  Whether  there 
are  any  internal  remedies  which  promote  the  secretion  of  bile  is  very  doubtful. 
The  drug  which  is  most  recommended  for  this  purpose,  and  is  much  employed  in 
catarrhal  jaundice,  is  salicylate  of  sodium,  in  the  dose  of  eight  to  fifteen  grains 
(gramme  0.5-1.0),  several  times  a  day.  The  biliary  acids  have  also  been  tried,  in 
the  form  of  purified  ox-gall,  and  also  salol,  podophyllin,  and  many  others.  We 
believe  that  all  these  remedies  may  be  perfectly  well  dispensed  with. 

The  effort  has  also  been  made  to  empty  the  gall-bladder  by  manipulation. 
Gerhardt  states  that  sometimes  the  distended  viscus  can  not  only  be  felt  through 
the  abdominal  walls  {vide  supra),  but  it  can  be  so  firmly  compressed  as  to  squeeze 
its  contents  into  the  duodenum.  Sometimes  the  obstruction  is  said  to  yield  sud- 
denly, as  if  a  plug  were  driven  out.  This  method  has  not  been  extensively 
adopted.  It  seems  applicable  only  in  a  limited  number  of  cases,  and  is  probably 
not  free  from  danger.  Several  authorities  have  recommended  external  faradiza- 
tion as  a  means  to  stimulate  the  gall-bladder  to  contract  and  discharge  its  eon- 
tents.     We  believe  that  iew  will  adopt  the  suggestion. 

Among  symptoms,  the  troublesome  itching  deserves  particular  attention.  The 
remedies  which  may  be  recommended  for  this  are  bathing  with  cold  water,  rub- 
bing the  skin  with  slices  of  lemon,  or  the  application  of  a  2-per-cent.  solution  of 
carbolic  acid,  or  of  salicylic  acid  or  thymol  dissolved  in  alcohol  (1  to  3  per  cent.) ; 
also  menthol  (headache  pencil)  and  chloroform  mixed  with  olive-oil.  Sometimes 
temporary  relief  is  afforded  by  a  dose  of  antipyrine  or  salicylate  of  soda  internally. 


CHAPTEE   II 


ACTJTE    FEBRILE    JAUNDICE 

{Infectious  Jaundice.      WeWs  Disease) 

There  is  a  peculiar  acute  infectious  disease  which  was  first  described  by  Weil, 
and  then  more  fully  by  Fiedler  and  others,  which  seems  to  be  always  associated 
with  an  acute  infectious  inflammation  of  the  gall-ducts,  and,  having  jaundice  for 
a  symptom,  it  may  properly  be  described  in  this  connection. 

The  disease  is  most  frequent  in  the  months  of  summer.  It  attacks  by  prefer- 
ence young  and  middle-aged  men.  Fiedler  was  struck  by  the  frequency  with 
which  butchers  suffered  from  it.  The  symptoms  usually  begin  suddenly.  Ex- 
treme chilliness,  fever,  headache,  and  malaise  are  almost  always  present  at  the 
onset.  Jaimdice  usually  appears  on  the  second  day,  or  soon  after,  and  it  may 
become  severe.  Its  immediate  cause  is  doubtless  obstruction  of  bile,  for  the 
stools  are  colorless,  and  the  urine  contains  an  abundance  of  bile-pigment.  The 
constitutional  symptoms  remain  for  several  days  quite  severe.  The  patient  com- 
plains of  violent  headache,  wakefulness,  and  vertigo.  Sometimes  there  is  evident 
stupor  or  mild  delirium.  Upon  physical  examination  we  not  infrequently  notice 
herpes  on  the  lips,  besides  the  icterus.  The  tongue  is  coated.  There  is  nothing 
unusual  about  the  lungs  or  heart,  except  that  the  pulse  is  apt  to  be  quite  rapid. 
The  abdomen  is  not  particularly  distended.  The  liver  is  often  enlarged,  but  not 
always.  An  acute  splenic  tumor  is  very  often,  but  not  invariably,  present.  There 
is  usually  diarrhoea.  Vomiting  may  occur.  The  urine  almost  invariably  con- 
tains albumen,  and,  as  a  rule,  we  find  blood,  epithelium,  and  casts,  indicating  a 
considerable  amount  of  nephritis.  In  a  few  cases  there  are  anuria  and  uraemia. 
Finally,  a  very  characteristic  symptom  is  the  violent  pain  in  the  muscles,  particu- 


BILIAKY   CALCULI  543 

larly  in  the  calves  of  the  legs,  of  which  most  patients  complain.  Epistaxis  and 
hsemorrhages  into  the  skin  have  also  been  repeatedly  observed. 

With  these  symptoms  the  disease  persists  for  from  five  to  eight  days,  during 
which  period  the  fever  is  often  very  considerable.  Temperatures  of  105° -107° 
(40°-41°  C.)  are  not  rare.  Then  the  fever  falls  by  crisis  or  rapid  lysis,  although 
seldom  with  perfect  regularity.  At  the  same  time  the  other  symptoms  abate  also, 
and  convalescence  ensues  after  an  illness  of  ten  to  fourteen  days  in  all.  Many 
of  the  milder  cases  recover  promptly,  while  others  are  prolonged  by  various 
sequelae  and  fresh  exacerbations.  An  unfavorable  termination  seems  to  be  excep- 
tional :  it  may  result  from  urtemia. 

It  is  highly  probable  that  this  perfectly  specific  disease,  the  most  important 
symptoms  of  which  are,  as  we  have  seen,  jaundice,  fever,  swelling  of  the  spleen, 
albuminuria,  and  pain  in  the  muscles,  is  an  acute  infectious  process,  with  a  spe- 
cial involvement  of  the  biliary  ducts ;  but  we  do  not  yet  possess  any  precise  infor- 
mation as  to  its  aetiology.  Possibly  we  do  not  always  have  to  deal  with  abso- 
lutely the  same  morbific  process,  but  with  several  allied  conditions.  We  have  no 
information  about  the  pathological  anatomy,  because  the  disease  is  too  benign 
to  furnish  autopsies,  and  the  few  bacteriological  examinations  which  have  been 
thus  far  reported  have  led  to  no  decisive  conclusion. 

The  treatment  must  be  purely  symptomatic.  In  the  beginning  calomel  is 
useful.  Later  we  prescribe  antipyretics,  hydrochloric  acid,  salicylate  of  sodium, 
and  stomachics.  The  headache  is  often  relieved  by  an  ice-bag;  the  muscular 
pain  by  the  inunction  of  chloroform  oil.  From  the  first  the  diet  must  be  such 
as  not  to  aggravate  the  nephritis  (milk,  simple  soups). 


CHAPTER   III 

BILIARY    CALCULI 

{Hepatic  Colic.     Cholelithiasis) 

.3itiology. — Gall-stones  are  of  verj^  frequent  occurrence;  Riedel  asserts  that 
some  two  millions  of  the  inhabitants  of  Germany  have  gall-stones,  although  this 
estimate  seems  to  be  very  high.  Despite  their  frequency,  we  have  little  positive 
knowledge  of  their  causation.  We  can  merely  state  certain  circumstances  which 
in  all  probability  favor  the  formation  of  these  concretions. 

Biliary  retention  certainly  acts  in  this  way,  both  directly  and  by  leading  to  an 
increased  consistency  and  increased  concentration  of  the  bile.  As  a  result,  certain 
constituents  which  were  before  held  in  solution  are  thrown  down.  And  yet  this 
cause,  however  potent  {vide  supra),  can  not  be  regarded  as  the  only  one.  The 
chemical  composition  of  gall-stones  suggests  that  their  formation  must  be  pre- 
ceded by  certain  abnormal  chemical  processes  of  decomposition  and  of  trans- 
formation. We  can  not  otherwise  explain  Avhy  the  constituents  of  gall-stones 
should  differ,  as  they  do  in  many  ways,  from  the  matters  which  nomial  bile  holds 
in  solution.  For  example,  the  pigment  in  gall-stones  is  never  found  unchanged, 
but  invariably  exists  in  composition  with  lime.  Now,  normal  bile  contains  only 
a  trace  of  lime,  so  that  long  ago  Frerichs  expressed  the  opinion  that  the  lime 
comes  from  the  mucous  membrane  of  the  gall-bladder.  It  is  an  important  fact 
that  the  cholesterine,  and  probably  also  a  portion  of  the  pigmentary  matters,  are 
held  in  solution  in  normal  bile  by  the  combination  of  sodium  with  the  biliary 
acids  which  it  contains.  If  this  sodium  salt  were  decomposed  from  any  cause, 
the  matters  named  would  naturally  be  precipitated.     The  decomposition  of  the 


544  DISEASES    OE   THE   DIGESTIVE    OEGANS 

salts  formed  by  the  bile-acids  is  greatly  promoted  if  the  bile  acquires  an  acid 
reaction ;  but  of  the  circumstances  in  which  this  last-mentioned  change  occurs  we 
do  not  yet  have  any  accurate  knowledge.  Lately  Naunyn,  after  extensive  inves- 
tigations, has  propounded  a  theory  that  the  formation  of  calculi  is  due  in  most 
cases  to  a  primary  disease  of  the  mucous  membrane  of  the  gall-bladder  and  the 
bile-ducts.  The  disease  causes  the  destruction  of  great  numbers  of  the  epithelial 
cells  of  the  mucous  membrane,  with  a  resultant  production  of  cholesterine,  and  of 
a  compound  of  lime  with  bilirubine.  Thus  are  formed  friable  masses  of  detritus, 
which  are  gradually  changed  into  gall-stones,  in  the  interior  of  which  it  is  still 
possible  at  an  early  stage  to  demonstrate  the  original  pultaceous  mass.  As  the 
cholesterine  and  the  compound  of  lime  with  bilirubine  continue  to  form  by  crys- 
tallization, and  fresh  deposits  of  firm  material  take  place,  the  stone  gradually 
grows  harder  and  larger.  Very  often  also  there  is  added  at  this  stage  a  deposit  of 
carbonate  of  lime.  The  cause  of  the  original  lithogenous  catarrh  is  not  known. 
Perhaps  the  mere  mechanical  obstruction  of  bile  is  causative,  perhaps  infection. 
In  particular,  the  bacterium  coli  commune,  which  originates  in  the  intestines, 
seems  to  be  important — or  at  least,  if  not  this,  a  very  similar  kind  of  bacillus. 
If  the  supposition  were  confirmed  that  infection  of  this  sort  is  a  factor,  it  would 
also  be  natural,  as  shown  by  what  has  been  previously  stated,  to  consider  that 
such  an  infection  would  have  an  influence  upon  the  bile  itself. 

We  have  rather  more  knowledge  as  to  predisposing  causes  than  about  the 
chemical  processes  involved  in  the  formation  of  gall-stones. 

Age  seems  to  be  an  important  factor.  The  great  majority  of  patients  are  over 
forty.  Gall-stones  are  much  less  frequent  between  twenty  and  forty  years  of  age ; 
and  in  children  they  are  very  rare,  although  they  have  been  observed  in  the  new- 
born. One  reason  why  elderly  people  are  so  liable  to  this  trouble  is  said  to  be  the 
senile  weakness  of  the  muscular  fibers  of  the  gall-bladder.  Thus  stagnation  and 
retention  of  bile  are  promoted.  It  has  also  been  suggested  that  in  old  age  the 
bile  may  contain  an  excessive  amount  of  cholesterine  and  lime.  It  must  be  con- 
fessed that  this  explanation  is  not  very  satisfactory. 

Sex  also  has  a  decided  influence.  All  authors  agree  that  gall-stones  are  more 
frequent  in  females  than  in  males,  the  proportion  being  about  three  to  two.  An 
explanation  of  this  fact  has  been  sought  in  the  sedentary  life  of  women,  and  par- 
ticularly in  the  mechanical  efl^ect  of  women's  clothes  and  tight  lacing,  impeding 
the  outflow  of  bile.  It  is  a  fact  which  certainly  deserves  consideration  that  we 
are  very  apt  to  find  gall-stones  and  a  corset-liver  in  the  same  individual.  Also, 
the  influence  of  pregnancy  can  not  be  denied.  Gall-stones  are  found  in  women 
who  have  borne  children  much  oftener  than  in  others. 

Much  has  been  said  abovit  certain  peculiarities  of  constitution,  in  their  rela- 
tion to  the  formation  of  gall-stones ;  and  it  is  asserted  that  the  mode  of  life  may 
favor  their  development — as  when  too  much  food  is  taken,  particularly  an 
excess  of  fat  and  meat,  and  when  there  is  insufiicient  bodily  exercise.  In  general, 
statements  of  this  sort  must  be  viewed  with  much  suspicion;  still,  we  can  not 
deny  that  cholelithiasis  is  seen  with  striking  frequency  in  obese  women,  and  that 
the  trouble  seems  to  be  somewhat  more  common  among  the  favored  classes  than 
among  the  poor.  There  often  seems  to  be  a  hereditary  predisposition  to  gall- 
stones. It  has  been  said  that  there  is  a  relation  between  cholelithiasis  and  gout, 
arterio-sclerosis,  and  other  diseases,  but  this  is  not  at  all  certain.  It  is  an  inter- 
esting fact  that  sometimes  the  same  individual  has  gall-stones  and  renal  calculi. 

In  many  cases  there  may  be  disease  of  the  liver  and  of  the  bile-ducts  them- 
selves, leading  to  persistent  obstruction,  and  thus  causing  gall-stones.  It  must  be 
confessed  that  it  is  often  very  difficult  to  decide  about  this  point,  for  gall-stones, 
as  we  shall  see  later,  may  themselves  lead  to  secondary  disease  of  the  liver,  such 
as  biliary  cirrhosis   and  carcinoma;  so  that  when  gall-stones   and   some   other 


BILIAEY   CALCULI  545 

hepatic  disease  are  both  present  it  is  often  impossible  to  decide  which  of  the  two 
lesions  was  iDrimary. 

Occurrence,  and  Chemical  and  Physical  Properties  of  Gall-stones. — Tlie 
place  where  gall-stones  are  most  frequently  formed  and  found  is  the  g-all-bladder. 
We  may  find  in  it  any  number,  from  one  or  two  up  to  a  hundred  and  more.  The 
size  varies  from  that  of  a  grain  of  sand  to  that  of  a  hen's  egg.  The  large 
stones  may  completely  fill  the  gall-bladder;  and  sometimes  the  smaller  stones  are 
numerous  enough  to  fill  it  also.  The  stones  usually  lie  free  in  the  bladder,  al- 
though exceptionally  they  may  be  found  adherent  to  its  walls.  Rarely  the  blad- 
der presents  a  diverticulum,  in  which  a  stone  has  been  formed.  The  lining  mem- 
brane of  the  viscus  often  presents  quite  a  severe  catarrhal  inflammation.  This 
may  have  preceded  the  formation  of  the  stone  (vide  supra),  but,  on  the  other 
hand,  it  may  have  developed  as  a  result  of  the  mechanical  irritation  of  the  mucous 
membrane  occasioned  by  the  concretions.  Very  often  the  wall  of  the  gall-bladder 
and  the  neighboring  tissues  are  afi'ected  by  mild  or  even  severe  inflammatory  pro- 
cesses, necrosis,  perforation,  and  similar  lesions  (vide  infra). 

Stones  which  are  found  in  the  larger  bile-ducts  are  not  formed  in  them,  but 
they  have  become  wedged  in  them  while  on  their  way  to  the  intestine.  Some- 
times, however,  stones  are  formed  in  the  liver  itself  ("hepatic  calculi")-  These 
are  seldom  primary,  but  are  usually  the  result  of  biliary  obstruction  because  of 
persistent  stenosis  of  the  common  duct.  Hepatic  gall-stones  of  this  sort  may 
reach  a  diameter  of  a  half  to  one  centimetre.  In  such  cases  the  small  intra- 
hepatic bile-ducts  are  usually  a  good  deal  widened;  or  occasionally  they  present 
niches  in  which  the  stones  lie.  As  a  rule,  the  hepatic  parenchyma  surrounding  the 
stone  is  in  a  state  of  chronic  or  acute  purulent  inflammation  (vide  infra). 

In  form,  gall-stones  vary  infinitely.  The  smallest  are  irregular  masses,  well 
described  by  the  name  of  "  gall-sand."  The  larger  stones  are  more  or  less  round, 
oval,  or  polyhedral.  The  polyhedra  are  usually  due  to  the  mutual  rubbing  and 
pressure  of  a  number  of  stones  upon  one  another.  In  color,  the  stones  vary  ac- 
cording to  the  amount  of  pigment  they  contain,  from  almost  black  or  dark  brown 
to  a  lighter  greenish  or  bright  yellow  shade.  A  fresh  gall-stone  always  sinks  in 
water;  but  when  dry,  gall-stones  contain  air  and  generally  float.  On  cross-sec- 
tion, the  hard  stones  are  found  to  be  either  homogeneous  or  composed  of  layers. 
As  a  rule,  there  is  a  nucleus,  darkly  pigmented,  which  is  surrounded  by  a  lighter- 
colored  envelope,  itself  either  made  up  of  concentric  layers  or  evidently  crystalline. 
Often  the  outermost  layers  are  still  distinguishable  as  peculiar  darker  and  harder 
strata.  If  we  examine  thin  scales  of  gall-stones  microscopically  we  shall  find  in 
them  (as  in  renal  calculi)  an  organic  cement  which  holds  the  minute  crystals 
together  (Posner). 

As  to  chemical  composition,  gall-stones  are  usually  divided  into  several 
groups.  By  far  the  most  frequent  variety  is  made  up  of  cholesterine  and  pigment 
(bilirubine)  mixed  together  in  greatly  varying  proportions.  The  pigment  is  in 
great  part  combined  with  lime.  On  the  average,  stones  contain  about  seventy 
to  eighty  per  cent,  of  cholesterine.  Besides  these  two  chief  ingredients,  most 
stones  also  contain  lime  and  magnesium.  In  color,  they  are  light  or  dark  ac- 
cording to  the  smaller  or  greater  proportion  of  coloring  matter  they  contain. 
Stones  of  pure  cholesterine  are  less  common.  These  are  usually  found  singly, 
are  soft,  and  often  are  almost  transparent.  Most  cholesterine  stones  have  a 
nucleus  of  pigment  and  lime  in  combination.  Pure  pigmentary  concretions  are 
rare,  and  are  generally  small,  like  coarse  sand.  A  still  greater  rarity  is  a  stone 
made  up  entirely  of  lime.     Such  a  stone  is  small  and  very  hard. 

Anatomical  and  Clinical  Results  of  Gall-stones. — It  is  by  no  means  rare 
for  gall-stones  to  be  present  even  in  considerable  number  and  size  without  caus- 
ing the  slightest  discomfort.  This  is  proved  by  the  fact  that  often  at  autopsy 
35 


546  DISEASES    OF   THE   DIGESTIVE    OEGA^S 

gall-stones  are  found  by  chance,  although  there  had  never  been  a  symptom  sug- 
gesting their  presence.  In  such  cases  it  is  evident  that  the  concretions  have 
formed  very  gradually  in  the  gall-bladder,  and  never  have  led  to  mechanical  or 
inflammatory  disturbance. 

In  other  cases,  probably  very  numerous,  the  gall-stones  occasion  certain  dis- 
turbances, but  these  are  comparatively  insignificant  and  not  of  such  a  character 
as  to  enable  the  physician  to  make  an  absolute  diagnosis.  Patients  of  this  sort 
complain  at  times  of  slightly  painful  or  disagreeable  sensations  in  the  stomach 
and  liver,  particularly  after  bodily  exertion,  and  they  may  also  have  other  symp- 
toms, such  as  slight  dyspepsia.  The  objective  examination  yields  nothing  posi- 
tive. The  physician  suspects  a  gastric  disorder,  a  floating  kidney,  or  a  neurosis. 
It  is  important  that  he  should  always  in  such  eases,  particularly  in  women, 
consider  the  possibility  of  gall-stones ;  for  it  is  possible,  if  there  is  an  actual  chole- 
lithiasis, that  at  any  time  there  may  be  severe  symptoms,  the  correct  interpreta- 
tion of  which  will  be  rendered  much  easier  if  these  mild  prodromata  have  been 
duly  appreciated. 

In  a  third  class  of  cases  the  gall-stones  cause  severe  and  sometimes  actually 
fatal  illness.  The  symptoms  may  be  very  characteristic,  so  that  they  can  be  rec- 
ognized easily  and  absolutely;  but  not  infrequently  the  condition  is  difiicult  to 
interpret,  and  misleading. 

The  form  of  the  disease  which  can  be  recognized  most  certainly  and  which 
has  been  longest  known  to  clinicians  is  characterized  by  the  occurrence  of  distinct 
and  peculiar  jjaroxysms.  These  are  usually  termed  biliary  colic.  An  attack  of 
this  sort  may  occur  suddenly,  while  the  patient  is  apparently  in  perfect  health. 
More  often,  however,  the  first  distinct  attack  is  preceded  for  a  long  time  by  mild 
disturbances  (vide  supra),  although  these  latter  often  receive  little  attention, 
and  are  apt  to  be  misinterpreted. 

The  typical  attack  of  biliary  colic  begins  either  with  absolute  suddenness  or 
after  some  slight  prodromata,  such  as  chilliness,  nausea,  and  malaise.  It  may 
occur  at  any  time,  day  or  night.  Usually  there  is  no  exciting  cause  to  be  dis- 
covered. Sometimes  the  paroxysm  is  preceded  by  a  slight  injury  or  some  other 
apparently  harmful  influence,  such  as  errors  in  diet  and  the  like.  The  chief 
symptom  of  the  attack  is  the  pain.  This  may  be  extreme  from  the  start,  or  it 
may  begin  mildly  and  then  rapidly  or  slowly  become  extreme.  Usually  the 
patient  refers  the  pain  chiefly  to  the  epigastrium  and  to  the  right  hypochondrium, 
but  from  here  it  radiates  into  the  left  side,  the  back,  the  shoulders,  and  even  the 
right  arm,  and  sometimes  ag'ain  down  into  the  hypogastrium  and  the  thighs. 
In  some  paroxysms  the  pain  increases  to  extreme  severity;  and  convulsive  move- 
ments have  been  repeatedly  observed,  particularly  in  nervous  persons,  as  a  result 
of  the  pain.  The  pain  may  be  accompanied  by  nausea,  eructations,  and  repeated 
vomiting.  The  bowels  are  usually  constipated,  but  sometimes  there  is  diarrhoea. 
The  constitutional  disturbance  is  marked;  the  patient  feels  extremely  feeble  and 
exhausted,  and  gives  the  impression  of  anguish  and  collapse.  The  pulse  is  small, 
usually  accelerated,  but  sometimes  infrequent.  The  bodily  temperature  is  normal 
in  a  minority  of  the  cases;  often  there  is  slight  fever,  and  sometimes  a  consider- 
able rise  of  temperature,  to  104°  (40°  C.)  and  more.  At  the  beginning  of  the 
attack,  and  also  later,  there  is  apt  to  be  chilliness,  or  a  well-marked  rigor;  and 
this  is  often,  but  not  invariably,  associated  with  high  fever. 

Upon  objective  examination  of  the  abdomen  we  find  its  upper  portion,  par- 
ticularly the  region  of  the  liver  and  gall-bladder,  slightly  prominent  or  even 
markedly  so.  The  same  region  is  sensitive  to  pressure,  and  this  tenderness  may 
be  diffuse  or  localized.  Sometimes  an  enlargement  of  the  liver  can  be  distinctly 
made  out  (vide  infra),  and  sometimes  when  the  abdominal  walls  are  yielding  we 
can,  upon  careful  palpation,  feel  the  enlarged,  tense,   and  tender  gall-bladder 


BILIAEY   CALCULI  547 

(vide  infra).  In  exceptional  cases  we  can  even  feel  the  grating  of  the  stones 
npon  one  another,  and  with  a  stethoscope  hear  the  crepitation  thus  produced; 
but  in  other  cases  it  is  impossible  to  make  out  with  certainty  any  change,  either 
in  the  liver  or  the  gall-bladder;  or  the  abdominal  walls  may  be  so  thick  and  rigid 
that  a  good  examination  is  impossible.  In  any  case  of  this  sort  the  physician  looks 
with  special  attention  for  the  appearance  of  jaundice.  Even  a  slight  icteric  hue 
of  the  eyes  and  the  skin  is  important,  for  the  appearance  of  jaundice  is  often 
decisive  in  leading  to  an  absolute  diagnosis.  Sometimes  the  jaundice  is  very 
marked;  in  such  cases  the  urine  contains  an  abundance  of  bile  pigment.  It 
can  not,  however,  be  too  much  insisted  upon  that  it  is  by  no  means  exceptional  to 
have  no  jaundice  at  all  in  an  attack  of  biliary  colic  (vide  infra).  With  regard 
to  finding  gall-stones  in  the  faeces,  vide  infra. 

The  duration  of  an  attack  of  biliary  colic  varies  greatly.  Extremely  mild 
attacks  may  last  merely  a  few  hours  or  a  day;  more  severe  attacks  continue 
two  to  four  days  and  even  much  longer.  It  is  equally  impossible  to  establish 
any  universal  rule  as  to  the  frequency  with  which  the  attacks  recur.  Sometimes 
a  second  attack  will  come  after  a  short  interval ;  sometimes  not  until  months  or 
years  have  elapsed.  Not  infrequently  there  will  be  several  attacks  in  close 
succession,  and  then  none  for  a  long  time;  or  there  may  never  be  any  more. 
Again,  the  early  attacks  of  simple  colic  may  be  followed  later  by  a  complicated 
disorder,  due  to  one  of  the  numerous  sequelae  to  which  gall-stones  may  lead. 

We  intend  to  discuss  the  remote  results  of  gall-stones,  but  we  must  first  answer 
the  question.  What  abdominal  processes  occasion  the  attacks  of  biliary  colic,  of 
which  we  have  just  presented  the  clinical  picture.  Until  within  a  few  years  the 
answer  to  this  question  seemed  very  simple.  Almost  all  authorities  conceived 
that  the  attack  was  due  mainly  to  the  moving  about  of  the  calculi  and  their 
expulsion.  It  was  said  that  the  stones  moved  into  the  cystic  duct  because  of 
their  own  weight,  the  pressure  of  the  diaphragm,  and,  above  all,  the  contractions 
of  the  gall-bladder ;  and  being  once  in  the  duct,  they  were  forced  along  through  the 
cystic  and  the  hepatic  ducts.  The  attack  was  successfully  ended  when  at  last 
the  concretion  escaped  from  the  common  duct  into  the  duodenum.  The  incar- 
ceration of  the  stone  in  the  common  duct  necessitated  jaundice.  If  the  stone 
stopped  in  the  cystic  duct,  or,  as  was  often  supposed  to  be  the  case,  went  back 
into  the  gall-bladder  again,  there  would  be  no  jaundice. 

This  old  doctrine  of  the  causes  of  biliary  colic  is  now  known  to  be  in  large 
part  incorrect,  a  better  understanding  having  been  obtained,  incidentally  to 
operations  upon  the  gall-bladder  and  the  bile-ducts.  In  particular,  Riedel  has 
made  extensive  and  careful  observations,  and  has  contributed  many  new  facts 
and  views  to  the  doctrine  of  cholelithiasis.  Still,  complete  insight  into  all  the 
conditions  has  been  by  no  means  attained. 

Even  now  it  must  be  confessed  that  small  stones  can  be  driven  from  the  gall- 
bladder through  the  cystic  and  common  ducts  into  the  intestine  in  the  way  above 
mentioned,  but  the  progress  of  the  small  stone  in  this"  manner  into  the  intestine 
usually  causes  no  symptoms  at  all,  or,  if  there  are  any,  they  are  slight  and 
ambiguous.  It  may  be  that  now  and  then  a  somewhat  larger  stone  is  forced  from 
the  gall-bladder  into  the  intestine  and  excites  a  genuine  attack  of  biliary  colic, 
in  the  old  sense  of  the  term;  but  in  most  cases  the  attack  which  we  clinically 
term  biliary  colic  is  probably  due,  only  to  a  very  slight  extent,  to  the  incnrcera- 
tion  of  a  calculus,  or  to  cramp-like  contractions  of  the  gall-bladder  and  biliary 
ducts,  but  it  is  rather  an  inflammatory  process.  So  long  as  the  stones  in  the  gall- 
bladder remain  there  without  exciting  any  secondary  change,  and  so  long  as  th'3 
bile  flows  freely  around  them,  in  and  out,  there  are  no  clinical  symptoms,  although 
there  is  very  often  a  gradual  development  of  what  is  called  dropsy  of  the  gall- 
bladder.    If  a  stone  enters  the  neck  of  the  bladder  and  there  increases  in  size,  or 


548  DISEASES    OF   THE   DIGESTIVE    OEGA]!^S 

if  the  cystic  duct  becomes  obstructed  by  the  swelling  of  its  membrane,  then  the 
entrance  of  the  bile  into  the  gall-bladder  is  impeded.  The  constituents  of  the 
bile  which  is  in  it  are  absorbed,  and  the  contents  of  the  gall-bladder  change  to  a 
3^ellowish  serum,  which  may  finally  be  almost  colorless.  This  process  often  goes 
on  without  any  symptoms,  but  frequently  there  are  slight  suggestions  of  chronic 
inflammation.  The  wall  of  the  gall-bladder  becomes  thickened;  there  may  be  a 
gradual  formation  of  manifold  adhesions  between  the  serous  coat  of  the  gall- 
bladder and  the  neighboring  parts,  such  as  the  omentum,  duodenum,  or  transverse 
colon ;  and  these  adhesions  are  in  many  cases  the  cause  of  the  mild  and  indefinite 
pains  and  other  unpleasant  sensations  of  which  many  patients  with  gall-stones 
complain  for  a  long  time  previous  to  their  first  genuine  attack.  When  a  gall- 
bladder has  been  changed  in  this  way,  there  is  liability  to  frequent  and  sudden 
acute  infiammatory  symptoms ;  acute  calculous  cholecystitis  is  the  true  anatom- 
ical basis  of  biliary  colic. 

We  do  not  possess  accurate  knowledge  as  to  the  cause  of  these  acute  inflam- 
matory attacks  or  exacerbations.  In  our  judgment,  it  is  more  probable  that  from 
the  start  infectious  germs  are  factors  in  promoting  the  inflammation — perhaps  the 
bacterium  coli  commune,  perhaps  other  bacteria.  These  usually  originate  in  the 
intestine,  and  opportunity  for  their  pathogenic  activity  is  afforded  by  the 
mechanical  irritation  and  pressure  of  the  gall-stones.  The  ordinary  brief  attacks 
of  biliary  colic  are  due  to  simple  cholecystitis  with  a  serous  exudation,  which 
usually  gets  well  of  itself  in  a  few  days.  This  serous  or  "  catarrhal "  chole- 
cystitis occasions  swelling  of  the  gall-bladder,  pain,  fever,  and  vomiting.  The 
calculus  caught  in  the  neck  of  the  gall-bladder  may,  of  course,  have  many  other 
stones  behind  it ;  but  it  is  not  pushed  onward  if  it  has  reached  a  certain  size ;  it 
remains  till  the  inflammation  passes  away.  We  have  in  this  case  a  so-called 
"unsuccessful  attack  of  biliary  colic"  (Eiedel).  These  attacks  are,  of  course, 
as  a  rule  not  associated  with  jaundice.  If,  however,  the  stone  is  small  and  the 
cystic  duct  patent,  the  stone  is  pushed  on  by  the  pressure  of  the  inflammatory 
exudation  which  collects  behind  it.  We  have  now  the  pain  due  to  the  inflam- 
mation and  also  that  due  to  the  incarceration  of  the  stone,  and  as  soon  as  the 
stone  reaches  the  common  duct,  and  for  a  time  blocks  the  discharge  of  bile,  we 
almost  invariably  have  obstructive  jaundice.  If  the  stone  is  successfully  driven 
through  the  common  duct  into  the  duodenum,  the  pain  and  inflammation  usually 
promptly  cease.  By  careful  search  we  may  find  one  or  more  stones  in  the  faeces. 
In  brief,  we  have  to  deal  with  a  so-called  "  successful "  attack  of  biliary  colic. 
The  distinction  between  unsuccessful  and  successful  attacks  is,  of  course,  not 
always  self-evident ;  but  it  should  be  noted  that,  according  to  Eiedel,  unsuccessful 
attacks  are  much  more  frequent  than  the  successful.  It  is  true  that  in  the  success- 
ful attacks  there  is  always  jaundice,  and  in  the  unsuccessful  attacks  there  is  usu- 
ally no  jaundice,  yet  this  criterion  is  not  absolute,  because,  as  Eiedel  was  the  first 
to  point  out,  jaundice  may  occasionally  be  present  in  the  unsuccessful  attacks. 
In  such  a  case  the  jaundice,  of  course,  is  not  due  to  closure  of  the  common  duct 
by  a  stone — that  is,  it  is  not  lithogenous,  but  it  is  inflammatory.  The  catarrhal 
inflammation  of  the  gall-bladder  may  sometimes  extend  to  the  bile-ducts  and  pro- 
duce jaundice,  because  of  inflammatory  swelling  of  the  common  or  hepatic  duct. 

This  simple  cholecystitis  or  cholangitis  (inflammation  of  the  bile-ducts)  does 
not  by  any  means  com-prise  all  of  the  pathology  of  cholelithiasis.  In  many  cases 
there  is  not  a  simple  cholecystitis  or  cholangitis,  but  a  purulent  inflammation, 
which  is  either  purulent  from  the  start  or  a  sequel  to  a  serous  exudation.  That 
bacteria  are  factors  in  this  process  there  can  be  no  doubt,  and  it  is  the  author's 
opinion  that  we  can  scarcely  draw  any  sharp  dividing  line  between  serous  and 
purulent  inflammation  of  the  bile-ducts.  The  danger  of  inflammation  varies 
according  to  the  power  of  the  infecting  bacteria,  and  the  greater  or  less  vulner- 


BILIARY   CALCULI  549 

ability  of  the  infected  tissue.  It  is  certain,  however,  that  the  purulent  inflam- 
mation will  cause  severer  clinical  symptoms.  The  condition  now  presented  is  no 
longer  a  simple  attack  of  colic,  but  a  far  more  severe  and  persistent  constitu- 
tional disturbance,  associated  with  pain  in  the  hepatic  region,  vomiting,  possibly 
jaundice,  and  very  likely  signs  of  enlargement  of  the  gall-bladder  and  the  liver. 
There  are  high  fever  (often  accompanied  with  rigors),  general  prostration,  and 
cerebral  symptoms.  In  milder  cases  there  is  only  a  purulent  cholecystitis.  In 
the  severer  cases  there  is  a  purulent  diffuse  cholangitis  alone,  or  combined  with 
purulent  inflammation  of  the  gall-bladder.  To  enumerate  here  all  the  possi- 
bilities of  the  condition  is  impossible.  Even  severe  derangement  of  this  sort  is. 
not  incompatible  with  spontaneous  recovery,  but  in  some  cases,  if  it  is  too  late 
for  surgical  aid,  there  is  a  general  septic  infection  and  death. 

We  shall  refer  to  a  great  number  of  other  sequelge  of  gall-stones  when  we  are^ 
considering  the  fate  of  the  calculi  after  they  have  left  the  gall-bladder  and: 
reached  the  bile-ducts.  As  above  mentioned,  the  smaller  stones  may  be  driyen  by 
a  successful  attack  of  biliary  colic  into  the  duodenum,  but  in  other  cases  the- 
stones  are  stopped  on  the  way,  either  in  the  cystic  or  in  the  common  duct.  If  the- 
stone  lodges  in  the  common  duct  there  is  usually  long-continued  jaundice  with 
secondary  changes  in  the  liver,  with  which  we  shall  later  become  better  acquainted. 
(vide  infra,  biliary  hepatic  cirrhosis).  The  inflammation  may,  however,  abate — 
the  stone  remaining  quietly  where  it  is  lodged,  and  the  duct  gradually  dilating 
and,  in  a  certain  measure,  accommodating  itself  to  the  stone;  but  the  mechanical 
effect  of  the  foreign  body  will  be  very  likely  eventually  to  occasion  fresh  attacks 
of  inflammation  and  the  gradual  formation  of  chronic  adhesions  and  distortions 
of  the  surrounding  parts.  There  is  special  danger  when  there  is  a  considerable 
pressure-necrosis  of  the  underlying  tissue.  This  immediately  opens  the  door  to 
inflammatory  germs,  and  results  in  secondary  suppuration,  which  may  be  either 
diffuse  or  localized.  In  the  worst  cases  there  may  be  purulent  phlebitis  of  an 
abdominal  vein,  with  metastatic  abscesses  in  other  organs. 

Precisely  similar  conseqviences  may,  however,  arise  from  stones  which  are 
situated  in  the  gall-bladder  itself  (usually  at  its  neck),  with  a  consequent  suppu- 
rative infection  of  the  neighboring  parts.  Perforation  into  the  abdominal  cavity 
leads  to  purulent  peritonitis.  If  adhesions  have  already  been  formed,  as  is 
usually  the  case,  there  may  be  perforation  in  any  one  of  many  directions,  either 
outward  with  escape  of  the  pus  and  often  the  gall-stones,  and  perhaps  with  the 
formation  of  a  biliary  fistula,  or  into  the  transverse  colon,  or  more  rarely  into  the 
stomach,  the  portal  vein,  or  the  urinary  tract;  but  chief  in  relative  frequency 
and  importance  is  perforation  from  the  neck  of  the  gall-bladder  into  the  duo- 
denum, for  this,  as  Virchow  and  Fiedler  have  pointed  out,  is  the  most  common 
way  by  which  large  gall-stones  reach  the  intestine  and  come  to  be  discharged  with 
the  faeces.  Many  of  these  processes  may,  imder  favorable  circumstances,  lead 
to  spontaneous  recovery  from  cholelithiasis.  The  gall-bladder,  under  the 
influence  of  suppuration,  may  finally  completely  shrivel  up,  perhaps  retaining  in 
its  folds  one  or  more  calculi;  but  much  oftener,  if  there  is  no  prompt  surgical 
intervention,  the  termination  is  unfavorable.  The  associated  clinical  conditions 
are  manifold  and  they  can  not  be  sketched  in  detail,  and  the  end  may  come  in  an 
acute  and  stormy  manner,  or  after  a  long  illness  marked  by  many  fluctuations. 
Still,  we  feel  bound  to  emphasize,  in  closing,  that  the  frequency  of  these  many 
grave  results  of  cholelithiasis  which  we  have  mentioned  must  not  be  over-esti- 
mated. In  comparison  with  the  extremely  great  number  of  gall-stones  which 
produce  either  no  symptoms  at  all,  or  none  which  suggest  danger  to  life,  the 
severe  cases  of  purulent  inflammation  after  cholelithiasis  are  few. 

Diagnosis. — It  is  evident  from  what  has  been  already  said  that  often  the  diag- 
nosis of  cholelithiasis  is  easy  and  indubitable,  while  in  other  cases  the  symptoms 


550  DISEASES    OF   THE   DIGESTIVE    OKGAls^S 

and  course  of  the  disease  are  obscure  and  ambiguous.  The  attacks  of  colic  are 
certainly  the  most  characteristic  symptom.  We  should  therefore  make  it  a  rule, 
in  case  of  severe  paroxysmal  pain  in  the  region  of  the  stomach  or  liver,  particu- 
larly in  middle-aged  women,  to  think  of  the  possibility  of  gall-stones.  If  an 
attack  of  this  sort  is  associated  in  even  a  slight  degree  with  jaundice,  the  diag- 
nosis is  usually  perfectly  clear.  If  there  is  no  jaundice — and  frequently  there  is 
none — the  diagnosis  is  less  certain,  but  still  it  can  often  be  made  because  of  the 
general  character  of  the  painful  attack;  the  indications  of  localized  peritoneal 
irritation,  such  as  slight  swelling  of  the  abdomen,  tenderness  on  pressure,  and 
vomiting;  and  finally  because  of  the  discovery  on  palpation  of  an  enlarged  gall- 
bladder. In  every  case  importance  must  be  laid  upon  a  careful  inquiry  of  the 
patient  or  his  friends  as  to  any  previous  attacks  or  any  mild  indefinite  prodrom- 
ata,  etc.  In  a  certain  number  of  eases,  however,  it  will  not  be  possible  to  get 
beyond  a  mere  suspicion  that  there  are  gall-stones,  and  occasionally  it  will  be 
impossible  to  avoid  confusion  with  cardialgia,  intestinal  colic,  renal  colic,  the 
pains  of  a  movable  kidney,  and  visceral  neuralgia.  This  is  particularly  apt  to 
happen  when  the  attack  is  not  a  well-developed  one  with  characteristic  symptoms, 
but  is  more  indefinite  and  suggests  cardialgia,  dyspepsia,  and  similar  conditions. 
A  careful  and  thorough  examination  of  all  the  organs  that  might  be  involved, 
such  as  the  stomach  and  kidneys,  may  in  many  cases  aid  us ;  and  often  the  truth 
is  revealed  by  the  further  course  of  the  disease;  but  many  cases  remain  obscure. 
The  hope  that  gall-stones  might  be  recognized  during  life  by  means  of  the 
Roentgen  rays  has,  unfortunately,  not  been  fulfilled. 

We  must  say  a  word  about  finding  the  gall-stones  in  the  iseces.  Of  course, 
the  discovery  of  the  corpus  delicti  in  the  evacuations  after  an  attack  of  colic 
makes  the  diagnosis  absolute.  They  are  to  be  searched  for  by  mixing  the  stools 
with  water,  and  then  passing  them  through  a  sieve.  But,  as  we  have  pointed  out 
above,  the  "  unsuccessful "  attacks  of  biliary  colic  are  probably  much  more  fre- 
quent than  the  "  successful."  We  can  not,  therefore,  be  surprised  that  in  many 
cases  of  cholelithiasis  no  stones  can  be  found  in  the  dejecta,  and  Eiedel  is  right 
in  maintaining  that  it  is  not  worth  while  to  search  for  the  stones  except  in  those 
attacks  which  are  associated  with  jaundice,  that  is,  those  that  are  not  unlikely  to 
be  "  successful."  It  should  be  pointed  out  further  that  we  should  be  on  our 
guard  not  to  mistake  for  gall-stones  hardened  portions  of  faeces — for  instance, 
compacted  vegetable  matter. 

Often  the  diagnosis  is  very  difiicult  in  cases  of  severe  purulent  inflammation, 
,  originating  from  gall-stones.  If  there  are  such  symptoms  as  indicate  a  peri- 
tonitis localized  in  the  hepatic  region,  associated  with  fever  and  rigors,  and 
suggesting  circumscribed  suppuration,  we  must  always  consider  the  possibility 
of  gall-stones  being  the  primary  cause.  We  should  make  a  careful  local  exami- 
nation and  consider  the  general  conditions,  such  as  age  and  sex,  and  we  shall 
often  be  greatly  helped  by  inquiring  carefully  into  the  previous  health  of  the 
patient — e.  g.,  with  regard  to  any  characteristic  colic.  It  must  be  confessed  that 
it  will  not  always  be  possible  to  avoid  confusion  between  this  and  other  suppura- 
tive processes,  particularly  those  originating  from  an  abnormally  situated  appen- 
dix, or  from  suppurating  echinococci.  No  special  diagnostic  rules  can  be  formu- 
lated, for  the  symptoms  are  peculiar  in  almost  every  single  case.  Even  when  we 
are  able  to  make  a  correct  diagnosis  of  cholelithiasis  we  are  often  unable  to 
estimate  the  exact  condition,  the  extent  of  the  secondary  inflammation,  the 
number  and  the  situation  of  the  stones,  or  the  presence  of  secondary  adhesions. 

Prognosis. — The  prognosis  of  gall-stones  must  really  be  termed  doubtful  in 
every  case,  that  is,  if  we  provisionally  exclude  the  possibility  of  cure  by  surgical 
means.  The  presence  of  gall-stones,  as  the  reader  already  knows,  may  entail  a 
number  of  dangerous  sequelae,  and  we  can  never  foretell  whether  the  patient  will 


BILIAEY   CALCULI  551 

suffer  from  these  or  escape  them;  still,  there  is  no  doubt  that  in  many  cases, 
particularly  when  the  stones  are  small  (vide  supra),  there  may  be  a  spontaneous 
and  pei*manent  recovery,  while  in  other  cases  there  may  be  disturbances  of  the 
most  varied  kind,  persistent,  or  constantly  recurrent,  and  yet  never  absolutely 
serious.  There  is  no  occasion  for  describing  here  a  second  time  the  numberless 
possibilities  of  cholelithiasis  and  their  prognostic  significance. 

There  is  one  important  symptom  which  is  interesting  from  the  standpoint  of 
general  pathology  and  which  must  be  noted  here — viz.,  the  development,  subse- 
quent to  cholelithiasis,  of  cancer  of  the  gall-bladder  and  bile-ducts.  This  possi- 
bility is,  of  course,  of  great  clinical  importance,  and  agrees  with  the  general 
observation  that  persistent  mechanical  irritation  of  the  mucous  membrane  and 
scar  formations  may  occasion  the  development  of  carcinoma.  The  formation  of 
secondary  cancer  after  cholelithiasis  is  precisely  analogous  to  the  growth  of  cancer 
after  ulcer  of  the  stomach,  or  secondarily  to  stone  in  the  kidney. 

Treatment. — Our  means  of  efficient  prophylaxis  against  the  formation  of 
gall-stones  are  very  limited.  The  most  we  can  assume  is  that  an  entirely  suitable 
regimen,  and  particularly  the  avoidance  of  any  tight  lacing  or  similar  mechanical 
interference  with  the  excretion  of  bile,  will  prevent  or  at  least  delay  the  develop- 
ment of  any  tendency  to  the  formation  of  calculi.  If  gall-stones  have  been  once 
formed,  our  task  as  physicians  consists  merely  in  moderating  the  disturbance 
which  they  produce;  in  guiding,  so  far  as  possible,  all  sequelae  to  a  favorable 
termination;  and  finally  in  effecting  the  removal  of  the  stones  from  the  body,  so 
far  as  this  is  necessary  and  within  our  power. 

If  the  symptoms  of  the  patient  remain  comparatively  slight,  and  especially  if 
the  diagnosis  of  gall-stones  has  not  yet  been  absolutely  established,  energetic 
treatment  is  not  demanded.  We  regard  it  as  important  that  in  such  cases,  as 
soon  as  we  conceive  the  possibility  of  cholelithiasis,  the  patients  should  enter 
upon  a  proper  rest-cure.  Very  often  female  patients  of  this  sort  are  regarded 
as  nervous,  are  sent  into  all  sorts  of  health-resorts,  and  treated  with  electricity 
and  massage,  and,  of  course,  without  success.  Instead  we  should  induce  such  a 
patient  to  spend  a  few  weeks  of  complete  rest  in  bed,  or  at  any  rate,  lying  on  a 
sofa  with  easy  clothing;  prescribe  a  cautious  and  nourishing  diet,  and  the  reg- 
ular application  of  warm  poultices  upon  the  hepatic  region;  and  administer 
before  breakfast  and  in  the  middle  of  the  forenoon  a  half  pint  of  warm  Carlsbad 
Miihlbrunnen  water.  We  may  then  hope  for  a  satisfactory  improvement  in  the 
symptoms  due,  in  our  judgment,  to  the  cessation  of  the  slight  inflammatory 
irritation.  Often  patients  of  this  sort  are  sent  to  Carlsbad.  We  will  not  deny 
that  Carlsbad  water  may  have  some  favorable  influence  upon  cholelithiasis,  but 
we  believe  that  the  exertion  of  the  journey  and  the  promenades  and  other  activi- 
ties in  which  the  patients  are  apt  to  indulge  after  their  arrival,  are  often  serious 
drawbacks.  That  Carlsbad  water,  as  such,  is  of  real  value  in  expelling  the  stones 
or  in  actually  dissolving  ( !)  them,  we  find  difficult  to  believe. 

Whenever  there  is  a  well-marked  attack  of  biliary  colic  we  have  special 
indications  for  treatment.  Of  course,  in  this  ease  also,  we  must  immediately 
enjoin  complete  rest  in  bed. 

The  pain  demands  the  prompt  employment  of  narcotics,  particularly  of  mor- 
Ijhine  or  opium.  If  the  suffering  is  extreme,  a  subcutaneous  injection  of 
morphine  is  by  far  the  best  and  quickest  remedy;  but  the  internal  use  of  opium 
is  also  to  be  recommended.  We  may  give  every  two  or  three  hours  fifteen  or 
twenty  drops  of  the  tincture,  or  half  a  grain  to  a  grain  of  powdered  opium  (gramme 
0.03-0.05).*     Other  narcotics,  such  as  chloral  or  belladonna,  are  scarcely  ever 

*  [When  oriving  repeated  doses  of  opium  for  biliary  or  renal  colic,  it  should  be  roiiiemberfd  tlint 
the  pain  will  cease  abruptly  as  soon  as  the  stone  ceases  to  obstruct  the  passage,  and  that  severe  toxic 


552  DISEASES    OF   THE   DIGESTIVE    OEGANS 

necessary,  but  we  may  sometimes  combine  extract  of  belladonna,  which  is 
much,  praised  by  many  physicians,  with  the  opium.  Of  external  applications 
upon  the  hepatic  region  the  best  is  a  warm  or  hot  poultice.  It  is  exceptional  for 
the  patient  to  prefer  an  ice-bag.  Usually,  gentle  rubbing  of  the  hepatic  region 
with  chloroform-oil  (a  mixture  of  equal  parts  of  chloroform  and  olive-oil)  does 
good.  In  a  few  cases  the  patient  experiences  relief  from  a  prolonged  warm  bath. 
If  there  is  violent  vomiting  we  give  tincture  of  opium,  bromide  of  potash,  cocaine, 
or  bits  of  ice.  If  there  is  marked  collapse,  such  stimulants  must  be  employed  as 
wine,  strong  black  coffee,  or  even  injections  of  ether  and  camphor.  When  the 
acute  symptoms  have  ceased,  we  must  still  persist  for  some  time  in  a  cautious 
diet  and  in  bodily  quiet,  and  it  is  often  well  to  prescribe  a  gentle  laxative,  such 
as  Carlsbad  salts  or  rhubarb. 

When  the  attack  is  completely  over,  the  question  arises  how  to  guard  against 
the  occurrence  of  others.  The  answer  to  this  question  depends  mainly  upon  the 
view  we  take  of  the  present  attack,  whether  we  regard  it  as  a  "  successful "  or  an 
"  unsuccessful "  one.  If  the  attack  was  successful — that  is,  if  calculi  were  found 
in  the  intestinal  evacuations  after  it — we  may  hope  that  in  case  there  are  more 
stones  present  they  also  may  be  discharged.  Whether  we  possess  artificial  means 
of  insuring  this  discharge  is  extremely  doubtful.  Still,  many  remedies  and 
methods  of  cure  have  been  recommended  as  exerting  a  favorable  influence  in  this 
direction.  Here  again  we  must  mention  first  the  use  of  Carlsbad  and  similar 
waters,  such  as  Homburg,  Ems,  and  Vichy.  Many  physicians  believe  that  they 
have  seen  good  results  from  the  persistent  use  of  turpentine,  particularly  in  the 
form  of  what  is  called  Durande's  remedy;  that  is,  a  mixture  of  ether  and  tur- 
pentine in  the  proportion  of  three  to  two,  of  which  two  or  three  times  a  day 
twenty  to  thirty  drops  are  given ;  and  the  same  is  true  of  salicylate  of  sodium,  of 
which  half  a  drachm  to  a  drachm  (grammes  2-4)  is  given  daily  for  a  consider- 
able period,  either  alone  or  in  combination  with  bicarbonate  of  sodium.  We 
should  also  mention  in  this  connection  the  administration  of  large  doses  of  olive- 
oil.  This  is  extremely  unpleasant  for  the  patient,  and  very  uncertain  in  its 
effect,  but  still  is  highly  praised  by  many  physicians.  A  mixture  of  six  or  seven 
ounces  (grammes  200)  of  olive-oil,  five  drachms  (grammes  20)  of  brandy,  and  the 
yolk  of  two  eggs,  with  a  few  drops  of  oil  of  pepperrnint,  is  given  in  two  portions 
at  a  short  interval.  [Most  of  the  oil  is  passed  in  lumps,  which  have  a  super- 
ficial resemblance  to  gall-stones,  and  are  sometimes  called  such.]  Of  course,  we 
should  also  regulate  the  diet  and  the  life  of  the  patient  in  a  suitable  manner,  and 
this  may  be  the  most  important  prescription  of  any. 

If,  however,  the  attack  was  unsuccessful,  or  particularly  if  several  unsuc- 
cessful attacks  have  occurred,  there  is  scarcely  room  to  hope  that  any  internal 
remedy  will  result  in  expulsion  of  the  stone.  It  may  be  too  large.  If,  then,  we 
do  not  choose  to  let  the  case  take  whatever  course  it  will,  there  is  only  one  remedy 
available,  and  that  is  the  operative  removal  of  the  stones  by  opening  the  gall- 
bladder. If  we  consider  the  dangers  which  are  entailed  by  the  presence  of  stones 
that  can  not  be  evacuated  by  the  natural  passages,  we  must  agree  with  Riedel 
when  he  says  a  "  single  unsuccessful  inflammation  of  the  gall-bladder  is  a  suffi- 
cient indication  for  immediate  operation."  To  be  sure,  no  one  will  fail  to 
recognize  that  the  circumstances  in  practice  may  prevail  over  purely  theoretical 
considerations,  however  lucid  the  latter  may  be.  Many  patients  will  not  consent 
to  an  operation  after  a  single  brief  attack  which,  although  painful,  has  ended  in 
apparently  complete  recovery,  and  the  conscientious  physician  will  consider  in 

effects  of  the  drug  may  then  appear.  In  bilious  colic  the  distance  to  be  traversed  by  the  stone  is 
relatively  short,  and  in  that  affection  especially  the  inhalation  of  ether  or  chloroform  is  sometimes  the 
best,  and,  indeed,  the  imperative  treatment.] 


SUPPURATIVE   HEPATITIS  553 

any  actual  case  the  indisputable  dangers  of  the  operation,  and  the  possible  doubt 
as  to  diagnosis.  It  is  a  very  different  matter  when  the  unsuccessful  attacks  are 
frequently  repeated  or  when  there  is  persistent  discomfort,  so  that  the  patient  is 
deprived  of  all  joy  in  life  and  all  personal  activity.  Then  we  ought  not  and  dare 
not  longer  delay  in  urging  him  to  operation.  The  surgical  treatment  of  chole- 
lithiasis in  such  cases  already  possesses  a  record  of  many  brilliant  successes. 

There  is  likewise  an  urgent  indication  for  prompt  operation  when  the  symp- 
toms indicate  a  purulent  cholecystitis  or  a  localized  abscess,  due  to  gall-stones. 
It  would  probably  be  better  if  such  complications  of  cholelithiasis  were  avoided 
by  anticipatory  surgical  interference,  but  this  desirable  result  will  never  be 
attained  in  practice,  because  in  many  cases  the  purulent  infection  of  the  gall- 
bladder or  the  bile-ducts  occurs  without  having  been  preceded  by  any  marked 
sjTnptoms'.  In  these  suppurative  cases,  surgical  intervention  often  not  only  saves 
life  but  works  a  permanent  cure,  unless  the  purulent  infection  has  already 
extended  to  the  bile-ducts  of  the  liver  itself,  or  has  led  to  general  pyaemia.  We 
can  not  in  this  place  enter  into  the  particulars  of  the  surgical  treatment  of  gall- 
stones, or  the  removal  by  operation  of  stones  fixed  in  the  cystic  or  common  ducts. 
Complete  information  will  be  found  in  surgical  monographs. 


CHAPTER   TV 

SUPPURATIVE    HEPATITIS 

{Ile/iatic  Ab-scesii) 

.etiology. — Exclusive  of  traumatism  there  are  two  ways  by  which  bacteria 
may  penetrate  into  the  liver,  there  to  excite  a  suppurative  inflammation — namely, 
by  the  blood  and  through  the  bile-ducts.  In  the  circulatory  system  the  main 
route  is  by  way  of  the  portal  vein,  by  which  pyogenic  organisms  from  the  intes- 
tines reach  the  liver.  This  explains  why  many  ulcerative  processes  in  the  intes- 
tine, such  as  severe  dysentery,  are  followed  by  hepatic  abscess ;  and  why  purulent 
pylephlebitis  (q.  v.)  and  other  suppurative  processes  within  the  portal  system  may 
have  a  similar  sequel.  In  general  pyaemia,  the  germs  must  take  a  very  circuitous 
route  in  order  to  reach  the  liver.  They  must,  on  leaving  the  primary  abscesses, 
first  enter  the  veins  and  the  lungs,  and  then  gain  the  liver  by  way  of  the  hepatic 
artery.  It  has  been  well  known  for  a  long  time  that  suppurating  wounds  of  the 
head  are  followed  by  hepatic  abscess  with  comparative  frequency.  Perhaps  it 
may  exceptionally  happen  that  infectious  matter  enters  the  hepatic  veins  by 
"  retrogressive  embolism  "  from  the  vena  cava. 

The  germs  which  make  their  way  into  the  liver  from  the  bile-ducts  invariably 
originate  in  the  intestine.  In  these  cases  the  hepatic  inflammation  is  almost 
always  preceded  by  disease  of  the  biliary  passages.  The  most  frequent  cause 
by  far  of  this  variety  of  hepatic  abscess  is  the  formation  of  gall-stones  in  the 
gall-bladder  and  in  the  liver.  This  has  been  fully  discussed  in  the  preceding 
chapter. 

Among  us,  hepatic  abscesses  are  rarely  occasioned  in  other  ways  than  those 
indicated;  but  in  the  tropics  it  is  said  that  quite  a  large  number  of  apparently 
primary  hepatic  abscesses  are  met  with.  Their  origin  is  not  yet  explained, 
although  in  this  case  also  there  is  most  probably  an  invasion  of  pyogenic  bacteria 
from  the  intestine. 

Pathology. — The  smallest  and  as  yet  imperfectly  developed  embolic  abscesses 
best  illustrate  the  mode  of  formation.     We  find  the  blood-vessels  choked  with 


554  DISEASES    OE    THE   DIGESTIVE    ORGAXS 

micrococci,  and  tlie  cells  of  the  surrounding  parencliyiaa  void  of  nuclei  and  in 
process  of  disintegration.  Along  the  course  of  the  blood-vessels  nuclei  are  very 
abundant.  These  are  due  to  white  corpuscles  which  have  escaped  through  the 
vascular  walls.  The  cells  and  the  liquid  exudation  rapidly  increase,  and  there  is 
complete  destruction  of  the  hepatic  parenchyma,  and  the  formation  of  an  abscess 
in  its  place.  This  extends  in  all  directions.  Large  abscesses  may  at  last  involve 
an  entire  lobe.  In  other  cases  the  suppurative  process  is  limited  by  encapsulation. 
Sometimes  quite  large  portions  of  the  liver  become  necrotic  and  slough  off,  under 
the  influence  of  what  is  called  "  sequestrating  "  suppuration.  "We  almost  invari- 
ably find  some  shreds  of  hepatic  tissue  in  the  pus  of  hepatic  abscesses.  When 
hepatic  abscess  has  been  occasioned  by  gall-stones,  the  suppuration  has  usually 
been  due  to  direct  extension  of  the  process  from  the  bile-ducts  to  the  parenchyma 
of  the  liver.     Not  infrequently  gall-stones  are  found  in  the  pus  of  such  cases. 

Small  abscesses  may  perhaps  be  absorbed,  but  they  are  in  most  cases  merely 
symptomatic  of  pyaemia  or  some  such  disease,  which  is  itself  incurable.  Larger 
abscesses  may  point  into  neighboring  organs.  If  they  are  discharged  into  the 
abdominal  cavity,  diffuse  peritonitis  follows.  The  most  favorable  termination, 
and  one  repeatedly  observed,  is  perforation  through  the  abdominal  walls,  after 
these  walls  and  the  liver  have  been  joined  by  adhesions.  They  may  also  break 
into  the  pleural  cavity,  the  pericardium,  the  intestine,  and  the  pelvis  of  the  right 
kidney. 

Clinical  History. — An  absolutely  complete  clinical  description  of  hepatic 
abscess  is  impossible,  because,  as  we  have  seen,  it  may  be  a  symptom  of  such 
diverse  pathological  processes.  Hepatic  abscesses  are  often  found  post  mortem 
which  had  given  no  previous  indication  of  their  presence ;  this  is  frequently  true 
in  pyaemia.  In  other  cases  there  are  symptoms,  in  part  directly  referable  to  the 
seat  of  inflammation,  and  in  part  due  to  its  influence  upon  neighboring  organs. 

Enlargement  of  the  liver  can  often  be  made  out  by  percussion  or  even  by  pal- 
pation. It  is  the  result  of  swelling  and  hypersemia  involving  the  entire  organ. 
Extensive  abscesses  may  give  much  more  definite  signs  of  their  presence,  however, 
if  situated  on  the  anterior  surface  of  the  organ.  They  are  sometimes  felt 
through  the  abdominal  walls  as  hemispherical  and  actually  fluctuating  tumors. 
It  is  not  so  very  rare  for  tropical  hepatic  abscess  to  attain  these  dimensions. 

Pain  in  the  right  hypochondrium,  although  it  may  be  entirely  absent  when 
the  abscesses  are  small,  even  if  they  are  numerous,  is  often  violent  and  persistent 
when  the  abscess  is  large.  It  is  excited  by  the  tension  of  the  peritoneal  covering 
of  the  liver,  or  by  perihepatitis.  The  pain  often  radiates — and  with  especial 
frequency,  it  is  said,  into  the  neighborhood  of  the  right  shoulder. 

The  course  of  the  fever  may  prove  a  strong  diagnostic  point.  "When  the 
abscess  is  chronic  and  encapsulated  there  may,  it  is  true,  be  no  fever  whatever; 
but,  as  a  rule,  fever  does  exist,  and  it  often  presents  a  very  characteristic  inter- 
mittent character.  There  are  great  elevations,  usually  ushered  in  by  a  chill, 
and  succeeded  by  deep  depressions  of  temperature  accompanied  by  perspiration. 
If  the  hepatic  trouble  is  merely  a  symptom  of  general  pyaemia,  then  the  fever  is 
to  be  ascribed  to  the  latter ;  but  if  there  are  signs  of  a  severe  local  hepatic  disease, 
such  as  pain,  enlargement,  and  perhaps  jaundice,  and  if  these  febrile  attacks 
come  on  at  irregular  intervals,  we  should  always  consider  the  possibility  of 
abscess  of  the  liver.  In  the  cases  of  large  tropical  abscess  this  sort  of  fever  is  the 
rule.  It  is  most  frequent  with  us  in  cases  of  purulent  pylephlebitis  and  of  abscess 
excited  by  gall-stones.  The  "  fievre  inter  mitt  ente  hepatique"  of  the  French  is 
in  most  instances  due  to  the  presence  of  gall-stones  in  the  liver,  with  secondary 
suppuration  and  abscess  formation. 

Among  the  secondary  symptoms  of  hepatic  abscess  jaundice  is  prominent.  It 
is  not  invariably  present,  however,  occurring  only  when  the  abscess  has  com- 


CIKEHOSIS    OF    THE   LIVER  555 

pressed  some  large  biliary  duct,  and  has  thus  given  occasion  to  the  absorption  of 
bile  by  the  lymphatics,  or  when  an  extensive  cholangitis  has  simultaneously 
developed,  sufficient  to  cause  jaundice.  In  rare  instances  the  abscess  compresses 
the  portal  vein  and  thus  causes  ascites.  There  may  be  pulmonary  symptoms  of 
considerable  importance,  even  when  there  are  no  actual  pulmonary  complications. 
This  is  because  the  right  half  of  the  diaphragm  is  crowded  up  by  abscesses  pro- 
jecting from  the  convex  surface  of  the  liver.  Hiccough  is  sometimes  a  source 
of  distress,  and  it  may  be  due  to  the  pressure  of  the  abscess  upon  the  stomach. 
Vomiting  is  also  a  rather  common  and  often  very  troublesome  symptom. 

There  is  almost  always  great  constitutional  disturbance.  The  patient  has  no 
appetite,  and  loses  flesh,  particularly  if  there  are  frequent  febrile  exacerbations. 
Often  there  are  severe  nervous  attacks.  Very  exceptionally,  the  disease  remains 
latent  for  a  long  time,  and  does  not  disturb  the  general  health  to  any  great 
extent. 

The  course  of  the  disease  depends  mainly  upon  the  nature  of  the  original  dis- 
turbance. Severe  pyaemic  cases,  in  which  hepatic  abscesses  develop,  are  generally 
brief,  and  are  almost  invariably  fatal.  Abscesses  due  to  gall-stones,  and  the  large 
abscesses  which  are  apparently  idiopathic,  are  generally  chronic,  lasting  for 
weeks,  or  even  for  many  months.  Cases  exhibit  manifold  diversities,  according 
to  the  position,  size,  number,  and  sequelae  of  the  abscesses.  Among  the  possible 
results,  we  would  once  more  call  attention  to  perforation  into  neighboring  organs. 
If  the  pus  is  discharged  externally,  recovery  m^y  ensue;  as  also  if  the  pus 
reaches  the  intestinal  canal  or  the  bronchi,  which  seldom  happens.  Perforation 
into  the  abdominal  cavity  always  excites  a  fatal  acute  peritonitis.  As  a  general 
rule,  hepatic  abscess  finally  proves  fatal,  recovery  being  exceptional.  Death  is 
due  either  to  the  gradual  loss  of  strength  or  to  some  complication. 

Treatment. — Local  bleeding,  counter-irritation,  purgatives,  and  emetics  are 
among  the  remedies  which  are  advocated,  but  we  can  hardly  expect  them  to  exert 
much  influence  upon  a  hepatic  abscess.  The  best  way  is  to  treat  the  case  purely 
symptomatically,  seeking  to  keep  up  the  patient's  strength  and  mitigate  his  suf- 
fering until,  if  we  are  very  fortunate,  we  have  a  chance  for  operative  interfer- 
ence. When  once  the  other  symptoms  are  re-enforced  by  the  discovery  on  palpa- 
tion of  a  fluctuating  tumor,  the  diagnosis  is  established,  and  the  pus  should  be 
evacuated  and  the  cavity  drained.  Particulars  about  the  operation  should  be 
sought  in  works  on  surgery.  More  than  one  case  of  the  large  tropical  abscess 
have  been  cured  in  this  way;  but  the  cases  which  are  most  common  among  us — 
namely,  embolic  abscesses  and  those  excited  by  gall-stones — hardly  ever  afford 
any  opportunity  for  surgical  interference. 


CHAPTER   V 


CIRRHOSIS    OF    THE    LIVER 

(Clcronic  Diffuse  Interstitial  Hepatitis.    Laennec's  Cirrhosis.     Gin-drinker's  Liver,    lloh-nailed  Liver) 

.aitiology  and  Pathology.— Cirrhosis  of  the  liver  is  usually  defined  as  a 
diffuse  interstitial  inflammation,  chronic  in  duration,  and  resulting  in  a  secondary 
atrophy  of  the  true  hepatic  parenchyma.  This  conception  makes  the  disease  per- 
fectly analogous  to  "  chronic  interstitial  inflammation  "  of  the  kidney  and  many 
other  organs.  Weigert's  careful  study  of  the  processes  of  "  chronic  interstitial 
nephritis  "  has  shown  that  at  least  a  large  part  of  the  changes  which  take  place 
in  the  connective  tissue  are  not  primary,  but  secondary,  and  the  consequence  of 


556  DISEASES    OF   THE   DIGESTIVE   OEGANS 

a  primary  destruction  of  the  genuine  renal  parenchyma.  The  question  naturally 
suggests  itself,  whether  the  same  may  not  be  true  of  the  apparently  closely  allied 
phenomena  of  hepatic  cirrhosis.  We  feel,  therefore,  that  in  most  cases  of  hepatic 
cirrhosis  the  origin  of  the  disease  consists  of  a  primary  injury  and  consequent 
partial  destruction  of  the  hepatic  cells,  whereupon  follow  a  secondary  prolifera- 
tion and  final  contraction  of  the  interstitial  tissue,  just  as  is  seen  in  lesions  of 
the  parenchyma  of  the  kidneys,  spinal  cord,  and  heart. 

Such  a  conception  would  be  extremely  compatible  with  one  fact  about  the 
setiology  of  the  disease — namely,  that  chronic  alcoholism  is  universally  regarded 
as  a  potent  predisposing  cause.  Hence  the  English  name,  "  gin-drinker's  liver." 
The  harmful  influence  of  alcohol  can  be  appreciated  if  we  remember  that  on  being 
absorbed  it  is  carried  directly  by  the  blood-vessels  through  the  portal  vein  to  the 
liver.  According  to  the  usual  view  of  the  disease,  the  poison  excites  a  chronic  in- 
flammation of  the  connective  tissue ;  while,  according  to  the  new  view,  the  alcohol 
exerts  a  specific  injurious  influence  upon  the  hepatic  cells  proper,  impairing  their 
nutrition,  and  finally  causing  their  destruction.  That  the  disease  attacks  the 
periphery  of  the  lobules  and  the  interlobular  connective  tissue  is  equally  conso- 
nant with  either  theory.  It  is  well  known  that  the  capillary  anastomoses  of  the 
portal  vein  are  situated  between  the  lobules. 

Hepatic  cirrhosis  is  most  common  in  those  who  drink  distilled  liquors,  while 
excessive  indulgence  in  less  strongly  alcoholic  beverages,  such  as  wine  and  beer, 
leads  less  frequently  to  cirrhosis.  Still,  we  have  repeatedly  seen  the  disease  in 
beer  drinkers. 

The  abuse  of  alcohol  is  surely  the  chief  but  by  no  means  the  only  cause  of 
cirrhosis,  for  quite  often  the  disease  attacks  persons  in  whose  case  no  such 
aetiology  is  possible.  In  such  instances  we  are  seldom  able  to  demonstrate  the 
real  cause.  The  excessive  use  of  spices,  and  other  analog-ous  substances,  has  some- 
times been  regarded  as  causative.  It  is  also  said  that  malaria  and  the  acute 
infectious  diseases  sometimes  leave  behind  them  a  tendency  to  cirrhosis.  In  our 
opinion  such  cases  are  due  to  the  long-continued  action  of  chemical  agents  and 
bacteria,  about  which  we  do  not  as  yet  possess  any  accurate  knowledge,  which 
are  conveyed  from  the  intestine  to  the  liver.  These  cases  of  "  genuine  hepatic 
cirrhosis  "  are  analogous  to  the  not  infrequent  cases  of  "  genuine  interstitial 
nephritis  "  of  unknown  origin.  Perhaps  in  many  instances,  also,  there  is  a  con- 
stitutional and  excessive  sensitiveness  of  the  hepatic  cells  to  the  injurious  influ- 
ences to  which  they  are  exposed  while  performing  their  normal  functions. — The 
form  of  cirrhosis  which  follows  diseases  of  the  bile-ducts,  and  also  "  syphilitic 
cirrhosis,"  will  receive  separate  consideration. 

Cirrhosis  of  the  liver  is  seen  much  oftener  in  men  than  in  women,  and  usually 
occurs  in  middle  life.  This  is  in  harmony  with  the  fact  that  the  chief  cause 
is  the  abuse  of  alcohol. 

The  anatomical  changes  are  generally  divided,  without  regard  to  the  way  in 
which  they  are  brought  about,  into  two  stages.  In  the  first  stage  the  liver  is 
uniformly  enlarged,  resistant,  with  its  edge  blunt,  and  its  surface  at  first  per- 
fectly smooth,  but  later  presenting  little  dimples.  On  section,  the  increased  con- 
sistency, or  "  interstitial  induration  "  of  the  liver,  can  be  readily  perceived.  The 
acini  are  separated  from  one  another  by  a  relatively  thick  band  of  grayish-red 
interstitial  tissue,  and  are  at  first  readily  distinguishable.  Later  on,  the  inter- 
stitial hyperplasia  invades  the  acini  themselves,  and  they  cease  to  be  discernible. 
The  microscope  shows  that  the  cause  of  this  increase  in  size  and  firmness  of  the 
organ  is  due  exclusively  to  the  abundant  cellular  infiltration  and  the  new  forma- 
tion of  connective  tissue  between  the  individual  lobules.  The  neighboring  cells 
of  the  parenchyma  exhibit  signs  of  disintegration,  undergoing  either  simple 
atrophy  or  else  fatty  degeneration. 


CIRRHOSIS    OF    THE   LIVER  557 

The  second  stage  corresponds  with  the  process  of  contraction  of  the  newly 
formed  connective  tissue,  but  in  this  stage  the  destruction  of  the  proper  hepatic 
tissue  has  already  assumed  grave  -proportions.  On  the  old  theory,  the  paren- 
chyma perishes  because  of  the  great  disturbance  of  circulation  in  the  portal 
capillaries,  great  numbers  of  which  are  obliterated  by  the  shrinking  of  the  con- 
nective tissue.  We  ourselves,  as  we  have  already  intimated,  incline  rather  to 
Weigert's  view,  that  the  atrophy  of  the  hepatic  cells  is,  as  a  rule,  the  direct  result 
of  a  primary  pathological  lesion  of  the  hepatic  tissue.  Under  this  process  of 
contraction  the  liver  undergoes  progressive  atrophy,  and  its  surface  becomes 
mammillated.  The  size  of  the  nodviles  varies.  The  size  of  the  whole  organ  may 
be  reduced  one  half,  or  even  more.  Frequently  its  general  contour  is  consider- 
ably modified.  Often  the  diminution  of  the  size  of  the  liver  is  confined  mainly  to 
the  left  lobe.  The  serous  coat  of  the  liver  is  usually  thickened  and  rendered 
opaque ;  the  hepatic  tissue  feels  very  resistant  and  cuts  with  difiiculty,  often  with 
a  grating  sound;  the  color  of  the  cut  surface  is  usually  a  rather  light  yellow 
(Kippos  =  yellow).  Upon  microscopic  examination,  we  find  merely  vestiges  of 
parenchyma,  embracing  which  are  wide,  firm  bands  of  connective  tissue.  Even 
within  the  acini  there  is  decided  interstitial  hyperplasia  along  the  blood-vessels. 
The  hepatic  cells  exhibit  various  stages  of  fatty  degeneration  and  simple  atrophy. 
Brown  masses  of  pigment  are  often  found  here  and  there,  which  have  been  left 
behind  by  the  hepatic  cells  now  destroyed.  Regenerative  changes  can  also  be  de- 
tected quite  frequently.  The  most  common  of  these  is  the  formation  of  small 
biliary  passages  in  the  broad  bands  of  interstitial  tissue. 

The  division  of  hepatic  cirrhosis  into  two  stages  is  somewhat  schematic, 
for  there  is  really  no  sharp  dividing  line  between  them.  The  same  liver  may  in 
different  places  illustrate  both  stages  simultaneously.  Thus,  the  surface  is  often- 
distinctly  granular,  while  the  liver  as  a  whole  remains  hypertrophic.  In  many 
cases  there  seems  to  be  no  so-called  "  first  stage  "  at  all,  and  the  previously  normal 
liver  is  directly  transformed  into  a  contracted  liver,  perhaps  comparable  to  the 
kidney  of  genuine  interstitial  nephritis. 

Clinical  History. — The  onset  of  the  disease  is  usually  insidious.  At  autop- 
sies quite  an  advanced  stage  of  cirrhosis  is  sometimes  found,  to  which  not  a 
single  clinical  symptom  had  pointed ;  and  it  is  often  observed  that  the  duration 
of  unambiguous  symptoms  is  much  shorter  than  the  degree  of  anatomical  change 
discovered  post  mortem  would  have  led  us  to  expect. 

It  is,  however,  true  that  certain  prodromata  may  appear  long  before  the  genu- 
ine cirrhotic  symptoms;  but  there  is  generally  room  for  doubt  whether  these  pro- 
dromata are  excited  by  the  incipient  hepatic  disease  or  whether  they  are  not  due 
to  other  coincident  affections,  such  as  the  chronic  gastric  or  intestinal  catarrh 
which  drunkards  so  often  have.  There  are  anorexia,  nausea,"  epigastric  uneasi- 
ness, eructations,  constipation,  and  sometimes  vomiting.  There  is  evident  con- 
stitutional disturbance  in  many  cases,  but  in  others  the  strength  is  unimpaired. 
The  severer  symptoms  usually  date  from  the  time  when  disturbance  of  the  portal 
circulation  arises.  We  have  already  stated  that  the  diseased  process  is  most 
active  in  the  interlobular  connective  tissue — that  is,  where  the  portal  capillaries 
are  situated.  When  the  contraction  of  the  connective  tissue  has  resulted  in  the 
destruction  of  a  large  number  of  these  portal  capillaries  and  the  minute  veins 
from  which  they  spring,  the  portal  circulation  is  inevitably  impeded,  and  there 
arises  a  passive  congestion  of  the  whole  portal  system.  The  signs  of  this  are  soon 
manifest. 

The  stasis  in  the  veins  of  the  peritoneum  is,  as  a  rule,  the  first  to  attract  atten- 
tion, from  the  ascites  which  it  occasions.  The  distention  of  the  abdomen  and  the 
sensation  of  weight  and  pressure  due  to  this  effusion,  are  often  the  first  things 
which  excite  the  patient's  attention  and  lead  him  to  seek  medical  advice.     Later 


o5S  DISEASES    OE   THE   DIGESTIVE    ORGANS 

on,  the  ascites  sometimes  becomes  enormous,  causing  immense  swelling  and 
extreme  tension  of  the  abdominal  walls,  and,  of  course,  proportionate  discomfort. 
Proper  nursing  and  internal  treatment  may  diminish  the  ascitic  effusion,  but 
they  will  seldom  wholly  remove  it.  It  quite  often  remains  nearly  uniform,  until 
finally,  for  some  reason,  there  is  a  change  for  the  worse. 

Next  to  ascites,  the  most  important  symptom  of  portal  obstruction  is  enlarge- 
ment of  the  spleen,  which  is  due  both  to  the  increased  amount  of  blood  in  the 
organ  and  to  a  diffuse  hyperplasia  of  its  tissues.  As  a  rule,  the  increase  in  size  is 
considerable,  amounting  sometimes  to  two  or  three  times  the  normal  dimensions. 
It  is  not  very,  exceptional  to  find  a  well-marked  splenic  tumor  in  hepatic  cirrho- 
sis, even  before  there  is  any  ascites.  In  such  eases  the  splenic  tumor  is  not  due 
at  all  to  portal  congestion  but  to  other,  perhaps  toxic,  influences,  just  as  in  biliary 
cirrhosis  (vide  infra).  At  any  rate,  the  discovery  of  splenic  tumor  is  invariably 
of  great  diagnostic  importance,  although  it  is  often  no  easy  matter  to  make  out 
the  size  of  the  spleen,  inasmuch  as  both  percussion  and  palpation  are  rendered 
very  difficult  by  the  presence  of  ascites.  On  the  whole,  palpation  is  the  more 
reliable.  Pain  or  other  subjective  symptoms  are  rarely  observed.  Exceptionally, 
there  is  no  enlargement  of  the  spleen.  This  may  be  due  to  the  firmness  and  thick- 
ness of  its  capsule,  or  to  the  general  marantic  condition  of  the  patient. 

The  venous  congestion  of  the  stomach  and  intestines  excites  catarrh,  which  is 
evinced  by  anorexia,  nausea,  and  irregularity  of  the  bowels.  Usually  there  is 
quite  obstinate  constipation,  but  there  may  be  persistent  diarrhoea.  None  of  these 
symptoms  occupies  the  foreground  of  the  clinical  picture,  however,  both  because 
such  symptoms  are  frequent  in  all  grave  chronic  diseases  and  because  many  pa- 
tients have  had  digestive  derangements  long  before  these  severer  troubles  began. 
A  more  significant  symptom,  if  it  occurs,  is  haemorrhage.  This  is  now  and  then 
occasioned  by  the  extreme  gastro-intestinal  congestion.  If  the  haemorrhage  is 
slight  and  comes  from  capillaries,  there  is  diarrhoea  with  blood-stained  stools,  or 
vomiting,  the  vomitus  being  dark-colored.  Probably  the  tendency  to  haemorrhage 
is  aggravated  by  the  general  cachexia  or  by  the  alcoholism.  Of  more  importance 
is  the  vomiting  of  large  amounts  of  pure  blood.  This,  as  the  author  knows  from 
repeated  observations,  may  be  sufiicient  of  itself  to  endanger  life.  Such  cases 
have  more  than  once  led  to  the  incorrect  diagnosis  of  gastric  ulcer,  but  at  autopsy 
we  usually  find  well-marked  varices  in  the  oesophagus,  due  to  passive  congestion. 
The  severe  haemorrhage  is  occasioned  by  the  bursting  of  a  varix.  We  surmise 
that  similar  conditions,  probably  mostly  in  the  rectum,  cause  the  severe  intestinal 
hgemorrhages  which  are  sometimes  seen. 

There  is  sometimes  a  slight  jaundice  in  ordinarj^  cirrhosis,  which  is  due  to  the 
existence  of  duodenal  catarrh,  or  perhaps  to  catarrh  of  the  smaller  bile-ducts.  In 
many  cases,  however,  there  is  no  jaundice  at  all,  or  the  skin  shows  merely  a  slight 
yellowish  tinge.  There  is  also  a  peculiar  dark  or  dirty-grayish  color,  which  is 
tolerably  characteristic  of  cirrhosis. 

The  above  signs  of  portal  obstruction  will  often  render  the  diagnosis  of 
hepatic  disease  extremely  probable,  but  we  shoiild  always  endeavor  to  confirm  our 
opinion  by  physical  examination  of  the  liver.  In  the  later  stages  of  the  disease, 
and  particularly  if  there  be  great  ascites,  our  efforts  may  be  fruitless;  but  at  first, 
or  after  paracentesis  has  been  performed,  percussion  and  palpation  may  yield 
valuable  information.  In  the  earliest  stages  the  liver  is  usually  large.  Hepatic 
dullness  reaches  some  way  below  the  edge  of  the  ribs,  and  we  can  often  feel  the 
lower  edge  and  anterior  surface  of  the  organ.  Later  on  we  find  the  surface  irreg- 
ular and  rough.  If  we  can  feel  these  little  nodules  or  prominences  through  the 
abdominal  walls,  as  we  sometimes  can,  of  course  the  diagnosis  of  cirrhosis  of  the 
liver  is  nearly  certain.  As  already  mentioned,  it  often  happens  that  irregular- 
ities are  already  to  be  felt  upon  the  surface  of  the  organ  while  it  still  remains 


CIREHOSIS    OF    THE   LIVER  559 

hypertrophic.  The  demonstration  of  atrophy  by  percussion  in  the  later  stages  of 
the  disease  is  less  reliable.  The  ascites  often  interferes  with  such  an  attempt. 
We  may  also  be  misled  by  coils  of  in^;estine  distended  with  gas  and  perhaps  lying 
in  front  of  the  liver.  If,  however,  after  guarding  against  error,  we  constantly 
find  the  area  of  hepatic  dullness  diminished,  the  sign  has  some  value.  Moreover, 
it  is  not  infrequently  possible  to  make  out  by  palpation  that  the  liver,  although 
reduced  in  size,  is  hard  and  uneven.  This  is  easier  after  the  removal  of  ascitic 
fluid,  when  the  abdominal  walls  are  lax,  and  also  if  the  attachments  of  the  liver 
have  been  loosened  so  that  it  sinks  downward. 

General  nutrition  is  usually  much  impaired  in  the  later  stages  of  the  disease. 
At  first  the  patient  may  retain  vestiges  of  his  former  corpulence,  but  finally  he 
grows  emaciated.  Anasarca  may  exceptionally  occur  toward  the  close;  but  there 
is  frequently  considerable  cedema  of  the  lower  extremities,  and  even  of  the  scro- 
tum and  the  dependent  portions  of  the  abdominal  walls.  The  cause  of  this  is  a 
purely  local  one — the  pressure  of  the  ascites  impedes  the  return  of  blood  from  the 
lower  limbs  to  the  heart.  Thus  arises  a  condition  which  is  characteristic  of  portal 
obstruction  in  general,  and  hepatic  cirrhosis  in  particular,  and  has  been  termed 
"  oedema  of  the  lower  half  of  the  body."  There  is  ascites  with  cedema  of  the  loins, 
the  scrotum,  and  the  lower  extremities;  while  the  upper  extremities,  the  upper 
half  of  the  trunk,  and  the  face  are  entirely  free  from  oedema. 

Occasionally  there  are  ecchymoses  into  the  skin,  the  mucous  membranes,  the 
retina,  and  other  parts.  These  arc  probably  due  to  malnutrition  of  the  vascular 
walls.    The  gastric  and  intestinal  haemorrhages  have  been  already  discussed. 

In  uncomplicated  cases  of  the  disease  there  is  no  fever.  The  pulse,  even 
when  there  are  no  cardiac  complications,  is  small  and  often  somewhat  rapid. 
Respiration  may  be  much  embarrassed,  as  a  result  of  the  upward  pressure  of  the 
diaphragm. 

At  first  the  urine  presents  no  characteristic  changes.  When  the  ascites  has 
become  considerable  and  there  is  oedema,  the  urine  grows  scanty,  dark,  and  con- 
centrated, and  often  has  an  abundant  sediment  of  urates.  It  should  be  men- 
tioned that  some  observers  have  found  a  diminished  excretion  of  urea.  This  is 
perhaps  due  to  a  disturbance  of  the  urea-generating  function  of  the  liver,  about 
which  both  earlier  and  more  recent  investigators  agree.  In  a  few  instances  the 
urine  has  been  found  to  contain  a  trace  of  sugar.  As  a  rule,  however,  the  urine 
contains  no  sugar  whatever,  not  even  when  an  attempt  is  made  to  induce  an 
alimentary  glycosuria. 

It  remains  for  us  to  describe  briefly  the  collateral  circulation  which  may  be 
developed  in  cirrhosis,  so  as  to  enable  the  blood  of  the  portal  system  to  reach  the 
systemic  veins.  The  clinical  history  of  the  disease  does  not  indicate  that  this 
attempt  at  compensation  is  very  successful.  We  may  have :  1.  Communications 
between  the  veins  of  the  mesentery  and  of  the  abdominal  walls.  2.  Communica- 
tions between  the  coronary  vein  of  the  stomach  and  the  veins  of  Glisson's  capsule 
on  the  one  hand,  and  the  phrenic  veins  on  the  other.  3.  Anastomoses  between 
the  internal  hsemorrhoidal  and  the  h\T50gastric  veins.  4.  As  pointed  out  by 
Baumgarten.  enlargement  of  the  not  yet  completely  obliterated  umbilical  vein  in 
the  ligamentum  teres.  Through  all  these  the  blood  may  flow  from  the  portal 
system  into  the  veins  of  the  abdominal  walls — that  is,  in  the  reverse  of  the  normal 
direction.  Then  in  a  few  exceptional  cases  the  veins  around  the  navel  become 
varicose,  a  phenomenon  which  has  been  termed  the  "  caput  Meduste."  Much  more 
frequent  and  more  important  is  the  finding  of  unnaturally  distended  and  tortuous 
veins  in  the  skin  of  the  abdominal  walls,  when  there  is  ascites.  These  veins 
usually  extend  upward  from  the  neighborhood  of  Poupart's  ligament.  This  phe- 
nomenon is  due  to  the  fact  that  because  of  the  ascites  the  flow  of  venous  blood 
from  the  lower  extremities  through  the  iliac  veins  is  im.peded  (vide  supra),  and 


560  DISEASES    OF   THE   DIGESTIVE    OEGANS 

consequently  a  part  of  the  venous  blood  takes  its  course  through  the  inferior  and 
superior  epigastric  veins  to  the  mammary  veins. 

The  complications  which  are  seen  in  many  cases  are  probably  due  in  part  to 
the  same  influences  which  occasion  the  cirrhosis.  In  this  list  belong,  for  exam- 
ple, cardiac  hypertrophy,  intestinal  nephritis,  and  chronic  pachymeningitis.  Of 
special  interest,  because  of  its  diagnostic  and  therapeutic  importance,  is  the 
combination  of  hepatic  cirrhosis  with  tubercular  peritonitis.  As  we  have  already 
seen  (page  531),  hepatic  cirrhosis  is  probably  in  most  cases  the  primary  disease, 
and  occasions  a  predisposition  to  the  development  of  tubercular  peritonitis.  The 
clinical  picture  in  these  cases  is  a  combination  of  the  symptoms  of  hepatic  cirrho- 
sis, such  as  a  palpable  granular  liver,  splenic  tumor,  and  yellowish  complexion, 
with  the  symptoms  of  tuberculosis,  such  as  irregular  distention  and  tenderness 
of  the  abdomen,  persistent  fever,  and  emaciation.  If  we  consider  the  aetiology 
(alcoholism),  we  may,  therefore,  sometunes  make  a  complete  diagnosis  of  this 
combination,  particularly  if  at  the  same  time  the  tuberculous  inflammation  at- 
tacks other  serous  membranes,  such  as  the  pleura. 

As  to  the  general  course  of  cirrhosis,  its  duration  can  not  easily  be  determined 
because  the  onset  is  usually  insidious.  As  a  rule,  the  disease  lasts  one  to  three 
years,  or  rarely  longer.  In  many  cases  the  symptoms  are  insignificant  for  the 
first  six  to  eighteen  months.  Then  the  disorder  takes  on  a  severer  form,  perhaps 
rather  suddenly.  Ascites  appears,  for  example.  These  graver  symptoms  persist, 
until  after  a  few  months  the  patient  dies.  The  course  of  the  disease  reminds  one 
of  cardiac  cases,  where  for  a  long  while  the  compensatory  changes  avert  any  dis- 
tress, until  on  a  sudden  the  circulatory  disturbances  become  pronounced  and  per- 
sist to  the  end. 

The  prognosis  is  always  unfavorable,  at  least  when  the  symptoms  have  once 
become  well  marked.  It  may  be  that  in  the  earlier  stages  the  disease  can  be 
cheeked  or  even  permanently  cured;  but  even  this  is  open  to  doubt.  No  case 
recovers  in  which  the  diagnosis  of  cirrhosis  is  certain. 

Death  is  due  either  to  intercurrent  disease,  or  more  often  to  gradually  increas- 
ing exhaustion.  In  some  few  cases  severe  cerebral  symptoms  suddenly  appear: 
there  are  coma,  general  convulsions,  and  delirium;  and  these  usually  are  soon 
fatal.  Just  how  these  nervous  phenomena  originate  we  do  not  certainly  know 
(see  the  chapter  on  acute  yellow  atrophy  of  the  liver). 

Diagnosis. — The  diagnosis  of  hepatic  cirrhosis  is  not  usually  self-evident.  It 
may  be  made  with  some  positiveness  if  a  patient  who  has  a  previous  history  of 
alcoholic  excess  gradually  develops  ascites  and  splenic  tumor,  and  if  upon  palpa- 
tion we  find  the  liver  unnaturally  firm  and  hard,  either  enlarged  or  shrunken, 
perhaps  with  a  roughened  surface,  and  in  any  case  distinctly  to  be  felt;  yet  in 
palpating  the  granular  surface  one  is  very  liable  to  errors,  and  particularly  the 
separate  kernels  of  fat  in  the  panniculus  adiposus  of  the  abdomen  are  apt  to  be 
mistaken  by  inexperienced  observers  for  irregularities  in  the  surface  of  the  liver. 
The  difficulties  in  the  percussion  of  the  liver  have  been  already  indicated.  Often 
a  patient  does  not  come  under  observation  until  a  considerable  ascitic  effusion 
has  already  taken  place,  so  that  physical  examination  of  the  liver  and  spleen  is 
rendered  very  difficult,  if  not  impossible.  Then  we  must  first  exclude  any  general 
disturbance  of  circulation  as  a  cause  of  the  ascites.  If  the  heart,  lungs,  and 
kidneys  are  found  to  be  normal,  and  if  there  is  no  oedema  in  the  upper  half  of 
the  body,  it  is  very  probable  that  there  is  a  local  derangement  of  the  portal  circu- 
lation, particularly  if  the  patient  is  positive  that  the  abdominal  enlargement  was 
the  first  evidence  of  dropsy;  but  we  have  still  to  determine  whether  the  cause  of 
this  derangement  is  cirrhosis  of  the  liver.  This  may  be  assumed  to  be  the  case 
if  the  whole  course  of  the  disease  warrants  the  assumption,  and  if  the  history 
furnishes  that  most  frequent  of  all  etiological  factors,  chronic  alcoholism.     0th- 


CIKEHOSIS    OF   THE   LIVER  561 

erwise  we  must  be  cautious,  for  portal  obstruction  with  precisely  similar  results 
may  be  due  to  other  causes — such  as  the  external  pressure  of  tumors  or  portal 
thrombosis.  Many  forms  of  hepatic  syphilis  (q.  v.)  can  not  be  differentiated  from 
cirrhosis  by  mere  clinical  observation  of  the  hepatic  disorder.  Here  it  is  only  the 
aetiology  and  the  demonstration  of  other  signs  of\syphilis  that  can  justify  the 
assumption  that  the  disease  in  hand  is  of  specific  origin.  It  is  often  a  great  aid 
in  diagnosis  to  examine  the  liver  directly  after  tapping.  The  abdominal  walls  are 
then  relaxed  and  soft,  so  that  the  liver  may  be  made  out  very  distinctly.  It 
should  be  borne  in  mind  that  irregularities  of  considerable  size  are  more  frequent 
in  hepatic  syphilis  ("  lobulated  liver  "),  while  cirrhosis  is  suggested  by  a  more 
uniform  granulation. 

It  is  also  very  difficult  in  many  instances  to  exclude  chronic  peritonitis.  The 
aetiology  may  aid  us.  Other  points  are,  that  in  chronic  peritonitis  there  may  be 
tenderness  on  pressure,  the  abdominal  distention  is  less  uniform,  and  there  is  no 
enlargement  of  the  spleen.  Another  point  is  that  the  specific  gravity  of  a  simple 
ascites  due  to  passive  congestion  is  often  below  1015,  while  an  inflammatory  exu- 
dation usually  reaches  higher  figures.  Hsemorrhagic  ascites,  as  a  rule,  indicates 
tuberculous  or  cancerous  peritonitis.  The  combination  of  hepatic  cirrhosis  and 
chronic  peritoneal  tuberculosis  (vide  supra)  may  be  diagnosticated  with  a  certain 
probability  if,  besides  sjonptoms  of  cirrhosis  and  peritoneal  disturbance,  there  are 
definite  indications  of  a  tuberculous  afi^ection;  such  are  a  phthisical  constitu- 
tion, persistent  fever,  and  the  existence  of  a  tuberculous  disease  in  some  other 
organ,  particularly  the  pleura. 

Treatment. — In  treating  hepatic  cirrhosis  the  first  necessity  is  a  strict  regu- 
lation of  the  diet.  The  earlier  in  the  disease  proper  diagnostic  rules  are  fol- 
lowed, the  more  likelihood  of  benefit.  The  most  important  principle  in  regulat- 
ing the  diet  is  to  avoid  all  ingesta  which  in  any  way  might  irritate  or  damage  the 
hepatic  cells.  We  forbid,  therefore,  all  alcoholic  beverages,  or  at  most  allow  very 
small  amounts  merely  to  stimulate  the  appetite.  We  likewise  forbid  sharp  spices, 
pepper,  mustard,  horse-radish,  onions,  and  similar  articles.  In  general,  the 
amount  of  meat  should  be  limited.  We  may  allow  milk,  buttermilk,  eggs, 
vegetables,  and  cereals.  In  suitable  cases  we  may  try  the  prescription  of  an 
exclusive  milk  diet  for  some  weeks.  Quite  a  number  of  authors  report  favorable 
results  from  a  milk-cure  of  this  sort,  but  the  individual  peculiarities  of  every  case 
must  be  considered. 

If  the  disease  has  already  developed  we  must  resign  ourselves  to  merely  symp- 
tomatic treatment :  at  least,  the  specific  benefit  which  iodide  of  potassium  is  said 
to  exercise  in  hepatic  cirrhosis  is  very  doubtful,  and  is  probably  based  merely 
upon  cases  of  syphilitic  disease  of  the  liver. 

The  symptomatic  treatment  of  hepatic  cirrhosis  has  to  deal  mainly  with  the 
disturbances  due  to  portal  congestion,  and  the  associated  gastro-intestinal  ca- 
tarrh. In  such  cases  experience  shows  that  the  best  results  are  obtained  by  the 
cautious  use  for  a  considerable  time  of  laxatives.  In  early  cases  we  should  resort 
first  to  salines,  particularly  Carlsbad  salts.  We  may  prescribe  artificial  Carlsbad 
salts,  dissolved  in  warm  water,  or  the  genuine  Carlsbad  water  to  be  drunk  at  all 
times.  If  the  patient's  circumstances  permit  we  may  even  recommend  in  suitable 
cases  a  visit  to  Carlsbad.  Other  appropriate  health-resorts  are  Marienbad,  Kis- 
singen.  Ems,  and  Neuenahr.  If  the  saline  remedies  are  ill-borne  we  employ  vege- 
table laxatives,  such  as  rhubarb  and  aloes.  In  case  there  is  already  a  consider- 
able degree  of  ascites,  good  results  may  sometimes  be  obtained  by  administering 
drastic  purgatives,  among  which  gamboge  has  earned  a  special  reputation.  Many 
observers  have  seen  benefit  from  calomel,  giving  three  times  a  day  three  grains 
(gramme  0.2)  for  a  period  of  two  to  three  days.  Calomel  may  be  given  repeatedly 
in  this  way  at  intervals  of  from  five  to  eight  days.  Of  course,  caution  is  necessary 
36 


562  DISEASES    OF   THE   DIGESTIVE   OEGAI^S 

in  its  employment.  Probably  it  does  good  both  as  a  laxative  and  also  as  a  diuretic 
(vide  infra).  Sasaki,  in  Japan,  lias  seen  excellent  results  in  hepatic  cirrhosis 
from  the  administration  of  cream  of  tartar  in  considerable  doses,  two  to  four 
drachms  (grammes  10  to  15)  a  day,  associated  with  a  nourishing  diet,  including 
milk  and  scraped  raw  meat.  After  all,  however,  laxatives  should  not  be  employed 
if  they  disturb  the  digestive  apparatus. 

If  ascites  has  already  developed,  we  may  administer  diuretics  besides  the 
drastic  purgatives ;  trial  may  be  made  of  acetate  of  potassium  or  sodium,  squills, 
diuretine,  and  the  species  diuretica3  of  the  German  Pharmacopoeia  (containing 
lovage,  rest-harrow,  licorice-root,  and  juniper  berries).  English  authorities ' rec- 
ommend the  balsam  and  the  resin  of  copaiba  as  particularly  efficient  in  the  vari- 
ous forms  of  ascites.  The  dose  is  about  fifteen  minims  (gramme  1)  a  day. 
The  best  mode  of  administration  is  in  gelatine  capsules.  This  remedy  occasions 
in  some  eases  a  rapid  increase  in  diuresis,  and  a  consequent  diminution  in  the 
ascites.  Sometimes,  also,  pure  urea  (2.5-4  drachms,  grammes  10-15,  daily,  dis- 
solved in  water)  acts  as  a  good  diuretic.  If  the  heart  is  feeble,  digitalis  may 
cause  a  decided  increase  in  the  amount  of  urine,  and  it  is  also  worth  while  to 
try  a  combination  of  digitalis  with  calomel. 

If  the  ascites  is  so  excessive  as  to  occasion  much  local  discomfort  and  to  im- 
pede respiration,  the  removal  of  the  fluid  by  paracentesis  may  afford  relief.  The 
details  of  this  proceeding  were  given  in  the  last  section.  Many  physicians  recom- 
mend tapping  as  early  as  possible,  before  it  is  absolutely  necessary.  The  relief 
is  said  to  be  more  lasting  in  that  case;  but  this  proposal  has  by  no  means  met 
with  universal  assent,  and,  as  a  rule,  the  physician  will  not  tap  until  the  abdom- 
inal tension,  the  dyspnoea,  and  other  symptoms  occasioned  by  the  ascites  render 
it  necessary.  Unfortunately,  the  relief  is  only  temporary,  for  the  fluid  collects 
again  with  great  rapidity  after  tapping ;  yet  it  is  sometimes  possible  to  delay  the 
reaccumulation  for  a  considerable  time  by  compressing  the  abdomen  with  an 
elastic  bandage,  and  by  using  the  above-mentioned  remedies  (diuretics  and  digi- 
talis) directly  after  tapping. 

[In  1896  Drummond  and  Morison  proposed  an  operation  to  relieve  the  venous 
stasis,  by  producing  adhesions  between  the  liver,  spleen,  and  omentum  and  the 
parietal  peritoneum.  A  few  successful  cases  have  been  reported.  Three  known 
to  one  of  the  translators  all  died. — V.] 


CHAPTEK  YI 

BILIARY    CmilHOSlS    AND    HYPERTROPHIC     CIRRHOSIS    OF    THE 

LIVER 

There  are  two  forms  of  cirrhosis  which  differ  in  many  respects  from  the  dis- 
ease just  described :  they  are  called  biliary  cirrhosis  and  hypertrophic  cirrhosis  of 
the  liver.  Charcot  and  Hanot  were  the  first  to  call  attention  to  them.  Since 
then  the  literature  of  the  subject  has  become  quite  extensive,  but  all  doubts 
and  differences  of  opinion  are  not  yet  settled. 

1.  Secondary  Biliary  Cirrhosis  of  the  Liver. — Whenever  there  is  retention  of 
bile  in  the  liver  for  any  length  of  time,  no  matter  what  causes  it,  certain  changes 
may  result.  The  small  and  the  medium-sized  bile-ducts  become  distended,  and 
granules  of  pigment  are  deposited,  both  in  the  interlobular  connective  tissue  and 
within  the  acini  themselves.  Besides  this,  however,  and  undoubtedly  because  of 
the  noxious  influence  of  the  retained  bile,  the  hepatic  cells  not  infrequently  un- 


BILIAEY   CIEEHOSIS  '   i  563 

dergo  destructive  changes.  In  accordance  with  the  general  rule,  connective  tis- 
sue gradually  jfills  the  gaps  thus  left  in  the  parenchyma,  and,  more  than  this,  the 
interstitial  hyperplasia  is  so  great  as  to  increase  the  size  of  the  organ.  If,  there- 
fore, there  is  ijersistent  obstruction  of  the  common  duct  by  a  gall-stone,  or  a  cica- 
tricial stenosis,  or  a  tumor  pressing  from  without  upon  the  duct,  the  liver  will,  in 
all  such  cases,  be  found  to  be  larger,  firmer,  and  richer  in  fibrous  tissue  than  nor- 
mal— in  a  word,  "  cirrhotic."  Hence  this  condition  does  not  represent  an  inde- 
pendent disease,  but  is  a  result  of  chronic  biliary  retention,  in  whatever  way 
occasioned.  It  is  appropriately  termed  "  secondary  biliary  cirrhosis."  That  re- 
tention is  really  the  cause  of  this  change  has  been,  proved  by  experiments,  for  it 
has  been  shown  that  ligature  of  the  common  duct  in  animals  causes  well-marked 
biliary  cirrhosis. 

2.  Primary  Hypertrophic  or  Biliary  Cirrhosis. — The  secondary  cirrhosis  just 
described  is  due  to  occlusion  of  the  large  bile-ducts.  There  is  also  a  not  very 
common  primary  form  of  biliary  cirrhosis,  usually  known  as  hypertrophic  cirrho- 
sis. French  authors  have  given  it  the  name  of  "  cirrhose  hypertrophique  sans 
ascite  avec  ictere,"  out  of  regard  to  its  most  important  clinical  symptom.  That 
there  is  an  essential  difference  between  this  form  and  the  ordinary  "  atrophic  " 
cirrhosis  of  Laennec  is  manifested  by  the  clinical  behavior  of  the  disease. 

The  specific  cause  of  hypertrophic  bilious  hepatic  cirrhosis  is  as  yet  entirely 
unknown.  We  can  merely  surmise  that  we  have  to  do  with  a  chronic  inflamma- 
tory process,  excited  by  some  toxic  or  infectious  agent,  and  that  the  process  prob- 
ably originates  in  the  small  bile-ducts  of  the  liver. 

Often  this  disorder  attacks  hard  drinkers,  but  they  are  not  by  any  means  its 
only  victims.  While,  in  the  common  form  of  cirrhosis,  ascites  is  usually  the 
earliest  grave  symptom  of  disease,  in  hypertrophic  cirrhosis  a  slight  jaundice  gen- 
erally appears  simultaneously  with  the  first  indefinite  symptoms^  of  pressure  in 
the  region  of  the  liver,  languor,  and  anorexia.  This  jaundice  rapidly  increases, 
and  persists  throughout  the  illness.  In  ordinary  cirrhosis  there  may  be,  as  we 
have  said,  hardly  any  jaundice,  or,  at  any  rate,  it  is  a  rather  late  symptom,  and 
even  then  it  is  seldom  extreme.  On  the  other  hand,  ascites,  as  a  rule,  is  slight  or 
absent  in  hypertrophic  cirrhosis.  It  is  true  that  there  have  been  cases  with  great 
ascitic  effusion,  but  it  never  comes  till  the  disease  is  quite  far  advanced. 

On  physical  examination  the  liver  is  usually  found  to  be  considerably  en- 
larged, and  its  surface  is  smooth,  as  a  rule,  or  rarely  it  displays  some  low  eleva- 
tions, due  perhaps  to  variations  in  the  fullness  of  the  blood-vessels.  In  general 
there  is  said  to  be  this  important  difference  between  the  ordinary  and  the  hyper- 
trophic forms,  that  in  the  latter  the  newly  formed  connective  tissue  evinces  little 
tendency  to  contraction,  so  that  the  liver  remains  large,  even  late  in  the  course 
of  the  disease,  and  does  not  shrink.  This  is  certainly  true  of  the  majority  of 
cases,  so  that  after  an  illness  of  two  or  three  years  the  liver  is  still  found  to  be 
large  and  smooth;  but  further  observations  are  necessary  in  order  to  determine 
whether  there  may  not  sometimes  be  contraction  toward  the  end  of  the  disease. 

Along  with  the  chronic  jaundice  and  the  marked  enlargement  of  the  liver 
there  is  a  third  important  symptom — viz.,  chronic  splenic  tumor,  usually  of  con- 
siderable size.  As  there  are  no  indications  of  portal  obstruction,  we  must  con- 
clude that  the  spleen  is  not  enlarged  from  passive  congestion,  as  is  usually  the 
case  in  ordinary  alcoholic  cirrhosis,  but  as  the  result  of  hyperplasia ;  and  post- 
mortem examinations  confirm  this  conclusion.  The  origin  of  the  hyperplasia  is 
not  clear.  In  one  case  we  found  not  only  splenic  tumor  but  a  distinct  hyper- 
plasia of  many  mesenteric  and  peritoneal  lymph-glands;  which  suggests  the  pos- 
sibility of  infectious  influences.  A  corroborative  fact  is  that  not  infrequently 
the  entire  course  of  the  disease  will  be  marked  by  slight  elevations  of  temperature. 
The  other  symptoms  of  the  disease  are  in  part  the  direct  result  of  the  jaundice. 


564  DISEASES    OF   THE   DIGESTIVE   OEGA^ts 

such  as  the  slow  pulse,  the  itching,  and  the  changes  in  the  urine;  while  others, 
such  as  languor  and.  weakness,  are  the  results  of  the  constitutional  disturbance. 
The  dejections  are  not  always  colorless  and  fatty,  as  in  case  of  obstruction  of  the 
large  bile-ducts.  Many  patients  have  a  noticeable  tendency  to  haemorrhage,  par- 
ticularly to  hgeniateniesis.  In  the  case  mentioned  above,  the  fatal  termination 
was  due  to  constantly  repeated  and  profuse  haemorrhages  from  the  stomach,  for 
which  the  autopsy  disclosed  no  anatomical  cause  in  the  stomach  or  intestine.  It 
seemed  as  if  the  haemorrhages  had  taken  place  by  diapedesis. 

The  entire  duration  of  the  disease  is  about  one  or  two  years;  but  it  may  last 
much  longer.  The  prognosis  is  almost  always  bad.  Occasionally  a  case  will 
exhibit  marked  temporary  improvement  or  an  apparent  arrest  of  the  disease,  so 
that,  in  spite  of  the  size  of  the  liver,  the  patient  is  able  to  do  light  work.  Death 
comes,  when  there  are  none  of  the  above-mentioned  hsemorrhages,  as  a  result  of 
gradual  exhaustion,  or  is  sudderJy  ushered  in  by  coma,  convulsions,  and  other 
grave  nervous  symptoms,  usually  ascribed  to  cholaemia  (vide  infra). 

That  a  chronic  hepatic  disease  of  so  peculiar  a  nature  should  be  marked  by 
peculiar  anatomical  changes  would  seem  certain,  even  from  clinical  observation. 
In  general,  this  view  is  confirmed,  although  further  and  careful  investigations  are 
much  needed.  Upon  microscopic  examination  there  is  always  found  an  abundant 
new  growth  of  a  tissue  containing  many  cellular  elements,  surrounding  the  small 
bile-ducts  of  the  liver.  In  other  particulars  the  histological  changes  are  very 
similar  to  those  of  ordinary  hepatic  cirrhosis.  The  new  growth  of  connective 
tissue  is  found  in  the  interior  of  the  hepatic  lobules,  but  this  can  scarcely  be 
regarded  as  a  radical  difference.  Still,  one  gets  the  impression  that  the  entire 
pathological  process  of  hypertrophic  cirrhosis  originates  in  the  bile-ducts  and  the 
tissues  surrounding  them,  while  the  changes  of  ordinary  alcoholic  hepatic  cirrho- 
sis start  from  tl^e  branches  of  the  portal  vein.  The  absence  of  contraction  in  the 
new  tissue  of  hypertrophic  cirrhosis  seems  to  be  consonant  with  the  fact  that  the 
anatomical  changes  suggest  hyperplasia  rather  than  inflammation  (compare  the 
changes  in  the  spleen  and  the  lymph-glands). 

The  diagnosis  of  hypertrophic  cirrhosis  can  sometimes  be  made  with  consider- 
able positiveness,  and  sometimes  can  merely  be  regarded  as  probable.  The  grad- 
ual development  and  persistence  of  jaundice  and  the  presence  of  an  enlarged  liver 
and  spleen,  but  usually  without  marked  ascites,  would  suggest  the  disease  strongly, 
especially  if  long-continued  observation  enabled  us  to  exclude  carcinoma  and 
other  diseases.  Sometimes,  however,  it  is  very  difiicult  to  decide  whether  the 
biliary  cirrhosis  is  primary  or  secondary,  for  the  conditions  giving  rise  to  sec- 
ondary biliary  cirrhosis  (occlusion  of  the  bile-ducts  from  sears,  new  growths,  or 
calculi)  may  be  obscure.  A  careful  investigation  into  the  history  of  the  case 
with  regard  to  biliary  colic  and  similar  symptoms  might  be  decisive.  Other  fac- 
tors are  the  general  course  of  the  disease  and  the  presence  of  a  splenic  tumor, 
unaccompanied  by  ascites.  An  enlarged  spleen  is  scarcely  ever  seen  in  this  way 
in  ordinary  chronic  jaundice  of  obstructive  origin. 

The  treatment  should  conform  to  the  principles  laid  down  in  the  chapters  on 
jaundice  and  ordinary  cirrhosis  of  the  liver.  Sacharjin  has  lately  recommended 
the  persistent  use  of  small  doses  of  calomel — one  grain  (gramme  0.06)  several 
times  a  day. 


ACUTE   YELLOW   ATROPHY   OF   THE   LIVER  5G5 

CHAPTER   Vn 
ACUTE    YELLOW    ATBOPHY    OF    THE    LIVER 

^Etiology. — Acute  fatty  degeneration  of  the  liver  occurs  both  as  a  primary  dis- 
ease and  as  secondary  to  other  hepatic  disorders,  or  as  a  symptom  of  constitu- 
tional diseases.  Secondary  acute  fatty  degeneration  in  rare  instances  accom- 
panies severe  acute  infectious  diseases,  such  as  typhoid  fever,  recurrent  fever, 
septicaemia,  and  puerperal  disease.  It  also  appears,  with  equal  rarity,  in  the 
course  of  cirrhosis  of  the  liver  or  of  persistent  biliary  retention ;  and  it  is  a  con- 
stant phenomenon  in  acute  phosphorus  poisoning.  Indeed,  the  effects  of  phos- 
phorus resemble  the  symptoms  of  primary  acute  yellow  atrophy  in  many  ways  so 
closely,  even  post  mortem,  that  formerly  the  two  were  often  confounded. 

Primary  acute  yellow  atrophy  of  the  liver  is  a  very  rare  but  extremely  severe 
disease  which  almost  invariably  leads  to  speedy  death.  There  is  generally  no 
determinable  cause,  and  its  victims  are  struck  down  in  blooming  health.  It  is 
most  common  in  young  adult  life  between  the  fifteenth  and  thirty-fifth  year. 
Children  and  elderly  people  have  been  occasionally  attacked.  Eemales  are  much 
more  liable  to  the  disease  than  males;  and  pregnancy  increases  the  predisposi- 
tion to  it. 

As  we  have  said,  we  can  not  as  a  rule  find  any  exciting  cause.  It  is  stated  that 
sometimes  the  onset  has  been  preceded  by  some  violent  emotional  excitement,  or 
excess  in  alcohol,  or  the  like;  but  how  important  these  factors  may  be  is  not  at 
all  clear. 

It  is  an  interesting  fact  that  sometimes  the  disease  becomes  rather  more  fre- 
quent than  usual,  and  endemic.  Eor  instance,  several  members  of  one  family 
may  be  attacked.  This  favours  a  theory  as  to  the  nature  of  acute  yellow  atrophy 
which  a  majority  of  the  present  investigators  seem  inclined  to  adopt.  The  theory 
referred  to  is  suggested  not  only  by  the  whole  course  of  the  disease,  but  by  the 
pathological  appearances,  and  places  it  in  the  category  of  acute  infectious  dis- 
eases. It  must  be  confessed  that  as  yet  we  know  nothing  about  the  intimate 
nature  of  the  infection. 

Pathology. — The  chief  change  found  post  mortem  is  in  the  liver,  and  it  has 
determined  the  name  given  to  the  disease. 

The  liver  is  much  atrophied,  sometimes  being  only  one  half  or  one  third  its 
normal  size.  This  makes  its  capsule  often  seem  contracted  and  wrinkled.  The 
organ  is  usually  soft  and  flabby,  so  that  in  some  places  it  seems  as  if  the  finger 
could  be  pressed  into  it.  The  color  of  the  surface,  and  for  the  most  part  of  the 
cross-section  also,  is  yellow,  like  ochre  or  saffron;  but  the  cut  surface  may  be 
parti-colored,  having  red  and  yellow  spots  interspersed.  Hence  the  names  "  red 
atrophy  "  and  "  yellow  atrophy."  The  arrangement  and  relative  extent  of  these 
patches  may  vary  exceedingly.  The  red  places  look  as  if  they  had  collapsed,  and 
seem  tougher  than  the  yellow.  They  correspond,  as  we  shall  soon  see,  to  the 
more  advanced  stages  of  the  affection,  while  the  yellow  spots  have  undergone 
less  change.  The  lobules  are.  as  a  rule,  no  longer  distinguishable  by  the  naked 
eye.  Such  lobules  as  can  still  be  made  out  seem  abnormally  small  and  have  a 
gray  periphery. 

On  microscopic  examination,  we  find  that  the  essential  change  is  an  intense 
and  uniform  fatty  degeneration  of  the  hepatic  cells,  affecting  the  entire  paren- 
chyma. Only  a  few  cells  still  retain  their  normal  condition.  The  others  are  filled 
with  large  and  small  fat-globules,  and  many  are  already  suffering  evident  disin- 
tegration and  absorption.  Where  the  degeneration  is  furthest  advanced,  fat, 
detritus,  and  pigment  alone  remain.     Inasmuch  as  the  lymphatics  rapidly  absorb 


566  DISEASES    OE   THE   DIGESTIVE   OEGANS 

and  remove  the  fatty  and  albiiminoid  granules,  there  is  finally  little  left  except 
blood-vessels  and  connective  tissue.  The  blood-vessels  are  frequently  quite  con- 
gested, and  thus  occasion  that  red  color  vhich  the  naked  eye  detects  in  the  mora 
advanced,  broken-do-mi  portions.  Frerichs  made  an  interesting  discovery,  which 
deserves  mention,  of  the  existence  of  leucine  and  tyrosine  crystals  both  in  the 
parenchyma  and  in  the  blood-vessels.  Bilirubine  crystals  also  are  sometimes 
found  in  the  detritiis,  and  more  rarely  in  the  interior  of  the  hepatic  cells. 

Not  only  the  liver,  but  many  other  organs  present  fatty  degeneration:  the 
heart  in  particular,  the  kidneys,  and  rarely  the  muscles ;  but  the  process  is  always 
most  intense  in  the  liver.  The  skin  (vide  infra)  and  most  of  the  viscera  are  evi- 
dently tinged  with  jaundice. 

Acute  splenic  tumor  is  invariably  present.  This  suggests  that  the  disease  may 
be  infectious.  That  the  disease  is  a  constitutional  one  is  also  to  be  inferred  from 
the  numerous  ecchymoses  in  the  skin  and  the  interior  of  the  body,  especially  in 
the  mucous  membrane  of  the  stomach  and  intestines,  in  the  serous  membranes, 
in  the  pelvis  of  the  kidneys  and  the  kidneys  themselves,  and  more  rarely  in  the 
brain  and  heart.  This,  again,  is  like  the  grave  septic  diseases.  The  blood  itself 
is  dark,  with  few  clots.  Leucine  and  tyrosine  have  repeatedly  been  detected  in  it. 
The  peritoneum  and  other  serous  cavities  sometimes  contain  a  considerable 
amount  of  serum. 

Clinical  History. — The  disease  is  ustially  divided  into  two  stages,  the  first  of 
which  corresponds  to  the  milder  prodromal  symptoms,  the  second  to  those  severe 
symptoms  which  are  alone  characteristic.  In  many  instances,  however,  the  first 
period  is  wanting,  or  is  so  brief  that  the  patient  is  plunged  almost  without  warn- 
ing into  the  gravest  condition. 

The  prodromata  in  most  cases  consist  of  constitutional  disturbances  and  mild 
gastro-intestinal  symptoms.  The  patient  is  languid,  without  appetite,  and  disin- 
clined to  exertion.  There  are  headache,  nausea,  vomiting,  slight  pains  in  the  gas- 
tro-hepatie  region,  and  sometimes  moderate  fever.  In  a  few  days  jaundice  usually 
appears.    This  is  almost  invariably  taken  for  an  ordinary  catarrhal  attack. 

After  some  days,  or  it  may  be  weeks,  the  second  stage  begins.  The  chief 
characteristic  of  this  is  the  occurrence  of  grave  nervous  symptoms.  First  there 
is  violent  headache,  with  sleeplessness  and  marked  restlessness.  The  intellect  is 
usually  somewhat  dulled  even  now,  and  articulation  is  slow  and  clumsy.  The 
mental  confusion  usually  advances  very  rapidly  to  a  noisy  and  violent  delirium. 
The  excitement  becomes  at  times  maniacal.  The  patient  screams  and  storms,  and 
he  can  hardly  be  kept  in  bed.  Often  there  are  convulsive  twitchings  of  individual 
muscles;  and  there  may  be  typical  epileptiform  attacks,  but  this  is  not  common. 
After  one  or  two  days,  or  rarely  longer,  the  excitement  abates,  and  is  followed  by 
sopor,  which  soon  passes  into  deep  coma.  At  death  the  patient  is  usually  per- 
fectly unconscious.  It  is  exceptional  for  the  excited  stage  to  be  wanting;  in  such 
cases  the  first  nervous  symptom  is  sopor. 

The  cause  of  the  nervous  symptoms  has  not  yet  been  explained  in  a  way  to 
silence  discussion.  The  same  theories  which  have  been  set  up  to  account  for  the 
grave  form  of  jaundice  in  general  (see  appendix  to  this  chapter)  have  also  been 
employed  to  elucidate  the  nervous  phenomena  of  acute  yellow  atrophy.  Thus, 
some  refer  them  to  cholsemia,  some  to  acholia.  In  acute  yellow  atrophy  of  the 
liver  it  might  also  be  that  the  primary  specific  processes  of  infection  or  intoxica- 
•tion  are  factors  in  the  development  of  the  severe  cerebral  symptoms. 

The  jaundice,  which  is  present  even  in  the  first  stage,  afterward  usually  deep- 
ens. The  urine  contains  bile-pigment,  and  many  investigators  have  also  found 
bile-acids  in  it.  If  these  latter  are  present,  it  suggests  that  the  jaundice  is  not 
(as  was  formerly  believed)  hsematogenous — that  is,  the  result  of  a  destruction  of 
red  blood-corpuscles  and  the  transformation  of  their  pigment  into  biliary  color- 


ACUTE   YELLOW   ATEOPHY   OF   THE   LIVER 


56^ 


ing  matter — but  is  due  rather  to  a  retention  of  bile.  Just  how  this  retention 
arises  we  do  not  yet  know  definitely.  The  obstruction  can  not  be  in  the  large 
bile-ducts,  for  the  gall-bladder  is  usually  found  empty.  Hence  the  cause  of  the 
retention  of  bile  and  of  the  jaundice  is  probably  a  derangement  of  the  smaller 
biliary  passages  within  the  liver.  We  should  add  that  in  a  few  rare  cases  there 
has  been  little  or  no  jaundice. 

On  physical  examination  of  the  liver  during  the  last  stage  of  the  disease,  there 
is  usually  a  striking  diminution  of  hepatic  dullness,  corresponding  to  the  atrophy 
of  the  organ.  Generally  the  first  change  to  be  detected  is  a  contraction  of  the 
left  lobe,  as  shown  by  the  development  of  tympanitic  resonance  in  the  epigastrium. 
At  the  commencement  of  the  illness,  the  hepatic  dullness  is  normal  or  slightly 
increased  in  area.  If  the  disease  proves  very  rapidly  fatal,  the  organ  may  never 
become  very  small.  In  most  cases,  though  by  no  means  in  all,  there  are  pain  and 
tenderness  in  the  hepatic  region,  but  these  are  seldom  so  great  as  in  phosphorus 
poisoning. 

The  enlargement  of  the  spleen  has  been  already  mentioned  as  an  almost  con- 
stant symptom  of  the  disease.     Even  during  life  some  increase  of  the  area  of 
splenic  dullness  can  usually  be  made  out,  and  some- 
times the  spleen  can  be  felt  under  the  edge  of  the 
ribs. 

The  occurrence  of  the  haemorrhages,  which  have 
already  been  referred  to  under  the  pathological  le- 
sions, can  often  be  demonstrated  during  life.  The 
cutaneous  ecchymoses  can,  of  course,  be  seen,  and 
the  haemorrhages  in  the  mucous  membranes  may 
give  rise  to  hsematemesis,  bloody  stools,  bleeding 
from  the  female  genitals,  or  epistaxis.  The  haem- 
orrhages are  due  probably  to  the  impaired  nutri- 
tion and  diminished  resisting  power  of  the  vascular 
walls  occasioned  by  the  grave  constitutional  disturb- 
ance. 

The  condition  of  the  urine  in  acute  yellow  atrophy  is  very  interesting.  The 
amount  is  either  normal  or  slightly  diminished,  and  the  specific  gravity  is  some- 
what increased.  Often  there  is  a  trace  of  albumen.  We  have  already  mentioned 
the  presence  of  bile-pigment.  The  point  of  chief  interest,  however,  is  one  that 
Frerichs  discovered  and  various  others  have  since  confirmed — namely,  the  great 
diminution  of  urea  and  the  appearance  in  its  place  of  several  other  substances, 
which  are  likewise  the  products  of  the  decomposition  of  albuminoid  matter,  and 
represent,  in  all  probability,  the  first  steps  in  the  formation  of  urea.  Of  these  sub- 
stances, the  most  important  are  leucine  and  tyrosine.  Their  characteristic  crys- 
tals can.  sometimes  be  detected  by  the  microscope  in  the  urinary  sediment  (see 
Fig.  63).  The  crystals  may  also  sometimes  be  obtained  by  allowing  a  drop  of 
the  fresh  urine  to  evaporate  slowly  upon  an  object-glass.  The  proper  way,  how- 
ever, to  demonstrate  these  crystals  is  to  precipitate  the  urine  with  basic  acetate 
of  lead,  to  remove  the  lead  from  the  filtrate  by  means  of  sulphuretted  hydrogen, 
and  then  to  evaporate  the  filtrate  thus  obtained  to  the  point  of  crystallization. 
There  are  some  other  abnormal  constituents  to  be  found  in  the  urine  besides 
leucine  and  tyrosine;  but  what  their  significance  is  we  do  not  know.  Among 
these  are  sarcolactic  acid,  oxymandelic  (paraoxyphenylglycolic)  acid,  peptonoid 
substances,  and  large  amounts  of  kreatine. 

It  at  once  suggests  itself  that  this  disappearance  of  urea  and  appearance  of 
leucine  and  tyrosine,  which  are  regarded  as  preparatory  stages  in  the  formation 
of  urea,  gives  valuable  support  to  Meissner's  and  Von  Schroder's  idea  that  this 
substance  is  manufactured  in  the  liver. 


Fig. 


63.— a.  Leucine  crystals. 
Tyrosine  crystals. 


568  DISEASES    OF   THE   DIGESTIVE   OEGAls^S 

As  to  the  other  organs  little  need  be  said.  Vomiting  is  very  frequent  in  the 
second  stage,  as  well  as  in  the  first.  It  usually  ushers  in  the  severe  cerebral  symp- 
toms. The  stools  are,  as  a  rule,  clay-colored,  as  is  usual  in  jaundice.  There  is 
generally  constipation.  The  pulse  is  rapid,  often  reaching  140  to  160  beats  per 
minute,  and  is  also  small  and  compressible.  It  is  this  acceleration  of  the  pulse, 
contrasting  with  its  usual  slowness  during  the  first  stage,  which,  along  with  the 
vomiting,  announces  the  onset  of  dangerous  symptoms.  The  pulmonary  signs 
are  seldom  marked,  although  there  may  be  bronchitis  or  a  pneumonia  due  to 
the  inhalation  of  foreign  substances.  During  the  coma  Avhieh  precedes  death 
respiration  is  usually  hurried,  and  often  deep  and  noisy.  Sometimes  it  is 
irregular. 

The  temperature  is  generally  approximately  normal.  Toward  the  fatal  termi- 
nation there  may  be  a  subnormal  temperature.  Still  more  frequently  the  tem- 
perature rises  before  death,  and  even  sometimes  grows  higher  after  death,  reach- 
ing 107.5°  (42°  C.)  or  more. 

In  case  the  disease  attacks  a  pregnant  woman,  abortion  or  premature  delivery 
is  almost  certain  to  occur. 

The  entire  duration  of  the  disease  depends  mainly  upon  the  length  of  the  first 
stage.  This  may  be  wholly  absent,  or  may  be  brief,  or  may  occupy  several  weeks. 
The  duration  of  the  second  stage,  reckoning  from  the  occurrence  of  grave  cere- 
bral symptoms,  is  generally  only  a  few  days  (two  to  four),  rarely  a  week.  The 
termination  is  almost  invariably  fatal.  In  a  few  cases  recovery  has  been  ob- 
served. 

The  diagnosis  can  not  be  made  till  the  second  stage.  The  symptoms  of  the 
first  stage  are  indistinguishable  from  those  of  simple  catarrhal  jaundice.  "With 
the  development  of  the  grave  symptoms  all  doubt  usually  vanishes.  The  general 
course  of  the  disease,  the  deep  jaundice,  the  cerebral  disturbances,  the  cutaneous 
ecchymoses,  and  the  character  of  the  urine,  form  a  clinical  picture  resembling  no 
other  disease.  The  only  cases  where  there  can  be  any  uncertainty  about  the  diag- 
nosis are  the  exceptional  ones  in  which  there  is  no  jaundice.  It  is  of  practical 
importance  to  distinguish  this  disease  from  acute  phosphorus  poisoning  {q.  v.^. 
The  differential  diagnosis  is  to  be  made  from  the  history  of  the  case  and  from 
the  following  factors : 

Acute  Yellow  Atrophy  of  the  Liver  Phosphorus  Poisoxixg 

1.  Prodromes  are  usually  present,  but  1.  Prodromes  are  almost  always  present. 
may  be  absent. 

2.  Jaundice  develops  early,  sometimes  be-  2.  Jaundice  does  not  appear  until  rather 
comes  marked.  late,  and  it  may  be  slight  to  the  end. 

3.  Liver  seldom  enlarged,  becomes  atro-  3.  Liver  much  enlarged  until  death,  and 
phic  from  the  start ;  pain  in  hepatic  region  very  painful. 

not  the  rule. 

4.  Maniacal  delirium  very  frequent.  4.  Seldom  marked  delirium. 

5.  Not  infrequently  fever,  sometimes  5.  Not  infrequently  fever  is  absent 
high  fever.  throughout. 

6.  Leucine  and  tyrosine  often  found  in  6.  Leucine  and  tyrosine  found  in  urine 
the  lu'ine.  exceptionally. 

7.  Spleen  often  enlarged.  7.  Usually  no  enlargement  of  the  spleen. 

After  what  has  been  said,  we  need  hardly  add  that  treatment  is  unavailing. 
Usually  laxatives  are  employed,  particularly  calomel.  The  nervous  symptoms  are 
combated  by  an  ice-cap  and  baths  and  narcotics ;  the  vomiting,  by  opium  and  bits 
of  ice;  and  the  cardiac  weakness,  by  stimulants. 


PEENICIOUS   JAUNDICE.    CHOL^MIA   AND  ACHOLIA        569 


APPENDIX 

PERNICIOUS  JAUNDICE.      CHOL.«MIA   AND   ACHOLIA 

Reference  lias  been  repeatedly  made  in  the  preceding  chapters  to  the  possibil- 
ity of  the  sudden  supervention  of  grave  nervous  derangements  in  the  course  of 
various  hepatic  diseases.  These  nervous  symptoms  resemble  one  another  so  much 
in  the  different  instances  of  their  occurrence  that  we  are  forced  to  believe  them 
always  due  to  the  same  cause. 

These  symptoms  are  relatively  most  frequent  when  there  is  chronic  biliary 
retention.  Whether  this  retention  be  the  result,  for  example,  of  obstruction  of  the 
common  or  the  hepatic  duct,  or  of  stenosis  of  the  biliary  passages  from  a  carci- 
noma involving  the  opening  of  the  common  duct  into  the  duodenum  or  that  duct 
itself,  the  patient  may  quite  suddenly  fall  into  a  condition  which  in  many  respects 
corresponds  to  the  second  stage  of  acute  yellow  atrophy  just  described.  Grave 
cerebral  disturbances  declare  themselves,  with  delirium,  convulsions,  and  coma. 
There  are  haemorrhages  into  the  skin  and  into  the  mucous  membranes,  and  in  a 
few  days  the  patient  dies.  Usually  the  end  is  attended  with  high  fever.  We  have 
ourselves  seen  a  temperature  of  107.4°  (41.9°  C.)  in  a  case  of  cancer  at  the  duo- 
denal extremity  of  the  common  duct.  It  is  this  group  of  symptoms  which  is  usu- 
ally termed  pernicious  jaundice;  but  almost  precisely  similar  phenomena  may 
suddenly  appear  in  hepatic  cirrhosis,  when  there  is  no  great  degree  of  jaundice, 
if  any. 

Exactly  what  produces  these  grave  results  in  acute  yellow  atrophy  and  the 
other  disorders  just  enumerated,  we  are  not  certain.  In  the  main  three  theories 
have  been  propounded  in  explanation.  The  first  theory,  the  latest  champion  of 
which  is  Leyden,  attributes  pernicious  jaundice  to  cholsemia — that  is,  to  the  accu- 
mulation in  the  blood  of  the  constituents  of  bile,  and  in  particular  of  the  biliary 
acids,  as  a  result  of  absorption.  This  accumulation,  it  is  said,  is  promoted  by  the 
paralyzing  effect  of  the  jaundice  upon  the  activity  of  the  kidneys.  Opposed  to 
this  theory  is  the  fact  that  these  same  symptoms  may  occur  when  there  is  no 
marked  hepatogenous  jaundice. 

Bouchard  and  other  French  physicians  ascribe  to  the  liver  the  function  of 
rendering  harmless  the  products  of  the  decay  of  albuminous  matters  developing 
in  the  intestine,  which  may  be  absorbed  and  enter  the  circulation.  Destruction  of 
the  hepatic  cells  would  consequently  lead  to  auto-intoxication  with  these  intes- 
tinal ptomaines.    In  Germany  this  doctrine  has  gained  few  adherents. 

The  view  which  we  are  most  inclined  to  accept  is  that  of  Frerichs.  He  has 
given  to  the  group  of  symptoms  under  discussion  the  name  of  acholia.  These 
symptoms  he  ascribes  to  the  pernicious  influence  of  those  substances  which  under 
normal  conditions  are  manufactured  by  the  liver  into  bile,  but  which  in  such  cases 
accumulate  in  the  blood  and  the  tissues.  As  Frerichs  himself  has  said,  and  we 
believe  very  justly,  this  view  should  be  extended  to  include  all  other  metabolic 
functions  of  the  liver,  and  especially  the  production  of  urea.  There  is  no  doubt 
that  the  processes  of  metamorphosis  are  very  active  in  the  liver.  That  these 
should  be  incomplete  when  there  is  a  severe  anatomical  lesion  of  the  liver,  or 
when  there  is  persistent  biliary  obstruction,  is  very  likely,  and  this  limitation  of 
activity  might  occasion  an  accumulation  of  all  sorts  of  material  in  the  blood. 
We  may,  therefore,  regard  acholia,  using  the  word  as  Frerichs  does,  as  entirely 
analogous  to  uraemia,  which  latter  appears  not  only  in  diseases  of  the  kidney  but 
also  when  the  ureters  are  obstructed.  In  this  sense  the  name  cholaemia  would 
be  preferable  to  the  term  acholia,  to  represent  a  condition  analogous  to  uraemia — 
taking  the  word  cholaBmia  to  mean  the  intoxication  of  the  blood  with  all  sorts  of 


570  DISEASES    OF   THE   DIGESTIVE    OEGANS 

substances  due  to  the  imperfect  metamorphosis  going  on  in  the  liver,  and  not,  as 
Leyden  formerly  held,  the  saturation  of  the  blood  with  the  completely  formed 
components  of  the  bile. 

The  termination  of  cholasmia  or  acholia  is  almost  always  unfavorable.  In 
cases  of  this  kind  there  is  usually  marked  fatty  degeneration  of  the  hepatic  par- 
enchyma to  be  found  post-mortem,  as  the  anatomical  expression  of  its  suspended 
function. 


CHAPTEE  VIII 

ICTERUS    NEOITATORUM 

{Jaundice  of  the  New-horn) 

Frequently  the  normal  red  color  of  the  skin  in  children  changes  on  the  sec- 
ond, third,  or  fourth  day  after  birth  to  a  distinctly  yellow,  jaundiced  hue.  The 
yellow  tinge  is  deeper  on  the  face  and  trunk  than  on  the  extremities.  There  are 
no  special  digestive  or  constitutional  disturbances.  Still  it  may  be  taken  for  the 
rule  that  weaklings  and  premature  infants  more  often  present  this  jaundice  than 
do  vigorous  babes.  The  abnormal  hue  is  almost  certain  to  vanish  in  a  week  or 
two,  and  leave  no  sequelae.  The  termination  is  unfavorable  in  those  instances 
alone  where  there  is  some  special  complication,  not  directly  connected  with  the 
jaundice  as  such. 

The  aetiology  is  a  disputed  matter.  A  large  number  of  theories  of  all  sorts 
have  been  set  up,  no  one  of  which  to  this  day  has  gained  universal  acceptance. 
Formerly  there  was  considerable  tendency  to  regard  the  jaundice  as  hematoge- 
nous— that  is,  as  due  to  the  transformation  of  the  pigment  of  broken-down  blood- 
corpuscles  into  bile-pigment.  Points  which  seemed  to  support  this  view  are  the 
light  (not  jaundiced)  color  of  the  urine  and  the  yellow  color  of  the  stools  (from 
bile).  But  more  accurate  examination  has  shown  that  the  urine  does  contain 
biliary  pigment,  as  do  also  the  kidneys  of  such  infants  as  happen  to  die  during 
the  existence  of  the  jaundice;  and  the  biliary  acids  have  been  clearly  shown  to 
be  present  in  the  serous  transudations.  It  is  therefore  assumed  at  present  by 
most  authors  that  icterus  neonatorum  is  hepatogenous;  but  how  the  biliary 
Tetention  and  consequent  absorption  are  caused  we  do  not  know.  Perhaps  the  bile 
is  not  ejected  properly,  from  weakness,  or  the  ducts  may  be  narrow,  or  temporarily 
plugged  by  desquamated  epithelium.  Birch-Hirschfeld  has  called  attention  to 
the  fact  that  after  birth  there  is  a  tendency  to  considerable  passive  congestion  of 
the  liver,  with  resultant  cedema  of  Glisson's  capsule  and  pressure  upon  the  inter- 
lobular bile-ducts.  Probably  more  importance,  however,  attaches  to  a  circum- 
stance which  Hofmeier  has  noted,  that  in  the  first  days  after  birth  many  red  cor- 
puscles are  disintegrated,  and  consequently  there  is  a  comparatively  large  secre- 
tion of  bile.  This  might  easily  lead  to  congestion  of  the  smallest  bile-ducts  and 
so  to  icterus;  but  it  should  be  said  this  view  has  its  opponents.  Quincke  has 
an  entirely  different  explanation  of  icterus  neonatorum.  He  goes  back  to  an  old 
theory  enunciated  by  Peter  Frank.  According  to  this,  the  jaundice  of  the  new- 
born is  due  to  the  absorption  by  the  intestine  of  a  large  amount  of  biliary  color- 
ing matter  from  the  meconium  in  the  large  intestine.  IsTow,  if  the  ductus  venosus 
remains  open  for  some  little  time  after  birth,  as  it  often  does,  this  biliary  pigment 
is  carried  not  to  the  liver,  but  by  means  of  the  vena  cava  inferior  directly  into 
the  systemic  circulation.  The  meconium  is  rich  in  bile  pigment,  and  moreover 
there  is  an  abundant  secretion  of  biliary  coloring  matter  in  the  new-born,  and 
in  them  bilirubine  is  not  changed  into  urobiline  in  the  intestine,  and  finally  the 


SYPHILIS    OF   THE   LIVEE  571 

renal  secretion  of  the  new-born  is  at  first  very  scanty.     Consequently,  the  absorp- 
tion of  the  bile-pigment  from  the  intestine  results  in  jaundice. 

It  is  well  to  mention  in  conclusion  that  in  very  rare  instances  there  is  complete 
congenital  stenosis,  or  even  entire  absence,  of  the  larger  bile-ducts.  Then  deep 
jaundice  comes  on  soon  after  birth,  and  is  persistent.  The  children  become  ex- 
tremely emaciated,  and,  after  a  few  weeks,  inevitably  perish. 


CHAPTER   IX 
SYPHILIS    OF    THE    LIVER 

.ffitiology  and  Pathology. — Syphilitic  disease  of  the  liver  occurs  both  when 
the  syphilis  is  acquired  and  when  it  is  congenital.  Congenital  syphilitic  disease 
of  the  liver  may  be  diffuse  or  localized,  and  it  causes  a  cellular  infiltration  in 
either  case.  If  the  changes  are  extensive,  the  organ  is  hard  and  considerably 
enlarged;  or,  if  the  newly  formed  connective  tissue  has  undergone  contraction, 
the  liver  is  smaller  than  normal,  and  its  surface  is  uneven.  In  some  cases  of 
hereditary  syphilis,  distinct  gummata  of  considerable  size  have  been  observed. 

In  acquired  syphilis,  hepatic  disease  is  one  of  the  so-called  tertiary  symptoms, 
and  does  not  usually  develop,  at  least  to  any  great  extent,  until  several  years  after 
infection.  Indeed,  it  may  be  a  very  late  result.  It  may  take  the  form  either  of 
a  diffuse  syphilitic  hepatitis,  or  of  circumscribed  gummata  or  syphilomata.  The 
diffuse  hepatatis  does  not  present  essentially  different  anatomical  appearances 
from  those  of  ordinary  cirrhosis,  although  in  syphilis  the  changes  are  seldom  so 
uniformly  distributed  throughout  the  organ.  The  gummata  are  the  most  char- 
acteristic, and  the  most  important  clinically.  They  may  form  separate  tumors 
the  size  of  an  apple  or  even  larger.  The  convex  surface  of  the  organ,  particularly 
that  portion  near  the  suspensory  ligament,  seems  to  be  a  favorite  location  for  the 
new  growth.  The  same  is  true  of  the  porta  hepatis,  where  Glisson's  capsule  enters 
the  liver.  At  the  autopsy  the  gummata  have  in  most  cases  already  begun  to 
undergo  contraction.  If  so,  the  liver  is  usually  smaller  than  normal,  and  trav- 
ersed in  various  directions  by  deep  furrows,  which  divide  it  into  lobes.  These 
furrows  are  due  to  firm  cicatricial  bands,  among  the  fibers  of  which  we  may 
sometimes  find  necrotic  and  cheesy  vestiges  of  the  gumma  proper.  Often  there  is 
evident  syphilitic  endarteritis  in  the  smaller  and  sometimes  also  in  the  larger 
branches  of  the  hepatic  artery  and  portal  vein. 

Clinical  History. — Circumscribed  syphilitic  changes  in  the  liver  often  give  rise 
to  no  symptoms  whatever.  It  is  only  when  the  disease  comes  to  disturb  the  portal 
circulation  that  a  series  of  symptoms  result,  which,  for  evident  reasons,  may  be 
analogous  in  all  essential  points  to  the  effects  of  ordinary  cirrhosis.  Whenever 
the  syphilitic  growths  contract  so  as  to  obliterate  a  large'  number  of  branches  of 
the  portal  vein,  or  whenever  a  gumma  happens  to  be  so  situated  as  to  compress 
the  trunk  of  the  portal  vein  itself,  then  the  well-known  results  of  portal  obstruc- 
tion are  inevitable,  the  chief  being  ascites  and  enlargement  of  the  spleen.  The 
disturbance  of  circulation  often  gives  rise  also  to  anorexia  and  digestive  disorders. 
Experience  shows  jaundice  to  be  rare  in  hepatic  syphilis,  but  it  may  appear  when 
the  lesions  involve  the  larger  bile-ducts  or  a  considerable  number  of  the  smaller 
biliary  passages. 

On  physical  examination,  the  results  vary  according  to  the  form  and  the  stage 
of  the  disorder.  Sometimes  the  larger  gummata  may  be  plainly  felt  through  the 
abdominal  walls,  usually  as  flattened  hemispheres.    Frequently,  also,  we  can  feel 


572  DISEASES    OF   THE   DIGESTIVE    OEGAISTS 

the  edge  of  tlie  enlarged  organ,  and  can  detect  that  the  edge  is  less  sharp  than  nor- 
mal. In  other  instances  the  separate  elevations  and  prominences  can  be  made 
out.     The  area  of  dullness  on  percussion  of  course  varies  in  different  cases. 

It  deserves  mention  that  hepatic  syphilis  quite  often  causes  severe  pain,  some- 
times over  the  entire  region  of  the  liver  and  sometimes  in  just  one  spot.  Pain  is 
by  no  means  felt  in  every  case.  With  the  pain  there  may  be  great  tenderness 
on  pressure. 

The  course  of  the  disease  is  usually  tedious,  and  it  may  occupy  many  years. 
Probably,  too,  lesions  exist  in  many  cases  long  before  there  are  any  symptoms. 
Just  as  in  cirrhosis,  ascites  is  usually  the  first  thing  to  attract  the  patient's  atten- 
tion. Improvement  and  temporary  arrest  of  the  disease  are  more  frequent  than 
in  ordinary  cirrhosis.  Still,  in  most  cases,  if  the  lesions  are  at  all  extensive, 
the  termination  is  unfavorable. 

The  diagnosis  is  not  always  easy.  Usually  the  objective  changes  in  the  liver, 
the  ascites,  and  the  enlarged  spleen,  indicate  hepatic  trouble,  but  we  are  often 
unable  to  determine  just  what  the  trouble  is,  Naturally,  the  setiological  factors 
are  of  great  importance.  In  a  toper  we  would  think  rather  of  the  common  form 
of  cirrhosis.  If  there  is  a  syphilitic  history,  or  if  we  find  scars  in  the  throat, 
irregularities  in  the  surface  of  the  bones,  or  other  signs  of  a  specific  dyscrasia, 
we  would  naturally  ascribe  the  hepatic  disorder  to  the  same  cause.  As  to  special 
signs,  if  the  prominences  on  the  liver  are  rather  large  in  contrast  to  the  smaller 
granulations  of  common  cirrhosis,  syphilis  is  somewhat  more  probable.  Severe 
pain  in  the  right  hyiiochondrium  also  suggests  syphilis  rather  than  cirrhosis.  It 
should  also  be  considered  that  the  course  of  hepatic  syphilis  is  usually  much  more 
protracted  than  that  of  ordinary  hepatic  cirrhosis. 

Treatment. — Whether  we  feel  certain  that  syphilitic  hepatitis  exists,  or  merely 
suspect  it,  specific  treatment  should  be  tried.  Mercury  and  potassic  iodide  should 
both  be  given,  but  probably  the  iodide  is  the  more  valuable  of  the  two.  These 
remedies  can  be  successful  only  when  the  gummata  are  still  in  process  of  forma- 
tion. Our  therapeutic  efforts  produce  no  impression  upon  the  cicatricial  bands, 
the  contraction  of  which  is  the  main  cause  of  derangement.  Indeed,  even  the 
absorption  of  gummata  may  not  always  have  a  favorable  infiuence  upon  the 
patient,  because  of  the  mechanical  disturbance  due  to  the  consequent  cicatricial 
change.  Hence,  in  general,  the  results  of  antisyphilitic  treatment  are  not  very 
favorable. 

For  symptomatic  treatment,  the  reader  is  referred  to  the  chapter  on  cirrhosis 
of  the  liver. 


CHAPTEE   X 
CANCER    OF    THE    LIVER    AND    BILE-DUCTS 

etiology  and  Pathology. — Primary  cancer  of  the  liver  is  very  rare,  but  sec- 
ondary or  metastatic  cancer  of  this  organ  is  met  with  often.  The  chief  explana- 
tion of  this  latter  fact  is  the  slowness  of  the  blood-current  in  the  liver,  which 
favors  the  deposition  of  the  cancerous  germs  suspended  in  the  blood. 

Secondary  hepatic  cancer  may  be  a  sequel  to  primary  cancer  of  any  organ.  It 
is  most  often  seen,  however,  when  the  primary  growth  lies  within  the  portal  sys- 
tem, in  the  stomach,  intestines,  rectum,  03Sophagus,  or  pancreas.  In  some  in- 
stances the  projection  of  the  primary  growth  into  the  lumen  of  a  branch  of  the 
portal  vein  has  been  directly  demonstrated,  thus  furnishing  an  obvious  source  for 
metastasis.    The  secondary  cancers  in  the  liver  may  be  very  numerous.    They  are 


CANCER   OF   THE   LIVER   AXD   BILE-DUCTS  573 

found  both  within  the  organ  and  upon  its  surface.  If  superficial,  they  form  flat- 
tened protuberances,  which  are  often  dimpled  in  the  middle.  If  the  new  growth 
is  extensive,  the  liver  may  be  greatly  enlarged,  so  as  to  occupy  a  great  part  of  the 
abdominal  cavity. 

As  we  have  said,  primary  cancer  of  the  liver  is  very  imusual.  It  may  occur 
either  in  the  form  of  separate  large  nodules,  or  as  a  more  diffuse  cancerous  infil- 
tration pervading  the  greater  part  of  the  organ.  Histologically  considered,  the 
primary  growths  are  of  cylindrical-cell  carcinoma,  apparently  originating  from 
the  epithelium  of  the  minute  bile-ducts,  but  also,  according  to  some  authors,  some- 
times starting  from  the  cells  of  the  parenchyma. 

Primary  cancer  of  the  larger  bile-ducts  is  of  more  frequent  occurrence  than 
genuine  primary  hepatic  cancer,  and  therefore  it  is  of  more  importance  clinically. 
The  gall-bladder  may  also  be  the  seat  of  primary  carcinoma.  Erom  these  sources 
may  proceed  abundant  metastatic  growths  in  the  liver  itself. 

As  to  the  aetiology  of  hepatic  cancer  we  can  be  brief.  The  disease  is  most  fre- 
quent in  advanced  life,  from  forty  to  sixty,  following  in  this  the  general  rule  for 
cancer.  Of  special  exciting  causes,  there  is  only  one  to  be  mentioned — that  is, 
biliary  calculi.  As  we  have  already  remarked  (see  page  551),  the  formation  of 
cancer  subsequent  to  cholelithiasis  has  been  observed  so  many  times  that  mere 
coincidence  is  out  of  the  question. 

Clinical  History. — Diagnosis. — Many  small  nodules  of  cancer,  as  well  as  large 
masses  which  are  favorably  situated,  may  exist  in  the  liver  without  exciting  any 
symptoms.  If  there  is  an  undoubted  primary  cancer  in  another  organ,  such  as 
the  stomach,  we  must  always  remember  the  possibility  of  metastatic  growths  in 
the  liver;  but  they  can  not  be  proved  to  exist,  unless  they  alter  appreciably  the 
size  or  shape  of  the  organ.  Sometimes  their  existence  may  be  inferred,  when  we 
observe  either  ascites  and  enlargement  of  the  spleen  from  pressure  on  the  portal 
vein,  or  jaundice  from  pressure  on  the  bile-ducts. 

On  palpation,  we  are  often  able  to  make  out  plainly  one  or  more  tumors  in 
hepatic  cancer.  These  tumors  are  in  the  region  of  the  liver,  and  they  are  directly 
connected  with  it,  as  we  can  prove  by  marking  out  its  limits  by  percussion  and 
palpation.  Another  characterstic  sign  is  that  almost  all  hepatic  tumors  can  be 
felt  to  move  with  respiration,  on  account  of  the  inspiratory  depression  of  the  dia- 
phragm pushing  down  the  liver  and  all  that  is  joined  to  it.  Percussion  over  a 
hepatic  tumor  almost  invariably  gives  flatness,  in  contrast  to  the  muffled  tym- 
panitic resonance  of  many  gastric  tumors. 

The  most  characteristic  condition  is  not  a  very  rare  one ;  in  it  the  liver  is  the 
seat  of  a  very  large  number  of  cancerous  nodules.  In  such  cases  the  organ  is 
usually  much  enlarged.  Often  we  can  detect  by  mere  inspection  a  great,  irregular 
prominence  in  the  hepatic  region,  pressing  forward  the  flabby,  atrophied  walls  of 
the  abdomen,  reaching  down  to  the  level  of  the  umbilicus,  or  even  lower,  and 
moving  with  respiration.  On  palpation,  we  can  feel  most  of  the  anterior  surface 
of  the  liver,  and  the  separate  cancerous  nodules  scattered  over  it.  These  usually 
are  as  large  as  walnuts,  or  even  apples,  and  they  are  often  umbilicated.  The 
lower  or  anterior  margin  of  the  liver  can  often  be  made  out  plainly,  and  it  also  is 
often  the  seat  of  nodules ;  and  we  can  sometimes  feel  nodules  on  the  lower  surface 
of  the  organ. 

The  other  clinical  phenomena  in  hepatic  cancer  have  several  causes :  (1)  The 
primary  disease,  such  as  cancer  of  the  stomach;  (2)  the  general  cancerous  ca- 
chexia, as  shown  by  languor,  emaciation,  and  possibly  a  slight  oedema  of  the 
ankles;  and  (3)  the  possible  compression  of  the  blood-vessels  or  bile-ducts.  This 
compression  is  not  infrequent,  and  produces  a  moderate  or  even  a  large  ascitic 
effusion.  Even  in  these  instances  the  spleen  is  seldom  much  enlarged  as  a  result 
of  the  passive  congestion,  because  the  universal  emaciation  and  anaemia  counter- 


574  DISEASES    OF   THE   DIGESTIVE   OEGANS 

act  the  tendency  to  increase  in  size.  Jaundice  is  relatively  more  frequent  in 
cancer  of  the  liver  than  is  ascites.  It  is  caused  by  compression  either  of  the 
hepatic  duct  or  of  the  minuter  bile-ducts.  On  the  other  hand,  however,  we  can 
easily  see  that  hepatic  cancer  may  exist  without  producing  either  icterus  or 
ascites. 

The  differential  diagnosis  of  hepatic  cancer  from  cancer  in  other  organs  is 
sometimes  extremely  difficult.  This  is  particularly  true  of  pyloric  cancer,  and 
especially  so  when  the  pylorus  has  become  adherent  to  the  liver,  which  often  is  the 
case.  Cancers  of  the  omentum  and  of  the  colon  sometimes  simulate  hepatic 
cancer,  but  they  seldom  move  so  decidedly  in  respiration  as  do  hepatic  tumors. 
Given  a  new  growth  in  the  liver,  it  is  usually  comparatively  easy  to  distinguish 
between  carcinoma  and  other  tumors.  In  case  of  syphilitic  new  growths,  we  have 
to  consider  the  previous  history  and  other  signs  of  syphilis,  also  the  eventual  con- 
tractions and  diminution  in  size  of  the  liver,  the  usually  longer  duration  of  the 
disease,  and  the  general  condition  of  the  patient.  Echinococci  have,  as  a  rule,  a 
much  more  regular  shape,  like  a  flattened  ball;  they  seldom  occasion  marked 
cachexia,  and  also  have  a  much  longer  clinical  history.  Large  abscesses  are  very 
rare  in  our  climate  and  they  can  usually  be  recognized  by  special  objective  condi- 
tions. Moreover,  they  cause  fever  (rigors),  which  is  exceptional  in  carcinoma. 
Other  primary  tumors  of  the  liver,  such  as  sarcoma  and  adenoma,  are  very  rare, 
and  therefore  of  no  great  clinical  importance.  There  is,  however,  one  rare  but  ira- 
portant  tumor  of  the  liver  which  we  must  mention — ^viz.,  melanotic  sarcoma,  which 
may  appear  as  a  secondary  growth  in  the  liver.  It  may  be  of  enormous  extent, 
either  diffuse  or  nodular,  and  secondary  to  melanotic  sarcoma  of  the  choroid  or 
of  the  skin. 

When  we  have  decided  that  cancer  of  the  liver  is  present,  the  question  arises. 
Is  it  primary  or  secondary  ?  In  the  first  place,  primary  cancer  here  is  so  rare  that 
the  probabilities  are  in  favor  of  a  secondary  growth.  Not  infrequently  the 
primary  tumor  can  not  be  detected  during  life.  Thus  a  small  cancer  of  the 
stomach,  or  a  flat  oesophageal  cancer,  or  carcinoma  of  the  pancreas,  are  all  easily 
overlooked.  Cancer  in  the  rectum  may  be  detected  by  digital  examination.  If 
we  find  many  nodules  in  the  liver  and  no  primary  trouble  elsewhere,  then  there 
comes  the  possibility  that  there  is  primary  cancer  in  the  gall-bladder  or  the  bile- 
ducts.  In  rare  instances  palpation  may  discover  the  gall-bladder  in  a  state  of 
cancerous  degeneration  close  underneath  the  liver ;  but  usually  the  viscus  will  be 
small  and  contracted,  and  the  flat  and  ulcerating  growth  is  not  noticeable,  except 
from  the  inside.  It  is  particularly  in  those  cases  of  hepatic  cancer  in  which  there 
is  at  an  early  period  great  and  persistent  icterus,  without  evidence  of  carcinoma 
in  any  other  organ,  that  we  should  be  most  apt  to  think  of  primary  cancer  of 
the  bile-ducts. 

The  duration  of  hepatic  cancer  is  usually  not  prolonged.  The  first  decided 
evidences  of  its  existence  no  sooner  present  themselves  than  marasmus  and  ca- 
chexia rapidly  develop.  The  fatal  end  comes  in  a  few  months,  or  at  latest  within 
a  year. 

The  prognosis  is  hopeless.  Treatment  can  avail  only  to  alleviate  somewhat 
the  patient's  sufferings. 


ECHINOCOCCUS    OF   THE   LIVER 


5T5 


CHAPTER  XI 
ECHINOCOCCTJS    OF    THE    LIVER 

Natural  History  and  Pathology. — Inasmuch  as  it  is  the  liver  which  suffers 
most  frequently  from  invasions  of  the  eehinococcus,  we  will  here  state  the  main 
general  points  relative  to  the  troubles  produced  by  this  parasite. 

The  tcenia  eehinococcus  (see  Fig.  64)  is  a  small  tape-worm  about  four  milli- 
metres long,  and  composed  of  four  joints.  It  inhabits  the  intestinal  canal  of  the 
dog.  The  head  is  small  and  bears  a  beak  which  is  provided  with  some  thirty  to 
forty  booklets,  arranged  in  two  rows.  Behind  the  circle  of  booklets  are  four 
suckers.  The  last  joint  of  the  taenia  is  by  far  the  largest, 
and  contains  some  five  hundred  eggs.  Man  is  infected  by 
ingestion  of  the  eggs.  The  great  frequency  of  the  eehino- 
coccus in  Iceland  is  explained  by  the  close  intimacy  of  the 
Icelanders  with  their  dogs.  In  Germany  the  eehinococcus 
is  most  frequent  in  Mecklenburg  and  Pomerania. 

If  a  human  being  has  become  infected,  the  embryo 
pierces  the  intestinal  wall,  and  is  carried  with  the  blood- 
current  or  the  lymph-current  to  some  remote  organ.  Most 
of  the  eggs  no  doubt  are  destroyed  in  the  stomach,  as  may 
be  inferred  from  the  fact  that  multiple  echinococci  are 
much  less  frequent  than  solitary  individuals.  In  a  great 
majority  of  cases  the  embryo  passes  through  a  branch  of  the 
portal  vein  into  the  liver  and  there  fastens  itself ;  but  the 
eehinococcus  may  be  developed  in  other  organs — including 
the  lungs  {vide  page  278),  the  bones,  the  brain,  the  kidneys, 
and  the  heart.  A  hydatid  cyst  develops  from  the  embryo, 
and  is  filled  with  a  non-albuminous  fluid.  The  cyst  is  com- 
posed of  an  external  cuticle  of  laminated  structure,  and 
an  inner,  parenchymatous  layer,  which  contains  muscular 
fibers  and  blood-vessels.  Surrounding  the  cyst,  as  it  lies  in 
the  infested  organ,  there  is  gradually  developed  a  thick 
capsule  of  connective  tissue. 

After  the  cyst  has  continued  its  growth  for  some  four 
to  six  months,  being  now  about  the  size  of  a  walnut,  there 
are  generated  upon  the  inner  surface  of  the  capsule,  from 
the  parenchymatous  layer,  so-called  breeding  capsules,  con- 
taining numbers  of  echinococcus-heads,  or  "  scolicesJ' 
Each  scolex  has  four  suckers  and  a  circlet  of  hooks.  It 
can  draw  itself  into  the  breeding  capsule  and  also  produce  a  prominence  upon  the 
outer  surface  of  the  latter  (see  Figs.  65,  66,  and  67).  The  number  of  new-formed 
scolices  in  an  eehinococcus  is  very  great.  The  sac  grows  very  slowly  up  to  about 
the  size  of  a  fist,  or  even  larger;  its  wall  has  a  pale,  yellow  color,  is  transparent, 
and  displays  an  extremely  characteristic  laminated  structure.  The  firmly  at- 
tached breeding  capsules  are  visible  from  the  outside  through  the  walls,  as  minute 
points. 

The  primary  cyst  often  gives  rise  to  secondary  "  daughter  vesicles,"  and  these 
to  "granddaughter  vesicles."  Some  of  these  are  formed  in  the  cuticle,  others 
from  the  breeding  capsules.  In  man  they  generally  grow  inward — that  is,  are 
endogenous  (eehinococcus  hydatidosus) — and  finally  become  detached.  Hun- 
dreds of  them  may  sometimes  be  found  free  in  the  liquid  contents  of  the  cyst. 
In  animals  the  daughter  vesicles  are  more  often  exogenous  (eehinococcus  veieri- 


',:n 


Fig.  64.— (From  Heller.J 
Taenia  eehinococcus, 
enlarged.  Above,  at 
the  right,  eehinococ- 
cus, of  natural  size. 


576 


DISEASES    OE   THE   DIGESTIVE    OEGANS 


norum  seu  granulosus).  A  peculiar  kind  of  eehinococcus,  which  was  formerly 
regarded  as  a  kind  of  new  growth,  is  that  called  by  Virchow  echinocoocus  multi- 
locularis.    This  is  a  resistant  tumor  containing  much  connective  tissue,  and  per- 


FiG.  65.  Fig.  66.  Fig.  67. 

Figs.  65  and  66.— (From  Heller.)    Eehinococcus  scolices,  free,  drawn  in  and  turned  outward. 
Fig.  67.— Eehinococcus  booklets. 

meated  with  numerous  small  alveoli.  The  gelatinous  contents  of  the  alveoli  con- 
sist of  eehinococcus  vesicles.  The  growth  probably  originates  from  a  single  germ, 
which  by  persistent  exogenous  proliferation  invades  the  lymph-vessels  (perhaps 
also  the  blood-vessels  and  the  bile-ducts). 

The  growth  of  a  hydatid  cyst  is  very  slow,  and  it  may  continue  for  years.  At 
last,  however,  the  eehinococcus  dies.  The  cyst  then  undergoes  considerable 
though  gradual  contraction,  and  both  walls  and  contents  become  fatty-degener- 
ated and  calcified.  In  the  mortar-like  detritus  it  is  usually  possible  to  find  some 
characteristic  booklets. 

Clinical  Symptoms. — As  long  as  the  cyst  in  the  liver  retains  moderate  dimen- 
sions, there  is  usually  no  discomfort.  Frequently  the  cysts  perish  and  become 
calcified,  without  having  ever  attracted  attention,  and  are  found  post-mortem 
merely  by  accident. 

If  the  cyst  becomes  very  large,  it  causes  a  sensation  of  pressure  and  pain  in  the 
hepatic  region.  In  rare  instances,  unusually  large  cysts,  if  situated  on  the  convex 
surface  of  the  liver,  may  crowd  up  the  diaphragm  so  as  to  compress  the  lower 
portions  of  the  lung  and  induce  dyspnoea.  In  such  cases  we  find  on  the  anterior 
or  posterior  wall  of  the  thorax  an  abnormal  protuberance,  with  dullness  and 
diminished  respiratory  murmur.  If  a  large  eehinococcus  grows  downward  into 
the  abdominal  cavity  it  occasions  pressure,  tension,  and  pain  in  the  abdomen. 
Compression  of  the  portal  vein  may  lead  to  ascites,  and  compression  of  the  bile 
duct,  in  rare  cases,  to  jaundice.  The  tvmior  can  usually  be  made  out  with  ease 
by  inspection  and  palpation.  It  is  approximately  hemispherical,  smooth,  not 
tender,  and  feels  rather  firm  and  elastic.  There  is  often  a  sense  of  fluctuation, 
while  the  so-called  hydatid  thrill — to  be  elicited  by  quick  pushes  with  the  flat  of 
the  hand — is  recognized  distinctly  in  but  few  cases. 

The  condition  may  be  complicated  (1)  by  rupture  of  the  echinocoecus-sac 
into  neighboring  parts,  and  (2)  by  secondary  suppuration.  Both  occurrences 
may  be  apparently  spontaneous,  or  the  result  of  traumatic  influences. 

Of  the  possible  directions  in  which  rupture  may  take  place,  penetration  of  the 
pleural  cavity  should  be  particularly  mentioned.  It  usually  results  in  an  acute 
empyema.  Here  we  have  to  do  partly  with  secondary  infection  occasioned  by 
pyogenic  bacteria,  and  partly  also,  as  it  seems,  with  the  influence  of  toxic  sub- 
stances (toxalbumens)  which  are  present  in  the  eehinococcus  fluid  {vide  infra). 
Penetration  into  the  lungs  with  rupture  of  the  echinococcus-sac  leads  to  severe 
pulmonary  symptoms.  The  patient  may  cough  up  constitutents  of  the  bile  and 
small  eehinococcus  vesicles,  or  portions  of  the  same.  Perforation  into  the  abdom- 
inal cavity  occasions  purulent  peritonitis.    If  viable  daughter-vesicles  are  set  free 


ECHINOCOCCUS   OF   THE   LIVEE  577 

in  the  abdominal  cavity,  they  may  settle  on  some  fresh  spot  and  continue  to  grow. 
As  extreme  exceptions  are  to  be  mentioned  rupture  of  the  echinococcus-sac  into 
the  pericardium,  the  bile-ducts,  the  intestine,  the  vena  cava,  and  the  pelvis  of  the 
kidney. 

Suppuration  of  an  eehinococcus  in  the  liver  leads  to  the  clinical  symptoms  of 
hepatic  abscess — increasing  tenderness  and  fliictuation  of  the  tumor,  fever,  aggra- 
vation of  the  constitutional  symptoms,  etc.  Perforation  of  the  abscess  into 
neighboring  structures  may  occur,  in  the  same  way  as  above  mentioned.  Spon- 
taneous recovery  is  possible  but  infrequent.  In  general,  suppuration  of  an 
echinococcus-sac  is  a  dangerous  condition,  unless  there  is  surgical  interference. 

We  must  devote  a  few  words  to  eehinococcus  muUilocularis  of  the  liver.  As 
has  been  said,  the  tumor  in  this  case  is  large,  very  firm  and  hard,  and  with  a 
surface  which  is  either  smooth  or  rough.  Tenderness  on  pressure  is  exceptional. 
On  the  other  hand  there  is  a  feeling  of  painful  distention  in  the  hepatic  region. 
Comparatively  often  (H.  Vierordt)  there  is  jaundice,  which  may  be  extreme. 
The  spleen  is  usually  enlarged.  The  bodily  condition  is  fairly  good  for  a  long 
while,  but  later  marasmus  develops,  particularly  if  ascites  or  oedema  occurs. 
Secondary  suppuration  in  the  interior  of  the  tumor  also  leads  to  fever  and  rapid 
loss  of  strength.    The  disease  lasts  one  to  two  years,  sometimes  much  longer. 

Diagnosis. — The  diagnosis  of  eehinococcus  of  the  liver  depends  chiefly  upon 
the  demonstration  of  a  very  slowly  developing  tumor  in  the  liver,  hemispherical, 
fluctuating,  and  painless,  with  no  marked  influence  at  first  upon  the  general 
health.  If  the  patient  comes  froui  a  country  where  the  eehinococcus  is  particu- 
larly frequent,  of  course  this  renders  the  diagnosis  easier.  Formerly  it  was  the 
custom  to  aspirate  the  tumor  for  diagnostic  purposes.  In  this  way  we  can,  in 
many  cases,  obtain  from  the  interior  of  the  sac  a  light  yellow  non-albuminous 
fluid,  which  often  contains  sugar  and  succinic  acid;  and  in  it  sometimes,  but 
of  course  not  invariably,  are  found  upon  microscopic  examination  the  charac- 
teristic hooklets,  or  little  pieces  of  the  laminated  membrane.  Lately,  however, 
physicians  have  become  miich  more  cautious  about  puncturing  eehinococcus-cysts, 
because  the  procedure  is  sometimes  followed  by  symptoms  which  are  probably  due 
to  the  poisonous  influence  of  the  escaping  contents  of  the  cyst  (vide  supra). 
!N'ot  infrequently  after  puncture  there  occurs  urticaria  or  severe  toxic  symptoms, 
such  as  collapse,  vomiting,  dyspnoea,  diarrhoea,  chills,  and  epileptiform  attacks; 
and  these  may  even  prove  quickly  fatal,  although  occurrences  of  this  sort  are 
infrequent.  They  have  brought  great  discredit  upon  the  practice  of  aspiration 
for  diagnostic  purposes  in  case  of  eehinococcus. 

The  diagnosis  of  the  multilocular  eehinococcus  of  the  liver  is  always  very 
difficult.  If  made  at  all,  it  demands  a  careful  consideration  of  all  the  separate 
symptoms,  and  particularly  of  the  general  course  of  the  disease,  in  order  to  dis- 
tinguish the  condition  from  hepatic  carcinoma,  cirrhosis,  or  syphilis. 

Treatment. — Inasmuch  as  internal  remedies,  such  as  iodine  and  mercury,  are 
absolutely  useless,  the  only  treatment  of  eehinococcus  is  by  surgical  means.  In 
case  the  eehinococcus  tumor  causes  little  if  any  discomfort,  the  patient  is  usually 
loath  to  consent  to  an  operation,  but  it  should  be  recommended  in  all  cases,  for  it 
protects  the  patient  from  the  possibility  of  later  dangerous  developments,  and  in 
itself  is  no  grave  matter.  A  description  of  the  many  methods  of  surgical  treat- 
ment will  be  found  in  the  text-books  on  surgery. 


37 


578  DISEASES    OF    THE   DIGESTIVE    OEGANS 

CHAPTEE   XII 
CIRCULATORY    DISTURBANCES    IN    THE    LIVER 

1.  Hepatic  ansemia  is  seldom  extreme  except  in  cases  of  profound  general 
anaemia,  and  it  has  no  clinical  importance,  so  far  as  we  are  aware. 

2.  Passive  congestion  of  the  liver  is  of  frequent  occurrence  and  is  of  impor- 
tance. It  may  arise  in  any  disorder  which  disturbs  the  systemic  circulation.  It 
is  oftenest  seen  in  connection  with  heart  disease,  particularly  mitral  disease.  It 
also  follows  pulmonary  emphysema  and  chronic  processes  which  result  in  con- 
traction of  the  lungs.  The  liver  is  enlarged  and  engorged.  The  hepatic  veins 
being  situated  in  the  center  of  the  lobules,  this  central  portion  becomes  darkly 
pigmented,  while  the  periphery  of  the  lobules  seems  lighter  colored.  The  periph- 
eral cells  may  even  appear  distinctly  yellow,  from  a  fatty  infiltration  which  is  not 
infrequent.  In  this  way  the  cut  surface  comes  to  present  that  variegated  appear- 
ance which  has  led  to  the  name  of  "  nutmeg  liver."  If  the  venous  stasis  be  per- 
sistent, there  is  considerable  atrophy  of  the  hepatic  parenchyma,  involving  espe- 
cially the  cells  near  the  center  of  each  lobule.  Thus  the  liver  is  somewhat  re- 
duced in  size  in  spite  of  the  secondary  increase  of  connective  tissue,  and  its 
surface  may  become  slightly  granular.  This  is  the  "  atrophic  nutmeg  liver  "  or 
"  contracted  liver  due  to  passive  congestion." 

The  clinical  phenomena  are  chiefly  those  caused  by  the  hepatic  enlargement. 
If  chronic  cardiac  disease,  emphysema,  or  some  analogous  trouble  has  occasioned 
congestion  of  the  liver,  the  area  of  hepatic  dullness  is  increased,  and  frequently 
we  can  feel  the  edge  or  even  a  portion  of  the  anterior  surface.  In  well-developed 
cases  the  liver  reaches  a  hand's-breadth  or  more  below  the  ribs  on  the  right  side. 
If  there  is  also  tricuspid  regurgitation  (g.  v.),  the  liver  is  usually  much  en- 
larged and  can  be  felt  to  pulsate  distinctly  if  the  palm  of  the  hand  is  laid  upon  it. 
ISTot  infrequently  in  passive  congestion  of  the  liver  there  is  jaundice,  which  may 
be  slight  or  quite  well-marked.  This  is  perhaps  due  to  the  pressure  exerted  by  the 
distended  blood-vessels  upon  the  small  bile-ducts  in  the  liver,  and  perhaps  also  to 
the  secretion  of  a  particularly  viscid  bile  containing  less  water  than  normal,  and 
tending  to  stagnate.  As  we  have  already  mentioned,  the  peculiar  mixture  of 
jaundice  and  cyanosis  in  the  complexion  of  many  cardiac  patients  is  very  char- 
acteristic. The  secondary  cirrhosis  of  the  congested  liver  leads  to  ascites.  We 
may  suspect  this  condition  of  the  liver  in  all  cases  of  heart  disease  in  which 
ascites  is  particularly  well  marked,  in  comparison  with  the  slight  oedema  in  other 
portions  of  the  body. 

Quite  often  the  congestion,  if  great,  produces  subjective  disturbances.  There 
is  a  feeling  of  pressure  and  weight  in  the  hepatic  region ;  and  if  the  capsule  of  the 
organ  is  tightly  stretched,  there  may  be  actual  pain. 

The  prognosis  and  treatment  depend,  of  course,  upon  the  primary  disorder. 

3.  About  active  hypersemia  of  the  liver  we  have  little  definite  information. 
Formerly  there  was  a  great  deal  said  about  it,  as  one  of  the  conditions  in  "  ab- 
dominal plethora."  Active  hypersemia  is  most  frequently  assumed  to  exist  in 
case  of  those  who  are  good  livers  and  of  sedentary  habit.  In  such,  we  are  told, 
the  temporary  physiological  h3T)ercemia  which  attends  digestion  passes  on  into  a 
permanent  congestion  of  the  liver.  Thereby  the  organ  is  enlarged,  there  are  pain- 
ful sensations  in  the  right  hypochondriura,  digestive  disturbances,  and  occasional 
slight  jaundice.  The  abnormal  condition  just  described  is  certainly  often  met 
with  in  practice,  but  it  would  seem  hardly  possible  to  draw  a  clear  dividing-line 


ATEOPHY  AND  HYPERTEOPHY  OF  THE  LIVEE     579 

between  active  laypersemia  of  the  liver  and  other  disturbances  which  give  rise  to 
similar  symptoms.  Such  are  chronic  gastric  and  intestinal  catarrhs;  cardiac 
hypertrophy  and  functional  cardiac  derangement,  with  passive  congestion  of  the 
liver ;  fatty  liver ;  and  incipient  cirrhosis. 

A  prominent  factor  in  the  production  of  active  hypersemia  of  the  liver  is  also 
ascribed  to  the  ingestion  of  such  matters  as  are  said  to  "  irritate  "  the  liver,  like 
the  various  spices,  coffee,  and,  above  all,  alcohol. 

It  should  also  be  noted  that  the  liver  may  be  much  engorged  in  many  acute 
infectious  diseases,  particularly  in  pernicious  malarial  diseases  and  in  typhus  or 
typhoid  fever. 

It  is  also  maintained  that  the  hj^persemia  may  result  from  the  cessation  of 
haemorrhages  elsewhere,  such  as  the  catamenia  or  bleeding  from  haemorrhoids. 
The  facts  that  have  been  brought  forward  to  sustain  this  view  are  none  of  them 
conclusive.  We  will  mention  that  the  "menstrual  jaundice"  which  occasionally 
appears  when  the  menses  are  scanty  or  absent  has  been  referred  to  a  vicarious 
hyperagmia  of  the  liver. 

It  is,  of  course,  impossible  to  make  general  statements  about  the  course  and 
duration  of  active  hypersemia  of  the  liver.  The  treatment  of  the  first  variety 
mentioned — namely,  that  arising  from  an  improper  mode  of  life — demands  care- 
ful regulation  of  the  diet,  abundant  exercise  in  the  open  air,  such  as  horseback- 
riding,  and  laxatives.  We  may  order  rhubarb,  aloes,  or  a  course  of  the  waters  at 
Carlsbad,  Marienbad,  Kissingen,  or  Homburg. 


CHAPTEE   XIII 
ATROPHY,    HYPERTROPHY,    AND    DEGENERATIONS    OF    THE    LIVER 

1.  Simple  Atrophy  of  the  Liver. — Simple  atrophy  is  not  of  rare  occurrence, 
being  seen  in  senile  marasmus,  and  in  malnutrition  from  almost  any  cause.  The 
degree  of  atrophy  varies.  The  borders  of  the  organ  are  much  wrinkled.  The 
lobules  seem  decidedly  smaller  than  normal,  and  even  the  individual  cells  that 
still  remain  are  atrophied  and  also  usually  deeply  pigmented. 

The  condition  does  not  of  itself  give  rise  to  any  special  symptoms.  The  area  of 
hepatic  dullness  is  usually  lessened,  but  this  sign  is  too  ambiguous  ever  to  justify 
us  in  making  from  it  a  diagnosis  of  hepatic  atrophy.  Perhaps  there  is  some  value  in 
the  alleged  lighter  color  of  the  stools,  as  indicating  a  diminished  secretion  of  bile. 

2.  Hypertrophy  of  the  Liver. — Even  under  normal  circumstances  the  liver 
undergoes  quite  marked  alterations  in  size.    The  exact  point,  therefore,  where  an 
abnormal  hypertrophy  begins  can  not  be  set.     Sometimes  the  autopsy  reveals  an 
unusually  large  liver,  of  which  there  had  been  no  indications  during  life,  and  for  ■ 
which  no  cause  can  be  made  out. 

There  are  certain  diseases  in  which  enlargement  of  the  liver  is  found  with 
comparative  frequency:  diabetes  mellitus,  chronic  malarial  poisoning,  leukaemia, 
and  sometimes  rachitis.  Topers  quite  often  have  enlarged  livers,  which  as  a  rule 
present  simple  hypertrophic  changes.  Occasionally  a  liver  has  been  reported  as 
showing  spots  of  localized  hyperplasia,  which  may  form  flattened  prominences 
upon  the  surface  of  the  organ. 

Hypertrophy  is  to  be  diagnosticated  only  when  palpation  and  percussion  give 
proof  of  an  enlargement,  and  yet  amyloid,  hypertrophic  cirrhosis,  and  other  dis- 


580  DISEASES    OF   THE   DIGESTIVE    ORGANS 

eases  whicL.  cause  an  increase  iji  the  size  of  the  liver,  can  be  excluded.    The  seti- 
ology  of  the  case  should  also  be  considered. 

3.  Fatty  Liver. — This  name  is  applied  to  excessive,  diffuse,  fatty  infiltration 
of  the  hepatic  cells.  The  size  of  the  organ  is  increased.  It  is  firm,  antemic,  and  of 
a  uniform  yellow  color,  both  externally  and  upon  section.  The  microscope  shows 
that  the  cells  of  the  parenchyma  are  filled  with  large  and  small  globules  of  fat. 
The  fat  is  most  abundant  toward  the  periphery  of  the  lobules. 

The  causes  of  fatty  liver  are  by  no  means  clear.  Sometimes  it  is  found  in 
cases  of  general  obesity,  where  we  may  assume  that  the  amount  of  fat  which  the 
liver  receives  as  nourishment  is  abnormally  great;  but  often  we  find  a  liver  that 
contains  comparatively  little  fat  in  those  who  have  a  well-developed  panniculus 
adiposus  and  much  fat  in  other  organs.  Topers  may  have  a  decidedly  fatty  liver. 
The  occurrence  of  fatty  liver  in  the  cachectic,  and  particularly  in  the  consump- 
tive, is  remarkable;  and  individuals  suffering  from  cancer,  or  marantic  children, 
may  also  exhibit  the  same  change.  We  have  no  intimate  knowledge  of  the  condi- 
tions that  prevent,  in  such  cases,  the  oxygenation  of  the  fat  which  comes  to  the 
liver  from  the  ingesta  or  from  other  organs. 

We  do  not  know  that  the  fatty  liver  is  in  any  way  functionally  impaired.  The 
only  clinical  indication,  therefore,  of  its  existence  is  the  increased  bulk  of  the 
organ.  In  phthisis  we  may  sometimes  feel  pretty  certain  that  the  liver  is  fatty,  if 
an  increase  in  bulk  can  be  demonstrated,  and  if  other  causes  for  this  enlargement, 
such  as  amyloid  degeneration,  appear  improbable.  If  the  anterior  edge  of  a  fatty 
liver  can  be  felt,  it  is  usually  found  to  be  noticeably  thick  and  blunt. 

The  treatment  of  fatty  liver  is  to  combat  the  original  disease. 

4.  Amyloid  Liver  (Waxy  Liver). — Amyloid  degeneration  of  the  liver  is  al- 
most invariably  a  part  of  extensive  amyloid  disease,  involving  also  the  spleen, 
kidneys,  intestine,  and  other  organs.  The  disease  occurs  chiefly  in  certain  cachec- 
tic conditions,  such  as  chronic  suppuration,  as  in  caries  and  persistent  empyema, 
and  also  in  chronic  pulmonary  tuberculosis,  and  constitutional  syphilis. 

The  amyloid  liver  is  usually  increased  in  bulk.  The  organ  may  even  become 
almost  double  its  normal  size.  It  feels  very  firm  and  hard,  its  surface  is  perfectly 
smooth,  and  its  edge  is  slightly  thickened.  The  cut  surface  presents  a  character- 
istic grayish-brown  "  waxy  "  appearance. 

The  microscope  shows  that  the  degenerative  process  attacks  chiefly  the  walls  of 
the  hepatic  capillaries,  the  hepatic  cells  proper  showing  infrequent  and  slight 
amyloid  changes.  Very  often  the  cells  of  the  parenchyma  are  atrophied  and 
somewhat  infiltrated  with  fat. 

The  diagnosis  of  amyloid  liver  requires  (1)  the  demonstration  by  palpation 
and  percussion  of  hepatic  enlargement.  We  can  often  feel  a  large  part  of  the 
anterior  surface  and  the  margin  of  the  hard  and  firm  organ.  The  liver  may  reach 
as  low  as  the  level  of  the  umbilicus.  The  diagnosis  further  demands  (2)  that 
some  disease  which  predisposes  to  amyloid  be  present,  and  (3)  that  there  be  evi- 
dence of  the  degenerative  process  in  other  organs :  the  spleen  should  be  enlarged, 
and  the  kidneys  secrete  an  abundance  of  albuminous  urine. 

The  other  symptoms,  as  well  as  the  prognosis  and  treatment,  are  determined 
mainly  by  the  nature  of  the  causative  affection.  The  use  of  iodide  of  iron,  iodide 
of  potassium,  the  alkaline  carbonates,  and  ammonic  chloride,  respectively,  has 
been  recommended  as  particularly  efilcient,  but  therapeutic  claims  of  this  sort  do 
not  withstand  a  rigorous  criticism.  The  chief  point  is  the  general  improvement 
of  nutrition  by  careful  diet  and  nursing.  Further  particulars  about  amyloid 
disease  in  general  will  be  found  in  the  chapter  on  amyloid  degeneration  of  the 
kidney. 


ANOMALIES   IN    THE    SHAPE   AND   POSITION   OF   LIVEE    581 

CHAPTER   XIV 
ANOMALIES    IN    THE    SHAPE    AND    POSITION    OE    THE    LIVER 

1.  Corset  Liver. — The  constant  pressure  of  the  lower  ribs  against  the  liver,  as 
a  result  of  tight  lacing,  often  produces  an  atrophy  of  the  hepatic  parenchyma 
from  pressure,  as  shown  by  a  deep  furrow  crossing  transversely  the  anterior  sur- 
face of  the  organ.  This  "  corset  furrow  "  lies  chiefly  in  the  right  lobe.  Its  usual 
situation  corresponds  to  the  margin  of  the  ribs,  and  the  atrophy  may  be  so  extreme 
that  the  liver  is  divided  into  a  large  upper  part  and  a  small,  usually  roundish, 
lower  portion,  connected  by  a  narrow  isthmus  of  tissue.  At  the  atrophic  place,  the 
connective-tissue  capsule  of  the  liver  is  almost  always  much  thickened.  Often 
the  lower  section  can  be  bent  upv^^ard  as  if  attached  by  a  hinge. 

This  deformity  of  the  liver  is  found  quite  often  in  elderly  females,  and  rarely 
in  men,  as  in  soldiers.  Unless  extreme,  it  can  not  be  detected  during  life,  and  it 
causes  no  discomfort.  Even  the  bad  cases  do  not,  as  a  rule,  occasion  any  special 
symptoras ;  but  they  can  be  clearly  made  out  if  the  abdominal  walls  are  lax.  The 
deep  transverse  furrow  can  be  felt,  and  also  the  lower  section,  with  its  usually 
blunt  edge.  Particularly  in  the  case  of  old  women  we  must  bear  this  condition 
in  mind,  else  we  might  easily  confound  it  with  some  enlargement  of  the  liver, 
such  as  amyloid  or  passive  congestion,  or  even  new  growths. 

In  some  few  cases  a  well-marked  corset  liver  seems  to  cause  especial  symptoms. 
It  occasions  a  constant  feeling  of  pressure  and  tugging  in  the  region  of  the  liver. 
Sometimes  there  are  attacks  of  violent  pain,  with  peritoneal  irritation  and  vomit- 
ing, and  a  mild  degree  of  collapse.  These  have  been  regarded  as  the  result  of  tem- 
porary congestion  and  swelling  in  the  portion  of  the  liver  below  the  constriction, 
but  we  should  view  this  explanation  with  reserve,  and  should  bear  in  mind  that 
in  corset  liver  gall-stones  are  remarkably  frequent  (vide  supra,  page  544),  and 
that  consequently  the  symptoms  mentioned  may  also  be  connected  with  chole- 
lithiasis. The  treatment  of  such  attacks,  even  when  the  diagnosis  is  doubtful, 
will  in  every  case  consist  chiefly  in  absolute  rest  in  bed,  the  employment  of  poul- 
tices or  perhaps  of  an  ice-bag,  and  a  restricted  diet.  If  there  is  violent  pain,  we 
must  resort  to  narcotics. 

2.  MovalDle  Liver. — This  name  has  been  applied  to  a  condition  exceptionally 
seen  in  women  with  very  lax  abdominal  walls,  in  which  the  liver  sinks  deep  down 
into  the  lower  portions  of  the  abdominal  cavity,  probably  as  a  result  of  an  unnat- 
ural length  of  the  suspensory  ligament.  The  organ  can  be  distinctly  felt  in  its 
new  situation,  and  can  usually  be  brought  back  to  a  normal  position  with  toler- 
able ease  by  means  of  external  pressure.  It  is  invariably  very  movable  and  it  can 
be  seen  to  change  its  place  v/hen  the  patient  lies  upon  the  side.  In  most  cases 
there  are  at  the  same  time  the  indications  of  universal  enteroptosis,  with  which 
we  have  already  become  acquainted  (see  page  462).  The  interpretation  of  the 
symptoms  present,  such  as  pain  and  digestive  disturbance,  is  consequently  difil- 
cult  in  most  cases,  especially  if  the  patient  is  also  neurasthenic  and  hysterical, 
which  is  not  infrequently  the  case.  The  reader  may  compare  on  this  point  the 
chapter  on  movable  kidney.  Treatment  is  governed  by  the  same  principles  as  in 
the  other  forms  of  enteroptosis.  Above  all,  trial  should  be  made  of  a  suitably 
applied  and  well-fitting  bandage. 


582  DISEASES    OF   THE   DIGESTIVE    ORGANS 


CHAPTER   XV 

SUPPURATIVE    PYLEPHLEBITIS 

(^Purulent  Inflammation  of  the  Portal  Vein  and  its  Brandies) 

etiology. — ^Purulent  pylephlebitis  is  seldom  a  primary,  idiopathic  disease.  In 
most  instances  it  is  due  to  the  propagation  of  a  suppurative  inflammation  of 
neighboring  tissues  to  the  walls  of  the  vein.  The  main  trunk  of  the  portal  vein 
is  rarely  directly  attacked.  Usually  the  process  originates  in  the  hepatic  branches 
of  the  vein  or  in  the  veins  of  the  portal  system,  and  thence  extends  to  the  larger 
vessel. 

Perityphlitic  abscess  is  the  most  frequent  source  of  suppurative  pylephlebitis. 
The  inflammation  involves  a  mesenteric  vein,  and  thence  extends  upward.  Other 
causes  are  gastric  ulcer,  intestinal  ulcers,  as  in  dysentery,  splenic  abscess,  and 
purulent  inflammation  at  the  porta  hepatis  or  within  the  liver  itself,  as  in  abscess 
due  to  gall-stones.  The  mode  of  production  in  these  cases  is  precisely  analogous 
to  that  in  peritj^jhlitic  abscess ;  but  they  are  rare. 

A  special  form  of  pylephlebitis  is  observed  in  the  new-bom.  Here  the  inflam- 
mation originates  in  the  umbilical  vein,  and  we  need  hardly  say  that  the  cause  is 
a  suppurative  infection  through  the  navel. 

In  rare  instances  it  has  been  found  that  pylephlebitis  has  resulted  from  the 
penetration  into  a  vein  of  some  foreign  body  that  had  been  swallowed,  such  as  a 
pin.  Here,  too,  the  true  factors  in  producing  the  inflammation  are,  of  course, 
the  bacteria  which  adhere  to  the  foreign  body. 

Pathology. — Where  the  inflammation  has  attacked  the  vascular  walls,  the 
vein  is  thickened,  and  often  the  surrounding  connective  tissue  is  infiltrated  with 
pus-cells  and  mottled  with  minute  ecchymoses.  If  the  vein  is  cut  open,  the  intima 
is  seen  to  be  opaque  and  often  superficially  ulcerated.  The  lumen  of  the  vessel 
is  filled  with  a  thrombus,  which  is  usually  to  a  great  extent  in  a  state  of  purulent 
softening,  so  that  offensive  purulent  fluid  flows  out.  The  course  of  events  is  as 
follows :  First,  the  wall  of  the  vein  becomes  inflamed.  As  a  consequence  of  this,  a 
thrombus  forms  at  the  same  place.  The  bacteria  penetrate  this  thrombus  and 
occasion  its  purulent  softening. 

The  extent  of  a  pylephlebitis  naturally  varies  in  different  cases.  As  a  rule, 
little  fragments  become  detached  from  the  thrombus  and  enter  the  liver,  produc- 
ing metastatic  abscesses.  Secondary  suppuration  may  occur  also  in  the  lungs, 
kidneys,  brain,  and  joints,  so  that  we  have  all  the  anatomical  characteristics  of  a 
general  pyaemia. 

Clinical  History. — Inasmuch  as  the  primary,  causative  disease  may  be  very 
different  in  different  cases,  it  is  impossible  to  delineate  the  disease  comprehen- 
sively. It  is,  however,  frequently  ushered  in  by  a  number  of  symptoms,  which 
render  a  diagnosis  possible,  at  least  in  some  cases,  if  the  original  disease  has 
been  recognized. 

The  symptoms  of  suppurative  pylephlebitis  are  in  part  due  directly  to  the  local 
disease  itself,  and  in  part  are  occasioned  by  the  general  pyaemia.  One  of  the  local 
symptoms  is  pain  in  the  epigastrium.  This  is  rare.  It  may  radiate  downward  or 
laterally,  according  to  the  starting-place  and  extent  of  the  inflammation.  An 
inevitable  result  of  the  portal  thrombosis  is  portal  obstruction.  The  spleen  be- 
comes considerably  swollen,  and,  if  the  disease  be  not  too  quickly  fatal,  there 
is  an  evident  effusion  into  the  peritoneal  cavity.  The  splenic  enlargement  can 
not  be  regarded  as  due  merely  to  venous  stasis,  but  is  in  part  the  "  acute  splenic 
tumor  "  of  constitutional  septic  conditions.  If  the  inflammation  spreads  from 
the  branches  of  the  portal  vein  to  the  neighboring  bile-ducts,  jaundice  results. 


THEOMBOSIS    OF   THE   POETAL   VEI]!T  583 

This  is  seen  quite  often.  Sometimes  it  is  due  also  to  the  hepatic  abscesses,  or  to  a 
gall-stone  which  happens  to  cause  trouble  simultaneously.  Now  and  then  there  is 
no  jaundice  whatever. 

Of  the  pyaemic  symptoms,  hepatic  abscesses  come  first.  They  are  due,  as  we 
have  said,  to  the  conveyance  of  infectious  matter  directly  into  the  liver  by  emboli. 
The  one  almost  constant  sign  of  their  occurrence  is  a  decided  enlargement  of  the 
liver.  When  there  are  no  hepatic  abscesses,  the  organ  usually  retains  its  normal 
bulk. 

The  course  of  the  fever  is  very  characteristic.  As  in  other  pysemic  conditions, 
there  are  almost  invariably  great  elevations,  to  106°  (41°  C),  or  higher,  accom- 
panied by  rigors,  and  followed  by  marked  remissions,  with  profuse  perspiration. 
These  onsets  of  fever  occur  at  irregular  intervals,  either  daily,  or  every  two  or 
three  days. 

There  are  at  the  same  time  indications  of  constitutional  septic  infection, 
which  keep  increasing  in  severity.  The  pulse  grows  rapid  and  small.  Intelligence 
is  impaired.    Somnolence  and  delirium  come  on,  and  the  strength  rapidly  fails. 

There  are  other  symptoms.  Vomiting  is  frequently  seen.  The  bowels  are  sel- 
dom constipated,  but  usually  relaxed.  The  dejections  may  contain  blood,  because 
of  the  venous  stasis.  In  some  cases  the  inflammation  extends  so  as  to  produce  a 
fatal  general  peritonitis.  It  is  noticeable  that  the  urine  is  generally  scanty,  and 
the  amount  of  urea  is  strikingly  diminished. 

The  disease  usually  runs  a  rather  acute  course.  On  the  average,  it  lasts  about 
two  weeks,  but  it  may  occupy  three  or  four  weeks,  or  even  a  longer  period.  It  is 
invariably  fatal.     At  least,  no  cases  of  recovery  are  known. 

The  diagnosis  can  sometimes  be  made  with  considerable  positiveness.  In  other 
instances  it  is  impossible  to  exclude  other  pysemic  conditions,  or  abscess  due  to 
gall-stones,  etc.  Important  factors  are  the  origin  of  the  trouble — if  it  can  be 
made  out — the  pysemic  rigors,  the  enlargement  of  the  spleen  and  liver,  jaundice, 
epigastric  pain,  and  the  evidences  of  general  sepsis. 

Treatment  is  unfortunately  almost  entirely  useless.  The  fever  is  not  affected 
even  by  large  doses  of  quinine.  All  we  can  aim  at  is  to  support  and  relieve  the 
sufferer  as  far  as  possible. 


CHAPTEE   XVI 

THROMBOSIS    OF    THE    PORTAL    VEIN 

(  Chronic  Adhesive  Pylephlebitis.     Pylethrombosis) 

-Etiology  and  Pathology. — Like  suppurative  pylephlebitis,  chronic  portal 
thrombosis  is  not  an  independent  disease,  but  is  the  sequel  of  a  great  variety  of 
pathological  conditions.  Marantic  thrombosis  is  of  rare  occurrence,  and  is  usu- 
ally formed  toward  the  close  of  life,  so  as  not  to  be  of  practical  interest.  Apart 
from  this,  almost  all  cases  of  thrombosis  of  the  portal  vein  are  due  to  a  compres- 
sion and  constriction  of  the  trunk  of  that  vessel  or  one  of  its  main  branches.  This 
most  often  occurs  in  certain  chronic  hepatic  diseases  which  involve  a  mechanical 
stenosis,  either  of  the  smaller  branches  of  the  portal  vein  within  the  liver,  or  of  the 
vein  itself,  with  resulting  coagulation  of  the  blood  within  it.  Chief  among  these 
diseases  are  cirrhosis  and  syphilis  of  the  liver,  which  have  repeatedly  been  ob- 
served to  entail  portal  thrombosis ;  but  other  diseases  in  the  neighborhood  of  the 
vein  may  produce  a  similar  effect.  New  growths  of  various  kinds  may  press  upon 
the  vessel,  or  chronic  inflammatory  hyperplasia  of  the  connective  tissue  at  the 
porta  hepatis  may  act  in  the  same  way.    This  is  illustrated  in  chronic  peritonitis, 


584  DISEASES    OF   THE   DIGESTIVE   OEGANS 

whether  circumscribed  or  diffuse,  an  example  of  the  former  being  sometimes  seen 
as  an  effect  of  duodenal  ulcer. 

It  was  formerly  held  that  many  forms  of  so-called  "  lobulated  liver  "  were  due 
to  a  primary  adhesive  pylephlebitis.  This  is  erroneous.  These  cases  are  probably 
all  due  to  some  primary  hepatic  disease,  usually  syphilitic.  The  size  of  the  liver 
is  little  influenced  by  obstruction  of  the  portal  vein,  even  if  long  continued,  for 
the  hepatic  artery  suffices  to  supply  all  the  blood  required  by  the  organ. 

The  anatomical  changes  in  pylethrombosis  do  not  differ  essentially  from  those 
seen  in  thrombosis  of  any  other  vein.  If  fresh,  the  thrombus  is  stillred;  later 
it  grows  harder,  paler,  and  more  friable.  If  the  thrombosis  has  existed  a  long 
while,  the  clot  becomes  completely  organized.  We  have  observed  this  even  in  the 
main  trunk  of  the  portal  vein. 

Clinical  History. — The  symptoms  of  portal  thrombosis  are  those  occasioned  by 
the  obstruction,  and  therefore  such  as  we  have  already  repeatedly  met  with,  in 
connection  with  various  hepatic  diseases.  The  intensity  and  extent  of  these  re- 
sults, as  well  as  the  time  occupied  in  their  development,  depend,  of  course,  upon 
the  place  and  size  of  the  clot.  If  it  is  the  portal  vein  itself  which  is  attacked,  and 
if  the  thrombus  is  extensive  enough  to  obstruct  the  flow  of  blood,  then  the  signs 
of  venous  stasis  are  evident  throughout  the  portal  system.  The  spleen  becomes 
much  enlarged,  as  can  be  easily  demonstrated  by  percussion  and  palpation.  Soon 
ascites  appears,  as  a  result  of  the  passive  congestion  of  the  peritoneal  veins ;  and 
from  a  similar  condition  of  the  gastro-intestinal  veins  arise  catarrhal  disorders, 
such  as  diarrhoea;  or,  not  so  very  exceptionally,  there  is  repeated  gastric  and  in- 
testinal hsemorrhage. 

As  we  have  seen,  a  collateral  circulation  may  be  developed  (vide  page  559),  by 
which  the  venous  blood  of  the  portal  system  is  enabled  to  reach  the  systemic 
veins.  This  explains  why  some  of  the  symptoms  of  venous  stasis  may  temporarily 
(perhaps  permanently)  vanish.  We  saw  one  case  of  portal  thrombosis,  the  sequel 
to  what  was  apparently  a  syphilitic  disease  of  the  liver,  in  which  quite  a  large 
ascitic  effusion  appeared  some  six  or  seven  times  at  intervals  of  three  to  six 
months,  and  under  proper  nursing  and  treatment,  without  aspiration,  as  often 
disappeared.  The  patient  did  not  die  till  the  illness  had  continued  six  years, 
and  tapping  had  been  required  in  all  some  fifteen  times.  At  the  autopsy  the 
trunk  of  the  portal  vein  was  found  to  be  converted  into  a  fibrous  cord,  with  a 
lumen  which  barely  admitted  a  knitting-needle. 

In  simple  pylethrombosis  there  are  no  local  symptoms  such  as  pain.  The  con- 
dition of  the  liver  depends  upon  the  primary  disease.  It  is  possible  that  a  moder- 
ate atrophy  of  the  entire  organ  might  at  length  ensue  if  the  portal  blood  were 
permanently  cut  off  from  it.  But,  as  we  have  said,  any  cirrhotic  changes,  or  any 
"  lobulation,"  are  not  to  be  regarded  as  the  result,  but  as  the  cause  of  the  throm- 
bosis, or  at  least  as  related  to  the  cause. 

The  course  and  duration  of  the  disease  are  according  to  the  nature  of  the 
original,  causative  trouble.    No  general  statements  can  be  made. 

The  diagnosis  of  thrombosis  of  the  portal  vein  is  usually  extremely  difficult, 
and  it  can  really  hardly  ever  be  made  with  absolute  certainty.  We  may,  indeed, 
'  recognize  readily  that  there  is  some  decided  obstruction  to  the  portal  circulation ; 
but  whether  this  be  due  to  a  thrombus,  or  to  compression  of  the  portal  vein,  or  to 
the  obliteration  of  a  large  number  of  the  smaller  branches  of  that  vein  within  the 
liver,  we  can  very  seldom  determine.  Pylethrombosis  may  be  regarded  as  prob- 
able, if  no  other  possible  cause  of  the  portal  obstruction  seems  likely,  and  if  we 
are  able  to  discover  a  cause  for  thrombosis. 

The  prognosis  is  always  unfavorable,  although  there  may  be,  as  we  have  said, 
great  temporary  improvement.  Treatment  must  be  symptomatic,  and  it  follows 
in  the  main  the  principles  set  forth  under  cirrhosis  of  the  liver. 


DISEASES    OF   THE   PANCEEAS  585 

APPENDIX 
DISEASES    OF    THE    PANCREAS 

The  few  facts  of  clinical  importance  that  are  known  about  tlie  pathology  of 
the  pancreas  are  given  below. 

1.  Hsemorrhages  into  the  Pancreas. — Small  haemorrhages  occur  in  the  pan- 
creas in  cases  of  general  hsemorrhagic  diathesis,  marked  passive  congestion,  severe 
acute  constitutional  infection,  and  trauma  of  the  abdomen.  These  do  not,  as  a 
rule,  cause  marked  clinical  symptoms.  On  the  other  hand,  Klebs,  Zenker,  and 
others  describe  cases  in  which  a  more  or  less  extensive  pancreatic  haemorrhage  has 
been  found  at  autopsy  as  the  only  demonstrable  cause  of  death.  The  patients 
were  previously  in  apparently  perfect  health  and  were  vigorous,  although  usually 
corpulent  individuals;  and  they  died  suddenly.  Perhaps  it  was  the  influence  of 
the  haemorrhage  upon  the  semilunar  ganglia  or  the  solar  plexus  which  occasioned 
the  speedy  death.  At  any  rate,  we  find  in  such  cases  the  cavities  of  the  heart  of 
usual  size  and  empty,  while  the  abdominal  vessels  are  distended  with  blood.  The 
special  causes  which  lead  to  the  haemorrhage  are  not  aways  clear.  In  general,  we 
probably  must  surmise  a  primary  disease  of  the  blood-vessels  (syphilis,  atheroma). 
It  is  noteworthy  that  a  comparatively  large  number  of  cases  have  occurred  in 
hard  drinkers.  Many  cases  also  seem  to  be  similar  to  those  first  described  by 
Balser.  These  have  an  uncertain  aetiology,  perhaps  infectious,  and  exhibit  a  mul- 
tiple necrosis  of  fat  and  of  the  pancreatic  tissue — there  being  numerous  minute 
necrotic  foci  in  the  pancreas  and  in  the  fat  tissue  of  the  mesentery.  Extensive 
disorder  of  this  kind  is  observed  particularly  in  obese  persons,  but  is  not  con- 
fined to  them.  Sometimes  in  cases  of  pancreatic  haemorrhage  death  is  extremely 
sudden  and  apoplectiform.  In  other  cases  the  symptoms  last  from  twelve  to 
twenty-four  hours  before  the  fatal  termination.  The  patient  suffers  from  violent 
abdominal  pain,  vomiting,  abdominal  distention,  and  general  collapse ;  treatment 
is  purely  symptomatic. 

2.  Atrophy  of  the  Pancreas. — The  organ  may  share  in  a  general  marasmus. 
There  is  sometimes  also  extreme  atrophy  of  the  pancreas  in  those  who  have  died  of 
diabetes  mellitus  (q.v.). 

3.  Pancreatitis.— A  few  cases  have  been  reported  of  what  would  seem  to  be  a 
primary  acute  pancreatitis,  usually  haemorrhagic.  The  disease  is  certainly  very 
rare.  It  begins  with  violent  colicky  pains  in  the  epigastrium.  Vomiting  and 
collapse  soon  follow.  The  pulse  grows  small,  the  extremities  become  cool,  and 
death  is  speedy.  At  the  autopsy  the  pancreas  is  found  to  be  much  enlarged,  and 
mottled  with  ecchymoses,  or  it  even  presents  scattered  foci  of  suppuration.  The 
aetiology  is  unknown.  It  is  most  likely  that  the  germs  which  excite  the  inflamma- 
tion originate  in  the  intestines.  Apparently  there  should  be  a  sharp  distinction 
made  between  primary  pancreatic  haemorrhage  and  acute  haemorrhagic  pancrea- 
titis, but  formerly  these  two  conditions  seem  often  to  have  been  confounded. 
Secondary  abscesses  of  the  pancreas  are  not  infrequent  in  pyaemia. 

[Fitz,  in  the  Middleton-Goldsmith  lecture  for  1889,  threw  much  light  on  the 
aetiology  and  diagnosis  of  acute  pancreatitis,  which  he  subdivides  into  three  ana- 
tomical forms — the  haemorrhagic,  the  suppurative,  and  the  gangrenous.  He  shows 
that  the  affection  is  not  so  rare  as  has  been  supposed ;  that  its  victims  are  usually 
in  middle  life,  fat,  and  good  livers ;  that  it  commonly  originates  by  the  extension 
of  a  gastro-duodenal  inflammation  along  the  pancreatic  duct. 

"  If  the  case  does  not  end  fatally  in  the  course  of  a  few  days,  recovery  is  pos- 
sible, or  a  recurrence  of  the  symptoms  in  a  milder  form  takes  place,  and  the  char- 
acteristics of  a  subacute  peritonitis  are  developed." 


586  DISEASES    OF   THE   DIGESTIVE   OEGANS 

In  the  differential  diagnosis  irritant  poisoning,  perforation  of  the  digestive  or 
biliary  tracts,  and  acute  intestinal  obstruction  are  to  be  considered.  The  location 
of  peritonitic  symptoms,  their  suddenness  of  onset,  the  absence  of  apparently 
sufficient  cause,  and  the  age  and  habit  of  the  individual  are  important  points.] 

Chronic  interstitial  pancreatitis  sometimes  results  from  the  extension  of 
chronic  inflammatory  processes  affecting  neighboring  parts.  Friedreich  states 
that  it  sometimes  is  a  primary  disease  in  topers.  Syphilitic  lesions  of  the  pan- 
creas have  been  observed,  occasioning  contraction  and  induration. 

There  are  no  characteristic  clinical  symptoms  which  correspond  to  these  vari- 
ous changes.  The  symptoms  observed  in  the  cases  belonging  in  this  category  are 
digestive  disturbances,  indefinite  pain,  bodily  weakness,  emaciation,  and  anaemia, 
and  they  are  so  ambiguous  that  a  diagnosis  of  the  true  condition  is  scarcely  ever 
possible.  If  there  were  a  single  distinctive  symptom,  it  would  be  one  common  to 
all  sorts  of  grave  pancreatic  disorder — namely,  the  appearance  of  a  large  amount 
of  fat  in  the  stools.  As  we  know,  the  pancreatic  juice  is  an  important  factor  in 
the  digestion  of  fat,  so  that  it  is  very  natural  for  any  great  derangement  of  the 
organ  to  have  this  result;  and  yet  the  bile  alone  may  render  the  ingested  fat 
capable  of  absorption,  so  that  in  repeated  instances  there  have  been  no  fatty  stools 
when  the  pancreas  has  been  completely  atrophied  or  degenerated. 

4.  Cysts  of  the  Pancreas. — After  closure  of  Wirsung's  duct  by  scars,  concre- 
tions, or  the  like,  cysts  of  the  pancreas  may  form,  as  a  result  of  the  damming  up 
of  the  secretion.  These  may  become  so  large  as  to  be  felt  as  great  tumors  through 
the  abdominal  walls.  In  some  instances  they  have  been  operated  upon  with 
success.  Rarely,  spaces  are  found  in  the  neighborhood  of  the  pancreas  filled 
with  a  thick,  slimy  fluid.  These  seem  to  be  associated  with  the  above-mentioned 
peculiar  multiple  necrosis  of  fat  and  pancreatic  tissue,  but  with  regard  to  them 
further  observations  are  desirable. 

5.  Cancer  of  the  Pancreas. — Primary  cancer  is  the  most  frequent,  and  there- 
fore clinically  the  most  important  disease  of  this  organ.  As  a  rule,  the  new 
growth  is  situated  in  the  head  of  the  pancreas.  It  is  usually  of  the  medullary 
variety,  though  occasionally  colloid.  It  may  involve  neighboring  parts  by  direct 
extension,  and  a  great  many  organs  by  metastasis;  for  example,  the  liver,  peri- 
toneum, and  lymph-glands. 

The  clinical  symptoms  of  cancer  of  the  pancreas  are  very  seldom  so  decided  as 
to  justify  a  positive  diagnosis.  Sometimes  the  secondary  nodules  can  be  detected 
in  the  liver,  peritoneum,  and  elsewhere.  Then  we  are  left  in  doubt  about  the  seat 
of  the  primary  growth.  Or  the  primary  tumor  may  be  plainly  felt  through  the 
abdominal  walls ;  but  then  we  can  hardly  ever  exclude  cancer  of  the  stomach  or 
of  the  omentum,  and  neighboring  parts. 

The  symptoms  of  pancreatic  cancer,  as  a  whole,  resemble  closely  those  occa- 
sioned by  most  cancers  of  abdominal  organs.  Usually  the  patient  is  elderly.  The 
first  symptoms  are  weakness,  emaciation,  and  indigestion,  or  they  are  the  result  of 
compression.  Often  there  is  complaint  of  a  persistent  dull  pain  in  the  epigas- 
trium. If  the  portal  vein  is  pressed  upon  by  the  tumor,  ascites  appears.  If  the 
common  duct  is  compressed,  there  is  jaundice.  Icterus  is  an  especially  frequent 
symptom  of  pancreatic  carcinoma.  The  dejections  have  repeatedly  been  observed 
to  contain  a  large  amount  of  fat  (vide  supra),  but  there  may  be  none  whatever. 
Osier  remarks  the  noticeable  frequency  and  large  amount  of  the  dejections, 
and  the  quantity  of  undigested  muscular  fiber  which  they  contain,  because  the 
pancreas  no  longer  performs  its  part  in  the  digestion  of  albuminoids.  Sugar  is 
sometimes  present  in  the  urine,  but  by  no  means  in  every  case.  Marasmus  in- 
creases, and  usually  at  the  end  of  six  months  or  a  year  the  patient  dies. 

The  diagnosis  is  difiicult.  It  can  be  made  with  a  certain  degree  of  probability 
when  there  is  a  slowly  growing  tumor  in  the  region  of  the  pancreas,  without 


DISEASES    OF   THE   PANCREAS  587 

enlargement  of  the  liver,  but  accompanied  by  jaundice,  deeply-seated  epigastric 
pain,  glycosuria,  and  the  above-mentioned  abnormalities  in  the  fasces.  Usually, 
however,  the  clinical  picture  is  by  no  means  so  characteristic,  and  it  is  often  im- 
possible to  avoid  confusing  cancer  of  the  pancreas  with  cancer  of  the  stomach, 
duodenum,  gall-bladder,  or  other  organs. 

The  prognosis  is  absolutely  bad.  The  treatment  is  merely  symptomatic,  with 
the  aim  of  lessening  the  patient's  suffering. 

6.  Pancreatic  Calculi, — In  the  excretory  ducts  of  the  pancreas  are  sometimes 
found  calculi  of  small  or  moderate  size,  consisting  essentially  of  carbonate  and 
phosphate  of  lime.  The  cause  of  their  formation  is  as  little  settled  as  that  of 
gall-stones  (which  see).  Because  of  the  obstruction  caused  by  these  calculi  we 
have  secondary  dilatation  of  the  ducts,  secondary  contraction  and  atrophy,  and  in 
some  cases  secondary  inflammation  and  suppuration;  these  probably  result  from 
processes  similar  to  those  with  which  we  have  become  acquainted,  while  consid- 
ering biliary  calculi.  There  may  be  no  symptoms.  Sometimes,  however,  there  is 
violent  pain,  either  continuous  or  paroxysmal,  also  digestive  disturbances,  and 
occasionally  the  above-mentioned  changes  in  the  dejecta,  and  glycosuria.  In  only 
a  very  few  cases  has  it  been  possible  to  find  pancreatic  calculi  in  the  fseces.  An 
absolute  diagnosis  can  rarely  be  made.  As  a  therapeutic  measure  Eichhorst  has 
recommended  the  stimulation  of  the  pancreatic  secretion  by  means  of  injections 
of  pilocarpine ;  as  a  rule,  treatment  will  be  purely  symptomatic. 


DISEASES   OF   THE    URINARY   ORGANS 


SECTION  I 

Diseases  of  the  Kidneys 


CHAPTEE   I 

GENERAL    PRELIMINARY    REMARKS    UPON    THE    PATHOLOGY 
OF    RENAL    DISEASE 

Although  some  knowledge  of  the  occurrence  and  significance  of  renal  affec- 
tions had  been  acquired  even  by  the  older  physicians,  still  the  service  of  having 
pointed  out  the  frequency  of  these  diseases,  and  of  having  clearly  recognized  their 
most  important  anatomical  forms  and  their  chief  clinical  symptoms,  belongs 
undoubtedly  to  the  English  physician  Eichard  Bright,  vpho  vpas  born  in  1788  and 
died  in  1858,  as  physicion  in  ordinary  to  Queen  Victoria.  Bright's  first  work  on 
this  subject  appeared  in  the  year  1827.  In  this  he  brought  forward  the  special 
discovery  that,  in  many  cases  of  general  dropsy,  which  are  associated  with  the 
secretion  of  an  albuminous  urine,  a  primary  affection  of  the  kidneys  must  be 
regarded  as  the  true  cause  of  the  disease.  Since  then,  the  disease  described  by 
him  has  been  almost  universally  called  "  Bright's  disease  "  ("  Morhus  Brightii  "), 
a  name  still  much  employed,  but  in  whose  stead  the  anatomical  terms  would  be 
more  proper,  since  many  forms  were  previously  classed  under  it  which,  according 
to  our  more  accurate  present  knowledge,  must  be  separated. 

Bright's  statements  were  either  confirmed  or  expanded  in  subsequent  times  by 
many  other  observers.  Christison,  Osborne,  and  E.  Willis  in  England,  and  Eayer 
and  M.  Solon  in  Erance,  were  the  chief  students  of  renal  diseases.  Ererichs  pub- 
lished the  first  great  work  in  Germany  in  the  year  1851.  His  division  of  Bright's 
disease  into  three  different  "  stages,"  based  on  Eeinhardt's  histological  investiga- 
tions, was  for  a  long  time  quite  generally  accepted,  until  gradually  further  clin- 
ical experience  showed  that  it  was  untenable.  A  more  accurate  division  of  renal 
diseases  was  substituted  for  it  first  in  England  (Johnson,  S.  Wilks,  and  others), 
and  then  in  Germany  (Traube,  Bartels).  However  admirable  these  labors,  espe- 
cially the  work  of  Bartels  in  1871,  renal  pathology  fell  into  subjection  to  the- 
ories, with  which  the  facts  of  experience  could  be  harmonized  only  by  force. 
Only  of  late  years  has  a  natural  theory  of  renal  diseases,  derived  from  general 
pathological  observations,  at  last  become  accepted — a  theory  which  is  based  chiefly 
upon  the  anatomical  work  of  Weigert. 

The  following  presentation  of  renal  pathology  is  intended  to  show  that,  from 
a  clinical  standpoint  as  well,  the  renal  diseases  may  be  viewed  comprehensively  as 
a  unit,  and  this  not  in  a  schematic  way,  but  vdth  due  regard  to  actual  conditions. 

The  chief  reason  why  the  kidneys  are  so  often  diseased,  either  alone  or  in  con- 
junction with  other  organs,  is  to  be  found  in  the  fact  that  the  body  must  eliminate 
all  forms  of  injurious  matter,  which  circulate  in  the  blood,  in  great  part  by  the 
kidneys..  Consequently  the  action  of  any  injurious  substance  is  often  manifested 
588 


KEMAEKS  UPOIT  THE  PATHOLOGY  OF  EENAL  DISEASE     589 

chiefly  in  tlie  kidneys,  and  they  must,  in  a  certain  measure,  suffer  for  the  service 
which  they  do  the  rest  of  the  body.  According  to  their  nature  and  character,  the 
injurious  substances,  which  are  here  to  be  considered,  are  divided  chiefly  into  two 
great  groups — the  chemico-toxic  and  the  organized  infectious  substances.  At  the 
same  time,  it  should  be  noted  that  in  case  of  infection  it  is  comparatively  excep- 
tional for  the  germs  themselves  to  reach  the  kidneys  and  there  fix  themselves. 
Most  cases  are  referable  to  toxines,  which  are  formed  in  the  body  as  the  result 
of  the  infectious  process,  and,  being  excreted  through  the  kidneys,  produce  a 
nephritis.  In  this  way  the  kidneys  may  be  involved  sympathetically  after  the 
ingestion  of  many  poisons,  both  organic  and  inorganic,  and  also  in  the  great 
majority  of  all  the  infectious  diseases.  In  these  cases,  of  course,  as  we  shall  see 
later,  certain  chemical  and  infectious  poisons  exert  their  action  in  a  particularly 
frequent  and  in  a  particularly  severe  or  definitely  characterized  fashion.  Besides 
these  forms  of  origin  for  many  renal  diseases,  which  are  the  chief  ones  to  be  con- 
sidered, we  must  consider  other  causes  of  disease  which  are  much  rarer.  One  way 
in  which  the  morbific  agents  may  also  enter  is  especially  important — namely, 
from  the  lower  urinary  passages,  the  bladder,  and  pelvis  of  the  kidney,  upward 
into  the  kidney.  In  this  way  those  renal  diseases  arise  which  come  on  secondarily 
to  cystitis,  pyelitis,  etc.  Finally,  of  course,  disturbances  of  circulation  and 
mechanical  injuries  may  also  make  themselves  manifest  in  the  kidneys. 

The  clinical  symptoms  which  are  caused  by  the  different  forms  of  renal  dis- 
ease are  referable  only  in  very  small  part  directly  to  the  diseased  organ  itself.  In 
renal  diseases  characteristic  subjective  local  symptoms — such  as  local  pain — are 
rare,  and  the  anatomical  position  and  the  physiological  conditions  of  the  kidneys 
make  it  almost  impossible  to  discover  any  changes  in  their  size,  their  physical 
consistency,  etc.,  by  a  direct  objective  examination.  In  the  diagnosis  of  renal  dis- 
eases we  are  therefore  confined  chiefly  to  the  investigation  of  two  groups  of  symp- 
toms :  in  the  first  place,  to  the  examination  of  the  secretion  from  the  kidneys,  the 
urine,  whose  character,  as  we  know  by  experience,  may  be  materially  altered  when 
there  is  renal  disease;  and,  in  the  second  place,  to  the  discovery  of  certain  phe- 
nomena in  other  portions  of  the  body,  which  are  immediately  dependent  upon 
the  renal  affection.  Since  both  the  pathological  changes  in  the  urine,  and  the 
symptoms  in  other  organs  occurring  in  renal  affections,  have  much  in  common 
in  almost  all  the  forms  of  renal  disease,  it  is  advisable  first  to  describe  the  main 
features,  at  least,  of  the  general  symptomatology  of  renal  diseases.  We  shall  then 
be  obliged,  in  the  following  chapters,  to  mention  only  the  precise  circumstances 
of  the  occurrence  and  onset  of  each  symptom — the  general  significance  of  the 
symptoms  being  already  known. 

1.  Albuminuria 
The  most  constant  symptom,  which  in  many  cases,  even  by  itself,  renders 
the  diagnosis  of  a  renal  affection  possible  with  complete  certainty,  is  albuminuria 
— that  is,  the  appearance  of  albumen,  and  especially  of  serum  albumen  and  serum 
globuline  (paraglobuline),  in  the  urine.  From  recent  investigations  (Leube, 
Fiirbringer,  and  others)  we  know  that  in  some  cases  the  urine  may  contain  a  very 
slight  amount  of  albumen  even  in  healthy  persons,  especially  after  physical  exer- 
tion, emotional  disturbance,  a  cold  bath,  a  hearty  meal,  etc.  Indeed,  we  find  occa- 
sionally in  some  few  individuals,  particularly  in  early  years,  marked  albuminuria, 
especially  in  the  urine  of  the  daytime,  while  the  night  tirine  never  contains  a 
trace  of  albumen ;  and  yet  these  persons  are  apparently  in  perfect  health.  This 
has  been  called  intermittent  or  functional  albuminuria  (vide  infra).  Yet  it  is 
at  least  questionable  if  such  a  condition,  even  if  no  symptoms  are  associated  with 
it,  can  be  regarded  as  physiological,  and  these  facts  do  not  impair  the  justice  of 
the  dictum  that  every  case  of  persistent  excretion  of  albumen  in  the  urine,  which 


590  DISEASES    OF   THE   UKIITAEY   OEGAITS 

can  be  demonstrated  clearly  by  ordinary  methods,  is  to  be  regarded  as  somewhat 
pathological. 

The  detection  of  albumen  in  the  urine  for  clinical  purposes,  wherein  no  regard 
need  be  paid  to  the  separation  of  serum  albumen  and  serum  globuline,  is  per- 
formed almost  exclusively  by  means  of  the  so-called  heat  test.  If  the  urine  is 
cloudy,  it  must  be  filtered  before  heating.  The  reaction  of  the  urine  must  always 
be  tested  fijst.  If  the  reaction  of  the  urine  is  acid,  as  it  ordinarily  is,  it  is  heated 
in  the  test-tube  without  any  further  addition.  If  the  urine  is  neutral  or  alkaline, 
then,  and  only  then,  we  acidify  it  slightly  before  boiling,  by  means  of  a  few  drops 
of  dilute  acetic  acid.  If  the  urine  contains  albumen  there  will  appear,  upon  boil- 
ing, a  distinct  flocculent  precipitate  of  coagulated  albumen.  The  possibility  of  an 
error  lies  in  the  fact  that  sometimes,  with  a  neutral  or  faintly  acid  urine,  upon 
heating  there  appears  a  cloudiness  because  of  the  phosphates  and  carbonates 
which  are  precipitated.  These  are  salts  of  lime  and  magnesia.  In  order  to  avoid 
confounding  such  phosphatic  deposit  with  a  deposit  of  albumen,  we  must  in  ever;^ 
case  after  the  urine  has  boiled  for  a  short  time,  if  there  is  any  deposit  formed,  add 
a  few  drops  of  nitric  or  acetic  acid.  By  this  means  the  deposit  of  phosphate  or 
carbonate  is  immediately  dissolved,  while  a  deposit  of  albumen  is  not  affected. 
The  change  in  the  color  of  the  urine,  which  is  sometimes  caused  by  the  addi- 
tion of  nitric  acid,  is  due  to  the  action  of  the  acid  upon  the  urinary  pigments. 
We  can  measure  the  amount  of  albumen  contained  in  the  urine  approximately 
by  the  height  of  the  settled  precipitate  in  the  test-tube.  "We  often  speak  of 
"  one-half  or  one-fourth  of  the  volume  being  albumen,"  but  we  can  not  state 
any  definite  relation  between  this  estimate  of  the  volume  and  the  precise  amount 
of  albumen.  Approximately,  however,  a  deposit  of  albumen,  which  upon  settling 
occupies  about  half  the  volume  of  the  urine,  corresponds  to  about  one  per  cent,  by 
weight  of  albumen ;  a  deposit  of  about  one-third  of  the  volume  to  about  one-half 
per  cent,  of  albumen,  and  so  on. 

Besides  the  test  by  boiling  there  is  a  very  distinct  test  which  can  be  highly 
recommended  to  practitioners,  in  which  acetic  acid  and  ferrocyanide  of  potassium 
are  employed.  A  rather  large  amount,  perhaps  one-tenth  of  the  volume,  of  acetic 
acid  is  added  to  the  urine,  and  then  a  few  drops  of  a  ten-per-cent.  solution  of 
ferrocyanide  of  potassium  are  added  to  the  mixture.  If  the  urine  contains  albu- 
men there  is  formed  a  distinct  deposit.  This  reaction  usually  takes  place  at 
once,  but  if  the  amount  of  albumen  is  very  small,  it  may  be  somewhat  delayed. 

If  we  have  found  out  that  the  urine  certainly  contains  albumen,  we  must  then 
decide  whether  we  have  really  a  true  renal  albuminuria — that  is,  whether  a  urine 
already  albuminous  is  secreted  in  the  kidneys,  or  whether  the  albumen  is  not 
mixed  with  a  perfectly  normal  or  at  least  non-albuminous  urine  later,  in  the  kid- 
neys themselves  or  in  the  urinary  passages,  the  pelvis  of  the  kidney,  or  the  bladder 
(spurious,  accidental  albuminuria).  Such  a  spurious  albuminuria  occurs  when 
the  urine  is  contaminated  with  blood  (as  in  hsemorrhages  from  the  kidneys,  the 
pelvis  of  the  kidney,  the  bladder,  or  the  urethra),  or  with  pus  (in  pyelitis,  cystitis, 
etc.).  In  these  cases,  of  course,  the  albumen  contained  in  the  serum  of  the  blood 
or  pus  is  found  in  the  urine.  Spurious  albuminuria  is  usually  easily  recognized, 
since  the  presence  of  pus  or  blood  in  the  urine,  which  is  shown  by  the  appear- 
ance of  the  urine  or  upon  microscopic  examination  (red  blood-corpuscles,  pus-cor- 
puscles), points  with  immediate  certainty  to  the  origin  of  the  albuminuria. 
Moreover,  the  amount  of  albumen  in  these  cases  is  usually  but  slight,  and  corre- 
sponds to  the  amount  of  pus  or  blood  in  the  urine.  A  disproportion  in  this  respect 
must  excite  the  suspicion  whether,  beside  the  spurious  albuminuria,  there  is  not 
perhaps  at  the  same  time  an  affection  of  the  kidneys  causing  a  true  renal  albu- 
minuria. The  determination  of  this  point  is  not  always  perfectly  easy,  but  we 
can  usually  come  to  a  decision  by  finding  abnormal  morphological  constituents 


KEMAEKS  IIP0:N'  THE  PATHOLOGY  OF  RENAL  DISEASE     591 

in  the  urine,  the  so-called  urinary  casts  (vide  infra),  which  give  indubitable  evi- 
dence of  the  existence  of  a  disease  of  the  kidneys. 

What  general  pathological  significance  has  the  true  renal  albuminuria,  and 
what  are  the  causes  of  its  origin  ?  According  to  our  present  theories,  the  answer 
to  these  questions  is  simply  this :  In  every  case  of  genuine  albuminuria  there  is 
an  abnormal  transudation  of  the  albumen  of  the  blood  into  the  urine.  The 
place  of  this  transudation  is  chiefly  the  glomeruli,  and  its  immediate  cause  is  the 
abnormal  permeability  of  the  walls  of  the  glomeruli,  due  to  disease  of  those  struc- 
tures, and  particularly  of  their  epithelium.  The  fact  that  the  easily  filtrated 
serum  albumen  of  the  blood,  as  well  as  the  water,  does  not  pass  through  the 
vascular  loops  of  the  glomeruli,  even  under  normal  conditions,  is  due  entirely  to 
the  circumstance  that  the  capillaries  of  the  Malpighian  bodies  are  not  inserted 
bare  into  the  beginning  of  the  uriniferous  tubules,  but  that  they  are  covered  with 
epithelium.  This  epithelium  of  the  glomeruli  has  the  physiological  task  and  the 
power  of  providing  for  the  retention  of  the  album.en  in  the  blood.  If  it  suffers  a 
pathological  change  in  any  way,  it  loses  this  power,  and  then  the  albumen  passes 
into  the  urine  (Heidenhain).  The  inflammatory  changes  which  the  walls  of  the 
blood-vessels  themselves  undergo  probably  facilitate  the  transudation  of  serum 
albumen,  as  is  suggested  by  what  we  know  about  inflammatory  exudations  in 
other  parts  of  the  body.  The  best  experimental  proof  of  the  theory  that  the 
changes  in  the  walls  of  the  glomeruli  are  the  chief  cause  of  the  appearance  of 
albumen  in  the  urine  is  furnished  by  the  albuminuria  which  appears  whenever 
the  supply  of  arterial  blood  to  the  kidney  is  checked  by  a  temporary  constriction 
of  the  renal  artery.  The  epithelium  of  the  glomeruli  thereby  suffers  a  visible 
microscopic  change.  If  the  kidneys  in  this  condition  are  removed  as  rapidly  as 
possible  and  boiled,  according  to  Posner's  suggestion,  we  can  discover  under  the 
microscope  in  the  capsules  of  the  glomeruli  the  albumen  that  is  thus  coagulated 
(Ribbert) — a  most  certain  sign  that  the  passage  of  the  albumen  from  the  blood- 
vessels into  the  urinary  passages  has  in  fact  taken  place  in  the  glomeruli. 

Almost  all  cases  of  albuminuria  may  readily  be  referred  to  analogous  disturb- 
ances of  nutrition  in  the  epithelium  of  the  glomeruli,  whether  they  be  excited  by 
anomalies  of  the  circulation,  such  as  arterial  anaemia  or  venous  stasis,  by  toxic  or 
infectious  influences  which  have  reached  the  glomeruli,  or  by  any  other  circum- 
stances. In  these  cases  the  changes  in  the  glomeruli  need  not  always  be  of  a 
very  severe  or  irreparable  nature;  for  we  often  see  a  slight  albuminuria  appear 
under  the  most  different  conditions,  and  rapidly  pass  off  again.  This  is  the  so- 
called  "  transitory  albuminuria,"  which  is  seen,  for  example,  in  various  febrile 
affections,  after  slight  intoxications,  after  epileptic  attacks  or  in  other  severe 
nervous  conditions,  in  lead-colic,  etc.  We  will  show  later  how  the  anatomical 
changes  in  the  glomerular  epithelium  explain  the  occurrence  of  albuminuria  in 
severe  renal  diseases. 

The  other  factors,  which  have  also  been  made  answerable  for  the  origin  of 
albuminuria,  are  without  doubt  quite  subordinate  to  the  changes  in  the  epithe- 
lium of  the  glomeruli,  and  at  most  they  can  affect  merely  the  amount  of  albumen 
eliminated.  The  changes  in  the  composition  of  the  blood,  on  which  formerly,  and 
again  by  some  investigators  recently,  great  stress  has  been  laid,  especially  the  hy- 
draemia  and  hypalbuminosis  (the  diminished  amount  of  albumen)  of  the  blood, 
have  probably  only  an  indirect  significance,  since  the  nutrition  of  the  walls  of 
the  glomeruli  suffers  from  such  a  faulty  condition  of  the  blood,  and  this  circum- 
stance again  is  the  true  cause  of  elimination  of  the  albumen. 

The  significance  of  the  blood-pressure  with  regard  to  the  occurrence  of  albu- 
minuria was  also  formerly  very  much  overrated.  According  to  the  older  hypoth- 
esis, it  was  believed  thct,  in  an  increase  of  the  blood-pressure,  the  molecules  of 
albumen  in  the  blood  could  be  pressed  through  the  filter  formed  by  the  membrane 


>92 


DISEASES    OF   THE   IIRINAEY   OEGAIStS 


of  the  glomeruli.  This  hypothesis  has  been  disproved,  especially  by  the  experi- 
ments of  Runeberg;  these  experiments  showed  that,  in  the  filtration  of  solutions 
of  albumen  through  animal  membranes,  a  rise  in  the  filtration  pressure  was  fol- 
lowed by  a  decrease,  and  a  fall  in  the  pressure  by  an  increase  of  the  percentage  of 
albumen  in  the  filtrate. 

Although  in  the  preceding  paragraphs  only  the  Malpighian  bodies  have  been 
regarded  as  the  spot  where  the  transudation  of  the  albumen  of  the  blood  into  the 
urine  takes  place,  we  must  also  note  that,  under  some  circumstances,  we  may 
admit  the  possibility  of  a  passage  of  albumen  directly  into  the  tubules  from  the 
capillaries  that  encircle  the  uriniferous  tubules;  but  we  must  also  necessarily 
assume  in  such  cases  that  there  is  a  disturbance  of  nutrition  in  the  membranse 
propriee,  or  at  least  in  the  epithelium  of  the  uriniferous  tubules.  Such  an  assump- 
tion seems  to  explain  the  albuminuria,  according  to  Senator's  experiments,  in 
venous  stasis  in  the  kidneys,  although  in  these  cases  the  epithelium  of  the  glome- 
ruli also  suffers  soon,  and  then  becomes  pervious  to  albumen. 

2.  Casts  and  other  Abnormal  Morphological  Constituents  of  the  Urine  in 

Eenal  Disease 

Beside  albuminuria,  certain  peculiar  morphological  constituents  of  the  urine, 
visible  under  the  microscope,  are  of  especial  importance  for  the  diagnosis  of  renal 
affections — the  urinary  casts,  whose  significance  was  first  correctly  recognized  by 

Henle  in  1842_.  These  are  cylindri- 
cal bodies,  whose  breadth  corre- 
sponds to  the  width  of  the  urinif- 
erous tubule,  and  whose  length  only 
exceptionally  reaches  a  millimetre, 
which  must  be  regarded  in  their 
chemical  nature  as  consisting  main- 
ly of  a  coagulated  albuminous  sub- 
stance. To  the  latter  circumstance 
we  owe  their  old  name  of  "  fibrine 
casts,"  or  "  fibrous  casts,"  a  name 
which  is  obsolete,  and  properly  so, 
since  the  coagulated  albuminous 
substance  of  casts  is  certainly  not 
identical  with  fibrine. 

Since  the  precise  conditions  of 
the  occurrence  and  the  character  of 
the  renal  casts,  in  the  different  dis- 
eases of  the  kidneys,  will  be  spoken 
of  later,  we  need  discuss  here  only 
the  general  properties,  the  origin,  and  the  significance  of  casts  (see  Fig.  68). 
1.  Hyaline  Casts. — The  hyaline  casts  are  the  commonest  and  most  important 
form  of  casts,  and,  to  a  certain  extent,  are  the  ground-form  for  different  varieties. 
They  are  perfectly  homogeneous,  clear  as  glass,  colorless,  soft,  and  flexible.  "We 
find  them  either  wide  or  narrow,  sometimes  broken  ofi  short,  sometimes  quite  long, 
usually  straight,  but  in  many  cases  partly  curved.  They  are  easily  stained  with 
carmine  or  gentian-violet.  On  heating  the  urine,  they  are  dissolved,  but  they  are 
quite  resistant  to  acids. 

The  hyaline  casts  are  very  often  covered  to  a  greater  or  less  extent  with  all 
sorts  of  deposits,  which  are  usually  affixed  to  the  soft  substance  of  the  cast  in  the 
kidney  itself,  but  which  may  often  be  attached  to  it  later.  These  deposits  are  as 
follows:  First,  red  blood-corpuscles.  This  condition  is  important,  because  it 
points  with  certainty  to  the  existence  of  htemorrhages  in  the  kidneys  themselves. 


Fig.  68. — Different  forms  of  casts,  a.  Hyaline  cast  with 
occasional  granules,  b.  Hyaline  cast  with  fat-drops 
and  granular  cells,  c.  Hyaline  cast  with  red  blood- 
corpuscles  attached,  d.  Hyaline  cast  with  white 
blood-corpuscles  attached,  e.  Cast  with  a  large 
number  of  fat-drops. 


KEMAEKS  UPON  THE  PATHOLOGY  OF  EENAL  DISEASE     593 


Second,  of  white  blood-corpuscles.  These  are  often  considerably  swollen,  so  that 
we  must  guard  against  mistaking  them  for  epithelium.  Third,  of  renal  epithe- 
lium, which  may  be  recognized  by  its  size,  its  more  angular  shape,  and  its  nuclei. 
Of  course,  we  often  find  the  epithelium  cloudcs"  and  granular,  or  shriveled  and 


lar  globules — that  is,  both  fatty-de- 
white  blood-corpuscles  which  are  filled 
generated  cells.  Fifth,  of  little  gran- 
always  be  easily  recognized.  They 
albumen,  or  fat-drops,  or  urates,  or 
hsematoidine,  which  have  come  from 


Fig.  70. 


atrophied.  Fourth,  of  fatty  granu- 
generated  epithelium  and  also 
with  fat-drops  from  the  fatty-de- 
ular  masses  whose  nature  can  not 
are  either  coagulated  granules  of 
bacteria,  or,  finally,  granules  of 
the  destruction  of  red  blood-cor- 
puscles, and  are  usually  easily  rec- 
ognized by  their  dark,  brownish- 
yellow  color.  Sixth,  we  rarely  find 
in  the  casts  drops  like  myeline,  as 
to  whose  precise  significance  noth- 
ing is  known. 

As  to  the  origin  of  hyaline 
casts,  despite  many  investigations 
the  question  has  not  been  fully 
answered.  Probably  they  are  due 
to  the  coagulation  of  the  excreted 
albumen  occasioned  by  the  dying 
epithelial  cells  and  the  escaped  leu- 
cocytes. It  may  be  questionable 
whether,  in  this  process  of  coagula- 
tion, the  albumen  excreted  with 
the  urine  by  the  glomeruli  is  in- 
volved, or  the  albumen  due  to  the 
inflammatory  exudation  and  origi- 
nating from  the  other  renal  blood- 
vessels.    From  analogy  with  other 

inflammations  which  lead  to  coagulable  exudates,we  regard  the  latter  as  the 
more  probable  supposition.  Furthermore,  many  investigators  assume  that  the 
desquamated  and  disintegrating  epithelium  is  transformed  into  hyaline  casts. 

2.  The  epithelial  casts  are  composed  exclusively  of  renal  epithelium,  although 
probably  hyaline  casts  not  infrequently  form  a  basis  to  which  the  epithelial  cells 
adhere.  Epithelial  casts  are  usually  easily  recognized,  and  always  indicate  an 
excessive  desquamation  of  epithelium  in  the  diseased  kidneys.  One  must  be  on 
one's  guard,  as  already  mentioned,  not  to  confound  renal  epithelium  with  swollen 
white  blood-corpuscles.  The  separate  epithelial  cells  and  the  epithelial  casts  may 
present  various  changes,  such  as  granular  opacity,  fatty  degeneration,  and 
atrophy. 

3.  The  so-called  waxy  casts  are  almost  always  rather  broad  and  usually  yellow- 
ish-colored, opaque  casts,  of  evidently  a  much  tougher  consistency  than  hyaline 
casts.  We  have  found  them  most  frequently  in  severe  acute  nephritis,  either 
primary,  or  secondary  to  scarlet  fever,  but  they  also  appear  in  the  severer  forms 
of  chronic  diffuse  nephritis.  As  to  their  origin,  we  are  convinced  that  they  cer- 
tainly in  many  eases  are  formed  out  of  epithelial  casts.  The  closely  apposed  renal 
epithelial  cells  degenerate  into  waxy  flakes,  and  gradually  coalesce.  One  can,  in 
fact,  observe  all  stages  of  transition  between  the  epithelial  casts  and  the  almost 
completely  homogeneous  waxy  casts.  Fiirbringer,  therefore,  terms  waxy  casts 
"  metamorphosed  " ;  and  he  insists,  correctly,  that  they  always  indicate  severe  dis- 
ease of  the  kidney. 

38 


a  b  c 

Fig.  69. 

Fig.  69. — a.  Waxy  cast.    b.  'Waxy  cast  bearino:  crystals  of 

calcic  oxalate,    c.  Fragments  of   waxy  casts. 

(From  von  Jaksch.) 

Fig.  70.— Epithelial  cast,  granular  in  its  lower  half. 

(From  von  Jaksch.) 


594  DISEASES  OF   THE   UEINAEY   OKGAKS 

4.  Granular  Casts. — ^A  kind  of  cast  "whicli  is  composed  of  coarse,  yellowish, 
flaky  granules  represents  the  just-mentioned  transition  of  epithelial  casts  into 
waxy  casts.  In  other  cases  the  waxy  casts  are  nothing  but  hyaline  casts  com- 
pletely covered  with  the  above-mentioned  granules  of  various  kinds.  Sometimes, 
also,  coagulated  masses  of  albumen  or  granules  of  hsematoidine  may  themselves 
be  formed  into  cylindrical  shapes. 

Genuine  blood  casts  are  not  very  frequent.  They  consist  of  coagulated  blood 
and  represent  casts  of  the  renal  canals  into  which  haemorrhage  has  taken  place. 

The  clinical  diagnostic  significance  of  renal  casts  is  very  great.  They  are,  in 
the  first  place,  always  a  sure  sign  of  the  existence  of  some  renal  disease,  since  in 
normal  urine  casts  are  not  found  at  all,  or,  at  most,  they  are  exceptional  and  are 
present  in  small  numbers.  The  consideration  of  the  special  forms  of  casts,  and 
of  the  deposit  upon  them,  is  also  of  great  diagnostic  importance,  although  from  it 
we  can  never  decide  immediately  upon  the  general  form  of  the  renal  disease,  but 
we  can  recognize  with  certainty  the  type  of  special  pathological  processes  in  the 
kidneys.  Frerichs  has  well  named  casts  "  messengers  from  the  kidneys."  The 
blood-casts  and  the  red  blood-corpuscles  sticking  to  the  cylinders  point  to  the 
occurrence  of  renal  haemorrhages;  the  epithelial  casts  to  a  desquamation  of  the 
epithelium  in  the  kidneys;  the  white  blood-corpuscles  to  an  emigration  of  the 
colorless  cells  from  the  vessels;  the  fatty  granular  cells  to  processes  of  fatty 
degeneration  in  the  kidneys. 

We  have  already  learned  to  recognize  in  a  great  measure  in  the  preceding,  as 
occasional  deposits  on  the  casts,  the  other  morphological  constituents  found,  be- 
side the  casts,  in  the  sediment  of  the  urine  in  renal  disease.  Briefly  recapitulated, 
they  are  as  follows : 

1.  Bed  hlood-corpuscles.  The  presence  of  a  large  amount  of  blood  in  the  urine 
(haematuria)  is  almost  always  to  be  recognized  by  its  blood-red  color.  The  blood 
may  be  made  out  with  certainty  by  the  microscope,  or  by  Heller's  blood-test.  The 
latter  is  performed  by  heating  the  urine  in  a  test-tube  with  sodic  or  potassic 
hydrate.  The  blood-corpuscles  are  thus  dissolved,  and  the  hsematine  formed 
from  the  blood-pigment  is  precipitated  with  the  phosphates,  giving  to  the  pre- 
cipitate o^  the  latter  a  very  characteristic  blood-red  color.  Van  Deen's  test  is  very 
distinct  and  easily  performed.  It  requires  a  freshly  prepared  mixture  of  equal 
parts  of  old  oil  of  turpentine  and  newly  m.ade  tincture  of  guaiac.  This  mixture 
is  poured  upon  the  urine  to  be  examined,  and  slightly  shaken.  At  the  place  of 
contact  of  the  two  fluids  there  will  immediately  form  a  beautiful  blue  ring,  if 
there  is  the  slightest  trace  of  blood  in  the  urine.  Finally,  of  course^  the  spectro- 
scope may  serve  for  the  detection  of  hsematuria.  Hsemoglobinuria  will  be  de- 
scribed in  a  special  chapter  later. 

2.  White  hlood-corpuscles.  Only  when  they  are  also  attached  to  the  casts  can 
we  assume  with  certainty  that  these  come  from  the  kidneys,  and  not  from  the 
lower  portions  of  the  urinary  tract. 

3.  Renal  epithelium. 

4.  Fat-drops  and  fatty  granular  cells. 

5.  Uric-acid  crystals,  urates  and  calcic  oxalate,  hacteria,  etc. 

For  microscopic  examination  of  the  urinary  .sediment,  we  let  the  urine  settle 
in  a  tall  beaker;  it  is  more  convenient,  and,  if  the  urine  contains  few  morpho- 
logical constituents,  far  more  reliable  to  employ  a  centrifugal  machine. 

3.  The  Dropsy  of  Eenal  Disease 

Although  the  changes  in  the  urine  must  be  alone  decisive  in  the  diagnosis 

of  any  renal  disease,  there  are  yet  certain  other  symptoms  which  are  also  due 

immediately  to  the  renal  affection,  and  which  may  first  direct  our  suspicions  to 

the  existence  of  a  disease  of  the  kidneys,  and  consequently  lead  to  a  careful  exam- 


EEMAEKS  UPON  THE  PATHOLOGY  OP  RENAL  DISEASE     595 

ination  of  the  urine.  Among  these  symptoms  the  dropsy  of  renal  disease  is  one  of 
the  commonest  and  most  important.  This  may,  indeed,  quite  frequently  be  en- 
tirely absent,  both  in  acute  and  chronic  nephritis,  and  in  other  diseases  of  the  kid- 
neys ;  but  in  many  cases  it  is  decidedly  prominent  in  the  whole  clinical  picture. 

If  we  ask  what  is  the  reason  of  the  frequent  occurrence  of  dropsy  in  renal  dis- 
ease, the  answer  at  first  does  not  seem  difficult.  Since  the  main  function  of  the 
kidneys  is  to  excrete  water  from  the  body,  and  since,  as  we  shall  see  later,  in  many 
cases  the  diseased  kidney  can  no  longer  fulfill  this  task,  or  can  fulfill  it  only  to 
a  slight  degree,  we  are  not,  in  fact,  veiy  much  out  of  the  way  in  considering  the 
retention  of  water  in  the  body  as  rhe  main  cause  of  the  consequent  oedema.  Clin- 
ical observation  seems  in  general  to  agree  completely  with  this  assumption.  The 
oedema  in  renal  disease  seldom  appears  until  the  daily  amount  of  urine  has  been 
below  the  normal  for  some  time,  while,  on  the  other  hand,  in  those  cases  where 
the  amount  of  urine  passed  is  normal,  or  even  abnormally  great,  in  spite  of  the 
existing  renal  disease,  oedema  is  usually  wholly  absent.  In  individual  cases, 
too,  we  very  often  see  a  decrease  of  the  oedema  associated  with  an  increase  in  the 
amount  of  urine,  and  an  increase  of  the  oedema  associated  with  a  corresponding 
diminution  in  the  excretion  of  urine.  The  pathological  process  accordingly  seems 
to  consist  of  an  accumulation  in  the  body  of  the  water  which  can  not  be  excreted 
from  it,  and  which  transudes  from  the  vessels  and  thus  gives  rise  to  the  develop- 
ment of  oedema. 

On  more  careful  consideration,  however,  there  are  some  objections  to  this 
theory,  which  is  apparently  so  simple.  In  the  first  place,  it  might  be  supposed 
that,  when  there  is  retention  of  water,  the  body  must  get  rid  of  the  surplus  water 
by  employing  to  a  greater  degree  the  other  channels  of  elimination  which  are  at 
its  service — the  skin  and  the  intestines.  Since  we  can  never  determine  accurately 
the  time  when  the  water  first  begins  to  be  retained  in  the  body,  the  clinical  experi- 
ence just  mentioned  may  also  be  thus  interpreted,  that  the  lessened  excretion  of 
urine  is  not  the  cause  of  the  oedema,  but  that,  on  the  contrary,  the  appearance  of 
oedema  is  rather  the  cause  of  the  diminished  elimination  of  water  by  the  kidneys. 
The  other  clinical  facts,  also,  are  inconsistent  with  the  view  that  the  oedema  de- 
pends upon  the  simple  accumulation  of  water  in  the  blood.  In  many  forms  of 
nephritis,  and  particularly  in  the  nephritis  of  scarlet  fever,  we  very  often  see 
extreme  oedema  appear  suddenly,  while,  on  the  other  hand,  many  severe  varieties 
of  nephritis — e.  g.,  those  associated  with  diphtheria,  septic  diseases,  and  pneu- 
monia, run  their  course  with  little  or  no  oedema,  although  they  are  characterized 
by  a  marked  diminution  in  the  amount  of  urine.  Moreover,  cases  have  been 
repeatedly  observed  in  which,  as  a  result  of  obstruction  of  the  ureters,  or  from 
pressure  on  these  canals,  there  has  been  complete  anuria  for  several  days  without 
a  trace  of  oedema  developing;  and  experimental  investigations  have  given  corre- 
sponding results.  The  bilateral  ligation  of  the  ureters  in  animals  does  not  lead 
to  the  development  of  oedema  even  after  several  days.  Cohnheim  and  Lichtheim 
introduced  large  amounts  of  a  one-half  to  one-per-cent.  solution  of  common  salt 
into  the  vascular  system  of  an  animal,  and  despite  this  great  artificial  "  hydrseraic 
plethora,"  observed  no  oedema,  even  when  the  renal  arteries  were  tied.  Nor 
can  oedema  be  provoked  by  slow  and  continuous  infusion  (Gartner,  Francotte). 

Consequently,  we  must  seek  some  other  cause  to  explain  the  oedema  of  nephri- 
tis, and  this  is  in  all  probability  the  peculiar  change  in  the  vascular  walls, 
which  renders  them  more  permeable  and  permits  the  water  accumulated  in  the 
blood  to  transude  into  the  tissues.  Just  what  this  change  in  the  vascular  walls 
may  be  and  what  produces  it  we  do  not  yet  know;  probably  there  are  chemical 
agents  which  change  the  vascular  walls,  either  the  same  substances  which  excite 
the  nephritis,  or  matters  secondarily  formed,  or  certain  products  of  metamor- 
phosis retained  in  the  blood  because  of  the  inefficiency  of  the  kidneys.     That 


596  DISEASES    OF   THE   UKIKAKY   OEGAXS 

dropsy  develops  because  of  direct  damage  to  the  blood-vessels  is  rendered  probable 
from  the  cases  of  so-called  "  acute  essential  dropsy,"  in  which,  there  develops  a 
considerable  general  dropsy,  just  as  in  acute  nephritis,  often  preceded  by  mild 
gastro-intestinal  symptoms,  and  yet  without  a  trace  of  albumen  in  the  urine  or 
any  other  demonstrable  cause  for  this  dropsy,  which  usually  soon  abates. 

Many  clinical  peculiarities  of  nephritic  oedema  harmonize  with  this  concep- 
tion of  its  origin.  In  general,  we  may  say  that  the  oedema  of  nephritic  patients 
appears  first  in  the  skin  ("  anasarca  "),  and  has  a  striking  tendency  to  show  first 
in  the  face,  in  contrast  with  the  oedema  due  to  the  passive  congestion  of  heart 
disease,  which  usually  begins  in  the  ankles.  The  puffy  and  noticeably  pale  coun- 
tenance of  the  patient  will  often  suggest  the  existence  of  kidney  trouble  at  the 
first  glance.  In  severe  cases  the  dropsy  often  develops  over  the  whole  body  in  an 
extreme  degree,  involving  the  skin  of  the  trunk,  and  particularly  the  dependent 
parts,  the  extremities,  and  scrotum,  so  that  the  patient  is  a  pitiable  object.  In 
such  cases  there  are  also  apt  to  be  dropsical  transudations  into  the  internal  cav- 
ities of  the  body,  causing  hydrothorax,  ascites,  and  hydropericardium ;  and  these 
aggravate  the  patient's  distress.  It  is,  however,  a  striking  fact  that  often  there 
will  be  marked  dropsical  effusions  (ascites,  hydrothorax),  and  yet  no  marked 
oedema  of  the  skin ;  and  hydrothorax  is  sometimes  much  greater  on  one  side  than 
on  the  other.  All  these  facts  indicate  special  local  conditions — viz.,  the  changes 
in  the  blood-vessels,  which  we  have  surmised.  Still  more  is  this  the  case  with 
regard  to  the  oedema  of  mucous  membranes  which  sometimes  occurs.  There  may 
be  oedema  of  the  conjunctiva,  of  the  soft  palate,  of  the  ary-epiglottic  ligaments 
(oedema  of  the  glottis),  and  other  parts.  (Edema  of  this  sort  is  apt  to  resemble 
a  mild  local  inflammation,  and  in  general  it  is  impossible  to  deny  a  certain  rela- 
tionship between  "  inflammatory  "  oedema  and  nephritic  oedema.  The  nephritic 
oedema  of  the  skin  may  in  places  have  suggestions  of  an  inflammatory  nature, 
such  as  slight  redness  and  tenderness.  (Edema  may  affect  the  internal  organs,  and 
nephritic  pulmonary  oedema  is  of  great  practical  importance.  The  question  of 
the  existence  of  cerebral  oedema  and  of  its  possible  importance  will  be  discussed 
below  (see  uraemia). 

The  preceding  remarks  relate  only  to  genuine  nephritic  oedema.  We  shall  see 
later  that  oedema  may  have  an  entirely  different  origin,  particularly  in  cases  of 
chronic  nephritis — that  is,  if  there  is  a  cardiac  hypertrophy  and  the  powers  of  the 
heart  become  impaired,  dropsy  may  at  last  develop.  This  oedema  is  of  course  a 
genuine  congestive  oedema,  and  exactly  similar  to  that  seen  in  failing  compensa- 
tion in  heart  disease. 

In  its  chemical  composition,  the  dropsical  fluid  corresponds  to  a  very  thin 
blood-serum.  The  amount  of  water  is  usually  97  to  98  per  cent.,  the  amount  of 
salts  one  to  one  and  a  half  per  cent.  The  amount  of  albumen  is  usually  very 
slight.    Urea  has  been  repeatedly  found  in  the  fluid. 

4.  IjR.rMIA 
If  the  diseased  kidneys  can  no  longer  perform  their  secretory  functions  in  a 
satisfactory  way,  not  only  does  the  elimination  of  water  from  the  body  thereby 
suffer,  but  the  soluble  constituents  of  the  urine,  the  salts,  the  urea,  and  the  other 
final  products  of  tissue  metamorphosis  may  also  be  retained  in  the  blood  and  ac- 
cumulate there.  Hence  we  often  find  the  blood,  in  patients  with  renal  disease,  not 
only  more  watery  than  under  normal  conditions,  so  that  the  specific  gravity  of 
the  serum  may  fall  from  1030  to  1020,  or  even  lower,  but,  in  almost  all  cases  where 
there  is  a  diminished  excretion  of  urine,  it  is  also  richer  in  urea,  as  many  experi- 
ments have  shown,  and  under  corresponding  conditions  it  is  probably  also  fre- 
quently richer  in  the  other  constituents  of  the  urine,  or  in  substances  correspond- 
ing to  them  but  not  completely  metamorphosed. 


EEMAEKS  UPON  THE  PATHOLOGY  OF  EEKAL  DISEASE     597 

This  accumulation  of  the  urinary  constituents  in  the  blood,  and  further,  per- 
haps, in  the  tissues  themselves,  is  the  cause  of  a  class  of  symptoms  which  are  often 
seen  in  diseases  of  the  kidneys,  and  which  are  termed  uraemic  symptoms  or 
uremia. 

Probably  no  one  to-day  doubts  that  uraemia  must  be  regarded  as  essentially  an 
intoxication  of  the  body  by  the  retained  products  of  tissue  metamorphosis.  Nu- 
merous experimental  investigations  have  proved  that  in  animals  extirpation  of 
the  kidneys,  or  ligation  of  the  ureters,  will  produce  a  symptom-complex,  charac- 
terized by  vomiting,  convulsions,  and  coma — almost  completely  analogous  to  the 
iTrsemia  of  Bright's  disease ;  but  if  we  inquire  what  constituents  of  the  urine  are 
the  particular  occasion  of  the  uraemic  phenomena,  we  can  not  as  yet  obtain  any 
definite  answer.  For  a  long  time  it  was  believed  that  urea  played  a  chief  part  in 
the  development  of  uraemia,  but  the  result  of  experiments  upon  animals  does  not 
support  this  view.  It  is  possible  to  inject  enormous  amounts  of  urea  into  the  cir- 
culation or  into  the  peritoneal  cavity  of  animals  without  any  symptoms  of  poison- 
ing. Voit  did,  indeed,  show  that  the  healthy  kidneys  remove  from  the  blood  the 
excessive  amount  of  urea  with  extreme  rapidity,  and  that  accordingly  uraemic 
symptoms  do  really  appear  if,  while  we  are  feeding  an  animal  with  large  amounts 
of  urea,  we  impede  the  excretion  of  the  urea  by  a  simultaneous  withholding  of 
water.  Yet  the  amount  of  urea  necessary  for  the  success  of  this  experiment  is 
greater  than  can  possibly  exist  in  the  ordinary  uraemia  of  Bright's  disease;  and, 
moreover,  the  withholding  of  water  might  also  prevent  the  excretion  of  other 
matters;  hence  we  must  seek  for  other  poisonous  substances  as  factors  in  the 
production  of  uraemia.  Many  experiments  seem  to  indicate  that  the  potassium 
salts  are  especially  poisonous,  while  some  authors  have  laid  the  blame  mainly  on 
the  extractive  matters,  such  as  creatinine.  Bouchard  has  sought  to  prove  that 
certain  alkaloid  substances  (urotoxines),  which  are  probably  developed  during  the 
digestion  of  albumens  and  are  always  demonstrable  in  normal  urine,  occasion  the 
phenomena  of  uraemia ;  but  to  all  these  suppositions  there  are  serious  objections, 
so  that  really  the  substances  which  occasion  uraemic  intoxication  are  as  yet  un- 
identified. It  might  be  possible  that  the  poison  corresponding  to  uraemia  is  not, 
in  every  case,  the  same. 

The  mode  of  action  of  the  toxic  material  is  as  unsettled  as  is  its  chemical 
nature.  This  much  only  is  certain,  that  in  uraemia  the  disturbances  are  almost 
exclusively  cerebral,  and  in  the  m_ain  located  in  the  cortex  of  the  brain ;  but 
whether  there  is  actually  a  direct  injury  of  the  nervous  elements,  or  whether  the 
immediate  action  is  upon  the  blood-vessels,  is  uncertain.  The  occurrence  of 
uraemic  focal  symptoms,  to  which  we  shall  refer  below,  renders  the  former  supposi- 
tion the  more  likely.  Fleischer  produced  uraemia  experimentally  in  animals,  and 
in  every  case  observed  an  extreme  anaemia  of  the  brain  and  spinal  cord,  so  that  he 
concludes  that  there  is  a  spasm  of  the  blood-vessels. 

Clinical  experience  also  agrees  perfectly  with  the  theory  that  uraemia  is  caused 
by  a  retention  of  urinary  constituents  in  the  body.  In  most  cases  the  uraemic 
symptoms  appear  only  when  the  daily  amount  of  urine  has  fallen  to  a  very  low 
figure,  or  when  the  secretion  of  urine  has  wholly  ceased  for  several  days.  That 
in  these  cases  not  only  the  elimination  of  water,  but  also  the  elimination  of 
an  amount  of  urea  corresponding  to  the  food  taken,  and  also  the  elimination  of 
the  other  urinary  constituents,  is  very  much  diminished,  is  shown  by  the  experi- 
ments in  regard  to  this  point  made  by  Fleischer  and  others.  Furthermore,  a 
great  increase  of  the  amount  of  urea  in  the  blood  in  uraemic  patients  has  been 
found  in  many  if  not  in  all  cases. 

Of  course  there  can  be  no  question  that  some  clinical  facts  can  not  be  brought 
into  exact  harmony  with  what  has  been  previously  said.  If  cases  are  repeatedly 
reported  in  which  no  uraemic  symptoms  have  appeared  in  spite  of  anuria  lasting 


598  DISEASES    OF   THE   URINARY   ORGANS 

several  days,  it  does  not  prove  very  much,  since  we  can  never  make  an  exact  esti- 
mate of  the  matter  accumulated  in  the  blood  which  ought  to  have  been  eliminated ; 
for  the  organism  can  certainly  get  rid  of  the  final  products  of  tissue  metamor- 
phosis in  other  ways  than  through  the  kidneys — for  instance,  through  the  skin 
or  the  intestines — and  we  must  also  bear  in  mind  that  different  individuals  show 
a  great  diversity  in  tolerating  the  action  of  any  poison  in  the  body,  particularly 
as  regards  the  nervous  system.  It  is  harder  to  explain  those  cases  which  are  some- 
times seen,  in  which  ureemic  symptoms  suddenly  appear  in  patients  with  renal  dis- 
ease, although  these  symptoms  are  not  preceded  by  any  noticeable  diminution  of 
the  secretion  of  urine.  We  may,  however,  assume  that,  despite  the  abundant  ex- 
cretion of  water  and  the  normal  amount  of  urine,  there  has  been  a  slight  retention 
of  solid  matters.  Analogy  with  other  kinds  of  poisoning  makes  the  supposition 
very  plausible  that  the  long  persistent  retention  of  even  extremely  small  portions 
of  toxic  matter  may  occasion  an  absolutely  sudden  explosion  of  the  severest  symp- 
toms. In  chronic  lead  and  mercurial  poisoning  the  symptoms  often  appear  with 
great  abruptness,  although  the  poisoning  has  taken  place  very  slowly  and  grad- 
ually. In  the  same  way  we  explain  to  ourselves  the  not  very  infrequent  cases  of 
the  sudden  development  of  severe  urfemic  symptoms,  as  seen  particularly  in 
patients  with  contracted  kidney  (vide  infra),  in  whom  it  may  seem  as  if  no  single 
prodromal  symptom  had  indicated  the  impending  outburst  of  intoxication.  Often, 
also,  peculiar  circumstances  may  favor  the  occurrence  of  ursemia — for  example, 
the  development  of  cardiac  weakness,  so  that  the  blood  tension  is  diminished  and 
the  excretion  of  urine  impeded.  In  some  cases  again  it  is  observed  that  the  devel- 
opment of  urasmia  coincides  with  the  absorption  of  previously  existing  oedema. 
This  is  explained  by  the  supposition  that  the  rapid  absorption  of  the  oedema  in- 
troduces into  the  blood  a  comparatively  large  amount  of  the  poisonous  products 
of  metabolism,  which  had  not  been  excreted,  but  had  been  contained  in  the 
cedematous  fluid. 

While  we  are  firmly  of  the  opinion  that  uraemia  is  to  be  regarded  as  a  poison- 
ing of  the  body  by  the  retained  constituents  of  the  urine,  yet  we  should  not  fail 
to  mention  that  attempts  have  been  made  to  explain  in  other  ways  the  ursemic 
phenomena.  In  particular,  Traube  has  propounded  the  theory  that  the  so-called 
ursemic  symptoms  are  dependent  upon  an  acutely  developing  cerebral  oedema,  and 
consequent  cerebral  anasniia.  This  theory  can  be  regarded  as,  on  the  whole,  unten- 
able. Still,  it  may  contain  a  certain  amount  of  truth,  for  we  can  not  wholly 
deny  that  sometimes  there  may  be  actual  anatomical  lesions,  such  as  inflamma- 
tory oedema  of  the  brain,  in  the  course  of  a  nephritis,  suflicient  to  occasion  severe 
cerebral  symptoms.  During  nephritis,  secondary  inflammation  may  appear  in 
almost  all  the  internal  organs,  and  often  suddenly;  and  this  sort  of  nephritic 
inflammation  is  especially  frequent  in  the  retina,  a  structure  composed  of  nervous 
elements,  so  that  the  possibility  of  similar  disease  in  the  brain  is  very  great.  If 
we  consider  that  cases  of  ursemic  hemiplegia  and  monoplegia  have  been  repeat- 
edly observed,  and  that  likewise  cases  have  been  described  of  ursemic  Jacksonian 
epilepsy,  hemianopsia  and  aphasia,  it  will  be  seen  that  the  supposition  of  an  ac- 
tual local  lesion  as  the  explanation  of  such  well-marked  focal  symptoms  is  very 
plausible.  Yet  we  must  also  consider  that  in  the  last  analysis  the  cause  of  such 
limited  cedematous — or  inflammatory-ffidematous — changes  in  the  brain  is  to  be 
sought  in  the  action  of  some  retained  products  of  metamorphosis. 

Finally,  we  may  mention  here  the  theory  advanced  by  Frerichs  in  the  ye^r 
1851,  which  at  first  found  much  favor,  but  which  at  present  is  almost  universally 
abandoned.  According  to  this,  the  urea  retained  in  the  blood  was  not  in  itself 
the  cause  of  the  ursemic  symptoms,  but  it  was  changed  into  carbonate  of  ammo- 
nium by  the  action  of  a  ferment  in  the  blood,  and  from  this  the  severe  nervous 
symptoms  arose.     This  theory  is  untenable,  because  carbonate  of  ammonium  is 


EEMAEKS  UPON  THE  PATHOLOGY  OF  EENAL  DISEASE     590 

scarcely  ever  found  in  the  blood  of  urnemic  patients.  It  is  much  more  probably 
formed  first  in  the  stomach  and  intestinal  canal  of  ursemic  patients  from  the  urea 
there  excreted  (vide  infra),  as  Claude  Bernard,  Treitz,  Voit,  and  others  have 
shown. 

In  regard  to  the  clinical  symptoms  of  uraemia  in  the  individual  case,  they  show 
all  possible  transitions  from  the  mildest  symptoms,  which  are  only  intimated,  up 
to  the  severest  nervous  symptoms,  which  may  be  the  immediate  cause  of  death. 
The  severe  forms  of  uraemia  may  sometimes  come  on  quite  suddenly,  while  in 
other  cases  they  may  be  preceded  for  a  long  time  by  milder  ursemic  symptoms, 
which  are  then  termed  prodromata.  The  severest  symptoms  may  not  appear  at 
all,  and  the  milder  symptoms  may  exist  alone  for  a  longer  or  shorter  time.  This 
latter  condition  is  called  chronic  ursemia. 

The  milder  ursemic  symptoms,  which  are  observed  either  alone  or  as  precursors 
or  as  sequelse  of  severe  uraemia,  consist  of  headache,  somnolence,  and  mental 
stupor,  of  a  peculiar  uneasiness,  or  of  a  feeling  of  anxiety  and  constraint  (some- 
times associated  with  hurried  respiration),  and  very  often  of  nausea,  spasmodic 
eructations,  and  repeated  vomiting;  and,  finally,  not  infrequently,  of  various 
symptoms  of  motor  irritation,  of  slight  twitchings  or  temporary  tonic  rigidity  of 
the  face  or  the  extremities,  etc. 

Among  the  characteristic  symptoms  of  this  milder  form  of  ursemia,  besides  the 
vomiting,  we  would  place  the  peculiar  restlessness  and  praecordial  distress  of 
patients  as  especially  important.  Not  infrequently,  observers  use  the  term 
uraemic  asthma  (vide  infra). 

The  most  characteristic  symptom  of  severe  uraemia  is  the  uraemic  convulsion, 
or  the  so-called  ursemic  eclampsia.  It  corresponds  almost  exactly  in  its  details 
to  an  epileptic  attack;  it  usually  begins  with  a  short  tonic  stage,  in  which  the 
whole  body  is  generally  in  a  position  of  extension  in  opisthotonos,  and  then  follow 
vigorous  clonic  contractions  in  the  face  and  extremities.  The  face  becomes  cya- 
notic, a  bloody  froth  comes  from  the  mouth,  the  pupils  are  usually  dilated  and 
almost  without  reaction,  the  respiration  is  accelerated  (but  at  times  it  is  intermit- 
tent from  spasm  of  the  respiratory  muscles),  the  pulse  is  small  and  accelerated, 
and  it  can  scarcely  be  felt  in  the  radial  artery,  and  the  temperature  is  sometimes 
raised.  In  other  cases  the  spasm  begins  with  short  jerky  contractions  in  one  ex- 
tremity, as  in  the  arm,  and  then  invades  the  trunk  muscles,  the  face,  and  the  legs. 
One  half  the  body  is  often  more  affected  in  the  attacks  than  the  other.  The 
spasms  usually  cease  in  a  few  minutes,  and  are  followed  by  deep  coma  and  stertor, 
which  last  for  several  hours  or  more.  There  is  only  rarely  a  single  attack.  The 
attacks  are  much  oftener  repeated  after  longer  or  shorter  intervals,  so  that  there 
may  even  be  twenty  or  more  in  the  twenty-four  hours,  during  the  whole  of  which 
time  a  complete  loss  of  consciousness  persists.  Severe  and  fully  developed  epilep- 
tiform attacks  often  alternate  with  slighter  convulsions. 

Some  other  uraemic  symptoms,  besides  the  convulsions,  which  have  already 
been  briefly  mentioned,  merit  a  somewhat  fuller  description. 

The  ursemic  amaurosis  occasionally  seen  is  especially  interesting.  It  is  usually 
left  after  recovery  from  the  convulsions.  Only  rarely  does  it  precede  them  or 
appear  without  them.  It  always  develops  quite  rapidly,  so  that  the  first  disturb- 
ance of  vision  soon  passes  into  complete  blindness.  The  reaction  of  the  pupils  to 
light  is  almost  always  retained,  and  the  ophthalmoscope  shows  a  perfectly  normal 
retinal  image.  At  what  spot  in  the  visual  apparatus  the  lesion  is  situated  is  not 
yet  known.  Many  investigators  assxime  that  there  is  an  osdcma  of  the  sheath  of 
the  optic  nerve;  while  others,  including  the  author,  think  it  more  probable  that 
there  is  disturbance  of  the  cerebral  visual  centers,  and  particularly  of  the  occip- 
ital cortex. 

Its  prognosis  is  on  the  whole  favorable,  since  the  disturbance  of  vision  \isually 


600  DISEASES  OF   THE   UEIXAKY   ORGANS 

disappears  completely  in  a  day  or  two,  though  sometimes  not  until  after  a  longer 
time.  Anomalies  are  only  rarely  seen  in  the  domain  of  the  other  nerves  of  special 
sense,  the  most  frequent,  comparatively,  being  a  difficulty  in  hearing,  or  even 
complete  deafness. 

Other  motor  disturbances,  except  twitchings  and  convulsions,  are  rare.  Only 
in  a  few  cases  have  hemiplegic  or  monoplegic  paralyses,  contractures,  trembling, 
etc.,  been  observed.  Mental  symptoms  are  more  common.  Delirium,  and  mani- 
acal or  sometimes  melancholic  states,  occasionally  follow  ursemic  coma. 

Those  ursemic  symptoms  have  also  a  great  interest,  which  are  to  be  regarded 
as  a  sort  of  self-help  on  the  part  of  the  organism,  since  they  often  lead  to  a  vica- 
rious elimination  of  urea  and  presumably  of  the  other  products  of  tissue  metamor- 
phosis. The  first  of  these  is  ursemic  vomiting,  which  is  a  frequent  and  often  an 
extremely  obstinate  symptom  both  in  acute  and  chronic  urasmia.  In  many  cases 
it  is  of  central  origin,  and  is  to  be  regarded  as  analogous  to  the  vomiting  so  fre- 
quent in  different  forms  of  cerebral  disease;  but  it  is  often  produced  by  the  irri- 
tation which  the  gastric  mucous  membrane  suffers  froin  the  urea  eliminated,  or 
rather  from  the  carbonate  of  ammonium  arising  from  it.  The  latter  is  always 
first  formed  from  the  urea  in  the  stomach  itself,  and  we  find  in  the  vomitus  of 
uraemic  patients  either  the  still  undecomposed  urea  or  the  carbonate  of  ammoni- 
um in  considerable  quantities.  Sometimes  there  is  quite  a  violent  hiccough 
besides  the  vomiting. 

Urasmic  diarrhoea  has  the  same  significance  as  uraemic  vomiting.  It  is  usually 
provoked  by  the  carbonate  of  ammonium  arising  from  the  urea  in  the  intestines. 
The  latter  often  causes  quite  a  severe  catarrhal,  and  even  at  times  a  diphtheritic, 
inflammation  of  the  intestinal  mucous  membrane. 

Another  way  in  which  the  organism  sometimes  tries  to  get  rid  of  the  large 
amount  of  urea  accumulated  in  it  is  by  the  sweat-glands.  Schottin  first  described 
the  remarkable  discovery  of  a  coating  of  urea  on  the  skin  in  the  uraemia  of  chol- 
era, an  observation  which  since  then  has  been  repeatedly  confirmed  in  other  cases 
of  uraemia.  This  coating  is  most  frequently  seen  on  the  face,  especially  on  the 
sides  of  the  nose,  to  which  little  faintly  lustrous  scales  are  seen  sticking  after  the 
evaporation  of  a  clammy  sweat.  Chemical  examination  shows  that  these  scales 
are  urea.  The  excretion  of  urea  is  much  more  rare  in  other  parts  of  the  skin, 
but  perhaps  the  occasional  severe  uraemic  itching  of  the  skin  is  due  to  an  irri- 
tation of  the  cutaneous  nerves  by  some  of  the  constituents  of  the  urine  that  are 
excreted. 

Other  organs  besides  the  skin  and  the.  digestive  tract  are  but  rarely  to  be  con- 
sidered as  a  means  of  the  vicarious  elimination  of  urea,  but  Fleischer  was  once 
able  to  discover  considerable  amounts  of  urea  in  the  saliva  and  sputum  of  a 
uiraemic  patient. 

In  conclusion,  we  must  describe  the  condition  of  the  pulse,  of  the  temperature, 
and  of  the  respiration  in  uraemia.  The  pulse  is  often  very  slow  before  the  appear- 
ance of  severe  symptoms,  sometimes  48  or  40,  but  it  is  almost  always  tense  and 
hard.  In  chronic  uraemia,  also,  a  moderate  slowness  of  the  pulse  is  not  infre- 
quent. When  uraemic  convulsions  appear,  however,  the  pulse  usually  becomes 
small  and  very  frequent,  especially  in  cases  that  terminate  unfavorably.  The 
temperature  but  rarely  remains  unchanged  in  severe  uraemia.  If  there  are  con- 
vulsions, it  usually  rises  several  degrees,  in  severe  oases  even  to  106°  or  108°  (41°- 
42°  C).  We  have  seen  these  high  temperatures,  especially,  as  a  terminal  rise  with 
an  imfavorable  issue,  although  there  may  sometimes  be  an  improvement  even  in 
such  cases.  On  the  other  hand,  there  are  also  great  declines  in  temperature,  down 
to  93°  or  91°  (34°-33°  C),  most  frequently  again  as  a  terminal  temperature  of 
collapse,  in  cases  which  end  in  deep  coma  without  marked  symptoms  of  motor 
irritation.    We  might  also  mention  the  "  uraemic  chills  "  which  we  have  seen  sev- 


EEMAEKS  UPOI^r  THE  PATHOLOGY  OF  EEiTAL  DISEASE     GOl 

eral  times — that  is,  a  chill  coming  on  suddenly  along  with  other  uremic  symp- 
toms, with  a  great  increase  of  temperature,  and  followed  by  a  rapid  fall  in  the 
temperature.  The  respiration  in  uraamic  patients  is  sometimes  very  much  accel- 
erated, and  is  especially  deep — a  symptom  which  recalls  the  peculiar  breathing  in 
diabetic  coma  {vide  infra).  Certain  severe  attacks  of  dyspnoea  in  patients  with 
renal  disease  have  been  described  as  "  ursemic  dyspnoea  "  or  "  ursemic  asthma  " ; 
but  it  is  not  always  easy  to  decide  whether  this  is  really  a  ursemic  nervous  symp- 
tom in  these  cases,  since  similar  conditions  of  sudden  dyspnoea  may  depend  upon 
coincident  heart  disease  and  insufficiency  of  the  left  ventricle  or  upon  inflamma- 
tory affections  of  the  lungs. 

In  regard  to  the  duration  of  urasmic  symptoms  and  to  the  different  forms  and 
ways  in  which  the  various  ursemic  symptoms  may  be  combined  in  the  clinical 
picture,  we  can  give  only  a  few  general  statements.  The  division  of  ursemia  into 
an  acute  and  a  chronic  form,  already  mentioned,  is  generally  very  useful  practi- 
cally. In  the  acute  form  we  usually  have  the  severe  ursemic  symptoms,  especially 
ursemic  convulsions  and  ursemic  coma.  This  condition  usually  lasts  some  days, 
while  chronic  ursemia,  in  which  the  milder  cerebral  symptoms — uremic  vomiting, 
difficulty  in  breathing,  etc. — are  most  prominent,  may  last  as  many  weeks.  The 
severe  acute  form  of  ursemia  may,  as  has  been  already  stated,  begin  with  almost 
absolute  abruptness.  Quite  often,  however,  there  are  first  mild  ursemic  symptoms, 
such  as  headache,  vomiting,  general  restlessness,  and  an  occasional  slight  twitch- 
ing of  the  muscles,  and  then  suddenly  ursemic  convulsions  or  other  ursemic 
symptoms. 

The  termination  of  ursemia  is  always  doubtful  in  every  severe  case,  but  it  is  by 
no  means  always  unfavorable.  Even  after  coma  lasting  for  several  days,  with 
very  severe  and  often-repeated  convulsions,  the  ursemic  symptoms  may  wholly 
disappear,  while  on  the  other  hand,  of  course,  ursemia  is  by  no  means  a  rare  cause 
of  death  in  the  most  diverse  forms  of  acute  and  chronic  renal  disease.  In  judging 
of  the  individual  case,  the  most  stress  is  to  be  laid  on  the  condition  of  the  pulse, 
the  respiration,  and  the  temperature ;  we  must  also  consider,  of  course,  the  char- 
acter of  the  urinary  secretion,  and  especially  the  other  morbid  symptoms  depend- 
ent upon  the  primary  disease. 

5.  The  Changes  in  the  Circulatory  Apparatus  in  Eenal  Disease 
Although  it  had  not  escaped  Bright's  observation  that  changes  in  the  heart  are 
also  present  in  diseases  of  the  kidney,  this  condition  was  first  generally  known 
when  Traube,  in  1856,  in  a  treatise  which  has  become  famous,  explained  that  a 
change  in  the  heart  was  very  common  in  certain  renal  affections,  and  thus  gave 
the  chief  impulse  to  the  numerous  clinical  and  experimental  investigations  that 
have  been  made  since  then  as  to  the  connection  between  cardiac  and  renal  disease. 
This  connection,  generally  considered,  may  be  accounted  for  in  three  ways : 
First,  the  heart  disease  may  without  doubt  be  the  primary  disease,  and  only 
secondarily  lead  to  a  disease  of  the  kidneys.    In  this  way  develop  the  kidney  of 
passive  congestion  (vide  infra,  and  page  331),  acute  nephritis  secondary  to  acute 
primary  or  recurrent  endocarditis,  and  the  embolic  processes  in  the  kidney  (vide 
infra). 

Secondly,  heart  disease  and  renal  affections  may  also  develop  independently  of 
each  other,  as  a  result  of  an  injurious  influence  that  affects  both  organs  at  the 
same  time.  Thus,  for  example,  a  general  arterio-sclerosis  leads  to  cardiac  hyper- 
trophy or  to  myocarditis,  and  also  to  a  granular  kidney  (vide  infra),  as  a  result 
of  an  implication  of  the  renal  vessels.  Certain  other  injurious  influences,  such  as 
toxic  and  constitutional  influences,  alcohol,  syphilis,  or  improper  living,  may  also 
cause  a  disease  of  the  heart  and  the  kidneys  at  the  same  time.  Later  on,  if  both 
affections  have  developed,  their  influence  upon  each  other  is  often,  of  course,  con- 


G02  DISEASES  OE    THE   TJEIXARY   OEGANS 

siderable — a  circumstance  whicli  may  render  our  judgment  as  to  the  condition 
decidedly  difficult. 

In  the  third  place — and  this  is  the  point  with  which  we  are  here  chiefly  con- 
cerned— the  renal  affection  may  be  the  primary  disease,  and  of  itself  the  cause 
of  a  change  in  the  heart,  and  especially  of  a  secondary  hypertrophy  of  the  left 
■ventricle.  At  present  there  can  no  longer  be  any  doubt  of  the  fact  of  this  depend- 
ence. We  also  know  now  that  the  secondary  development  of  cardiac  hypertrophy 
is  not  confined  to  one  form  of  chronic  nephritis,  the  so-called  contracted  kidney, 
as  was  at  first  believed,  but  that  it  is  almost  as  constant  in  all  other  forms  of 
chronic,  and  also  even  in  prolonged  acute,  nephritis.  Opinions  are  at  present  still 
much  divided  as  to  the  precise  nature  of  this  connection,  and  as  to  the  causal 
factors. 

The  theory  which  Traube  himself  advanced  for  the  explanation  of  the  cardiac 
hypertrophy  in  nephritis  rested  on  the  assumptions  that,  in  the  first  place,  less 
water  is  withdrawn  from  the  blood  in  nephritis  for  the  formation  of  the  renal 
secretion,  and  that,  in  the  second  place,  the  fiow  of  arterial  blood  into  the  venous 
system  is  hindered  by  the  changes  in  the  kidneys,  particularly  by  the  destruction 
of  many  of  the  smaller  blood-vessels.  Both  circumstances  must  raise  the  pressure 
in  the  arterial  system,  and  therefore  gradually  lead  to  cardiac  hypertrophy. 
Traube's  theory  can  not  be  maintained.  The  first  claim  especially  is  untenable, 
because  in  many  cases  of  chronic  contraction  of  the  kidney  with  co-existing  car- 
diac hypertrophy  there  is  never  a  diminution  of  the  elimination  of  water  by  the 
kidneys,  and,  besides,  this  can  never  of  itself  cause  an  increase  of  the  arterial  pres- 
sure. The  second  supposition,  that  the  destruction  or  the  narrowing  of  a  large 
number  of  the  small  blood-vessels  of  the  kidneys  must  produce  a  general  rise  in 
arterial  tension,  is  disproved  by  the  fact  that  even  the  complete  ligation  of  both 
renal  arteries  does  not  raise  the  tension  in  the  arterial  system,  because  the  blood 
at  once  passes  off  into  other  vessels  which  dilate. 

In  place  of  the  "  mechanical  theory,"  therefore,  there  have  been  of  late  many 
supporters  of  the  "  chemical  theory  "  of  cardiac  hypertrophy,  which  was  in  a  cer- 
tain sense  propounded  by  Bright  himself,  and  later  by  Johnson  and  others.  Ac- 
cording to  this  view  which,  with  some  modifications,  is  held  by  the  author,  the 
retention  of  urinary  constituents  in  the  blood  is  the  cause  of  the  cardiac  hyper- 
trophy because  the  retained  material  occasions  a  rise  in  arterial  tension,  and  this 
increased  tension,  if  it  persists  for  a  sufficiently  long  time,  must  occasion  a  hyper- 
trophy of  the  left  ventricle.  Clinical  experience  shows  beyond  a  doubt  that  any 
severe  case  of  acute  nephritis  occasions  in  a  few  days  an  increase  in  the  arterial 
tension,  which  can  usually  be  easily  perceived  in  the  pulse.  This  increased  ten- 
sion, which  certainly  precedes  the  cardiac  hypertrophy,  is  best  explained  by  the 
supposition  that  the  matters  which  ought  to  be  but  are  not  excreted  occasion  a 
contraction  of  the  smaller  arteries.  It  is  also  possible  to  conceive  that  there 
may  be  a  direct  irritation  of  the  cardiac  muscle.  At  any  rate,  the  occurrence  of 
a  rise  in  arterial  tension  is  of  decided  benefit  to  the  body,  as  it  promotes  the  ex- 
cretion of  urine.  If,  in  the  course  of  a  nephritis,  the  normal  conditions  return, 
after  a  few  days  or  weeks,  the  increased  tension  is  relaxed  and  the  heart  suffers 
no  noticeable  change;  but  if  the  nephritis  and  consequent  impairment  in  urinary 
secretion  and  increased  arterial  pressure  persist  for  a  considerable  tinie,  jve  often 
see,  even  after  six  or  eight  weeks,  a  hypertrophy  of  the  left  ventricle  develop, 
under  our  own  eyes,  in  a  way  that  can  be  demonstrated  most  distinctly  at  the 
bedside.  This  is  the  necessary  consequence  of  the  increased  effort  which  the  heart 
is  obliged  to  make  in  order  to  overcome  the  abnormal  resistance  in  the  systemic 
arteries. 

We  have  precisely  the  same  conditions  in  the  chronic  forms  of  nephritis,  ex- 
cept that  they  develop  more  slowly  and  insidiously.    In  these,  also,  the  first  fac- 


ACUTE   :N^EPHEITIS  603 

tor  is  the  insufficiency  of  the  kidneys,  occasioned  by  the  disease — that  is,  failure 
to  excrete  all  the  products  of  metabolism.  To  this  the  body  responds  immedi- 
ately by  a  rise  in  arterial  tension,  "which  is  intended  to  serve,  and  does  actually 
serve,  as  a  compensation  of  the  impairment;  then,  thirdly,  hypertrophy  of  the 
left  ventricle  develops,  and  enables  the  heart  for  a  long  while  to  supply  the  de- 
mands put  upon  it.  This  hypertrophy  is  consequently  the  most  important  and 
indispensable  compensatory  arrangement  by  means  of  which  the  body  is  pro- 
tected from  the  onset  of  ursemic  intoxication.  Just  as  any  patient  with  valvular 
heart  disease  would  invariably  fail  much  earlier  if  his  heart  did  not  become 
hypertrophied  in  portions  corresponding  to  the  lesion,  so,  also,  in  chronic  nephri- 
tis, the  unfavorable  termination  would  occur  much  earlier  if  the  body  were  not 
in  a  position  to  effect  and  maintain  an  increase  in  the  arterial  tension,  and  thus 
for  a  time,  at  least,  ward  off  the  threatening  enemy.  Viewed  in  this  light,  the 
chemical  theory  of  cardiac  hypertrophy  not  only  gives  us  an  insight  into  the 
clinical  phenomenon  as  such,  but  also  enables  us  to  perceive  its  true  significance. 

The  question  naturally  arises  here,  just  as  when  we  were  considering  the 
theory  of  ursemia,  what  substances  are  the^chief  occasion  of  the  rise  in  arterial 
tension.  This  question,  however,  can  not  at  present  be  answered.  We  can  merely 
say  that  the  results  of  experiment  indicate  that  urea  probably  does  not  play  the 
most  essential,  and  certainly  not  the  sole,  part  in  the  matter.  The  question 
whether  the  hypertrophy  of  the  left  ventricle  associated  with  nephritis  is  mainly 
simple  (concentric),  or  whether  it  may  not  sometimes  be  accompanied  by  dilata- 
tion of  the  cardiac  cavities  (eccentric),  we  do  not  regard  as  of  any  special  impor- 
tance. It  should,  however,  be  noted  that  while  the  hypertrophy  always  affects  the 
left  ventricle  chiefly,  and  often  it  alone,  yet  not  infrequently  the  right  ventricle 
is  also  found  to  be  hypertrophied.  If  we  assume  that  there  is  a  direct  irritation 
of  the  myocardium  (vide  supra),  this  condition  will  not  seem  remarkable.  Oth- 
erwise, the  hypertrophy  of  the  right  ventricle  might  be  regarded  as  a  compensa- 
tory hypertrophy,  supplementing  failure  of  the  left  ventricle. 

The  relation  between  certain  diseases  of  the  vessels  and  diseases  of  the  kidneys 
will  be  spoken  of  in  the  chapter  on  contracted  kidney. 


CHAPTEE  II 

ACUTE    NEPHRITIS 

{Amite  Brighfs  Disease) 

.3Stiology. — Acute  nephritis,  like  most  of  the  other  forms  of  nephritis,  is  not 
a  disease  whose  aetiology  is  uniform.  The  same  anatomical  change,  which  we 
term  "nephritis,"  and  which  is  attended  by  about  the  same  morbid  phenomena, 
may  be  excited  by  influences  of  very  different  kinds.  Almost  all  these  influences 
have  one  thing  in  common,  namely,  that,  as  we  have  stated  in  the  preceding  chap- 
ter, they  reach  the  kidneys  by  way  of  the  circulation  and  are  here  in  part  elimi- 
nated, ai^^thus  exert  their  specific  injurious  action  upon  the  parenchyma  of 
the  kidne^^  but  they  differ  considerably  from  one  another  in  their  precise  chem- 

(      ical  nature.     Since  the  pathological  change  in  the  kidneys  depends  upon  the 

amount  of  the  noxious  material,  upon  the  intensity  of  its  action  and  the  duration 

of  its  influence,  we  see  that  the  cases  of  nephritis  that  arise  in  this  way  must 

present  a  perfectly  continuous  series  from  the  mildest  to  the  severest,  from  those 

f  that  pass  off  rapidly  to  those  that  last  perhaps  for  years  and  years.  The  history 
of  renal  py;hology  teaches  us  In  the  plainest  way  that  all  attempts  to  divide  the 


604  DISEASES    OF    THE   FEINAEY   ORGANS 

forms  of  nephritis  into  different  clinical  and  pathological  "  varieties  "  can  not 
be  strictly  carried  out.  The  more  scientific  experience  increases,  the  more  numer- 
ous must  be  the  forms  established,  and  still  we  only  too  frequently  have  to  assume 
all  sorts  of  "  transitional  forms  "  merely  to  bring  the  reality  into  harmony  with 
the  scheme.  It  therefore  corresponds  merely  to  our  practical  needs  if  we  take 
certain  types  from  this  whole  list  and  divide  nephritis  into  various  groups;  for, 
from  the  nature  of  the  case,  there  can  be  no  question  of  a  sharp  separation  of  the 
various  forms. 

We  accordingly  call  those  inflammatory  renal  affections  acute  nephritis  which 
arise  comparatively  rapidly  from  any  of  the  injurious  influences  soon  to  be  enu- 
merated, and  which  terminate,  after  a  few  days  or  a  few  weeks,  either  fatally  or 
with  recovery;  or  occasionally,  after  a  rapid  onset  of  this  sort,  pass  gradually  into 
a  chronic  form.  Acute  nephritis,  on  the  one  hand,  follows  immediately,  without 
any  fixed  boundary,  the  mildest  morbid  changes  in  the  kidney,  which  are  usually 
not  termed  actual  nephritis,  but  simple  "  parenchymatous  degeneration  " ;  while 
on  the  other  hand  it  shows  a  continuous  transition  to  those  forms  which  last  for 
several  weeks  or  months,  or  longer,  aitd  hence  are  called  subacute  or  subchronic 
nephritis. 

Let  us  now  consider  more  minutely  the  conditions  under  which  acute  nephritis 
develops.  In  the  first  place,  it  occurs  with  very  great  frequency  as  a  sequel  or 
complication  of  all  sorts  of  infectious  diseases.  We  may  assert  that  there  is 
really  no  acute  infectious  disease  in  which  a  secondary  acute  nephritis  may  not 
occasionally  appear.  There  are,  however,  many  diseases  in  which  this  complica- 
tion is  peculiarly  frequent  and  characteristic.  The  exact  causes  of  its  develop- 
ment are  as  yet  imperfectly  known.  Formerly,  authorities  were  inclined  to  as- 
sume that  the  original  germs  had  directly  invaded  the  kidney  itself,  but  probably 
this  is  true  in  only  a  few  cases,  if  we  except  genuine  metastatic  pyonephritis. 
According  to  the  views  of  the  present  day,  it  is  much  more  likely  that  abnormal 
chemical  substances,  toxines,  which  develop  in  the  body  under  the  influence  of  the 
infection,  reach  the  kidneys  and  excite  disease  in  them.  The  amount  and  char- 
acter of  these  substances  determine,  of  course,  the  severity  of  the  renal  disease. 
Since  we  have  already  dwelt  upon  the  occurrence,  the  frequency,  and  certain 
peculiarities  of  secondary  nephritis  in  the  description  of  the  different  infectious 
diseases,  a  brief  recapitulation  of  the  facts,  which  have  already  been  for  the  most 
part  discussed,  will  suffice  here. 

The  infectious  disease  which  most  frequently  gives  rise  to  an  acute  nephritis 
is  scarlet  fever.  As  has  been  shown  previously  (see  page  43),  the  renal  affection 
appears  but  rarely  at  the  beginning  of  the  disease,  and  then  in  a  very  mild  form, 
while  the  special  severe  scarlatinous  nephritis  usually  attains  its  development 
only  toward  the  end  of  the  third  week  of  the  disease.  In  measles,  secondary 
nephritis  is  very  much  rarer  than  in  scarlet  fever;  in  rotheln  it  is  only  of  very 
exceptional  occurrence.  It  is  commoner  again  in  small-pox,  especially  in  the 
severe  hsemorrhagic  forms.  In  varicella,  renal  affections  are  very  rare,  but  they 
have  been  occasionally  observed.  They  are  always  of  but  slight  intensity.  In 
typhoid  fever  a  slight  albuminuria  is  very  common,  but  genuine  acute  nephritis 
is  quite  rare.  There  are  some  cases,  however,  where  a  nephritis  appears  very 
early,  and  where  the  other  typhoid  symptoms  are  so  crowded  into  the  J^kkground 
by  it  that  we  have  decided  difficulty  in  making  the  diagnosis  of  typh^TO;  this  is 
called  the  "  renal  form  of  typhoid  fever."  In  typhus  and  recurrent  fevers  severe 
cases  of  nephritis  are  not  especially  common,  but  they  are  seen  more  frequently 
than  in  typhoid  fever. 

The  nephritis  that  often  comes  on  in  cholera  is  of  great  practical  importance.- 
This  is  seen  in  the  earlier  stages,  anU  is  especially  one  of  the  most  frequent 
causes  of  the  so-called  cholera  typhoid  (see  page  89).    Of  course  it  may  appear 


ACUTE   NEPHEITIS  605 

questionable  whether  the  renal  affection  here  is  always  of  a  genuine  inflammatory 
nature,  or  develops  only  in  consequence  of  the  disturbance  of  circulation. 

^Nephritis  develops  quite  frequently  in  the  course  of  diphtheria,  especially  in 
severe  cases  of  this  disease;  but  the  renal  affection  only  rarely  reaches  a  high 
degree.  We  sometimes  see,  however,  very  severe  forms  of  nephritis  in  all  the  so- 
called  septic  diseases  (septic  nephritis,  see  page  120),  in  acute  ulcerative  endocar- 
ditis and  endocarditis  verrucosa,  and  allied  affections,  such  as  puerperal  fever, 
septic  wounds,  etc. 

Erysipelas  also  is  very  often  associated  with  nephritis,  and  likewise  croupous 
pneumonia;  while,  on  the  other  hand,  acute  articular  rheumatism  is  seldom  ac- 
companied by  albuminuria.  It  is  not  very  exceptional  for  sore  throat,  particularly 
follicular  tonsillitis,  to  occasion  acute  nephritis,  and  the  same  is  true  of  acute 
intestinal  diseases.  It  is  of  great  practical  importance  to  know  that  a  severe 
secondary  nephritis  may  follow  primary  diseases  of  this  sort,  even  if  the  latter 
seem  to  be  very  mild. 

We  ought  also  to  speak  of  the  acute  nephritis  sometimes  seen  in  patients  with 
pustular  eruptions,  such  as  impetigo,  pustular  eczema,  severe  scabies,  etc.  Prob- 
ably we  have  to  do  in  most  of  these  cases  with  a  mild  septic  infection,  which 
has  found  ingress  through  one  of  the  many  minute  scratches  or  other  lesions  of 
the  skin.  We  must  also  bear  in  mind  the  possibility  (vide  infra)  of  damage  done 
by  external  applications  which  are  absorbed  by  the  skin. 

There  are  many  chronic  infectious  diseases  besides  these  acute  ones,  in  the 
course  of  which  acute  nephritis  may  appear.  We  see  this  complication  most  fre- 
quently in  the  case  of  primary  tuberculosis,  but  it  seems  to  us  highly  probable 
that  the  nephritis  in  this  instance  is  not  directly  connected  with  the  tubercu- 
losis, but  is  the  result  of  absorption  of  septic  matters  from  the  pulmonary  cavities 
and  similar  places.  Syphilis  should  also  be  mentioned  in  this  connection.  We 
have  ourselves  repeatedly  seen  mild  and  even  severe  acute  nephritis  develop  in 
the  secondary  stage  of  syphilis.  Finally,  malaria  might  be  mentioned,  although 
the  nephritis  which  occurs  in  this  connection  usually  takes  a  chronic  form. 

Besides  the  infectious  forms  of  nephritis  just  described,  there  is  a  second  great 
group,  which  may  be  classed  under  the  general  heading  of  toxic  nephritis.  In 
these  cases  we  are  dealing  with  the  deleterious  action  of  definite  chemical  sub- 
stances which  enter  the  body  from  without  and  are  excreted  from  it  by  the  kid- 
neys. It  is  wholly  impossible  to  enumerate  all  the  substances  which  have  this 
injurious  effect;  we  will  therefore  confine  ourselves  to  mentioning  those  of  the 
greatest  practical  importance.  Among  the  poisons  proper  we  may  mention  the 
mineral  acids,  sulphuric,  hydrochloric,  and  nitric  acids,  oxalic  acid,  phosphorus, 
arsenic,  lead,  mercury  (corrosive  sublimate),  and  chromate  of  potassium.  Among 
remedies  used  internally,  which  may  excite  nephritis  when  given  in  too  great 
doses,  we  may  mention  cantharides,  squills,  balsam  of  copaiba,  turpentine,  sali- 
cylic acid,  and  chlorate  of  potassium.  This  last  causes  hsemoglobinuria  as  well 
as  nephritis.  It  is  also  very  important  to  know  that  many  remedies  applied  exter- 
nally are  absorbed  by  the  skin,  and  that  in  this  way  they  may  reach  the  kidneys 
and  excite  severe  changes  there.  Among  these  are  cantharidal  plaster,  prepara- 
tions of  tar,  petroleum,  styrax,  naphthol,  and  pyrogallic  acid.  We  must  men-, 
tion,  in  addition  to  these,  the  nephritis  which  may  arise  from  the  too  abundant 
use  of  cUbolic  acid  or  iodofonn  on  the  surface  of  open  wounds.  Under  some 
circumstances  renal  affections  may  even  arise  in  individual  cases  from  taking 
excessive  amounts  of  certain  foods  and  drinks,  such  as  spices,  alcohol,  horse- 
radish, or  very  acid  foods. 

The  many  cases  of  nephritis  thus  far  discussed  are  directly  referable  to  some 
definite  cause,  but  in  a  comparatively  small  number  of  instances  acute  nephritis 
appears  as  an  apparently  ;^imary  disease  in  persons  previously  healthy.    In  many 


♦3u6  DISEASES    OE    THE   UELN^AKY   OEGAXS 

such,  cases  vre  are  absolutely  unable  to  make  out  any  causative  factor,  while  in  otli- 
ers,  again,  we  do  find  certain  unfavorable  influences  affecting  the  patient,  such  as 
hard  drinking  or  severe  labor  in  the  open  air.  It  can  not  be  doubted  that  expo- 
sure to  severe  cold  and  thorough  wetting  promote  the  development  of  acute  ne- 
phritis. The  author's  experience  has  convinced  him  of  this  fact.  Thus,  the 
disease  may  occur  when  a  man  works  in  the  snow  or  in  cold  water.  We  possess 
as  yet,  however,  scarcely  any  knowledge  of  the  conditions  which  bring  about  this 
resTolt.  Many  investigators  assume  that  cold  interferes  with  the  excretory  fim.c- 
tion  of  the  skin;  others  imagine  that  the  blood  is  damaged  as  it  circulates  in  the 
cutaneous  vessels.  We  have  repeatedly  seen  cases  of  apparently  primary  acute 
nephritis  in  great  beer  drinkers.  We  suppose  that  in  such  cases  the  effect  of  the 
long-continued  chronic  intoxication  with  alcohol  is  cumulative,  and  finally  leads 
to  the  apparently  spontaneous  acute  development  of  nephritis  (acute  alcoholic 
nephritis).  Sometimes,  however,  even  in  such  cases  there  seems  to  be  some  other 
factor,  such  as  catching  cold,  which  gives  the  final  impulse  to  the  development 
of  the  disease.  A  considerable  number  of  cases  of  apparently  primary  acute 
nephritis  must,  however,  be  regarded  in  the  last  analysis  as  the  results  of  a  septic 
infection  of  some  sort.  If  we  question  the  patient  closely,  we  learn  in  such  cases 
that  the  appearance  of  the  nephritic  phenomena  has  often  been  preceded  by 
symptoms  of  a  mild  sore  throat  which  scarcely  attracted  the  patient's  attention, 
or  an  insignificant  gastro-intestinal  disturbance,  etc.  Such  statements  are  in- 
dicative of  the  possible  place  of  infection.  Again,  slight  purulent  affections  of 
the  skin,  such  as  furuncuiosis,  phlegmon  of  a  finger  or  toe,  and  eczema  may  some- 
times furnish  a  gate  of  entrance  for  infection.  In  considering  all  cases  of  appar- 
ently primary  idiopathic  and  acute  nephritis,  it  is  very  important  to  remember 
that  not  infrequently  a  chi-onic  nephritis  may  exist  for  a  long  while,  perhaps 
without  any  symptoms  whatever,  and  suddenly  flame  up  into  an  acute  disease 
(acute  recurrent  nephritis  of  Wagner),  and  thus  simulate  a  primary  acute  nephri- 
tis. We  can  not  get  at  the  correct  interpretation  of  such  cases  without  careful  in- 
quiry into  the  previous  history,  and  sometimes  only  after  observing  the  subsequent 
course  of  the  disease. 

In  conclusion,  we  have  an  especial  form  of  acute  renal  disease  to  mention  in 
this  connection — ^viz.,  the  nephritis  of  pregnancy  (nephritis  gravidarum).  This 
does  not  usually  appear  until  the  last  months  of  pregnancy.  It  may  attack 
women  whose  health  was  previously  perfect,  and  it  is  much  more  frequent  in 
primiparffi  than  in  multipara.  The  precise  causes  of  the  nephritis  of  pregnancy 
are  very  obscure.  The  earlier  explanations,  according  to  which  the  renal  dis- 
turbance was  occasioned  by  pressure  of  the  pregnant  uterus  upon  the  renal  arte- 
ries, the  renal  veins,  or  the  ureters,  are  entirely  unsatisfactory.  Perhaps  there 
are  special  toxic  influences,  the  origin  and  nature  of  which  are  as  yet  entirely 
unknown. 

Pathological  Anatomy. — The  anatomical  changes  of  acute  nephritis  show  a 
continuous  series  from  the  mildest  to  the  severest  degrees,  according  to  the  in- 
tensity of  the  injurious  action.  The  mildest  changes,  which,  as  we  have  said,  are 
not  called  actual  "  inflammation,"'  but  usually  simple  parenchymatous  degenera- 
tion, affect  exclusively  the  parenchyma  of  the  kidney — that  is,  the  epitbelium — 
while  the  interstitial  tissue,  the  connective  tissue,  and  the  vessels  remain  per- 
fectly normal.  This  fact  is  of  prime  importance,  since  it  implies  that,  in  almost 
all  the  injurious  influences  acting  on  the  kidneys,  the  specific  renal  parenchyma 
itself  is  diseased  first  and  before  any  other.  On  macroscopic  examination,  the 
kidneys  of  "  parenchymatous  degeneration  "  may  show  scarcely  any  plainly  per- 
ceptible changes,  but  it  sometimes  strikes  the  practiced  eye  that  the  kidneys  are  a 
little  enlarged,  that  the  cortex  on  section,  shows  either  a  more  reddish-gray, 
dimmed  coloring  (cloudy  swelling),  or  a  more  grayish- white,  yellowish  hue  (fatty 


ACUTE   XEPHEITIS  607 

degeneration).  The  microscopic  examination  gives  more  accurate  information 
as  to  the  degree  and  the  extent  of  the  disease.  We  distinguish  different  condi- 
tions according  to  the  form  of  change  in  the  epithelium,  of  which  the  three  fol- 
lowing are  most  important:  1.  Cloudy  Swelling:  It  is  most  easily  made  out  in 
the  epithelium  of  the  cortical  tubules,  but  it  may  also  be  seen  in  the  epithelium 
of  the  glomeruli.  The  cells  swell,  their  contents  become  uniformly  granular  and 
cloudy,  the  nuclei  swell,  and  finally  disappear.  Such  changes  are  often  found  in 
acute  infectious  diseases,  such  as  typhoid,  small-pox,  and  diphtheria.  2.  Fatty 
Degeneration:  This  may  proceed  from  the  cloudy  swelling,  or  may  develop  inde- 
pendently. Many  fat-drops  appear  both  in  the  cells  of  the  uriniferous  tubules 
and  also  in  the  epithelium  of  the  glomeruli,  and  they  may  finally  lead  to  the  dis- 
integration of  the  cells.  Simple  fatty  degeneration  of  the  kidneys  is  sometimes 
found  in  acute  infectious  diseases,  after  certain  poisons,  such  as  phosphorus,  and 
-finally  in  antemic  conditions.  3.  Necrosis  of  the  Renal  Epithelium:  The  nuclei 
of  the  cells  disappear,  and  the  cells  are  changed  to  clear  homogeneous  flakes, 
while  in  some  cases  they  are  greatly  swollen  ("  dropsical  degeneration  "  of  Nau- 
werck-Ziegler).  Genuine  epithelial  necrosis  is  found  in  the  kidneys,  chiefly  after 
the  action  of  toxic  substances — cantharides,  the  chromic  and  chloric  salts,  etc. 
— but  sometimes  also  in  infectious  diseases.  Combinations  of  simple  necrosis 
with  granular  cloudiness  and  fatty  degeneration  are  not  infrequent.  Both  the 
last-named  states  may  undergo  resolution  if  they  have  not  reached  a  high  degree. 
Otherwise  all  the  degenerations  mentioned  lead  to  the  destruction  and  disinte- 
gration of  the  cells;  nevertheless,  a  complete  restoration  is  possible,  from  the 
regeneration  of  new  epithelial  cells  from  epithelium  that  is  still  present. 

We  term  those  changes  in  the  kidneys  genuine  acute  nephritis,  in  which  not 
only  the  renal  parenchyma  proper,  the  epithelium,  but  also  the  interstitial  tissue, 
especially  the  vessels,  is  affected;  so  that  we  can  make  out  the  exudative  changes 
characteristic  of  all  inflammatory  processes — the  escape  of  fluid  and  cells  from 
the  vessels.  In  these  cases  the  different  histological  processes  may  be  combined 
in  the  most  varied  ways,  so  that  the  anatomical  picture  presents  quite  great  vari- 
ations, although  it  is  almost  always  seen  on  analysis  to  display  the  same  pro- 
cesses. 

If  we  begin  with  the  histological  lesions  in  acute  nephritis,  in  order  to  learn  to 
recognize  at  once  the  essential  changes,  we  have  first  precisely  the  same  processes 
of  degeneration  in  the  epithelium  which  have  been  already  described,  but  they  are 
usually  present  here  in  a  more  marked  degree.  In  some  cases  the  simple  ne- 
crotic processes  predominate;  in  others,  the  fatty  degeneration.  We  often  find 
degenerated  cells,  and  not  infrequently  a  more  or  less  marked  desquamation  of 
epithelium.  We  see  also  the  special  infiammatory  changes.  We  find  a  fluid 
inflammatory  exudation,  rich  in  fibrine,  and  therefore  soon  coagulating  in  the  in- 
terstitial connective  tissue,  which  is  dilated  and  swollen  by  it — inflammatory 
oedema.  The  same  exudation  is  also  found  in  the  uriniferous  tubules,  and,  by  the 
proper  methods,  by  alcohol  or  by  boiling  the  fresh  kidney,  the  albuminous  effusion 
can  be  made  out  both  in  the  capsules  of  the  glomeruli  and  in  the  uriniferous 
tubules.  The  interpretation  of  the  exudation  is,  of  course,  made  very  difficult,  or 
often  wholly  impossible,  by  the  presence  of  albuminous  urine  in  the  uriniferous 
tubules.  The  second  characteristic  of  inflammation,  the  "  cellular  exudation  " — 
that  is,  the  emigration  of  white  blood-corpuscles — is  also  present.  In  the  inter- 
stitial tissue  we  find  accumulations  of  round  cells,  usually  distributed  in  foci, 
and  white  blood-corpuscles  in  greater  or  less  numbers  also  enter  the  interior  of 
the  uriniferous  tubules.  We  often  find  many  hyaline  casts  in  the  lumen  of  the 
straight  tubules  or  of  Henle's  loops,  whose  origin  is,  in  all  probability,  connected 
with  the  albuminous  exudation  and  the  emigrated  white  blood-corpuscles  (see 
page  593).     The  vessels  themselves  are  often  hj-pera^mic  and  dilated,  but  in  some 


608  DISEASES    OF   THE   UEINAEY   OKGANS 

cases  they  are  compressed  by  the  interstitial  inflammatory  oedema.  It  is  of  spe- 
cial significance  that  in  very  many  cases  there  are  haemorrhages,  either  into  the 
interstitial  tissue  or  into  the  interior  of  the  uriniferous  tubules,  or  even  into 
Malpighi's  capsules. 

Special  care  has  been  recently  devoted  to  the  study  of  the  minute  changes  in 
the  glomeruli,  although  at  present  there  is  a  conflict  in  the  views  regarding  them. 
Klebs  called  attention  to  the  fact  that  in  scarlatinal  nephritis  the  lesions  may  be 
almost  exclusively  confined  to  the  glomeruli  (glomerulo-nephritis).  Sometimes 
kidneys  of  this  sort  seem  almost  normal  to  the  naked  eye,  although  during  the 
life  of  the  patient  there  have  been  the  severest  symptoms,  such  as  anuria  and 
uraemia.  Eriedlander,  Eibbert,  Langhans,  and  others  have  pursued  the  study  of 
the  histological  changes  in  the  glomeruli.  In  part  there  are  degeneration,  hyper- 
plasia, and  desquamation  of  the  glomerular  epithelium;  in  part  changes  in  the 
walls  of  the  blood-vessels  themselves.  With  regard  to  the  secretion  of  urine,  and, 
in  particular,  the  development  of  albuminuria,  these  changes  in  the  glomeruli  are 
certainly  of  the  greatest  importance,  and  it  is  not  improbable  that  in  many  cases 
of  acute  nephritis  the  disease  begins  chiefly  in  the  glomeruli;  but,  on  the  other 
hand,  it  is  not  proper  to  suppress  too  completely  the  other  changes  in  the  renal 
parenchyma  as  compared  with  the  glomerulo-nephritis. 

In  regard  to  the  extent  of  all  these  changes  which  have  been  described,  it 
should  be  noted  that  not  infrequently  certain  portions  of  the  kidney  are  more 
severely  diseased  than  others,  so  that  sometimes  the  nephritis  tends  to  develop 
in  separate  foci.    In  general,  however,  acute  nephritis  is  diffuse. 

If  the  histological  processes  have  been  made  clear,  the  understanding  of  the 
macroscopic  appearance  of  the  inflamed  kidney  is  very  simple.  We  can  under- 
stand that  either  this  or  that  "  form  "  of  acute  nephritis  must  be  present  accord- 
ing to  the  predominance  of  this  or  that  histological  process.  If  an  abundant 
interstitial  exudation  is  present,  the  kidney  is  much  enlarged;  if  this  exudation 
is  slight,  the  kidney  varies  but  little,  or  not  at  all,  from  its  normal  size,  not- 
withstanding any  other  severe  changes.  In  the  first  ease  it  usually  feels  soft, 
from  inflammatory  oedema;  in  the  second  case,  it  is  comparatively  firm.  If 
there  is  a  marked  hypersemia  of  the  kidney,  it  appears  much  reddened;  if  the 
kidney  is  anaemic,  it  is  paler ;  and  if  an  extensive  fatty  degeneration  is  also  pres- 
ent, it  is  yellowish-white  or  yellow.  If  haemorrhages  are  present,  they  can  easily 
be  recognized  with  the  naked  eye  on  the  outer  surface  beneath  the  capsule  as  dark- 
red  points  that  can  not  be  wiped  away.  We  speak  then  of  an  "  acute  haemor- 
rhagic  nephritis."  On  section,  the  medullary  substance  is  more  or  less  dilated, 
often  projecting  somewhat  above  the  general  level  of  the  cut  surface,  its  normal 
striated  appearance  is  almost  always  obliterated,  and  its  color  shows  the  same 
variations  as  the  outer  surface  of  the  kidney.  Not  infrequently  the  diseased 
Malpighian  corpuscles  can  be  recognized  by  the  naked  eye  as  grayish-red  or  whit- 
ish points.  Since,  as  we  have  said,  the  nephritic  changes  often  show  not  a  uniform 
and  diffuse,  but  a  nodular  arrangement,  we  can  understand  that  the  kidneys  some- 
times have  quite  a  mottled  appearance,  since  hyperaemic  or  heemorrhagic  red  spots 
alternate  with  the  lighter  anaemic  and  the  yellow  fatty-degenerated  parts. 

There  are,  accordingly,  cases  of  nephritis  which  show  almost  nothing  abnor- 
mal to  the  naked  eye,  while,  on  the  other  hand,  there  are  haemorrhagic  and  non- 
haemorrhagic  forms,  appearing  pale,  yellow,  red,  or  variegated,  none  of  which 
can  in  the  essential  features  be  separated  from  one  another,  but  which  are  com- 
bined with  one  another  in  all  conceivable  ways.  The  forms  of  nephritis  that 
differ  in  aetiology  have,  to  a  certain  degree,  definite  and  characteristic  anatomical 
types,  but  strict  rules  can  not  be  laid  down  in  regard  to  this. 

Clinical  History. — The  most  essential  symptom  of,  acute  nephritis  is  the  ab- 
normal character  of  the  urine.    In  most  of  the  milder,  and  even  in  many  of  the 


ACUTE   IS^EPHEITIS  609 

severer  cases  of  nephritis,  the  change  in  the  urine  is  the  sole  ohjective  clinical 
symptom  which  renders  the  diagnosis  possible.  The  physician  must,  therefore, 
make  it  his  practice  to  submit  the  urine  to  repeated  examinations  in  every  case  of 
disease  where  there  is  any  possibility  of  the  presence  of  a  nephritis. 

The  simple  parenchymatous  degeneration  of  the  kidneys,  cloudy  swelling, 
fatty  degeneration,  etc.,  may  probably  sometimes  exist  without  being  followed 
by  any  discoverable  change  in  the  urine;  but  they  often  lead  to  a  slight  albu- 
minuria, which  is  easily  explained  from  the  change  in  the  epithelium  of  the 
glomeruli.  If,  then,  the  urine  contains  a  slight  amount  of  albumen  (which  usu- 
ally soon  passes  off)  in  the  course  of  any  febrile  infectious  disease  or  other  affec- 
tion (the  so-called  febrile  albuminuria,  etc.),  we  .are  justified  in  assuming  some 
of  these  mild  conditions  of  degeneration  in  the  kidneys.  Usually  the  urine  shows 
no  other  peculiarities,  but  sometimes  we  find  in  the  sediment  a  few  hyaline  easts, 
a  few  white  blood-corpuscles,  etc.  As  we  have  repeatedly  stated,  these  conditions 
pass  into  nephritis  proper  without  any  sharp  limitations. 

Character  of  the  Urine  in  Acute  ISTephritis. — In  almost  every  case  of  severe 
nephritis  the  amount  of  urine  for  the  twenty-four  hours  is  more  or  less  dimin- 
ished. This  is  caused  directly  either  by  the  lessened  elimination  of  water  by  the 
kidneys,  or  by  the  plugging  of  many  uriniferous  tubules  by  casts,  desquamated 
epithelium,  etc.  The  amount  evacuated  daily  is  often  only  fifteen  or  twenty 
ounces  (400-700  cubic  centimetres),  but  it  sometimes  falls  to  a  much  lower  figure, 
two  or  three  ounces  (100-50  cubic  centimetres), and  there  may  finally  be  even  com- 
plete anuria.  In  general,  though  not  without  exceptions,  the  diminution  of  the 
amount  of  urine  runs  parallel  to  the  severity  of  the  anatomical  changes  in  the 
kidney.  Improvement  in  the  disease  is  very  often  first  seen  in  an  increase  of  the 
amount  of  urine.  If  there  was  a  previous  oedema,  and  this  is  absorbed,  the  daily 
amount  of  urine  often  rises  during  convalescence  to  a  very  considerable  quantity, 
eighty  to  a  hundred  ounces  (2,500-3,000  cubic  centimetres).  Even  in  cases  in 
which  there  had  been  no  decided  oedema,  we  have  often  seen  during  recovery  from 
acute  nephritis  very  abundant  diuresis.  In  so  far  as  this  symptom  did  not  relate 
to  the  excretion  of  water  that  had  been  retained  in  the  system,  it  might  perhaps 
be  referable  to  an  abnormal  permeability  of  the  glomeruli,  similar  to  the  condi- 
tion sometimes  seen  after  a  severe  attack  of  typhoid  fever. 

The  specific  gravity  of  the  urine  is  at  first  usually  increased,  since  the  urine  is 
poor  in  water,  but  comparatively  rich  in  solid  constituents,  especially  in  albumen 
(vide  infra).  Of  course  there  are  great  differences  here,  and  a  urine  secreted  in 
an  abnormally  small  amount  may  show  a  specific  gravity  of  only  1010  or  1015, 
while,  on  the  other  hand,  urines  with  a  specific  gravity  of  1020  to  1030,  or  even 
more,  have  been  observed.  If  during  convalescence  a  very  abundant,  watery  urine 
is  passed,  it  of  course  usually  has  a  low  specific  gravity,  about  1005  to  1008. 

In  many  cases,  but  of  course  not  in  all,  we  may  suspect  the  abnormal  character 
of  the  urine  from  its  appearance.  This  depends  chiefly  upon  an  admixture  of 
abnormal  morphological  constituents.  If  these  are  present  in  large  numbers,  as  is 
usually  the  case,  the  freshly  passed  urine  is  cloudy,  and  deposits  a  more  or  less 
abundant  floccular  sediment.  The  appearance  of  the  urine  is  most  altered  if 
blood  be  mixed  with  it  (hasmorrhagic  urine).  According  to  the  amount  of  blood, 
the  urine  is  a  light  or  dark  red,  or  even  a  dark  black-red,  and  often  has  a  greenish 
reflection  when  the  light  falls  on  it. 

The  microscopic  examination  of  the  sediment  gives  more  accurate  informatioji 
upon  the  different  morphological  constituents.  We  can  not,  of  course,  enumerate 
all  the  possibilities  that  may  exist  (see  page  592  et  seq.).  In  general,  it  may  bo 
said  that  in  most  of  the  severe  cases  of  acute  nephritis  the  urine  contains  numer- 
ous casts  of  the  hyaline  and  other  varieties.  As  has  been  already  mentioned,  the 
epithelial  casts  and  the  firm,  waxy  casts  are  especially  common  in  the  severer 
39 


610  DISEASES    OF   THE   URINAEY   OEGAE^S 

forms  of  acute  nephritis.  The  hyaline  casts  have  usually  adherent  to  them  red 
and  white  blood-corpuscles,  as  well  as  epithelium,  fat-drops,  and  detritus.  These 
morphological  constituents  are  also  found  free  in  greater  or  less  amount.  The 
sediment  is  apt  to  contain  also  numerous  beautiful  crystals  of  uric  acid. 

Individual  cases  are  often  characterized  by  a  striking  predominance  of  some 
one  constituent — epithelium,  white  blood-corpuscles,  or  red  blood-corpuscles — - 
but  no  special  rules  in  regard  to  this  can  be  given.  We  have  spoken  previously 
(page  594)  of  the  special  conclusions  we  can  draw  from  the  different  objects 
found  in  the  sediment.  We  can  accordingly  distinguish  an  acute  hgemorrhagie, 
or  non-ha3morrhagic,  an  acute  desquamative,  and  a  fatty  degenerative  nephritis, 
but  we  must  always  bear  in  mind  that  all  these  forms  pass  into  one  another  with- 
out sharp  boundaries. 

The  chemical  examination  of  the  urine  gives,  as  the  most  important  and  con- 
stant result,  usually  a  considerable  amount  of  albumen.  Since  the  reaction  of  the 
urine  is  almost  invariably  acid,  the  albumen  is  inxmediately  precipitated  on  heat- 
ing the  urine,  and  sinks  to  the  bottom  of  the  test-tube,  where  it  usually  takes  up 
about  one  half  or  three  fourths  of  the  volume  of  urine  used  for  the  heat-test. 
More  accurate  quantitative  determinations  of  albumen  give  most  frequently  in 
acute  nephritis  an  amount  of  albumen  of  from  three  tenths  to  one  per  cent. ; 
higher  percentages  are  rare.  The  daily  total  amount  of  albumen  eliminated 
amounts  to  about  one  or  two  drachms  (grammes  5-8),  or  sometimes  more,  but  the 
daily  loss  of  albumen  from  the  body  hardly  ever  exceeds  the  amount  of  five 
drachms  (grammes  20).  The  variation  in  the  amount  of  albumen  eliminated 
in  different  cases  is  quite  noticeable. 

The  examination  of  the  other  solid  constituents,  which  is  not  generally  em- 
ployed in  practice,  usually  gives  a  diminished  secretion  of  urea,  phosphoric  acid, 
etc.,  corresponding  to  the  diminution  in  the  whole  amount  of  urine. 

The  other  Symptoms  of  Acute  Nephritis. — Local  symptoms  in  the  kidneys 
themselves  are  only  rarely  present.  There  is,  of  course,  a  certain  tenderness  in 
the  region  of  the  kidneys,  which,  however,  is  too  ambiguous  to  have  very  great 
symptomatic  importance.  It  is  more  often  the  case  that  the  abnormally  concen- 
trated urine  causes  frequent  micturition,  associated  with  a  disagreeable  burning 
sensation — a  sort  of  vesical  tenesmus. 

The  subsequent  symptoms  of  acute  nephritis,  which  appear  in  the  rest  of  the 
body,  and  among  which  dropsy  takes  the  first  place,  are  far  more  important  than 
the  local  symptoms.  CEdema  may  be  entirely  wanting  in  acute  nephritis,  particu- 
larly in  cases  of  secondary  nephritis  after  pneumonia,  erysipelas,  diphtheria,  and 
usually  in  cases  of  septic  nephritis.  On  the  other  hand,  oedema  is  especially  char- 
acteristic of  many  cases  of  acute  nephritis,  including  cases  due  to  scarlet  fever,  to 
catching  cold,  to  alcoholic  excess,  and  to  pregnancy,  as  well  as  the  so-called  pri- 
mary nephritis  and  the  nephritis  which  follows  cutaneous  diseases,  such  as 
scabies  or  pustulous  eczema.  This  oedema  is  not  infrequently  the  most  promi- 
nent clinical  symptom.  We  must  always  be  prepared  for  its  appearance,  espe- 
cially when  the  amount  of  urine  shows  a  considerable  and  persistent  dimi- 
nution. 

The  oedema  is  usually  discovered  first  in  the  face,  which  has  a  bloated,  and 
often  a  pale  and  somewhat  shiny  appearance.  The  eyelids  are  usually  most 
swollen  at  first.  Besides  the  face,  the  ankles,  the  legs,  the  scrotum,  and  the  depend- 
ent parts  of  the  trunk  may  be  the  chief  seat  of  the  oedema,  the  severity  and  extent 
of  which  may  of  course  vary  greatly  in  different  cases.  If  a  high  degree  of  gen- 
eral dropsy  develops,  this  is  a  source  of  great  distress  to  the  patient.  The  move- 
ments of  the  body  are  much  restrained,  and  all  changes  of  position  are  difficult, 
associated  with  great  exertion,  and  painful.  In  the  severest  degrees  of  dropsy 
small  fissures  may  form  here  and  there  in  the  excessively  tense  skin,  from  which 


ACUTE   NEPHRITIS  611 

the  dropsical  fluid  oozes.  Such  little  wounds  are  sometimes  the  starting-point  for 
disagreeable  erysipelatous  inflammations,  etc. 

If  great  o-dema  of  the  skin  is  present,  we  usually  find  at  the  same  time  a  more 
or  less  marked  dropsy  of  the  serous  cavities.  It  is  often  hard,  however,  to  make 
out  ascites  or  hydrothorax  on  physical  examination,  owing  to  the  oedema  of  the 
skin  that  is  present.  The  symptoms  mentioned  acquire  their  chief  clinical  signifi- 
cance from  the  difliculty  of  respiration  necessarily  associated  with  them,  since  the 
diaphragm  is  pressed  upward  by  ascites,  and  the  lungs  are  compressed  by  hydro- 
thorax.  If  a  hydrothorax  is  more  marked  on  the  left,  or  especially  if  hydroperi- 
cardium  sets  in,  the  activity  of  the  heart  is  materially  impaired. 

A  marked  oedema  of  the  mucous  membranes  develops  but  rarely;  in  a  few 
cases  we  have  seen  oedema  of  the  conjunctivae,  oedema  of  the  soft  palate,  and 
oedema  of  the  glottis.  Of  the  cedemas  of  internal  organs,  oedema  of  the  brain  has 
already  been  mentioned  as  a  possible  cause  of  severe  nervous  ursemic  symptoms. 
Qildema  of  the  lungs,  which  often  comes  on  toward  the  end  of  the  disease,  when 
it  terminates  unfavorably,  is  usually  not  to  be  regarded  as  a  part  of  the  general 
oedema,  but  as  a  result  of  the  final  cardiac  weakness. 

In  regard  to  the  other  symptoms  in  the  different  organs,  the  symptoms  on  the 
part  of  the  circulatory  apparatus  must  first  be  mentioned.  The  pulse  is  often 
abnormally  tense,  hard,  and  full  (see  page  600).  In  the  beginning  of  the  disease 
it  is  often  somewhat  slow;  later  it  is  usually  accelerated.  A  beginning  cardiac 
hypertrophy  can  often  be  made  out  post  mortem,  and  sometimes  clinically,  in 
cases  which  have  lasted  a  rather  long  time,  four  to  six  weeks.  It  seems 
to  develop  most  rapidly  in  children  who  were  previously  well  and  strong.  We 
pay  especial  regard  to  the  condition  of  the  apex-beat,  and  to  the  accentuation  of 
the  aortic  second  sound.  The  occasional  nose-bleeds  are  probably  connected  with 
the  increased  arterial  tension.  Pericarditis  is  seen  as  a  rare  complication — a 
complication  which  is  connected  with  the  general  fact  that  in  all  forms  of  nephri- 
tis the  different  internal  organs,  especially  the  serous  membranes,  have  a  tendency 
to  inflammation.  Whether  this  circumstance  is  connected  with  the  retention  of 
urinary  constituents,  as  has  been  repeatedly  surmised,  can  not  at  present  be  de- 
cided with  certainty. 

Of  the  symptoms  in  the  respiratory  apparatus,  we  have  mentioned  above  the 
dyspnoea  consequent  upon  the  dropsical  symptoms.  In  severe  cases  the  lungs 
themselves  are  often  drawn  into  sympathy,  as  shown  by  the  development  of  a  dif- 
fuse bronchitis  or  a  peculiar  form  of  pneumonia.  The  latter  stands  midway 
between  a  catarrhal  and  a  croupous  inflammation.  It  exhibits,  to  a  certain  degree, 
a  form  of  stiff  inflammatory  oedema,  and  occurs  in  just  the  same  way  in  the 
chronic  forms  of  nephritis  as  in  acute  nephritis.  When  it  involves  both  lungs  to  a 
great  extent,  it  may  be  the  immediate  cause  of  death.  The  development  of  gen- 
eral pulmonary  oedema  is  usually  a  sign  of  beginning  weakness  of  the  left  ven- 
tricle, as  we  have  said  above,  although  here,  too,  inflammatory  factors  may  have 
some  influence. 

Vomiting  is  the  most  important  symptom  in  the  digestive  apparatus.  If  it 
appears  in  a  marked  degree,  it  may  almost  always  be  considered  as  a  ura3mic 
symptom,  and  then  is  often  the  precursor  of  severe  nervous  symptoms.  The  appe- 
tite is  almost  always  diminished  in  acute  nephritis ;  the  bowels  are  usually  consti- 
pated, but  there  may  be  quite  severe  diarrhoea  (see  page  600).  We  may  mention 
peritonitis,  which  is  sometimes  purulent,  as  a  very  rare  complication  (vide  supra). 

The  temperature  is  jnarkedly  influenced  by  acute  nephritis  only  in  those  cases 
where  the  disease  develops  in  previously  healthy  persons,  or  at  least  in  those  free 
from  fever.  Then  we  see  quite  frequently  a  moderate  fever,  with  an  irregular 
rise  of  temperature  of  about  100°  to  102°  (38°-39°  C).  It  is  quite  rare  that  an 
apparently  primary  acute  nephritis  begins  suddenly  with  a  chill  and  high  fever, 


612  DISEASES    OE    THE   UKIisTAEY   ORGAI^S 

104°  (40°  C).  Tiie  condition  of  the  temperature  on  tlie  onset  of  ursemic  symp- 
toms has  already  been  described  (page  600). 

The  state  of  the  general  nutrition  suffers  in  quite  a  noticeable  degree  in  most 
of  the  severe  cases  of  acute  nephritis.  The  emaciation  is  often  concealed  by  the 
oedema;  but  the  anaemia  is  the  more  prominent,  and  often  lends  to  the  bloated 
face  a  peculiar  aspect. 

Urasmic  symptoms  may  come  on  at  any  time  in  the  course  of  acute  nephritis. 
We  are  often  prepared  for  the  onset  of  uraemia  by  a  previous  marked  decrease  in 
the  secretion  of  urine,  or  by  the  well-known  prodromal  symptoms,  but  in  other 
cases  it  begins  very  suddenly  with  severe  symptoms  of  eclampsia.  In  regard  to 
all  further  details  we  may  refer  to  what  was  said  on  page  5U6  et  seq. 

The  Course  and  Different  Forms  of  Acute  ISTephritis. — The  whole  clinical 
picture  of  acute  nephritis  depends  very  materially  upon  the  form  of  its  develop- 
ment. If  an  acute  nephritis  comes  on  in  the  course  of  a  severe  infectious  general 
disease,  as  in  the  course  of  a  septic  affection,  of  ulcerative  endocarditis,  or  of 
severe  typhoid,  the  changes  in  the  urine  are  often  the  sole  indication  of  the  occur- 
rence of  the  complication.  The  type  of  the  severe  febrile  general  disease  is  in  no 
way  materially  modified  by  the  added  renal  affection ;  oedema  and  uraemic  symp- 
toms do  not  iTSually  appear,  often  because  the  primary  disease  soon  ends  in  death. 

Also  when  nephritis  comes  on  in  previously  healthy  persons  or  in  chronic 
invalids,  the  tuberculous,  etc.,  in  many  cases  the  changes  in  the  urine  are  the 
chief  symptom,  while  the  other  general  and  secondary  symptoms  are  scarcely  evi- 
dent at  all,  or  at  least  only  in  a  very  slight  degree.  Such  mild  cases  are  associated 
only  with  more  or  less  general  dullness  and  loss  of  appetite.  (Edema  is  entirely 
absent,  or  present  only  to  a  very  slight  degree.  Of  course  such  cases  demand 
great  caution,  since  even  in  them  we  may  have  a  sudden  outbreak  of  severe 
uraemic  symptoms. 

The  fully  developed  type  of  severe  acute  nephritis  is  seen  especially  in  scar- 
latinous nephritis  (g.  v.),  which  comes  on  in  children  who  are  fully  convalescent 
or  apparently  wholly  well ;  it  is  also  seen  in  many  cases  of  apparently  idiopathic 
nephritis  (vide  supra),  or  nephritis  coming  on  after  exposure  to  cold,  etc.  In  these 
cases  there  is  often  the  development  of  a  general  dropsy,  secondary  pulmonary 
affections,  ursemic  Symptoms,  the  symptoms  mentioned  in  the  circulatory  appa- 
ratus, etc.  In  these  cases,  too,  the  examination  of  the  urine  affords  the  only  cer- 
tain means  of  judging  accurately  of  the  condition,  but  the  other  morbid  symptoms 
which  appear  early — oedema,  anaemia,  and  vomiting — may  direct  our  suspicions 
to  the  developing  renal  affection. 

Scarcely  any  general  statements  can  be  made  as  to  the  course  and  the  dura- 
tion of  acute  nephritis,  since  the  variations  in  this  respect  are  too  great.  To 
describe  here  in  particular  all  the  different  forms  of  nephritis  according  to  the 
aetiological  conditions  in  question  would  lead  us  too  far.  We  will  therefore  refer 
to  the  description  of  the  different  primary  diseases,  in  which  the  characteristic 
marks  of  any  renal  complication  are  always  stated.  A  few  remarks  must  be 
added  about  some  of  the  simple  forms  of  acute  nephritis. 

The  so-called  primary  idiopathic  nephritis  usually  appears  rather  suddenly 
without  any  demonstrable  cause,  or  it  may  follow  a  marked  chill  ("  nephritis  due 
to  catching  cold")-  The  first  symptoms  of  the  disease  are  sometimes  insignifi- 
cant, but  at  other  times  they  are  quite  severe — chills,  fever,  renal  pain,  etc.  Some- 
times other  "  rheumatic  symptoms,"  such  as  angina  or  articular  pains,  are  also 
present.  Often  the  first  thing  which  attracts  the  attention  of  the  patient  is  the 
occurrence  of  oedema,  the  pufflness  of  the  face,  or  slight  shortness  of  breath  due  to 
hydrothorax.  Sometimes  the  first  symptom  is  vomiting.  The  further  course  of 
the  illness  may  be  mild  or  severe.  In  the  former  case  the  oedema  that  has  ap- 
peared is  but  slight,  the  changes  in  the  ui'ine  (albuminuria,  hcematuria,  etc.),  do 


ACUTE   XEPHRITIS  613 

not  attain  a  very  high  degree,  and  after  a  few  weeks  complete  recovery  ensues. 
In  other  cases,  however,  the  type  of  a  severe,  acute,  and  very  often  hasmorrhagic 
nephritis  develops,  with  great  general  dropsy,  uraemia,  etc.,  which  in  three  or 
four  weeks,  or  sooner,  may  lead  to  death;  but  improvement  may  follow  in  spite 
of  the  severest  symptoms.  Then  the  amount  of  urine  gradually  increases,  and  the 
abnormal  constituents  of  the  urine,  the  (jedema,  and  the  other  morbid  symptoms, 
gradually  disappear.  Of  course,  it  is  often  a  long  time  before  complete  recovery 
ensues,  since,  even  when  the  patient  feels  perfectly  well  subjectively,  the  urine 
may  still  sometimes  contain  some  albumen,  a  few  casts,  or  a  few  red  blood-corpus- 
cles. In  such  cases  one  must  think  of  the  possibility  of  a  transition  of  acute 
into  chronic  nephritis.  Xot  infrequently  there  is  apparently  complete  recovery, 
but  several  weeks  or  months  later  there  appears  suddenly,  perhaps  after  some  spe- 
cial cause,  such  as  catching  cold,  or  over-exertion,  or  some  febrile  disease,  a  fresh 
attack  of  acute  nephritis  ("  acute  recurrent  nephritis,"  vide  supra). 

The  XEPHPJTis  OF  PREGNANCY  usually  begins  gradually.  Erequent  micturition 
and  oedema  of  the  lower  extremities  make  their  appearance,  and  beside  these  there 
are  often  nausea  and  even  vomiting.  If  we  examine  the  urine,  we  usually  find 
it  quite  rich  in  albumen,  but  comparatively  poor  in  morphological  elements.  The 
slight  sediment  consists  of  hyaline  casts,  a  few  white  blood-corpuscles,  and  some 
epithelium.    Only  rarely  does  the  urine  assume  a  hsemorrhagic  character. 

The  condition  described  almost  always  lasts  to  the  end  of  pregnancy.  In  the 
cases  that  proceed  favorably  a  verj-  rapid  recovery  often  follows  after  the  birth 
of  the  child;  but  the  onset  of  eclampsia  gravidarum  is  to  be  dreaded  as  a  not 
infrequent  and  a  dangerous  complication.  This  is  to  be  regarded  as  entirely  anal- 
ogous to  uremia.  It  begins  after  mild  prodromal  symptoms,  or  even  quite  sud- 
denly, with  violent  general  convulsions,  during  which  the  child  is  usually  born. 
A  more  or  less  persistent  coma  follows  the  convulsions.  The  convulsions  may  be 
very  frequently  repeated.  Death  ensues  in  about  one  third  of  the  cases ;  the  other 
cases  usually  recover,  only  rarely  passing  into  chronic  nephritis.  A  slight  albu- 
minuria may,  however,  persist  for  months  after  delivery.  The  prognosis  is  still 
more  unfavorable  for  the  child  than  for  the  mother,  inasmuch  as  the  child  dies  in 
nearly  one  half  of  the  eases. 

Moreover,  it  should  be  noted  that  eclampsia  sometimes  occurs  without  any 
preceding  albuminuria,  and  perhaps  of  itself  leads  to  a  mild  albuminuria  because 
of  the  circulatory  disturbances  incident  to  the  convulsive  seizures. 

The  anatomical  changes  in  the  nephritis  of  pregnancy  are  hardly  ever  very 
striking  to  the  eye.  The  kidneys  are  usually  pale  and  but  little  enlarged.  Under 
the  microscope  we  usually  find  a  slight  interstitial  cedema  and  degenerative 
changes  in  the  epithelium.  Only  rarely  are  more  marked  nephritic  appearances 
present. 

Acute  alcoholic  nephritis  is  a  term  which  we  apply  to  that  form  of  the  disease 
which  we  have  repeatedly  observed  in  excessive  beer  drinkers — for  instance,  in 
brewers.  The  appearance  of  the  disease  seems  to  be  favored  by  coincident  excit- 
ing causes,  such  as  catching  cold,  but  beyond  this  it  is  to  be  regarded  as  the  sud- 
den development  of  a  renal  disease,  resulting  from  the  toxic  influences  of  alcohol 
habitually  ingested.  There  is  a  rapid  and  great  development  of  general  dropsy. 
The  amount  of  urine  is  moderately  diminished.  The  urine  contains  much  albu- 
men, but  usually  remains  rather  clear  and  contains  no  blood.  As  a  rule,  the 
patients  are  obese,  and  their  discomfort  is  great.  A  favorable  termination  is  pos- 
sible under  suitable  treatment,  but  yet  there  is  always  danger  of  a  transition  into 
chronic  nephritis. 

Diagnosis. — Acute  nephritis  can  be  overlooked  only  when  the  examination  of 
the  urine  is  neglected  or  when  it  is  impracticable.  The  latter  sometimes  happens, 
for  example,  when  the  patient  does  not  come  under  observation  until  after  the 


614  DISEASES    OF   THE   UEINARY   OEGANS 

onset  of  severe  ursemic  symptoms.  Otherwise,  however,  the  changes  in  the  urine 
always  furnish  evidence  enough  to  recognize  the  existence  of  the  affection  of  the 
kidneys.  We  can,  of  course,  decide  that  the  nephritis  is  acute  only  by  considera- 
tion of  the  history,  the  setiological  conditions,  and  the  whole  course  of  the  dis- 
ease. We  must  also  bear  in  mind  the  possibility  that  there  may  be  an  acute  ex- 
acerbation in  a  chronic  nephritis  that  has  already  existed  for  a  long  time,  and  has 
been  perhaps  without  symptoms — acute  recurrent  nephritis,  usually  heemorrhagic. 

Prognosis. — The  prognosis  of  acute  nephritis  depends  in  many  cases  not  only 
upon  the  renal  affection,  but  also  upon  the  underlying  primary  disease.  We  caii 
not  here  describe  in  detail  the  numerous  conditions  that  must  be  considered,  but 
they  are  to  be  found  in  the  appropriate  chapters. 

Many  cases  of  primary  nephritis  from  toxic  action,  or  exposure  to  cold,  and 
also  many  cases  of  secondary  nephritis  after  scarlet  fever,  in  pneumonia,  typhoid 
fever,  or  syphilis,  during  pregnancy,  etc.,  recover  perfectly  in  a  short  time  or 
after  several  weeks,  according  to  the  severity  of  the  individual  case.  On  the 
other  hand,  however,  it  must  be  said  that  every  case  of  nephritis  must  be  viewed 
with  great  caution,  partly  because  it  may  be  the  starting-point  of  a  subsequent 
chronic  renal  disease,  and  partly  because  dangerous  sequelae  may  sometimes  de- 
velop in  cases  that  at  first  are  apparently  mild.  The  dangers  of  acute  nephritis 
are  chiefly :  First,  the  appearance  of  severe  general  dropsy,  especially  in  the  inter- 
nal cavities  of  the  body.  Of  the  forms  of  dropsy  hydrothorax  is  the  most  danger- 
ous, as  it  may  produce  suffocation  by  compression  of  the  lungs.  Second,  ursemia, 
especially  in  its  severe  convulsive  forms,  with  high  temperature  and  finally  car- 
diac paralysis.  Third,  the  inflammation  of  internal  organs,  among  which  second- 
ary pneumonia,  in  particular,  is  a  frequent  cause  of  death,  while  secondary  peri- 
carditis and  peritonitis,  as  we  have  said,  are  seen  in  but  very  few  cases.  We  mus^ 
bear  in  mind,  however,  that  in  individuals  otherwise  healthy  the  severe  sequelae 
just  mentioned  may  also  be  recovered  from.  The  most  extreme  dropsy  may  be 
re-absorbed,  and  we  sometimes  see  recovery,  especially  in  children,  after  the 
worst  ursemic  symptoms. 

Treatment.— With  regard  to  prophylaxis,  the  reader  should  be  reminded  that 
in  all  diseases  which  experience  has  shown  to  be  prone  to  lead  to  secondary  ne- 
phritis— for  instance,  scarlet  fever — the  kidneys  should  be  guarded  as  much  as 
possible,  from  the  start,  by  suitable  diet  (milk)  ;  by  promoting  the  secretion  of  the 
kidneys  ("flushing  the  kidneys''),  by  administering  an  abundance  of  liquids, 
such  as  mineral  waters,  milk,  and  lemonade ;  and  by  stimulating  the  cardiac  activ- 
ity by  warm  clothing,  warm  baths,  and  rubbing  with  alcohol. 

If  nephritis  has  already  developed  we  can  scarcely  hope  to  influence  directly 
the  inflammatory  process.  The  remedies  recommended  for  this  purpose  are  tan- 
nin, uva  ursi,  fuchsine,  and  methyl  blue,  but  to  an  unprejudiced  observer  they 
seem  absolutely  useless. 

We  expect  as  little  result  at  present  from  "  external  antiphlogosis  "  as  from  the 
internal  remedies  mentioned — that  is,  from  local  blood-letting,  applications  of  ice 
to  the  region  of  the  kidneys,  etc.  Only  in  the  rare  cases  where  severe  pain  in  the 
region  of  the  kidneys  comes  on  at  the  beginning  of  nephritis,  in  an  otherwise 
robust  individual,  are  we  at  present  justified  in  trying  leeches  or  a  few  dry  cups. 
The  warm  baths,  to  be  described  more  fully  below,  have  perhaps  an  indirect 
favorable  action  on  the  process  in  the  kidneys,  since  they  produce  a  hyperaemia 
of  the  skin,  and  thus  lessen  the  flow  of  blood  to  the  kidneys. 

Although  we  must  accordingly  admit  that  there  is  scarcely  any  remedy  at  our 
service  which  has  a  direct  therapeutic  influence  upon  the  diseased  kidneys,  the 
treatment  of  nephritis  may  nevertheless  produce  very  significant  results,  since 
both  a  number  of  hygienic  measures  and  the  fulfillment  of  certain  symptomatic 
indications  are  of  the  greatest  importance. 


ACUTE   NEPHEITIS  615 

Among  the  general  hygienic  measures  we  must  mention  first  strict  confine- 
ment to  bed.  In  the  severe  cases  its  necessity  is  self-evident;  but,  even  in  the 
milder  cases,  which  run  their  course  without  any  severe  subjective  symptoms, 
constant  rest  in  bed  is  necessary  throughout.  In  this  way  we  not  only  avoid  the 
unfavorable  action  of  cold  upon  the  external  skin,  but  the  activity  of  the  skin, 
which  must  act  vicariously  for  the  kidneys,  is  also  excited  by  the  uniform  warmth 
of  the  bed;  while  any  useless  muscular  exertion,  which  would  tax  the  heart's  ca- 
pacity for  work,  is  also  avoided  by  staying  in  bed.  In  general  it  is  advisable  to 
cover  the  patient  quite  warmly,  so  as  to  keep  him  in  a  constant  slight  perspiration. 

The  regulation  of  the  diet  is  very  important.  All  those  foods  and  drinks  which 
may  irritate  the  kidneys  are  to  be  strictly  avoided,  especially  spices,  very  sour 
substances,  strong  tea  and  coffee,  or  alcoholic  drinks.  Milk  has  for  a  long  time 
proved  itself  to  be  by  far  the  most  suitable  and  best  food.  It  has  won  for  itself 
the  reputation  of  a  remedy  in  renal  disease,  and  the  best  results  have  often  been 
seen  from  a  methodical  "  milk-cure  " — that  is,  from  feeding  the  patient  almost 
exclusively  with  milk.  The  great  aversion  of  some  patients  toward  milk,  how- 
ever, is  sometimes  an  obstacle  to  its  use.  We  may  often  be  aided,  then,  by  mak- 
ing the  milk  more  acceptable  to  the  patient  by  the  addition  of  a  little  coffee,  salt, 
a  little  cognac,  or  soda-water.  Among  other  foods  to  be  recommended  are  but- 
termilk, milk-gruel  with  rice  or  groats,  and  flour-gruel.  We  should  be  very  cau- 
tious about  giving  meat  as  long  as  there  are  severe  symptoms. 

Less  harmful  are  light  broths  made  from  pigeons,  fowls,  or  veal,  with  eggs.  In 
every  case  of  acute  nephritis,  even  when  there  is  dropsy,  we  regard  the  abundant 
ingestion  of  liquids  as  advantageous.  For  beverages,  besides  milk  we  may  give 
Seltzer,  Wildinger,  or  Fachinger  water,  tea,  and  lemonade.  The  last  is  particu- 
larly to  be  recommended.  Alcoholic  beverages  must  be  entirely  withheld,  or,  at  the 
most,  we  may  allow  a  little  claret.  The  stronger  wines  are  given  only  when  the 
heart  becomes  weak,  and  even  then  their  usefulness  is  dubious. 

The  chief  object  in  the  symptomatic  treatment  consists  in  preventing  the  in- 
jurious results  of  the  defective  elimination  of  the  water  and  the  solid  constituents 
of  the  urine  by  the  kidneys,  or  in  remedying  these  results  if  they  have  already 
occurred.  This  purpose  can  be  attained  only  by  exciting,  as  far  as  possible,  the 
activity  of  other  organs  which  in  this  respect  may  act  vicariously  for  the  kidneys. 
The  skin  deserves  the  first  attention  here,  through  which,  by  means  of  the  sweat- 
glands,  large  amounts  of  water,  and  also,  to  a  certain  extent,  the  solid  constituents 
of  the  urine,  which  have  been  retained,  may  be  eliminated.  The  diaphoretic  treat- 
ment of  renal  diseases  has,  therefore,  been  generally  in  vogue  for  a  long  time.  If 
the  patient's  general  condition  permits,  we  always  begin  with  it  as  early  as  possi- 
ble, even  before  there  have  been  any  signs  of  oedema,  uraemic  symptoms,  etc.  For- 
merly we  employed,  like  most  other  physicians,  hot  baths  from  95°  to  105°  (36°- 
40°  C).  The  patient  stays  about  half  an  hour  or  an  hour  in  the  bath,  is  then 
rapidly  dried  somewhat,  wrapped  up  in  bed  in  a  previously  warmed  sheet,  and 
well  covered  up  to  the  neck  with  blankets.  In  order  to  make  the  procedure 
somewhat  easier  for  the  patient,  it  is  a  good  plan  to  cover  the  forehead  with 
a  cold  compress,  always  to  wipe  the  sweat  carefully  from  the  face,  and  fre- 
quently to  give  a  little  swallow  of  fresh  cold  water.  The  production  of  sweat 
is,  of  course,  better  excited  during  the  pack  if  the  patient  takes  some  hot  drink, 
hot  milk  with  soda-water,  or  hot  elder-tea.  It  sometimes  seems  to  aid  diaphoresis 
if  an  internal  diaphoretic  be  given  at  the  same  time,  the  best  being  five  to  ten 
grains  of  Dover's  powder  (gramme  0.3-0.5),  or  a  teaspoonful  or  two  (grammes 
5-10)  of  liquor  ammonii  acetatis  [U.  S.  P.]  (spiritus  Mindereri)  in  a  cup  of 
elder-tea.  We  have  also  found  a  good  rubbing  of  the  whole  body  with  dilute 
warm  French  brandy  of  service  before  the  pack.  The  pack  may  last  two  or  three 
hours.     Of  late  years,  particularly  in  severe  cases  with  marked  dropsy,  we  have 


616  DISEASES    OF   THE   URINAKY   ORGANS 

almost  entirely  abandoned  baths  and  in  their  stead  employed  with  the  best  re- 
sults the  hot,  wet  pack,  or  dry  heat  (vide  infra).  For  the  pack,  the  patient  is 
completely  wrapped  up  in  a  hot,  wet  sheet;  on  both  sides  are  arranged  several 
jugs  filled  with  hot  water,  and  likewise  enveloped  in  moist  cloths;  then  the  pa- 
tient is  covered  with  several  dry  blankets  and  is  given  two  or  three  cups  of  some 
hot  drink.  The  duration  of  a  pack  of  this  sort  is  about  two  or  three  hours.  In- 
stead of  moist  heat,  dry  heat  may  be  applied  with  the  purpose  of  sweating  the 
patient.  There  are  complicated  arrangements,  such  as  sweat-boxes  and  a  patent 
sweat-bed,  but  these  can  seldom  be  employed  outside  of  hospitals,  and  we  have  for 
a  considerable  time  adopted  with  good  results  the  arrangement  made  by  Quincke. 
A  tin  pipe  is  bent  at  an  angle  and  fastened  upon  a  board,  and  its  upper  end  is 
introduced  under  the  bed-clothes,  which  should  be,  if  possible,  somewhat  raised 
up,  while  under  its  lower  open  end  a  lighted  alcohol  lamp  is  placed  upon  the  floor ; 
the  warm  air  rises  and  is  conducted  beneath  the  bed-clothes,  where  the  heat 
becomes  so  great  that  the  upper  end  of  the  pipe  must  always  be  wrapped  in  a  cloth 
wet  in  cold  water. 

In  this  way  we  succeed  in  many  cases  in  causing  a  considerable  sweat,  so  that 
the  patient  loses  several  pounds  in  weight  at  each  pack,  and  an  existing  dropsy 
may  sometimes  be  made  to  disappear  completely  in  a  comparatively  short  time. 
On  the  other  hand,  however,  we  can  not  deny  that  it  is  very  hard  sometimes  to 
make  patients  sweat,  even  when  there  is  oedema  of  the  skin,  and  also  that  many 
patients  do  not  bear  hot  baths  and  packs  at  all.  The  latter  is  especially  true  if 
the  patient  has  dyspnoea,  and  if  signs  of  cardiac  weakness  have  already  set  in. 
In  such  cases  we  must  be  very  cautious  about  sweating  the  patient,  and  we  should 
employ  merely  warm  baths ;  or  if  we  put  the  patient  in  a  pack,  it  should  be  for 
a  brief  time. 

Of  internal  diaphoretics  there  is  one  remedy  which  is  particularly  useful  in 
renal  disease—viz.,  the  hydrochlorate  of  pilocarpine,  prepared  from  jaborandi. 
This  is  best  employed  subcutaneously,  one  sixth  to  one  third  of  a  grain  at  one 
dose  (gramme  0.01-0.02),  but  the  drug  may  also  be  given  internally  in  pills  in  the 
same  dose.  Its  effect  consists  in  the  production  of  a  rather  profuse  perspiration, 
and  likewise  a  marked  increase  in  the  salivary  secretion,  which  latter  is  often 
a  great  annoyance  to  the  patient.  For  this  reason,  and  because  it  sometimes 
induces  cardiac  weakness,  pilocarpine  is,  on  the  whole,  scarcely  to  be  recom- 
mended. We  ourselves  employ  it  only  occasionally  when  the  hot  baths  are  not 
used  or  when  they  do  not  have  a  satisfactory  effect. 

Next  to  the  skin,  the  intestinal  mucous  membrane  is  the  organ  from  which  we 
may  soonest  expect  to  produce  a  vicarious  elimination  of  water,  and  also  of  urea. 
It  is  sometimes,  therefore,  of  distinct  service  to  prescribe  drastic  cathartics  in 
nephritis  with  a  diminished  secretion  of  urine,  especially  if  there  is  a  tendency 
to  constipation  besides  the  dropsy,  dyspnoea,  etc.  The  drastic  cathartics  chiefly 
used  are  infusion  of  senna,  extract  of  colocynth,  gamboge  in  two-grain  powders 
(gramme  0.1),  tamarinds,  Epsom  salts,  etc. 

Finally,  it  may  be  asked  whether  we  should  not  excite  the  secretory  function 
of  the  kidneys  themselves  by  the  exhibition  of  diuretics.  Certainly  the  employ- 
ment of  vigorous  diuretics  is  opposed  by  the  consideration  that  we  might  still 
further  irritate  and  consequently  damage  the  renal  epithelium.  The  milder 
diuretics,  particularly  the  acetates  of  potash  and  of  sodium,  in  doses  of  about  one 
to  two  and  a  half  drachms  (grammes  5-10)  in  the  course  of  twenty-four  hours, 
and  diuretine,  one  to  one  and  a  half  drachms  (grammes  4—6)  a  day,  are  usually 
well  borne  and  are  often  efficient.  The  use  of  calomel  in  renal  disease  has  been 
repeatedly  commended,  but  we  would  warn  against  its  employment  because  very 
disagreeable  symptoms  of  mercurial  poisoning,  such  as  stomatitis,  are  apt  to 
occur. 


ACUTE   InTEPHRITIS  617 

The  therapeutic  measures  so  far  spoken  of  are  intended  to  prevent  as  far  as 
possible  the  retention  of  urinary  constituents  in  the  body.  They  are  also  very 
much  employed  when  the  signs  of  this  retention  have  already  appeared.  The 
dropsy  especially  is  best  treated  by  methodical  sweating-,  with  the  aid,  eventually, 
of  drastic  and  diuretic  remedies.  If  there  is  persistent  and  extreme  dropsy  we 
may  determine  to  remove  the  dropsical  fluid  by  direct  mechanical  means  from  the 
subcutaneous  cellular  tissue.  Better  than  the  so-called  capillary  trocars  and 
similar  apparatus  (such  as  aspiration  through  a  funnel  placed  like  a  wet  cup 
upon  the  incised  skin)  are  simple  scarifications  of  the  skin  made  longitudinally 
in  the  dependent  parts  (scrotum  and  posterior  surface  of  the  thigh  and  calf). 
Erom  these  the  dropsical  fluid  is  allowed  to  escape  into  pads  made  of  peat, 
[gauze],  or  similar  substances.  Absolute  antisepsis  and  asepsis  are  demanded, 
for  there  is  a  great  tendency  to  erysipelatous  inflammation. 

When  urEemia  is  threatening,  and  often  even  when  it  has  broken  out,  we  may 
try  to  produce  an  elimination  of  the  injurious  products  of  tissue  metamorphosis 
from  the  body  in  the  well-known  ways  above  described,  by  sweating  or  drastic 
purgatives.  Beside  this,  the  ursemic  symptoms,  however,  often  demand  a  special 
symptomatic  treatment.  If  very  violent  and  frequent  uraemic  convulsions  appear, 
we  consider  it  advisable  to  try  to  suppress  the  attacks  by  chloroforming  the  pa- 
tient. At  any  rate,  it  seems  to  us  to  be  better  to  use  chloroform  in  ursemia  than 
to  give  narcotics  internally,  because  with  this  we  can  watch  the  action  of  the  rem- 
edy better,  especially  with  regard  to  the  pulse  and  respiration.  Chloroform  is 
also  generally  used  by  the  obstetricians  as  the  main  remedy  in  the  eclampsia  of 
pregnancy.  If  the  attacks  are  not  very  frequent,  but  if  there  is  marked  somno- 
lence or  coma,  tepid  baths  with  cold  shower-baths  are  often  employed  with  dis- 
tinct advantage.  Cool  baths  are  also  serviceable  when  there  is  a  great  increase 
of  the  temperature.  If  we  are  treating  a  robust  individual  with  a  full  pulse,  and 
during  severe  ursemia  there  is  a  decided  redness  or  cyanosis  of  the  face,  venesec- 
tion may  be  indicated.  This  sometimes  has  a  striking  and  instant  effect,  as  has 
lately  been  confirmed  by  various  observers.  Great  attention  is  to  be  paid  to  the 
condition  of  the  heart.  As  soon  as  the  pulse  becomes  small  and  weak,  energetic 
stimulants,  such  as  strophanthus  or  subcutaneous  injections  of  camphor,  must  be 
used.  If  the  signs  of  cardiac  weakness  appear  before  the  beginning  of  severe 
uraemic  symptoms,  infusion  of  digitalis  must  be  used,  two  or  three  parts  to  three 
hundred  of  water.  Through  its  action  in  raising  the  blood-pressure — it  being  ad- 
visable under  some  circumstances  to  combine  with  it  acetate  of  potassium — free 
diuresis  sometimes  comes  on,  and  with  it  a  disappearance  of  the  danger  from 
uraemia ;  but  meanwhile  we  must  watch  for  symptoms  of  the  toxic  action  of  digi- 
talis. The  tinctura  nervina  Bestuschefiii  [nearly  equivalent  to  the  tincture  of  the 
chloride  of  iron,  U.  S.  P.]  may  also  be  sometimes  used  to  advantage  in  uraemia. 
We  are  not  apt  to  interfere  with  uraemic  vomiting  or  uraemic  diarrhoea,  because 
these  symptoms,  as  we  have  said,  are  to  be  regarded  as  a  form  of  self-help  by  the 
organism.  Only  when  such  symptoms  are  very  distressing  do  we  give  cracked  ice, 
morphine,  opium,  cocaine,  chloroform,  etc.  If  the  vomitus  contains  ammonia,  it 
is  a  good  plan  to  give  ten  or  fifteen  drops  of  dilute  hydrochloric  acid  in  water  sev- 
eral times  a  day.  An  abundance  of  liquids  is  always  to  be  prescribed  upon  the 
appearance  of  uraemic  symptoms,  because  in  this  way  it  is  probable  that  the  poi- 
sonous blood  is  diluted  and  also  the  excretion  of  the  toxines  promoted. 

[A  method  of  treatment  of  uraemic  convulsions,  whether  post  partum  or  con- 
nected in  no  way  with  parturition,  which  gives  excellent  and  prompt  results,  is  the 
administration  of  pilocarpine  hypodermically — grain  I,  and  repeat  in  twenty 
minutes — followed  by  the  hot-air  bath,  to  maintain  the  action  of  the  skin  after 
it  has  once  been  started.  PilocariDine  sometimes  acts  as  a  decided  cardiac  depress- 
ant, so  one  must  be  ready  to  administer  stimulants — brandy  or  ether — under  the 


618  DISEASES    OF    THE   URINAEY   ORGANS 

skin  if,  as  is  apt  to  be  the  case,  there  is  doubt  as  to  the  readiness  with  which  they 
will  be  absorbed  from  the  stomach  or  rectum.] 

In  severe  cases,  the  patient's  dyspnoea  often  demands  prompt  relief.  If  the 
dyspnoea  be  caused,  or  at  least  increased,  by  hydrothorax,  and  we  do  not  succeed 
in  removing  the  hydrothorax  in  any  other  way,  it  is  necessary  to  evacuate  it  by 
puncture.  In  acute  nephritis,  indeed,  we  may  hope  by  this  means  sometimes  to 
preserve  the  patient's  life  until  improvement  sets  in.  Great  ascites  must  also  be 
relieved  by  tapping.  Against  "  renal  pneumonia  "  our  remedies  are  powerless. 
Tepid  baths,  shower-baths,  and  wet  packs  sometimes  procure  relief.  In  "  ureemic 
asthma,"  morphine  injections  may  act  beneficially.  If  pulmonary  oedema  ensues, 
the  heart  again  is  chiefly  to  be  considered.  We  may  try,  besides  the  remedies 
already  mentioned,  large  mustard  plasters,  baths,  and  acetate  of  lead. 

We  accordingly  see  that  many  remedies  are  at  our  service  in  the  treatment  of 
nephritis,  the  choice  of  which  in  the  individual  case  must  be  committed  to  the 
personal  judgment  of  the  physician.  In  the  main,  we  should  always  begin  with 
the  necessary  hygienic  measures,  and,  if  possible,  with  a  methodical  diaphoretic 
treatment,  and  govern  ourselves  otherwise  by  symptomatic  indications.  After 
recovery  has  set  in,  great  caution  is  still  necessary  for  a  long  time.  The  patient 
must  guard  against  physical  over-exertion,  errors  in  diet,  and  exposure  to  cold. 
Preparations  of  iron  are  to  be  prescribed  when  there  is  a  secondary  anaemia. 

In  regard  to  the  influence  of  the  onset  of  an  acute  nephritis  on  the  treatment 
of  the  primary  disease,  we  may  mention  that  cold  baths  are  in  general  not  to 
be  freely  used,  as  in  typhoid  fever  with  nephritis,  but  still  they  may  be  tried  if 
they  are  otherwise  urgently  desirable.  We  would  also  suggest  that  certain 
internal  remedies,  especially  calomel  and  salicylic  acid,  must  be  used  only  with 
great  caution  when  there  is  nephritis.  In  the  eclampsia  of  lying-in  women  the 
induction  of  premature  labor  is  only  rarely  indicated,  since  the  child  is  usually 
born  during  the  paroxysms  without  interference. 


CHAPTER   III 

THE   SUBCHRONIC  AND   CHRONIC   FORMS   OF   NEPHRITIS,    WITH   THE 
EXCEPTION    OF    THE    GENUINE    CONTRACTED    KIDNEY 

{Chronic   Diffuse  Nephritis^   Chrqnic  Parenchymatous  Ntphritis,  Chronic    Hmmoi'rhagic   JVe^^hritis, 
Large  White  Kidney^  Secondary  Contracted  Kidney) 

.ffitiology. — While  the  acute  nephritis  described  in  the  preceding  chapter  runs 
its  course  in  several  days  or  weeks,  and  only  rarely  extends  over  some  months, 
we  will  now  speak  of  inflammatory  degenerative  affections  of  the  kidneys  which 
last  at  least  several  months,  and  often  go  on  for  a  year  or  two.  The  term  "  sub- 
acute "  or  "  subchronic  "  is  chosen  for  the  cases  that  last  a  comparatively  short 
time.    As  we  must  once  more  repeat,  there  is  no  sharp  limit  in  this  respect. 

In  regard  to  the  aetiology  of  these  forms  of  nephritis,  they  do  arise  from  an 
acute  nephritis,  but  this  is  quite  rare.  Formerly  such  an  origin  was  erroneously 
regarded  as  the  rule,  and  this  is  the  reason  why  the  changes  in  the  kidney  in  these 
cases  were  described  as  the  "second  stage  of  Bright's  disease"  (Frerichs).  The 
English  clinical  observers  Wilks  and  Johnson,  whom  Bartels  followed  in  Ger- 
many, first  pointed  out  the  fact  that  in  most  cases  the  disease  shows  a  chronic 
character  from  the  start,  and  that  we  can  only  exceptionally,  as  after  scarlet 
fever,  recognize  an  acute  "  first  stage."  The  name  "  chronic  parenchymatous  ne- 
phritis," since  frequently  used,  is  chosen  entirely  from  practical  reasons,  inasmuch 


SUBCHEONIC  AND    CHEOXIC   FOEMS    OF   NEPHEITIS       619 

as  it  briefly  states  the  distinction  from  the  genuine  contracted  kidney;  but  it  is 
incorrect  in  principle,  as  will  be  shown  from  the  description  of  the  anatomical 
conditions  later.  It  is  more  correct,  therefore,  to  employ  the  term  "chronic  diffuse 
nephritis,"  because  we  have,  in  fact,  to  deal  with  what  is  essentially  a  chronic  uni- 
versal or  diffuse  disease  of  the  kidneys,  as  contrasted  with  the  "  contracted  kid- 
ney "  in  which  there  are  always  bits  of  normal  tissue  interspersed  between  the 
numerous  separate  foci  of  disease. 

If  we  look  for  the  setiological  conditions  in  cases  that  have  a  chronic  course 
from  the  beginning,  we  can  often  discover  nothing  definite  at  all.  The  disease 
seems  to  have  developed  "  of  itself  "  in  previously  healthy  persons.  Most  probably 
we  have  here  some  toxic  or  infectious  agency  that  acts  on  the  kidneys,  whose 
detection,  however,  is  at  present  impossible.  In  malarial  regions  the  malarial 
poison  may  often  lead  to  chronic  nephritis.  It  is  also  attributed  to  syphilis  and 
tuberculosis,  but  the  cases  met  with  are  usually  combinations  of  these  diseases 
with  amyloid  kidney  (vide  infra).  Frequent  exposure  to  wet  and  cold,  damp 
dwellings,  etc.,  seem  sometimes  to  be  of  more  material  significance.  That  hard 
drinkers,  particularly  beer  drinkers,  are  especially  liable  to  nephritis  seems  to  the 
author  indubitable,  because  of  his  personal  observations  (vide  supra)  ;  but  it  is,  of 
course,  difficult  to  form  a  definite  opinion  on  all  these  points. 

Persons  in  early  middle  life  are  most  frequently  affected  by  the  disease,  and 
men  more  often  than  women.    In  children  and  old  people  the  disease  is  quite  rare. 

Pathological  Anatomy. — There  is  no  essential  distinction  between  the  ana- 
tomical lesions  of  the  kidney  in  acute  and  in  chronic  nephritis.  The  changes  that 
are  seen  in  both  are  essentially  the  same,  only  they  develop  and  extend  more 
slowly  in  the  chronic  forms;  and  they  also,  during  their  longer  duration,  lead  to 
certain  sequelse  in  the  kidney,  which  can  not  develop  at  all  in  acute  nephritis, 
owing  in  part  to  the  lack  of  time.  Even  in  chronic  nephritis  the  individual  cases 
differ  from  one  another  in  many  respects.  First  this  and  then  that  histological 
process  is  especially  prominent,  and  thus  lends  certain  peculiarities  to  the  macro- 
scopic appearance  of  the  kidneys.  Certain  sequelse — such  as  contractions — have 
also  developed  but  little  in  many  cases  that  soon  end  fatally,  but  they  develop 
far  more  in  other  cases  of  longer  duration.  Hence  it  happens  that  we  can  quite 
well  regard  certain  anatomical  forms  that  are  more  frequently  observed  as  types, 
although  we  must  never  lose  from  sight  the  important  fact  that  there  is  a  patho- 
logical unity  in  all  these  forms  and  types.  Then  we  shall  not  lose  the  clew  to  the 
understanding  of  the  morbid  process  if  the  individual  case  does  not  always  har- 
monize with  the  scheme  of  the  text-books. 

We  distinguish  the  three  following  chief  anatomical  types  of  subchronic  and 
chronic  nephritis: 

1.  Chronic  H/emorrhagic  Nephritis  in  the  form  of  the  Large  Eed  or  Varie- 
gated Kidney. — The  kidney  is  at  least  of  normal  size,  and  often  a  little  or  a  good 
deal  enlarged.  It  feels  firmer  than  normal;  its  capsule  is  often  adherent  to  the 
surface  in  some  places.  The  surface  looks  either  uniformly  a  more  gray  red  or 
more  mottled,  while  dai'k-red  spots  alternate  with  lighter  gray  or  even  yellow 
spots.  The  red  spots  on  the  surface  can  not  be  wholly  wiped  off,  and  thus  they 
prove  to  be  htemorrhages.  The  gray  or  yellow  parts  correspond  to  the  anaemic  or 
fatty-degenerated  portions.  On  section,  the  cortical  substance  is  usually  broader, 
its  normal  boundary  is  obliterated,  and  its  color  is  a  uniform  gray  red,  or  mottled 
and  striated. 

Under  the  microscope  we  find  in  part  the  same  changes  as  in  acute  nephritis — 
parenchymatous  and  fatty  degeneration  of  the  epithelium,  casts  or  haemorrhages 
in  the  uriniferous  tubules,  inflammatory  oedema  or  granular  infiltration  of  the  in- 
terstitial tissvie,  the  capsules  of  the  glomeruli  sometimes  thickened,  the  epithelium 
of  the  glomeruli  sometimes  proliferated  or  desquamated,  etc.     The  special  char- 


620  DISEASES    OF   THE   UEINAEY   ORGANS 

acteristic  of  this  chronic  form,  in  contrast  with,  acute  nephritis,  is  that  in  many 
places  a  complete  destruction  of  the  uriniferous  tubules  has  occurred,  and  that 
a  genuine  interstitial  connective  tissue,  more  or  less  rich  in  cells,  has  taken 
their  place.  In  this  lies  the  anatomical  evidence  of  the  longer  duration  of  the  dis- 
ease, since  the  two  processes — both  the  complete  atrophy  of  the  epithelium,  and 
especially  the  secondary  proliferation  of  connective  tissue — of  course  need  a  cer- 
tain time  for  their  development.  The  atrophy  and  the  consequent  proliferation  of 
connective  tissue  usually  predominate  in  some  parts,  while  in  others  nothing  but 
fresher  inflammatory  and  degenerative  changes  are  perceived. 

2.  The  Inflammatory  Fatty  Kidney,  or  the  Large  White  Kidney  {yellow 
would  be  more  exact). — In  this  form  of  chronic  nephritis  the  kidney  is  usually 
enlarged,  or  at  least  of  normal  size.  Its  outer  surface  is  smooth  and  of  a  yellow 
or  an  alternating  yellow  and  gray-yellow  color  throughout.  The  broader  cortical 
substance  shows  a  yellow  and  usually  somewhat  mottled  appearance,  while  the 
pyramids  almost  always  appear  considerably  reddened.  Haemorrhages  are  also 
almost  always  present  in  this  form,  usually,  of  course,  in  smaller  numbers  than 
in  the  variegated  kidney,  but  they  are  sometimes  quite  abundant,  as  in  the  hsem- 
orrhagic  fatty  kidney. 

The  microscope  shows  the  great  affinity  between  this  form  of  nephritis  and  the 
preceding.  We  have  almost  precisely  the  same  changes,  including  always  a  par- 
tial destruction  of  renal  tissue  with  a  subsequent  increase  of  interstitial  con- 
nective tissue.  The  macroscopic  appearance  of  the  kidney  is  due  to  the  fact  that 
it  is  ansemic,  and  that  the  fatty  degeneration  preponderates  in  the  epithelium. 
It  is  worthy  of  note  that  in  these  kidneys  marked  changes  in  the  glomeruli  are 
usually  present. 

3.  The  Secondary  Contracted  Kidney. — While  in  the  two  forms  of  nephritis 
thus  far  described  the  outer  surface  of  the  kidney  is  still  smooth,  and  the  kidney, 
on  the  whole,  is  somewhat  enlarged,  we  have  to  do  here  with  kidneys  of  about 
normal  size,  on  whose  surface  there  are  granulations,  which  as  yet  are  slight,  but 
which  still  are  already  plain.  This  granulation  signifies  nothing  more  than  that 
the  destruction  of  the  renal  tissue  has  here  advanced  farther,  and  that  the  newly 
formed  connective  tissue  has  in  part  undergone  cicatricial  contraction.  These 
kidneys,  therefore,  represent  a  later  stage  of  the  two  forms  first  named.  They 
usually  come  under  observation  when  the  nephritis  has  lasted  about  a  year  and  a 
half  or  two  years,  or  even  somewhat  longer.  The  first  beginnings  of  granulation 
may,  of  course,  show  themselves  earlier,  while,  on  the  other  hand,  when  the 
process  lasts  a  longer  time,  a  completely  contracted  kidney  may  develop. 

The  color  of  these  kidneys  is  usually  reddish  or  mottled,  the  red  spots  corre- 
sponding to  the  sunken  atrophic  parts,  and  the  gray  or  yellowish  spots  to  the  ele- 
vated parts.  Yellow  kidneys,  however,  may  also  show  at  times  decided  granu- 
lations. Microscopically,  we  find  already  marked  atrophy  of  the  renal  paren- 
chyma, with  a  corresponding  increase  of  the  interstitial  connective  tissue. 

Formerly  these  kidneys  were  called  the  "  transition  between  the  second  and 
third  stages  of  Bright's  disease."  As  follows  from  the  above,  they  are  to  be 
regarded  only  as  a  more  advanced  form  of  chronic  nephritis.  Since  the  kidneys, 
in  spite  of  their  granulation,  have  on  the  whole  a  normal  size,  we  can  infer 
from  this,  and  from  the  clinical  course,  that  they  were  previously  enlarged. 
Therefore  the  name  of  "  secondary  contracted  kidney  "  is  quite  suitable,  in  oppo- 
sition to  the  genuine  contracted  kidney,  which  represents  a  much  more  chronic 
form  of  renal  atrophy.  In  the  latter  the  contraction  takes  place  in  an  extremely 
chronic  manner  in  a  kidney  which  was  previously  normal,  while  in  the  "  secondary 
contracted  kidney"  the  cicatricial  process  develops  in  a  kidney  which  was  pre- 
viously the  subject  of  diffuse  disease. 

Of  other  pathological  lesions,  apart  from  the  changes  in  the  kidney,  we  will 


SUBCHRONIC  AND    CHROKEC   FORMS    OF   NEPHRITIS       021 

mention  here  only  the  hypertrophy  of  the  left  ventricle,  which  is  found  (vide 
infra)  in  all  the  above-mentioned  forms  of  nephritis.  The  chronic  parenchym- 
atous nephritis  without  cardiac  hypertrophy,  assumed  by  Bartels  in  his  time, 
does  not  exist.  Such  cases  were  probably  instances  of  unrecognized  amyloid  dis- 
ease. Exceptionally  it  may  happen  that  when  a  patient  with  chronic  nephritis  is 
very  much  debilitated  and  enfeebled,  the  cardiac  hypertrophy  is  not  developed. 

Clinical  History. — Only  in  the  comparatively  rare  cases  when  the  renal  affec- 
tion begins  acutely,  do  the  symptoms  of  chronic  nephritis  follow  immediately  on 
the  first  acute  stage.  In  most  cases,  however,  the  disease  develops  slowly  and 
gradually  from  the  start,  as  we  have  said,  so  that  it  is  usually  impossible  to  deter- 
mine accurately  the  moment  when  the  disease  begins.  Still  we  may  assume  that 
the  onset  is  decidedly  more  rapid  in  chronic  diffuse  nephritis  than  in  genuine 
contracted  kidney. 

The  first  signs  of  the  disease  consist  of  certain  general  symptoms,  pallor, 
dullness,  loss  of  appetite,  nausea  and  headache,  and  later  of  oedema.  The  latter 
is  often  the  first  symptom  which  sends  the  patient  to  the  physician,  since  in 
the  beginning  he  is  apt  to  pay  little  attention  to  the  symptoms  first  named.  The 
oedema  usually  appears  first  in  the  ankles  and  legs,  more  rarely  at  an  early  period 
in  the  face.  It  often  disappears  at  first  after  a  night's  rest,  but  always  develops 
afresh  during  the  day,  gradually  increasing  in  intensity.  The  patient  himself 
now  sometimes  notices  a  change  in  the  urine,  either  an  abnormal  color  or  cloudi- 
ness or  a  diminished  amount.  The  accurate  examination  of  the  urine  by  the 
physician  first  establishes  the  diagnosis. 

In  regard  to  the  more  special  symptomatology  of  chronic  nephritis,  we  meet 
exactly  the  same  symptoms  as  have  been  described  in  the  preceding  chapter  on 
acute  nephritis.  The  characteristic  distinction  is  based  merely  upon  the  whole 
course  of  the  affection  and  the  order  of  development  of  the  different  symptoms, 
and  not  upon  the  symptoms  themselves. 

The  urine  almost  always  is  diminished.  Of  course  the  figures  vary  con- 
siderably both  in  different  cases  and  at  different  times  in  the  same  case.  A 
small  amount  of  urine,  ten  to  twenty-five  ounces  (300-700  cubic  centimetres)  a 
day,  is  almost  always  an  unfavorable  sign,  while  a  free  diuresis  signifies  an  ab- 
sorption of  the  dropsy  and  an  improvement  of  the  condition.  There  is  also  a 
persistent  increase  in  the  amount  of  urine  when  the  chronic  nephritis  passes  into 
a  secondary  contracted  kidney.  Under  such  circumstances  the  daily  amount  of 
urine  may  rise  to  1,500  or  2,000  cubic  centimetres  or  more. 

The  specific  gravity  of  the  urine  is  often  increased  to  about  1015  to  1025,  cor- 
responding to  the  amount  of  albumen  and  of  other  solid  constituents.  It  is  of 
course  correspondingly  lower  when  there  is  a  more  abundant  elimination  of  water 
by  the  kidneys. 

The  amount  of  albumen  in  the  urine  is  quite  marked  in  all  severe  cases,  being 
one  third  to  three  fourths  of  its  volume.  It  amounts  to  about  1.5-3  per  cent,  by 
weight,  so  that  the  patient's  daily  loss  of  albumen  may  reach  half  an  ounce  to  an 
ounce  (grammes  15-30). 

The  examination  of  the  sediment,  which  is  usually  abundant,  is  of  the  great- 
est importance  for  the  accurate  determination  of  the  form  of  the  anatomical 
changes  in  the  kidneys.  Above  all,  the  question  arises  as  to  the  presence  or  ab- 
sence of  blood  in  the  urine.  If  abundant,  hfematuria  may  be  recognized  by  the 
naked  eye  from  the  color  of  the  urine.  The  detection  of  smaller  amounts  of  blood 
can  be  made  only  by  the  aid  of  the  microscope.  It  goes  without  saying  that  the 
amount  of  blood  in  the  urine  varies  considerably  in  the  different  cases,  and  in 
the  same  case  the  urine  often  contains  much  more  blood  during  certain  periods 
in  the  c  Jurse  of  the  disease  than  at  other  times.  The  portions  of  urine  passed  at 
different  times  taken  separately  often  show  quite  marked  variation  in  this  respect ; 


622  DISEASES    OF    THE   UEIXAEY   OKGAKS 

tlie  day's  urine  113113117  contains  more  blood  than  the  night's.  From  the  detec- 
tion of  renal  haemorrhages,  of  course  in  connection  with  other  symptoms, 
"we  can  always  make  with  certainty  the  diagnosis  of  a  "  chronic  hsemorrhagic  " 
nephritis. 

In  most  cases  casts  are  quite  abundant  in  the  sediment  of  the  urine,  but  natu- 
rally their  amount  and  variety  undergo  quite  great  variations  in  different  cases 
and  at  different  times  in  the  same  case.  They  are  the  direct  sign  of  the  presence 
of  an  inflammatory  exudative  process  in  the  kidneys,  although  the  deposits  on  the 
casts  are  more  important  for  the  diagnosis  of  the  special  form  of  renal  disease 
than  are  the  casts  themselves.  Those  formed  constituents  of  the  sediment  are 
most  characteristic  in  this  respect  which  point  directly  to  the  processes  of  fatty 
degeneration  in  the  kidneys :  the  fatty  granules  and  fatty  granular  cells,  free  or 
attached  to  the  casts.  The  number  of  these  elements  is  especially  great  in  the 
chronic  inflammatory  fatty  kidney,  the  "  large  white  kidney."  The  usually  clear, 
non-heemorrhagic  urine  may  in  some  cases  have  even  a  fatty  lustrous  surface. 
Eenal  epithelium  is,  on  the  whole,  more  rarely  present  in  the  sediment  in  chronic 
nephritis  than  in  acute,  but  it  occurs  in  some  cases. 

Of  the  other  symptoms,  the  one  that  usually  most  strikes  the  eye  is  dropsy.  It 
usually  come  on,  as  we  have  said,  in  the  beginning  of  the  disease,  and  slowly  or 
rapidly  reaches  a  great  extent  and  intensity.  A  medium  or  even  a  high  degree  of 
general  dropsy  may  often  persist  almost  unchanged  for  months.  In  other  cases 
it  shows  either  spontaneous  variations  or  variations  influenced  by  treatment ;  it 
decreases  for  a  time  only  to  increase  anew.  The  severer  and  more  comparatively 
acute  the  case,  the  greater  in  general  is  the  dropsy.  In  the  more  chronic  cases,  in 
secondary  contracted  kidney,  its  intensity  may  be  slight  for  a  time  or  even  perma- 
nently. The  dropsy  may  even  be  absent  in  some  cases,  as  we  learn  especially 
from  the  observations  reported  by  Wagner  under  the  name  of  "  chronic  hsemor- 
rhagic Bright's  disease  without  oedema  "  (vide  infra).  In  regard  to  the  different 
localizations  of  the  dropsy,  and  to  dropsy  of  the  internal  cavities,  hydrothorax, 
ascites,  and  hydropericardium,  and  their  results,  the  same  holds  true  as  in  acute 
nephritis. 

Of  the  internal  organs,  the  condition  of  the  heart  lays  claim  to  the  most  inter- 
est. In  all  cases  of  chronic  nephritis,  in  which  we  do  not  have  to  do  with  espe- 
cially weak  and  run-down  patients,  who  can  not  save  the  necessary  nutritive 
material  for  the  formation  of  a  cardiac  hypertrophy,  we  find  a  pronounced  and 
often  a  very  marked  hypertrophy  of  the  left  ventricle,  either  with  or  without  a 
co-existing  dilatation  of  its  cavity.  The  detection  of  cardiac  hypertrophy  during 
the  patient's  life  is  sometimes  difiicult,  especially  when  there  is  general  dropsy,  but 
the  diagnosis  can  usually  be  correctly  made  with  proper  attention  to  the  abnor- 
mally tense  radial  pulse,  the  accentuated,  valvular  aortic  second  sound,  and  the 
displacement  outward  of  the  apex-beat,  or  at  least  its  increased  strength.  We 
often  find  in  the  cadaver,  and  can  sometimes  make  out  during  life,  a  hypertrophy 
of  the  right  ventricle  (vide  supra,  page  603). 

A  second  important  sequel  of  chronic  nephritis  consists  of  the  changes  in  the 
retina — albuminuric  retinitis.  Although  very  rare  in  acute  nephritis,  these 
changes  are  present  in  the  majority  of  the  cases  of  this  class.  Sometimes  the  pa- 
tient's subjective  visual  disturbance  (dimness  of  vision,  defects  in  the  field  of 
vision)  points  to  a  disease  of  the  retina,  but  the  existence  of  disease  can  be  estab- 
lished with  certainty  only  by  ophthalmoscopic  examination.  In  tnese  cases  we 
find  two  kinds  of  changes,  in  varying  numbers  and  combinations :  first,  retinal 
haemorrhages ;  and,  second,  white  spots  and  streaks,  especially  in  the  vicinity  of 
the  optic  nerves.  The  origin  of  the  spots,  which  may  appear  and  disappear  again, 
is  not  yet  entirely  clear.  At  any  rate,  they  are  circumscribed  fatty  dege  aerations 
of  the  special  retinal  elements.     The  degree  of  amblyopia  depends,  0:  course, 


SUBCHKON'IC  AND    CHRONIC   FORMS    OF   NEPHRITIS       623 

chiefly  upon  the  localization  of  the  changes,  whether  in  the  macula  lutea,  or  other 
parts. 

We  need  say  little  in  regard  to  the  other  symptoms,  since  they  agree  essen- 
tially with  those  of  acute  nephritis.  The  general  anaemia  is  very  pronounced  in 
many  cases,  but  it  is  less  marked  in  the  very  chronic  forms.  The  cerebral  symp- 
toms, especially  the  headache  and  the  mild  vertigo,  may  depend  in  part  upon  the 
cerebral  anaemia;  otherwise,  they  are  due  to  urasmia  (vide  infra).  Cerebral 
haemorrhages  have  been  observed  in  a  very  few  cases.  Ha3morrhages  on  the 
inner  surface  of  the  dura  mater  are  more  frequent,  but  they  are  usually  without 
clinical  significance.  The  mouth,  larynx,  and  pharynx  usually  show  nothing 
particular,  except  accidentally  complicating  inflammations.  We  must,  however, 
remember  the  occasional  occurrence  of  a  very  distressing  or  even  dangerous 
oedema  of  the  soft  palate,  or  of  the  arytseno-epiglottic  ligaments — oedema  of  the 
glottis.  Forms  of  bronchitis  and  pneumonia  occur,  similar  to  those  seen  in  acute 
nephritis.  Bronchitis  and  chronic  oedema  of  the  lungs  also  make  their  appear- 
ance in  the  more  advanced  stages  of  the  disease,  as  a  result  of  cardiac  insufii- 
ciency.  Finally,  we  must  remember  the  hindrance  to  respiration  from  hydro- 
thorax,  and  also  from  uraamic  dyspnoea.  The  changes  in  the  heart  have  already 
been  spoken  of.    Endocarditis  or  pericarditis  may  occur,  but  they  are  very  rare. 

As  to  digestive  disturbances,  loss  of  appetite  is  a  very  common  symptom.  Very 
persistent  vomiting  is  usually  to  be  regarded  as  a  chronic  uraemic  symptom.  The 
bowels,  as  a  rule,  are  constipated,  but  there  may  also  be  severe  diarrhoea,  as  in 
acute  nephritis.  In  severe  cases,  especially  in  the  last  stages  of  the  disease,  ulcer- 
ative and  dysenteric  processes  have  repeatedly  been  observed  in  the  large  intestine 
and  the  ileum.  Peritonitis  may  occur,  but  it  is  at  all  events  extremely  rare.  The 
liver  and  spleen  usually  show  no  peculiarities. 

Uremic  symptoms,  both  of  the  milder  chronic  variety  and  also  in  their  severest 
acute  form,  may  come  on  at  any  time,  although  they  do  not  by  any  means  attain 
their  full  development  in  all  cases,  and  are  somewhat  rarer  than  in  genuine  con- 
tracted kidney. 

The  temperature  remains  normal,  as  a  rule,  as  long  as  it  is  not  influenced  by 
complicating  inflammations,  or  by  the  appearance  of  uraemia. 

Course,  Duration,  and  Termination  of  Chronic  Nephritis. — In  general,  the 
whole  course  of  chronic  nephritis  presents  quite  a  great  uniformity.  The  different 
symptoms  may  show  certain  variations  within  long  periods,  but  the  patient  often 
presents  almost  the  same  appearance  day  after  day  for  months.  The  duration  of 
the  disease  varies  greatly,  from  three  to  six  months,  in  the  subacute  cases,  to 
two  or  three  years,  or  even  more,  in  the  very  chronic  cases.  The  cases  of  long 
duration  are  almost  all  cases  of  secondary  contracted  kidney.  They  some- 
times show  in  their  clinical  relations  the  transition  from  the  enlarged  to  the 
granular  kidney,  since  the  picture  in  many  of  its  details  is  more  like  that  in  the 
genuine  contracted  kidney:  the  oedema  decreases,  disappears  completely,  or,  at 
least,  continues  in  a  lesser  degree;  the  amount  of  urine  becomes  more  abundant, 
and  the  specific  gravity  and  the  amount  of  albumen  become  correspondingly  less. 
The  condition  thus  lasts  for  a  long  time  until  it  grows  worse  again,  through 
ursemia,  or  disturbance  of  the  compensation  in  the  heart. 

The  final  termination  of  chronic  nephritis  is  in  most  cases  unfavorable.  In 
the  severe  forms  death  ensues  in  from  three  months  to  a  year,  either  in  conse- 
quence of  general  dropsy  or  from  uraemia,  from  complicating  inflammations,  etc. 
The  conditions  when  the  nephritis  goes  on  to  secondary  contraction  are  com- 
paratively more  favorable,  inasmuch  as  the  patient  may  then  find  himself  in  a  tol- 
erable state,  for  a  time  at  least.  Complete  recoveries  doubtless  occur  in  chronic 
nephritis,  but  they  are  rare.  The  longer  the  disease  lasts  beyond  the  first  six 
months  the  less  likely  is  recovery.     The  development  of  secondary  contraction 


624  DISEASES    OF   THE   UEINARY   OEGAiTS 

may  simulate  recovery  or,  at  any  rate,  the  subjective  condition  of  the  patient  may 
be  almost  perfect.  Even  after  signal  improvement,  however,  relapses  are  always 
to  be  feared.  There  are  even  genuine  acute  attacks  in  the  course  of  chronic 
nephritis. 

Different  Forms  of  Chronic  Diffuse  Nephritis. — ^Diagnosis. — By  means  of 
careful  examination  of  the  urine  in  all  suspicious  cases — for  example,  those  pre- 
senting oedema,  anaemia,  and  similar  symptoms — we  may  in  general  be  certain  of 
making  a  correct  diagnosis  of  chronic  nephritis,  but  all  experienced  observers  will 
acknowledge  that  the  diagnosis  of  the  particiilar  form  of  chronic  nephritis  is  diffi- 
cult and  uncertain,  even  when  the  examination  of  the  case  is  most  painstaking. 
Still,  the  following  schematic  resume  may  at  least  furnish  some  indications : 

Chronic  Hcomorrhagic  Nephritis  (large  variegated  or  mottled  kidney). — Dura- 
tion from  six  to  eighteen  months.  Urine  ha3morrhagic ;  usually  quite  rich  in  red 
blood-corpuscles  and  casts.  (Edema.  Cardiac  hypertrophy.  Retinal  changes. 
Quite  frequently  uraemia. 

Inflammatory  Fatty  Kidney  (large  white  kidney). — Duration  also  six  to  eight- 
een months,  but  usually  somewhat  shorter  than  in  the  preceding  form.  Urine  not 
at  all,  or  only  slightly,  hsemorrhagic.  Frequently  many  white  blood-corpiiscles, 
and  especially  signs  of  fatty  degeneration  in  the  kidneys,  fatty  granular  cells,  fat- 
drops  in  the  urine,  etc.  Large  amount  of  albumen  in  the  urine.  Marked  oedema. 
Cardiac  hypertrophy.    Very  often  retinal  ch'^nges.    Death  by  uraemia  frequent. 

Secondary  Contracted  Kidney. — Longer  duration  of  the  disease,  from  a  year 
and  a  half  to  three  years.  At  first  the  svmptoms  of  the  preceding  forms;  later, 
urine  more  abundant,  less  oedema,  etc.  Death  from  an  increase  of  the  dropsical 
symptoms  due  to  cardiac  insufficiency,  uraemia,  etc. 

Chronic  Hwmorrhagic  Nephritis  without  CEdema. — This  form  has  been  already 
mentioned  (page  622),  but  it  should  receive  somewhat  further  consideration.  Up 
to  this  time  it  has  been  too  little  regarded,  although  we  ourselves  have  observed 
not  a  few  cases  of  this  variety  of  chronic  nephritis.  The  disease  has  a  rather 
chronic  course.  For  a  long  time  the  patient  is  but  slightly  inconvenienced,  par- 
ticularly if  he  has  good  care.  The  urine  is  usually  quite  abundant,  and  contains 
very  little  albumen,  but  has  always,  or  almost  always,  small  amounts  of  blood 
mixed  with  it,  and  this  continues  for  many  months  or  even  longer.  From  time  to 
time  there  will  appear  a  more  or  less  considerable  hsematuria,  so  that  the  urine 
has  an  abundant  dark,  brownish-red  sediment.  This  is  especially  likely  to  occur  if 
the  mode  of  life  has  been  indiscreet,  but  it  may  also  happen  without  exciting 
cause.  The  urinary  sediment  is  composed  of  red  blood-corpuscles,  some  of  which 
are  entire  and  some  already  disintegrated,  together  with  a  moderate  number  of 
hyaline  casts.  The  latter  usually  have  red  blood-globules  or  granules  of  hfematoi- 
dine  and  detritus  adherent  to  them.  The  amount  of  urine  temporarily  diminishes, 
but  it  soon  increases  again.  Little,  if  any,  increase  in  the  size  of  the  heart  can  be 
demonstrated;  oedema  is  entirely  absent,  nor  have  we  yet  observed  retinitis  in 
association  with  this  form  of  nephritis.  Uraemia  does  occur,  but  it  is  rare.  The 
course  of  the  disease  is  very  tedious,  as  we  have  said.  Whether  recoverv  may  take 
place  is  uncertain.  Usually  apparent  recovery  is  followed  by  the  sudden  appear- 
ance of  a  fresh  haemorrhage.  It  is  probable  that  in  most  cases  the  final  result  is  a 
secondary  contracted  kidney. 

With  regard  to  the  aetiology  of  this  form  of  chronic  nephritis,  it  is  our  opinion 
that  in  most  cases  there  is  a  chronic  septic  infection  or  intoxication ;  at  any  rate, 
it  is  noticeable  that  such  patients  not  very  infrequently  give  a  history  of  some 
suppurative  process. 

Treatment. — The  treatment  of  chronic  nephritis  corresponds  in  all  its  details 
so  closely  to  that  of  acute  nephritis  that  we  can  refer  almost  entirely  to  the  pre- 
ceding chapter. 


CONTEACTED   KIDNEY  625 

The  main  thing  here  also  is  regimen  and  symptomatic  treatment.  The  patient 
must  always  keep  himself  warm,  wear  flannels,  or  stay  in  bed.  The  diet  mvist  be 
unirritating.  At  first,  for  a  time,  we  may  try  giving  milk  alone;  it  is  always 
advantageous  to  give  an  abundance  of  liquids,  except  that  alcoholic  beverages 
should  be  avoided  so  far  as  possible.  It  is  well  to  pay  careful  attention  to  the 
skin — bathing,  or  sponging  with  warm  water  and  alcohol.  Under  some  circum- 
stances climatic  treatment,  in  Italy,  Egypt,  etc.,  are  indicated  in  the  more  chronic 
forms. 

The  treatment  of  dropsy  follows  entirely  the  methods  previously  described,  and 
so  does  the  treatment  of  any  uraemic  symptoms.  If  there  is  persistent  hsematuria, 
ergotine  may  be  tried,  but  it  seldom  seems  to  do  any  good. 

In  the  more  chronic  cases  with  great  anaemia,  preparations  of  iron,  such  as 
iodide  of  iron,  are  often  to  be  used,  and  also  frequently  stomachics,  cathartics,  etc. 
The  condition  of  the  heart  always  deserves  careful  attention  (digitalis!).  The 
retinitis  rarely  demands  special  treatment. 


CHAPTER  TV 

CONTRACTED    KIDNEY 

(Genuine  Contracted  Kidney.    Granular  Atrophy  of  the  Kidney.     Granular  Kidney.     Chronic  Inter- 
stitial Nephritis) 

Definition  and  .^Etiology. — The  genuine  contracted  kidney  is  the  result  of  an 
extremely  chronic  and  very  slowly  but  constantly  progressive  atrophy  of  the 
renal  tissue.  The  term  "  chronic  nephritis  "  is  also  used  for  contracted  kidney, 
but  the  special  inflammatory  processes  are  very  subordinate  here,  for  the  anatom- 
ical change  consists  essentially  in  nothing  but  a  simple  degenerative  atrophy  of 
the  renal  parenchyma,  and  in  a  corresponding  gradual  increase  of  the  interstitial 
connective  tissue.  From  a  general  pathological  point  of  view  the  process  is  to  be 
regarded  as  wholly  analogous  to  the  corresponding  changes  in  the  liver  in  cirrhosis 
of  that  organ,  in  the  spinal  cord  in  the  chronic  degenerations  of  the  different  sys- 
tems of  fibers,  etc.  In  all  these  cases  we  have  a  primary  destruction  of  the  special 
tissue-elements  as  a  result  of  some  deleterious  action,  and,  following  a  general 
pathological  law  (Weigert),  a  partial  replacement  of  the  parts  destroyed  by  a 
newly  formed  cicatricial  connective  tissue. 

In  the  "  genuine "  contracted  kidney  the  atrophy  of  the  renal  parenchyma 
begins  in  a  previously  healthy  kidney.  Cell  after  cell  of  epithelium,  islet  after 
islet  of  tissue,  are  slowly  attacked,  while  other  parts  still  remain  intact.  It  was 
therefore  an  error  of  the  older  pathologists  to  regard  the  contracted  kidney  as  the 
"  third  stage  of  Bright's  disease,"  as  if  every  granular  kidney  were  first  found  in 
the  stage  of  acute  inflammation,  and  then  passed  into  the  stage  of  chronic  enlarge- 
ment, and  lastly  into  that  of  contraction.  This  theory,  of  course,  suits  certain 
cases  in  part,  for  chronic  nephritis  at  least  may  often  finally  pass  into  contraction, 
but  these  "  secondary  contracted  kidneys  "  {vide  supra)  can  clinically,  and  almost 
always  anatomically,  be  differentiated  from  the  genuine  contracted  kidneys.  The 
contracted  kidney  may  arise  from  an  acute  nephritis  in  some  cases,  and  careful 
investigation  indicates  that  such  cases  are  not  very  rare;  but  then  the  process 
hardly  ever  passes  through  the  three  stages  mentioned  above,  for  the  acute  ne- 
phritis apparently  recovers.  A  slight  remnant  of  it  is  left — a  little  fire,  as  it 
were,  smouldering  under  the  ashes;  its  work  of  destruction  advances,  wholly  in 
secret,  and  perhaps  only  after  many  years  do  the  symptoms  of  a  pronounced  renal 
contraction  appear. 
40 


626  DISEASES    OF   THE   URINARY   ORGANS 

If  ^ve  inquire  into  the  causes  wliicli  produce  the  atrophy  of  the  renal  tissue  in 
the  ordinary  cases  of  contracted  kidney,  which  are  chronic  from  the  first,  we  are 
very  often  unable  to  make  out  any  special  etiology.  Of  course,  one  of  the  first 
things  to  consider  in  this  disease  is  chemical  or  toxic  agents,  whether  these  are 
introduced  directly  as  such  into  the  body,  or  whether  they  are  manufactured  in 
the  body  because  of  abnormalities  in  metabolism,  or  as  a  result  of  infectious  pro- 
cesses. 

Experience  teaches  us  that  there  are  three  chemical  substances  to  be  mentioned 
which  may  favor  the  development  of  contracted  kidney:  alcohol,  lead,  and  uric 
acid.  Chronic  alcoholism  is  often  to  be  regarded  as  the  most  probable  cause  of 
renal  contraction,  especially  in  people  who  have  "  lived  well  "  otherwise,  and  have 
become  corpulent.  In  these  cases  contracted  kidney  is  to  be  viewed  as  a  sort  of 
atrophy,  due  to  wearing  out,  or  to  strain.  It  is  difiicult  to  decide  how  much  influ- 
ence should  be  ascribed  to  the  alcohol  itself  and  how  much  to  the  excessive  inges- 
tion of  food.  The  specific  effect  of  alcohol  is  almost  indubitable  in  those  cases  in 
which  contracted  kidney  and  hepatic  cirrhosis  are  both  present,  a  combination 
repeatedly  observed. 

We  are,  therefore,  strongly  inclined  to  assume  that  the  chief  cause  of  inter- 
stitial nephritis  is  an  improper  mode  of  life,  but  yet  it  can  not  be  denied  that  the 
disease  is  also  frequently  observed  in  individuals  whose  lives  are  not  open  to 
criticism.  There  are  cases  of  genuine  contracted  kidney  in  youthful  patients, 
twenty-five  to  thirty-five  years  old,  and  of  both  sexes,  for  which  not  the  slight- 
est cause  c?,n  be  discovered.  One  might  suppose,  under  such  circumstances,  that 
there  are  kidneys  which  are  peculiarly  vulnerable  and  which  can  not  permanently 
meet  even  the  ordinary  demands  of  life.  The  connection  between  contracted 
kidney  and  chronic  lead-poisoning,  in  type-setters,  painters,  etc.,  is  also  incon- 
testable. It  is  a  remarkable  circumstance,  and  one  not  yet  fully  explained,  that 
in  these  cases  we  very  often  see  at  the  same  time  genuine  gout  (arthritis 
uratica  saturnina).  Gout,  however,  alone,  without  any  co-existing  chronic  lead- 
poisoning,  often  leads  to  the  development  of  contracted  kidney,  "  gouty  kidney," 
in  Avhich  we  probably  have  to  do  with  the  noxious  action  of  an  abnormal  amount 
of  uric  acid  on  the  renal  parenchyma ;  but  it  always  seems  to  be  especially  unfa- 
vorable to  have  an  accumulation  of  several  injurious  factors — for  instance,  lead- 
poisoning  associated  with  chronic  alcoholism. 

Infectious  influences  are,  probably,  first  to  be  considered  in  those  cases  where 
the  contracted  kidney  can  be  referred  to  a  former  acute  infectious  nephritis,  as 
after  scarlet  fever.  We  may  also  mention  here  the  appearance  of  contracted 
kidney  sometimes  observed  after  severe  acute  articular  rheumatism.  We  may 
perhaps  imagine  a  similar  connection  in  the  cases  where  contracted  kidney  is 
found  combined  with  chronic  endocarditis  (valvular  heart  disease),  or  with 
chronic  arthritis  not  of  gouty  origin.  Of  the  chronic  infectious  diseases,  which 
sometimes  have  a  connection  with  the  origin  of  contracted  kidney,  we  may  men- 
tion malaria  and  syphilis.  The  latter  ought  especially  to  be  considered  more 
than  it  is  at  present,  because  we  may  have  either  an  immediate  action  of  syphilitic 
toxines,  or  a  renal  atrophy  as  the  result  of  a  specific  disease  of  the  renal  arteries. 

We  must  here  devote  a  little  time  to  a  consideration  of  the  connection  between 
renal  contraction  and  primary  disease  of  the  vessels,  which  has  been  much  dis- 
cussed. It  is  true  that  we  often  find  general  arterio-sclerosis,  and  also  atheroma, 
especially  in  the  renal  arteries,  in  the  bodies  of  persons  who  have  died  from  con- 
tracted kidney,  but  this  frequent  coincidence  can  not  be  remarkable  in  such  cases, 
because  contracted  kidney  is  seen  chiefly  in  elderly  persons,  and  those  in  whom 
atheroma  of  the  arteries  is  also  a  very  common  symptom.  The  theory  advanced 
by  the  English  authors.  Gull  and  Sutton  and  others,  that  the  vascular  disease, 
"  arterio-capillary  fibrosis,"  always  represents  the  primary  process,  to  which  the 


CONTEACTED   KIDNEY  G27 

renal  atrophy  is  only  secondaiy,  is,  however,  utterly  untenable.  We  often  find  the 
most  pronounced  contraction  of  the  kidneys  without  any  vascular  changes  suffi- 
cient to  explain  the  atrophy ;  and  where  the  latter  can  be  found  in  the  small  renal 
arteries,  we  usually  have  not  a  primary  but  a  secondary  process — namely,  the  well- 
known  obliterating  arteritis,  which  is  seen  in  almost  all  chronic  inflammations 
and  degenerative  atrophies  of  various  organs. 

Of  course,  it  can  not  be  denied  that  primary  disease  of  the  arteries  in  the  kid- 
ney may  check  the  flow  of  blood  to  certain  portions  of  the  tissue,  and  thus  occasion 
secondary  atrophy  in  limited  areas  (arterio-sclerotic  contracted  kidney),  just  as, 
for  example,  interstitial  myocarditis  results  from  primary  arterio-sclerosis  of  the 
coronary  arteries.  This  is  particularly  true  of  the  so-called  senile  kidney — that 
is,  the  granulated  kidney  of  old  persons,  due  to  atheromatous  changes  in  the  blood- 
vessels, and  perhaps  also  certain  other  cases  of  nephritis  subsequent  to  syphilis, 
and  especially  the  rare  cases  of  unilateral  contracted  kidney,  which  have  been 
seen  chiefly  in  association  with  syphilis. 

With  relation  to  the  age  and  sex  of  patients  with  contracted  kidney,  it  has 
already  been  repeatedly  stated  that  the  disease  occurs  mainly  in  later  life.  The 
explanation  of  this  fact  lies  in  the  peculiar  circumstances  which  occasion  the 
renal  process.  For  the  same  reason,  also,  the  male  sex  is  much  oftener  attacked 
than  the  female ;  yet  the  causes  which  lead  to  contracted  kidney  are  so  numerous 
that  it  is  easy  to  understand  why  the  disease  is  not  infrequently  seen  even  in 
younger  individuals  and  in  women.  Contracted  kidney  does  occur  in  children, 
though  rarely.  In  all  cases  in  youthful  persons  we  must  make  careful  inquiry  as 
to  any  previous  attack  of  acute  nephritis,  subsequent  perhaps  to  scarlet  fever, 
diphtheria,  or  measles. 

The  relations  of  contracted  kidney  to  amyloid  disease  of  the  kidney  (so-called 
amyloid-contracted  kidney),  and  to  chronic  disease  of  the  urinary  passages,  par- 
ticularly of  the  pelvis  of  the  kidney,  will  be  discussed  later  in  the  appropriate 
chapters. 

Pathological  Anatomy. — In  the  genuine  contraction  of  the  kidney,  both  kid- 
neys are  always  diminished  in  about  the  same  degree.  Their  size  is  sometimes 
reduced  to  one  half  or  even  one  third  of  the  normal,  so  that  it  is  almost  difficult  to 
find  the  Uttle  kidney  in  the  very  abundant  and  thick  fatty  capsule  that  is  often 
present.  The  kidneys  feel  firm  and  dense,  and  show  on  their  surface  a  very  plain, 
coarse  or  fine,  uniform  or  irregular,  granulation.  On  pulling  off  the  somewhat 
thickened  fibrous  capsule,  these  granulations  become  more  prominent,  and  the  cap- 
sule usually  adheres  quite  firmly  to  the  depressed  portions.  The  raised  portions 
are  almost  always  darker  and  redder — that  is,  richer  in  blood — than  the  lighter 
and  grayer  depressions.  Whether  the  whole  kidney  appears  more  red  or  more 
white  depertds  only  upon  the  amount  of  blood  in  the  organ,  and  there  is  no  reason 
for  separating  the  "  small  red  "  from  the  "  small  white  "  contracted  kidney. 

On  section  of  the  contracted  kidney,  we  find  the  cortex  very  thin,  and  pale 
atrophic  streaks  alternating  with  the  darker  portions.  The  pyramids  are  also 
rather  small,  and,  as  a  rule,  are  darker  than  the  cortex.  In  the  pelvis  of  the  kid- 
ney, which  is  often  somewhat  dilated,  there  are  sometimes  a  number  of  uric-acid 
concretions.  Striated  uric-acid  infarctions  in  the  pyramids  are  a  very  character- 
istic mark  of  the  gouty  contracted  kidney.  The  microscope  shows  an  advanced 
destruction  of  the  renal  parenchyma,  which  is  replaced  by  a  cicatricial  connective 
tissue  in  which  the  nuclei  are  still  numerous  or  else  have  already  become  scanty. 
We  can  always  make  out  signs  of  degeneration  and  atrophy  of  the  epithelium,  and 
the  formation  of  casts  in  the  uriniferous  tubules  which  still  remain,  but  which  are 
already  diseased.  Atrophy,  thickening  of  the  capsule,  etc.,  are  found  in  many  of 
the  glomeruli.  The  uriniferous  tubules  that  are  still  preserved  in  some  places  are 
often  in  part  dilated.     We  can  not  here  go  more  fully  into  the  manifold  histo- 


628  DISEASES    OE    THE   UHIIS^AEY   OEGAXS 

logical  details,  especially  the  formation  of  cysts,  the  changes  in  the  vessels  {vide 
supra),  the  deposition  of  lime-salts,  etc.  Haemorrhages  are  only  very  rarely 
present. 

Thus  the  contracted  kidney  may  be  regarded  as  the  form  of  chronic  nephritis 
with  by  far  the  longest  course  (lasting  from  three  to  five  years,  and  even  much 
longer),  and  also  the  form  with  the  widest  extent.  Its  essential  nature  can  in  no 
way  be  contrasted  with  "  chronic  parenchymatous  nephritis  "  as  a  "  chronic  inter- 
stitial nephritis  " ;  for  we  always  find  interstitial  processes  in  the  former,  which 
have  reached  a  far  higher  degree  in  the  contracted  kidney  only  because  the  slow 
atrophy  of  tissue  is  compatible  with  a  much  longer  duration  of  life,  and  hence  can 
attain  a  much  greater  extent. 

The  anatomical  changes  in  the  other  organs  of  the  body  beside  the  kidneys 
will  be  spoken  of  in  connection  with  the  symptomatology  of  contracted  kidney. 

Clinical  Symptoms, — Except  in  the  comparatively  rare  cases  where  we  can 
refer  the  origin  of  a  contracted  kidney  to  a  previous  acute  or  chronic  nephritis, 
the  clinical  symptoms  of  contracted  kidney  develop  as  gradually  and  insidiously 
as  the  anatomical  process  itself.  There  is  no  doubt  but  that  a  contraction  of  the 
kidney  may  exist  for  years,  without  calling  the  patient's  attention  to  his  disease  by 
a  single  serious  subjective  symptom.  This  is  evident  from  the  chance  discov- 
eries on  autopsy  of  a  contraction  of  the  kidney  in  people  who  have  lost  their 
lives  in  some  other  way,  but  especially  from  the  cases  where  the  severest  symp- 
toms, such  as  uraemia,  cerebral  haemorrhage,  etc.,  which  often  lead  immediately  to 
death,  suddenly  come  on  in  persons  previously  regarded  as  perfectly  healthy, 
while  the  autopsy  shows  a  quite  far  advanced  contraction  of  the  kidney  as  the 
special  cause  of  these  symptoms.  The  less  prominent  the  subjective  symptoms  of 
renal  contraction  are  in  the  earlier  stages  of  the  disease,  the  more  we  should  con- 
sider the  objective  changes,  which  in  fact  usually  permit  the  diagnosis  of  the  dis- 
ease quite  early  on  careful  examination  of  the  patient. 

The  condition  of  the  urine  is  most  important  in  this  respect.  As  soon  as 
changes  have  taken  place  in  the  epithelium  in  different  parts  of  the  kidneys,  the 
results  previously  spoken  of  must  make  themselves  manifest  in  the  secretion  of 
the  urine,  although  still  in  a  slight  degree,  and  the  diseased  portions  will  secrete  a 
urine  diminished  in  amount  and  in  solid  constituents,  but  containing  albumen. 
Since,  however,  many  normal  uriniferous  tubules  and  glomeruli  are  still  present, 
and  since  the  whole  process,  as  we  have  seen,  develops  only  very  slowly,  the  body 
gains  time  for  the  development  of  one  of  those  apt  compensatory  arrangements 
which  we  recognize  in  so  many  pathological  processes,  and  which  we  must  regard 
in  a  teleological  sense.  This  compensatory  process  consists  of  an  increase  in  the 
arterial  pressure,  coming  on  as  gradually  as  the  renal  contraction  itself,  and  con- 
stantly increasing,  and  of  a  hypertrophy  of  the  left  ventricle  dependent  upon  it. 
The  blood  therefore  courses  through  the  many  normal  glomeruli  of  the  contracting 
kidney  under  an  increased  pressure,  and  the  consequence  is  that  in  these  portions 
the  secretion  of  the  urine,  especially  of  the  water,  is  much  more  abundant.  It  is 
possible,  also,  that  the  incipient  disease  of  the  glomerular  walls  which  tends  to 
increase  their  permeability  contributes  to  the  polyuria.  At  any  rate,  it  is  a  fact 
that  in  cases  of  contracted  kidney  there  is  usually  an  abnormally  large  amount  of 
pale,  watery  urine  of  low  specific  gravity,  containing  merely  a  trace  of  albu- 
men (originating  from  the  diseased  portions  of  the  organ).  The  daily  amount 
of  urine  is  often  seventy  to  a  hundred  and  twenty  ounces  (2,000-3,500  cubic  cen- 
timetres) or  more;  the  urine  looks  light-yellow  and  clear,  contains  scarcely  any 
morphological  constituents,  has  a  specific  gravity  of  1010  to  1005  or  even  lower, 
and  gives,  on  heating,  only  a  slight  precipitate  of  albumen,  the  amount  excreted 
in  the  twenty-four  hours  being  about  half  a  drachm  to  a  drachm  (two  to  five 
grammes).    On  careful  microscopic  examination  of  the  urine,  we  usually  succeed 


CONTEACTED   KIDNEY  629 

in  finding  a  few  hyaline  casts,  whicli  only  exceptionally  may  be  more  abundant. 
The  urine  also  frequently  contains  some  white,  and  more  rarely  a  few  red  blood- 
corpuscles.  In  rare  but  definitely  attested  cases  it  may  happen  that  for  a  time, 
or  even  during  the  main  part  of  the  disease,  the  urine  contains  no  albumen  at  all, 
or  only  a  trace  of  it.  This  is  probably  explained  by  the  fact  that  the  diseased 
glomeruli  have  wholly  ceased  secreting,  and  that  therefore  the  urine  is  secreted 
only  by  the  healthy  portions  of  the  kidney.  As  to  the  character  of  the  urine  in 
arterio-sclerotic  contracted  kidney,  vide  supra. 

It  is  apparent  of  how  great  significance  this  abundant  secretion  of  water,  as  a 
result  of  the  abnormally  high  blood-pressure,  must  be  for  the  whole  morbid  pro- 
cess; for,  in  spite  of  the  renal  disease,  there  is  now  absolutely  no  retention  of 
water  in  the  body,  and  we  therefore  understand  why  there  is  often  no  oedema  in 
contracted  kidney,  even  after  a  course  of  years.  The  secretion  of  the  solid  con- 
stituents of  the  urine  is  not  quite  in  such  a  favorable  condition  as  the  secretion  of 
water.  It  is  self-evident  that  the  percentage  of  the  former  decreases  with  the 
increased  amount  of  urine,  but  the  whole  amount  of  urea,  uric  acid,  phosphoric 
acid,  etc.,  eliminated  is  also  at  times  somewhat  less  than  normal  in  relation  to  the 
food.  This  diminution,  however,  is  not  very  great,  as  long  as  the  work  of  the 
heart  is  sufficient,  and  at  certain  times,  especially  in  the  earlier  periods  of  the  dis- 
ease, a  normal  amount  may  be  secreted.  We  accordingly  see  that  the  symptoms 
dependent  upon  an  accumulation  of  the  urinary  constituents  in  the  blood  do  not 
appear  at  all  for  a  long  time.  Thus  it  happens  that  the  patient  may  still  feel  per- 
fectly well  up  to  a  time  when  the  objective  examination  of  the  urine  indicates 
marked  pathological  changes.  Many  patients,  of  course,  notice  the  polyuria,  but 
often  no  special  attention  is  paid  to  it,  and  it  is  attributed  to  drinking  a  good 
deal  of  fluid.  The  patient  gets  accustomed  to  it,  even  if,  as  often  happens,  he 
has  to  pass  his  urine  much  more  frequently  than  formerly,  and  even  during  the 
night. 

We  need  not  go  into  detail  here  in  regard  to  the  special  causes  of  cardiac 
hypertrophy  (compare  page  602).  It  was  with  regard  to  contracted  kidney  that 
Traube  advanced  his  mechanical  theory  of  cardiac  hypertrophy,  which,  however, 
rested  upon  the  considerations  previously  mentioned,  and  therefore  was  properly 
replaced  by  the  chemical  theory,  which  was  also  very  applicable  to  this  form  of 
renal  disease.  In  its  clinical  relations  it  is  an  important  fact  that  the  cardiac 
hypertrophy  causes  no  subjective  symptoms  at  all,  as  long  as  the  heart  can  suffice 
for  the  work  put  upon  it  without  strain,  a  condition  which  is  perfectly  analogous 
to  that  of  any  fully  compensated  valvular  disease.  We  can  usually  recognize  the 
condition  correctly  only  by  a  careful  physical  examination  of  the  heart  and  the 
vascular  apparatus,  although  in  contracted  kidney  the  percussion  and  palpation  of 
the  heart  are  often  rendered  difficult  by  a  co-existing  pulmonary  emphysema. 
We  can  often  perceive,  however,  the  displacement  and  the  increased  strength  of 
the  apex-beat,  the  extension  of  the  cardiac  dullness  to  the  left,  and  almost  invari- 
ably the  abnormal  tension  of  the  radial  pulse,  and  the  accentuation  of  the  aortic 
second  sound.  In  the  later  stages  of  the  disease  a  hypertrophy  of  the  right  ventri- 
cle is  often  added  to  that  of  the  left  (compare  page  603).  Complete,  or  almost 
complete,  absence  of  the  cardiac  hypertrophy  is  observed,  as  we  have  said,  only 
in  weak  and  cachectic  patients. 

As  long,  therefore,  as  the  high  arterial  pressure  kept  up  by  the  cardiac  hyper- 
trophy regulates  the  renal  secretion  in  the  way  above  described,  the  condition  of 
the  patient  as  a  rule  shows  no  special  abnormality.  At  most  it  happens  that  cer- 
tain cerebral  symptoms  now  appear,  especially  attacks  of  headache  and  occasional 
vertigo,  which,  unless  they  are  ursemic,  are  probably  to  be  referred  to  active  cere- 
bral bypersemia.  Frequent  nose-bleed  also  sometimes  results  from  the  abnor- 
mally high  blood-pressure. 


630  DISEASES  OF   THE   UEEN-AEY   OEGAI^S 

The  clinical  picture  is  completely  transformed,  however,  upon  the  appearance 
of  the  first  signs  of  incipient  cardiac  insufficiency — that  is,  the  moment  that  the 
hypertrophy  of  the  left  ventricle  ceases  to  he  sufficient  to  overcome  the  obstacles 
to  the  secretion  of  urine  occasioned  by  the  deficiency  in  the  renal  parenchyma. 
The  disturbance  is  evident  either  when  the  left  ventricle  itself  grows  weak,  or 
when  the  gradual  advance  of  the  diseased  process  has  reached  such  a  point  that 
even  the  most  vigorous  efforts  of  the  heart  are  no  longer  sufficient  to  bring  aboijt 
compensation.  In  the  latter  ease  the  symptoms  which  appear  are  to  be  regarded 
as  ursemic,  in  the  broadest  sense  of  that  word.  The  pulse  is  frequent,  but  it  still 
remains  unusually  full  and  hard.  On  the  other  hand,  in  case  there  is  a  diminu- 
tion in  the  cardiac  energy  the  pulse  becomes  more  compressible,  smaller,  more 
frequent,  and  sometimes,  toward  the  termination  of  the  disease,  irregular.  The 
heart-sounds  remain  pure,  but  the  first  sound  often  becomes  indistinct.  When 
there  is  a  decided  disturbance  of  compensation  we  hear  a  well-marked  hruit  de 
galop.  In  all  these  cases  the  symptoms  result  from  the  disturbance  to  the  circula- 
tion, and  from  the  consequent  retention  of  urinary  constituents. 

Ordinarily,  the  subjective  symptoms  of  contracted  kidney  begin  very  gradually, 
then  disappear  for  a  time,  then  appear  again,  and  grow  worse  slowly  but  stead- 
ily. Apart  from  the  feeling  of  general  languor  and  weariness,  it  is  usually 
the  dyspnoea  which  first  calls  attention  to  the  disease.  The  patient  grows  short 
of  breath,  is  much  disturbed  by  even  slight  physical  exertion,  and  is  perhaps 
subject  to  attacks  of  palpitation.  Xot  infrequently  the  dyspnoea  occurs,  in  the 
later  stages  of  the  disease,  in  distinct  paroxysms  which  suggest  asthma.  This 
nephritic  asthma  has  long  been  recognized.  It  does  not  have  the  same  origin 
in  every  case ;  often  it  is  undoubtedly  the  result  of  the  attacks  of  cardiac  weak- 
ness, and  is  then  a  merely  cardiac  asthma  and  corresponds  in  its  individual 
symptoms  to  angina  pectoris  (see  page  355).  In  other  cases  the  asthma  seems  to 
be  connected  with  the  retention  of  the  products  of  metabolism  (ursemic  asthma, 
vide  supra).  The  clinical  picture  is  most  peculiar  in  those  cases  in  which  the 
dyspnoea  is  associated  with  the  signs  of  acute  pulmonary  oedema,  and  is  attended 
with  the  expectoration  of  a  large  amount  of  foamy,  serous  sputum,  which  is  often 
tinged  with  blood.  These  conditions,  which  may  pass  off  and  reappear  at  stated 
intervals,  are  mainly  those  to  which  the  name  of  humid  asthma  was  formerly 
given.  It  may  seem  questionable  whether  we  should  regard  the  pulmonary  oedema 
in  such  cases  as  a  purely  congestive  transudation  due  to  cardiac  weakness,  or 
as  an  oedema  occasioned  by  nephritis  and  in  a  certain  degree  inflammatory.  In 
the  last  stage  of  the  disease  there  is  often  constant  dyspnoea,  and  this  may  be  the 
chief  complaint  of  the  patient.  It  is  in  such  cases  often  referable  to  various 
causes  acting  simultaneously — for  instance,  pulmonary  congestion,  diffuse  bron- 
chitis, pneumonia  (vide  infra),  and  liydrothorax. 

Another  result  of  beginning  cardiac  failure  in  the  later  course  of  the  disease 
may  be  oedema  of  various  portions  of  the  body.  This  is  certainly  in  many  cases 
to  be  regarded  as  a  purely  congestive  oedema,  particularly  when  associated  with 
contracted  kidney;  but,  on  the  other  h?.nd,  we  can  not  always  exclude  conditions 
which  occasion  nephritic  oedema  (vide  supra).  It  has,  indeed,  been  repeatedly 
observed  that  dropsy  may  be  entirely  absent  in  contracted  kidney;  but  this  is  the 
case  only  when  death  ensues  from  some  intercurrent  attack  before  the  pronounced 
cardiac  insufficiency.  Otherwise  oedema  is  by  no  means  rare  in  contracted  kidney. 
It  usually  appears  first  in  the  ankles,  the  eyelids,  or  the  prepuce,  disappears  again 
when  the  pptient  remains  pt  rest,  and,  after  a  longer  or  a  shorter  pause,  comes 
on  anew,  until  finally,  in  the  last  period  of  the  disease,  a  high  degree  of  gen- 
eral dropsy  may  develop. 

Among  the  disturbfinces  of  the  internal  organs  we  must  mention  first  the 
cerebral  symptoms.    TVliile  at  first,  as  we  hr.ve  said,  these  have  more  of  an  active 


CONTEACTED   KIDNEY  631 

hypersemic  character,  the  frequent  and  very  violent  headaches  that  come  on 
later  in  part  are  of  a  ursemic  nature  and  in  part  depend  upon  the  passive  hyper- 
semia,  or  the  arterial  anaemia  of  the  brain.  The  pain  sometimes  shoots  into  the 
back  of  the  neck,  and  sometimes  is  localized  chiefly  in  one  half  of  the  head ;  it  is 
often  associated  with  symptoms  of  vertigo,  with  a  gloomy  or  morose  mood, 
with  troubled  sleep,  etc.  The  stasis  is  usually  also  apparent  in  the  abdominal 
organs.  Chronic  dyspeptic  disturbances  appear,  the  appetite  fails,  the  bowels 
become  irregular,  and  we  can  even  make  out  a  moderate  enlargement  of  the  liver. 
The  influence  which  the  altered  activity  of  the  heart  exerts  upon  the  function  of 
the  kidneys  themselves  is,  however,  particularly  important.  From  what  has  been 
previously  said  of  the  dependence  of  the  secretion  of  urine  upon  the  arterial  pres- 
sure, it  follows  directly  that  any  compensatory  activity  of  the  still  normal  renal 
territory  must  at  once  experience  a  reduction,  as  soon  as  the  blood-pressure  falls. 
Corresponding  to  this  we  see,  in  fact,  that  the  secretion  of  urine  also  usually 
suffers  a  decline  at  the  same  time  with  the  other  symptoms  of  stasis.  The 
amount  of  urine  is  less  abundant:  it  drops  to  forty  or  fifty  ounces  (1,500-1,000 
cubic  centimetres),  and  even  lower;  the  specific  gravity  rises,  rarely  to  a  high 
figure,  but  still  up  to  1010  or  1012,  or  over.  The  urine  often  retains  its  light 
color  for  quite  a  long  time,  but  it  may  finally  more  and  more  resemble  the 
genuine  urine  of  stasis.  The  point,  however,  which  is  especially  to  be  consid- 
ered, is  the  simultaneous  and  increasing  retention  of  the  solid  constituents  of 
the  urine  in  the  blood,  and  the  consequent  possibility  of  the  onset  of  ursemic 
symptoms. 

It  must  be  stated  that,  in  contracted  kidney,  the  immediate  exciting  causes  of 
uraemia  are  not  always  clear.  Thus,  it  is  a  well-known  and  very  important  fact, 
clinically,  that  very  severe  and  often  fatal  uraemic  convulsions  may  sometimes 
attack  the  patient  quite  suddenly,  apparently  when  in  the  best  of  health.  Cases 
have  been  repeatedly  seen,  by  other  observers  and  by  ourselves,  where  the  daily 
amount  of  urine  has  shown  no  discoverable  diminution  in  the  days  preceding  the 
uraemia.  Probably  the  explanation  of  this  is  that  for  a  long  time  very  minute 
amounts  of  toxic  material  are  daily  retained  in  the  blood,  and  that  these  of  them- 
selves occasion  no  noticeable  disturbance  until  suddenly  the  severe  symptoms  of 
uraemia  develop  as  a  cumulative  result  of  long-continued,  though  slight,  injurious 
influences.  These  cases  of  suddenly  developing  uraemia  always  remind  us  of  the 
similar  phenomena  in  chronic  poisoning  from  lead  or  mercury.  In  these  cases, 
also,  after  a  long-continued  absorption  of  trifling  amounts  of  poison,  the  symp- 
toms of  intoxication  may  finally  appear  abruptly.  In  other  cases  of  uraemia 
associated  with  contracted  kidney,  the  condition  of  the  heart  is  of  great  impor- 
tance. The  uraemic  symptoms  develop  in  different  ways,  according  to  the  slowness 
or  rapidity  with  which  the  cardiac  insufiiciency  causes  diminution  in  the  urinary 
secretion.  If  the  amount  of  urine  is  slowly  diminished,  we  observe  the  symptoms 
of  chronic  uraemia  (page  596),  consisting  of  headache,  vomiting,  diarrhoea,  severe 
pruritus  of  the  skin,  etc.,  but  these  symptoms  are,  of  course,  often  combined  with 
the  immediate  symptoms  of  stasis,  and  are  not  always  to  be  easily  and  distinctly 
separated  from  them.  Such  a  condition  of  chronic  uraemia,  in  patients  with  con- 
tracted kidney,  often  presents  a  very  mournful  picture,  since  the  unrestrainable 
and  constantly  recurring  vomiting,  the  headache,  and  the  general  mental  anxiety 
may  last  for  weeks.  The  severe  acute  uraemia  either  is  preceded  by  chronic 
uraemic  symptoms,  or  comes  on  at  once  in  the  severest  form,  with  general  and 
often-recurring  convulsions,  and  coma.  The  uraemia  may  pass  off  again,  even  in 
contracted  kidney,  but  quite  frequently  it  is  the  immediate  cause  of  death  (vide 
infra). 

Beside  the  symptoms  so  far  described,  we  must  now  mention  a  set  of  anatom- 
ical complications  which  may  appear  in  the  course  of  contraction  of  the  kidney. 


632  DISEASES    OF   THE   UEINAEY   OEGANS 

Erom  its  diagnostic  and  clinical  importance  the  albuminuric  retinitis,  already 
known  to  us  from  the  preceding-  chapter,  takes  the  first  place.  It  may  come  on 
at  any  time  in  the  course  of  the  disease;  but  it  often  develops  so  early  that  the 
patient,  up  to  this  time,  knows  nothing  at  all  of  his  other  disease.  He  merely 
consults  an  oculist,  who  often  first  recognizes,  from  the  ophthalmoscopic  image 
(see  page  622),  the  special  seat  of  the  primary  disease.  Even  in  the  cases  where 
no  subjective  visual  disturbance  is  present,  the  retinal  examination  sometimes 
discloses  retinitis.  In  general,  the  contracted  kidney  is  that  form  of  renal  dis- 
ease in  which  retinal  changes  are  decidedly  most  frequent. 

Another  rarer  but  clinically  important  complication  consists  of  the  hsemor- 
rhages  in  internal  organs,  whose  cause  is  to  be  found  either  in  the  increased  arte- 
rial pressure,  or  in  an  abnormal  weakness  of  the  walls  of  the  vessels — arterio- 
sclerosis in  older  persons,  defective  nutrition  of  the  vascular  walls  in  young  and 
ansemic  patients.  Hemorrhages  into  the  brain  are  comparatively  the  most  fre- 
quent. They  cause  both  mild  and  severe  apoplectic  attacks,  which  pass  off  com- 
pletely or  leave  a  hemiplegia  behind,  and  sometimes  they  are  the  direct  cause  of 
death.  Beside  the  haemorrhages  into  the  brain  itself,  there  may  also  be  hsemor- 
rhages  on  the  inner  surface  of  the  dura  mater — hsematoma.  ISTose-bleed  is  also  of 
significance ;  in  many  patients  it  is  frequent  and  very  stubborn ;  we  have  ourselves 
seen  two  cases  where  the  fatal  termination  was  caused  directly  by  an  unrestrain- 
able  nose-bleed.  Haemorrhages  into  the  other  organs  are  more  rare,  but  they 
have  been  observed  in  the  skin,  the  stomach,  the  intestines,  and  the  lungs.  -In 
a  few  cases,  indeed,  a  sort  of  hsemorrhagic  diathesis  seems  to  develop.  We  must 
remind  the  reader  again,  in  this  connection,  of  the  general  truth  that  in  renal 
disease  all  the  internal  organs  display  a  somewhat  increased  tendency  to  sec- 
ondary inflammation;  thus  the  mucous  membranes  often  present  an  accom- 
panying catarrhal  inflammation,  such  as  chronic  bronchitis,  gastritis,  gastric 
catarrh,  and  intestinal  catarrh.  These  catarrhal  troubles  are  in  part  to  be  re- 
garded as  due  to  congestion,  but  in  part  they  certainly  result  from  the  retention 
of  the  products  of  metabolism.  In  serous  membranes  we  often  observe  pleurisy, 
pericarditis,  etc.  The  surface  of  the  body  sometimes  displays  a  tendency  to 
obstinate  eczema.  Of  the  inflammations  of  internal  organs,  pneumonia  is  the 
most  frequent  and  important.  Some  cases  are  croupous  or  lobar,  and  some  are 
of  that  diffuse  lobular  variety  which  is  peculiar  to  all  sorts  of  nephritis.  We  have 
already  mentioned  that  the  kidney  itself  may  suffer  from  inflanmaatory  exacerba- 
tions, in  addition  to  the  chronic  disease. 

Quite  great  variations  appear  in  regard  to  the  general  nutrition.  In  most 
cases  where  the  disease  develops  quite  gradually  in  persons  in  middle  or  advanced 
life,  the  general  nutrition  for  a  long  time  shows  no  striking  anomaly.  The  patient 
is  often  very  well  nourished,  and  even  corpulent,  at  the  period  when  the  first 
cardiac  symptoms  begin.  To  the  more  practiced  and  attentive  eye,  of  course,  he 
shows  a  certain  appearance  of  suffering,  which  later  becomes  more  pronounced. 
He  becomes  emaciated,  and  has  a  sallow  and  often  cyanotic  complexion.  Marked 
anaemia  usually  develops  only  in  younger  individuals,  who  then  show  the  pallor 
characteristic  of  so  many  patients  with  renal  disease. 

We  desire  to  append  a  few  remarks  with  regard  to  arterio-sclerotic  contracted 
kidney.  This  may  pursue  precisely  the  characteristic  course  of  the  ordinary 
disease,  but  in  many  cases  its  symptoms  are  very  obscure.  If  we  examine  care- 
fully, from  day  to  day,  the  urine  of  old  persons  who  present  other  signs  of  gen- 
eral arterio-sclerosis,  we  shall  be  likely  to  find  at  many  times  a  small  trace  of 
albumen,  and  at  other  times  none  at  all.  In  such  cases  we  may  be  almost  cer- 
tain that  there  is  an  arterio-sclerotic  contracted  kidney.  Still,  the  renal  symp- 
toms are  usually  of  minor  importance  in  the  clinical  picture  of  senile  marasmus, 
senile  emphysema,  senile  dementia,  or  the  other  changes  of  old  age. 


CONTEACTED   KIDNEY  633 

General  Course,  Duration,  and  Termination. — The  most  important  peculiar- 
ities in  the  course  of  renal  contraction  have  already  been  spoken  of  above.  We 
have  stated  that  the  disease  may  be  latent  for  a  long-  time ;  that  the  severest  symp- 
toms— such  as  uraemia  or  apoplexy — sometimes  come  on  suddenly  and  unexpected- 
ly; that  in  other  cases  the  disturbances  of  compensation  in  the  heart,  dyspnoea, 
palpitation,  or  slight  cedema,  are  the  first  symptoms;  that,  under  some  circum- 
stances, certain  complicating  conditions,  such  as  retinitis,  or  frequent  nose-bleed, 
first  direct  suspicion  to  a  renal  disease,  and  suggest  an  examination  of  the  urine ; 
while,  finally,  in  a  last  class  of  cases,  only  general  disturbances,  loss  of  appetite, 
pallor,  general  physical  weakness,  and  similar  symptoms  induce  the  patient  to 
consult  a  physician.  It  is  usually  hard  to  decide  how  long  the  disease  has  lasted 
before  a  diagnosis  is  made.  "We  must  especially  inquire  into  the  existence  of 
polyuria,  which  patients  may  not  notice,  however,  even  if  it  exists. 

The  further  course  may  vary  according  to  the  onset  of  complications,  the 
external  conditions  under  which  the  patient  lives,  etc.  In  general,  as  we  must 
repeatedly  emphasize,  much  depends  upon  the  heart's  capacity  for  work  and  its 
staying  qualities.  If  death  does  not  ensue  sooner  from  some  intercurrent  dis- 
ease, the  last  stage  of  the  disease  almost  always  presents  itself  under  the  picture 
of  cardiac  insufficiency  with  predominant  symptoms  of  dyspnoea  and  general 
dropsy. 

As  has  been  said,  we  usually  can  not  determine  with  any  accuracy  the  dura- 
tion of  the  disease.  It  may,  at  any  rate,  last  many  years,  probably  even  ten  years 
or  more,  although  there  may  be  many  variations  in  its  course.  It  is  not  impos- 
sible that,  during  the  earlier  period  of  the  disease,  there  may  be  a  cessation  in 
the  process  of  renal  atrophy,  but  it  is  hard  to  decide  with  cert^iinty.  At  all  events, 
the  disease  must  generally  be  termed  absolutely  incurable,  although  life  may  not 
only  be  preserved  for  a  long  time,  but  the  patient  may  even  exist  without  much 
discomfort.  "We  need  not  refer  especially  here  to  the  different  intercurrent  at- 
tacks, the  possibility  of  which  must  always  be  kept  in  mind  in  regard  to  prognosis. 

Diagnosis. — The  diagnosis  of  contracted  kidney  can  be  made  with  certainty 
only  by  examining  the  urine.  We  must,  therefore,  dwell  again  on  the  necessity 
of  making  this  examination  in  all  suspicious  cases,  because  only  in  this  way  can 
we  avoid  overlooking  the  condition.  The  suspicion  of  a  developing-  renal  contrac- 
tion should  demand  an  examination  of  the  urine,  especially  in  all  cases  where  the 
patient  complains  of  frequent  headache,  of  congestive  conditions,  of  palpitation 
and  dyspnoea,  asthmatic  attacks,  disturbances  of  vision,  general  dullness,  and  dvs- 
peptic  symptoms,  without  finding  any  other  reason  for  these  symptoms.  The  poly- 
uria, the  clear  urine  of  low  specific  gravity,  containing-  a  slight  amount  of  albu- 
men, in  connection  with  the  signs  in  the  circulatory  apparatus,  the  tense  pulse, 
and  the  hypertrophy  of  the  left  ventricle,  permit  us  to  recognize  the  disease  cor- 
rectly in  most  cases.  If  retinal  changes  are  present,  they  may  sometimes  be  of 
much  aid  in  confirming  the  diagnosis.  The  agtiological  conditions — lead,  gout, 
alcoholism,  etc. — of  course  also  merit  attention. 

The  diagnosis  presents  great  difficulty  in  the  quite  rare  cases  where  albumin- 
uria is  absent.  In  these  cases  we  are  sometimes  able  to  reach  the  correct  interpre- 
tation of  the  morbid  condition  only  by  repeated  examinations  of  the  urine.  Other- 
wise we  can  scarcely  avoid  mistaking  it  for  chronic  affections  of  the  heart,  such 
as  myocarditis  or  idiopathic  hypertrophy. 

The  diagnosis  is  also  very  difficult  if  the  patient  does  not  come  under  observa- 
tion until  the  stage  of  fully  developed  disturbance  of  compensation.  The  chnrac- 
teristic  features  of  the  urine  of  contracted  kidney  are  then  absent,  the  urine  is 
scantier,  darker,  richer  in  albumen,  and  it  is  often  scarcely  possible  to  decide 
whether  we  have  a»primary  renal  affection  with  secondary  cardiac  hypertrophy 
or  a  primary  heart  disease  with  a  secondary  congested  kidney.    If  general  arterio- 


634  DISEASES    OF   THE   UEINAEY   OEGANS 

sclerosis  or  marked  pulmonary  emphysema  is  present  at  the  same  time,  the  judg- 
ment as  to  the  condition  is  still  more  difficult.  In  such  cases  a  correct  diagnosis 
is  possible  only  by  very  carefully  balancing  all  the  different  symptoms,  and  con- 
sidering the  whole  course  of  the  disease. 

Finally,  the  diagnosis  of  contracted  kidney  is  very  difficult  in  cases  where  the 
first  examination  of  the  patient  is  made  during  a  sudden  attack  of  uraemia  or 
after  an  apoplectic  seizure.  Here  the  albuminuria  is  the  symptom  which  points 
most  to  the  existence  of  a  renal  disease,  although,  in  spite  of  this  symptom,  the 
judgment  as  to  the  condition,  and  its  differentiation  from  other  acute  cerebral 
affections,  often  presents  great  difficulties. 

We  must  devote  a  few  words  to  those  not  very  infrequent  cases  in  which  a 
small  amount  of  albumen  is  found,  often  quite  by  chance,  in  the  urine  of  youthful 
individuals  who  are  apparently  in  perfect  health;  thereupon  the  question  is  pro- 
pounded, which  is  often  of  extreme  practical  importance,  whether  we  are  dealing 
with  a  so-called  physiological  or  intermittent  albuminuria  (vide  supra,  page  589), 
or  with  an  actual  renal  disease — viz.,  an  unsuspected  contracted  kidney.  The 
diagnosis  is  never  easy.  In  the  first  place,  it  is  necessary  to  make  careful  obser- 
vations for  a  considerable  period,  at  the  same  time  varying  the  conditions  as  to 
nourishment  (nitrogenous  diet,  milk  diet,  use  of  beer),  and  activity  (complete 
physical  rest,  persistent  exercise)  ;  then  we  must  carefully  investigate  all  the  pos- 
sible setiological  circumstances,  such  as  previous  disease  and  mode  of  life;  and 
finally,  take  into  consideration  the  associated  phenomena — for  instance,  of  the 
circulatory  apparatus.  From  a  practical  point  of  view  it  is  advisable  to  be  most 
cautious  in  all  these  cases,  and,  at  any  rate,  to  give  such  advice  as  to  regimen 
with  the  aim  of  preventing  damage  to  the  kidneys,  as  if  there  were  an  actual 
renal  disease. 

Treatment. — As  soon  as  the  diagnosis  of  renal  contraction  is  established,  the 
whole  hygienic  condition  of  the  patient  must  be  regulated  so  as  to  prevent  the 
advance  of  the  affection  in  every  possible  way.  In  this  respect  two  indications 
are  to  be  fulfilled,  to  guard  against  any  irritation  which  may  have  an  injurious 
action  on  the  kidneys,  and  to  relieve  the  work  of  the  heart  as  much  as  possible,  in 
order  to  keep  off  cardiac  insufficiency  as  long  as  we  can.  The  diet  must  be  care- 
fully regulated,  and  must  be  of  scant  measure  or  abundant  and  strengthening, 
according  to  the  patient's  physical  constitution.  In  these  cases,  too,  milk  is  a 
food  of  great  value.  The  use  of  meat  is,  in  general,  to  be  limited,  while  easily 
digestible  dishes  made  from  cereals  and  eggs,  and  vegetables  and  fruits,  are  to 
be  recommended.  Alcoholic  beverages  should  be  allowed  in  only  limited  amounts, 
their  place  being  supplied  by  mineral  waters  (Fachinger,  Wildunger,  Wernarzer), 
and  water  with  lemon-juice  or  the  juice  of  other  fruits.  Great  care  of  the  skin 
is  an  important  matter.  We  should  recommend  the  regular  employment  of 
warm  baths  or  salt  baths,  and  daily  sponging  of  the  whole  body  with  brandy  or 
warm  vinegar.  All  physical  over-exertion  is  to  be  avoided,  although  moder- 
ate methodical  exercise  is  to  be  recommended  for  corpulent  patients.  We  should 
always  provide  for  regular  evacuation  of  the  bowels  by  appropi'iate  remedies, 
dietetic  prescriptions,  fruits,  bitter  mineral  waters,  etc.  The  general  condition 
is  often  materially  improved  by  proper  air  and  recreation,  and  in  this  way  resort 
to  a  bath  may  be  of  service,  chosen  according  to  the  individual  conditions,  such 
as  Briickenau,  Marienbad,  Carlsbad,  Kissingen,  ISTauheim,  Ems,  or  Baden-Baden. 
In  appropriate  cases,  a  winter  residence  in  the  south  is  advisable. 

If  disturbances  of  compensation  appear,  we  must  be  still  more  strict  in  our 
dietary,  and  must  enjoin  the  utmost  physical  rest,  at  the  same  time  employing 
other  treatment  according  to  the  symptoms  which  may  be  present.  Above  all,  we 
must  endeavor  to  impart  new  vigor  to  the  heart  by  means  ©f  digitalis,  though 
unfortunately  such  efforts  often  prove  unavailing.    The  minutiie  of  treatment  in 


AMYLOID   KIDNEY  635 

this  connection  are  almost  precisely  the  same  as  in  chronic  heart  disease  {q.  v.'), 
and  in  other  renal  diseases.  The  treatment  of  the  dyspnoea  and  chronic  ura3mia, 
which  develop  in  the  last  stages  of  the  disease,  is  apt  to  be  most  unsatisfactory; 
but  we  can,  sometimes  at  least,  remove  the  symptoms  by  various  external  appli- 
cations upon  the  chest  and  the  head  (ice-bags  or  hot  compresses),  by  various 
drugs  to  combat  the  nervous  symptoms,  bromide  of  potassium,  antipyrine,  nitro- 
glycerine, and  by  the  combination  of  cardiac  stimulants,  such  as  digitalis  and 
strophanthus,  with  diuretics,  such  as  caffeine  and  diuretine.  In  the  worst 
cases  narcotics  are  indispensable,  particularly  subcutaneous  injections  of  mor- 
phine. As  yet  we  are  unable  to  exert  a  direct  beneficial  influence  by  drugs  upon 
the  interstitial  process  in  the  kidneys.  The  only  ones  recommended  for  this  pur- 
pose and  worth  a  trial  are  the  preparations  of  iodine — viz.,  iodide  of  potassium,  or 
iodide  of  sodium,  in  daily  amounts  of  three  to  eight  grains  (gramme  0.2-0.5), 
and,  in  anaemic  patients,  iodide  of  iron.  We  do  not  need  to  go  minutely  into  the 
treatment  of  the  numerous  complications  which  occur. 

The  prophylaxis  of  renal  contraction  is  evident;  we  should  avoid  so  far  as 
we  can  the  known  setiological  conditions. 


CHAPTEE   V 
AMYLOID    KIDNEY 

.33tiology. — The  amyloid  kidney  is  invariably  associated  with  the  more  or 
less  extensive  amyloid  degeneration  of  other  organs  in  the  body.  In  its  clinical 
relations,  however,  it  claims  the  most  interest  of  all  amyloid  diseases,  since  it 
has  by  far  the  greatest  significance  for  the  whole  clinical  picture  of  amyloid 
degeneration. 

As  is  well  known,  we  understand  by  amyloid  degeneration  a  peculiar  change 
which,  under  certain  pathological  conditions,  is  observed  in  the  connective  tissue, 
and  especially  in  the  smaller  vessels.  The  walls  of  the  vessels  are  thickened,  they 
have  a  lustrous,  homogeneous  appearance,  and  they  show;  peculiar  reactions  on 
treatment  with  certain  coloring  agents.  These  reactions  are  due  to  the  presence 
of  an  albuminoid  substance — amyloid — which  either  is  deposited  in  the  tissue 
from  the  blood,  or,  as  is  much  more  probable,  is  developed  in  that  spot  from 
the  albuminoid  substances  there  present.  In  marked  amyloid  degeneration  the 
diseased  organs  often  show  macroscopically  an  altered,  "  bacon-like  "  appearance, 
and  assume  a  characteristic  red-brown  color  on  treating  the  affected  parts  with 
Lugol's  solution  of  iodine,  changingto  violet  on  the  addition  of  sulphuric  acid. 
The  microscopic  examination  alone  affords  more  accurate  conclusions  as  to  the 
presence  and  distribution  of  the  degeneration.  For  this  purpose  we  usually  stain 
the  tissues  with  methyl-violet  or  gentian-violet.  The  amyloid  portions  thus 
take  on  a  very  characteristic  and  clearly  defined  red  color.  In  this  way  we  can 
discover  that  the  amyloid  degeneration  begins  everywhere  in  the  walls  of  the 
small  vessels,  that  the  interparenchymatous  connective  tissue  may  also  be  affected 
later,  but  that  the  parenchymatous  cells  proper,  liver  cells,  renal  epithelium,  etc., 
almost  always  remain  perfectly  free.  The  latter  often  show  atrophic  and  fatty 
degenerative  changes  {vide  infra),  but  little  if  any  amyloid  degeneration. 

Nothing  is  known  as  to  the  special  causes  which  efl^ect  this  peculiar  metamor- 
phosis of  the  albumen  of  the  connective  substance  into  amyloid.  We  know  only 
that  there  are  a  number  of  primary  diseases  in  which  experience  has  shown  that 
amyloid  degeneration  quite  frequently  develops  as  a  secondary  condition  in  the 


626  DISEASES    OF    THE   UEI^AET   OEGANS 

different  organs.  These  conditions  have,  for  the  most  part,  the  common  charac- 
teristic of  being  associated  with  general  cachexia  and  debility,  and  of  being  con- 
nected with  some  localized  chronic  morbid  process  in  some  part  of  the  body,  from 
which  abnormal  chemical  matters  may  be  constantly  carried  into  the  blood.  We 
suppose  that  the  normal  albuminous  material  is  transformed  into  amyloid  by 
means  of  such  influences.  With  regard  to  the  relations  which  may  exist  between 
the  so-called  hyaline  degeneration  of  Recklinghausen,  and  amyloid  disease,  the 
investigations  are  not  yet  complete. 

The  conditions  in  which  amyloid  degeneration  in  general,  and  consequently 
amyloid  disease  of  the  kidney  also,  are  chiefly  observed,  are  the  following,  ar- 
ranged in  about  the  order  of  their  frequency: 

1.  Chronic  pulmonary  tuberculosis,  particularly  the  ordinary  ulcerative  phthi- 
sis. Tubercular  ulcers  of  the  intestines,  with  or  without  co-existing  marked  pul- 
monary tuberculosis,  may  also  lead  to  amyloid  disease. 

2.  Long-continued  chronic  suppuration  in  the  bones  or  soft  parts,  especially 
chronic  fungous  processes  with  fistulse  into  the  bones  or  joints,  empyema  with 
fistulse,  vertebral  caries,  etc. 

3.  Constitutional  syphilis,  chiefly  the  cases  with  ulcerative  and  usually  ter- 
tiary processes  in  the  bones  and  mucous  membranes. 

4.  Other  ulcerative  processes,  or  processes  associated  with  chronic  suppura- 
tion: saccular  bronchiectases,  chronic  intestinal  ulcers  (for  example,  of  dysen- 
teric origin),  purulent  pyelo-cystitis,  vesico-vaginal  fistulas,  ulcerated  new 
growths,  such  as  cancer,  etc. 

5.  In  rare  cases  amyloid  has  also  been  observed  in  other  chronic  diseases,  as  in 
malaria,  gout,  and  other  chronic  articular  affections.  In  the  medical  clinique 
at  Leipsic  we  once  saw  a  case  of  marked  amyloid  kidney  in  a  girl  of  twenty-one 
with  aortic  insufficiency. 

6.  Finally,  in  a  small  class  of  cases,  of  which  we  have  ourselves  seen  some 
examples,  so  discoverable  cause  at  all  may  be  found  at  the  autopsy  for  quite 
extensive  amyloid  degeneration.  In  such  cases,  therefore,  there  seems  to  be 
a  primary  intoxication  with  resultant  amyloid  disease. 

Pathological  Anatomy. — With  regard  to  the  anatomical  lesions  of  amyloid 
disease  in  other  organs,  we  shall  refer  to  handbooks  on  pathological  anatomy.  As 
to  amyloid  liver,  see  page  580.  Here  we  shall  discuss  merely  the  pathological 
anatomy  of  amyloid  kidney. 

In  very  slight  and  limited  amyloid  degeneration  of  the  kidneys,  the  latter 
present  a  perfectly  normal  appearance  to  the  naked  eye.  Careful  microscopic 
examination  alone  shows  amyloid  degeneration  of  the  walls  of  different  vessels  in 
the  cortex,  and  especially  in  the  medullary  substance. 

The  commonest  and  most  characteristic  form  of  amyloid  kidney  is  the  so-called 
large  white  amyloid  kidney  (waxy  kidney,  lardaceous  kidney).  The  kidney  is 
usually  enlarged,  and  the  surface  is  smooth  and  of  a  grayish-white  or  yellowish 
color,  and  usually  somewhat  mottled.  On  section,  the  cortex  is  wide  and  also  of 
a  yellowish-white  color,  and  the  glomeruli  may  often  be  recognized  with  the  naked 
eye  as  dull,  lustrous,  translucent  points.  Haemorrhages  are  scarcely  ever  seen. 
The  medullary  substance  may  be  also  pale,  or  darker.  In  many  cases  the  cortex 
may  itself  have  a  darker  reddish  or  mottled  appearance,  which  is  due  merely  to 
the  greater  amount  of  blood  in  the  organ.  The  pale-yellow  color  is  due  either  to 
the  ansemia  or  to  the  fatty  degeneration,  while  the  amyloid  spots  show  a  more 
translucent  character  with  a  bacon-like  luster. 

If  we  examine  the  kidney  microscopically,  we  find  first  the  amyloid  degenera- 
tion, which,  in  varying  extent  and  combination,  affects  most  frequently  the  glo- 
meruli and  also  the  capillaries  of  the  cortex,  the  vasa  recta,  and  sometimes  the 
membrana3  proprise  of  the  uriniferous  tubules.     In  pure  amyloid  kidney  the  rest 


AMYLOID   KIDNEY  637 

of  the  renal  tissue  is  normal,  but  in  many  cases  we  find  changes  in  the  epithe- 
lium— fatty  degeneration,  desquamation  and  disintegration — and  also  not  infre- 
quently interstitial  cellular  infiltration.  We  see,  therefore,  that  amyloid  degen- 
eration of  the  kidney  is  not  infrequently  associated  with  degenerative  changes  of 
an  inflammatory  nature.  Thus  we  observe,  not  infrequently,  the  combination  of 
chronic  diffuse  nephritis  (large  white  kidney)  with  amyloid. 

If  the  process  has  lasted  for  a  long  time,  it  leads,  as  in  ordinary  nephritis,  to  a 
complete  atrophy  of  tissue  in  some  parts,  with  a  corresponding  increase  of  con- 
nective tissue.  Then  the  renal  tissue  sinks  in  at  the  affected  spots,  and  there  is  a 
decided  unevenness  to  the  surface  of  the  kidney.  There  is  even  a  completely 
developed  red  or  white  contracted  kidney,  in  which  we  find  abundant  amyloid,  and 
which  is,  therefore,  termed  amyloid  contracted  kidney.  In  this  form  the  paren- 
chymatous and  interstitial  changes  correspond  precisely  to  those  in  ordinary  con- 
tracted kidney,  only  the  amyloid  degeneration  is  added  to  them. 

At  present  differences  of  opinion  prevail  as  to  the  precise  connection  between 
amyloid  and  the  inflammatory  degenerative  processes  in  the  kidney.  In  our  opin- 
ion there  is,  in  most  cases,  an  actual  combination  of  both  conditions,  they  being 
co-effects  of  simultaneously  acting  causes.  We  have  seen  that  in  tuberculosis 
chronic  suppuration  and  genuine  nephritis  develop,  as  well  as  amyloid  disease,  so 
it  can  not  be  surprising  that  sometimes  with  these  diseases  both  sequelae,  nephritis 
and  amyloid,  should  develop  side  by  side,  and  that  we  should,  consequently,  find 
in  the  kidney  not  only  the  changes  associated  with  an  inflammatory,  large,  white 
kidney,  a  secondary  contraction,  or  a  genuine  contracted  kidney,  but  also  a  more 
or  less  extensive  amyloid  degeneration.  On  the  other  hand,  it,  of  course,  can  not 
be  questioned  that  the  disturbance  of  circulation,  which  must  arise  in  conse- 
quence of  a  marked  amyloid  of  the  vessels,  is  of  influence  on  the  nutrition  of  the 
renal  tissue,  and  that,  therefore,  many  changes  in  it,  especially  fatty  degenera- 
tion of  the  epithelium,  are,  under  some  circumstances,  the  direct  result  of  the 
amyloid  disease. 

Clinical  History. — If  we  consider  the  great  diversity  which  the  distribution 
of  the  amyloid  in  the  kidneys  shows,  and  its  manifold  combinations  with  inflam- 
matory processes,  it  is  clear  from  the  outset  that  we  can  not  set  up  a  uniform 
picture  of  the  symptoms  of  amyloid  disease  in  general.  To  this  we  must  add  that 
the  symptoms  of  amyloid  disease,  which  is  almost  always  a  secondary  condition, 
are  also  modified  in  various  ways  by  the  primary  disease. 

We  must  first  state  that  many  cases,  where  the  amyloid  in  the  kidneys  is  of 
comparatively  slight  extent,  can  not  be  recognized  by  any  clinical  symptom.  The 
albuminuria  in  particular  may  be  entirely  absent,  as  has  been  repeatedly  proved 
(Rosenstein,  Litten,  and  others).  That  in  such  cases  the  vasa  recta  and  not  the 
glomerui  are  chiefly  affected  by  the  amyloid  degeneration  has  been  affirmed  but 
not  proved. 

Except  in  these  instances,  however,  the  urine  secreted  from  the  amyloid  kid- 
neys shows  marked  changes,  which,  of  course,  present  considerable  variations  ac- 
cording to  the  form  of  the  individual  case.  The  amount  of  urine  is  most  fre- 
quently about  normal,  or  somewhat  diminished — in  some  cases  much  diminished 
— but  in  others  it  is  decidedly  increased,  so  that  the  patient  may  pass  eighty  to  a 
hundred  and  twenty  ounces  (2,500-3,500  cubic  centimetres)  in  the  twenty-four 
hours.  We  quite  frequently  see  considerable  variations  in  the  amount  of  the 
urine  in  the  same  patient  at  different  times.  All  these  differences  are  easily  ex- 
plained if  we  remember  how  many  circumstances  may  affect  the  amount  of  urine 
— the  presence  or  absence  of  inflammatory  changes  in  the  kidney,  the  presence  or 
absence  of  cardiac  hypertrophy,  co-existing  perspiration,  diarrhoea,  oedema, 
fever,  etc. 

The  color  of  the  urine  is  almost  always  light  yellow.     Only  exceptionally,  in 


638  DISEASES    OF   THE   UEII^AKY   OEGANS 

amyloid  nephritis,  does  it  contain  an  abundant  sediment;  usually  it  is  entirely, 
or  almost  entirely,  clear.  The  very  considerable  amount  of  albumen  in  the  urine, 
which  is  often  one  or  two  per  cent.,  is  also  characteristic  of  amyloid  kidney. 
In  many  cases,  indeed,  particularly  in  the  combination  of  amyloid  with  contracted 
kidney,  the  amount  of  albumen  is  smaller,  although  usually  decidedly  more  abun- 
dant than  in  pure  interstitial  nephritis.  Senator  has  pointed  out  that  the  com- 
parative amount  of  the  globuline  which  is  contained  in  the  urine  besides  the 
serum  albumen  is  often  particularly  large  in  amyloid  kidney.  The  specific  gravity 
of  the  urine  varies  very  much  according  to  the  amount  of  water  and  albumen  in 
it.    It  may  be  increased  (1015-1020)  or  diminished  (1010-1005). 

If  we  examine  the  urine  under  the  microscope,  we  usually  find  only  a  few 
hyaline  casts,  and  also  most  frequently  a  small  number  of  white  blood-corpuscles. 
In  general,  it  is  very  characteristic  of  amyloid  kidney  that  there  is  an  abundance 
of  albumen,  contrasting  with  the  scanty  or  scarcely  appreciable  microscopic  sedi- 
ment. In  the  combination  of  amyloid  with  more  marked  nephritic  changes  the 
sediment  is  more  abundant,  so  that  the  urine  is  cloudy.  The  microscope  then 
shows  more  numerous  hyaline  or  moderately  fatty  casts,  more  abundant  white 
blood-corpuscles,  sometimes  a  little  renal  epithelium,  and  in  quite  rare  cases  even 
red  blood-corpuscles.  Amyloid  reaction  is  said  to  occur  in  the  casts,  but  it  is  very 
rare,  and  therefore  of  no  value  in  diagnosis. 

The  other  morbid  symptoms  which  are  observed  in  amyloid  kidney  depend 
either  upon  the  change  in  the  kidneys  themselves,  or  upon  co-existing  amyloid 
degeneration  in  other  organs;  or,  lastly,  upon  the  primary  disease.  The  symp- 
toms of  the  latter  are,  of  course,  extremely  varied,  but  in  many  cases  they  may  be 
entirely  subordinate. 

In  regard  to  the  directly  resulting  symptoms  of  amyloid  kidney,  their  occur- 
rence is  of  interest,  especially  in  comparison  with  the  analogous  conditions  in 
acute  nephritis.  Dropsy  of  a  moderate,  or  even  a  severe  degree,  is  often  present  in 
amyloid  kidney,  but  it  may  also  be  entirely  absent.  We  must  remember  that  an 
oedema  independent  of  a  renal  affection  may  be  produced  by  marantic  venous 
thrombosis,  Urasmic  symptoms  are  distinctly  rare  in  amyloid  kidney,  but  they 
are  sometimes  observed,  especially  in  their  milder  forms,  such  as  vomiting.  It  is 
a  very  important  point  that  a  hypertrophy  of  the  left  ventricle  is  absent  in  most 
cases  of  amyloid  kidney.  This  is  explained  partly  by  the  fact  that  the  disease  usu- 
ally affects  feeble,  cachectic  individuals  who  have  no  superfluous  material  for  the 
manufacture  of  cardiac  hypertrophy,  and  partly  by  the  fact  that  in  pure  amyloid 
kidney  there  is  no  appreciable  retention  of  urinary  constituents  in  the  blood.  This 
latter  fact  explains,  also,  the  infrequency  of  ursemic  symptoms  (vide  supra).  If, 
however,  the  amyloid  degeneration  is  combined  with  genuine  nephritic  changes, 
the  condition  of  things  is  altered.  In  amyloid  contracted  kidney  we  have  repeat- 
edly observed  hypertrophy  of  the  left  ventricle. 

Albuminuric  retinitis  hardly  ever  appeal's  in  pure  amyloid  kidney.  In  the 
amyloid  contracted  kidney  it  has  sometimes  been  observed,  however,  in  cases 
where  there  has  probably  been  originally  a  pure  contracted  kidney,  with  amyloid 
coming  on  later.  The  secondary  inflammations  in  the  internal  organs,  such  as 
renal  pneumonia,  and  the  haemorrhages,  such  as  cerebral  haemorrhage,  are  also  rare. 

The  patient's  general  condition  is  dependent  in  part  upon  the  renal  disease, 
and  in  part  upon  amyloid  degeneration  in  other  organs,  but  mainly  upon  the 
primary  disease.  The  patient  with  amyloid  kidney  is  usually,  therefore,  cachectic, 
and  shows  in  high  degree  a  pallid,  anaemic  color  of  the  skin.  If,  also,  general 
dropsy  develops,  we  have  an  external  appearance  very  characteristic  of  amyloid 
disease ;  still,  in  some  few  cases  of  syphilis,  bronchiectasis,  and  unilateral  pulmo- 
nary contracture,  the  general  nutrition  remains  tolerably  good  for  a  consider- 
able time. 


AMYLOID   KIDNEY  639 

The  symptoms  which  point  to  a  co-existing  amyloid  degeneration  in  other 
organs  beside  the  kidneys  are  of  great  diagnostic  significance.  The  symptoms  in 
the  liver  (enlargement,  abnormal  firmness,  and  a  hard,  sharp  lower  edge  to  the 
organ),  the  spleen  (enlargement  and  hardness),  and  intestines  (obstinate  diar- 
rhoea not  yielding  to  any  remedy)  are  clinically  important  in  this  respect.  The 
interpretation  of  the  diarrhoea  is,  of  course,  usually  difficult,  since  it  may  often 
depend  upon  tubercular  intestinal  ulcers  as  well  as  upon  amyloid  of  the  intes- 
tines. 

We  can  scarcely  make  general  statements  in  regard  to  the  whole  course  and 
the  duration  of  amyloid  kidney,  since  the  form  of  the  primary  disease  is  to  be  es- 
liecially  considered  in  these  cases.  In  regard  to  the  time  that  it  takes  for  an 
amyloid  degeneration  to  develop  in  an  existing  primary  disease,  the  degeneration 
is  certainly  present  sometimes  after  a  few  months.  Of  course,  it  is  hardly  ever 
possible  to  determine  its  onset  accurately,  since  the  first  beginnings  of  amyloid 
degeneration  in  the  kidneys  do  not  usually  permit  themselves  to  be  recognized  at 
once  by  the  appearance  of  albuminuria  (vide  supra).  The  duration  of  amyloid 
kidney  varies  very  much  according  to  the  severity  of  the  case;  it  may  last  only 
a  few  weeks  or  months  before  death,  while  other  cases  have  certainly  lasted  for  a 
year,  especially  in  amyloid  contracted  kidney. 

The  prognosis  of  amyloid  kidney  is  in  most  cases  utterly  unfavorable,  which  is 
due  mainly  to  the  incurability  of  the  primary  disease ;  but  trustworthy  observers 
have  repeatedly  proved  that,  when  the  primary  disease  is  curable,  as  with  syphilis 
and  many  chronic  suppurations,  an  already  developed  amyloid  kidney  may  excep- 
tionally be  completely  restored. 

The  diagnosis  of  amyloid  kidney  can  be  made  with  considerable  certainty 
when  the  evident  signs  of  a  renal  affection  are  added  to  those  of  a  disease  which 
we  know  by  experience  to  promote  the  development  of  amyloid  degeneration. 
Whether  in  such  cases  we  have  a  pure  amyloid  or  a  pure  nephritis,  or  a  combina- 
tion of  the  two,  can  be  decided  with  some  certainty  only  from  the  condition  of  the 
urine :  a  clear  urine,  containing  but  few  morphological  elements,  but  rich  in  albu- 
men, points  to  pure  amyloid,  while  a  large  number  of  casts  and  red  and  white 
blood-corpuscles  in  the  urine  points  to  the  presence  of  inflammatory  changes  in 
the  kidney.  The  diagnosis  of  amyloid  contracted  kidney  is  justified  when  the 
symptoms  of  contracted  kidney  (abundance  of  pale  urine,  secondary  cardiac 
hypertrophy)  are  seen  in  association  with  such  morbid  conditions  as  are  likely 
to  occasion  amyloid  disease.  Of  great  importance,  as  we  have  already  pointed  out, 
is  the  comparatively  large  amount  of  albumen  and  the  consequently  somewhat 
higher  specific  gravity  of  the  urine.  Of  many  cases  of  amyloid  kidney  it  is  very 
characteristic,  and  so  of  diagnostic  value,  that  there  is  a  rapid  and  frequent 
variation  in  the  amount  of  urine  and  the  percentage  of  albumen  (Wagner). 

A  very  material  support  for  the  diagnosis  of  amyloid  kidney,  and  therefore  one 
which  should  always  be  looked  for,  is  the  discovery  of  amyloid  in  other  organs. 
We  have  briefly  mentioned  above  the  most  important  symptoms  in  the  liver,  the 
spleen,  and  the  intestines  referable  to  this  point. 

Treatment. — Only  the  treatment  of  the  primary  disease  can,  of  course,  be  con- 
sidered, both  as  a  prophylactic  and  also  as  a  causal  indication.  In  many  surgical 
cases,  and  also  in  the  cases  of  amyloid  in  syphilis,  there  is  a  possibility  of  this  (as 
by  iodide  of  potassium) ;  but  otherwise  we  try  to  improve  the  primary  disease  as 
far  as  we  can. 

In  other  respects  the  treatment  is  purely  hygienic  and  symptomatic.  We  must 
try  to  strengthen  the  patient  as  much  as  possible  by  good  food  and  the  exhibition 
of  preparations  of  iron  and  quinine.  The  use  of  iodide  of  iron  or  small  doses  of 
iodide  of  sodium  is  to  be  recommended.  In  a  symptomatic  point  of  view  the 
same  remedies  are  used  as  in  other  renal  diseases. 


640 


DISEASES    OF   THE   UEIKAEY   OEGANS 


We  insert  here  a  synopsis  of  the  condition  of  the  urine  and  of  the  left  ven- 
tricle in  the  most  important  varieties  of  renal  disease. 


Amount  of  urlue. 

Specific  gravity. 

Amount  of  albumen. 

Morphological  constituents. 

Condition  of  left 
ventricle. 

1.  Acute  nephritis 

Diminished. 

High. 

Considerable. 

Numerous  casts ;  blood- 
corpuscles  ;     epitheli- 
um. 

Numerous  casts  ;  blood- 
corpuscles  ;  epitheli- 
um; compound  granu- 
lar cells. 

Few  casts ;  small  num- 
ber of  blood-corpuscles. 

Few  casts. 

Few   casts  ;    blood- cor- 
puscles. 

Not     hyper- 
trophied. 

2.  Chronic  diffuse  ne- 

Normal     or 
s  0  m  ewhat 
diminished. 

Increased. 

Variable, 
normal,  or 
increased. 

Increased. 

Diminished. 

High. 

Low. 
Variable. 

Rather  low. 
High. 

Slight. 
Considerable. 

Moderate. 

Absent     or 
scanty. 

Hy  p  e  r  t  r  0  - 

3.  Contracted  kidnej' . 

4.  Amyloid  liidney 

5.  Amyloid  contracted 

phied. 

Hy  p  e  r  t  r  0  - 

phied. 
Not     hyptr- 

trophied. 

Hypertro- 

6.  Passive  congestion  . 

phied. 

CHAPTER   VI 
PURULENT    NEPHRITIS    AND    PERINEPHRITIS 

1.  Purulent  Nephritis 

.31tiolog^. — Although  in  the  forms  of  nephritis  so  far  described  the  occurrence 
of  large  numbers  of  nuclei  in  the  interstitial  tissue  has  been  repeatedly  mentioned, 
none  of  them  ever  come  to  genuine  suppuration — that  is,  to  a  purulent  liquefac- 
tion of  tissue,  a  true  abscess-formation.  The  origin  of  a  purulent  nephritis  is, 
rather,  always  associated  with  the  entrance  of  perfectly  definite  morbid  irritants 
into  the  kidneys.  These  are  invariably  organized  and  their  special  peculiarity  is 
to  excite  a  purulent  inflammation. 

There  are  two  chief  ways  through  which  the  morbid  irritants  may  reach  the 
kidneys — the  arterial  blood-current  and  the  urinary  passages.  The  first-men- 
tioned means  of  entrance  is  to  be  considered  in  all  the  cases  of  purulent  nephritis 
which  come  on  as  one  symptom  of  pysemic  processes  and  certain  forms  of  ulcera- 
tive endocarditis  (see  pages  116  and  307  on  the  point).  Far  more  rarely  purulent 
nephritis  develops  in  this  way  as  a  complication  in  other  diseases,  such  as  dysen- 
tery.   Purulent  nephritis  also  occurs  in  actinomycosis  (Israel). 

The  excitants  of  inflammation  take  the  second  path  in  those  cases  where  a 
purulent  nephritis  follows  an  inflammation  of  the  lower  urinary  passages,  the 
pelvis  of  the  kidney,  the  bladder,  etc.  Here  the  bacteria,  which  almost  always 
enter  directly  into  the  urinary  passages  (the  urethra  and  bladder)  from  without, 
pass  gradually  upward  from  the  bladder  through  the  ureter  to  the  pelvis  of  the 
kidney ;  from  this  they  enter  the  apertures  of  the  collecting  tubes  and  the  urinif- 
erous  tubules  of  the  kidney,  everywhere  exciting  a  purulent  inflammation.  We 
therefore  term  these  forms  of  purulent  nephritis — ^with  regard  to  their  origin — 
purulent  pyelo-nephritis. 

We  must  remark  in  conclusion  that  a  purulent  nephritis  and  perinephritis 
(vide  infra)  may  arise  in  direct  wounds  of  the  kidney  from  infection  of  the 
wound. 

Pathology. — Purulent  nephritis  shows  quite  characteristic  peculiarities  and 
differences  according  to  its  mode  of  origin.     (We  omit  traumatic  abscesses  here.) 


PUEULEl^T   NEPHRITIS    AND   PERINEPHRITIS  641 

The  renal  abscesses  in  pyaemia  and  analogous  diseases  are  usually  focal  suppu- 
rations, which  only  exceptionally  attain  a  great  extent,  but  which  are  usually  to 
be  recognized  with  the  naked  eye  as"  numerous  little  yellowish  dots  or  lines,  scat- 
tered over  the  whole  kidney,  about  half  a  millimetre  or  a  millimetre  in  diameter. 
On  microscopic  examination,  these  nodules  prove  to  be  genuine  little  abscesses,  in 
whose  territory  the  renal  tissue  proper  is  completely  destroyed.  In  the  middle 
of  them  we  often  find  the  originating  colony  of  micrococci,  the  "  micrococci 
embolus,"  seated  in  a  central  vessel.  The  conditions  are  still  plainer  if  we  exam- 
ine an  earlier  stage  of  the  process.  We  find  vessels  (the  loops  of  the  glomeruli, 
or  the  encircling  capillaries),  which  are  completely  plugged  with  micrococci,  and 
in  whose  vicinity  the  renal  tissue  is  still  perfectly  normal.  We  further  see  analo- 
gous spots  where  the  renal  tissue  is  already  necrosed  in  the  vicinity  of  the  colony 
of  micrococci,  and  is  infiltrated  with  emigrated  cells.  These  nodules  show,  finally, 
a  continuous  transition  to  the  completed  abscess,  which  is  often  surrounded  by  a 
hypersemic  or  even  a  hsemorrhagic  areola. 

In  purulent  pyelo-nephritis  the  renal  abscesses  appear  somewhat  different. 
The  abscesses  also  have  a  characteristic  striated  appearance,  corresponding  to  the 
distribution  of  the  inflammation  along  the  straight  tubules.  They  often  extend 
from  the  point  of  the  renal  papilla  through  the  cortex  to  the  surface  of  the  organ, 
so  that  from  the  outside  we  see  the  abscesses,  showing  through  as  yellowish 
points.  The  broader  abscesses  arise  from  the  confluence  of  neighboring  striae. 
The  microscope  shows  that  the  purulent  inflammation  arises  from  the  vessels  of 
the  interstitial  tissue,  in  whose  territory  the  uriniferous  tubules  are  of  course 
destroyed.  The  clusters  of  micrococci  form  the  most  interesting  feature.  These 
settle  originally  in  the  uriniferous  tubules  and  are  the  special  cause  of  the  necrosis 
of  epithelium  and  the  inflammation.  Pyelo-nephritis,  indeed,  was  one  of  the  first 
diseases  for  which  a  bacterial  origin  was  discovered   (Klebs). 

Clinical  Symptoms. — We  can  speak  very  briefly  here  in  regard  to  the  clinical 
symptoms  of  purulent  nephritis,  since  they  can  never  be  sharply  separated  from 
the  symptoms  of  the  primary  disease.  The  pysemic  renal  abscesses,  and  the  ab- 
scesses in  ulcerative  endocarditis,  hardly  ever  cause  special  clinical  symptoms,  so 
that  their  presence  is  first  recognized  on  the  autopsy-table.  Since  the  abscesses 
do  not  as  a  rule  communicate  with  the  uriniferous  tubules,  there  is  usually  no 
great  amount  of  pus  in  the  urine. 

The  clinical  symptoms  of  pyelo-nephritis  also  depend  less  upon  the  nephritic 
abscesses  than  upon  the  previous  and  accompanying  pyelitis  and  cystitis.  We 
will  therefore  return  to  renal  abscesses  in  the  description  of  these  diseases. 

2.  Perinephritic  (Paranephritic)  Abscess 
Perinephritic  abscess  is  the  name  given  to  suppurations  in  the  vicinity  of  the 
kidney,  especially  in  its  fatty  capsule  or  in  the  peri-renal  connective  tissue.  Apart 
from  any  traumatic  origin  for  such  abscesses,  they  develop  most  frequently  as  a 
result  of  purulent  nephritis  or  purulent  pyelitis.  The  escape  of  pus,  which  in- 
volves the  surrounding  tissue  in  the  inflammation,  may  come  from  the  ureter  or 
pelvis  of  the  kidney,  or  from  the  kidney.  The  special  form  of  primary  disease  dif- 
fers very  much;  it  may  be  either  simple  purulent  pyelitis,  or  pyelitis  from  renal 
calculi,  or  sometimes  tubercular  processes  and  new  growths  that  finally  suppurate, 
such  as"  cancer,  or  echinococci.  The  peri-renal  suppuration  may  also  take  its  start 
from  the  other  organs  in  the  neighborhood.  Thus  cases  have  been  seen  in  which 
the  perinephritis  followed  a  perityphlitic  abscess,  a  hepatic  abscess,  or  a  psoas  ab- 
scess after  vertebral  disease.  Perinephritic  suppuration  may  also  be  due  to  actino- 
mycosis. It  is  a  very  important  fact,  however,  that  paranephritic  abscesses  may 
develop  as  a  primary  disease  in  persons  in  apparently  perfect  health,  particularly 
in  middle-aged  men,  and  this  without  any  discoverable  cause.  It  is  usually  abso- 
41 


642  DISEASES    OF   THE   UEINARY   ORGAITS 

lutely  impossible  to  determine  how  and  by  what  path  the  inflammatory  germs 
reach  the  peri-renal  connective  tissue,  unless  possibly  they  migrate  from  the 
intestine.  These  cases  of  abscess  are  very  important  from  a  clinical  standpoint, 
because  the  symptoms  are  at  first  difficult  of  interpretation.  There  is  fever,  usu- 
ally of  a  decidedly  intermitting  pyaBmic  type,  and  there  are  also  dull,  indefinite 
pains  in  the  loins  or  abdomen,  constipation,  and  constitutional  symptoms.  The 
cause  of  all  these  symptoms  is  gradually  made  apparent  by  the  development  of 
distinct  local  changes. 

In  almost  all  cases  of  perinephritic  abscess  the  accumulation  of  pus  finally 
becomes  so  great  that  a  swelling  appears,  usually  in  the  lumbar  region,  and  this 
grows  more  and  more  prominent;  at  first  it  is  scarcely  noticeable;  but  later  the 
skin  becomes  oedematous  there,  it  constantly  protrudes  more  and  more,  it  assumes 
an  inflammatory  hypersemic  redness,  until  finally  a  definite  fluctuation  shows  the 
advance  of  the  abscess  up  to  the  skin.  In  other  cases  the  inflammatory  swelling 
extends  forward  into  the  iliac  fossa;  then  there  is  also  abnormal  resistance  and 
dullness  above  Poupart's  ligament.  The  swelling  may  also  extend  upward  toward 
the  diaphragm,  so  that  the  diaphragm  is  crowded  upward,  giving  rise  to  marked 
dyspnoea.  The  relations  of  the  swelling  to  the  descending  colon  are  sometimes  the 
same  as  in  new  growths  of  the  kidney  (compare  Chapter  VIII). 

Besides  the  swelling,  there  is  almost  invariably  a  very  great  pain  in  the 
affected  region,  either  spontaneous  or  on  pressure.  If  the  swelling  presses  on 
the  large  nerve-trunks  in  the  vicinity,  it  produces  severe  shooting  pains  in  the 
leg  of  the  same  side,  and  sometimes  a  numb  feeling  and  paresis.  The  leg  is 
then  often  kept  in  a  position  similar  to  that  in  coxitis. 

The  fever  is  persistent,  and  usually  of  an  intermittent  character  and  associ- 
ated with  rigors.  It  and  the  pain  make  the  patient  thin  and  feeble,  even  to  an 
extreme  degree.  The  urine  does  not  contain  pus  unless  the  abscess  has  some  con- 
nection with  the  urinary  passages. 

Recovery  may  occur  if  the  pus  finds  some  way  out  of  the  body.  Apart  from 
operative  interference,  the  most  favorable  termination  is  the  spontaneous  dis- 
charge of  the  pus  into  the  intestine  (colon),  or  into  the  urinary  tract  (pelvis  of 
the  kidney,  bladder).  The  course  of  the  disease  is  much  more  tedious  if  the  pus 
finds  its  way  through  the  skin.  If  renal  abscesses  discharge  outwardly,  they  most 
frequently  point  in  the  loins,  less  often  like  a  psoas  abscess,  below  Poupart's  liga- 
ment. They  may  also  discharge  into  the  pleural  or  peritoneal  cavities,  with  a 
consequent  empyema  or  quickly  fatal  peritonitis.  In  other  cases,  if  prompt  surgi- 
cal aid  is  impossible,  death  occurs  from  exhaustion. 

The  diagnosis  is  made  chiefly  from  the  swelling,  pain,  and  fever,  and  a  con- 
sideration of  the  aetiological  factors.  We  can  settle  any  doubts  in  most  cases  by 
exploratory  puncture.  The  condition  may  be  confounded  with  hydronephrosis, 
psoas  abscess,  and  solid  tumors  of  the  kidney. 

The  only  treatment,  apart  from  the  fulfillment  of  any  symptomatic  indica- 
tions, is  surgical,  and  consists  in  opening  and  draining  the  abscess.  The  result 
depends  chiefly  upon  the  patient's  general  condition,  and  the  character  of  the 
primary  disease.    The  details  are  to  be  found  in  the  text-books  of  surgery. 


DISTURBANCES    OF   CIRCULATION  IN"   THE     KIDNEYS     643 

CHAPTER   VII 
DISTURBANCES    Or    CIRCULATION    IN    THE    KIDNEYS 

1.  The  Congested  Kidney. — Although  local  impediments  to  the  flow  of  venous 
blood  from  the  kidneys,  such  as  thrombosis  of  the  renal  veins,  hardly  ever  attain 
a  clinical  significance,  the  participation  of  the  kidneys  in  a  general  venous  stasis, 
as  is  seen  chiefly  in  heart  disease  (compare  page  331),  pulmonary  emphysema, 
etc.,  is  of  great  diagnostic  importance,  since  we  possess  in  the  condition  of  the 
urine  quite  an  accurate  measure  of  the  intensity  as  well  as  of  the  increase  and 
decrease  of  the  stasis. 

The  congested  kidney  is  easily  recognized  anatomically:  The  organ  is  often 
somewhat  enlarged,  it  feels  firmer  than  normal,  and  shows,  both  on  its  surface 
and  on  section,  a  dark,  bluish-red  color — "  cyanotic  induration."  The  medullary 
substance  is  usually  darker  than  the  cortex.  Under  the  microscope  we  see  con- 
siderable dilatation  and  a  tense  fullness  of  the  veins  and  capillaries.  The  paren- 
chyma is  normal,  but  in  more  advanced  cases  it  may  show  a  beginning  fatty 
degeneration  of  the  epithelium,  which  is  a  result  of  the  defective  arterial  blood- 
supply.  At  first  the  interstitial  tissue  is  little  changed,  but  if  the  congestion  per- 
sists for  a  long  while  there  may  be  a  gradual  destruction  of  the  renal  parenchyma, 
to  a  certain  degree,  with  the  formation  of  an  abundance  of  contractile  interstitial 
tissue  (congested  and  contracted  kidney). 

The  clinical  symptoms  of  congested  kidney  concern  only  the  changes  in  the 
urine.  The  amount  of  urine  diminishes,  corresponding  to  the  diminution  of  the 
arterial  pressure  and  the  diminished  rapidity  of  the  blood-current.  Only  twenty- 
five  to  twenty  ounces  (800-500  cubic  centimetres),  or  less,  ten  to  six  ounces  (300- 
200  cubic  centimetres),  are  secreted  daily.  The  urine  is  also  more  concentrated 
and  darker  than  normal,  and  often  has  an  abundant  sediment  of  urates.  If  nutri- 
tive disturbances  have  begun  in  the  epithelium  of  the  glomeruli  as  a  result  of 
stasis,  the  urine  is  also  albuminous,  but  the  amount  of  albumen  in  pure  congested 
kidney  is  always  slight — about  one  tenth  to  one  sixth  of  the  volume.  The  urine 
often  contains,  besides,  a  few  hyaline  casts,  and  a  few  white  and  red  blood-corpus- 
cles, the  latter  pointing  to  little  congestive  haemorrhages. 

If  the  changes  mentioned  come  on  as  one  symptom  of  a  general  venous  stasis, 
and  are,  accordingly,  associated  with  cyanosis  and  dropsy,  the  diagnosis  of  con- 
gested kidney  can  be  made  with  certainty.  If  we  succeed  in  restoring  the  cir- 
culation by  appropriate  remedies,  such  as  digitalis,  the  urine  at  once  becomes  more 
abundant  and  clearer  and  its  albumen  disappears.  Otherwise  the  characteristics 
of  the  urine  of  passive  congestion  last  until  the  patient's  death. 

2.  Embolic  Infarction  in  the  Kidneys. — Since  the  renal  infarction,  although 
it  has  great  pathological  interest,  is  hardly  ever  of  clinical  significance,  we  will 
limit  ourselves  here  to  a  brief  description  of  the  most  essential  points. 

If  one  of  the  smaller  renal  arteries  is  plugged  by  an  embolus  in  heart  disease, 
the  affected  portion  of  the  organ  cut  off  from  the  circulation  must  perish,  since 
all  the  renal  arteries  are  terminal  arteries.  The  epithelium  undergoes  the  well- 
known  changes  of  coagulation  necrosis,  disappearance  of  the  nuclei  of  the  cells, 
and  disintegration,  and  the  tissue  becomes  entirely  or  in  part  a  haemorrhagic 
infarction  (compare  page  331).  In  this  way  arise  the  characteristic  wedge- 
shaped,  red,  hsemorrhagic  infarctions  in  the  kidney,  or  far  more  frequently  the 
yellowish-gray,  anaemic  infarctions  (often  surrounded  by  a  hfemori-hagic  areola), 
the  base  of  which  is  at  the  surface  of  the  kidney;  the  base  may  reach  a  width  of 
half  a  centimetre  to  a  centimetre  or  more,  while  the  apex  extends  a  varying  dis- 
tance into  the  cortex,  or  even  into  the  medullary  substance.    Later  on  the  grad- 


614  DISEASES    OF    THE   UHINAEY   OEGANS 

ually  disintegrated  tissue  of  tlie  infarction  is  absorbed,  round  cells  emigrate  from 
without  into  the  region  destroyed,  and  a  shrunken  connective-tissue  cicatrix  grad- 
ually develops  in  place  of  the  former  infarction.  Many  kidneys  may  have  such  a 
granular  surface  from  numerous  infarction  cicatrices  that  they  may  be  appro- 
priately termed  "  embolic  contracted  kidneys." 

The  anatomical  processes  just  briefly  described  cause  in  most  cases  no  special 
clinical  symptoms  at  all.  Sometimes,  however,  a  slight  amount  of  blood  in  the 
urine  seems  to  depend  on  the  development  of  a  hsemorrhagic  infarction  in  ths 
kidneys,  so  that  when  a  cause  for  embolic  ijrocesses,  such  as  heart  disease,  is  pres- 
ent, we  may  entertain  the  suspicion  of  the  development  of  a  renal  infarction  dur- 
ing life.  In  rare  cases  the  development  of  a  rather  large  infarction  of  the  kidneys 
is  associated  with  a  sudden  and  violent  pain  in  that  region,  with  marked  subse- 
quent hsematuria  or,  as  we  observed  in  one  case,  hsemoglobinuria. 

The  embolic  processes  in  the  kidney  never  demand  special  treatment. 


CHAPTER   VIII 
NEW    GROWTHS    IN    THE    KIDNEYS 

Of  the  primary  forms  of  tumor  occurring  in  the  kidney,  two  especially  claim 
our  interest:  cancer  of  the  kidney  and  congenital  sarcoma.  The  latter  is  of  great 
importance  in  regard  to  the  g^eneral  theory  of  tumors,  since  it  points  definitely  to 
the  development  of  the  new  growth  from  scattered  portions  of  embrj^onic  tissue. 
Striped  muscular  fibers  have  been  repeatedly  found  in  tumors  consisting  otherwise 
of  round  or  spindle  cells,  from  which  the  name  of  rhabdomyoma  or  myosarcoma 
striocellulare  has  been  chosen  for  these  tumors.  Since  there  are  no  muscular 
fibers  in  the  kidney  itself,  their  occurrence  in  the  tumors  points  undeniably  to  dis- 
turbances of  embryonic  development.  This  theory  obtains  a  further  interesting 
confirmation  from  our  own  observation  of  the  development  of  left-sided,  and, 
probably,  congenital  renal  sarcoma  in  two  brothers.  Both  children  died  wh^n 
between  two  and  three  years  of  age,  and  the  autopsy  gave  almost  precisely  the 
same  lesions  in  both :  numerous  metastases  in  the  liver  and  lungs,  beside  a  new 
growth  almost  as  large  as  a  child's  head  in  place  of  the  left  kidney. 

Eenal  cancer  is  also  remarkably  frequent,  comparatively  speaking,  in  children 
under  four  years  of  age,  and  about  equally  common  in  the  trsvo  sexes.  Of 
course,  we  find  renal  cancer  in  persons  of  more  advanced  years;  in  some  cases 
of  this  sort  renal  calculi  seem  to  occasion  the  development  of  carcinoma.  This  is 
like  the  relation  between  gall-stones  and  cancer  of  the  biliary  passages.  Usually 
only  one  kidney  is  affected,  chiefly  the  left,  as  it  seems,  but  the  new  growth  has 
sometimes  been  found  in  both  kidneys.  In  its  character,  renal  cancer  belongs 
either  to  the  denser  or  to  the  softer,  medullary  form.  It  may  permeate  the  whole 
kidney  and  change  it  to  a  large  tumor,  weighing  fifteen  or  twenty  pounds  (five  or 
ten  kilogrammes).  Softening  and  h93morrhage  very  often  take  place  within  th? 
tumor.  The  proliferation  has  been  repeatedly  observed  to  extend  to  the  neighbor- 
ing parts,  especirlly  the  pelvis  of  the  kidney,  and  metastases  also  form  in  other 
organs,  as  in  the  lymph-glands,  liver,  or  lungs.  It  should  also  be  mentioned  that 
several  times  renal  cancer  and  cancer  of  the  testicle  have  been  combined. 

The  clinical  symptoms  of  renal  tumor  are  entirely  absent,  or  of  a  very  indefi- 
nite nature,  in  the  first  period  of  the  disease.  Dull  pain  in  the  renal  region  is 
repeatedly  given  as  the  first  symptom,  but,  of  course,  this  is  hardly  ever  of  definite 
significance.     The  diagnosis  almost  always  first  takes  a  definite  direction  by  the 


NEW   GEOWTHS   IN   THE   KIDNEYS  645 

appearance  of  a  palpable  tumor.  This  develops  in  the  lumbar  and  lower  lateral 
abdominal  region,  constantly  extending  from  this  point  upward  and  inward.  As 
stated  above,  both  carcinoma  and^  sarcoma  of  the  kidney  may  cause  enormous 
tumors,  especially  in  children,  which  may  make  the  whole  abdomen  protrude  to  a 
marked  degree.  The  tumor  feels  firm  and  sometimes  smooth,  sometimes  uneven ; 
it  does  not  usually  move  with  respiration,  but  this  rule  has  exceptions,  particularly 
in  the  case  of  tumors  of  the  right  kidney.  In  tumors  of  the  left  kidney  some 
diagnostic  importance  attaches  to  the  relation  of  the  new  growth  to  the  descend- 
ing colon,  inasmuch  as  the  latter  is  pushed  forward  by  the  growth  of  the  tumor 
and  comes  to  lie  between  it  and  the  anterior  abdominal  wall.  It  is  quite  often 
possible  to  demonstrate  that  portion  of  the  intestine  which  traverses  the  tumor 
by  means  of  percussion,  and  sometimes  even  by  means  of  palpation.  For  this  pur- 
pose the  colon  may  be  examined  alternately  when  empty  and  when  artificially  dis- 
tended with  water,  or,  still  better,  with  air.  In  the  case  of  tumors  of  the  right 
kidney,  there  may  be  corresponding  relations  to  the  ascending  colon,  but  this  is 
less  frequent.  Almost  all  larger  tumors  of  the  kidney  occasion  displacement  of 
the  diaphragm  upward,  and  of  neighboring  organs  laterally.  Another  factor  in 
diagnosis  is  the  hallottement  renal  described  by  Guyon:  when  a  gentle  thrust  is 
made  in  the  renal  region  the  tumor  is  felt  to  strike  softly  upon  the  anterior  ab- 
dominal wall. 

There  may  be  scarcely  any  pain  for  a  long  while,  but  in  some  cases  there  is 
violent  and  persistent  pain.  Often  the  pressure  of  the  tumor  upon  neighboring 
nerve-trunks — for  instance,  the  sciatic — occasions  obstinate  neuralgia,  sometimes 
associated  with  paresis. 

In  many  cases  of  renal  tumor  the  urine  shows  no  abnormal  conditions  at  all, 
since  its  secretion  is  performed  vicariously  by  the  other  healthy  kidney.  In 
carcinoma  of  the  kidney  it  sometimes  presents,  however,  one  sign  valuable  for 
diagnosis — namely,  an  admixture  of  blood.  This  hsematuria  often  comes  on  very 
early,  even  before  there  is  any  tumor  to  be  felt.  It  is  repeated  either  frequently 
or  only  rarely  in  different  cases,  and  sometimes  it  is  entirely  absent.  The  haem- 
orrhage is  associated  with  colicky  pains  only  when  large  clots  have  to  pass  through 
the  urinary  passages.  Sometimes,  but  very  rarely,  small  particles  and  shreds  of 
tissue  from  the  disintegrated  new  growth  may  be  found  in  the  urine. 

The  general  symptoms  are  often  very  late  at  first,  especially  in  children;  but 
finally  a  general  condition  of  marasmus  almost  always  develops.  A  constant  and 
great  frequency  of  the  pulse  is  often  striking.  We  must  also  mention  the  peculiar 
symptom  several  times  observed  in  girls  with  congenital  renal  tumors — viz.,  an 
abnormally  early  development  of  the  pubic  and  axillary  hair,  and  sometimes 
a  peculiar  pigmentation  of  the  skin  (Kiihn). 

The  diagnosis  of  renal  tumors  is,  in  many  cases,  quite  evident,  but  in  others 
very  difficult.  The  position  of  the  new  growth,  its  limited  mobility,  its  relations 
to  the  colon,  and,  above  all,  our  knowledge  as  to  the  occurrence  of  renal  tumors 
in  children,  often  suggest  the  correct  interpretation  of  the  case.  In  older  persons 
renal  haemorrhages  which  can  not  be  otherwise  explained  must  direct  our  sus- 
picions to  the  possibility  of  a  cancer  of  the  kidney.  Often,  however,  the  disease 
has  been  confounded  with  tumors  of  the  retro-peritoneal  glands  and  of  the  ovaries, 
with  large  psoas  abscess,  tumor  of  the  liver,  and  splenic  tumor. 

The  prognosis  is,  of  course,  unfavorable.  The  disease  sometimes  lasts  only  a 
few  months,  sometimes  a  year  or  two,  rarely  longer. 

The  treatment  must  in  most  cases  be  purely  symptomatic.  The  only  expecta- 
tion of  success  lies  in  the  operative  removal  of  the  new  growth,  the  details  of 
which  are  to  be  found  in  recent  monographs  on  renal  surgery. 


64:6  DISEASES    OF   THE   UELN^aeY   OEGAXS 


CHAPTEE   IX 

PARASITES    OF    THE    KIDNEYS    AND    OF    THE    URINAIIY    PASSAGES— 

CHYLTJRIA 

1.  EcMnococcus  of  the  Kidney.* — Eeliinocoecus  cysts  have  been  repeatedly 
found  in  the  kidney,  although  much  more  rarely  than  in  the  liver.  Usually  only 
one  kidney  is  affected,  and  the  parasite  is  generally  situated  in  the  renal  substance 
itself,  only  exceptionally  between  it  and  the  capsule  of  the  kidney.  The  size  of 
the  echinococcus  cysts  may  be  very  considerable,  the  diameter  reaching  to  tvrenty 
centimetres  or  more. 

Clinical  symptoms  usually  first  appear  when  the  tumor  can  be  felt  through  the 
abdominal  walls.  Subjective  symptoms  may  even  then  be  entirely  wanting.  Pain 
on  pressure  develops  gradually  later.  The  tumor  usually  has  an  approximately 
globular  shape.  Its  relations  to  the  neighboring  organs,  especially  to  the  colon, 
are  the  same  as  we  have  learned  to  recognize  in  the  preceding  chapter,  in  the 
description  of  cancer  of  the  kidney.  The  so-called  hydatid  thrill  which  is  said  to 
be  characteristic,  and  which  is  obtained  by  giving  the  tumor  a  little  push  with  the 
flat  of  the  hand,  can  be  distinctly  felt  in  only  the  rarest  instances. 

It  is  a  comparatively  frequent  occurrence  for  the  echinococcus  cyst  to  burst  into 
the  pelvis  of  the  kidney.  Then  single  echinococcus  cysts,  or  at  least  bits  of  mem- 
brane, hooks,  etc.,  are  passed  with  the  urine,  usually  with  severe  colicky  pains, 
which  are  exactly  like  the  renal  colic  from  the  passage  of  a  calculus.  Such  at- 
tacks may  be  often  repeated,  and  may  form  a  very  severe  type  of  disease  by  ob- 
structing the  urinary  passages — the  bladder  and  urethra.  In  such  cases  the  symp- 
toms of  a  secondary  pyelitis  and  cystitis  are  often  added. 

Perforations  in  other  directions  are  much  rarer.  The  rupture  of  a  renal  echi- 
nococcus into  the  lungs  has  sometimes  been  observed,  the  patient  coughing  up 
echinococcus  cysts. 

Sometimes,  especially  after  injuries,  the  sac  of  the  echinococcus  becomes  in- 
flamed, suppurates,  and  leads  to  a  general  pysemic  condition. 

The  diagnosis  of  renal  echinococcus  is  possible  only  when  a  tumor  can  be  made 
out  belonging  to  the  kidney,  and  when  portions  of  echinococcus  are  passed  with 
the  urine,  or  through  an  exploratory  puncture.  It  has  already  been  stated  that 
one  shovild  be  cautious  about  employing  this  procedure  (see  page  577).  The  cysts 
are  most  frequently  confounded  with  hydronephrosis  {vide  infra),  and,  in  women, 
with  ovarian  tumors. 

The  prognosis  is  not  wholly  unfavorable.  Permanent  recovery  has  been  re- 
peatedly observed,  especially  after  the  rupture,  or  single  or  repeated  evacuations, 
of  the  sac  of  the  echinococcus;  but,  of  course,  echinococcus  of  the  kidney  may 
also  be  attended  with  numerous  dangers,  such  as  suppuration  of  the  sac.  The 
course  of  the  disease  is  always  very  tedious. 

A  radical  treatment  is  possible  only  by  surgical  means.  Symptomatically,  ice 
'and  local  blood-letting  are  used  when  there  are  symptoms  of  local  inflammation ; 
and  morphine,  warm  baths,  and  sometimes  mechanical  aids,  e.  g.,  the  catheter, 
when  there  are  symptoms  of  colic. 

2.  Distoma  hsematobium  (bilharzia  haematobia — hlood-ftul-e,  see  Fig.  71)  is  a 
parasite  which  belongs  to  the  flukes  or  trematodes,  and  which  occurs  especially  in 
Egypt,  Abyssinia,  and  East  Africa.  Infection  is  said  to  take  place  partly  by  means 
of  the  drinking-water  and  food,  and  partly,  perhaps,  by  the  parasite  creeping  into 
the  urinary  passages  and  the  rectum  during  bathing.    ^STatives  are  much  of  tener  at- 

*  In  regard  lo  the  general  natural  historv  of  the  cchinocoeeus,  compare  page  575. 


PAEASITES    OF   THE    KIDNEYS    AND    IJEINAEY   PASSAGES     Gi7 

tacked  than  Europeans.  The  distoma  has  its  chief  abode  in  the  branches  of  the 
portal  vein,  and  particularly  in  the  venous  plexuses  of  the  bladder  and  the  rec- 
tum. Its  eggs  are  often  deposited  in  great  numbers  in  the  mucous  membrane  of 
the  pelvis  of  the  kidney,  the  ureter,  and  the  bladder,  and  they  excite  in  these 


Fig.  71.— Distoma  hsematobium  (from  Leuckart).  a.  Male  and  female,  the  latter  in  the  canalis  gynae- 
cophorus  of  the  former.  Ten  diameters,  b.  Egg  with  a  terminal  spine,  c.  Egg  with  a  lateral  spine. 
150  diameters. 


places  a  severe  inflammation  with  ulceration  and  consequent  strictures,  or  the 
formation  of  concretions.  Similar  violent  inflammation  occurs,  also,  in  the  rec- 
tum and  in  the  sexual  organs.  The  course  of  the  disease  is  very  chronic.  The 
main  symptom  is  persistent  hsematuria.  Many  cases  of  so-called  tropical  hema- 
turia are  due  to  the  distoma,  and  later  we  have  the  symptoms  of  local  inflamma- 
tion and  of  severe  cystitis.  The  diagnosis  may  be  established  by  the  discovery  of 
the  eggs  in  the  urine  or  the  fseces.    Treatment  is  merely  symptomatic. 

3.  Strongylus  or  Eustrong^lus  G-ig-as  (palisade  worm)  is  a  parasite  occurring 
in  the  pelvis  of  the  kidney  in  many  animals — the  dog,  the  wolf,  the  marten — and 
very  rarely  in  man.  In  size  and  color  it  is  not  unlike  an  ordinary  earth-worm. 
It  may  produce  symptoms  of  severe  pyelitis,  with  haemorrhages,  and  colicky 
pains.    No  well-established  cases  have  been  reported  of  late. 

4.  Filaria  Sanguinis.  Chyluria. — The  blood  filaria  of  man,  belonging  to  the 
round-worms,  has  obtained  a  special  clinical  interest,  since  it  is  recognized,  from 
the  investigations  of  Wucherer  in  Bahia  in  1868,  and  of  Lewis  in  the  East  Indies 
in  1870,  as  the  cause  of  the  tropical  chyluria  and  some  allied  diseases,  such  as 
lymph  scrotum,  elephantiasis  Arabum,  and  chylous  ascites. 

The  full-grown  filaria,  "  filaria  Bancrofti,"  a  very  thin  worm,  about  three  or 
four  inches  long,  has  been  found  only  a  few  times  in  man.  Its  seat  is  in  the 
larger  lymphatics,  where  it  gives  rise  to  chronic  stasis  of  the  lymph  with  its  conse- 
quences— chronic  hyperplasia  of  the  connective  tissue,  etc.  In  chyluria,  the  para- 
sites are  probably  situated  in  the  main  branches  of  the  thoracic  duct — at  any 
rate,  in  such  a  place  that  a  stasis  of  the  lymph  ensues  in  the  lymphatics  of  the 
bladder,  or  perhaps,  in  some  cases,  of  the  pelvis  of  the  kidney  and  the  other  urinary 
passages.  If  the  distended  lymph-sac  ruptures,  the  lymph  or  chyle  is  poured  out 
into  the  urinary  passages  and  is  evacuated  with  the  urine.  Since  this  process  may 
be  often  repeated,  the  intermittent  course  of  chyluria  is  thus  explained.  The  indi- 
vidual attacks  of  the  disease  may  come  on  during  years  at  intervals  of  weeks  or 
months.     They  are  often  associated  with  pain  and  febrile  symptoms. 

The  condition  of  the  urine,  which  in  many  cases  may  look  almost  exactly  like 
milk,  is  most  characteristic.  A  creamy  layer  of  fat  forms  upon  the  surface.  If  we 
shake  the  urine  with  ether,  the  greater  part  of  the  fat  can  be  removed,  and  the 
urine  rendered  clear.  The  fat  in  the  urine  may  amount  to  two  or  three  per  cent. 
The  chyluria  is  often  associated  with  a  hsematuria  coming  from  the  ruptured 
veins.  The  urine  then  looks  bloody  red,  and  shows  under  the  microscope  many 
red  blood-corpuscles  beside  the  fat-drops.    Large  clots  often  form  in  the  urine. 


648 


DISEASES    OF   THE   UEHSTART   OEGANS 


The  embryos  of  filaria,  found  in  the  urine  in  very  many  eases,  although  not  in 
all,  form  the  most  important  diagnostic  feature  in  the  urine.    These  (see  Fig.  72) 

are  objects  two  to  three  tenths  of  a  milli- 
metre long,  with  a  diameter  about  equal 
to  that  of  a  red  blood-corpuscle.  They  are 
usually  imbedded  in  a  very  delicate  sheath, 
which  often  projects  at  the  end  of  the  ani- 
mal, and  show  a  constant,  vigorous  vibrat- 
ing motion.  They  have  also  been  found  in 
the  blood  of  the  patient,  as  well  as  in  the 
urine,  and,  strange  to  say,  esi^ecially  during 
the  night. 

The  course  of  the  filaria  disease  may 
vary  considerably.  Many  patients  reach  an 
advanced  age;  in  others,  severe  general 
symptoms,  like  anaemia  and  emaciation, 
finally  come  on.  The  different  forms  in 
which  the  disease  occurs — chyluria,  elephan- 
tiasis, etc. — are  combined  in  manifold  ways. 
The  region  of  the  geographical  distribu- 
tion of  the  disease  lies  almost  wholly  in 
hot  countries.  It  has  so  far  been  most  fre- 
quently observed  in  Brazil,  the  Antilles,  the 
East  Indies,  China,  Japan,  Egypt,  Cape 
Colony,  and  Australia.  Nothing  definite  is 
yet  known  of  the  precise  mode  of  invasion 
of  the  parasites.  According  to  Hansen's 
investigations,  mosquitoes  play  an  important  part  here.  [This  view  is  now  well 
established. — V.] 

In  regard  to  treatment,  apart  from  any  surgical  interference,  we  may  try 
picro-nitrate  of  potassium,  three  to  ten  grains  (gramme  0.2-0.5),  in  pills  or  cap- 
sules, several  times  a  day  (Scheube). 


Fig.  72.— (From  Schecbe.)  Embryos  of  filaria. 


CHAPTEE  X 
MOVABLE    KIDNEY    (FLOATING    KIDNEY,    REN    MOBILIS) 

.ZEtiology. — With  some  practice  the  physician  can  frequently  palpate  the  kid- 
neys, particularly  the  right  kidney,  even  under  absolutely  normal  conditions 
("palpable  kidney").  This  is  much  oftener  the  case  in  women  with  lax  and 
yielding  abdominal  walls  than  in  men.  With  every  inspiration  the  kidney  is 
pushed  somewhat  downward.  In  many  cases,  therefore,  the  kidney,  or  at  least  its 
lower  half,  is  felt  only  upon  deep  inspiration.  If  the  kidney  is  not  only  palpable, 
but  also  capable  in  greater  or  less  degree  of  being  moved  about  by  the  hand,  and 
if,  consequently,  we  do  not  always  find  the  kidney  in  the  same  place,  then  we  de- 
scribe it  as  an  abnormally  movable  kidney;  or,  if  the  case  is  extreme,  a  floating 
kidney.  What  may  be  the  causes  of  this  extreme  mobility  of  the  kidney  is  not  set- 
tled. Often  it  may  be  due  to  the  congenital,  anatomical  relations  of  the  perito- 
neum, and  other  tissues  around  the  kidney.  This  is  indicated,  particularly,  by  the 
occasional  occurrence  of  movable  kidney  in  children.  Certain  external  mechan- 
ical factors,  however,  undoubtedly  play  the  most  important  role.  First  among 
these  is  the  distention  and  relaxation  of  the  abdominal  walls  as  a  result  of  preg- 


MOVABLE   KIDNEY    (FLOATING   KIDNEY,   EEN  MOBILIS)  619 

nancy;  and,  secondly,  the  influence  of  clothing,  waist-bands  and  corsets.  This  ex- 
plains the  fact  that  movable  kidney  is  found  mainly  in  women,  and  particularly  in 
married  women.  At  the  same  time,  the  abnormal  mobility  and  downward  dis- 
placement of  the  kidney  are  often  merely  a  part  of  a  general  "  enteroptosis  "  (see 
page  465),  and  are  therefore  associated  with  gastroptosis,  coloptosis,  and  cor- 
set liver.  That  the  movable  kidney  is  far  more  often  the  right  than  the  left,  is 
probably  due  to  the  fact  that  the  right  kidney  is  originally  less  firmly  fastened, 
and  is  placed  lower,  and  also  that  it  is  affected  by  the  great  mass  of  the  liver  which 
lies  above  it.  Numerous  other  causative  influences  have  been  mentioned,  but  none 
of  them  is  as  important  as  the  preceding:  they  are  severe  physical  labor  with 
frequent  tension  of  the  abdominal  muscles;  injuries  involving  the  region  of  the 
kidneys;  diseases  of  the  neighboring  organs,  particularly  displacement  of  the 
uterus,  and  finally  emaciation,  causing  absorption  of  the  fat  which  supports  the 
kidneys  and  makes  tense  the  abdominal  walls.  After  death  a  movable  kidney 
can  not  be  recognized,  unless  it  is  found  in  an  abnormal  position — e.  g.,  in  front 
of  the  vertebral  column,  or  close  to  the  anterior  abdominal  walls.  In  such  cases 
its  external  edge  may  be  directed  downward  and  its  inner  edge  upward. 

Symptoms. — The  clinical  importance  of  movable  kidney  is  estimated  very  dif- 
ferently by  different  physicians.  Many  conceive  that  it  is  a  very  frequent  cause 
of  manifold  abdominal  disturbances ;  others  are  almost  inclined  to  deny  it  any 
influence  on  the  health.  We  ourselves  believe  that  a  movable  kidney  as  such  may, 
in  fact,  excite  disagreeable  symptoms,  but  that  this  is  the  exceptional  occurrence. 
As  we  have  already  mentioned,  palpability  and  slight  movability  of  the  right  kid- 
ney are  so  frequent  in  women  that  as  soon  as  one's  attention  is  directed  to  the 
matter,  one  finds  this  condition  in  a  large  proportion  of  all  cases  in  which  there  is 
occasion  to  make  a  careful  abdominal  examination.  The  pains  and  abnormal 
sensations  in  the  abdomen,  of  which  women  so  frequently  complain,  are  difficult 
of  interpretation,  and  it  is,  of  course,  very  seductive  and  convenient  to  refer  them 
to  a  movable  kidney;  but  if  we  consider  how  often  we  find  an  exactly  similar 
movable  kidney  in  women  who  are  entirely  free  from  abdominal  symptoms,  we 
can  not  avoid  suspicion  as  to  the  importance  of  the  condition. 

It  is  difficult  to  form  a  characteristic  group  of  symptoms  which  may  be  un- 
hesitatingly referred  to  movable  kidney.  Eirst,  pain  should  be  named.  This  is 
to  a  certain  extent  local,  but  it  often  radiates  into  the  epigastrium  and  the  sacral 
and  lumbar  regions,  and  sometimes  is  colicky.  Not  infrequently  the  pain  is  asso- 
ciated with  nausea.  The  discomfort  is  aggravated  by  any  decided  motion  of  the 
patient,  or  by  riding,  driving,  and  the  like ;  but  during  repose  it  becomes  slight, 
or  entirely  disappears.  In  rare  cases  we  have  symptoms  of  strangulation.  These 
occur  periodically,  and  are  said  to  be  especially  frequent  at  the  time  of  the  menses. 
They  consist  of  the  sudden  onset  of  violent  pain;  chilliness  which  seldom 
amounts  to  a  rigor;  great  tenderness  and  tenseness  of  the  abdomen;  slight 
fever;  vomiting;  and  collapse.  During  this  time  the  urine  is  usually  scanty,  and 
the  amount  does  not  increase  again  till  the  attack  is  over,  about  three  to  five  days. 
The  precise  cause  of  these  symptoms  is  supposed  to  be  a  sudden  damming  up  of  the 
urine  by  a  kink  or  twist  in  the  ureter.  This  occasions  acute  hydronephrosis,  and 
resultant  phenomena,  which  last  until  the  urinary  channels  are  free  again.  In 
certain  cases  floating  kidney  seems  actually  to  be  the  cause  of  persistent  hydro- 
nephrosis, with  secondary  pyelitis. 

The  discovery  of  floating  kidney  by  palpation  is  usually  easy.  The  physician 
examines  the  patient  lying  on  her  back,  applying  his  left  hand  on  the  right  lum- 
bar region  and  pressing  forward,  while  his  right  hand  presses  from  in  front  in  the 
opposite  direction.  It  is  then  often  possible,  especially  upon  deep  inspiration 
(vide  supra),  to  catch  the  kidney  between  both  hands,  and  so  form  an  opinion 
as  to  its  position  and  mobility. 


650  DISEASES    OF   THE   UKINAEY   OEGANS 

The  next  point  is  to  determine  whether,  in  any  particular  case,  the  symptoms 
which  may  be  present  are  actually  due  to  the  movable  kidney  which  has  been  dis- 
covered, or  whether  the  latter  is  an  unimportant  matter.  This  question  demands 
a  careful  and  complete  physical  examination  and  a  consideration  of  all  the  symp- 
toms. In  the  first  place,  we  should  determine  accurately  the  position  of  the  stom- 
ach (g-astroptosis,  etc.),  and  we  should  also  think  of  the  possibility  of  gall-stones, 
which  may  produce  a  very  similar  group  of  symptoms.  Gall-stones  are  especially 
apt  to  occur  in  women  with  corset  liver  and  enteroptosis,  and  this  explains  why  a 
movable  kidney  is  not  infrequently  found  in  cases  of  biliary  colic,  although  it 
has  nothing  to  do  with  the  attack. 

In  a  g-reat  majority  of  cases  of  "  floating-  kidney  "  we  have  to  do  with  those 
familiar  and  frequent  conditions  of  a  "  nervous  "  character  which  are  termed 
hysteria  or  neurasthenia.  Women  of  this  kind  suffer  very  frequently  from  all 
sorts  of  painful  sensations  in  the  abdomen,  and  from  dyspeptic  disturbances  and 
the  like,  and  of  course  we  very  often  find  in  them  a  movable  kidney.  In  such 
cases  the  abdominal  symptoms  are  also  of  a  nervous  character,  as  can  usually  be 
easily  determined  from  the  general  condition  of  the  patient,  from  her  psychical 
and  cerebral  symptoms,  and  the  indications  of  a  cardiac  neurosis,  and  also  from 
the  results  of  suggestive  ti'eatment.  Still,  a  certain  number  of  cases  may  be  very 
difiicult  of  diagnosis.  If  we  find  a  movable  kidney  in  a  nervous,  hysterical 
woman,  it  is  not  always  advisable  to  apprise  the  patient  of  the  fact,  for  with  a 
person  of  this  sort  the  mere  idea  of  possessing  a  "  floating  kidney  "  is  enough  to 
stir  up  a  host  of  subjective  symptoms.  On  the  other  hand,  it  may  be  said  that  the 
floating  kidney  may  serve  as  a  very  handy  instrument  for  suggestive  therapeutics. 
If  we  say  to  such  a  patient  that  her  annoyance  would  immediately  vanish  after 
the  application  of  a  suitable  bandage,  we  may  sometimes  attain  great  therapeutic 
success,  although  this  is  apt  to  be  but  temporary. 

Treatment. — If  we  deem  that  the  movable  kidney  requires  treatment,  the  first 
thing  to  recommend  is  the  wearing  of  a  suitable  support.  The  bandages,  with 
special  pads  and  the  like,  we  regard  as  usually  of  no  value,  while  a  good  elastic 
abdominal  bandage,  with  thigh-straps,  or  a  well-fitted  "  abdominal  corset,"  is 
sometimes  decidedly  efficient,  particularly  in  all  cases  of  general  enteroptosis. 
We  should  also  see  that  the  patient  is  properly  nourished.  If  she  is  emaciated, 
we  should  prescribe  rest  with  the  largest  possible  amount  of  food,  so-called  over- 
feeding. As  more  and  more  fat  is  deposited  in  the  abdomen,  the  abdominal  walls 
regain  their  tension  and  the  kidneys  receive  better  support.  It  is  also  advisable  to 
sponge  the  abdomen  with  cold  water  or  brandy. 

If  there  are  any  symptoms  of  strangulation,  we  should  of  course  put  the  patient 
to  bed  and  order  hot  poultices  and  opium.  We  may  also  make  a  cautious  attempt 
to  replace  the  organ.  If  severe  attacks  of  this  sort  recur,  the  possibility  of  surgical 
treatment  should  be  considered  (nephrorrhaphy  or  nephropexy).  In  a  fairly  large 
number  of  cases  the  patients  are  said  to  have  been  entirely  freed  of  their  discom- 
fort by  this  method. 


APPENDIX 


THE    DISEASES    OF    THE    SUPRA-IIENAL    CAPSULES    AND     ADDISOIST'S 
DISEASE    (BRONZED    SKIN) 

.ffitiology  and  Pathological  Anatomy. — In  the  year  1855  the  English  physi- 
cian Addison  published  for  the  first  time  a  list  of  cases  in  which,  besides  the  symp- 
toms of  a  general  bodily  weakness  and  ansemia,  a  peculiar  dark  pigmentation  of 


ADDISON'S   DISEASE  651 

the  skin  liad  gradually  developed.  Since  disease  of  the  supra-renal  capsule  was 
found  at  the  autopsy  in  all  cases,  Addison  concluded  that  this  was  the  immediate 
cause  oi  the  bronze  coloring  of  the  skin.  Observations  similar  to  Addison's  were 
soon  made  in  greater  numbers,  so  that  the  fact  itself  can  not  be  doubted ;  but  even 
at  present  nothing  definite  is  known  as  to  the  special  cause  of  the  disease  or  the 
true  nature  of  this  remarkable  connection  between  disease  of  the  supra-renal 
capsules  and  pigmentation  of  the  skin. 

Attempts  have  been  made  in  difterent  quarters  to  obtain  an  explanation  from 
experiments  on  animals.  Prom  these  it  has  appeared  that  the  complete  extirpa- 
tion of  both  adrenals  in  animals  usually  results,  after  a  short  time,  in  death,  but 
if  vestiges  of  the  adrenals,  or  if  so-called  accessory  adrenals  are  left  behind,  there 
is  no  unfavorable  result;  or,  if  any,  it  is  much  delayed.  The  symptoms  of  the 
extirpation  of  the  adrenals  consist  m  emaciation,  paretic  weakness  of  the  muscles, 
indigestion,  and  nervous  disturbance.  It  has  not  yet  been  possible  to  obtain  by 
experimental  methods  such  an  abnormal  pigmentation  of  the  skin  as  is  seen  in 
Aadison's  disease  (JSTothnagel  and  others).  Very  many  experiments  have  been 
made  with  regard  to  the  enect  of  extract  of  the  adrenal  gland;  it  affects  chiefly 
the  vaso-motor  system,  as  shown  by  the  increase  of  blood-pressure  and  slowing  of 
the  heart's  action.  The  results  thus  obtained  do  not  as  yet,  however,  justify  abso- 
lute conclusions.  Chemical  examination  of  the  gland  shows  an  abundance  of 
lecithine,  also  brenzcatechine,  and  a  substance,  sphyg-mogenine,  which  raises  the 
blood-pressure.  Most  investigators  are  at  present  inclined  to  the  opinion  that  the 
adrenals  have  the  task  of  destroying,  or  rendering  innocuous,  certain  poisons 
which  are  formed  in  the  body,  particularly  in  connection  with  muscular  activity. 
It  may  also  be  that  the  adrenal  gland  secretes  some  material  of  physiological 
importance.    We  are  as  yet  far  from  a  clear  understanding  of  the  matter. 

ihe  anatomical  lesions  found  in  man  up  to  the  present  time  are  not  calculated 
to  add  clearness  to  the  case,  since  they  seem  to  contradict  one  another  in  various 
points.  In  the  first  place,  some  observations  must  be  mentioned  in  which  the 
supra-renal  capsules  were  found  perfectly  normal  in  spite  of  an  existing  pigmen- 
tation of  the  skin.  Such  cases,  however,  prove  little,  since  it  of  course  can  not  be 
put  in  question  that  a  staining  of  the  skin  may  sometimes  develop  from  some 
other  reason  besides  disease  of  the  supra-renal  capsules.  On  the  other  hand,  it  has 
been  asserted  that  extensive  changes  are  sometimes  found  in  the  supra-renal  cap- 
sules on  autopsy  without  the  existence  of  the  symptom  of  bronzed  skin  during  the 
patient's  life;  but  these  cases  are  also  open  to  the  objection  that  the  disease  has 
perhaps  not  been  extensive  and  intense  enough  to  cause  the  bronze  coloring  of  the 
skin.  The  contradictions  just  mentioned,  however,  have  led  to  many  other  at- 
tempts at  an  explanation  of  Addison's  disease,  of  which  one  especially  deserves 
consideration.  According  to  this,  the  symptoms  met  with  are  produced  not  by  the 
disease  of  the  supra-renal  capsules  themselves  but  by  the  invasion  of  the  solar 
plexus  and  the  semilunar  ganglia  of  the  sympathetic  by  the  morbid  process  (Rise), 
Burger,  and  others).  According  to  this  theory,  the  symptoms  of  Addison's  disease 
may  arise  when  the  aforesaid  nervous  parts  are  diseased  independently,  or  by  the 
extension  of  a  pathological  process  from  some  other  neighboring  orgiin;  but 
pathological  anatomy  has  not  furnished  any  corroboratory  evidence  of  this  view. 
On  the  contrary,  the  more  recent  investigations  of  the  sympathetic  nervous  sys- 
tem in  Addison's  disease  have  had  ambiguous  results. 

Addison  himself  has  pointed  with  emphasis  to  the  fact  that  the  precise  form 
of  disease  in  the  supra-renal  capsules  is  by  no  means  always  the  same.  At  any 
rate,  the  disease  named  from  him  is  not  to  be  regarded  as  a  definite  anatomical 
afl'ection,  but  rather  as  a  particular  group  of  symptoms.  By  far  the  most  fre- 
quently it  is  tuberculosis  of  the  supra-renal  capsules  which  lies  at  the  bottom  of 
Addison's  disease.    The  capsules  then  are  either  enlarged  and  studded  with  case- 


652  DISEASES    OE   THE   UEINAEY   OEGAXS 

ous  tubercular  new  growths,  or  they  are  in  part  cicatricially  contracted.  Other 
tubercular  affections  are  almost  always  present  in  the  body  at  the  same  time,  espe- 
cially caseation  of  the  mesenteric  lymph-glands  and  pulmonary  tuberculosis. 
Other  morbid  processes  besides  tuberculosis  may  also  be  found  in  the  supra-renal 
capsules:  tumors  (adenoma  or  struma,  carcinoma,  sarcoma),  haemorrhage,  atro- 
phy, etc.  It  is  self-evident,  from  what  has  been  said  above,  that  in  every  case  we 
must  consider  some  implication  of  the  neighboring  sympathetic  ganglia,  by  com- 
pression, cicatricial  contraction,  or  chronic  inflammation.  Both  supra-renal  cap- 
sules are  almost  always  diseased  at  the  same  time,  rarely  only  one  is  affected. 

Of  the  lesions  in  other  organs  we  must  also  mention  that  Peyer's  patches  and 
the  solitary  follicles  of  the  intestine  are  as  a  rule  swollen.  The  spleen  is  some- 
what enlarged  in  some  cases,  but  not  in  others.  There  is  no  striking  pigmentation 
of  the  internal  organs.  The  changes  in  the  skin  and  in  certain  mucous  membranes 
will  be  mentioned  below. 

Considering  the  variety  of  the  anatomical  causes  there  can  be  no  question  of  a 
uniform  aetiology  of  the  disease.  Among  the  causal  factors,  those  most  frequently 
reported  are  defective  nutrition,  care  and  anxiety,  and  finally  injury  of  the  abdo- 
men. The  majority  of  cases  are  met  with  in  the  male  sex  and  in  middle  life. 
Addison's  disease,  however,  must  be  regarded  as  a  rare  affection,  of  which  but 
few  cases  are  observed  even  in  the  larger  cliniques. 

Symptomatology.- — The  purest  type  of  Addison's  disease  appears  in  those  cases 
where  the  symptoms  are  apparently  primary  in  their  development,  and  do  not 
come  on  in  the  course  of  some  other  disease,  such  as  phthisis  or  cancer. 

The  first  symptoms  of  the  disease  are  usually  of  a  general  nature,  and  are 
referable  to  a  gradually  increasing  anaemia  and  to  general  weakness  and  physical 
lassitude.  The  anaemia  shows  itself  objectively  through  the  pallor  of  the  skin 
and  the  diminution  in  the  number  of  red  blood-corpuscles,  but  without  other  defi- 
nite anomalies  of  the  blood  that  can  be  made  out.  Moreover,  there  are  a  number 
of  symptoms  which  depend  in  part  upon  the  cerebral  ansemia,  and  in  part  upon 
nervous  disturbance.  In  this  number  are  the  mental  torpor  and  lack  of  energy, 
the  headache  and  tendency  to  syncope,  and  the  tinnitus  aurium.  Sometimes 
there  are  marked  psychical  disturbances,  such  as  impairment  of  memory,  feeble- 
ness of  mind,  or  exaltation.  The  patient's  general  nutrition  often  suffers  very 
considerably;  but  it  must  be  added  that  in  Addison's  disease,  as  in  other  anaemias, 
the  fatty  layer,  especially  over  the  abdomen,  often  remains  remarkably  well  de- 
veloped. 

The  great  muscular  weakness,  asthenia,  of  the  patient  is  still  more  character- 
istic than  the  anaemia.  This  is  shown  less  in  inability  to  make  a  few  vigorous 
contractions  than  in  extremely  rapid  exhaustion  of  the  separate  muscles.  As  a 
consequence,  all  long-continued  muscular  exertion,  such  as  walking  for  any  length 
of  time,  standing,  continuous  labor,  becomes  absolutely  impossible. 

Beside  the  symptoms  which  have  been  enumerated  there  is  often  gastric  dis- 
turbance. The  appetite  is  poor,  and  there  is  very  often  vomiting.  The  latter  may 
sometimes  be  almost  uncontrollable,  and  then  it  is  one  of  the  most  distressing 
symptoms  of  the  disease.  It  is  usually  due  not  to  an  anatomical  change  in  the 
stomach,  but  probably  to  the  anemia  of  the  brain,  or  to  other  nervous  influences. 
Cardialgic  symptoms  are  also  frequent.  The  bowels  are  sluggish  as  a  rule,  but 
there  is  sometimes  diarrhea.  We  sometimes  hear  functional  murmurs  in  the 
heart,  but  as  a  rule  its  sounds  are  pure  though  feeble.  The  pulse  is  usually  mod- 
erately accelerated.  The  liver  and  spleen  do  not  show  any  special  changes.  Albu- 
minuria is  exceptional  and  depends  upon  complications,  such  as  amyloid  kidney; 
the  bodily  temperature  is  not  elevated,  and  not  infrequently,  indeed,  it  is  decid- 
edly subnormal. 

The  special  characteristic  symptom,  which  alone  renders  the  diagnosis  possible, 


ADDISON'S   DISEASE  653 

is  the  gradual  onset  of  a  peculiar  pigmentation  of  the  skin.  This  usually  shows 
itself  first  in  the  face  and  on  the  backs  of  the  hands,  and  also  in  those  parts  -which 
normally  present  a  greater  pigmentation  (the  areola  of  the  nipples,  the  axillae, 
and  the  genitals),  or  which  are  exposed  to  greater  pressure  by  the  clothing,  as 
the  hips  and  shoulders.  It  is  especially  noteworthy  that  dark  pigmented  spots 
and  stripes  usually  develop  on  the  mucous  membrane  of  the  lips,  particularly  at 
the  comers  of  the  mouth,  and  inside  the  cheeks.  The  intensity  of  the  coloring 
differs  in  different  cases.  It  usually  increases  as  the  general  condition  grows 
worse.  In  the  most  intense  cases  almost  the  whole  skin  may  become  dark  brown 
or  black,  like  that  of  a  mulatto  or  negro.  Sometimes,  however,  the  pigmentation 
remains  limited  to  separate  large  or  small  spots,  and  in  other  parts  of  the  skin 
there  may  then  be  even  a  marked  loss  of  pigment.  The  nails  and  the  sclera  always 
remain  white,  and  frequently  the  palms  of  the  hands  and  the  soles  of  the  feet  also. 
The  -hair  is  usually  not  changed.  The  pigmentation  of  the  skin  usually  increases 
during  the  whole  disease;  only  exceptionally  does  the  skin  become  light  again  in 
the  later  stages. 

The  real  cause  of  the  accumulation  of  pigment  in  the  skin  is  wholly  unknown. 
We  find  on  microscopic  examination  of  the  skin  that  the  pigment  lies  not  only 
in  the  cells  of  the  rete  Malpighii,  but  also  in  the  corium,  especially  along  its  blood- 
vessels. It  is  probably  formed  from  the  blood-pigment,  and  is  carried  by  wander- 
ing cells  from  the  cutis  into  the  epithelial  layers  of  the  skin  (Demieville,  jSToth- 
nagel). 

The  course  of  Addison's  disease  is  almost  always  chronic,  and  may  last  for 
years,  but  cases  have  been  described  with  a  rather  acute  course.  The  disease 
sometimes  begins  with  violent  initial  febrile  symptoms,  vomiting,  and  diarrhoea. 
The  disease  then  has  a  comparatively  rapid  termination  after  a  few  months,  or  a 
second  chronic  stage  may  follow  the  first  acute  one. 

The  final  termination  of  Addison's  disease  is  always  unfavorable.  Temporary 
remissions  are  often  observed,  but  the  disease  always  becomes  worse  again  after 
them.  Death  usually  ensues  gradually  amid  the  signs  of  increasing  general 
uragmia  and  weakness.  In  some  cases  severe  nervous  symptoms  also  come  on 
toward  the  end  of  the  disease — coma,  delirium,  or  epileptiform  attacks.  Condi- 
tions of  this  sort  may  develop  comparatively  suddenly  and  unexpectedly;  indeed, 
they  seem  to  support  the  hypothesis  of  toxic  influences  (vide  supra). 

Treatment. — Organo-therapy  has  been  repeatedly  tried  in  Addison's  disease, 
on  the  same  lines  as  the  treatment  of  diseases  of  the  thyroid  gland.  The 
adrenals  of  the  sheep  have  been  administered,  either  as  fresh  glands,  finely 
minced  and  eaten  with  bread,  or  as  an  extract,  or  in  the  form  of  tablets  of  the 
dried  glands.  In  some  cases  excellent  results  seem  to  have  been  obtained  in  this 
manner,  even  to  diminution  in  pigmentation,  but  in  many  other  cases  this  pre- 
scription has  no  beneficial  effect.  We  ourselves  administered  adrenal  tablets  in 
one  case  for  a  long  time  without  any  advantage.  Still,  it  would  be  proper  to  con- 
tinue these  trials.  Whether  treatment  with  Koch's  tuberculine  might  cause  per- 
manent benefit  in  those  cases  which  are  due  to  tuberculosis,  is  as  yet  doubtful. 
A  cautious  trial  might  be  made  under  proper  circumstances.  As  to  other  reme- 
dies, tonics  are  generally  employed — nourishing  food,  iron,  quinine,  and  arsenic ; 
iodide  of  potassium,  bromide  of  potassium,  and  electricity  have  also  been  tried. 
but  without  success.  Symptomatic  treatment  is  needed  for  the  vomiting,  diar- 
rhoea, and  nervous  attacks.  Experience  has  shown  that  great  caution  should  be 
exercised  in  prescribing  laxatives,  because  in  repeated  instances  such  remedies 
have  had  decidedly  luifavorable  results. 


654  DISEASES    OF   THE   UEINAEY   OEGANS 

SECTION  II 

Diseases  of  the  Pelvis  of  the  Kidney  and  of  the  Bladder 

CHAPTER   I 

INFLAMMATION    OF    THE    PELVIS    OF    THE    KIDNEY.     PYELITIS 

Etiology. — Isolated  primary  pyelitis  hardly  ever  occurs  as  an  independent 
disease.  Pyelitis  is  rather  in  most  cases  either  a  complication  or  a  result  of  other 
diseases,  and  in  such  cases  often  attracts  but  little  clinical  attention. 

We  sometimes  find  a  rather  moderate  pyelitis  in  the  bodies  of  persons  :who 
have  died  of  severe  areneral  infectious  diseases,  typhoid  fever,  sm.all-pox,  diph- 
theria, or  pysemia.  The  affection  depends,  in  all  probability,  upon  the  elimination 
by  the  kidneys  of  substances  that  excite  inflammation,  and  is  thus  to  be  regarded 
as  analogous  to  the  renal  changes  which  often  coexist.  Toxic  substances,  such  as 
cantharides  and  copaiba,  which  pass  through  the  kidneys,  may  also  cause  pyelitis 
as  well  as  other  disturbances. 

Pyelitis  very  often  arises  from  a  direct  extension  of  inflammation  from  the 
neighboring  organs.  In  many  cases  of  acute  and  chronic  nephritis  the  pelvis  of 
the  kidney  takes  part  in  the  inflammation  to  a  greater  or  less  degree;  but  an 
ascending  extension  of  the  inflammation  from  primary  diseases  of  the  urethra  or 
bladder  is  still  more  common.  Any  case  of  urethritis  or  cystitis  may,  if  it  lasts 
long,  advance  upward  to  the  ureters  and  the  pelvis  of  the  kidney,  so  that  in  severe 
cases  we  often  find  an  inflammation  of  the  whole  urinary  tract,  a  pyelo-cystitis, 
and  even  a  "  ureteritis."  It  has  been  already  mentioned  (page  640)  that  the  in- 
flammation may  extend  still  farther  to  the  kidneys  themselves  (pyelo-nephritis), 
and  we  shall  refer  to  this  repeatedly.  Of  all  these  varieties  of  ascending  inflam- 
mation in  the  urinary  passages,  none  is  so  frequent  or  of  so  great  practical  impor- 
tance as  that  which  results  from  persistent  narrowing  of  the  urethra  (stricture, 
hypertrophy  of  the  prostate),  and  the  consequent  obstruction  to  the  flow  of  urine. 
We  shall  revert  to  this  important  variety  when  discussing  hydronephrosis.  Very 
frequently  the  ascending  pyelitis  is  a  sequel  to  cystitis  in  disease  of  the  spinal 
cord,  with  paralysis  of  the  bladder. 

Another  form  of  pyelitis  is  that  caused  by  the  presence  of  foreign  bodies  in 
the  pelvis  of  the  kidneys — e.  g.,  calculous  pyelitis  due  to  the  mechanical  irritation 
of  renal  calculi.  This  also  will  have  a  special  consideration  below.  Much  less 
frequent  causes  are  retained  blood-clots,  parasites  {vide  supra),  and  genuine 
foreign  bodies. 

Primary  idiopathic  pyelitis,  as  a  result  of  catching  cold  or  similar  influences, 
is,  as  we  have  already  said,  of  extremely  infrequent  occurrence.  We  have  our- 
selves seen  a  few  cases  which  did  not  seem  to  be  capable  of  any  other  interpreta- 
tion, and  yet  we  must  strongly  emphasize  the  necessity  of  regarding  all  such  cases 
of  pyelitis  with  great  suspicion,  from  a  diagnostic  point  of  view.  It  is  only  too 
often  that  the  "  simple  "  pyelitis  will  prove  to  be  renal  tuberculosis,  or  an  inflam- 
mation due  to  calculi  or  other  causes.  The  pyelitis  coming  on  in  women  in  child- 
bed, or  following  different  sorts  of  diseases  of  the  sexual  organs,  may  in  all  cases 
be  referred  to  an  infection  of  the  pelvic  mucous  membrane  from  the  bladder  or 
from  the  kidneys. 

Pathological  Anatomy. — In  simple  catarrhal  inflammation  the  mucous  mem- 
brane of  the  pelvis  of  the  kidney  is  reddened,  swollen,  and  covered  with  an  abun- 
dant secretion,  which  contains  varying  amounts  of  pus-corpuscles  and  epithelium. 


INFLAMMATIOIT   OF   THE   PELTIS    OF   THE   KIDNEY        655 

In  severer  inflammations  we  often  find  quite  numerous  little  li?emorrliages  in  the 
mucous  membrane,  and  sometimes  little  gray  nodules,  which  correspond  to  the 
swollen  lymph-follicles. 

In  severe  cases,  which  are  seen  almost  solely  as  a  complication  of  a  more 
extensive  affection  of  the  urinary  passages,  such  as  pyelo-cystitis,  we  have  a  puru- 
lent, ulcerative  inflammation,  which  may  even  assume  a  diphtheritic  character. 
In  these  cases  the  kidneys  are  almost  always  coincidently  involved — pyelo-ne- 
phritis.  If  the  nephritic  abscesses  break  into  the  pelvis  of  the  kidney,  there  arises 
an  ulcerative  destruction  of  the  renal  tissue,  so  that  the  pelvis  of  the  kidney  is 
filled  with  pus  and  bounded  by  extensive  ulcers,  which  often  penetrate  deeply 
into  the  substance  of  the  kidney — pyonephrosis.  The  pyelo-nephritic  abscesses 
reaching  to  the  outer  surface  of  the  kidney,  and  usually  giving  a  striated  appear- 
ance to  a  section  of  the  organ,  have  already  been  described  (see  page  641),  and 
their  bacterial  origin  mentioned. 

The  condition  differs  when  the  kidney  is  involved,  as  in  many  cases  of  chronic 
pyelitis.  This  appears  most  frequently  as  a  result  of  retention  of  urine,  and  hence 
it  is  usually  associated  with  a  dilatation  of  the  pelvis  of  the  kidney.  In  these  cases 
we  sometimes  find  pronounced  processes  of  contraction  in  the  kidneys — that  is,  a 
partial  atrophy  of  the  renal  tissue,  increase  of  the  interstitial  connective  tissue, 
and  evident  cicatricial  depressions  on  the  surface — in  a  word,  a  secondary  con- 
tracted kidney,  arising  as  a  result  of  pyelitis,  which  differs  from  genuine  contrac- 
tion of  the  kidney  only  in  its  aetiology. 

Clinical  Symptoms. — Since  in  most  cases  pyelitis  develops  only  as  one  symp- 
tom of  a  more  extensive  morbid  process,  its  clinical  symptoms  are  usually  but 
slightly  prominent  in  the  general  course  of  the  illness.  In  what  follows,  there- 
fore, we  can  not  give  any  complete  description  of  the  clinical  course  of  pyelitis, 
but  we  must  mention  only  those  symptoms  from  which,  when  there  is  an  affection 
of  the  urinary  passages,  we  may  conclude 
that  the  pelvis  of  the  kidney  takes  part  in 
the  morbid  process. 

The  most  essential  sign  which  the  urine 
presents  in  all  inflammatory  affections  of  the 
urinary  passages,  the  presence  of  mucus  and 
pus,  will  be  described  more  fully  in  the  chap- 
ter on  cystitis  (vide  infra).    In  pyelitis,  also, 

^1  ;       ,  ,•  !•    j_i  1    •  Fig.  73.— Epithelium  from  the  pelvis  of  the 

the   muco-purulent   secretion   ot   the   pelvic  kidney, 

mucous  membrane  must  mix  with  the  urine, 

and  in  every  severe  purulent  inflammation  the  amount  of  pus  in  the  urine  must  be 
considerable.  We  can  never  decide  with  certainty,  from  the  mere  presence  of  pus 
in  the  urine,  as  to  the  place  where  the  pus  mixes  with  the  urine,  whether  in  the  pel- 
vis of  the  kidney  or  in  the  bladder,  or  even  in  the  urethra.  If  only  we  were  able  to 
demonstrate  other  morphological  elements  besides  the  pus-corpuscles,  so  charac- 
teristic that  their  origin  might  be  affirmed  with  certainty  to  be  the  pelvis  of  the 
kidney,  we  might,  by  means  of  them,  make  our  diagnosis  of  pyelitis  absolute.  Un- 
fortunately, however,  the  microscopic  sediment  of  the  urine  leaves  much  in  this 
regard  to  be  desired.  The  greatest  weight  was  formerly  ascribed  to  the  discovery 
of  pelvic  epithelium;  especially  the  triangular,  long-tailed  epithelial  cells,  some- 
times arranged  one  upon  the  other,  like  the  tiles  of  a  roof  (see  Fig.  73),  were  re- 
garded as  an  indication  that  the  pelvis  of  the  kidney  was  involved  in  the  inflam- 
mation; but  the  diagnostic  significance  of  these  cells  is  by  no  means  indubitable, 
for,  on  the  one  hand,  they  may  be  absent  in  a  severe  case  of  pyelitis;  and,  on  the 
other  hand,  precisely  similar  epithelium  comes  from  the  mucous  membrane 
of  the  bladder.  Greater  value  is  given  of  late  to  the  discovery  of  certain  casts 
from  the  mouths  of  the  urinary  canaliculi  (ductus  papillares) — structures  which 


656  DISEASES    OE   THE   UEIISTAEY   OKGANS 

are  almost  invariably  involved  in  all  but  the  milder  cases  of  pyelitis.  Tubuliform 
epithelial  casts,  cylindrical  formations  composed  of  pus-corpuscles,  and,  above  all, 
casts  composed  of  micrococci,  have  been  repeatedly  found  in  the  urinary  sediment 
in  cases  of  pyelitis,  and  possess  some  diagnostic  importance  (Eiirbringer  and 
others). 

With  regard  to  the  other  characteristics  of  the  urine,  it  should  be  mentioned 
that  it  is  often  remarkably  abundant  in  pyelitis,  and  that  it  then  of  course  is 
pale  and  has  a  comparatively  low  specific  gravity.  The  reaction  of  the  urine  is 
usually  acid,  despite  the  admixture  of  pus.  That  this  acid  reaction  is  an  effectual 
distinction  from  the  urine  of  cystitis  can  by  no  means  be  maintained  (vide  infra). 
We  may,  however,  say  that  the  tendency  of  the  urine  to  ammoniacal  fermentation 
is  decidedly  greater  in  cases  of  cystitis  than  in  cases  of  pyelitis.  The  amount  of 
albumen  in  the  urine  corresponds  to  the  amount  of  pus.  If  there  is  a  very  large 
aiQOunt  of  albumen,  it  arouses  suspicion  of  a  coincident  nephritis.  The  only  de- 
cisive proof  of  such  a  complication  lies  in  the  finding  of  genuine  urinary  casts. 
In  cases  of  simple  pyelitis  it  is  exceptional  for  the  urine  to  be  bloody,  while  in 
calculous  pyelitis  (q.  v.)  blood  is  often  present. 

Besides  the  quality  of  the  urine,  another  symptom  is  pain  in  the  region  of  the 
kidneys.  This  is  present  in  many  cases  of  pyelitis.  The  pain  is  often  very  severe, 
and  radiates  along  the  ureters  to  the  bladder.  In  some  cases,  however,  there  may 
be  no  pain  at  all,  so  that  while  its  presence  is  one  symptom  of  pyelitis,  its  absence 
does  not  weigh  against  the  disease. 

All  the  other  symptoms  may  be  directly  dependent  upon  the  pyelitis,  but  they 
may  usually  be  referred  in  great  degree  to  the  other  co-existing  affections.  Eirst 
among  these  is  fever,  which  either  shows  an  irregularly  remitting  course,  or  ap- 
pears in  single  high  elevations  of  temperature,  usually  associated  with  rigors. 
The  fever,  however,  seldom  shows  this  latter  pysemic  character  except  in  the 
severe  purulent  forms,  where  we  usually  also  have  the  formation  of  renal  abscesses 
— that  is,  a  pyelo-nephritis.  Besides  the  fever  there  are  often,  in  severe  cases, 
general  nervous  symptoms,  such  as  headache,  delirium,  and  sopor,  which  are  to  be 
referred  partly  to  the  general  pyasmic  infection  of  the  body  and  partly,  perhaps, 
to  the  absorption  of  ammonia  from  the  decomposing  urine  into  the  blood — the 
"  ammonisemia  "  of  Treitz  and  Jaksch. 

The  whole  course  of  pyelitis  differs  so  much  according  to  the  primary  disease 
present  that  nothing  of  general  application  can  be  said  about  it.  The  milder 
forms,  which  often  pass  off  rapidly,  are  found  most  commonly  in  childbed,  and 
sometimes  in  acute  infectious  diseases,  poisonings,  and  as  a  result  of  mild  cystitis. 
The  severe  forms  are  chiefly,  as  we  have  said,  pyelo-cystitis  and  pyelo-nephritis, 
as  a  result  of  strictures  of  the  urinary  tract  (vide  infra),  of  severe  cystitis  in  dis- 
eases of  the  spinal  cord,  and  in  other  severe  diseases  of  the  kidney  and  of  the  pel- 
vis of  the  kidney,  such  as  new  growths,  and  parasites.  They  usually  constitute  a 
very  tedious  and  incurable  affection,  which  lasts  until  the  patient's  death. 

The  important  factors  in  the  diagnosis  of  pyelitis  have  been  already  pointed 
out.  The  main  thing  in  every  case  is  a  careful  consideration  of  the  cause  and  the. 
course  of  the  disease,  and,  with  regard  to  the  special  involvement  of  the  pelvis  of 
the  kidney,  a  study  of  the  changes  in  the  urine,  and  the  local  symptoms  if  there 
be  any.  If  the  bladder  itself  is  unaffected  there  will  be  no  special  bladder  symp- 
toms, such  as  tenesmus  and  frequent  micturition.  If  there  is  severe  disease  of  the 
urinary  passages,  and  especially  if  the  patient  has  considerable  fever,  we  may 
often  be  justified  in  diagnosticating  pyelitis,  or  pyelo-nephritis,  even  when  there 
are  no  direct  indications,  because  experience  has  shown  that  such  an  extension  of 
the  disease  is  the  rule  in  all  severe  and  long-continued  cases. 

The  implication  of  the  kidneys  is  shown  by  the  presence  of  casts  in  the  urine 
in  addition  to  the  pus-corpuscles.     In  the  cases  above  mentioned,  in  which  a 


NEPHEOLITHIASIS  657 

chronic  pyelo-cystitis  is  complicated  with  a  contracted  kidney,  the  condition  of 
the  urine  is  the  same  in  many  respects  as  in  genuine  contracted  kidney.  It  is 
abundant,  usually  has  a  low  specific  gravity,  and  contains,  besides  the  pus-corpus- 
cles, a  few  short  hyaline  casts.  In  such  cases  there  may  be  developed  a  secondary 
hypertrophy  of  the  left  ventricle,  unless  the  general  nutrition  of  the  patient  is  too 
much  impaired. 

Treatment. — The  treatment  of  pyelitis  coincides  mainly  with  the  treatment  of 
the  primary  disease — for  example,  renal  calculi — and  therefore  it  needs  no  de- 
tailed description  here.  Ordinarily  only  the  accompanying  cystitis  (vide  infra) 
is  accessible  to  a  direct  local  treatment,  and  here  an  important  prophylactic  factor 
is  discovered,  since  by  a  timely  treatment  of  the  cystitis  we  can  certainly  hinder 
the  advance  of  the  inflammation  to  the  pelvis  of  the  kidney. 

Among  the  internal  remedies  to  which  we  ascribe  a  favorable  influence  on  the 
mucous  membrane  of  the  urinary  tract,  which  are  therefore  used  in  like  man- 
ner both  in  pyelitis  and  in  cystitis,  we  may  mention  the  astringents,  tannin, 
alum,  and  acetate  of  lead.  Their  therapeutic  effects,  however,  are  usually  very 
slight,  and  often  they  are  ill-borne,  so  that  certain  antiseptic  remedies  are  prefer- 
able, particularly  salol  in  capsules  of  eight  grains  (gramme  0.5)  three  to  five  times 
a  day ;  [urotropine,  ten  grains  three  times  a  day] ;  also,  camphoric  acid  and  chlo- 
rate of  potash.  Balsamic  remedies  are  sometimes  useful,  including  turpentine, 
sandalwood,  and  copaiba.  The  details  in  regard  to  all  these  remedies  will  be 
found  in  the  treatment  of  cystitis.  The  copious  ingestion  of  fluids  usually  acts 
favorably,  especially  the  use  of  certain  mineral  waters,  among  which  the  waters  of 
Carlsbad,  Vichy,  Ems,  Neuenahr,  and  Wildungen  have  obtained  the  most  reputa- 
tion. A  methodical  milk  cure  is  also  greatly  to  be  recommended,  especially  when 
there  are  symptoms  of  irritation,  such  as  pain  on  micturition. 

Local  applications  to  the  region  of  the  kidneys,  warm  poultices,  or  exception- 
ally local  blood-letting,  are  indicated  only  when  there  is  severe  pain,  and  then,  of 
course,  narcotics  must  also  be  used  under  some  circumstances.  In  this  respect 
warm  baths  also  do  good  service  at  times. 


CHAPTEE  11 


NEPHROLITHIASIS 

{Eenal  Calculus,     lienal  Gravel.     Pyelitis  Calculosa) 

Occurrence,  Chemical  Composition,  and  etiology  of  Renal  Concretions. — 
The  precipitated  concretions  of  the  urinary  constituents  which  form  in  the  pelvis 
of  the  kidney,  and  which,  under  some  circumstances,  may  be  passed  from  it  with 
the  urine,  are  designated,  according  to  their  size  and  nature,  as  renal  sand,  a  fine, 
pulverized  precipitate;  renal  gravel,  gravel-like,  granular  concretions  about  the 
size  of  the  ordinary  coarse  grains  of  sand,  which  can  usually  pass  through  the 
ureters  without  special  difficulty;  or  renal  calculi,  the  larger  concretions.  The 
last  are  about  the  size  of  a  millet  seed  or  a  pea,  but  larger  stones  are  occasionally 
seen  which  may  even  resemble  actual  casts  of  the  pelvis  of  the  kidney.  We  usually 
find  a  calculus  in  only  one  kidney,  although  both  kidneys  may  be  affected. 

In  regard  to  the  chemical  nature  of  renal  concretions,  they  consist  most  fre- 
quently of  uric  acid.  They  then  are  hard,  have  a  brown-red  or  blackish  color,  and 
a  crystalline  fracture,  which  in  large  stones  is  usually  plainly  laminated ;  and,  on 
the  whole,  a  smooth  although  irregularly-shaped  surface.  More  rarely  the  renal 
concretions  consist  of  calcic  oxalate.  The  oxalate  calculi  are  extremely  hard, 
42 


658  DISEASES    OF   THE   URINAET   ORGAINtS 

have  a  dark-brown  color  and  a  rougli  surface,  often  fumished  with  many  prickles, 
from  which  reason  they  are  often  called  "  mulberry  calculi."  Their  fracture 
sometimes  has  a  radiated  but  never  a  laminated  arrangement.  Stones  are  also 
frequently  seen,  which  consist  of  alternating-  layers  of  uric  acid  and  calcic  oxalate, 
or  which  have  a  nucleus  of  uric  acid  and  a  coating  of  calcic  oxalate.  The  phos- 
phatic  calculi  are  another  variety  of  renal  concretions.  We  only  rarely  have  to 
do,  however,  with  stones  which  consist  exclusively  of  basic  calcic  phosphate  or 
ammonio-magnesic  phosphate,  but  we  oftener  have  secondary  deposits  of  layers 
of  phosphate  which  are  precipitated  on  uric  acid  or  mulberry  calculi  in  urine 
which  has  become  alkaline.  The  pure  phosphatic  calculi  are  grayish-white  and 
rather  soft,  so  that  they  can  be  crushed  with  the  finger.  The  largest  specimens 
of  this  kind  are  not  found  usually  in  the  pelvis  of  the  kidney,  but  in  the  bladder ; 
still,  as  we  have  ourselves  observed,  large  and  pure  phosphatic  calculi  do  occur  in 
the  pelvis  of  the  kidney,  without  any  uric-acid  nucleus.  All  the  other  calculous 
formations  are  so  rare  that  they  scarcely  possess  clinical  interest.  We  may 
mention  the  light-yellow  cystine  calculi  with  a  surface  of  waxy  luster,  the  xanth- 
ine calculi,  and  the  indigo  calculi. 

As  to  the  precise  causes  of  all  these  concretions  we  have  as  yet  no  certain 
knowledge.  The  uric  acid  probably  originates  from  the  nucleines.  An  increase 
in  the  destruction  of  leucocytes  seems  to  be  associated  with  an  increased  excretion 
of  uric  acid.  The  formation  of  a  solid  deposit  of  uric  acid  is  usually  associated 
with  marked  acidity  of  the  urine.  Yet,  we  do  not  know  at  all  in  what  way  these 
circumstances  bring  about  the  development  of  renal  calculi.  There  is  much  prob- 
ability in  the  assumption  that  some  solid  substance  or  other  usually  forms  the  nu- 
cleus, and  gives  the  impulse  to  the  formation  of  at  least  the  larger  renal  calculi. 
Such  nuclei  may  be  coagulated  mucus,  bits  of  epithelium,  and  perhaps  bacteria. 
It  is  an  interesting  fact,  although  we  can  not  completely  explain  it,  that,  as 
Meckel,  Ebstein,  and  others  have  shown,  the  microscopic  examination  of  minute 
scales  of  calculi  disclose  the  crystalline  uric  acid  deposited  in  a  supporting  struc- 
ture of  an  albuminous  character.  With  regard  to  the  formation  of  oxalate  cal- 
culi, likewise,  we  possess  no  exact  knowledge.  Oxalic  acid  in  the  urine  probably 
is  due  in  part  to  the  oxalic  acid  which  is  introduced  into  the  system  in  vegetables, 
and  in  part  is  probably  "formed  from  the  decomposition  of  albuminous  substances. 
The  deposits  of  crystals  of  calcic  oxalate  from  acid  urine  is  well  known  to  be  a 
very  frequent  occurrence,  while  the  actual  formation  of  calculi  is,  as  has  been 
said,  comparatively  rare.  The  cause  of  the  deposit  of  phosphatic  concretions  must 
lie  in  the  urine  becoming  alkaline.  In  such  cases,  therefore,  the  development  of 
concretions  is  probably  preceded  by  disease  of  the  pelvis  of  the  kidney,  and  the 
ingress  of  bacteria  capable  of  exciting  an  allcaline  fermentation  of  the  urine. 

In  regard  to  the  predisposing  causes  of  calculus  formation  we  must  mention, 
first  of  all,  that  stones  are  often  found  in  children,  and  next  in  frequency  in  ad- 
vanced life.  Men  show  a  greater  disposition  to  renal  calculi  than  women.  He- 
redity also  seems  to  play  a  certain  part,  since  the  disease  has  been  repeatedly 
observed  in  different  members  of  the  same  family.  The  many  relations  which 
have  been  imagined  between  the  formation  of  calculi  and  certain  conditions  in 
the  manner  of  life  and  in  the  food  taken,  all  lack  definite  proof.  As  to  mode  of 
life,  the  chief  blame  is  laid  upon  an  excessive  meat-diet,  drinking  copiously  of 
new  sour  wines,  and  drinking  water  containing  lime.  It  is  remarkable  that  cal- 
culi are  much  more  frequent  in  some  countries  (England)  and  regions  than  in 
others.  In  regard  to  the  occurrence  of  uric-acid  concretions  in  gouty  patients, 
compare  the  chapter  on  gout. 

The  Anatomical  Changes  caused  by  Renal  Calculi. — The  usual  change  which 
the  presence  of  concretions  in  the  pelvis  of  the  kidney  excites  is  pyelitis.  This 
may  exhibit  all  degrees,  from  a  simple  catarrhal  inflammation  to  a  diphtheritic  or 


NEPHROLITHIASIS  659 

severe  purulent  inflammation  of  the  pelvic  mucous  membrane.     As  a  result  of 
the  mechanical  irritation,  there  are  quite  frequently  large  or  small  haemorrhages. 

If  a  severe  purulent  pyelitis  has  developed,  this  may  bring  with  it  all  the 
sequelae  with  which  we  have  previously  become  acquainted.  In  severe  cases  the 
process  may  involve  the  kidneys,  when  there  arises  a  pyelo-nephritis,  with  a  pui-u- 
lent  breaking  down  of  the  renal  tissue,  and,  under  some  circumstances,  even  a 
perinephritis,  with  extensive  suppuration  in  the  vicinity  of  the  kidney,  and  with 
occasional  perforation  into  the  neighboring  organs.  If  the  renal  calculi  have 
previously  passed  outward,  they  are  not  found  at  the  autopsy,  although  they  form 
the  special  starting  point  of  the  disease.  Sometimes,  however,  the  pus-cavity  is 
entirely  filled  with  calculi. 

A  second  important  sequel  of  a  renal  calculus,  which  sometimes  develops,  is 
hydronephrosis  {vide  infra).  It  arises  when  a  large  stone  blocks  the  passage  from 
the  pelvis  of  the  kidney  into  the  ureter,  or  when  a  smaller  stone  remains  fast 
in  the  ureter  and  completely  shuts  off  the  passage  of  the  urine.  In  the  latter  case 
there  may  also  arise  a  pressure  necrosis  and  perforation  of  the  ureter.  It  goes 
without  saying  that  inflammation  and  hydronephrosis  or  pyonephrosis  may  be 
combined. 

Clinical  Symptoms. — If  there  is  merely  the  formation  of  renal  sand  or  renal 
gravel  in  the  urinary  tract,  this  condition  is  sometimes  associated  with  no  symp- 
toms at  all.  The  little  granules  are  washed  away  by  the  urine  and  evacuated, 
and  at  most  they  may  give  rise  to  slight  pain  in  the  region  of  the  kidney. 
Larger  stones,  however,  may  sometimes  be  wholly,  or  almost  wholly,  without 
symptoms,  if  their  position  and  their  smooth  surface  are  such  that  they  are  com- 
paratively harmless. 

The  characteristic  clinical  symptoms  of  nephrolithiasis  do  not  appear  until  the 
results  of  mechanical  irritation  of  the  pelvis  of  the  kidney  arise,  or  until  there  is 
an  incarceration  of  a  calculus  in  the  ureter.  It  is  the  latter  circumstance  which, 
after  the  analogy  of  gall-stones,  causes  the  most  important  symptom  in  the  diag- 
nosis of  renal  calculi — the  pain,  the  so-called  renal  colic.  Such  an  attack  of  colic 
sometimes  comes  on  quite  suddenly  and  unexpectedly;  in  other  cases  it  is  pro- 
duced by  some  exciting  cause — ^jumping,  running,  walking,  or  riding.  The  pain 
often  becomes  frightful ;  it  radiates  from  the  lateral  portions  of  the  abdomen  along 
the  course  of  the  ureters  upward  and  downward,  spreading  particularly  toward  the 
bladder,  testicles,  and  thighs,  and  also  up  the  back.  In  severe  attacks  there  may 
be  a  general  state  of  collapse  with  a  small  rapid  pulse,  cold  sweat,  and  attacks  of 
fainting.  The  temperature  may  be  somewhat  raised.  We  often  see  nausea  and 
repeated  vomiting.  The  urine  is  often  scanty  but  sometimes  entirely  normal, 
inasmuch  as  it  comes  exclusively  from  the  other  free  kidney ;  but  oliguria,  or  even 
complete  anuria,  with  its  consequences,  invariably  sets  in  if  both  ureters  be 
stopped.  Still,  even  when  one  kidney  is  normal  the  amount  of  urine  secreted  by 
it  may  be  scanty,  as  a  result  of  a  reflex  inhibitory  influence  reaching  it  in  some 
unknown  way.  If  there  is  at  the  same  time  an  inflammatory  process,  the  urine 
may  contain  blood  and  pus.  The  'duration  of  renal  colic  depends  upon  the  dura- 
tion of  the  incarceration;  it  may  last  for  a  few  hours  or  several  days.  The  attack 
often  ends  with  the  passage  of  the  stone  outward  into  the  bladder. 

The  other  symptoms  occurring  in  nephrolithiasis  refer  mainly  to  the  results  of 
the  mechanical  irritation  of  the  pelvis  of  the  kidney.  In  most  of  the  severer  cases 
there  is  pain  in  the  region  of  the  kidneys,  which  is  persistent,  although  of  varying 
severity.  The  urine  then  shows  an  admixture  of  pus,  and  contains  pelvic  epithe- 
lium and  often  blood.  The  frequent  appearance  of  blood  in  the  urine,  which  usu- 
ally has  its  cause  in  purely  mechanical  lesions  of  the  mucous  membrane,  is  a  char- 
acteristic symptom  of  pyelitis  calculosa.  If  we  find,  as  sometimes  happens,  the 
urine  at  many  times  perfectly  clear  and  normal,  but  at  other  times  purulent,  we 


660  DISEASES    OE   THE   UKIi^ARY   ORGANS 

may  suspect  an  occasional  blocking  of  the  ureter  coming-  from  tlie  diseased  kidney 
by  a  renal  calculus. 

Tbe  symptoms  are  much  more  severe  if  the  trouble  goes  on  to  a  severe  purulent 
pyelitis  and  pyelo-nephritis.  We  need  not  describe  the  details  again  here — the 
pain,  fever,  swelling,  and  perforation  internally  or  externally — since  they  agree 
completely  with  what  has  been  said  before  (see  the  previous  chapter  and  Chapter 
VI  in  the  previous  section).  A  special  chapter  will  be  devoted  to  the  symptoma- 
tology of  hydronephrosis. 

The  course  of  nephrolithiasis  is,  as  a  rule,  very  tedious.  Since  the  disposition 
to  the  formation  of  calculi  usually  persists,  and  since  also  the  sequelae  which  have 
once  developed  may  last  for  a  long  time,  a  very  chronic  state  often  develops, 
which,  in  varying  ways  and  with  manifold  exacerbations  and  remissions,  is  com- 
posed of  attacks  of  colic,  haemorrhages,  and  symptoms  of  pyelo-cystitis. 

In  many  cases,  of  course,  complete  recovery  may  finally  ensue.  The  calculi 
present  are  passed,  new  ones  are  not  formed,  the  pyelitis  that  has  arisen  disappears, 
and  all  the  morbid  symptoms  cease;  but,  on  the  other  hand,  nephrolithiasis  has 
also  a  number  of  dangers  in  itself,  which  threaten  life  very  seriously.  These  are, 
besides  the  rare  occurrence  of  uraemia,  first  of  all  the  development  of  pyelo- 
nephritis and  of  still  more  extensive  suppurations,  with  a  general  decline  in 
strength,  pyaemic  states,  etc.  There  is  also  a  possible  danger  in  such  chronic 
suppurations  that  a  general  amyloid  degeneration  of  the  internal  organs  may 
ensue.  With  regard  to  complications  on  the  part  of  other  organs,  there  is  only 
one  point  of  special  interest — viz.,  that  sometimes  gall-stones  and  renal  calculi 
are  found  in  one  and  the  same  patient. 

Diagnosis. — Diagnosis  is  rendered  absolutely  certain  by  the  discovery  of 
renal  calculi  in  the  urine.  Eor  this  purpose  the  urine  must  be  examined  as  soon 
as  possible  after  its  evacuation,  and  the  best  method  is  by  pouring  it  through  a 
fine  sieve.  In  many  cases,  however,  we  can  make  a  tolerably  certain  diagnosis  of 
nephrolithiasis,  without  the  direct  demonstration  of  concretions,  by  means  of 
the  characteristic  clinical  symptoms,  particularly  the  periodical  renal  haemor- 
rhages, the  attacks  of  colic,  and  in  most  cases  the  early  appearance  of  pyelitis. 
If  these  symptoms  are  not  well  marked,  it  must  be  confessed  that  it  is  not  always 
easy  to  distinguish  renal  colic  from  intestinal  colic,  biliary  colic,  neuralgia,  or 
other  painful  abdominal  diseases.  It  is  possible  to  confound  the  condition  with 
renal  carcinoma  and  renal  echinococeus.  It  is  of  great  importance,  particularly 
with  regard  to  any  operative  treatment,  to  determine  which  kidney  is  the  seat  of 
the  trouble,  and  whether  one  kidney,  at  any  rate,  is  perfectly  healthy  or  not.  In 
considering  these  questions  we  must  be  guided  by  the  chief  seat  of  the  pain ;  the 
appearance  of  the  urine — for  instance,  observing  whether  there  is  an  increase  in 
the  amount  of  pus  if  pressure  is  made  upon  the  diseased  kidney,  and  whether 
from  time  to  time  normal  urine  is  evacuated  as  a  result  of  occlusion  of  the  ureter 
upon  the  diseased  side;  and  by  the  results  of  external  examination  with  regard 
to  tenderness,  or  the  discovery  of  a  tumor  due  to  hydronephrosis.  In  difficult 
cases  the  special  catheterization  of  each  ureter  is  sometimes  practiced.  Numer- 
ous methods  of  performing  this  have  been  devised,  some  of  them  involving  an 
incision  into  the  bladder,  and  cystoscopy  has  of  late  become  so  perfected  that  im- 
portant information  may  be  obtained  by  its  means.  With  regard  to  the  minutiae 
as  to  these,  methods  and  their  employment,  we  must  refer  the  reader  to  special 
monographs. 

In  a  few  cases  admirable  diagnostic  results  have  been  obtained  in  case  of  renal 
calculi  by  examination  with  the  Rontgen  rays.  It  appears,  however,  that  only  the 
phosphatic  calculi  can  be  recognized  in  this  manner,  while  the  concretions  of 
urates,  which  are  of  much  more  frequent  occurrence,  do  not  throw  any  distinct 
shadow. 


XEPHEOLITHIASIS  661 

Treatment. — Since  the  uric-acid  concretions  are  by  far  tlie  commonest,  tlie 
methods  of  treatraent  most  in  use  for  nephrolithiasis  refer  especially  to  these. 

If  the  tendency  to  the  formation  of  urinary  gravel  be  confirmed  in  a  patient,  or 
if  the  severer  s^onptoms  of  nephrolithiasis  have  already  appeared,  we  must  first 
give  a  number  of  general  dietetic  directions,  in  order  to  check  the  formation  of 
uric  acid  in  general,  and  promote  the  solution  of  the  uric  acid  already  formed  as 
far  as  possible.  "Without  entering  too  much  on  theoretical  reasoning,  we  will  give 
in  what  follows  the  measures  which  have  won  general  approval.  In  the  first  place, 
the  patient  must  avoid  immoderate  indulgence  in  any  sort  of  food,  and  particu- 
larly in  meat.  Articles  of  diet,  such  as  liver,  sweetbread,  and  calf's  kidneys,  which 
contain  an  abundance  of  nucleine,  should  be  forbidden.  The  patient  should  be 
advised  to  choose  a  chiefly  vegetable  diet,  with  milk  and  a  moderate  amount  of 
meat;  spirituous  beverages  are  to  be  used  little,  if  at  all,  and  acid  viands  and 
liquids  are  inadmissible.  It  is  advantageous  to  weigh  the  patient  regularly  in 
order  to  keep  watch  on  the  nutrition,  and  to  avoid  any  further  increase  of  weight 
in  such  individuals  as  are  well  nourished;  and  in  the  obese,  to  bring  about  a 
diminution  of  weight.  ilEoreover,  so  far  as  the  general  condition  of  the  patient 
allows,  he  should  have  regular  exercise  in  the  gymnasium,  or  at  sawing  wood,  or 
gardening.  He  should  also  promote  the  assimilation  of  his  food  by  the  frequent 
use  of  warm  baths  or  mud  baths ;  and  an  abundance  of  liquid  must  be  ingested,  so 
as  to  dilute  the  urine,  and  thus  increase  its  solvent  power. 

This  last  indication  is  usually  met,  in  conjunction  with  that  of  diminishing 
the  acid  reaction  of  the  urine,  by  the  ingestion  of  alkalies,  so  as  to  prevent,  as  far 
as  possible,  the  deposit  of  uric  acid;  consequently,  alkalies  and  alkaline  mineral 
waters  are  very  extensively  employed  in  nephrolithiasis.  Pfeiffer  and  others  h.'^.A'e 
been  able  to  demonstrate  by  direct  experiment  that  the  urine  secreted  after  the 
use  of  such  waters  and  drugs  does  possess  an  increased  power  to  dissolve  uric  acid. 
The  simplest  way  is  to  have  the  patient  use  phosphate  of  soda  in  a  daily  dose  of 
one  to  four  drachms  (grammes  5-15)  ;  or,  better,  carbonate  of  soda,  one  drachin 
to  two  drachms  and  a  half  (grammes  5-10)  ;  or,  finally,  the  specially  recommended 
carbonate  of  lithia,  two  to  eight  grains  (gramme  0.1-0.5),  several  times  a  day, 
dissolved  in  a  large  amount  of  simple  water  or  carbonated  water,  or  lemonade. 
Also,  mixtures  of  these  remedies  are  often  used  with  good  results;  thus  Cantani 
recommends  bicarbonate  of  soda,  eight  grains  (grammes  0.5) ;  effervescing  car- 
bonate of  lithia,  four  grains  (gramme  0.25)  ;  citrate  of  potash,  fifteen  grain? 
(gramme  1)  ;  also  the  so-called  uricedine,  which  is  composed  of  the  citrates  of 
sodium  and  lithium,  sulphate  of  sodium,  and  chloride  of  sodium.  Of  this,  fifteen 
grains  are  to  be  given  several  times  a  day.  Another  remedy  is  borocitrate  of  mag- 
nesium, of  which  a  teaspoonful  may  be  taken  in  soda-water  with  syrup,  three 
times  a  day.  Of  the  natural  mineral  waters,  the  results  of  experiment  point  out 
the  springs  of  Fachingen,  Vichy,  and  Vals  as  specially  efilcient,  but  good  results 
are  also  obtained  in  Carlsbad,  Salzbrunn,  Xeuenahr,  and  Wildungen.  The  natu- 
ral lithia  waters  of  Assmanshausen  and  Salzschlirf  contain  such  minute  amounts 
of  lithia  salts  that,  in  general,  the  artificial  waters  are  to  be  preferred  to  them. 

The  attempt  has  been  often  made  to  promote  the  solution  of  uric  acid  by 
administering  certain  chemical  substances,  but  unfortunately  the  results  have  not 
been  brilliant.  The  conditions  which  obtain  in  the  human  organism  are  esseii- 
tially  different  from  those  in  a  test-tube.  Piperazine,  fifteen  to  forty-five  grains 
(grammes  1-3)  daily,  has  been  much  recommended,  but  has  not  proved  at  all  efil- 
cient, and  the  same  may  be  said  of  lysidine,  fifteen  to  sixty  grains  (grammes  1^) 
a  day,  and  urotropino,  fifteen  to  twenty-five  grnins  (gramme  1-1.5)  daily,  in 
water.    Still,  further  trial  of  these  remedies  would  not  be  unjustifiable. 

The  symptomatic  treatment  is  very  important.  In  so  far  as  this  relates  to 
the  accompanying  pelvic  and  vesical  catarrh,  we  may  refer  to  the  appropriate 


662  DISEASES    OF   THE   UEIFAEY   OEGANS 

chapters  in  this  book.  For  renal  haemorrhages  some  internal  remedies,  such 
as  erg-otine  or  tannin,  have  been  recommended,  but  their  action  is  quite  doubtful. 
The  treatment  of  the  attacks  of  colic  is  of  great  practical  significance.  The 
chief  remedies  are  the  narcotics,  opium,  and  morphine,  internally,  or,  with  very- 
severe  pains,  better  subcutaneously.  In  severe  cases  chloral  and  inhalations  of 
chloroform  may  be  employed.  Warm  baths,  warm  poultices,  or  narcotic  em- 
brocations, such  as  chloroform  liniment,  also  frequently  give  relief.  Local  blood- 
letting is  only  rarely  indicated.  An  abundant  supply  of  fluid  is  always  advisable, 
in  order  to  aid  the  washing  out  of  the  incarcerated  stone  by  an  increased  secretion 
of  urine. 

Since  the  initiative  of  Simon  in  1871  the  operative  treatment  of  renal  disease 
has  made  continuous  progress,  and  it  has  been  eminently  successful  in  many  cases 
of  renal  calculi.  It  is,  therefore,  most  important  in  all  instances  of  nephrolithiasis 
with  severe  symptoms,  and  particularly  with  secondary  purulent  inflammation,  to 
consider  the  possibility  of  surgical  interference  by  nephrotomy  or  nephrectomy. 
Particulars  in  these  matters  must  be  sought  in  special  treatises  on  renal  surgery. 

What  has  been  said  thus  far  refers,  as  we  have  stated,  chiefly  to  the  treat- 
ment of  uric-acid  calculi.  If  there  are  calculi  made  up  of  oxalate,  the  amount 
of  vegetables  eaten  must  be  limited,  but  the  use  of  alkaline  waters  is  advisable. 
We  do  not  know  any  special  directions  to  give  in  case  there  Avere  cystine  calculi. 
On  the  other  hand,  when  phosphatic  stones  are  present,  inasmuch  as  these  can 
not  be  deposited  unless  the  urine  is  alkaline,  we  should  recommend  the  employ- 
ment of  acids,  particularly  lactic  acid,  eight  to  fifteen  grains  (gramme  0.5-1),  and 
salicylic  acid;  also,  hydrochloric  acid  and  phosphoric  acid.  Of  course,  in  most 
cases  there  is  some  disease  of  the  urinary  passages  which  has  occasioned  the  for- 
mation of  the  calculi,  and  if  such  disease  is  discovered  its  treatment  is  of  para- 
mount importance. 


CHAPTEE  III 
TUBERCULOSIS    OP    THE    GENITO-UBINARY    APPARATUS 

.ffitiology  and  Pathological  Anatomy. — It  does  not  seem  remarkable  that, 
with  the  presence  of  many  tubercular  processes  in  the  body,  tubercle  bacilli  should 
quite  easily  reach  the  kidneys  by  way  of  the  blood-current,  and  there  give  rise  to 
an  eruption  of  tubercle.  Accordingly,  we  quite  frequently  find  a  few  or  many 
miliary  tubercles  in  the  kidneys  in  acute  miliary  tuberculosis,  in  pulmonary  tuber- 
culosis, etc.,  which  are  distributed  over  the  whole  kidney,  or  sometimes  only  in  the 
territory  of  one  arterial  branch. 

While  miliary  tuberculosis  of  the  kidney,  however,  is  without  any  clinical  sig- 
nificance, there  is  also  an  extensive  local  tuberculosis  of  the  kidney,  as  well  as  of 
the  urinary  tract  and  the  sexual  org'ans.  Such  affections  sometimes  occur  as  a 
result  of  pronounced  pre-existing  tuberculosis  of  other  organs,  especially  the 
lungs,  or  they  arise  as  an  apparently  independent  disease,  which  is  termed  genito- 
urinary tuberculosis.  In  such  cases  the  infection  with  the  tubercle  bacilli  often 
seems  to  take  place  by  means  of  the  blood  from  some  previously  existing — perhaps 
concealed — tubercular  focus  in  the  body,  such  as  a  gland,  tubercular  bone  or  joint 
disease,  etc.  In  other  cases,  the  tubercle  bacilli  perhaps  enter  the  urinary  tract 
from  without,  but  the  point  of  the  first  anatomical  lesion  need  not,  apparently, 
always  be  the  same.  The  kidneys  often  seem  to  be  first  diseased,  in  other  cases 
the  bladder,  and  quite  frequently,  as  it  seems,  tbe  prostate,  and  sometimes  perhaps 
the  vesiculae  seminales  or  the  testicles.    From  the  organ  first  affected  the  process 


'        TUBEECULOSIS    OF   THE   GENITO-UKINAEY  APPAEATUS  663 

then  extends  continuously  or  by  leaps  to  the  neighboring  parts.  If  the  cases  come 
to  autopsy,  the  tuberculosis  is  often  so  extensive  that  we  can  no  longer  make  out 
Avith  certainty  the  place  where  it  first  began.  In  women  the  urinary  apparatus  is 
only  very  rarely  affected  by  tuberculosis,  while  uterine  and  ovarian  tuberculosis 
represents  a  localization  of  the  tubercular  poison  of  clinical  importance. 

In  the  kidneys  the  tubercular  infiltration  develops  either  chiefly  from  the  pel- 
vis of  the  kidney  or  in  the  renal  substance  itself.  Yellow  cheesy  nodules  arise, 
which  finally  break  down  and  thus  lead  to  an  actual  "  nephro-phthisis."  If  the 
disease  arise  from  the  pelvis,  the  infiltrated  renal  papilla  are  usually  first  affected. 
Ulcerative  recesses  are  formed  in  the  pelvis  of  the  kidney,  and  finally  the  entire 
lining  of  the  pelvis  is  transformed  into  a  raw  surface  covered  with  necrotic  tissue 
and  cheesy  detritus.  In  very  advanced  cases  almost  the  whole  kidney  is  destroyed. 
The  process  is  usually  bilateral,  but  it  is  often  more  advanced  on  one  side  than  on 
the  other. 

If  the  process  invade  the  ureters,  their  walls  also  are  infiltrated  with  tubercular 
deposits,  and  hence  they  are  thickened,  while  the  mucous  membrane  is  often 
changed  in  great  part  to  a  necrotic  ulcerating  surface.  Precisely  analogous  con- 
ditions are  found  in  the  bladder,  and  in  some  cases  even  in  the  urethra;  while 
in  the  prostate,  the  vesiculse  seminales,  and  the  testicles  there  is  more  frequently 
the  formation  of  cheesy  tubercular  nodules,  and  rarely  disintegration  and  per- 
foration. 

Clinical  Symptoms, — The  picture  of  genito-urinary  tuberculosis  corresponds 
in  most  of  its  details  completely  to  that  of  a  severe  chronic  pyelo-cystitis.  The 
occasional  local  symptom  is  pain  in  the  region  of  the  kidneys  and  bladder. 
This  may  sometimes  assume  great  severity,  like  colic,  if  the  ureter  become  plugged 
by  a  broken-down,  crumbling  mass;  yet  in  other  cases  the  pain  is  but  slight  during 
the  whole  disease. 

The  urine  shows  the  most  important  changes.  It  almost  invariably  contains 
an  abundant  sediment,  consisting  of  pus-corpuscles  and  detritus.  Its  amount 
usually  remains  normal  for  a  long  time ;  its  reaction  is  faintly  acid,  but  in  severe 
cases  it  may  become  alkaline  through  complication  with  an  alkaline  fermentation 
of  the  urine.  The  discovery  of  shreds  of  tissiie  in  the  urine,  elastic  fibers  and 
connective  tissue,  is  sometimes  possible,  and  is  of  diagnostic  value  because  it  is 
direct  evidence  of  an  ulcerative  process.  The  discovery  of  tubercle  bacilli  in  the 
purulent  urinary  sediment  (Eosenstein  and  others)  is,  however,  far  more  impor- 
tant. This  is  possible  in  almost  all  cases,  and  is  a  reliable  and  absolutely  decisive 
factor  in  diagnosis.  There  is,  however,  one  unfortunate  circumstance  about 
the  demonstration  of  tubercle  bacilli  in  the  urine,  for  not  infrequently  other  ba- 
cilli (smegma  bacilli)  are  stained  by  the  ordinary  method  of  staining,  which  is 
that  employed  for  sputum,  and  are  thus  mistaken  for  tubercle  bacilli.  As  yet, 
no  easy  and  certain  method  of  distinguishing  these  two  varieties  of  bacilli  has 
been  discovered,  and  hence  in  doubtful  cases  it  is  necessary  to  resort  to  pure  cul- 
tures and  to  inoculation,  in  order  to  reach  a  decision.  [Stain  with  carbol-fuch- 
sine;  decolorize  with  twenty  per  cent,  nitric  acid;  wash  in  water;  and  still 
further  decolorize  in  seventy  per  cent,  alcohol  for  at  least  ten  minutes.  This  will 
bleach  the  smegma  bacilli. — V.] 

Admixtures  of  blood  in  the  urine  are  also  seen  in  genito-urinary  tuberculosis, 
but  they  may  often  be  entirely  absent.  In  several  of  our  cases  a  slight  hsematuria 
was  the  first  symptom  which  called  the  patient's  attention  to  the  trouble  with  the 
bladder.  ' 

The  local  objective  examination  of  the  kidneys  usually  gives  a  negative  result. 
Only  in  a  few  cases  have  we  been  able  to  feel  the  diseased  kidney  as  a  tumor 
through  the  abdominal  walls.  This  is  usually  due  less  to  the  tubercular  infiltra- 
tion of  the  kidney  itself  than  to  the  dilatation  of  the  pelvis  of  the  kidney  from 


6Q4.  DISEASES    OF    THE   UEINAEY   OEGAl!^S 

hydronephrosis.  We  can  sometimes  feel  the  thickened  walls  of  the  bladder.  The 
local  examination  of  the  prostate  and  the  testicles  is  far  more  important  in  diag- 
nosis. Especially  in  the  latter  we  often  feel  the  hardening  corresponding  to  tho 
tubercular  infiltration,  and  manifesting  itself  chiefly  in  the  epididymis,  while  the 
hardening  and  enlargement  of  the  prostate  and  seminal  vesicles  can  usually  be 
easily  detected  by  rectal  palpation. 

Among  the  general  symptoms  we  must  mention,  first  of  all,  fever,  which  is 
only  exceptionally  absent,  and  usually,  in  the  severe  cases,  shows  a  pronounced 
remitting,  hectic  character.  The  other  general  symptoms  are  the  same  as  in  most 
of  the  other  tubercular  diseases — ana3mia,  emaciation,  loss  of  appetite,  increasing 
bodily  weakness,  etc.  We  have  a  special  sign  in  the  occasional  co-existence  of 
other  tubercular  diseases  in  the  body,  the  lungs,  the  intestines,  the  bones,  etc., 
but  these  may  also  be  wholly  absent,  so  that  we  may  have  to  do  with  a  purely  local 
genito-urinary  tuberculosis. 

The  course  of  the  disease  is  steadily  progressive.  Recovery  does  not  occur,  at 
least  not  in  any  cases  where  the  disease  has  attained  any  extent.  The  disease 
lasts  from  a  few  months  to  a  year  or  two,  but  sometimes  much  longer.  The  fatal 
termination  usually  ensues  from  the  increasing  general  weakness,  more  rarely 
under  the  symptoms  of  ammonisemia,  or  sometimes  from  a  miliary  tuberculosis 
or  some  other  tubercular  disease,  such  as  pulmonary  tuberculosis,  tubercular 
meningitis,  etc. 

Diagnosis. — The  diagnosis  of  genito-urinary  tuberculosis  is  now  seldom  diffi- 
cult in  fully  developed  cases,  since  it  can  be  made  with  complete  certainty  by  the 
discovery  of  the  tubercle  bacilli  joined  to  the  presence  of  pus  in  the  urine.  Of 
course  this  gives  no  information  as  to  the  exact  distribution  of  the  process.  In 
order  to  judge  of  this,  we  must  add  the  local  symptoms  and  the  physical  examina- 
tion of  the  different  organs.  We  are  aided  in  the  confirmation  of  our  first  sus- 
picion of  a  tubercular  disease  chiefly  by  the  consideration  of  the  general  condi- 
tion and  the  habit  of  the  patient ;  the  discovery  of  a  hereditary  taint,  or  at  least 
the  probability  of  tubercular  infection ;  and  also  the  discovery  of  other  tubercu- 
lar affections,  especially  in  the  testicles;  the  hectic  fever;  and  the  tedious 
course,  upon  which  nothing  has  a  favorable  influence.  At  any  rate  we  must 
make  it  a  rule,  in  every  case  of  persistent  pyuria  which  can  not  be  otherwise 
explained,  to  examine  the  purulent  sediment  for  tubercle  bacilli  {vide  supra). 
We  may  then  often  be  able  to  recognize  with  certainty  the  milder  and  incipient 
cases  of  this  not  very  rare  affection.  [Another  valuable  diagnostic  method,  briefly 
referred  to  by  the  author,  is  by  inoculation  of  eight  to  fifteen  minims  of  the 
urinary  sediment  into  the  peritoneal  cavity  of  a  guinea-pig.  If  tubercle  bacilli 
are  present,  the  animal  will  develop  tuberculosis  in  six  to  eight  weeks. — V.] 

Treatment. — Whether  specific  treatment  of  genito-urinary  tuberculosis  with 
Koch's  tuberculine  is  likely  to  have  permanent  success  can  not  yet  be  determined, 
as  so  few  trials  have  been  made.  ^Nevertheless,  it  would  be  justifiable  to  make  a 
cautious  trial  of  the  remedy,  although  we  can  hardly  cherish  the  hope  that  it 
would  prove  very  beneficial.  Beyond  this  we  must  resort,  in  the  treatment  of  tu- 
berculosis of  the  urinary  passages,  to  the  same  remedies  as  in  ordinary  chronic 
pyelitis  and  cystitis.  Of  internal  remedies  we  have  most  frequently  used  chlorate 
of  potassium  and  turpentine,  and  have  sometimes  seen  good  results,  especially  from 
the  latter.  The  internal  exhibition  of  creasote  sometimes  seems  to  us  to  act  well. 
[Urotropine  has  also  been  recommended. — V.]  In  vesical  tuberculosis  it  is  well 
to  wash  out  the  bladder.  As  an  operative  procedure  we  may  remove  tubercular 
testicles  and  epididymes  and  one  kidney,  but  we  must  remember  that  in  such 
cases  there  is  usually  co-existing  disease  of  other  parts  of  the  genito-urinary  appa- 
ratus, such  as  the  prostate,  the  other  kidney,  etc. 


HYDRONEPHROSIS  665 


CHAPTER   IV 

HYDRONEPHROSIS 

{Dilatation  of  the  Pelvis  of  the  Kidney) 

^tiolog'y. — If  a  contraction  arises  in  any  part  of  the  urinary  tract  and  checks 
the  flow  of  urine,  there  is  a  stasis  of  the  urine  in  the  portion  behind  the  stenosis, 
which  gradually  leads  to  a  constantly  increasing  dilatation  of  the  tract  as  a  result 
of  the  pressure  of  the  retained  fluid. 

In  general,  it  is  evident  that  gradual  constrictions  of  the  urinary  tract  and 
periodic  obstructions,  as  from  calculi,  interrupted  by  free  intervals,  lead  to  more 
marked  degrees  of  hydronephrosis  than  rapid  and  complete  obstructions.  Under 
the  first-named  circumstances  the  renal  secretion  persists  much  longer  and  is  more 
abundant  than  in  the  latter  case,  when  it  usually  soon  ceases.  Nevertheless,  there 
may  be  even  then  a  very  slow  distention  of  the  pelvis  of  the  kidney,  particularly 
if  its  mucous  membrane  continues  to  secrete.  If  the  obstruction  is  located  in  the 
ureter,  the  proximal  portion  of  that  canal  dilates,  and  still  more  the  pelvis  of  the 
kidney,  giving  rise  to  what  is  called  hydronephrosis;  but  if  the  obstruction  is 
located  in  the  urethra  there  is  a  gradual  dilatation  of  the  bladder,  both  ureters, 
and  finaly  there  develops  a  bilateral  hydronephrosis, 

A  closure  of  the  ureter  arises  most  frequently  in  adults  from  impacted  renal 
calculi,  and  also  from  new  growths  in  the  vicinity,  in  the  uterus  or  ovaries,  which 
compress  the  ureter  from  without.  So  great  a  pressure  may  also  be  exerted  on 
the  ureters  by  the  gravid  uterus  as  to  be  followed  by  a  hydronephrosis,  which 
is  usually  bilateral.  Cicatricial  strictures,  valve-formations  and  bends,  also  are 
found  in  the  ureter,  and  form  an  obstacle  to  the  flow  of  urine.  Finally,  in  can- 
cer of  the  bladder  the  lower  opening  of  the  ureter  may  be  contracted  or  entirely 
closed.  Constrictions  of  the  urethra,  which  finally  lead  to  a  bilateral  hydronephro- 
sis, arise  most  frequently  from  strictures  as  a  result  of  gonorrhoea,  and  also  from 
enlargements  of  the.  prostate.    In  rare  cases  phimosis  may  form  the  obstacle. 

It  is  worthy  of  note  that  hydronephrosis  may  also  be  congenital,  and  then  it  is 
usually  due  to  congenital  defects  of  development  in  the  ureters  or  other  urinary 
passages.  In  later  life  hydronephrosis  is  in  general  more  frequently  observed  in 
women  than  in  men. 

Pathological  Anatomy. — The  pathological  anatomy  of  hydronephrosis  is  on 
the  whole  very  simple.  We  have  a  dilatation  of  the  pelvis  of  the  kidney,  which 
is  associated  with  a  pressure  atrophy  of  the  renal  tissue.  The  papilla  are  flattened, 
the  uriniferous  tubules  and  the  glomeruli  are  gradually  more  and  more  obliter- 
ated, and  finally  the  whole  kidney  may  be  changed  to  a  connective-tissue  sac 
filled  with  fluid,  and  displaying  in  its  walls  a  few  vestiges  of  the  renal  paren- 
chyma. The  size  of  such  a  hydronephrotic  sac  may  sometimes  be  sufiicient  to  con- 
tain ten  or  fifteen  quarts  (litres)  of  fluid.  The  latter  consists,  of  course,  at  first 
of  urine,  but  the  farther  the  atrophy  of  the  kidney  advances,  the  more  it  merely 
represents  the  secretion  of  the  mucous  membrane.  Inflammatory  conditions 
are  found  in  hydronephrosis  only  when  they  have  existed  previously,  as  in  pyelitis 
calculosa,  or  when  excitants  of  inflammation  in  addition  have  reached  the  pelvis 
of  the  kidney.    We  then  have  a  pyonephrosis. 

Clinical  Symptoms. — Since  the  whole  type  of  the  disease  is,  of  course,  depend- 
ent in  many  respects  upon  the  nature  of  the  primary  disease,  we  have  here  to 
describe  only  those  symptoms  which  point  to  the  development  of  hydronephrosis. 
Such  a  condition  often  causes  no  special  clinical  symptoms  at  all,  so  that  we  can 
at  most  suspect  its  existence  from  the  prepenee  of  an  a^tiological  factor. 

The  appearance  of  a  visible  and  palpable  tumor  is  the  first  definite  point  in  the 


Q66  DISEASES    OF   THE   UKL^AET   OEGAl^S 

diagnosis  of  hydronephrosis.  This  first  shows  itself  in  the  region  of  the  affected 
kidney,  but  then  it  gradually  enlarges  toward  the  hypochondrium  and  the  median 
line  of  the  body,  and  it  may  finally  reach  very  considerable  dimensions.  Hydro- 
nephrosis on  the  left  side  does  not  usually  move  with  respiration.  On  the  right 
side,  however,  there  may  be  a  distinct  downward  motion  upon  deep  inspiration. 
The  resistance  of  the  hydronephrotic  tumor  is  usually  quite  considerable,  but 
there  may  sometimes  be  a  distinct  sense  of  fluctuation.  On  percussion,  the  tumor 
gives  a  dull  note,  from  which  the  tympanitic  note  of  the  colon  in  front  of  the 
tumor  is  sometimes  distinct  (see  page  645).  It  is  an  important  diagnostic  sign 
if  the  tumor  show  variations  in  its  size  at  times — decreasing  in  size  with  a  simul- 
taneous increase  in  diuresis,  and  increasing  again  when  the  amount  of  urine  be- 
comes smaller  ("intermittent  hydronephrosis").  In  such  cases  there  is  usually 
a  very  peculiar  alternation  in  the  other  clinical  symptoms.  At  the  time  of  the 
scanty  secretion  of  urine  the  patient  suffers  from  violent  pain,  vomiting,  chills, 
and  similar  symptoms,  while  upon  the  appearance  of  an  abundant  urinary  secre- 
tion, all  these  symptoms  quickly  vanish.  In  doubtful  cases  an  exploratory  punc- 
ture of  the  tumor  may  also  be  of  significance  in  diagnosis.  It  of  course  favors  the 
assumption  of  hydronephrosis  if  urinary  constituents,  especially  urea,  can  be 
found  in  the  fluid  evacuated ;  but  if  the  hydronephrosis  be  of  long  standing,  its 
contents,  as  we  have  said,  will  be  simply  sero-mucous,  and  then  chemical  examina- 
tion gives  no  definite  data  for  distinguishing  hydronephrosis  from  ovarian  tumors, 
or  other  cystic  tumors  of  the  kidney. 

The  secretion  of  urine  in  unilateral  hydronephrosis  may  be  completely  normal 
if  the  other  healthy  kidney  acts  vicariously.  In  stricture  of  the  urethra,  and  also 
in  bilateral  constrictions  of  the  ureters,  however,  there  is,  of  course,  an  obstacle 
to  the  passage  of  urine,  so  that  the  amount  of  urine  may  be  abnormally  small. 
There  may  be  at  times  complete  anuria,  and  even  ursemic  symptoms.  The  com- 
position of  the  urine  depends  entirely  upon  the  form  of  the  primary  disease.  If 
the  healthy  kidney  alone  secretes,  the  urine  passed  is  normal.  If  there  be  at  the 
same  times  pyelitis  or  cystitis,  the  urine  may  contain  pus  or  blood.  If  the  urine 
can  also  come  from  the  diseased  kidney  at  one  time  and  not  at  another,  the  urine 
also  exhibits  a  varying  composition,  as  we  have  said  before  (page  660). 

In  many  eases  of  hydronephrosis  quite  severe  local  symptoms  are  constantly 
present ;  there  are  frequently  severe  pains  in  the  tumor,  which  shoot  chiefly  toward 
the  thigh.  Still,  these  local  symptoms  are  sometimes  surprisingly  slight.  In  re- 
gard to  the  symptoms  on  the  part  of  other  organs,  gastric  disturbances  appear  t& 
be  of  the  most  frequent  occurrence;  among  them  are  nausea,  loss  of  appetite, 
vomiting,  and  eructations.  In  some  cases  the  bowels  are  constipated,  in  others 
there  is  obstinate  diarrhcea.  It  is  a  very  interesting  fact  that,  particularly  in  case 
of  bilateral  hydronephrosis,  there  may  be  developed  a  distinct  hypertrophy  of 
the  left  ventricle,  with  all  its  sequelae.  The  explanation  of  its  occurrence,  in  our 
opinion,  is  precisely  the  same  in  this  case  as  in  chronic  nephritis  (vide  supra,  page 
602) — viz.,  the  toxic  effect  of  the  urinary  constituents  retained  in  the  blood. 

The  whole  course  of  the  disease  is  always  chronic.  There  are  often  variations 
in  its  course,  but  no  general  statements  can  be  given,  because  the  conditions  vary 
in  the  different  cases  according  to  the  form  of  the  primary  disease.  Most  cases 
of  hydronephrosis  end  fatally,  either  in  consequence  of  the  primaiy  disease  or 
in  consequence  of  secondary  pyelonephritic  or  perinephritic  inflammations,  of 
uraemia,  etc.  Recovery  takes  place  in  rare  cases,  especially  if  one  kidney  be  per- 
fectly normal,  and  there  be  no  incurable  primary  disease.  Recovery  may  ensue 
spontaneously  from  perforation  or  obliteration,  or  it  may  be  brought  about  arti- 
ficially from  operative  procedures. 

In  the  diagnosis  of  hydronephrosis,  the  points  especially  to  be  considered  have 
already  been  mentioned.    The  diagnosis  is  usually  not  easy,  especially  if  the  seti- 


CYSTITIS  667 

ological  factors  be  unknown;  and  the  disease  is  often  confused  with  other  renal 
tumors  and  echinococci  of  the  kidneys,  with  ovarian  tumors,  and  even  with  splenic 
and  hepatic  tumors. 

Treatment. — Except  for  the  symptomatic  treatment  of  the  pain  and  any  ac- 
companying' pyelo-cystitis,  an  efficient  treatment  of  hydronephrosis  can  be  at- 
tempted only  by  surgical  means,  the  details  of  which  are  to  be  found  in  the  spe- 
cial surgical  treatises. 


CHAPTER   V 

CYSTITIS 

(  Vesical  Catarrh) 

.3!tiology. — ^In  most  cases  of  vesical  catarrh  the  agents  of  inflammation  reach 
the  bladder  from  without  through  the  urethra.  The  most  unequivocal  demonstra- 
tion in  this  regard  is,  unfortunately,  often  made  by  the  physician  himself,  when 
he  excites  a  cystitis  by  the  use  of  an  insufficiently  purified  and  disinfected  cath- 
eter or  bougie.  The  development  of  the  vesical  catarrh  is  generally  aided  in  such 
cases  by  the  fact  that  there  is  usually  a  defective  evacuation  of  urine,  from 
stricture  of  the  urethra  or  paralysis  of  the  detrusor,  with  a  consequent  reten- 
tion of  urine,  in  which  the  bacteria  can  develop  undisturbed.  The  agents  of 
inflammation  may  also  enter  from  the  urethra  into  the  bladder  in  incontinence 
of  urine.  On  account  of  the  imperfect  closure  of  the  sphincter,  a  stagnating 
column  of  urine,  directly  connected  with  the  contents  of  the  bladder,  forms  in  the 
urethra,  and  to  this  column  the  air  and  the  bacteria  that  excite  decomposition  of 
the  urine  have  direct  access.  In  this  way  many  cases  of  cystitis  arise  in  patients 
with  nervous  disease  who  have  paralysis  of  the  bladder,  and  also  many  cases  of 
cystitis  arise  in  this  way  in  persons  who  are  severely  ill  and  stupid  from  some 
other  disease,  such  as  typhoid  fever. 

Cystitis  often  follows  diseases  of  the  neighboring  portions  of  the  urinary  tr_Tct. 
Among  these,  gonorrhoeal  urethritis  is  the  most  common,  and  this  invades  the 
bladder  directly  and  leads  to  a  gonorrhoeal  cystitis.  In  this  case,  it  has  not  yet 
been  absolutely  determined  whether  the  gonococci  themselves  invade  the  bladder 
and  occasion  cystitis,  or  whether  the  inflammation  is  due  to  the  secondary  intro- 
duction and  dissemination  of  other  pyogenic  cocci,  such  as  staphylococci  {vide 
infra).  It  is,  moreover,  a  fact  of  great  importance  that  the  development  of  cys- 
titis is  decidedly  promoted  by  the  unskilful  employment  of  urethral  injections. 
In  women,  the  agents  of  inflammation  may  quite  easily  enter  the  bladder  from  the 
vagina  through  the  short  female  urethra.  Thus  arise  especially  the  frequent 
cases  of  cystitis  in  childbed.  In  some  cases  communication  may  develop  between 
the  bladder  and  certain  neighboring  organs,  as  in  vesico-rectal  or  vesico-vaginnl 
fistulse,  by  which  again  access  to  the  bladder  is  opened  to  the  agents  of  inflam- 
mation. 

Another  group  of  cases  is  due  to  the  presence  of  foreign  bodies,  which  irritate 
the  vesical  mucous  membrane  mechanically.  Among  these  is,  first  of  all,  the  cys- 
titis which  so  often  accompanies  stone  in  the  bladder.  It  must  be  stated,  however, 
that  probably  these  cases  of  vesical  catarrh  are  not  directly  dependent  upon  the 
calculi,  but  are  first  excited  by  examination  with  catheters  and  sounds,  and  in 
brief  are  due  to  secondary  infection. 

In  distinction  from  the  methods  of  origin  of  cystitis  so  far  described,  the  pro- 
duction of  inflammation  by  way  of  the  blood-supply  is  much  rarer.  Certain 
chemical  substances,  already  mentioned  (page  654),  which  are  eliminated  by  the 


668  DISEASES    OF    THE   UEINAEY   OEGANS 

kidneys  and  provoke  an  inflammation  of  the  tirinary  tract,  are  tlie  most  important 
in  this  respect.  Cantharides  shows  the  most  intense  action  of  this  sort,  and  it  may- 
cause  an  actual  croupous  cystitis.  Slight  irritative  states  of  the  bladder  also  fre- 
quently appear  after  taking  certain  foods  and  drinks,  as  after  drinking  new  beer. 
Infectious  substances  only  rarely  come  under  consideration  in  this  regard.  Most 
of  the  cases  of  cystitis  in  severe  acute  infectious  diseases  are  secondary  complica- 
tions due  to  germs  reaching  the  bladder  through  the  urethra  (vide  supra).  It 
can  not  be  doubted  that  in  some  cases  an  apparently  idiopathic  primary  cystitis 
appears  after  exposure  to  cold,  but  it  is  very  rare.  In  such  cases  we  usually  have 
to  do  with  acute  exacerbations  of  an  old  chronic  cystitis — ^for  example,  of  gonor- 
rhceal  origin. 

As  to  the  special  variety  of  inflammatory  germs  in  cystitis,  our  knowledge  is 
as  yet  incomplete.  In  many  cases,  particularly  in  the  cystitis  of  puerperal  women, 
the  germs  are  perhaps  the  ordinary  pyogenic  cocci  (streptococcus  and  staphylo- 
coccus pyogenes).  In  gonorrhoeal  cystitis  the  invasion  of  the  gonococcus  into 
the  bladder  has  been  absolutely  demonstrated  in  some  cases.  Moreover,  the  bac- 
terium coli  commune  seems  to  play  a  great  role  in  cystitis.  The  development  of 
ammoniacal  fermentation  of  the  urine  (vide  infra)  is,  nevertheless,  not  due  to 
the  bacterium  coli,  but  in  most  instances  to  special  micro-organisms  (formerly 
termed  by  Cohn  "micrococcus  urese  ")»  among  which  the  proteus  deserves  promi- 
nence. The  staphylococcus  pyogenes  also  has  the  power  of  exciting  ammoniacal 
fermentation. 

It  has  been  stated  in  the  previous  chapters  how  frequently  cystitis  is  only  one 
symptom  of  a  more  extensive  disease  of  the  urinary  tract.  As  cystitis  may  invade 
the  pelvis  of  the  kidney  through  the  ureters,  so,  on  the  other  hand,  any  pyelitis 
of  primary  origin  may  extend  downward  and  involve  the  bladder. 

Pathological  Anatomy. — The  pathological  anatomy  of  cystitis  presents  the 
same  conditions  as  the  inflammation  of  any  other  mucous  membrane.  In  simple 
catarrhal  cystitis  the  mucous  membrane  is  swollen  and  covered  with  pus,  and  is 
often  studded  with  haemorrhages.  In  chronic  cystitis  the  mucous  membrane  some- 
times takes  on  a  granulated  appearance,  because  of  the  swelling  of  numerous  fol- 
licles, and  in  other  cases  assumes  a  slaty,  grayish-black  color,  because  of  the  pig- 
mentation resulting  from  numerous  small  hemorrhages.  The  severer  forms  of 
cystitis,  such  as  are  often  observed  in  diseases  of  the  spinal  cord,  are  termed  vesi- 
cal diphtheria.  These  cases  come  to  a  necrotic  destruction  of  the  superficial  lay- 
ers of  the  mucous  membrane,  ulcerations,  etc.  In  such  severe  cases  submucous 
and  pericystitic  abscesses  sometimes  develop,  which  may  perforate  into  the  sur- 
rounding parts  in  various  ways.  The  incrustation  of  the  mucous  membrane  with 
urinary  salts,  especially  with  ammonio-magnesic  phosphate,  is  also  frequently 
found  in  chronic  cystitis,  and  is  worthy  of  mention.  .  If  the  disease  of  the  bladder 
is  associated  with  a  stricture  of  the  urethra,  the  bladder  is  usually  much  dilated, 
and  the  muscular  layer  is  hypertrophied  and  stands  out  in  ridges  on  the  inner  sur- 
face of  the  bladder. 

Clinical  Symptoms. — The  local  symptoms  are  sometimes  quite  severe  in  cys- 
titis, but  in  other  cases  they  are  only  slight.  In  general,  they  show  a  greater  in- 
tensity in  acute  cases  than  in  chronic  cystitis.  The  pain  in  the  region  of  the 
bladder  is  rarely  continuous ;  it  usually  occurs  only  on  micturition,  but  it  is 
often  very  distressing  then,  and  shoots  to  the  opening  of  the  urethra.  Since 
the  inflamed  vesical  mucous  membrane  shows  an  increased  irritability,  and  since 
the  morbidly  altered  urine  (vide  infra)  also  exerts  an  abnormal  irritation  on  the 
mucous  membrane,  there  is  very  often  an  increased  desire  to  micturate.  The 
patient  has  to  empty  the  bladder  much  oftener  than  normal,  and  in  severe  eases 
there  is  an  almost  constant,  painful  "  vesical  tenesmus,"  and  at  every  attempt 
to  micturate,  only  a  very  small  amount  of  urine  is  passed,  with  severe  burning. 


CYSTITIS 


669 


As  a  result  of  the  increased  irritability  of  the  vesical  mucous  membrane,  there 
sometimes  comes  on  a  very  troublesome  reflex  spasm  of  the  sphincter,  by  which 
the  symptoms  are  increased. 

The  character  of  the  urine  is  alone  decisive  in  the  diagnosis.  This  is  secreted 
in  a  perfectly  normal  amount  and  quality,  in  case  there  is  no  complication  on  the 
part  of  the  kidneys ;  but  in  the  bladder  it  is  mixed  with  the  products  of  the  dis- 
eased mucous  membrane,  and  it  is  here  exposed  to  the  action  of  the  bacteria  in  a 
way  that  will  presently  be  described.  The  abnormal  constituents  of  the  urine  are 
chiefly  pus-corpuscles,  bladder  epithelium,  and  mucus  secreted  by  the  mucous 
membrane.  As  a  rule,  the  urine  of  cystitis  contains  innumerable  bacteria,  under 
the  influence  of  which  develops  that  important  chemical  transformation  of  urea 
into  carbonate  of  ammonia,  which  is  characteristic  of  all  severe  cases  of  cystitis, 
and  which  has  been  termed  the  alkaline  (ammoniacal)  fermentation.  This  for- 
mation of  carbonate  of  ammonia  decidedly  aggravates  the  inflammation.  As 
Lepine  and  Roux  have  shown,  we  can  produce  a  severe  cystitis,  and  even  nephritis, 
by  injecting  very  small  amounts  of  a  pure  culture  of  micrococcus  urese  into  the 
bladder  of  a  guinea-pig.  The  stagnation  is  a  factor  which  greatly  aids  the  whole 
process,  since  the  activity  of  the  bacteria, 
as  we  have  said,  can  develop  much  better 
than  if  the  bladder  were  to  a  certain  de- 
gree constantly  purified  and  washed  out 
by  the  urine;  but  cystitis  can  not  be  pro- 
duced by  mere  retention  of  urine. 

As  soon  as  a  part  of  the  urea  is 
changed  to  carbonate  of  ammonia,  the 
urine  must  be  less  acid  in  reaction. 
The  urine  has  a  faintly  acid  or  neutral 
reaction,  and  sometimes  it  is  decidedly 
alkaline  when  passed.  The  latter,  how- 
ever, is  only  rarely  the  case,  but  it  is 
often  simulated  by  the  fact  that  the 
urine  is  not  examined  until  it  has  stood 
for  some  time.  Since  during  this  time 
the  alkaline  fermentation  makes  rapid 
progress,  the  urine  that  has  stood  is  very 
often    alkaline.      Many   crystals    of    am- 

monio-magnesic  phosphate  and  urate  of  ammonium  then  form  in  it ;  the  former 
are  easily  recognized  by  their  "  cofiin-lid  shape,"  and  the  latter  by  their  "  thorn- 
apple  shape"  (see  Fig.  74).     There  is  also  a  deposit  of  amorphous  phosphates. 

If  we  then  briefly  sum  up  what  has  been  said,  the  urine  is  passed  in  about 
the  normal  amount  in  cystitis.  It  usually  looks  pale,  and  has  an  abundant  sedi- 
ment, which  can  often  be  recognized  as  purulent  with  the  naked  eye,  and  in  which, 
microscopically,  we  can  find  pus-corpuscles,  often  bladder  epithelium,  and  con- 
stantly innumerable  bacteria — usually  short  rods  in  vigorous  motion.  The  alka- 
line fermentation  may  usually  be  recognized  by  the  strong  ammoniacal  odor,  and 
also,  as  we  have  said,  by  the  reaction  of  the  urine.  In  the  severe  diphtheritic 
forms  of  cystrtis  we  find  shreds  of  necrotic  tissue  in  the  urine.  If  there  are 
haemorrhages  in  the  bladder,  the  urine  often  contains  red  blood-corpuscles  and 
sometimes  even  large  blood-clots.  The  mucus  in  the  urine  appears  in  milder  cases 
as  a  cloudy  opacity — "  mihecida."  The  viscid  masses  which  can  be  drawn  out  into 
threads,  and  which  are  usually  abundant  in  the  urine  in  severe  cystitis,  and  some- 
times form  gelatinous  casts  corresponding  in  shape  to  the  bottom  of  the  vessel 
containing  the  urine,  are  not  mucine,  but  they  arise  from  the  pus-corpuscles  and 
the  epithelium,  changed  and  dissolved  in  the  alkaline  urine,  and  hence  give  the 


Fig.  74. 


Crystals  of  triple  phosphate  and  am- 
monic  urate.    (.From  Funke.) 


670  DISEASES    OF   THE   UEmARY   ORGAN'S 

reactions  for  albumen.  It  goes  without  saying  (compare  page  590)  that  cystitic 
urine  is  always  albuminous  from  its  mixture  with  pus-serum.  The  presence  of 
slimy  threads  in  the  urine — the  so-called  "^  clap-threads  "  {Tripperfdden) — is 
characteristic  of  gonorrhceal  cystitis. 

There  can  be  no  doubt  that,  as  already  stated,  the  decomposing  alkaline  urine 
acts  as  a  chemical  irritant  on  the  vesical  mvicous  membrane.  Hence  cystitis  often 
arises  perhaps^  in  this  way,  that  the  bacteria  which  have  entered  the  bladder  first 
excite  only  an  alkaline  fermentation,  and  that  then  the  mucous  membrane  is 
affected  by  the  irritation  of  the  ammonia  salts  that  are  formed.  Sometimes,  how- 
ever, the  mucous  membrane  endures  this  irritation  for  a  long  time,  and  this  ex- 
plains the  fact  that  alkaline  fermentation  may  be  observed  in  cases  which,  upon 
autopsy,  present  an  almost  normal  condition  of  the  vesical  mucous  membrane. 
In  addition  to  the  alkaline  fermentation  of  the  urine,  it  seems  probable  that 
many  other  processes  of  disorganization  may  develop  in  the  urine,  as  is  indicated 
by  the  various  sorts  of  bad  odors  which  the  urine  of  severe  cystitis  may  have. 
In  a  few  cases- there  is  even  a  formation  of  gas  (carbonic  dioxide,  nitrogen,  hydro- 
gen), giving  rise  to  pneumaturia.  This  indicates  the  development  of  special  bac- 
teria which  generate  gas.  If  the  patient  is  also  suffering  from  diabetes  mellitus, 
the  pneumaturia  may  be  due  to  the  fermentation  of  the  sugar  in  the  bladder. 

The  other  morbid  symptoms  associated  with  cystitis  usually  depend  only  in 
part  upon  the  disease  itself  and  in  part  upon  some  existing  primary  disease.  The 
most  important  symptom  is  the  fever,  which  is  often  to  be  referred  directly  to  the 
cystitis.  In  severe  cases  it  may  be  very  intense,  and  often  assumes  a  pysemic 
intermittent  character,  especially  if  there  have  arisen  pericystitic  suppurations  or 
if  the  cystitis  has  extended  to  the  pelvis  and  parenchyma  of  the  kidney  (see  page 
654).  An  acute  cystitis  also  may  begin  with  a  chill  and  high  fever.  If  the  escape 
of  the  purulent  urine,  however,  is  absolutely  free,  fever  may  be  entirely  absent  in 
spite  of  the  existence  of  cystitis. 

Sometimes  in  severe  cystitis  with  a  marked  alkaline  fermentation  certain  nerv- 
ous symptoms  appear,  such  as  headache,  vertigo,  stupor,  and  nausea.  The  idea  has 
been  advanced  tJiat  in  these  cases  we  have  to  do  with  an  auto-intoxication  of  the 
body,  since  ammonia  and  perhaps  other  products  of  decomposition,  such  as  sulphu- 
retted hydrogen  ( '0>  are  absorbed  from  the  bladder  into  the  blood  (ammonisemia), 
and  in  this  way  excite  the  symptoms  of  poisoning  mentioned. 

According  to  the  course  of  the  disease  we  distinguish  an  acute  and  a  chronic 
cystitis.  The  former,  which  may  come  on,  for  example,  after  catheterization,  in 
gonorrhoea,  etc.,  often  terminates  favorably  after  a  few  days  or  weeks.  The 
amount  of  mucus  and  pus  in  the  urine  is  never  great.  Chronic  cystitis  is  observed 
especially  as  a  complication  in  other  diseases  of  the  urinary  tract,  such  as  stric- 
ture, chronic  diseases  of  the  spinal  cord  with  paralysis  of  the  bladder,  etc.  It  is 
very  often  incurable  because  the  primary  disease  is  incapable  of  improvement  and 
the  cause  of  the  disease  therefore  persists.  The  longer  a  cystitis  lasts,  the  greater 
is  the  possibility  of  the  development  of  severe  and  dangerous  complications,  espe- 
cially the  development  of  a  pyelo-nephritis,  and  the  formation  of  pericystitic 
suppurations.  In  this  way  cystitis,  especially  in  chronic  nervous  diseases,  may 
become  the  immediate  cause  of  death. 

Treatment. — The  dangers  last  mentioned  must  urgently  impress  upon  us  the 
prophylaxis  of  cystitis,  i  ortunately,  a  good  deal  can  be  done  in  this  respect,  in 
the  first  place,  by  the  avoidance  of  all  unnecessary  use  of  bougies  and  catheters, 
by  the  greatest  care  for  cleanliness  in  the  use  of  all  instruments  of  this  sort,  and 
by  the  timely  treatment  of  all  those  conditions  which  may  lead  to  cystitis. 

The  treatment  of  cystitis  is,  in  the  milder  and  acute  cases,  hygienic  and  medic- 
inal, but  the  severer  cases  demand  careful  local  treatment. 

In  any  severe,  and  especially  in  any  acute  cystitis,  the  greatest  bodily  rest  (if 


CYSTITIS  671 

possible  rest  in  bed)  is  urgently  desirable,  since  otherwise  an  increase  of  the  symp- 
toms and  a  prolongation  of  the  course  of  the  disease  is  the  almost  inevitable 
result.  The  diet  must  be  mild  and  unirritating.  Spiced  food  and  alcoholic  drinks 
are  to  be  avoided,  but  we  should  recommend  an  abundant  supply  of  fluid,  by 
which  the  urine  is  diluted  and  the  bladder  washed  out.  We  have  the  patient 
drink  plenty  of  ordinary  water,  tea  (made  from  uva  ursi,  etc.),  or  a  suitable  min- 
eral-water, like  Wildunger  or  Fachinger.  A  diet  mainly  of  milk  is  very  good; 
under  it,  improvement  is  often  surprisingly  rapid. 

Among  internal  remedies  those  are  to  be  considered  which  are  eliminated  with 
the  urine,  and  are  thus  able  to  act  on  the  diseased  mucous  membrane,  or  directly 
upon  the  agents  of  inflammation  and  the  ammoniacal  fermentation.  One  of  the 
most  efficient  drugs,  which  never  does  harm  if  proper  caution  is  exercised,  is  chlo- 
rate of  potassium,  of  whose  favorable  influence  on  vesical  catarrh  we  have  often 
convinced  ourselves.  It  is  prescribed  in  an  aqueous  solution,  forty  to  seventy-five 
grains  a  day  (grammes  3-5),  and  it  should  never  be  taken  on  an  empty  stomach. 
Far  less  efficient  than  chlorate  of  potash  are  the  true  astringents,  such  as  tannin 
and  uva  ursi,  which  were  formerly  much  employed.  The  latter  drag  is  said  by 
Lewin  to  contain  a  glucoside,  arbutine,  which  is  itself  recommended  in  doses  of 
forty-five  to  sixty  grains  a  day  (grammes  3-4),  but  its  efficacy  is  doubtful.  Of 
metallic  astringents,  acetate  of  lead  in  powders  of  half  a  grain  to  a  grain  and  a 
half  (gramme  0.03-0.1),  repeated  several  times  a  day,  is  at  present  seldom  em- 
ployed. In  cases  with  a  decided  purulent  secretion,  if  the  initial  symptoms  of 
irritation  have  abated,  we  may  often  prescribe  with  good  results  resinous  drug-s, 
of  which  the  best  are  oil  of  turpentine,  in  capsules  or  in  milk,  or  balsam  of  copaiba. 
If,  on  the  other  hand,  the  ammoniacal  fermentation  is  more  prominent,  salicylic 
acid  in  daily  doses  of  thirty  to  sixty  grains  or  more  (grammes  2-4)  in  capsules, 
and  salol,  in  powders  of  eight  grains  (gramme  0.5),  repeated  several  times  a  day, 
are  specially  to  be  recommended;  naphthaline,  a  grain  and  a  half  to  five  grains 
(gramme  0.1-0.3),  repeated  several  times  a  day,  has  also  been  recommended,  but 
it  may  produce  decidedly  disagreeable  symptoms.  [In  the  same  class  with  the 
remedies  just  named,  but  far  superior  to  them,  is  urotropine,  which  may  be  given 
in  doses  of  ten  to  fifteen  grains  in  water,  after  meals. — V.] 

If  there  are  severe  local  symptoms,  we  prescribe  warm  compresses  and  poul- 
tices to  the  region  of  the  bladder.  In  robust  persons  with  acute  cystitis,  local 
blood-letting  (three  to  six  leeches  to  the  perineum)  sometimes  has  a  decidedly 
favorable  symptomatic  action  in  such  a  case.  In  other  respects  narcotics,  espe- 
cially subcutaneous  injections  of  morphine,  are  the  best  remedy  when  there  is 
severe  pain  and  tenesmus.  Camphor,  extract  of  belladonna,  etc.,  are  much  more 
uncertain  in  their  action.  The  frequent  use  of  protracted  warm  baths  may,  how- 
ever, be  greatly  recommended. 

In  chronic  cystitis  all  the  remedies  previously  mentioned  are  also  to  be  con- 
sidered ;  but  they  are  usually  not  sufficient  alone,  and  at  any  rate  they  are  far  less 
effective  than  a  methodical  local  treatment.  This  consists  in  a  regular  daily 
washing  of  the  bladder  by  means  of  an  elastic  catheter.  A  rather  long  rubber 
tube  is  attached  to  the  catheter  at  one  end,  and  to  a  funnel  at  the  other,  and  by 
raising  or  lowering  this  funnel  the  bladder  can  be  filled  or  emptied.  We  allow  a 
moderate  amount,  say  three  to  seven  ounces  (100  to  200  cubic  centimetres), 
of  the  warm  fluid  to  run  into  the  bladder  and  escape,  repeating  the  process 
until  the  wash-water  is  clean.  For  this,  perhaps  we  employ  either  a  simple 
one-half  to  one-per-cent.  solution  of  common  salt,  or  preferably  a  warm  and  weak 
solution  of  acetate  of  lead,  1  to  1,000;  permanganate  of  potash,  1  to  1,000;  or  a 
combination  of  boracic  and  salicylic  acids.  By  treatment  of  this  sort  many  cases 
of  chronic  vesical  catarrh  may  be  cured,  while  the  most  obstinate  may,  at  any  rate, 
be  kept  within  bounds.    In  rebellious  cases  of  purulent  cystitis  it  is  advantageous 


672  DISEASES    OF    THE   UEIAtAEY   0EGA:S'S 

to  employ  lunar  caustic.  The  bladder  is  rinsed  out,  and  then  about  five  ounces 
(grammes  150)  of  a  weak  solution  of  nitrate  of  silver,  at  first  1  to  3,000,  later  as 
strong-  as  1  to  1,000  or  1  to  500,  are  injected  through  a  catheter.  The  solution  is 
allowed  to  remain  two  or  three  minutes  in  the  bladder  and  then  withdrawn.  What 
is  called  the  Janet  method  of  irrigating  the  bladder  is  also  very  useful.  The 
fluid  is  placed  in  a  fountain  syringe,  and  made  to  enter  the  bladder  from  the 
urethra,  by  raising  the  reservoir  high  enough  to  give  a  pressure  which  overcomes 
the  sphincter  of  the  bladder.  The  advantage  of  this  method  lies  in  the  coincident 
dilatation  and  lavage  of  the  posterior  portion  of  the  urethra. 

It  is  very  important,  in  treating  chronic  catarrh  of  the  bladder,  to  consider 
the  possible  cause  of  the  condition — for  instance,  stricture,  or  vesical  calculi,  or 
paralysis  of  the  bladder. 

In  pericystitic  suppuration  surgical  treatment  is  only  rarely  possible.  We 
■must,  therefore,  confine  ourselves  to  purely  symptomatic  procedures. 


CHAPTEE  YI 
NEW    GROWTHS    IN"    THE    BLADDER 

1.  Cancer  of  the  Bladder. — Primary  carcinoma  of  the  bladder  is  rare.  It 
forms  localized  tumors,  sometimes  with  a  pedicle ;  or  it  extends  diffusely  over  the 
wall  of  the  bladder,  and  in  that  case  leads  to  such  thickening  that  the  bladder  can 
sometimes  be  felt  through  the  abdominal  walls  as  a  firm  tumor.  Secondary  car- 
cinoma of  the  bladder  is  not  infrequently  due  to  direct  involvement  by  extension 
from  neighboring  parts,  such  as  the  uterus,  prostate,  or  rectum. 

The  early  symptoms  of  primary  cancer  of  the  bladder  consist  of  disturbances 
of  micturition,  which  are  often  difficult  to  explain.  Usually  the  first  indication 
of  the  special  local  disease  consists  of  a  change  in  the  character  of  the  urine,  which 
is  probably  coincident  with  the  beginning  of  ulceration  in  the  tumor.  Then  the 
complete  picture  of  severe  chronic  cystitis  is  rapidly  developed,  a  particularly 
characteristic  symptom  being  the  frequent,  though  irregular,  appearance  of  blood 
in  the  urine.  The  condition  becomes  most  distressing  if  the  vesical  termination 
of  the  urethra  is  occluded  by  the  new  growth.  In  the  cases  which  we  have  seen, 
cancerous  cachexia  did  not  develop  until  rather  late.  One  case  was  in  the  person 
of  a  quite  young  man.  In  general,  the  entire  course  of  the  disease  seldom  occu- 
pies more  than  one  or  two  years. 

The  diagnosis  of  vesical  cancer  is  not  always  easy,  particularly  at  first.  The 
main  point  is,  that  when  there  is  a  chronic  disease  of  the  bladder  and  no  other 
sufficient  reason  for  it  is  discovered,  we  should  think  of  the  possibility  of  tuber- 
culosis or  cancer,  and  make  a  careful  examination  with  these  severe  conditions  in 
mind.  It  is  sometimes  possible  to  confirm  the  diagnosis  by  finding  bits  of  the 
tumor  in  the  urine,  but  this  is  not  invariably  possible ;  consequently  a  number  of 
methods  have  been  elaborated  to  facilitate  early  recognition  of  vesical  tumors  by 
means  of  a  direct  and  careful  examination  of  the  bladder — thus  we  have :  cystos- 
copy (ISTitze) ;  exploratory  cystotomy ;  and  in  women  dilatation  of  the  urethra 
and  digital  examination  of  the  bladder.  Particulars  with  regard  to  these  pro- 
cedures and  their  value  are  to  be  found  in  monographs,  and  in  them  the  reader 
can  also  inform  himself  as  to  the  results  of  the  attempts  which  have  thus  far  been 
made  to  remove  vesical  tumors  by  operation. 

2.  Papilloma  of  the  bladder  is  usually  a  very  soft  fibroma,  which  is  located  in 
the  trigonum  or  fundus  and  has  delicate  waving  papillae,  which  are  covered  with 


EmJEESIS    NOCTUENA  673 

several:  layers  of  cylindrical  epithelium.  The  local  discomfort  which  this  not 
very  rare  form  of  tumor  occasions  is  often  slight,  but  the  haemorrhage  it  causes 
may  be  very  important,  being  chronic  and  obstinate;  for  months  and  years  the 
ligematuria  may  be  more  or  less  continuous.  The  clotted  blood  as  it  passes  through 
the  urethra  often  assumes  the  shape  of  a  worm.  There  is  not  much  disturbance  of 
micturition  unless  portions  of  the  tumor  obstruct  the  inner  end  of  the  urethra. 
Any  one  who  has  had  the  experience  which  we  have  had  of  seeing  an  otherwise 
liealthy  and  vigorous  man  die  because  of  persistent  haemorrhage  from  a  papilloma 
hardly  as  big  as  a  walnut,  can  not  insist  enough  upon  the  value  of  an  early  and 
■certain  diagnosis  (reached  by  examining  portions  of  the  tumor,  or,  still  better,  by 
■cystoscopy)  and  of  surgical  treatment. 


CHAPTEE   VII 

ENURESIS    NOCTURNA 

(^Nocturnal  Incontinence  of  Crine) 

Enuresis  noctuma  is  a  nervous  affection  of  the  bladder  by  no  means  rare  in 
•children  of  both  sexes,  and  therefore  quite  important  in  its  practical  relations. 
Of  course,  in  small  children  there  is  no  shai-p  boundary  to  be  drawn  between 
normal  and  pathological  conditions ;  but  it  is  decidedly  pathological  if  larger  chil- 
■dren,  from  four  to  ten  years  of  age  and  even  older,  pass  their  urine  in  bed  more 
or  less  frequently  during  sleep,  in  spite  of  well-developed  reasoning  powers  and 
professedly  the  best  intentions.  This  may  extend  to  the  years  of  puberty  and  even 
beyond,  and  then  it  frequently  produces  a  very  depressing  mental  influence  upon 
the  patient.  Special  causes  for  it  are  not  to  be  discovered  in  most  cases.  We  are 
■compelled  to  assume  either  an  abnormal  weakness  of  the  sphincter,  which  is  prob- 
ably sometimes  congenital,  or  an  abnormal  irritability  of  the  detrusor.  Some- 
times, but  not  invariably,  the  child  has  a  neurotic  constitution.  At  any  rate,  in 
wetting  the  bed  at  night  the  process  of  micturition  comes  on  in  a  purely  reflex 
way,  but  it  is  often  accompanied  by  certain  ideas  in  dreams  referable  to  micturi- 
tion. It  does  not  hold  in  all  cases  that  the  sleep  is  especially  deep.  Many  patients, 
of  course,  do  not  notice  the  mishap  till  morning,  but  others  almost  always  wake 
•directly  after.  The  involuntary  micturition  usually  occurs  in  the  first  hours  after 
going  to  sleep,  but  sometimes  it  is  later,  and  even  toward  morning.  By  day  mic- 
turition is  often  perfectly  normal ;  but  in  many  cases  there  is  even  then  a  notice- 
able weakness  of  the  bladder,  so  that  the  child  has  to  make  water  oftener  than 
usual,  and  sometimes  even  wets  its  clothes. 

Although,  as  we  have  said,  we  can  usually  find  no  special  cause  for  the  trouble, 
still,  in  some  cases,  certain  morbid  changes  in  the  urinary  organs  may  give  rise  to 
the  incontinence.  We  should,  therefore,  in  every  case  at  least  think  of  the  pos- 
sibility of  stone  in  the  bladder,  of  congenital  phimosis  and  adhesions  of  the  pre- 
puce to  the  glans  penis,  of  ascarides,  of  inflammatory  conditions,  and  foreign 
bodies  in  the  vagina,  and  make  a  special  examination  into  these  points.  We  must 
also  bear  in  mind  polyuria  caused  by  diabetes  or  renal  disease,  and  finally,  of 
•course,  in  the  diagnosis  of  a  purely  nervous  nocturnal  incontinence  of  urine,  we 
must  exclude  the  existence  of  any  actual  anatomical  spinal  affection. 

In  all  the  cases  just  mentioned,  the  treatment  must  be  directed  first  to  the 

primary  disease;  but  in  the  ordinary  nocturnal  incontinence  the  treatment  must 

be  aimed  at  the  symptom  of  nocturnal  micturition  as  far  as  possible.     The  child 

must  take  only  a  very  little  fluid  in  the  evening,  and  he  should  be  made  to  empty 

43 


674:  DISEASES    OF    THE  TJErN"AEY   OEGA^ts 

his  bladder  immediately  before  going  to  sleep,  and  perhaps  once  again  later.  He 
should  not  be  covered  up  too  warmly,  and,  if  possible,  he  should  not  lie  on  his  back 
during  sleep.  Tying  a  brush  to  the  back  is  therefore  a  well-known  domestic  rem- 
edy. It  is  strongly  recommended  that  the  child  should  be  made  to  lie  in  bed,  with 
the  hips  elevated  and  the  head  low.  A  somewhat  strict  mental  treatment  is  often 
effective,  since  thus  the  attention  to  the  process  is  increased,  although  uncon- 
sciously, and  the  child  often  learns  to  wake  up  at  the  right  time.  We  have  seen 
many  cases  of  enuresis,  which  did  not  recover  when  treated  at  home,  get  well 
quite  rapidly  when  the  children  were  isolated  in  the  hospital.  The  employment 
of  the  rod  is  rarely  allowable ;  on  the  other  hand,  we  often  must  shield  the  child 
from  injudicious  parents. 

Internal  remedies,  such  as  belladonna  and  tincture  of  nus  vomica,  were  for- 
merly recommended,  but  they  seldom  do  good.  Lately  the  tincture  of  rhus  aro- 
matica  has  been  employed  again ;  of  this,  fifteen  drops  are  given  in  the  afternoon 
and  in  the  evening  before  going  to  bed.  In  ansemic  children  preparations  of  iron 
are  indicated.  It  is  often  useful  to  employ  electricity,  although  it  may  be  that  the 
only  influence  it  has  is  psychical.  We  put  the  broad  anode  over  the  lumbar  cord,. 
and  the  smaller  kathode  over  the  region  of  the  bladder  or  on  the  perineum,  and 
let  quite  a  strong  constant  current  pass  through  for  two  or  three  minutes.  The 
current  may  also  be  interrupted  and  closed  a  few  times.  Then  we  pass  the  wire 
end  of  one  conducting  cord,  which  we  make  the  kathode,  into  the  mouth  of  the 
urethra  for  one  or  two  centimetres,  while  we  place  the  other  broad  electrode  on  the 
perineum  or  above  the  symphysis,  and  let  quite  a  strong  and  somewhat  painful 
faradic  current  act  for  one  or  two  minues  (Seeligmiiller).  The  sittings  must  at 
first  be  repeated  daily.  It  is  also  a  very  good  plan  to  let  the  whole  body  be  well 
rubbed  with  cold  water  before  going  to  sleep.  It  is  said  that  in  obstinate  cases 
the  introduction  of  large  bougies  and  the  consequent  distention  of  the  posterior 
portion  of  the  urethra  are  often  attended  with  rapid  improvement. 

Even  in  cases  in  which,  despite  careful  treatment,  no  permanent  success  is 
attained,  we  have  this  consolation  with  regard  to  the  prognosis,  that  in  simple 
enuresis  the  abnormal  condition  usually  undergoes  gradual  and  spontaneous  im- 
provement as  the  patient  grows  older. 

[Belladonna,  strychnia,  or  nux  vomica,  or  a  combination  of  the  two,  are  often 
of  unquestionable  service.  If  the  enuresis  is  only  nocturnal,  belladonna  alone 
may  be  used,  either  in  a  single  dose  at  bedtime  or  three  times  a  day.  If  the 
enuresis  is  diurnal  also,  the  two  drugs  should  be  combined  and  given  three  or  four- 
times  a  day.] 


DISEASES   OF    THE   ORGANS   OF   LOCOMOTION 


CHAPTEE   I 
ACUTE    ARTICITLAIl    RHEUMATISM 

Etiology. — Acute  articular  rheumatism  is  an  infectious  disease.  This  is 
shown  by  all  its  clinical  and  anatomical  characteristics,  and  although  we  are  not 
yet  definitely  acquainted  with  the  specific  organized  poison  which  gives  rise  to  it 
(vide  infra),  still,  it  is  impossible  to  come  to  a  correct  understanding  of  the  symp- 
toms and  the  course  of  the  disease,  unless  we  assume  that  it  is  caused  by  an  infec- 
tious germ. 

Like  many  other  infectious  diseases,  acute  articular  rheumatism  is  often  indis- 
putably endemic  and  epidemic.  According  to  Hirsch,  the  disease  is  most  preva- 
lent in  the  temperate  zones,  being  much  rarer  in  cold  and  tropical  latitudes ;  but 
even  in  Europe  it  is  by  no  means  uniform  in  its  frequency,  and  certain  districts  of 
England,  Belgium,  and  Russia  are  said  to  be  almost  exempt  from  it.  It  is  also 
possible  to  observe  epidemic  influences  with  regard  to  the  frequency  of  its  appear- 
ance, as  already  intimated.  In  Leipsic,  where  articular  rheumatism  is  one  of 
the  most  frequent  of  acute  diseases,  we  observed  for  years  that  at  certain  times 
there  were  only  a  few  cases,  while  at  others  there  was  a  striking  increase  in 
their  number.  Usually  attacks  are  most  prevalent  in  the  winter  and  spring 
months,  but  again  it  is  sometimes  in  summer  that  the  disease  is  especially 
common. 

Among  the  exciting  causes  of  the  disease,  taking  cold  is  always  mentioned  as 
of  first  importance ;  and  in  fact  it  can  not  be  denied  that  the  influence  of  cold  does 
often  seem  to  contribute  to  the  occurrence  of  the  disease.  This  result,  however, 
seldom  follows  a  single  severe  exposure,  but  it  much  more  frequently  follows  long- 
continued  "  rheumatogenous  influences,"  as  we  may  call  them,  and  in  particular 
the  long-continued  influence  of  wet  and  cold,  certain  occupations — for  example, 
washing  and  scrubbing — inhabiting  unhealthy  damp  dwellings,  and  the  like. 
This  explains  why  those  who  follow  certain  callings  are  especially  subject  to 
articular  rheumatism;  thus  servant-girls  and  coachmen  are  frequently  victims  to 
the  disease.  And  yet  it  is  possible  to  regard  all  these  injurious  influences  as  being 
merely  indirect  causes,  assuming  that  they  favor  the  development  or  action  of  the 
specific  micro-organisms;  and,  furthermore,  it  is  by  no  means  exceptional  to  see 
a  case  of  articular  rheumatism  in  which  no  history  of  exposure  to  cold  can  be 
obtained. 

Sex  exerts  no  special  influence  upon  the  frequency  of  the  disease.  As  to  age, 
acute  articular  rheumatism  is  most  frequent  in  young  adults  between  fifteen  and 
thirty-five  years  old.  In  later  life,  and  particularly  in  old  age,  it  is  much  rarer. 
In  children  six  years  old  or  more  the  disease  is  not  especially  infrequent,  but  in 

675 


676  DISEASES    OF   THE    OEGAXS    OF   LOCOMOTIOJST 

younger  children  it  occurs  only  exceptionally.  We  may  be  permitted  to  mention 
a  single  interesting  case  which  we  met  with  in  Leipsic,  where  a  child  who  died 
when  only  a  few  days  old,  and  whose  mother  at  the  time  of  its  birth  was  suffering 
from  a  severe  attack  of  acute  articular  rheumatism,  was  found  to  have  multiple 
purulent  arthritis. 

Of  precisely  what  variety  the  special  germ  of  acute  rheumatism  may  be  we  do 
not  yet  know.  Still,  many  recent  investigations  (Sahli  and  others)  seem  to  prove 
that,  at  least  in  many  cases,  the  chief  role  is  played  by  the  staphylococcus  pyo- 
genes. If  this  claim  is  confirmed  it  will  deprive  acute  articular  rheumatism  of  the 
m.ost  part  of  its  specific  character,  from  an  astiological  point  of  view.  In  that 
case,  we  would  have  to  regard  it  merely  as  a  special  clinical  form  of  staphylococcus 
infection,  and  place  it  among  the  mild  varieties  of  septic  infection.  Indeed,  upon 
more  careful  consideration,  this  conception  of  articular  rheumatism  seems  very 
probable.  It  is  well  known  that  in  all  varieties  of  constitutional  sepsis  the  joints 
are  particularly  apt  to  be  involved.  It  has  also  been  shown  by  numerous  observa- 
tions that  staphylococci  are  most  frequently  found  to  be  the  infectious  germs  in 
cases  of  acute  benign  endocarditis,  consequently  we  should  expect  that  a  constitu- 
tional infection  with  the  staphylococcus  would,  as  a  rule,  display  itself  by  fever 
and  multiple  serous  arthritis.  Very  often  there  are  at  the  same  time  other  local 
disturbances.  These  are  the  so-called  "  complications  "  of  articular  rheumatism, 
which,  however,  would  be  more  correctly  termed  special  localizations  of  the  infec- 
tious germs  (vide  supra,  endocarditis,  pericarditis,  pleurisy,  etc.).  USTot  infre- 
quently these  localizations  in  the  other  serous  membranes  may  appear  previous  to 
the  swelling  of  the  joints,  or  even  without  any  articular  swelling,  and  yet  they 
may  be,  in  an  ^etiological  point  of  view,  precisely  analogous  to  articular  rheuma- 
tism. If,  however,  we  are  not  yet  inclined  to  accept  the  designation  of  acute 
articular  rheumatism  as  a  mild  septic  infection,  then  it  would  seem  advisable  to 
speak  of  all  the  forms  of  disease  which  belong  in  this  class  and  which  are  closely 
related  to  one  another,  as  due  to  a  "  rheumatic  infection,"  employing  the  word 
rheumatic  with  a  special  idea  of  aetiology. 

If  we  conceive  of  articular  rheumatism  in  the  way  just  indicated  as  a  clinically 
well-characterized  constitutional  infection — perhaps  with  staphylococci— the  next 
question  is  the  place  of  infection,  and  its  gate  of  entrance.  It  seems  probable 
that  the  place  is  not  the  same  in  every  case.  Very  often  it  is  impossible  to  deter- 
mine the  path  by  which  infection  entered;  yet  we  may  sometimes  ascertain  by 
careful  questioning  that  the  arthritis  was  preceded  by  a  mild  sore  throat,  or  a 
laryngitis,  or  an  intestiiial  disturbance.  Indeed,  we  often  find  even  small  abra- 
sions of  the  skin  and  similar  lesions.  It  is  probable  that  such  statements  of  the 
patient  and  discoveries  of  the  physician  indicate  the  starting-point  of  the  infec- 
tion in  the  individual  case. 

!N^ow  that  we  have  become  clear  as  to  the  mode  of  development  of  articular 
rheiimatism,  we  have  grained  also  a  satisfactory  conception  of  the  so-called  second- 
ary rheumatism  which  occurs  subsequently  to  scarlet  fever,  meningitis,  and  other 
acute  diseases.  It  is  probable  that  in  most  instances  these  are  due  to  secondary 
infection  with  the  staphylococcus,  although,  of  course,  it  can  not  be  denied  a  priori 
that  other  varieties  of  germs  may  produce  inflammation  of  the  joints — e.  g.,  multi- 
ple purulent  arthritis  is  probably  due  in  most  cases  to  streptococci.  Very  fre- 
quently, however,  the  primary  disease  itself  is  occasioned  by  staphylococci.  This 
is  the  case  in  many  instances  of  chronic  valvular  disease.  If  a  "  secondary  "  acute 
articular  rheumatism  occurs  in  such  diseases,  as  it  often  does,  the  process  is  to  be 
regarded  merely  as  a  fresh  acute  infection,  starting  from  the  old  focus. 

A  very  noteworthy  fact  is  that  acute  articular  rheumatism  can  not  be  num- 
bered among  those  infectious  diseases  which  usually  occur  but  once  in  the  same 
individual.    On  the  contrary,  the  disease  has  the  same  peculiarity  as  pneumonia 


ACUTE   AKTICULAE   EHEUMATISM  67Y 

and  erysipelas,  of  appearing  with  noticeable  frequency  several  times  in  the  same 
individual,  so  that  when  a  person  has  once  had  articular  rheumatism,  even  though 
it  has  left  no  sequelae  behind  it,  he  seems  to  be  more  liable  than  before  to  the 
disease.  It  is  not  exceptional  to  meet  persons  who  have  had  five  or  more  attacks 
of  acute  articular  rheumatism. 

Symptomatology. — The  chief  symptom  of  acute  articular  rheumatism  is  an 
acute  febrile  synovitis,  which  almost  always  affects  several  joints.  The  synovitis 
is  associated  with  the  usual  local  phenomena  of  swelling  and  tenderness  in  the 
parts  affected.  Often  this  articular  affection  is  the  first  symptom,  and,  indeed,  it 
may  be  the  only  symptom  of  the  disease.  It  is,  however,  by  no  means  exceptional 
for  the  arthritic  trouble  to  be  preceded  by  certain  prodromal  or  initiatory  symp- 
toms, as  is  true  of  other  infectious  diseases.  These  prodromata  consist  either  of  a 
slight  general  malaise,  or  of  certain  local  symptoms.  It  is  not  rare,  as  already 
mentioned,  to  have  sore  throat,  or,  as  we  have  repeatedly  had  opportunity  to  ob- 
serve, laryngitis.  Still,  the  precursors  are  usually  mild;  and  they  may,  as  we 
have  said,  fail  to  appear  at  all,  or  at  any  rate  they  may  easily  escape  notice.  In 
some  few  cases  the  only  symptoms  at  first  are  febrile;  there  may  be  no  other 
marked  constitutional  symptoms,  or  there  may  be  a  typhoidal  condition  with  en- 
larged spleen,  and  diarrhoea.  Then,  some  days  later,  the  characteristic  swelling 
of  the  joints  appears  (Wagner).  Taken  in  connection  with  the  view  of  the  nature 
of  articular  rheumatism  which  we  have  elaborated  above,  this  behavior  has  noth- 
ing inexplicable  about  it — merely,  the  constitutional  symptoms  develop  some  little 
time  before  the  local  manifestations  of  the  disease. 

The  articular  disturbance  is  almost  always  very  rapid  in  its  development. 
Some  of  the  larger  joints  are  usually  first  affected,  and  perhaps  those  of  the  lower 
extremities  somewhat  oftener  than  those  of  the  upper.  It  is  extremely  exceptional 
for  all  the  joints  that  are  affected  to  be  attacked  at  one  and  the  same  time.  It  is 
somewhat  characteristic  of  acute  articular  rheumatism  that  it  "  jumps  from  one 
joint  to  another."  To-day  this  joint  will  be  affected  and  to-morrow  that,  while  the 
joint  first  attacked  may  still  remain  diseased  or  undergo  rapid  recovery.  Thus, 
there  may  be  either  a  few  joints  affected  or  many,  in  varying  sequence,  and  they 
may  sometimes  be  affected  rapidly  and  at  other  times  more  slowly.  In  many 
of  the  milder  cases  the  disease  is  an  extremely  temporary  one,  while  in  others  it 
may  attach  itself  most  persistently  to  some  one  or  more  joints. 

There  is  usually  fever  in  addition  to  the  arthritis;  but  it  is  not  usually  very 
high,  seldom  exceeding  103°  (39.5°  C).  The  fever,  on  the  whole,  corresponds  with 
the  arthritic  phenomena,  and  does  not  present  an  especially  typical  curve,  but 
one  which  is  irregularly  remittent.  We  have  scarcely  ever  seen  the  disease  begin 
with  an  initial  rigor ;  and  the  so-called  "  general  febrile  symptoms  "  of  headache, 
stupor,  and  subjective  feeling  of  heat  are  as  a  rule  ill  marked  in  acute  rheuma- 
tism. This  indicates  that  the  constitutional  infection  does  not,  owing  to  the 
peculiar  nature  of  rheumatic  infection,  attain  great  severity.  The  skin  is  notice- 
ably inclined  to  perspiration,  but  the  perspiration  is  not  at  all  a  result  of  any 
sudden  fall  in  temperature  such  as  is  seen  in  other  diseases. 

The  course  of  the  disease  is  marked  by  alternate  ameliorations  and  aggrava- 
tions of  the  local  symptoms  and  of  the  fever,  and  lasts,  particularly  if  it  is  not 
treated,  one  or  more  weeks,  or  a  still  longer  period.  Often  the  entire  course  of 
the  disease  under  such  circumstances  is  made  up  of  separate  "  attacks "  (vide 
infra),  there  being  repeated  improvement  followed  by  articular  swelling  and  fever. 
At  last,  however,  the  symptoms  entirely  disappear,  and  the  patient  enters  upon  a 
tedious  but  complete  convalescence. 

In  contrast  with  this  simple  course  the  clinical  picture  may  be,  in  other  cases, 
much  more  complex,  for  the  peculiar  infectious  character  of  articular  rheuma- 
tism renders  possible  many  complications  and  peculiarities.     The  protean  char- 


678  DISEASES    OF   THE   OEGAls^S    OF   LOCOMOTIOlSr 

acter  of  the  disease  "n-ill  be  evident  upon  a  perusal  of  the  following  description  of 
the  sjTnptoms  referable  to  the  different  organs  of  the  body. 

Symptoms  referable  to  tlie  Different  Organs,  and  Peculiarities  in  the  Course 
of  the  Disease. — 1.  Joints  asb  Sheaths  of  the  Tendons. — The  favorable  termina- 
tion of  most  cases  of  acute  articular  rheumatism  prevents  us  from  often  examin- 
ing the  anatomical  changes  in  the  affected  joints;  but  there  can  be  no  doubt  that 
in  most  instances  the  trouble  is  merely  a  simple  serous  synovitis — that  is,  an  in- 
flammation of  the  synovial  membrane,  with  an  exudation  into  the  cavity  of  the 
joint,  composed  mainly  of  serum  with  but  little  admixture  of  fibrine  and  pus.  The 
synovial  membrane  itself,  in  the  cases  which  do  come  to  autopsy,  is  usually  very 
little  affected.  It  is  somewhat  injected,  opaque,  and  thickened.  Xecrosis  of  the 
cartilages  is  seen  only  in  severe  cases,  or  in  those  which  have  lasted  a  rather  long 
time.  From  a  clinical  standpoint,  the  articular  disturbance  is  noticeable  chiefly 
for  the  pain  which  it  causes  the  patient  upon  every  movement  of  the  joint  and 
any  pressure  upon  it.  The  tenderness  is  often  in  striking  contrast  with  the 
slight  objective  signs  of  inflammation,  for  a  joint  which  is  extremely  sensitive 
may  appear  to  be  scarcely  at  all  diseased.  Usually,  however,  the  joints  exhibit 
the  signs  of  synovitis.  The  effusion  into  the  joint  produces  an  evident  swelling, 
which  can  be  seen  particularly  well  in  the  knees,  but  also  in  the  joints  of  the 
ankle,  wrist,  shoulder,  and  elbow,  and  sometimes  even  in  the  smaller  joints  of  the 
fingers  and  toes,  particularly  the  great  toe.  It  is  rather  exceptional  to  detect  swell- 
ing of  the  hip-joint.  It  should  be  remembered,  however,  that  the  swelling  in  the 
region  of  the  joint,  particularly  the  ankle  or  wrist,  is  often  less  the  result  of  a 
synovial  effusion  than  of  an  inflammatory  periarticular  oedema.  This  oedema, 
for  example,  may  extend  over  almost  the  whole  posterior  surface  of  the  hand. 
The  joints  are  by  no  means  invariably  the  only  parts  attacked.  ^ISTot  infrequently 
there  are  analogous  inflammatory  changes  visible  in  the  sheaths  of  the  tendons, 
the  bursEe,  and  perhaps,  in  many  cases,  even  the  fasciae  and  muscles.  The  skin 
over  the  affected  joints  often  has  an  inflammatory  blush,  which  is  usually  pale- 
red  and  spotted,  and  can  be  best  seen  at  the  ankle,  knee,  and  wrist.  It  has  been 
maintained  that  the  cutaneous  sensibility  is  diminished  over  the  joints  affected, 
but  we  regard  this  as  a  mistake. 

«_^  As  might  be  expected,  the  number  of  joints  attacked  and  the  sequence  in  which 
they  are  attacked  differ  greatly  in  different  cases ;  but  almost  invariably  a  number 
of  joints  suffer,  so  that  any  monarticular  arthritis  should  not  be  regarded  as  rheu- 
matic except  after  careful  deliberation  (vide  infra,  diagnosis).  It  should  be  said 
that,  in  mild  cases,  there  may  be  only  two  or  three  joints  affected,  these  being 
usually  some  of  the  larger  joints  of  the  extremities;  and  of  these,  one  may  be  so 
much  worse  than  the  otheK  that  their  participation  in  the  trouble  can  be  ascer- 
tained only  by  careful  questioning  and  examination.  In  severe  cases,  on  the  other 
hand,  the  number  of  joints  attacked  is  often  very  great.  Such  patients  become 
extremely  helpless,  because  any  movement  is  possible,  if  at  all,  only  under  the 
penalty  of  very  severe  suffering.  The  patient  usually  lies  with  bended  knees  and 
feet  curved  so  as  to  be  concave  on  the  plantar  surface,  and  screams  with  pain  at 
any  attempt  to  change  his  position.  The  joints  of  the  trunk  sometimes  participate 
in  the  disease,  but  hardly  ever  except  in  the  severe  cases ;  the  articulations  of  the 
vertebrae,  the  sterno-clavicular  joint,  the  articulation  of  the  lower  jaw,  and  the 
symphysis  pubis,  are  then  particularly  apt  to  be  affected. 

The  fugitive  character  of  the  arthritis  has  been  spoken  of  as  characteristic  of 
acute  articular  rheumatism,  and,  indeed,  it  is  not  infrequently  the  case  that  com- 
paratively large  swellings  of  the  joints  soon  abate  and  yield  to  new  disturbances  in 
other  joints;  but,  on  the  other  hand,  the  disease  may  persist  very  obstinately  in 
a  single  joint.  In  this  case  one  joint  or  rarely  several  joints  are  attacked  with 
marked  severity,  either  from  the  start  or  subsequently  to  milder  affections  of 


ACUTE   AETICULAR   RHEUMATISM  679 

other  joints,  and  often  remain  for  weeks  swollen  or  painful,  long  after  all  other 
symptoms  have  vanished. 

2.  Cardiac  Symptoms. — The  condition  of  the  heart  in  acute  articular  rheuma- 
tism is  next  in  importance  to  that  of  the  joints.  The  physician  should  therefore, 
in  every  case,  even  the  mildest,  maintain  a  continuous  watch  over  this  organ.  In 
1836  Bouillaud  made  careful  auscultatory  investigations  in  this  disease,  and  was 
thus  the  first  to  discover  that  the  course  of  acute  articular  rheumatism  is,  with 
noticeable  frequency,  accompanied  by  endocarditis,  and  sometimes  even  by  peri- 
carditis. Complications  of  this  sort  may  occur  in  any  case,  whether  mild  or  severe, 
or  may  be  absent  in  any  case,  even  the  worst.  They  may  develop  at  the  beginning 
or  later  on  in  the  course  of  the  disease.  Their  development  is  often  unattended 
by  any  subjective  symptoms,  so  that  they  can  be  recognized  only  by  careful  phys- 
ical examination.  In  many  cases,  however,  the  onset  of  cardiac  disease  is  marked 
by  a  fresh  exacerbation  of  the  fever,  or  possibly  by  palpitation,  or  by  painful  sen- 
sations in  the  prsecordia,  or  by  dyspnoea. 

We  will  consider  first  rheumatic  endocarditis.  This  is  almost  always  the  be- 
nign verrucous  variety  (see  page  306).  It  is  far  more  prone  to  attack  the  mitral 
than  the  aortic  valve,  and  is  accordingly  usually  betrayed  by  a  blowing  systolic 
murmur  at  the  heart's  apex.  Uncertainty  may  be  cast  upon  the  diagnosis  by  the 
fact  that  functional  murmurs  are  not  very  infrequent  at  the  apex  or  at  the  base 
of  the  heart  in  cases  of  acute  articular  rheumatism.  We  once  observed  a  case  of 
^^  hyperpyretic  rheumatism  "  (vide  infra)  in  which  there  was  an  evident  murmur 
of  this  sort  during  life,  and  yet  at  the  autopsy  we  were  able  to  assure  ourselves 
of  the  normal  condition  of  the  cardiac  valves.  Even  an  expert  may  for  a  time  be 
in  doubt  as  to  the  significance  of  many  cardiac  murmurs,  and  this  explains  in  part 
the  conflicting  statements  as  to  the  frequency  of  cardiac  complications  in  acute 
rheumatism.  In  general,  one  may  say  that  such  complications  occur  in  twenty- 
five  to  thirty-three  per  cent,  of  the  cases.  The  ultimate  results  of  this  endocar- 
ditis we  do  not  need  to  describe  over  again  in  this  connection  (see  the  chapters  on 
acute  and  chronic  endocarditis).  Complete  recovery  is  possible.  Often,  however, 
the  lesion  gives  rise  to  a  chronic  endocarditis — that  is,  to  a  cardiac  valvular  dis- 
ease, which  lasts  through  life. 

The  close  connection  between  endocarditis  and  the  arthritis  must  formerly 
have  seemed  very  puzzling,  despite  the  many  hypotheses  made  to  explain  it.  Our 
present  conception  of  articular  rheumatism  as  a  septic  (staphylococcus)  infec- 
tion renders  the  frequent  development  of  endocarditis  easily  explicable.  It  is 
due  to  a  settlement  of  the  germs,  which  are  circulating  in  the  blood,  upon  the 
cardiac  valves  (see  page  304).  As  a  matter  of  fact,  staphylococci  are  almost 
invariably  found  in  the  inflammatory  deposits  of  "  rheumatic "  endocarditis. 
The  endocarditis,  therefore,  is  not  strictly  a  "  complication,"  but  a  symptom  of 
the  disease. 

Rheumatic  pericarditis  is  not  infrequent,  although  less  common  than  endocar- 
ditis. The  only  certain  way  to  recognize  it  is  by  a  characteristic  friction-sound; 
and  even  when  this  is  heard  there  may  be  a  doubt  as  to  its  significance,  inasmuch 
as  functional  murmurs  are  not  infrequently  heard  at  the  base  of  the  heart.  The 
pericarditis  is  of  a  sero-fibrinous  nature.  Sometimes  it  is  of  slight  severity;  but  it 
may  be  extremely  severe,  with  a  large  effusion  and  the  most  urgent  dyspnoea 
(see  page  359).  In  rare  instances  this  pericarditis  proves  fatal.  Usually,  however, 
recovery  ensues,  although  in  severe  cases  there  may  be  obliteration  of  the  peri- 
cardial sac,  with  the  consequences  described  on  page  364. 

As  to  the  way  in  which  pericarditis  develops,  it  is  probable  that  in  most  cases 
there  is  a  direct  infection  of  the  pericardium  from  the  blood.  In  some  cases,  how- 
ever, we  are  inclined  to  assume  that  the  infection  of  the  pericardium  comes  from 
the  endocardium,   and  probably  in  most   instances  from  the  aortic  valves    (see 


680  DISEASES    OF   THE    OEGANS    OF   LOCOMOTION 

page  359).  We  liave  repeatedly  found  a  distinct  aortic  insufficiency  to  have  been 
left  behind  after  rheumatic  pericarditis,  the  heart  having  previously  been  healthy. 
We  should  also  mention  that  there  may  be  functional  cardiac  derangement 
without  any  grave  anatomical  lesion.  We  have  already  spoken  of  the  functional 
murmurs.  There  may  also  be  a  rapid  and  irregular  pulse,  and,  in  rare  instances,, 
attacks  of  angina  pectoris  of  apparently  purely  nervous  origin. 

3.  Serous  and  Mucous  Membranes. — We  have  not  only  pericarditis  in  associa- 
tion with  articular  rheumatism,  but  also  pleurisy  and  peritonitis,  so  that  we  may 
say  that  in  acute  articular  rheumatism  the  incidence  of  the  disease  is  mainly  upon 
all  serous  membranes,  inclusive  of  the  joints.  It  should  be  said  that  rheumatic 
pleurisy,  and  particularly  rheumatic  peritonitis,  are  much  less  frequent  than  endo- 
carditis and  pericarditis,  but  we  have  repeatedly  seen  in  severe  cases  rheumatic 
pleurisy,  with  serous  effusion,  on  one  or  even  on  both  sides.  In  such  severe  attacks- 
it  is  not  exceptional  to  find  several  serous  cavities  simultaneously  involved — -for 
instance,  the  pericardium  and  pleura ;  so  that  in  such  instances  the  inflammation 
may  have  extended  directly  from  the  pericardium  to  the  pleura,  or  vice  versa, 
although  direct  infection  of  the  pleura  by  the  blood  is  perfectly  possible.  Rheu- 
matic peritonitis,  indicated  by  distention  of  the  abdomen  with  a  moderate  exuda- 
tion and  by  tenderness,  has  been  absolutely  diagnosticated  in  a  few  cases.  Here, 
also,  the  inflammation  may  appear  independently,  or  may  be  due  to  extension 
from  the  pleura  through  the  diaphragm. 

The  mucous  membranes  are  seldom  greatly  affected  in  acute  articular  rheuma- 
tism. As  we  have  already  mentioned,  in  the  beginning  of  the  disease  there  may 
be  catarrhal  affections  of  the  pharynx,  larynx,  stomach,  or  intestines;  which 
lesions  probably  facilitate  the  "  rheumatic  "  infection.  Bronchitis  is  spoken  of  by 
the  older  authors  as  frequent,  but  it  is  probably  in  many  cases  not  due  directly 
to  the  rheumatism,  but  is  a  complication,  just  as  in  any  disease  attended  by  great 
prostration. 

4.  Skin. — Cutaneous  phenomena  are  not  infrequent  in  the  course  of  acute 
articular  rheumatism.  A  prominent  symptom  of  the  disease  is  the  tendency  to 
profuse  perspiration.  The  perspiration  often  has  a  strongly  acid  odor  and  reac- 
tion. Many  patients  exhibit  an  abundant  crop  of  sudamina,  the  back  in  particu- 
lar being  sometimes  entirely  covered.  Sometimes  there  are  other  cutaneous 
eruptions.  In  a  whole  series  of  cases  we  observed  erythema  nodosum.  This  af- 
fected the  lower  extremities  more  than  the  upper.  Urticaria  is  not  very  infre- 
quent, while  herpes  labialis  has  been  very  rare  in  our  experience.  It  is  well 
known  that  arthritic  affections  and  the  so-called  "  hsemorrhagic  diseases  "  are  in 
many  ways  related  to  each  other;  and  it  is  therefore  an  interesting  fact  that 
extensive  hsemorrhagic  disturbance  of  the  skin  also  occurs  in  connection  with 
acute  articular  rheumatism,  as  we  have  repeatedly  had  opportunity  to  observe. 
We  have  seen  several  cases  of  htemorrhagic  urticaria :  wheals  appear  upon  the 
skin,  and  a  haemorrhage  takes  place  into  their  centers  and  spreads  gradually. 
There  may  also  be  simple  cutaneous  ecchymoses.  These  may  in  severe  cases  be 
merely  one  symptom  of  a  general  hsemorrhagic  diathesis,  with  haemorrhages 
from  mucous  membranes.  The  occurrence  of  all  these  symptoms  shows  clearly 
that  no  sharp  dividing  line  can  well  be  drawn  between  the  various  disorders. 

5.  The  Muscles  and  Nervous  System. — The  condition  of  the  muscles  is  very 
important  in  many  cases  of  acute  polyarthritis.  They  are  often  quite  painful  on 
pressure,  and  apparently  somewhat  swollen  about  a  joint  that  has  been  long  af- 
fected. The  muscular  atrophies  and  muscular  paralyses  that  often  remain  after 
the  arthritis  has  disappeared  are  especially  important. 

According  to  a  general  law,  there  are  certain  definite  trophic  relations  between 
a  joint  and  the  muscles  belonging  to  it,  whereby  almost  every  severe  and  persistent 
disease  of  the  joint  is  necessarily  followed  by  an  atrophy  of  the  affected  muscles. 


ACUTE   AETICULAE   EHEUMATISM  681 

The  extensors  of  the  joint  are  often  most  afiected  by  this  atrophy.  This  atrophy 
has  long  been  recognized,  and  it  was  formerly  regarded,  particularly  by  surgeons,, 
as  merely  the  result  of  inactivity  of'the  muscles— " atrophy  from  disuse";  but  this 
view  is  certainly  erroneous.  We  do  not  know  its  precise  cause,  but  it  is  without 
doubt  the  result  of  the  disease  of  the  joint,  and  may  therefore  be  termed  "  muscu- 
lar atrophy  of  arthritic  origin."  If  an  attack  of  acute  articular  rheumatism 
affects  any  one  joint  for  a  long  period  there  is  a  secondary  atrophy  of  the  corre- 
sponding muscles.  This  is  seen  most  often,  and  in  its  most  typical  form,  when 
there  is  obstinate  trouble  in  the  shoulder-joint,  the  deltoid  becoming  extremely 
atrophied.  This  atrophy  of  the  muscles  may  contribute  largely  to  the  sum-total 
of  functional  derangement.  We  have  repeatedly  seen  cases  where  the  patient, 
could  hardly  lift  his  arm  at  all,  although  the  inflammation  of  the  shoulder-joint 
had  passed  away,  and  that  without  leaving  any  anchylosis.  It  is  therefore  en- 
tirely justifiable  to  speak  of  a  rheumatic  paralysis.  We  have  seen  similar  muscu- 
lar paralyses  after  acute  articular  rheumatism  in  the  rest  of  the  muscles  of  the 
upper  arm,  also  in  the  quadriceps  extensor,  and  once  in  the  serratus  magnus.  The 
explanation  given  by  Charcot,  that  the  cause  of  the  atrophy  is  a  "  reflex  "  implica- 
tion of  the  trophic  centers  in  the  cord  due  to  the  disturbance  in  the  joint,  seems  to 
us  hardly  satisfactory.  There  are  probably  local  disturbances  of  nutrition,  and 
sometimes  apparently  a  direct  extension  of  the  inflammatory  process  from  the- 
joint  to  the  neighboring  muscles.  It  is  noteworthy  that  the  atrophied  muscles 
respond  promptly  to  the  faradic  current,  and  never  exhibit  the  reaction  of  degen- 
eration. 

Chorea  (vide  infra,  page  1152)  may  be  a  sequel  of  acute  articular  rheumatism,. 
and  it  is  one  of  the  nervous  symptoms  which  may  arise  in  connection  with  it. 
This  complication  is  seen  most  frequently  in  children.  Endocarditis  may  accom- 
pany it,  but  it  does  not  always  do  so. 

There  are  certain  peculiar  eases  of  acute  articular  rheumatism  which  excite  the 
greatest  interest.  In  these,  very  severe  cerebral  symptoms  are  developed,  often 
most  acutely.  They  are  therefore  called  "  cerebral  rheumatism  " ;  or,  as  they  are 
almost  always  characterized  by  an  extraordinarily  high  temperature,  another 
name  is  "  hyperpyretic  articular  rheumatism."  In  these  eases  the  disease  may 
exhibit  severe  nervous  symptoms  from  the  start,  particularly  delirium;  or  it  may 
at  first  run  an  apparently  favorable  course,  and  not  change  for  the  worse  until 
after  several  days,  or  even  at  a  later  period.  The  change  may  be  quite  abrupt. 
The  temperature  rises  to  104°  or  106°  (40°^1°  C).  There  are  great  uneasiness,, 
delirium,  and  sometimes  also  signs  of  motor  irritation,  such  as  general  convul- 
sions, or  tonic  spasm  of  the  extremities,  or  trismus.  The  face  grows  pale  and 
cyanotic,  the  pulse  small  and  extremely  rapid.  With  slight  interruptions,  the 
temperature  continues  to  rise,  and  attains  107.5°  to  109.5°  (42°-43°  C).  This 
great  rise  is  most  apt  to  occur  just  before  death,  and  there  may  be  a  still  further 
increase  of  temperature  after  death  occurs.  As  has  been  implied,  the  termi- 
nation is  usually  unfavorable.  It  is  only  in  exceptional  cases  that  recovery  takes 
place. 

It  has  been  stated  that  cerebi'al  rheumatism  attacks  mainly  hard  drinkers  and 
other  individuals  whose  nervous  system  has  been  previously  impaired ;  but  our 
own  experience  does  not  confirm  this  view.  No  ease  is  absolutely  secure  from  the 
occurrence  of  hyperpyrexia ;  but  it  is  a  very  rare  phenomenon,  occurring  perhaps 
once  in  several  hundred  cases.  On  post-mortem  examination,  the  brain  seldom 
shows  any  change  in  these  cases  of  cerebral  rheumatism.  We  are  therefore 
obliged  to  regard  the  condition  as  the  result  of  an  unusually  severe  infection, 
affecting  chiefly  the  intellectual,  motor,  and  thermal  centers. 

Cases  have  also  been  reported  which  presented  actual  anatomical  lesions  of  the 
brain — in  particular,  purulent  meningitis.    Probably,  however,  most  of  these  cases 


682  DISEASES    OF   THE    OEGANS    OF   LOCOMOTION 

were  falsely  diagnosticated,  the  observer  having  confounded  articular  rheumatism 
with  epidemic  meningitis,  pyaemia,  and  similar  diseases.  "  Of  course,  if  there  be 
endocarditis,  cerebral  embolism  is  possible. 

Mental  derangements  deserve  a  brief  mention.  They  rarely  occur  during  the 
course  of  the  disease,  but  are  somewhat  more  frequent  after  it  has  terminated. 
We  may  have  either  melancholia  attended  with  marked  excitement  or  anxiety,- 
or  a  more  general  insanity.    The  prognosis  is  usually  favorable. 

6.  Other  Viscera. — Other  parts  of  the  body  than  the  heart,  the  serous  mem- 
branes, and  the  brain,  are  seldom  much  affected  in  articular  rheumatism.  Lobar 
pneumonia  occurs  only  in  especially  severe  cases,  but  in  such  it  may  attain  quite  a 
considerable  development  and  occasion  great  dyspnoea.  It  usually  requires  quite 
a  long  while  to  recover  from  it.  Whether  we  actually  have  to  do  in  these  cases 
with  a  specific  pneumonia,  or  with  an  ordinary  lobar  pneumonia  as  a  complication, 
has  not  yet  been  determined.  It  is  also  possible  for  lobular,  deglutition  pneumonia 
to  develop  in  severe  articular  rheumatism.  Acute  nephritis  has  been  demonstrated 
in  some  instances,  but  this  is  very  rare.  The  spleen,  as  already  mentioned,  may 
be  somewhat  swollen;  but  as  a  rule  we  do  not  find  the  distinct  splenic  tumor 
which  is  present  in  other  acute  infectious  diseases. 

7.  General  Symptoms. — In  many  cases  the  general  condition  of  the  patient  is 
but  little  affected,  but  in  others  the  disease  seems  to  exert  a  peculiar  influence 
upon  the  constitution.  This  may  show  itself  in  a  striking  anaemia ;  and  we 
have  observed  this  repeatedly  where  there  was  no  cardiac  complication.  Ordi- 
narily, there  is  a  slight  leucocytosis.  A  dangerous  but  extremely  rare  compli- 
cation has  already  been  briefly  referred  to,  namely,  the  occurrence  of  a  general 
haemorrhagic  diathesis.  This  is  almost  always  associated  with  high  fever  and 
great  prostration,  and  is  usually  fatal.  In  all  such  cases  there  is  probably  pro- 
found sepsis. 

Course,  Duration,  and  Prognosis. — Acute  articular  rheumatism  may  be  de- 
scribed as  generally  a  benign  disease,  for  it  usually  terminates  in  recovery.  It  is 
only  in  very  few  cases  that  an  unfavorable  termination  takes  place  immediately, 
whether  as  the  result  of  pericarditis  or  other  severe  cardiac  complication,  or  from 
hyperpyrexia,  or  the  development  of  a  general  haemorrhagic  diathesis. 

The  entire  duration  of  the  disease  varies  greatly  according  to  its  severity. 
There  are  mild  cases,  which  terminate  in  a  few  days ;  and,  on  the  other  hand,  the 
disease  may  be  very  tedious,  lasting  for  weeks  and  months.  This  latter  form 
is  seen,  upon  careful  consideration  of  the  whole  course  of  the  disease,  and  par- 
ticularly of  the  temperature-curve,  to  be  made  up  of  separate  attacks,  which  can 
often  be  very  clearly  distinguished.  In  each  attack  of  this  sort  (see  Fig.  76)  the 
temperature  rises  for  some  days  and  then  slowly  abates,  so  that  the  entire  length 
of  an  attack  is  about  seven  to  thirteen  days.  Then  there  is  an  afebrile  interval  of 
a  few  days,  followed  by  a  fresh  rise  of  temperature,  etc.  The  recurrence  of  the 
fever  is  usually  associated  with  new  trouble  in  one  or  more  joints,  or  with  some 
additional  rheumatic  disorder,  such  as  endocarditis  or  pleurisy,  while  during  the 
afebrile  period  the  local  symptoms  abate,  and  the  patient  feels  almost  well.  Fried- 
lander  has  tried  to  deduce  a  series  of  general  laws  about  the  course  of  the  disease, 
based  upon  this  typical  behavior  of  articular  rheumatism,  but  in  our  opinion  he 
has  gone  too  far  in  this  direction,  although  we  have  ourselves  frequently  observed 
this  interesting  course  of  acute  articular  rheumatism,  with  a  series  of  separate 
attacks,  and  regard  it  as  very  characteristic  of  individual  cases;  still,  there  are 
many  other  forms  which  the  disease  may  assume. 

Quite  often  the  violent  symptoms  experienced  at  first  disappear  promptly, 
but  only  to  be  replaced  by  such  milder  ones  as  pain  and  stiffness  of  the  joints — 
these  latter  persisting  for  a  long  time.  It  is  a  general  rule,  that  the  severity  and 
persistency  of  the  case  correspond  with  the  number  of  joints  affected;  but  to  this 


ACUTE   ARTICULAR  RHEUMATISM 


683 


rule  there  are  numerous  exceptions.     The  disease  may  persist  with  great  obsti- 
nacy in  a  single  joint.    It  need  hardly  be  said  that  the  duration  of  the  disease  is 
greatly   modified   by   the   occurrence   of 
complications,  cardiac  or  otherwise,  and 
such  sequelae  as  muscular  atrophy,  an- 
chylosis of  the  joints,  or  chorea.     The 
most  important  of  all  sequelae  is  cardiac 
disease,  and  this  must  always  be  consid- 
ered in  giving  a  prognosis ;  for,  although 
the   disease   as   such   does   in   most   in- 
stances  terminate   m  recovery,  yet  too     5 
often  it  gives  rise  to  a  tedious  and  usu-      ^ 
ally  incurable  disease  of  the  heart.     It     " 
is,  however,  true  that  complete  recovery     J 
from    the    acute    endocarditis    seen    in     t 
articular  rheumatism  is  possible,  but  in     -z 
a  large  majority  of  cases  recovery  is  not      f 
complete,  and  the  acute  passes  into   a     a 
chronic  endocarditis.    In  these  cases  the 
cardiac  symptoms  may  be  developed  di- 
rectly, so  that  the  patient  at  once  begins 
to  complain  of  palpitation  and  shortness 
of  breath;  or  he  may  seem  to  regain  his 
health  completely,  and  a  murmur  which 
the  physician  alone  can  detect  may  be 
the   only   sign   of   the   incurable   injury 
which  the  body  has  suffered.     The  pa- 
tient may  feel  perfectly  well  for  years 
after,  and  then  at  last  begin  to  suffer 
from  the  failure  of  compensation   (see 
page  326  et  seq.).     Finally,  we  should 
again   call    attention   to    the    important     .i 
fact  that  after  recovery  from  rheuma-     1 
tism,  there  may  be  a  tendency  to  fresh      \ 
attacks  of  arthritis  for  the  rest  of  the     ■; 
patient's  life.  '\ 

Diagnosis. — Most  cases  of  articular     ^ 
rheumatism   can   be   easily   recognized,     i 
for  the   acute   occurrence   of  pain   and      I 
swelling  in  several  joints  is  sufficiently 
characteristic  of  the  disease.    It  should 
nevertheless  be  borne  in  mind  that  ar- 
ticular swelling  may  also  take  place  in 
the  course  of  other  diseases,  and  that 
mistakes  in  diagnosis  are  by  no  means 
impossible.    When  there  are  grave  con- 
stitutional  symptoms   with   fever   from 
the  start,  we  should  not  forget  the  pos-     .; 
sibility  of  pyaemia,  or  of  acute  osteomye-     j 
litis,  since  these  affections  occasionally     ] 
give    rise    to    the    swelling    of    several     ■; 
joints.     In  such  cases,  however,  careful     ' 
attention  to  the  further  course  of  the 
disease  will  generally  enable  us  to  see 


684:         ,    DISEASES    OF   THE    OEGAl^S    OF   LOCOMOTIOi;!" 

that  we  can  not  be  dealing  with  a  simple  acute  articular  rheumatism.  Again^ 
after  childbirth  there  may  be  swelling  of  the  joints,  of  septic  origin,  and  but 
distantly  related  to  genuine  rheumatism. 

If  a  single  joint  be  attacked,  the  diagnosis  of  articular  rheumatism  must  be 
made  with  extreme  caution.  These  monarticular  inflammations  often  prove  to  be 
something  entirely  different,  namely,  fungous  disease  of  the  joint,  or  an  osteo- 
myelitis. The  arthritis  which  follows  gonorrhoea  is  usually  [though  not  invari- 
ably] monarticular  (affecting  especially  the  knee-joint  or  wrist).  In  conclusion, 
it  should  be  stated  that  it  is  not  very  rare  to  observe  pain  and  swelling  in  various 
muscles  and  joints  at  the  commencement  of  the  secondary  stage  of  syphilis,  simu- 
lating an  acute  articular  rheumatism. 

Sometimes  the  diagnosis  is  doubtful  in  those  cases  which  present  cutaneous 
ecchymoses  (purpura  and  peliosis)  and  erythema  nodosmn,  because  we  may  be 
unable  to  determine  which  should  be  regarded  as  the  primary  symptoms  and 
which  the  secondary.  Until  we  become  acquainted  with  the  specific  germs  which 
cause  all  these  diseases,  it  will  be  merely  a  dispute  about  words,  whether  we  shall 
call  a  particular  case  by  one  name  or  another.  In  our  opinion,  all  these  conditions 
have  a  close  setielogical  relation  to  one  another. 

Genuine  gout  (q.  v.)  can  usually  be  readily  diagnosticated  from  articular  rheu- 
matism by  its  localization  in  the  toe,  and  by  the  gastric  and  other  symptoms 
which  attend  it. 

Finally,  we  must  mention  that  acute  multiple  neuritis  (q.  v.),  beginning  with 
fever  and  severe  pain  in  the  extremities,  may  sometimes,  if  we  are  not  sufficiently 
careful,  be  mistaken  for  polyarthritis. 

Treatment. — Acute  articular  rheumatism  is  one  of  the  few  diseases  for  which 
we  possess  an  undoubtedly  specific  and  universally  accepted  remedy.  Kolbe  sug- 
gested its  use,  and  since  1876  it  has  been  largely  employed  upon  the  recommenda- 
tion of  Strieker,  Buss,  and  others,  for  articular  rheumatism.  This  remedy  is  sali- 
cylic acid.  Although  this  medicine  does  not  in  all  cases  produce  its  surprisingly 
favorable  results  with  equal  rapidity  and  completeness,  yet  it  almost  invariably 
does  produce  a  decided  and  beneficial  effect  upon  the  disease.  We  might  even 
say  that  this  influence  is  so  constant  that  when  salicylic  acid  proves  entirely 
inefficient  in  a  fresh  case,  such  failure  throws  doubt  upon  the  correctness  of  the 
diagnosis.  Thus,  where  there  is  monarticular  arthritis  dependent  upon  some  local 
cause,  the  remedy  has  hardly  any  beneficial  influence.  The  same  is  true  with 
regard  to  affections  of  the  joints  connected  with  gonorrhoea,  pyaemia,  and  similar 
troubles.  In  genuine  acute  articular  rheumatism,  on  the  other  hand,  the  salicylic- 
acid  treatment  is  so  superior  to  any  other  that  it  is  the  first  duty  of  the  physician 
in  every  case  to  give  this  remedy  a  fair  trial. 

There  are  but  two  preparations  of  salicylic  acid  used  in  rheumatism — the  pure 
acid  and  its  sodium  salt,  salicylate  of  sodium.  Each  of  these  two  remedies  has  its. 
peculiar  advantages,  but  the  specific  influence  of  each  is  about  the  same.  Sali- 
cylic acid  should  never  be  prescribed  in  solution,  but  always  in  wafers  or  capsules, 
usually  containing  ten  grains  (gramme  0.50).  In  this  way  the  salicylic  acid  can 
be  taken  by  almost  any  patient  quite  easily,  especially  if  a  little  water  or  milk  be 
drunk  after  each  dose.  Adults  should  receive  ten  grains  every  hour  until  about 
one  or  two  drachms  (grammes  5-8)  have  been  administered.  Usually  there  will  by 
this  time  be  a  very  decided  abatement  of  the  articular  pain  and  swelling,  while  on 
the  other  hand  there  will  also  usually  be  such  toxic  "  salicylic  symptoms  "  {vide- 
infra)  as  to  forbid  its  further  use.  The  salicylate  of  sodium  is  best  exhibited  in 
single  large  doses  of  a  drachm  to  a  drachm  and  a  half  (grammes  4—6),  each  dose 
being  given  with  about  an  ounce  (grammes  20-30)  of  peppermint  water,  or  still 
better,  in  wafers.  The  quite  disagreeable  taste  of  the  medicine  is  only  exagger- 
ated by  the  addition  of  such  substances  as  syrup  or  fluid  extract  of  licorice,  adde(J 


ACUTE   ARTICULAR   RHEUMATISM  685 

for  the  sake  of  elegance ;  but  the  simple  solution  in  peppermint  water  is  quite  well 
taken,  at  least  by  most  patients.  It  is  a  very  good  plan  to  give  salicylate  of 
sodium  in  a  glass  of  Hungarian  wine,  or  in  strong  black  coffee  without  sugar. 
The  advantage  of  the  salicylate  over  the  pure  acid  consists  in  its  being  possible 
to  give  a  larger  dose  at  one  time,  so  that  it  need  not  be  taken  more  than  two  or 
three  times  a  day.  In  general,  the  amount  given  in  twenty-four  hours  should  not 
exceed  two  and  a  half  drachms  (grammes  10)  ;  one  and  a  half  to  two  drachms 
(grammes  6-8)  may  suffice.  For  children  the  dose  is,  of  course,  smaller,  about  five 
g-rains  of  salicylic  acid  (gramme  0.30),  or  in  twenty-four  hours,  half  a  drachm  to 
a  drachm  (grammes  2-5)  of  the  sodium  salt. 

Which  of  these  two  preparations  shall  be  employed  is,  as  has  been  stated,  of 
little  consequence.  We  ourselves  usually  prescribe,  at  first,  capsules  of  salicylic 
acid  to  be  taken  hourly,  as  being  most  agreeable  to  the  patient;  but  if  our  first 
visit  be  made  in  the  evening,  we  prescribe  a  single  large  dose  of  a  drachm  to  a 
drachm  and  a  half  (grammes  4-6)  of  salicylate  of  sodium,  so  that  the  patient  may 
not  be  disturbed  every  hour  through  the  night  in  order  to  take  medicine.  It  is 
■often  possible  to  give  the  two  remedies  in  alternation.  This  is  a  good  way  later 
on  in  the  disease,  when  the  patient  has  already  acquired  a  distaste  for  the  medi- 
cine. In  such  cases  also  it  may  be  desirable  to  give  the  salicylate  of  sodium  as  an 
•enema.  About  two  and  a  half  drachms  (grammes  10)  should  be  given,  in  two 
ounces  of  water  (grammes  60).  There  is  no  doubt  that  the  specific  effects  can  be 
obtained  in  this  manner. 

The  benign  influence  of  this  remedy  upon  the  disease  is  apparent  in  many 
fresh  cases  as  early  as  ten  to  eighteen  hours  after  treatment  begins ;  and  it  is  often 
astonishing  to  see  how  soon  a  jiatient,  who  before  lay  helpless  and  complaining, 
becomes  free  from  pain  and  able  to  move  his  limbs.  It  must  be  confessed,  how- 
ever, that,  apart  from  its  taste,  salicylic  acid  may  produce  disagreeable  incidental 
•effects.  In  the  first  place,  there  may  be  nausea  with  epigastric  distress,  and  even 
vomiting.  Tinnitus  aurium  may  be  exceedingly  troublesome,  and  may  be  at- 
tended with  marked  vertigo.  In  somewhat  rarer  instances  the  mind  is  especially 
affected.  Young  girls  in  particular  are  often  peculiarly  excited;  but  the  frame 
of  mind  is,  however,  in  general  a  cheerful  one.  After  large  doses  there  may  be 
an  actual  "  salicylic  delirium."  It  should  also  be  said  that  respiration  may  be 
affected,  becoming  very  deep  and  rapid  (salicylic  dyspnoea).  All  these  incidental 
effects,  and  particularly  the  nausea  and  ringing  in  the  ears,  render  difficult  the 
•employment  of  the  remedy  in  those  large  doses  which  alone  are  of  any  benefit. 
This  is  the  more  unfortunate,  as  it  is  often  very  desirable  to  employ  salicylic  acid 
persistently. 

Although  it  is  not  exceptional  to  have  the  symptoms  almost  entirely  vanish 
at  the  end  of  one  or  two  days,  yet  it  is  only  in  the  minority  of  cases  that  the 
entire  process  ends  with  this  release  from  pain.  There  is  very  often,  sooner  or 
later,  a  relapse,  with  fresh  pain  or  even  fresh  swelling  in  one  or  more  joints.  It 
has  been  recommended  to  continue  the  salicylic  acid  in  smaller  doses  for  some 
time,  in  order  to  avert  such  relapses;  but  of  late  we  have  rather  abandoned  this 
method,  for  the  reason  that  these  small  doses  do  not  prevent  the  return  of  the 
•disorder,  but  are  calculated  to  give  the  patient  a  strong  dislike  to  the  remedy, 
and  lessen  his  confidence  in  it.  We  therefore  recommend  to  stop  the  medicine 
•  entirely  as  soon  as  the  pain  is  wholly  gone,  and  to  guard  the  patient  as  much  as 
possible  from  relapses  by  preventing  his  catching  cold  (vide  infra).  If  there  be 
fresh  pain,  we  should  at  once  resume  the  acid  or  its  salt  in  large  doses,  and  thus 
we  shall  very  frequently  be  able  to  cut  short  the  relapse  at  once.  In  case  there  is 
persistent  discomfort  in  the  joints,  small  doses  may  be  kept  up  for  some  time. 

[One  other  salicylic  compound  deserves  mention — the  oil  of  wintergreen;  this 
ias  been  used  largely  by  Kinnicutt,  who  finds  it  efficacious,  easy  to  take,  and  not 


686  DISEASES    OF   THE    OEGAITS    OF   LOCOMOTION" 

likely  to  produce  the  unpleasant  symptoms  whicti  sometimes  follow  tlie  com- 
pounds in  more  general  use.  It  is  given  in  doses  of  ten  to  fifteen  minims  every  two 
hours,  either  in  milk,  on  sugar,  or  in  capsules. 

The  salicylic  treatment  markedly  diminishes  the  ;^ain  and  fever,  shortens  the 
time  spent  in  bed  by  four  or  five  days,  does  not  shorten  the  time  spent  in  hospital, 
and  seems  to  have  little  or  no  influence  on  the  cardiac  complications.  The  full 
alkaline  treatment  does  not  curtail  the  pain  and  fever  in  the  same  degree,  but 
does  seera  to  afford  some  protection  against  the  heart  affection,  and  to  shorten  the 
stay  in  hospital  several  days. 

A  combination  of  the  salicylic  and  alkaline  treatments  seems  therefore  ra- 
tional, and  it  has  been  adopted  by  the  editor  for  some  years.  Citrate  of  potash  is 
given  in  sufficient  doses  to  produce  and  maintain  alkalinity  of  the  urine.  The 
salicylic  compound  is  given  at  first  in  full  doses,  which  are  diminished  in  size  and 
frequency  with  the  control  of  the  articular  symptoms,  but  are  not  omitted  entirely 
until  recovery  is  practically  complete.  The  editor  is  inclined  to  believe  that  re- 
lapse is  less  common  if  the  system  be  kept  somewhat  under  the  influence  of  the 
drug.  Salicine  is  often  perfectly  well  borne  when  the  sodium  salt  causes  gastric 
irritability,  and  the  oil  of  wintergreen  is  another  form  which  has  advantages  in 
some  cases.] 

Despite  the  admirable  qualities  of  salicylic  acid,  it  must  be  confessed  that  we 
can  not  always  bring  about  a  rapid  and  complete  cure  of  the  disease  by  this  rem- 
edy. There  are  cases  in  which,  although  at  first  evident  improvement  follows  its 
use,  relapses  continually  recur,  or  the  disease  fastens  itself  obstinately  in  single 
joints.  In  such,  the  continued  use  of  salicylic  acid  proves  almost  unavailing,  and 
indeed  the  patient  can  hardly  be  persuaded  to  take  it.  In  these  cases,  and  also 
when  the  salicylic  preparations  are  ill  borne  or  cause  unpleasant  attendant  symp- 
toms, antipyrine  is  the  best  substitute.  Many  physicians  therefore  often  prescribe 
it  from  the  first  in  place  of  salicylic  acid,  although  we  think  the  action  of  the 
latter  upon  acute  articular  rheumatism  is  greater  than  that  of  antipyrine.  We 
should  give  antipyrine  in  doses  of  fifteen  to  thirty  grains  (grammes  1-2)  several 
times  a  day  in  water  or  wine.  Its  attendant  symptoms  (sweating,  nausea,  and 
sometimes  an  eruption  like  measles)  are  usually  without  special  significance,  and 
its  influence  on  the  articular  pains  is  often  so  favorable  that  the  remedy  is  of  much 
value  in  the  treatment  of  protracted  rheumatism.  We  have  also  often  used  sali- 
pyrine  (salicylate  of  antipyrine)  with  good  results,  and  likewise  phenacetine,  and 
salol  (phenyl-salicylate),  which  last  was  recommended  by  Sahli,  and  which  is  ad- 
ministered in  powders  up  to  fif  tefen  grains  (gramme  1)  several  times  a  day,  the  total 
daily  dose  being  seventy- five  to  ninety  grains  (grammes  5-6).  Antifebrine  or  acet- 
anilide  is  decidedly  less  efficient,  but  it  has  the  advantage  of  being  inexpensive. 

From  the  other  remedies  which  may  be  sometimes  tried  in  obstinate  cases, 
we  can  seldom  expect  satisfactory  results;  at  least,  we  have  ourselves  never  seen 
any  decided  benefit  from  iodide  of  potassium,  prepa^rations  of  colchicum,  the 
alkalies,  trimethylamine,  or  veratrine.  Far  more  important  in  refractory  cases  is 
the  local  treatment  of  the  diseased  joints.  This  means  chiefly  massage,  the  re- 
sults of  which,  when  scientifically  performed,  are  often  admirable.  Electricity 
also  may  have  a  beneficial  effect,  particularly  the  galvanic  current.  We  would 
caution  against  the  too  early  use  of  warm  baths,  as  these  often  aggravate  the 
pain  instead  of  mitigating  it.  Steam  baths  are  sometimes  very  beneficial,  but 
they  may  also  do  harm,  and  they  should  therefore  be  given  only  when  the  acute 
inflammatory  sj^mptoms  have  entirely  vanished,  leaving  behind  only  stiffness  and 
tenderness  in  the  joints.  On  the  other  hand,  it  is  advantageous  to  give  the  patient 
a  sweat  in  bed.  This  is  a  favorite  remedy  of  the  author's,  and  may  be  accom- 
plished by  introducing  heated  air  lander  the  bed-clothes,  or  in  other  ways. 

The  application  of  an  ice-bag  in  geniiine  articular  rheimiatism  is  seldom  neces- 


ACUTE   AETIGULAR   RHEUMATISM  687 

sary,  but  it  may  sometimes  be  desirable  when  there  are  violent  and  obstinate  symp- 
toms of  acute  inflammation.  Warm,  moist  applications  are  seldom  beneficial  in 
acute  cases.  In  the  advanced  stages  of  subacute  cases  poultices  or  a  wet-pack  may 
afford  some  relief.  Painting  the  skin  over  the  joints  with  tincture  of  iodine  pro- 
duces no  effect  in  acute  cases,  and  even  in  the  chronic  ones  it  is  probably  mainly 
a  subjective  remedy.  Some  observers  report  that  injections  of  carbolic  acid  be- 
neath the  skin  of  the  affected  joints  greatly  relieve  the  pain.  A  Pravaz's  syringe- 
ful  (thirteen  minims)  of  a  one-per-cent.  solution  may  be  injected  one  to  three 
times  a  day.  We  have  had  no  personal  experience  with  this  remedy.  In  all  severe 
cases  careful  attention  should  be  given  from  the  start  to  maintaining  a  correct 
position  of  the  diseased  joints,  because  of  the  possibility  of  anchylosis.  Before 
salicylic  acid  was  introduced,  "  the  treatment  of  articular  rheumatism  with 
splints  "  was  largely  and  very  advantageously  employed.  The  use  of  salicylic  acid 
has  greatly  diminished  the  necessity  of  such  procedure,  but  even  now  it  is  some- 
times required.  It  is  often  possible  to  give  the  patient  great  relief  by  applying  a 
suitable  pasteboard  or  wooden  splint  to  an  affected  extremity. 

General  hygienic  and  dietetic  treatment  should  not  be  undervalued.  An 
equable  temperature  should  be  carefully  maintained  in  the  sick-room,  inasmuch 
as  cold,  or  draughts,  or  moisture  have  very  often  been  found  to  exert  an  evil 
influence  upon  the  disease  and  excite  fresh  pain.  The  patient  should  therefore 
be  kept  warm,  and  it  is  sometimes  advantageous  to  wrap  up  the  affected  joints  in 
cotton  batting.  It  is  of  great  importance  that  even  in  the  mildest  cases  the  pa- 
tient should  be  strictly  confined  to  bed,  and  he  should  by  no  means  get  up  too  soon. 
If  possible,  we  keep  our  own  patients  in  bed  for  a  week  after  the  pain  has  ceased. 
Getting  up  too  early  will  very  often  bring  on  a  relapse.  With  regard  to  diet,, 
milk  is  the  best  food.  We  may  also  allow  soup,  eggs,  and  a  little  meat.  In 
France,  great  weight  is  laid  upon  an  exclusive  milk  diet ;  but  this  would  seem  to 
us  an  extreme  view. 

We  do  not  need  to  speak  at  length  about  the  treatment  of  the  complications 
and  sequelae,  since  we  should  merely  repeat  what  has  already  been  said  in  the 
appropriate  chapters  of  this  work.  There  has  been  much  said  on  both  sides  as  to 
the  influence  of  salicylic  acid  in  preventing  complications,  particularly  cardiac 
complications.  This  much  is  certain,  that  cardiac  complications  are  not  abso- 
lutely prevented  by  the  salicylic  treatment,  and  that  they  too  frequently  occur 
while  it  is  being  employed;  but  we  do  believe  that  this  treatment  decidedly 
shortens  the  course  of  the  disease  as  a  whole,  in  many  instances,  and  thus  lessens 
the  liability  to  endocarditis.  If,  however,  a  cardiac  complication  has  made  its 
appearance,  salicylic  acid  does  not  exert  any  appreciable  influence  upon  it. 

Another  important  question  is  in  regard  to  the  efficiency  of  salicylic  acid  in 
the  graver  forms  of  articular  rheumatism,  particularly  in  cerebral  rheumatism. 
It  may  be  stated,  in  the  first  place,  that  in  Leipsic  cerebral  rheumatism  has 
apparently  become  much  less  frequent  since  the  salicylic  treatment  was  intro- 
duced. At  any  rate,  not  a  single  case  of  hyperpyrexia  occurred  in  the  clinique  in 
that  city  out  of  many  hundred  cases  treated,  where  the  salicylic  acid  was  properly 
employed  from  the  first.  We  had  an  opportunity  to  observe  a  case  in  which  hyper- 
pyretic  symptoms  had  already  appeared  when  we  first  saw  it,  and  which  had  ni)t 
been  treated  with  salicylic  acid.  Here  large  doses  of  that  remedy  produced  no 
effect.  We  should  nevertheless  be  inclined  to  employ  it,  first  of  all,  in  such  cases ; 
and  the  energetic  use  of  cool  baths  would  probably  be  the  most  speedy  way  of 
modifying  the  dangerously  high  temperature.  Stimulants,  in  particular  camphor, 
are  also  required  in  these  severe  cases. 

In  the  severe  hemorrhagic  varieties  of  rheumatism  we  should  also  give  sali- 
cylic acid  a  trial.  The  milder  hsemorrhagic  cases  (hsemorrhagic  urticaria)  do  well 
tinder  ordinary  methods  of  treatment. 


SS8  DISEASES    OE    THE    OEGAXS    OF   LOCOMOTION 

If  the  acute  affection  merge  into  a  chronic  condition  of  stiffness  and  swelling 
•of  certain  joints,  such  as  the  wrist  or  shoulder,  we  must  employ  the  same  remedies 
as  in  chronic  articular  rheumatism.  Passive  movements  and  massage  furnish  the 
best  results.  Warm  baths  may  also  be  ordered  in  such  cases  (see  the  following 
chapter).  The  patient  might  be  sent  to  Teplitz  or  Wiesbaden.  These  baths  are 
good  resorts  for  convalescents.  The  subsequent  muscular  atrophies  and  paralyses 
recover  most  rapidly  under  electricity. 

Prophylaxis  requires,  first  of  all,  that  one  should  avoid  cold  or  wet,  and  other 
"  rheumatogenous  influences."  Persons  who  have  already  had  one  attack  of 
articular  rheumatism  must  be  especially  careful,  inasmuch  as  they  are  more  than 
-ever  liable  to  the  disease,  as  has  already  been  said.  It  is  not  inconsistent,  how- 
ever, with  the  exercise  of  due  caution,  to  endeavor  to  lessen  the  sensitiveness  of 
the  skin  by  such  procedures  as  cold  sponging,  followed  by  friction. 


CHAPTEE   n 


CHRONIC     ARTICULAR     RHEUMATISM     (CHRONIC     POLYARTHRITIS) 
AND    ARTHRITIS    DEFORMANS 

.3itiology. — The  two  diseases  known  as  "  chronic  articular  rheumatism  "  and 
■*'  arthritis  deformans  "  are  considered  together  here,  because  it  is  impossible  to 
draw  a  sharp  distinction  between  them.  It  is,  indeed,  not  unlikely  that  the  above 
names  are  sometimes  applied  to  diseases  which  differ  essentially  from  each  other; 
but  as  we  do  not  yet  understand  the  nature  or  the  eetiology  of  many  chronic 
diseases  of  the  joints,  we  must  provisionally  be  guided  by  the  external  changes 
they  produce.  We  shall  therefore  embrace  all  chronic  inflammatory  processes 
affecting  the  joints  under  the  name  of  chronic  arthritis.  It  is  not  intended  to  in- 
clude traumatic  arthritis,  much  less  those  chronic  affections  of  the  joints  which 
are  evidently  of  tubercular  origin,  and  which  have  ordinarily  been  termed  fungous 
arthritis.  These  belong  to  the  domain  of  surgery.  We  would  also  exclude  chronic 
syphilitic  diseases  of  the  joints,  about  which,  indeed,  there  is  still  less  known  than 
about  the  tubercular  affections ;  besides,  they  are  rare.  Chronic  articular  affec- 
tions from  gonorrhcea  are  more  frequent,  and  of  great  practical  importance. 

The  aetiology  of  those  eases  of  chronic  arthritis  where  the  disease  is  a  direct 
sequel  of  acute  articular  rheumatism  is  evident  enough.  It  is  hardly  possible  to 
•doubt  that  the  same  specific  poison  which  excited  the  acute  arthritis  maintains 
possession  of  the  joints,  and  produces  the  chronic  inflammatory  changes.  Cases 
of  this  sort  especially  deserve  the  name  of  chronic  articular  rheumatism.  They 
are  not  very  infrequent,  and  may  be  of  slight  or  great  severity.  The  worst  cases 
produce  macroscopic  changes  which  fully  justify  the  other  appellation  of  arthritis 
•deformans. 

It  is  also  possible  that  many  cases  which  are  chronic  from  the  start  have  the 
•same  setiology — that  is,  are  due  to  the  same  pathogenic  agents.  This  might  be 
inferred  from  analogy  with  numerous  other  diseases,  and  it  is  rendered  still 
more  probable  by  the  fact  that  the  same  exciting  causes  which  promote  acute 
articular  rheumatism  often  play  a  conspicuous  part  in  chronic  arthritis.  Such 
causes  are  exposure  to  cold  and  wet,  and  working  in  cold  or  draughty  places,  or 
dwelling  in  newly  built  and  damp  houses.  This  explains  why  those  who  follow 
certain  callings — for  instance,  washerwomen — are  more  apt  to  suffer  from  the 
disease  than  others,  and  why  arthritis  deformans  has,  with  some  justice,  been 
■called  a  disease  of  the  poor,  in  contrast  with  the  gout  of  the  wealthy.    Many  of  the 


CHEONIC   EHEUMATISM   A^^d   aKTHRITIS    DEFORMANS    689 

laity,  and  even  some  physicians,  believe  that  gout  and  arthritis  deformans  are  in 
some  way  related,  but  this  view  is  erroneous. 

It  is  very  questionable  whether  all  cases  of  chronic  multiple  arthritis  are  refer- 
able to  the  causes  already  enumerated.  Such  other  influences,  however,  as  are 
concerned  in  its  production  are  not  at  all  understood.  Various  authorities  have 
maintained  that  arthritis  deformans  is  the  result  of  a  primary  disease  of  the  nerv- 
ous centers,  and  in  particular  of  the  spinal  cord.  We  regard  this  statement  as 
entirely  unwarranted.  It  originated  at  a  time  when  there  was  a  tendency  to 
ascribe  all  sorts  of  ills  to  disease  of  the  "  trophic  centers,"  but  there  is  no  doubt 
that  this  tendency  was  carried  very  much  too  far.  We  may  state  in  this  connec- 
tion that  a  careful  microscopic  exaraination  of  the  spinal  cord  in  one  case  of  very 
severe  arthritis  deformans  yielded  an  entirely  negative  result. 

[Some  striking  cases  are  reported  by  Blake,  which  go  to  show  that  the  arthritic 
■changes  may  be  set  up  by  chronic,  though  slight,  suppuration,  in  analogy,  perhaps, 
with  the  synovitis  of  gonorrhoea.  Careful  examination  should  consequently  be 
made  of  all  the  mucous  membranes,  especially  in  cases  which  seem  to  have  no 
connection  with  true  rheumatism.] 

Chronic  arthritis  is  mainly  a  disease  of  advanced  years.  Certain  monarticular 
varieties,  about  whose  etiology,  it  must  be  confessed,  we  know  little  as  yet,  have 
been  termed  arthritis  senilis — in  particular  the  malum  coxoe  senile.  Even  the 
common  and,  in  a  certain  sense,  typical  form  of  arthritis  deformans  (vide  infra) 
is  not  apt  to  occur  in  people  under  thirty-five  years  of  age.  This  rule,  however, 
has  exceptions,  and  we  have  ourselves  seen  a  few  perfectly  characteristic  cases  of 
arthritis  deformans  in  children  between  ten  and  fifteen  years  of  age.  Women  are 
much  oftener  attacked  than  men.  It  is  often  said  that  trouble,  anxiety,  and  other 
emotional  influences  favor  the  outbreak  of  the  disease;  but  the  proof  of  this  is 
lacking.    The  disease  does  not  often  seem  to  be  hereditary. 

Pathology. — The  process  is  described  as  simple  chronic  arthritis  (or  synovitis) 
so  long  as  it  is  conflned  mainly  to  the  synovial  membrane  of  the  joint  and  the 
periarticular  connective  tissue.  These  parts  often  undergo  decided  inflammatory 
thickening  (synovitis  hyperplastica)  ;  the  synovial  membrane  becomes  cloudy; 
and  the  amount  of  synovial  fluid  is  more  or  less  increased  (synovitis  serosa) — 
that  is,  we  have  chronic  dropsy  of  the  joint.  Sometimes  different  parts  of  the 
synovial  membrane  are  connected  by  adhesions,  which  considerably  interfere  with 
the  movements  of  the  joint.  There  may  even  be  complete  anchylosis :  for  exam- 
ple, in  the  shoulder  or  knee. 

Chronic  synovitis  may  pass  imperceptibly  into  arthritis  deformans.  In  this, 
not  only  the  capsules  of  the  joint,  but  the  articular  cartilages  and  the  articular 
extremities  of  the  bones,  are  so  much  affected  as  to  produce  the  most  striking 
deformity.  These  changes  almost  always  originate  in  the  articular  cartilages. 
In  many  cases  the  morbid  process  consists  merely  in  a  flbrillation,  destruction 
and  wearing  away  of  the  articular  cartilage,  beginning  usually  on  its  outer  edge ; 
finally,  the  bone  is  exposed  and  itself  undergoes  ulceration.  All  this  while,  the 
articular  capsule  may  escape  involvement,  and  there  may  be  no  serous  effusion 
into  the  joint  (arthritis  sicca).  In  other  cases,  however,  there  are  soon  added 
proliferative  changes  affecting  not  only  the  cartilage  itself,  but  also  the  synovial 
membrane.  The  inner  surface  of  the  synovial  membrane  becomes  tufted,  and 
many  of  these  tufts  may  undergo  secondary  calcification,  break  off,  and  become 
loose  bodies  in  the  joint.  The  articular  cartilages  are  also  affected  by  inflamma- 
tory new  growth  and  proliferation ;  these  in  part  become  disintegrated,  and  lead 
to  deeper  and  deeper  excavations  of  the  cartilage.  Erom  the  cartilage  the  pro- 
cess extends  to  the  bones,  and  thus  at  last  the  articular  extremities  of  the  bones 
become  almost  completely  destroyed.  Sometimes,  also,  the  periosteum  near  the 
joints  undergoes  ossific  periostitis.  On  microscopic  examination,  we  flnd  flbrous 
44 


690 


DISEASES    OE   THE   OEGANS    OF   LOCOMOTIOIT 


disintegration  of  tlie  matrix  of  the  cartilage,  and  proliferation  and  subdivision  of 
the  cartilage-cells,  at  the  same  time  that  there  is  destruction  of  the  newly  formed 
cells  by  simple  or  fatty  degeneration. 

Of  course  the  normal  structure  of  the  joint  is  at  last  completely  destroyed  by 
these  various  processes.  The  articular  extremities  of  the  bones  waste  away  more 
and  more,  and  take  new  relative  positions,  as  the  parts  which  impinge  upon  each 
other  are  worn  away.  Externally,  the  joint  usually  becomes  larger  and  larger; 
and  this  is  the  more  evident  because  the  surrounding  muscles  undergo  great 
atrophy.  There  is  often  no  collection  of  synovial  fluid  in  the  joints  during  the 
entire  illness,  but  sometimes  the  joints  are  swollen — e.  g.,  the  knee  joint — and 
even  to  a  considerable  degree.  There  is  a  tendency  for  the  affected  joints  to 
suffer  more  or  less  complete  anchylosis  and  contracture  (vide  infra). 

Symptomatology. — The  clinical  symptoms  of  chronic  arthritis  are  very  simple 
and  uniform.     They  relate  almost  exclusively  to  the  local  disturbances,  and  to 

these  they  are  directly  due.  The  gen- 
eral course  of  the  disease,  however,  pre- 
sents great  diversities.  Often  the  ar- 
thritis limits  itself  to  a  single  joint  or 
to  a  few  joints;  in  other  cases  almost 
all  the  joints  become  finally  involved. 

Except  in  the  cases  which  are  pre- 
ceded by  acute  articular  rheumatism, 
the  disease  usually  begins  quite  gradu- 
ally and  insidiously.  The  first  subjec- 
tive symptoms  are  stiffness  and  pain  in 
the  joints,  the  pain  being  aggravated  by 
pressure  or  movement.  The  stiffness  is 
most  noticeable  when  the  joint  has  re- 
mained quiet  for  some  time  previous, 
and  is  therefore  ordinarily  greatest  on 
waking  up  in  the  morning.  The  pain 
often  shoots  from  the  joints  upward  and 
downward,  and  is  of  a  burning  character, 
or  less  often  neuralgic.  Even  in  ad- 
vanced cases  the  pain  usually  occurs 
only  when  the  affected  joints  are  moved, 
although  then  it  may  be  very  severe. 
When  the  body  is  entirely  at  rest  there 
is  little  or  no  pain.  Besides  actual  pain 
there  are  apt  to  be  at  the  onset  of  the 
disease  peculiar  parsesthesias  and  other 
nervous  symptoms,  particularly  in  the 
fingers.  Motion  is  impaired  very  early. 
This  is  due  at  first  to  the  pain,  and  to 
a  certain  reflex  inhibition  and  ataxia  of  the  muscles ;  to  which  are  later  added  the 
purely  mechanical  hindrances  and  the  ever-increasing  atrophy  of  the  muscles. 
The  objective  changes  in  the  affected  joints  begin  to  appear  soon  after  the 
symptoms  just  mentioned,  at  least  in  cases  of  any  severity.  The  joints  often  seem 
enlarged  and  thickened.  If  we  attempt  to  move  them,  we  not  only  cause  pain 
and  meet  with  mechanical  obstruction,  but  we  may  hear  and  feel  the  cracking  and 
grating  produced  by  the  rubbing  of  the  denuded  and  uneven  surfaces  upon  each 
other.  This  is  often  noticed  by  the  patient  himself.  In  chronic  arthritis  sicca 
there  may  be  no  great  swelling  of  the  joints;  still,  there  are  usually  marked 
pain,  crepitation,  and  impairment  of  motion. 


Fig.  76. — Appearance  of  the  hand  in  a  case  of  "pro- 
tracted arthritis  deformans  (personal  observation). 


CHEONIC   EHEUMATISM   AND   AKTHKITIS    DEFOEMAl^TS    691 

As  the  disease  gradually  progresses,  there  are  usually  developed  certain  char- 
acteristic deformities,  which  are  apt  to  be  most  strikingly  exhibited  in  the  hands 
(see  Fig.  76).  The  metacarpo-phalangeal  joints  are  thickened  and  swollen,  and 
are  made  all  the  more  prominent  because  the  interossei  upon  the  back  of  the  hand 
are  atrophied.  The  bases  of  the  first  phalanges  are  directed  obliquely  toward  one 
side,  so  that  the  fingers  assume  more  and  more  the  appearance  of  subluxation. 
They  are  bent  over  toward  the  back  of  the  hand,  and  are  also  displaced  toward 
the  ulnar  side,  so  that  they  often  actually  come  to  rest  one  upon  the  other.  The 
palm  of  the  hand  is  frequently  deeply  hollowed  out.  Often  the  phalangeal  joints 
also  are  distorted,  so  that,  for  example,  there  will  be  an  obtuse  angle  on  the  dorsal 
surface  of  the  fingers  between  the  first  and  second  phalanx,  while  the  terminal 
phalanx  is  apt  to  be  flexed,  although  the  second  phalanx  preserves  a  position  of 
extension.  Despite  these  changes,  many  patients,  if  only  the  thumb  remains 
tolerably  movable,  are  able  to  use  their  hands  for  quite  delicate  work,  although 
at  the  expense  of  much  time  and  effort.  Arthritis  deformans  scarcely  ever  causes 
anchylosis  of  the  small  joints  of  the  fingers.  The  elbow-joints  are  often  decidedly 
enlarged.  The  forearms  usually  assume  a  position  of  pronation,  combined  with 
more  or  less  flexion.  Even  the  mobility  of  the  shoulder- joints  progressively 
diminishes,  so  that  at  last  the  arms  can  not  be  raised  at  all.  At  the  same  time 
there  is  contracture  of  the  adductor  muscles. 

With  regard  to  the  lower  extremities,  the  hip-  and  knee-joints  usually  suffer 
more  than  the  ankle.  Sometimes  there  are  thickenings  of  the  joints  and  serous 
effusions,  and  sometimes  arthritis  sicca.  If  the  joints  of  the  lower  extremities 
are  much  involved,  of  course  standing  and  walking  grow  more  and  more  painful 
and  difficult,  and  finally  require  crutches,  or  an  assistant.  Very  often  there  is 
marked  contracture  of  the  flexor  muscles  of  the  hip,  and  still  oftener,  of  the 
knee.  This  is  not  associated  with  anchylosis  of  the  joints,  but  is  of  purely  mus- 
cular origin.  In  such  cases  the  patient  can  not  sit  in  bed  with  the  knees  ex- 
tended (see  Fig.  77).  There  is  sometimes  subluxation  of  the  hip-joints,  so  that 
the  head  of  the  femur  slides  backward  and  upward.  The  same  thing  is  observed 
also  in  very  severe  cases  in  the  knee-joint. 

There  are  monarticular  and  polyarticular  forms  of  the  disease.  The  mon- 
articular form  is  usually  regarded  as  a  surgical  trouble,  and  is  most  often  located 
in  the  hip-joint  {malum  coxw  senile),  or  more  rarely  in  the  knee-  and  shoulder- 
joints.  The  polyarticular  form  is  the  characteristic  one.  In  most  of  the  typical 
cases  it  begins  in  the  small  joints  of  the  hand  and  fingers.  At  a  later  period 
the  larger  joints  are  also  invaded,  one  after  the  other,  the  invasion  taking  place 
symmetrically  on  both  sides  of  the  body,  although  the  disturbance  is  not  in- 
frequently greater  on  one  side  than  on  the  other.  In  severe  cases  the  joints  of 
the  spinal  column  also  are  involved.  This  impairs  particularly  the  movement 
of  the  head.  The  articulation  of  the  lower  jaw  is  usually  very  little  affected, 
if  at  all. 

In  less  frequent  instances  the  arthritis  is  confined  principally  to  the  lower 
extremities,  while  the  upper  escape  intact  for  a  long  while,  or  even  permanently. 
It  is  very  possible  that  such  cases  often  have  a  different  aetiology  from  ordinary 
arthritis  deformans ;  and  the  same  is  true  of  the  cases  which  are  confined  mainly 
to  the  vertebral  column,  and  are  termed  spondylitis  deformans.  A  remarkable 
and,  as  it  seems  to  us,  unique  disorder  may  be  mentioned  in  passing.  It  leads 
very  gradually  and  painlessly  to  a  complete  anchylosis  of  the  entire  spinal  column 
and  the  hip-joints  (chronic  spondylitis  and  coxitis,  with  anchylosis),  so  that  head, 
trunk,  and  thighs  are  firmly  united  and  completely  stiffened,  while  all  the  other 
joints  retain  their  normal  mobility.  It  need  scarcely  be  said  that  this  necessarily 
causes  a  peculiar  modification  of  the  carriage  and  gait  of  the  sufferer.  We  have 
ourselves  seen  two  typical  cases  of  this  peculiar  disease,  and  recently  other  physi- 


692 


DISEASES    or   THE    OEGANS    OF   LOCOMOTIOl^ 


eians  have  reported  precisely  similar  observations.     Marie  has  proposed  for  them 
the  name  "  spondylose  rhizomelique." 

There  is  hardly  any  affection  of  parts  of  the  body  other  than  the  joints  in 
arthritis  deformans.  The  muscles  should  be  excepted,  for  they  always  undergo 
that  muscular  atrophy  which  we  have  already  described  (vide  page  680)  as  the 
result  of  joint  disease.    This  atrophy  is  most  marked  in  the  interossei,  the  shoulder 


Fig.  77.— Chronic  arthritis  deforuiaus  with  coutraeture  of  the  hip-  aud  kuee-joiuts. 

muscles,  and  the  muscles  of  the  calf  and  thigh.  The  associated  muscular  con- 
tractures (vide  supra)  are  also  of  great  importance.  Sometimes  the  skin  over  the 
wrist  and  other  affected  joints  appears  peculiarly  wrinkled  and  flabby.  The  inter- 
nal organs  almost  always  perform  their  functions  in  a  perfectly  normal  manner. 
Appetite  and  digestion  remain  good,  although  there  is  often  some  tendency  to 
constipation.  Rarely  there  is  valvular  disease  of  the  heart,  but  usually  only  in 
such  cases  as  originate  in  an  acute  articular  rheumatism.  Still,  we  have  seen 
valvular  disease,  exceptionally,  in  cases  which  had  been  chronic  from  the  start,  a 
fact  which  is  not  without  interest  from  an  setiological  point  of  view.  Certain 
attendant  symptoms  which  are  sometimes  observed,  such  as  headache,  congestive 
states,  psychical  depression,  and  bronchitis,  probably  are  not  directly  connected 
with  the  disease,  but  are  easily  explicable  sequelae. 

General  Course  of  the  Disease. — Arthritis  deformans  is  an  extremely  chronic 
trouble.     It  may  last  even  ten  or  twenty  years,  or  more.     Sometimes  there  is  an 


CHRONIC   RHEUMATISM   AND   ARTHRITIS   DEFORMANS    693 

apparent  arrest  of  the  process  extending  over  months,  or  even  longer.  Sometimes 
the  progress  of  the  disease  is  marked  by  remissions  and  exacerbations,  affecting 
either  the  general  or  the  local  manifestations.  In  general,  however,  the  disease 
continually  advances. 

The  prognosis  is  therefore  unfavorable.  Recovery,  if  it  ever  occurs,  is  ex- 
tremely rare,  and  is  possible  only  in  the  early  stages.  For  the  encouragement  of 
the  patient,  it  may  be  said  that,  under  proper  care  and  treatment,  the  disease  often 
runs  so  gradual  a  course  that  the  general  condition  remains  at  least  bearable  for  a 
very  long  while,  although  there  may  be  considerable  local  disturbance.  The  dis- 
ease is  not  directly  dangerous  to  life.  The  eventual  fatal  termination  ensues 
either  from  general  debility,  or  because  of  some  intercurrent  disease. 

The  prognosis  is  somewhat  more  favorable  in  the  milder  cases  of  "  chronic 
articular  rheumatism,"  where  the  anatomical  changes  are  less  severe,  and  are 
completely  limited  to  the  synovial  membrane.  Even  here,  however,  recovery  is 
by  no  means  frequent,  and  it  is  always  to  be  feared  that  grave  deformities  of  the 
joints  will  gradually  be  developed. 

Treatment.^With  regard  to  regimen,  it  is  requisite  in  the  first  place  to  avoid 
all  unfavorable  external  influences.  If  possible,  the  dwelling  should  be  dry  and 
warm;  and  it  may  ofteu  seem  advisable  to  make  a  change  of  climate.  The  patient 
must  dress  warmly,  without,  however,  undermining  his  powers  of  resistance  too 
much,  as  he  will  be  in  danger  of  doing.    The  diet  must  be  abundant  and  nutritious. 

Internal  remedies  may  be  tried,  with  the  hope  of  modifying  the  disease,  but  our 
chief  reliance  must  be  upon  local  treatment  of  the  joints.  Among  internal  reme- 
dies, the  most  important  are  iodine  and  arsenic.  Iodine  may  be  given  in  the  form 
of  tincture  (a  few  drops  in  mucilage  several  times  a  day),  or  a  better  form  is  in 
combination  with  potassium.  As  yet,  we  ourselves  have  not  seen  any  great  benefit 
from  iodine,  but  we  have  in  repeated  instances  witnessed  a  quite  striking  result 
from  the  use  of  arsenic.  It  is  best  administered  in  pills  containing  one  thirtieth 
to  one  fifteenth  of  a  grain  (gramme  0.002-0.004)  of  arsenious  acid,  one  pill  two 
or  three  times  a  day.  If  this  remedy  prove  beneficial,  it  must  be  continued  for  at 
least  months,  perhaps  with  occasional  brief  intermissions.  The  persistent  use  of 
small  doses  of  salicylic  acid  or  salicylate  of  soda,  thirty  to  forty-five  grains  a  day 
(grammes  2-3),  and  similar  remedies,  is  recommended  by  many  ijhysicians.  We 
have  ourselves  seen  no  special  advantage  from  their  employment,  and  therefore 
usually  prescribe  them  only  during  acute  exacerbations  of  the  disease.  The  prep- 
arations of  colchicum  may  be  tried,  but  they  will  seldom  be  found  efficient.  Iron, 
quinine,  and  cod-liver  oil  are  sometimes  indicated  by  the  general  condition. 

First  among  local  methods  of  treatment  comes  massage,  although  the  g'ood  it 
accomplishes  is,  of  course,  apt  to  be  evanescent.  It  will,  however,  do  much  to 
hasten  the  absorption  of  inflammatory  exudations,  and  also  to  loosen  up  the 
joints,  invigorate  the  miiscles,  and  improve  the  general  health.  The  Swedish 
movement  cure  will  be  found  of  great  benefit  in  all  cases  if  begun  early  and 
methodically  persevered  in.  It  preserves  the  mobility  of  the  joints  as  long  as 
anything  can.  Electricity  also  has  a  beneficial  influence.  The  galvanic  current 
is  applied  to  the  affected  joints,  and  the  faradic  current  to  the  atrophied  muscles. 

Baths  are  universally  employed  in  chronic  arthritis.  Their  value  should  not  be 
overestimated,  but,  notwithstanding,  their  usefulness  is  undeniable  in  many  cases. 
Simple  warm  baths,  or  salt-baths  (five  to  ten  poimds  of  salt  for  each  bath),  are 
practicable  in  almost  any  household.  As  health-resorts  in  arthritis  deformans,  ex- 
perience shows  the  following  to  be  most  desirable :  The  simple  warm  baths,  such 
as  Teplitz,  Wildbad,  Ragatz,  and  Baden  in  Switzerland;  the  warm  chloride-of- 
sodium  baths  in  Wiesbaden;  the  acidulated  baths  of  Oeynhausen  and  Nauheim; 
and  the  mud-baths  of  Elster,  Marienbad,  Franzensbad,  and  Schmiedeberg. 
Steam-baths  are  admissible  only  in  the  early  stages  of  the  disease,  and  for  pa- 


694  DISEASES    OE   THE    OEGAls'S    OE   LOCOMOTIOE" 

tients  whose  general  condition  is  still  vigorous.  Even  then  they  should  be  em- 
ployed cautiously. 

[The  mineral  springs  within  the  limits  of  our  own  country  chiefly  to  be  recom.- 
mended  are  Sharon  and  Richfield,  in  Xew  York  State,  the  Sulphur  Springs  and 
Hot  Springs  of  Virginia,  and  the  Hot  Springs  of  Arkansas.  At  the  two  former, 
particularly,  there  is  every  provision  for  comfort  as  well  as  for  the  use  of  the 
waters.] 

We  have  repeatedly  seen  quite  excellent  results  follow  the  employment  of  hot 
sand-baths.  These  also  can  be  easily  used  at  home,  particularly  if  applied  merely 
to  the  hands  or  feet.  They  are  employed  more  elaborately  in  Kostritz  and  Blase- 
witz.  These  hot  sand-baths  seem  to  do  good,  not  only  from  the  temperature, 
but  also  from  the  uniform  and  persistent  compression  which  they  exert.  Some- 
times, also,  the  long-continued  local  application  of  warmth,  of  hot  compresses  and 
packs,  is  very  efPective.  Recently  special  apparatus  has  been  constructed  (fii*st  in 
England)  for  the  local  application  of  hot  air.  The  diseased  parts  are  thus  ex- 
posed for  about  an  hour,  in  closed  copper  chambers,  to  a  heat  of  150°-212°  (65"^- 
100°  C.)  and  higher.  The  reports  as  to  the  success  obtained  in  this  way  are  very 
favorable  [but,  unfortunately,  they  are  not  fully  confirmed  by  experience. — Y.] . 

Stimulating  or  narcotic  remedies  may  be  rubbed  into  the  joints,  but  they  are 
beneficial  only  because  of  the  massage  which  accompanies  their  emplojTuent.  In 
practice  it  is  not  always  possible  to  omit  their  use.  The  application  of  tincture  of 
iodine  is  usually  entirely  without  effect.  As  to  morphine  and  other  narcotics,  the 
disease  is  so  chronic  that  it  is  desirable  to  employ  them  as  little  as  possible.  A 
considerable  number  of  those  who  suffer  from  chronic  arthritis  become  opium- 
eaters.  We  should  try,  therefore,  if  there  is  severe  pain,  to  give  relief  as  long  as 
possible  with  antipyrine,  phenacetine,  and  similar  remedies. 

We  may  say,  therefore,  that  the  use  of  the  various  remedies  which  have  been 
suggested  one  after  another  will  enable  us  to  oppose  some  obstacles  to  the  progress 
of  the  disease.  Persistent  treatment  will,  in  many  cases,  be  rewarded  by  consider- 
able, at  least  temporary,  improvement. 


CHAPTER   m 

ACUTE    AND    CHRONIC    MTJSCTJLAR    RHEUMATISM 

{ITi/ositis^  or  Myalgia,  RJieumatica) 

Definition  and  .ffitiolo^. — Certain  acute  ajffections  may  originate  primarily 
in  the  muscles.  These  are  to  all  appearance  inflammatory  in  their  nature,  and 
not  infrequently  result  from  taking  cold,  or  other  causes  similar  to  those  which 
produce  acute  articular  rheumatism.  These  affections  are  classed  as  "  acute  mus- 
cular rheumatism  "  or  rheimiatic  myositis.  It  is  possible  that  this  disease  also  is 
an  infectious  one,  but  the  question  remains  entirely  undecided.  The  analogy 
which  this  trouble  bears  to  acute  articular  rheumatism  is  not  complete.  It  is  sel- 
dom that  the  two  processes  are  seen  in  combination;  and,  furthermore,  acute 
myositis  is  not  "  polymuscular,"  but  is  usually  confined  to  one  muscle,  or  to  a  sin- 
gle group  of  muscles;  it  is  attended  with  little  if  any  fever;  and  it  is  never  fol- 
lowed by  acute  endocarditis.  The  two  diseases,  therefore,  are  alike  only  in  certain 
symptoms  (pain  and  impairment  of  motion),  and  in  the  fact  that  they  are  often, 
although  not  always,  ascribable  to  cold  or  the  like. 

There  are  many  cases  in  which  pain  suddenly  occurs  in  the  muscles  ("  my- 
algia ")  without  any  attendant  objective  change.     These  cases  can  not  be  called 


ACUTE   AND    CHKONIC   MUSCULAR   RHEUMATISM  695 

genuine  acute  myositis.  Indeed,  it  is  sometimes  difficult  to  know  how  to  regard 
them.  In  practice  they  are  usually  termed  muscular  rheumatism,  especially  when 
they  are  referable  to  exposure;  and  it  is  possible  that  many  such  cases  are  really 
a  very  mild  form  of  the  genuine  inflammatory  disease.  Yet  in  our  opinion  it  is 
perfectly  possible  that  some  chemical  change  in  the  substance  of  the  muscle  occa- 
sions the  local  disturbance.  That  the  influence  of  cold  is  often,  though  not  always, 
important  in  this  connection,  seems  to  us  indubitable.  There  are  individuals  who 
are  almost  certain  to  have  a  stiff  neck  if  they  are  exposed  to  any  decided  draught 
npon  the  back  of  the  neck ;  and  others  who,  every  time  they  get  chilled,  are  liable 
to  lumbago.  However,  other  injurious  influences  may,  of  course,  be  important. 
Thus,  traumatic  pain  in  the  muscles  is  the  result  of  some  excessive  strain,  and  in 
many  instances  is  apparently  due  to  laceration  of  some  of  the  muscular  fibers. 
This  is  generally  occasioned  by  too  violent  muscular  exertion.  Any  physician 
who  sees  many  patients  from  the  laboring  classes  meets  with  an  abundance  of 
cases  of  this  sort.* 

The  limitations  of  acute  muscular  rheumatism  are  obscure;  but  still  more  so 
^re  those  of  "  chronic  muscular  rheumatism."  This  disease  also  is  a  frequent  one, 
and  only  imperfectly  understood.  It  does  not  bear  a  close  analogy  to  chronic 
articular  rheumatism,  except  in  this  unimportant  point,  that  chronic  muscular 
rheumatism  seems  to  be  quite  often  occasioned  by  meteorological  influences. 
While  the  anatomical  changes  in  chronic  articular  rheumatism  are  almost  always 
striking,  analogous  lesions  are  very  exceptional  in  chronic  muscular  rheumatism. 
On  the  contrary,  the  name  is  usually  applied  to  cases  where  there  is  pain  in  various 
muscles  all  over  the  body,  but  where  there  is  no  discoverable  objective  disturb- 
ance. Older  authorities  used  to  sjjeak  of  "  rheumatic  induration  "  of  the  muscles, 
hut  this  or  any  other  actual  anatomical  change  is  very  exceptional. 

These  facts  justify  a  doubt  as  to  whether  all  cases  of  chronic  muscular  rheu- 
matism actually  deserve  their  name.  It  is  certainly  quite  appropriate  in  those 
jiot  infrequent  cases  which  seem  to  be  due  to  "  rheumatogenous  influences,"  and 
are  so  evidently  aggravated  upon  every  exposure  to  cold,  or  every  period  of  bad 
weather,  that  the  patient  often  asserts  that  he  carries  in  his  bones  the  best  of 
Taarometers.  Such  is  the  "  old  rheumatism  "  of  those  who  have  passed  a  large  part 
of  their  lives  in  the  open  air,  regardless  of  wind  or  weather.  There  are  other  cases, 
the  character  of  which  is  different.  In  them  the  muscular  pain  is  associated  with 
a  general  neurasthenic  condition,  or  with  corpulence  (when  it  is,  perhaps,  the 
result  of  circulatory  disturbance),  or  possibly  with  chronic  poisoning.  An 
important  instance  is  the  "  rheumatic  pain  "  sometimes  complained  of  by  topers, 
which  we  are  inclined  to  ascribe  not  to  changes  in  the  muscles  but  to  nutritive 
•disturbances  of  the  nerves.  For  these  and  similar  disorders  there  are  no  special 
names,  and  the  practicing  physician  often  terms  them  all  "  muscular  rheuma- 
tism," a  diagnosis  with  which  the  patient  is  usually  quite  contented. 

Clinical  History. — Genuine  acute  muscular  rheumatism  is  ordinarily,  as  has 
been  said,  limited  to  some  one  definite  group  of  muscles.  The  affected  muscles 
often  seem  somewhat  swollen  and  infiltrated,  are  very  sensitive  to  pressure,  and, 
if  not  quite  useless,  are  nearly  so,  greatly  impairing  the  motion  of  the  correspond- 
ing member  of  the  body.  All  these  symptoms  are  best  illustrated  in  acute  myo- 
■sitis  of  the  deltoid  (omalgia).  The  whole  shoulder  is  swollen,  the  muscle  is  very 
painful,  and  the  upper  arm  is  almost  incapable  of  voluntarj^  motion,  although,  if 
caution  be  exercised,  passive  movement  can  be  made  without  causing  any  pain. 

The  various  forms  of  acute  muscular  rheumatism  have  received  names  descrip- 

*  Some  time  ago  the  author  saw  an  organ-  player  who  had  to  work  the  pedals  for  many  hours  a 
•day ;  he  had  an  extremely  painful  affection  of  the  lower  extremities  associated  with  swelling,  which 
could  be  regarded  only  as  an  acute  myositis. 


696  DISEASES    OE   THE    OEGA^Tg    qY   LOCOMOTION 

tive  of  the  locality  of  the  affection.    We  have,  besides  the  omalgia  already  men- 
tioned— 

1.  Rheumatism  of  the  cervical  muscles  (splenius,  trapezius,  sterno-cleido-mas- 
toid,  etc.).  Myalgia  cervicalis,  or  rlieumatic  torticollis.  The  pain  is  located  in 
the  back  and  side  of  the  neck,  and  is  usually  unilateral.  The  head  is  held  stiffly 
to  one  side,  the  occiput  inclines  toward  the  painful  side,  and  the  chin  is  turned 
toward  the  healthy  side.  All  active  and  passive  motions  which  tend  to  stretch  the- 
painful  parts  are  much  impaired,  and  cause  suffering. 

2.  Myalgia  lurnbalis,  or  lumbago.  This,  the  most  acute  form  of  muscular  rheu- 
matism, known  among  the  common  people  in  Germany  because  of  its  sudden  onset 
as  "  witch's  shot,"  or  "  dragon  shot,"  is  a  well-known  disease.  The  region  of  the 
sacrum  and  loins  in  a  greater  or  less  extent  (erector  spin^,  quadratus  lumborum, 
etc.)  is  very  sensitive.  All  motions  of  the  trunk,  such  as  bending  and  twisting,  are 
very  painful  and  difficult.  The  disease  is  more  frequent  in  men  than  in  women.. 
Certain  persons  seem  to  be  especially  predisposed  to  it.  It  should  also  be  stated 
that  lumbago  is  not  always  of  a  rheumatic  character,  but  of  traumatic  origin,  as 
from  lifting  a  heavy  weight,  or  from  sudden  stooping.*  [It  is  very  common  in 
the  traumatic  neuroses,  where  it  was  once  regarded  as  indicative  of  spinal  in- 
jury.— ^K.] 

3.  Rheumatism  of  the  thoracic  m,uscles,  and  particularly  of  the  intercostals. 
This  may  cause  great  discomfort,  as  it  renders  breathing,  coughing,  and  sneezings 
very  painful.  It  is  comparatively  rare ;  and  caution  should  be  exercised  in  diag- 
nosticating it,  to  avoid  confusion  with  pleurisy  and  periostitis  of  the  ribs.  Very 
often,  also,  thoracic  disturbance  is  regarded  as  rheumatic  when  it  is  really  trau- 
matic, being  the  result  of  stretching  or  laceration  of  the  fibers  of  the  pectoral  or 
other  muscles. 

4.  Rheumatism  of  the  head  also,  probably,  belongs  in  this  category,  although 
the  affection  is  seldom  confined  to  the  muscles  of  the  scalp,  but  involves  also  the 
fasciae,  and  may  even  be  almost  confined  to  them.  It  is  not  infrequently  excited 
by  exposure  to  cold.  The  pain  is  quite  violent,  and  greatly  increased  by  any 
movement  of  the  scalp.  Of  course,  the  diagnosis  requires  the  previous  exclusion 
of  the  various  forms  of  headache  described  on  pages  824  and  905. 

The  duration  of  acute  muscular  rheumatism  is  brief.  Usually  the  pain  abates 
in  a  few  days;  but  a  tendency  to  relapse  persists  for  some  time.  Constitutional 
symptoms  in  addition  to  the  local  disorder  are,  as  a  rule,  absent  or  slight ;  still,  we 
sometimes  meet  cases  in  which  acute  muscular  rheumatism  is  associated  with 
fever  and  marked  general  disturbance. 

In  chronic  rauscular  rheumatism  there  are,  as  a  rule,  no  objective  lesions  dis- 
coverable. The  statements  of  masseurs  as  to  palpable  nodes  and  indurations  are, 
in  our  opinion,  to  be  received  with  very  great  skepticism.  The  pain  is  seldom 
located  permanently  in  any  one  place,  but  it  is  felt  first  here  and  then  there.  It 
is  usually  increased  during  bad  weather,  and  is  less  severe  when  the  weather  is 
warm.  The  pains  are  often  described  as  "  wandering."  Motion  is  seldom  much 
impaired.  Sometimes,  however,  there  may  be  a  certain  stiffness  of  the  muscles, 
most  marked  after  a  period  of  repose. 

The  diagnosis  of  chronic  muscular  rheumatism  rests,  therefore,  mainly  upon 
the  rational  signs.    Hence  it  is  often  impossible  to  avoid  the  suspicion  of  malin- 

*  Lately,  S.  Erben  has  sought  to  prove  tliat  lumbacro  and  torticollis  are  not  at  all  muscular  diseases,, 
but  probably  in  most  cases  due  to  an  affection  of  the  joints  of  the  vertebrae.  He  bases  this  belief  upon 
the  result  of  painstaking  investigations.  One  who,  like  the  author  of  this  text-book,  has  often  him- 
self suffered  from  acute  muscular  rheumatism,  will  be  scarcely  inclined  to  adopt  this  view,  for  the  sub- 
jective sensation  of  pain  is  referred  decidedly  to  the  muscles,  or  to  the  attachments  and  fascite  of  the^ 
muscles. 


ACUTE   AND    CHEONIC   MUSCULAE   EHEIJMATISM  69^ 

gering,  particularly  where  certain  applicants  for  hospital  care  are  concerned.  We 
should  not,  however,  be  too  uncharitable,  since  without  doubt  there  are  cases 
in  which  quite  severe  pain  is  felt,  now  in  one  set  of  muscles  and  now  in  another, 
without  any  anatomical  basis  for  such  pain  being  discoverable.  Nor  should  we 
ever  forget  that  other  diseases  may  have  pain  for  their  first  symptom.  It  is  not 
at  all  exceptional  for  the  lancinating  pains  of  locomotor  ataxia  to  be  for  a  long 
time  regarded  as  "  rheumatic."  Lumbago  may  be  confounded  with  insidiously 
developing  tumors,  diseases  of  the  vertebrae,  renal  calculi,  or  with  various  hypo- 
gastric disorders  (particularly  in  women).  We  should  therefore  never  omit  to 
make  a  careful  physical  examination. 

Treatment. — Acute  muscular  rheumatism  has  this  in  common  with  acute 
articular  rheumatism,  that  it  is  usually  very  favorably  affected  by  salicylic  acid. 
In  cases  of  genuine  acute  rheumatic  myositis  the  employment  of  this  remedy  in 
the  manner  already  described  will  often  give  surprising  relief  in  as  short  a  time 
as  twelve  or  twenty-four  hours.  We  also  see  good  results  from  antipyrine  or  sali- 
pyrine,  etc.  Local  treatment  of  the  affected  muscles  also  may  be  followed  by  great 
and  speedy  improvement.  Massage  is  particularly  valuable.  It  is  not  infrequently 
the  case  that  a  single  properly  conducted  massage  will  cause  a  violent  lumbago  or 
omalgia  to  disappear  almost  completely,  and  like  favorable  results  are  witnessed 
when  there  is  traumatic  pain  in  the  muscles.  Most  of  the  external  applications 
which  are  so  frequently  prescribed  for  rheumatism — such  as  spirits  of  camphor  or 
chloroform  liniment — accomplish  less  through  the  cutaneous  irritation  they  pro- 
duce than  by  the  massage  incident  to  their  employment.  ISText  in  value  comes 
electricity.  Both  the  constant  and  the  faradic  current  may  be  enaployed.  Often, 
also,  the  local  application  of  warmth  is  very  beneficial ;  thus  hot  dry  cloths  or  hot 
poultices  may  be  applied.  Simple  stimulation  of  the  skin  by  mustard  is  often 
palliative,  but  less  so  than  the  first-mentioned  remedies.  Often  great  relief  is 
given  by  sweating,  by  means  of  a  hot  wet-pack,  or  by  a  steam-bath,  the  employ- 
ment of  which  is  so  common  that  patients  often  use  it  of  their  own  accord. 

In  chronic  muscular  rheumatism  the  benefit  of  salicylic  acid  and  antipyrine  is 
merely  temporary,  and  therefore  is  to  be  sought,  if  at  all,  only  when  there  is  an 
acute  exacerbation.  Massage  and  electricity  are  more  effective,  and,  if  persevered 
in  for  some  time,  will  often  accomplish  good  results  even  in  obstinate  cases. 
Treatment  by  sweating  and  bathing  is  frequently  prescribed  with  advantage. 
Steam-baths  are  often  beneficial,  but  their  use  requires  great  caution  when  the 
patient  is  corpulent  and  has  a  tendency  to  congestion  or  cardiac  failure.  There 
is  also  value  in  mud-baths,  pine-needle-baths,  and  in  the  baths  given  at  Teplitz, 
Wiesbaden,  and  other  places. 

In  many  case  of  chronic  muscular  rheumatism  constitutional  treatment  is  of 
great  importance.  Particularly  when  the  patient  is  overfed,  and  intemperate  in 
the  use  of  alcohol,  much  benefit  will  often  be  accomplished  by  a  proper  regulation 
of  the  ingesta  and  the  prescription  of  a  sufficient  amount  of  muscular  exercise. 
Such  patients  may  also  be  helped  by  a  cautiously  conducted  cold-water  treatment. 
This  lessens  their  great  sensitiveness  to  cold. 

[In  acute  cases  with  localized  pain  I  have  found  useful  a  thick  flaxseed  poul- 
tice, applied  as  hot  as  it  can  be  borne,  renewed  once  or  twice,  and  followed  by 
the  application  of  a  thick  layer  of  cotton.  A  dry  cup  or  two  is  also  often  pro- 
ductive of  great  relief.  In  chronic  cases,  plasters  and  the  iodide  of  potassium  are 
often  of  benefit. 

Muscular  rheumatism  is  a  common  and  often  very  troublesome  affection  in 
those  whose  occupation  calls  for  decided  muscular  exertion.  A  muscle  is  strained, 
pain  settles  in  and  is  apt  to  recur  in  the  part ;  and,  while  the  general  health  is  suf- 
ficiently good,  the  man  is  compelled  to  remain  idle.  Quack  advertisements  dwell 
so  much  upon  pain  in  the  back  as  a  symptom  of  Bright's  disease,  that  we  are  fre- 


698  DISEASES    OF   THE    OEGAl^S    OF   LOCOMOTIOIT 

quently  consulted  by  those  wlio,  suffering  from  muscular  pain  and  soreness,  think 
themselves  the  subjects  of  serious  disease  of  the  kidneys.] 


CHAPTEE   IV 
ACUTE    POLYMYOSITIS 

From  some  recent  obsei'vations  (E.  Wagner,  Unverricht,  and  others)  we  have 
obtained  knowledge  of  a  disease  which  consists  essentially  in  an  acute  inflamma- 
tion of  most,  or  even  of  all,  the  muscles  of  the  body.  The  disease  appears  chiefly 
in  persons  in  early  or  middle  life,  but  it  has  also  been  repeatedly  observed  in  the 
elderly.  The  disease  may  begin  either  quite  suddenly  or  gradually.  Sometimes 
polymyositis  is  a  sequel  of  some  other  disease,  most  often,  as  it  seems,  of  septic 
infections,  such  as  puerperal  fever  and  erysipelas.  This  circumstance  seems  to 
indicate  that  polymyositis  is  associated  with  severe  constitutional  intoxication. 

The  disease  usually  begins  with  decided  constitutional  disturbance,  including 
languor,  headache,  anorexia,  and  vomiting.  Very  soon  the  characteristic  muscu- 
lar pains  commence,  there  are  dragging  pains,  and  often  cramps  in  the  arms,  legs, 
and  trunk,  and  these  sooner  or  later  decidedly  impede  motion.  If  we  examine 
the  painful  places  we  find  a  marked  tenderness  upon  pressure  and  upon  passive 
motion.  Soon  we  can  perceive  a  distinct  swelling  of  the  parts  involved.  This  de- 
pends somewhat  upon  the  inflammatory  swelling  of  the  muscle,  and  still  more  upon 
a  firm  inflammatory  oedema  of  the  corresponding  skin,  which  usually  appears  very 
early.  As  a  rule,  the  upper  extremities  are  most  severely  attacked,  and  in  them, 
too,  the  inflammatory  oedema  is  most  marked.  The  forearm  swells,  particularly 
in  the  region  of  the  belly  of  the  muscles,  and  so  comes  to  have  a  characteristic 
spindle  shape,  provided  the  region  of  the  wrist-joint  is  not  involved.  The  face, 
the  trunk,  and  the  lower  extremities  also  present  similar  though  less  marked 
swellings  of  the  skin,  or  of  the  different  soft  parts,  particularly  on  the  extensor 
surfaces.  At  the  same  time,  the  skin  is  apt  to  be  distinctly  reddened  with  inflam- 
mation, so  that  it  almost  suggests  erysipelas  ("  dermatomyositis  ")•  Other  ex- 
anthems  also  may  appear — ^viz.,  erythema,  urticaria,  and  herpes.  If  the  disease 
lasts  some  time  the  swelling  gradually  disappears,  and  there  may  be  distinct 
atrophy  of  the  muscles.  The  patellar  reflex  is  usually  abolished  from  the  start. 
The  electric  excitability  of  the  muscles  rapidly  diminishes,  and  is  finally  de- 
stroyed. In  some  few  muscles  we  sometimes  observe  the  reaction  of  degeneration, 
but  a  careful  electrical  examination  is  always  very  difficult  because  of  the  great 
pain  it  causes.  The  sensibility  of  the  skin  in  cases  of  polymyositis  (vide  infra) 
remains  unimpaired. 

The  general  condition  becomes  very  much  aggravated  if  the  muscles  of  deg- 
lutition and  respiration  are  attacked ;  the  ingestion  of  food  is  rendered  more  and 
more  difficult,  and  there  is  severe  dyspnoea.  Soon  bronchitis  and  lobular  pneu- 
monia develop,  and  these  are  the  more  distressing  to  the  patient  because  expec- 
toration grows  increasingly  difficult  and  finally  quite  impossible.  ISTutrition  is 
often  interfered  with  by  stomatitis.  Tonsillitis  has  been  repeatedly  observed. 
Perspiration  is  decidedly  increased,  and  the  urine  may  contain  a  small  amount 
of  albumen.  Splenic  tumor  has  been  repeatedly  found  in  the  acute  cases.  The 
bodily  temperature  is  often  elevated,  101°-103°  (38.5°-39.5°  C.)  ;  the  pulse-rate 
may  rise  to  100  or  120  beats  per  minute. 

With  regard  to  the  clinical  course  of  the  disease,  we  should  make  a  distinc- 
tion between  the  acute  and  the  more  chronic  cases.    The  acute  may  end  in  recovery 


EACHITIS  699 

after  two  or  three  weeks.  Often,  however,  after  a  shorter  or  longer  course  of  from 
three  weeks  to  three  months,  a  fatal  termination  occurs,  probably  in  most  instances 
the  result  of  respiratory  disturbances,  secondary  pneumonia,  and  the  like. 
Chronic  cases  may  last  a  year  or  more. 

In  the  cases  observed  thus  far  there  has  been  found  on  examination  a  true 
acute  inflammation  of  the  muscles.  N"ot  only  do  the  muscular  fibers  show  all 
forms  of  degeneration  and  destruction,  but  also  in  the  interstitial  connective 
tissue  we  find  true  inflammatory  foci  (accumulation  of  nuclei  about  the  vessels, 
etc.).  In  a  case  which  we  examined  these  changes  were  apparently  to  be  found  in 
all  the  muscles,  even  in  the  tongue,  the  ocular  muscles,  etc.  In  genuine  poly- 
myositis the  peripheral  nerves  are  perfectly  normal.  Yet  recently  there  have  been 
repeated  observations  of  cases  in  which  a  genuine  polyneuritis  was  demonstrated 
along  with  genuine  polymyositic  lesions  (neuro-myositis) .  These  cases  indicate  a 
close  setiological  relation  between  polymyositis  and  polyneuritis  (q.v.).  At  the 
bedside  the  appearance  of  polyneuritis  as  a  complication  may  be  recognized  by 
slight  disturbances  in  sensation,  and  by  tenderness  along  the  nerve-trunks. 

The  diagnosis  of  polymyositis  is  not  difiicult,  on  the  whole.  The  pain  in  the 
muscles,  their  swelling,  the  impairment  of  motion,  the  inflammatory  changes  in 
the  skin,  etc.,  present  a  characteristic  clinical  picture.  It  is  important  to  exclude 
a  possible  trichinosis.  In  this  regard  we  must  consider  the  aetiology,  the  initial 
gastro-intestinal  symptoms,  and  the  oedema  of  the  face.  [It  is  not  yet  certain 
whether  eosinophilia  is  peculiar  to  the  myositis  occasioned  by  trichinae  or  common 
to  all  forms  of  it. — V.]  That  there  does  not  seem  to  be  any  sharp  dividing-  line 
between  polymyositis  and  polyneuritis  has  been  already  noted.  "We  would  like 
to  point  out,  also,  that  a  group  of  symptoms  very  similar  to  polymyositis  is  some- 
times excited  by  a  peculiar  disease  first  described  by  Kussmaul  and  Maier,  which 
is  as  yet  very  imperfectly  understood.  It  attacks  the  small  arteries  and  is  termed 
"  periarteritis  nodosa."  If  the  smaller  arteries  of  the  muscles  are  attacked,  with 
resultant  inflammation  of  the  vascular  wall,  thrombosis,  and  similar  changes, 
then  degeneration  of  the  muscular  fibers  ensues,  with  consequent  swelling,  pain, 
and  impairment  of  function.  At  the  same  time  there  are  usually  severe  con- 
stitutional symptoms,  such  as  fever,  anaemia,  nephritis,  and  severe  abdominal  pain. 

Treatment. — In  early  cases  of  acute  polymyositis  trial  should  be  made  of 
salicylic  acid  and  its  compounds,  antipyrine,  and  similar  remedies;  beyond  this, 
treatment  must  be  purely  symptomatic,  including  inunctions  of  chloroform  oil, 
the  administration  of  narcotics,  and  the  like.  Some  cases  may  be  benefited  by 
galvanism. 


CHAPTEE   y 

RACHITIS 

(Eickets) 


.ffitiology. — The  first  accurate  description  and  the  now  universal  name  of 
"  rachitis  "  (from  pacts',  the  spinal  column)  is  to  be  ascribed  to  the  Englishman 
Glisson,  who  published  a  comprehensive  monograph  upon  this  disease  in  1650.  It 
was  his  opinion  that  it  first  appeared  in  England,  in  the  beginning  of  the  seven- 
teenth century;  and  for  this  reason  rachitis  is  still  often  called  by  Germans  "  the 
English  disease." 

Although  the  clinical  and  anatomical  phenomena  of  rachitis  have  been  often 
and  accurately  investigated  since  Glisson's  time,  its  true  cause  still  remains  en- 
tirely unknown.    It  is  certain  only  that  its  development  is  promoted  by  all  unfa- 


TOO  DISEASES    OF   THE    OKGANS    OF   LOCOMOTION 

vorable  external  circumstances  affecting  the  nonrishment  and  health  of  the  child- 
It  is  therefore  more  frequent  among  the  poor  than  the  "wealthy,  in  the  damp  and 
crowded  quarters  of  large  cities  than  in  the  country,  and  among  artificially  fed,, 
and  therefore  weakly  and  ansemic  children,  than  such  as  receive  the  mother's 
milk.  Nevertheless,  the  essential  cause  of  the  disease  is  not  to  be  sought  among 
these  various  influences,  for  rickets  undoubtedly  does  occur,  although  rarely,  in 
children  whose  circumstances  seem  in  every  respect  most  favorable. 

Guerin,  Friedleben,  E.  Yoit,  Wagner,  Baginsky,  and  many  others  have  made 
very  exhaustive  experimental  researches  with  regard  to  the  development  of 
rachitis.  It  has  been  found  possible  to  produce  certain  changes  in  the  bones  of 
growing  animals  by  giving  them  as  little  lime  as  possible  in  their  ingesta,  or  by 
administering  very  large  amounts  of  lactic  acid,  with  the  purpose  of  dissolving 
the  calcium  salts,  or  by  giving  small  quantities  of  phosphorus.  The  changes  thus, 
caused  have  been,  with  more  or  less  correctness,  regarded  as  analogous  to  those 
of  rachitis.  These  investigations  are  of  great  interest  with  regard  to  the  physiol- 
ogy of  bony  structures  in  general,  but  in  our  opinion  they  throw  little  light  upon 
the  clinical  question  which  here  concerns  us.  It  is  indeed  natural  enough  to  sup- 
pose that  rachitis  in  childhood  may  be  due  to  an  insufficient  proportion  of  lime  in. 
the  food;  or  to  a  defective  absorption  of  the  lime-salts,  on  account  of  intestinal 
catarrh;  or  to  an  abnormally  abundant  production  of  lactic  acid,  or  even  of  car- 
bonic acid,  which  may  dissolve  the  lime-salts  in  the  system;  but  every  one  of 
these  theories  is  contradicted  by  the  facts  of  experience,  for  it  is  wholly  improper 
to  assume  that  the  food  of  children  with  rachitis  contains  less  lime  than  the  food 
of  healthy  children,  and  the  hypothesis  of  a  mere  poverty  in  lime  of  the  bony  tis- 
sues is  by  no  means  adequate  to  explain  the  whole  complicated  rachitic  process. 
In  our  opinion  everything  seems  to  indicate  that  some  special,  specific,  aetiological 
factor  is  requisite  for  the  development  of  rachitis.  This  factor,  however,  is  as  yet 
entirely  unknown  to  us.  The  thought  had  occurred  to  many  that  the  disease 
bears  some  relation  to  congenital  syphilis;  but  this  assumption  has  long  since- 
been  proven  to  be  entirely  without  foundation.  It  is  also  claimed  that  heredity 
plays  an  important  part  in  rachitis.  The  proof  of  this  is  lacking.  It  is,  however,, 
noteworthy  that  quite  often  several  children  of  the  same  family  are  attacked  by 
the  disease. 

Rickets  is  most  common  in  children  two  or  three  years  old.  According  to 
Kassowitz,  the  disease  usually  begins  in  the  first  months  of  life,  while  the  severe 
symptoms,  of  course,  appear  only  at  the  age  of  two  or  three  years.  Congenital 
rachitic  changes  (foetal  rachitis)  have  been  repeatedly  observed,  but  the  cases  of 
so-called  rachitis  tarda,  where  the  disease  is  said  to  develop  in  children  of  eight 
or  ten  years  of  age  and  over,  are  at  least  extremely  rare. 

Sex  exercises  no  great  influence  upon  the  occurrence  of  the  disease. 

Pathology. — Rachitis  consists  of  a  peculiar  disturbance  of  the  processes  con- 
nected with  the  growth  of  the  bones.  As  a  result  of  an  increased  absorption  of  the 
already  formed  bony  tissue,  and  especially  as  a  result  of  an  insufficient  or  an 
almost  wholly  deficient  deposition  of  lime-salts,  the  bones  become  or  remain 
abnormally  flexible  and  soft,  so  that  they  can  easily  be  cut  with  a  knife. 

Upon  minute  examination,  we  find  both  the  periosteum  and  the  marrow  much 
reddened  and  congested.  If  we  try  to  detach  the  thickened  periosteum  from  the- 
bone,  not  infrequently  a  few  bits  of  bone  adhere  to  the  membrane.  The  most 
striking  changes,  however,  are  exposed  upon  making  a  longitudinal  section  of  the 
bone.  They  are  located  at  the  bases  of  the  epiphyses,  because  here  is  the  place 
where  the  normal,  and  therefore  the  abnormal,  processes  of  ossification  are  most 
active.  Under  normal  circumstances,  the  epiphyseal  cartilage  of  the  bones  in 
childhood  is  separated  from  the  main  shaft  by  two  narrow  layers :  first,  an  outer 
one,  nearest  the  epiphyseal  cartilage,  of  a  bluish  color,  and  one  or  two  millimetres- 


EACHITIS  701 

thick;  this  is  the  proliferative  layer,  or  hyperplastic  zone,  where  the  cartilage-cells 
become  divided  and  arrange  themselves  in  rows.  Secondly,  an  inner,  dull  yellow 
layer,  only  about  half  a  millimetre  thick,  known  as  the  ossific  layer,  or  zone 
of  calcification,  in  which  the  real  process  of  ossification  takes  place — that  is, 
blood-vessels  grow  into  it,  osteoblasts  develop,  lime  is  deposited,  and  medullary 
spaces  are  hollowed  out.  In  healthy  bone  these  two  layers  are  parallel  to  each 
other,  and  are  limited  by  perfectly  straight  lines.  In  rachitic  bone,  on  the  other 
hand,  they  are  both  much  enlarged,  and  their  naturally  sharp  boundaries  are 
replaced  by  an  irregular  serrated  edge,  so  that  the  two  zones  encroach  mutually 
upon  each  other.  These  changes  affect  both  layers,  but  are  most  marked  in  the 
proliferative  layer.  Upon  microscopical  examination,  the  details  of  which  can 
not  be  given  here,  we  can  see  most  plainly  the  complete  confusion,  if  we  may  be 
permitted  to  use  the  expression,  into  which  the  growth  of  the  bone  has  fallen. 
The  proliferation  of  the  cartilage-cells  has  increased  beyond  all  bounds,  and  the 
scanty  matrix  of  the  cartilage  displays  a  fibrous  character.  In  the  bony  layer  are 
.seen  irregularly  scattered  foci,  which  are  already  undergoing  incomplete  calcifica- 
tion, or  else  marrow  formation,  breaking  down  the  cartilage.  The  latter  is  due  to 
an  invasion  of  the  vessels,  which  always  undergo  an  active  new  growth ;  they  per- 
meate the  cartilage  like  lacunar  spaces,  and  are  surrounded  by  a  so-called  osteoid 
tissue. 

The  periosteum  presents  analogous  changes.  The  innermost  osteoblastic  layer 
-of  the  periosteum  is  thickened ;  but  the  newly  formed  tissue  does  not  become  com- 
pletely calcified,  but  remains  in  large  part  soft  and  spongy.  Finally  an  increased 
absorption  of  bone  takes  place  inside  the  bones.  The  bony  partitions  disappear, 
and  the  cortical  layer  of  bone  often  becomes  much  thinner  than  normal. 

These  various  processes  furnish  a  direct  explanation  of  the  macroscopic  changes 
presented  by  rachitic  bones.  The  proliferative  process  causes  marked  swelling  of 
the  epiphyses  of  the  long  bones,  and  thickening  of  the  flat  bones  of  the  skull. 
The  abnormal  softness  of  the  bones  is  due  to  the  increased  absorption  of  bone, 
their  insufficient  calcification,  and  it  in  turn  causes  various  deformities,  which 
are,  for  the  most  part,  very  characteristic  (vide  infra).  If  recovery  takes  place, 
the  whole  bone  becomes  firm  at  last,  but  often  remains  permanently  deformed. 

The  deficient  development  of  rachitic  bones  can  also  be  recognized  upon  chem- 
ical examination.  While  normal  bones  in  a  dry  state  contain  about  sixty-three 
to  sixty-five  per  cent,  of  lime,  rachitic  bones  have  only  about  twenty  to  thirty 
per  cent. 

Clinical  History. — Rachitis  often  begins  so  insidiously  that  it  can  hardly  be 
detected.  Attention  is  not  called  to  the  disease  until  the  deformity  of  the  bones 
becomes  very  obvious,  or  it  is  noticed  that  the  child  does  not  learn  to  walk  as 
■early  as  other  children,  or,  having  already  learned,  is  no  longer  able  to  do  so. 
At  last  the  anxiety  of  the  parents  is  excited ;  and,  on  seeking  medical  advice,  they 
:find  their  fears  only  too  well  grounded. 

In  other  cases  the  appearance  of  the  characteristic  changes  in  the  bones  is 
preceded  by  certain  prodromes,  either  inflammatory  symptoms,  referable  to  the 
respiratory  tract,  or,  what  is  especially  frequent,  signs  of  acute  intestinal  disease. 
The  child  suffers  from  diarrhoea,  has  some  fever,  looks  pale,  and  grows  weak  and 
wretched.  At  night  he  is  restless,  screams,  bores  the  back  of  his  head  into  the 
pillow,  and  evinces  a  tendency  to  excessive  perspiration.  Often  there  is  a  slight 
■enlargement  of  the  spleen  even  at  this  period  (Oppenheim). 

The  diagnosis  of  rachitis  can  not  be  definitely  established  until  the  character- 
istic changes  in  the  bones  have  been  developed.  These  anomalies  vary,  of  course, 
in  their  severity  and  extent  in  different  cases.  We  append  a  list  of  the  most 
important : 

The  head  is  often  noticeable  for  its  great  size  and  somewhat  square  shape. 


702  DISEASES    OF   THE    OEGANS    OF   LOCOMOTION 

due  to  the  thickening-  of  the  parietal  and  frontal  eminences.  In  striking  contrast 
with  this  the  occiput  is  often  thin  and  soft,  so  that  it  can  be  pressed  in  like  parch- 
ment (Elsasser's  craniotahes).  This  is  particularly  noticeable  in  places  near  the 
lambdoidal  suture.  At  the  same  time  the  occiput  usually  becomes  bald,  because  of 
its  pressure  against  the  pillow.  The  fontanelles  remain  open  till  the  second  or 
third  year  of  life,  and  their  edges  seem  soft  and  yielding.  There  is  often  a  pecul- 
iar change  in  the  shape  of  the  jaws,  particularly  of  the  lower  jaw.  This  is  not 
rounded,  but  angular,  being  sharply  bent  in  the  neighborhood  of  the  canine  teeth ; 
so  that  the  incisors  stand  in  a  perfectly  straight  line,  besides  being  somewhat 
inclined  inward.  Fleischmann  was  the  first  to  describe  this  condition,  and  re- 
ferred it  to  the  action  of  the  mylohyoid  and  masseter  muscles  upon  the  soft  bone. 
Dentition  in  rachitic  children  is  usually  tardy,  irregular,  and  tedious.  More- 
over, the  teeth  are  soft  and  easily  worn  away. 

The  thorax  presents,  even  in  the  mildest  cases,  very  characteristic  and  notice- 
able changes.  There  is  a  swelling  at  the  junction  of  the  cartilages  with  the  ribs, 
which  can  be  felt  and  seen  through  the  skin,  and  produces  what  is  called  the 
"  rosary  of  rickets."  In  severe  cases  the  lateral  portions  of  the  thorax  are  often 
drawn  inward,  particularly  at  the  parts  which  correspond  with  the  insertion  of 
the  diaphragm.  This  change  is  due  mainly  to  the  action  of  the  diaphragm  during 
inspiration  upon  the  abnormally  soft  and  therefore  yielding  ribs.  The  changes 
are  greatest  when  the  respiratory  efforts,  and  particularly  abdominal  respiration, 
are  exaggerated  because  of  bronchitis,  pneumonia,  or  some  other  disease  of  the 
air-passages.  In  such  cases  the  entrance  of  air  into  the  lungs  is  impeded,  so  that 
it  is  possible  that  the  external  atmospheric  pressure  also  contributes  to  produce 
the  deformity  of  the  thorax.  Deep  hollows  may  finally  be  developed  on  each  side 
of  the  chest,  while  the  sternum  becomes  unusually  prominent,  giving  the  whole 
chest  that  shape  which  has  been  termed  pigeon-breast,  or  pectus  carinatum. 
When  once  this  deformity  has  been  developed,  of  course  it  in  turn  contributes  to 
render  respiration  difficult. 

The  clavicles  are  sometimes  distorted,  and  may  even  be  partially  fractured 
(vide  infra).  The  spinal  column  is  usually  unaffected  if  the  child  remains  quiet 
in  bed;  but  if  it  sits  up,  or  is  carried  about,  or  tries  to  walk,  the  traction  and 
pressure  thus  exerted  often  produce  curvature  of  the  spinal  column  (rachitic  scoli- 
osis and  kyphosis).  These  deformities  may  become  extreme.  Changes  in  the 
bones  of  the  pelvis  are  of  no  special  clinical  importance  at  this  period  of  the 
patient's  life;  but  in  women  the  consequent  shortening  of  the  antero-posterior 
diameter  of  the  pelvis  may,  as  is  well  known,  prove  a  great  obstacle  to  childbirth. 

The  extremities  not  only  present  swelling  of  the  epiphyses,  but  are  liable  to 
curvature.  This  latter  change  is  most  marked  in  the  lower  limbs,  inasmuch  as 
they  have  to  support  the  weight  of  the  body.  The  swelling  is  especially  well 
developed  at  the  lower  ends  of  the  bones  of  the  forearm  and  of  the  tibia  and  fibula. 
The  curvature  is  almost  invariably  greatest,  and  therefore  most  easily  recognized, 
in  the  tibia,  which  becomes  convex  outward,  giving  the  rachitic  child  its  "  bow- 
legs." Similar  curvature  of  the  femur  is  less  often  seen,  although  it  may  be 
obvious  enough  in  severe  cases.  The  same  is  true  of  the  humerus.  The  deformity 
of  the  lower  limbs  causes  that  waddling  gait  which  can  be  so  often  seen  on  the 
streets  of  any  large  city.  Sometimes  the  limbs  present  a  sharp  bend,  the  result  of 
partial  fracture.  These  "  green-stick  fractures  of  rachitis  "  are  invariably  refer- 
able to  some  slight  traumatism,  and  are  most  often  seen  in  the  lower  third  of  the 
tibia,  although  sometimes  visible  in  the  clavicles,  ribs,  and  bones  of  the  lower  arm. 
The  infraction  usually  takes  place  upon  one — generally  the  concave — side,  so  that 
it  is  often  compared  to  the  partial  fracture  of  a  quill  or  an  osier  rod. 

Symptoms  in  Other  Parts  of  the  Body. — Apart  from  the  changes  in  the  bones, 
a  rachitic  child  may  seem  to  be  perfectly  well.     Even  the  general  nutrition  may 


EACHITIS  T03 

be  unimpaired.  As  a  rule,  however,  rickets  is  associated  with  anjemia  and  im- 
paired nutrition.  The  muscles,  in  particular,  are  small  and  flabby.  The  child 
seems  pale,  thin,  and  feeble,  and  may  present  swollen  lymph-glands  and  other 
"  scrofulous  "  symptoms.  Sometimes  there  is  a  tendency  to  profuse  perspiration, 
especially  from  the  scalp.  Very  frequently  there  is  chronic  intestinal  catarrh, 
and  sometimes  there  is  chronic  bronchitis  or  lobular  pneumonia.  The  abdomen 
is  usually  prominent,  the  liver  and  spleen  are  frequently,  but  not  invariably,  en- 
larged. The  reader  should  also  be  remilided  that  rachitic  children  are  particularly 
liable  to  spasm  of  the  glottis  (laryngismus  stridulus)  and  convulsions,  due  per- 
haps to  the  rachitic  lesions  of  the  skull. 

The  faeces  and  urine  have  been  repeatedly  subjected  to  careful  chemical  inves- 
tigation in  the  hope  of  gaining  some  information  as  to  the  pathogenesis  of  the 
disease.  The  results  have  been,  however,  in  many  respects,  contradictory;  the 
most  accurate  of  these  investigations  have  shown  that  the  absorption  and  excre- 
tion of  the  calcium  salts  ingested  with  the  food  are  not  much  different  in  healthy 
and  in  rachitic  children. 

The  disease  almost  invariably  runs  a  chronic  course.  Usually  months,  or  even 
years,  pass  before  the  process  ends.  Its  termination  is  to  be  recognized  by  closure 
of  the  fontanelles,  increase  in  the  length  of  the  bones,  and,  above  all,  by  the  fact 
that  the  patient  becomes  stronger  and  makes  attempts  to  walk.  Unfortunately, 
many  results  of  the  disease  persist  through  life.  The  legs  are  crooked,  the  thorax 
deformed,  the  spinal  column  curved,  and  the  pelvis  narrowed.  Even  in  the  most 
favorable  cases  persons  who  have  once  had  rachitis  usually  remain  somewhat 
smaller  than  those  who  are  perfectly  healthy. 

Some  authorities  describe  an  "  acute  rachitis,"  in  which  painful  swelling  of  the 
epiphyses  is  said  to  be  developed  in  the  course  of  a  few  weeks.  At  the  same  time 
the  child  becomes  emaciated,  and  it  may  also  suffer  from  diarrhoea  or  vilcerative 
stomatitis.  Recovery  takes  place  in  a  few  months.  How  far  cases  of  this  sort  are 
related  to  genuine  rickets  has  not  yet  been  determined. 

Rachitis  does  not  involve  direct  danger  to  life,  although  many  rachitic  chil- 
dren fall  victims  to  the  attendant  intestinal  catarrh,  or  to  such  complications  as 
catarrhal  pneumonia  or  tuberculosis.  The  prognosis  is,  therefore,  not  unfavorable 
when  the  worldly  circumstances  of  the  child  permit  of  good  care  and  nourish- 
ment. The  remote  influences  of  the  thoracic,  spinal,  and  pelvic  deformities  can 
be  readily  inferred. 

The  diagnosis  of  rachitis  is  but  seldom  difficult  if  the  characteristic  changes  in 
the  bones  exist.  In  case  cranial  changes  have  occurred,  we  should  guard  against 
confounding  rickets  with  hydrocephalus,  but  we  can  usually  avoid  error.  The 
rachitic  child  holds  its  head  erect,  and  is  free  from  mental  or  other  functional 
nervous  disturbances. 

Treatment. — The  most  experienced  specialists  agree  that  the  first  aim  in  treat- 
ing most  cases  of  rachitis  is  to  improve  the  general  nutrition.  It  is  often  possible 
to  bring  about  recovery  simply  by  means  of  proper  diet  (milk,  the  yolk  of  eggs, 
and  perhaps  meat),  good  air  (in  the  coimtry),  and  baths  (brine,  malt,  and  medi- 
cated baths).  Digestive  disturbances  should  be  corrected  by  such  remedies  as 
hydrochloric  acid  or  tincture  of  rhubarb;  and  iron  should  be  administered  if  the 
patient  be  ansemic. 

It  is  very  important  that  the  child  should  be  placed  upon  a  good  mattress,  and 
should  neither  attempt  to  walk  too  early,  nor  be  needlessly  taken  up  and  carried 
about.  The  best  way  to  avoid  the  development  of  deformities  in  the  bones  is  to 
avoid  all  such  unfavorable  mechanical  influences. 

Attempts  have  also  been  made  to  check  the  disease  by  specific  remedies.  Upon 
doubtful  theoretical  grounds,  lime  has  been  very  frequently  prescribed,  in  the 
form  of  phosphate  of  calcium,  of  which  fifteen  to  forty-five  grains  may  be  given  in 


704  DISEASES    OE    THE    OEGAXS    OE   LOCO]^:©^^^ 

powder  several  times  a  day ;  or  in  the  form  of  lime-water,  of  which  one  or  two  tea- 
spoonfuls  are  added  to  the  milk  which  the  child  drinks.  The  benefit  of  these  reme- 
dies is  seldom  veiy  obvious.  Kassowitz  has  given  a  fresh  impetus  to  the  employ- 
ment of  phosphorus.  To  support  his  belief  he  brings  forward  numerous  clinical 
observations,  as  well  as  facts  obtained  from  experiment.  We  may  either  dissolve 
the  phosphorus  in  cod-liver  oil  (0.01-100),  giving  one  or  two  small  teaspoonfuls  of 
this  solution  every  day,  or  we  may  write  for  the  following  mixture,  which  is  more 
elegant,  but  is  also  more  apt  to  spoil : 

B   Phosphori 0.01; 

Olei  amygdalse  expressi  10.0. 

Misce,  deinde  adde : 

Pulv.  acaci^e, 

Syrupi  simplicis aa     5.0 ; 

Aquffi  destillata? 80.0. 

]\r.     Sig. :  Two  to  four  small  teaspoonfuls  a  day. 

We  can  state  from  our  own  experience  that  the  remedy  is  usually  very  well  borne, 
and,  in  fact,  often  shows  its  beneficial  action  after  a  few  weeks,  the  fontanelles 
growing  smaller  and  the  bones  becoming  firm.  Yet  there  are  cases  in  which  phos- 
phorus does  not  seem  to  do  any  good. 

It  may  be  eventually  necessary  to  resort  to  orthopaedic  or  surgical  treatment 
in  order  to  correct  the  deformities  of  the  bones. 

[The  comparative  rarity  of  rickets,  especially  in  its  extreme  degrees,  in  this 
•country  strikes  all  observers  who  have  studied  in  Germany.  With  a  fairly  exten- 
sive experience  among  the  poorer  classes  of  the  city,  the  writer  can  recall  scarcely 
half  a  dozen  cases  of  craniotabes.  The  colored  race  furnishes  a  large  contingent 
of  cases  of  rickets,  although,  as  is  shown  hy  Haven,  in  attention  to  diet  and  fresh 
air  its  members  are  superior  to  the  Irish  laboring  classes,  as  a  rule.  The  more 
pure  the  negro  blood,  the  greater  does  the  liability  to  rickets  seem  to  be  in  this 
latitude — an  indication,  perhaps,  that  a  noi'thern  climate  is  unsuitable  to  the 
African  race.] 


CHAPTER    VI 
OSTEOMALACIA 

.ffitiology  and  Pathology. — Osteomalacia  does  not,  like  rachitis,  consist  in  a 
disturbance  of  development.  The  growing  bones  are  not  prevented  from  ossifying, 
but,  having  already  undergone  normal  development  and  acquired  normal  firmness, 
they  afterward  become  soft.  It  is  mainly  a  disease  of  adults,  occurring  between 
thirty  and  forty  years  *  of  age,  but  sometimes  earlier.  The  female  sex  is  notice- 
ably predisposed  to  the  disease,  although  occasionally  it  has  been  observed  in  men. 

The  true  cause  of  osteomalacia  has  not  yet  been  ascertained.  It  is  a  remark- 
able fact  that  the  disease  is  much  more  frequent  in  certain  regions  than  in  others. 
It  is  very  common  along  the  Rhine,  and  in  Westphalia,  in  eastern  Flanders,  and 
northern  Italy.  This  suggests  that  there  is  some  specific  cause  for  the  disease, 
endemic  in  certain  localities.  Among  exciting  causes,  child-bearing  is  certainly 
the  most  important,  for  both  the  first  signs  of  osteomalacia,  and  also  fresh  exacer- 

*  Eehu  maintains  that  genuine  osteomalacia  may  occur  in  children  ;  but  his  statement  has  not  yet 
been  fully  corroborated. 


OSTEOMALACIA  705 

bations  of  the  disease,  usually  date  from  a  pregnancy.  There  is  no  doubt,  how- 
ever, that  occasionally  a  case  of  osteomalacia  occurs  in  a  woman  who  has  never 
had  children.  In  such  instances  the^  appearance  of  menstruation  seems  invariably 
to  have  an  unfavorable  influence  upon  the  disease.  In  brief,  the  relations  of  osteo- 
malacia to  the  sexual  processes  are  so  close  that  there  is  some  justification  for  the 
supposition  that  osteomalacia  is  directly  dependent  for  its  development  upon  dis- 
turbances of  metabolism  in  the  ovaries.  Moreover,  certain  therapeutic  experi- 
ences {vide  infra)  can  well  be  reconciled  with  this  assumption.  It  should  also  be 
mentioned  that  unfavorable  hygienic  surroundings,  damp  houses,  and  the  like, 
promote  the  development  of  the  disease. 

The  anatomical  process  of  osteomalacia  consists  of  a  disappearance  of  the 
earthy  salts  of  the  bone,  which  begins  interiorly  and  spreads  outward,  and  causes 
a  corresponding  softening  of  the  bony  structure. .  The  marrow  is  at  first  extremely 
hypersemic;  and  extravasations  of  blood  are  not  infrequently  found  here  and 
there.  The  bony  substance  surrounding  the  myeloid  spaces  and  the  Haversian 
canals  becomes  transformed  into  a  soft  fibrous  tissue,  while  the  irregularly 
arranged  bone-corpuscles  either  are  destroyed  or  lose  their  characteristic  shape. 
The  softening  process  gradually  extends  from  the  spongy  substance  outward  to  the 
cortex.  The  central  cavity  grows  larger  and  larger,  so  that  finally  the  cortical 
substance  is  as  thin  as  paper,  and  the  whole  bone  like  an  "  infiated  and  dried  coil 
of  intestine."  At  this  stage  the  original  hyperemia  of  the  marrow  has  vanished. 
The  marrow  acquires  a  yellow  color,  and  may  finally  be  entirely  transformed  into 
a  yellow,  viscid  fluid.  The  affected  bones  are  now  flexible  and  soft,  they  can  be 
easily  cut,  and  they  are  of  less  specific  gravity  than  normal.  The  periosteima  is 
also  at  first  thickened  and  hypersemic,  as  if  inflamed.  When  it  is  removed,  the 
surface  of  the  bone  beneath  it  is  found  to  be  rough  and  uneven.  The  attendant 
alterations  in  the  shape  of  the  bones  which  can  be  seen  during  life  will  be  men- 
tioned below. 

Upon  chemical  examination  of  the  bones  in  osteomalacia,  we  naturally  find  a 
marked  diminution  in  the  proportion  of  lime-salts.  It  is  also  stated  that  lactic 
acid  has  been  discovered  in  the  bones.  This  is  an  interesting  fact,  as  it  may  be 
that  the  acid  plays  an  important  chemical  part  in  the  process  of  decalcification. 

Clinical  History. — Osteomalacia  begins  very  gradually  in  most  cases.  Usually 
the  first  thing  noticed  is  an  ill-defined,  deep-seated  pain,  most  often  felt  in  the 
sacral  region,  the  nape  of  the  neck,  and  the  back  and  thighs.  The  affected  parts 
are  also  sensitive  upon  pressure. 

The  pain  is  persistent.  "While  it  still  keeps  on,  motion  becomes  gradually 
impaired.  The  patient  experiences  more  and  more  difficulty  in  walking,  partly 
because  of  the  pain  and  partly  because  of  muscular  weakness.  The  gait  is  either 
uncertain  and  slow,  or  characterized  by  short  painful  steps,  the  lower  limb  and 
the  pelvis  being  jerked  forward  as  if  in  one  piece.  This  peculiar  gait  in  which, 
with  every  short,  hobbling  step,  the  body  makes  a  slight  twist  inward,  is  so  char- 
acteristic that  often  the  disease  may  be  immediately  recognized  by  this  alone.  In 
other  instances  the  gait  is  more  waddling.  After  a  shorter  or  longer  time  walking 
becomes  absolutely  impossible,  and  the  patient  is  permanently  bedridden.  Even 
then  severe  pain  persists  in  most  cases.  It  is  not  precisely  spontaneous,  but  is 
produced  by  the  mere  pressure  of  the  mattress  or  the  bed-clothes,  and  similar 
causes. 

In  the  meanwhile,  there  has  probably  been  distortion  of  many  of  the  bones, 
sufficient  to  occasion  a  decided  alteration  in  the  appearance  of  the  skeleton.  Usu- 
ally the  first  to  be  noticed  is  the  deformity  of  the  spinal  column  (see  Fig.  78). 
As  a  rule,  there  is  kyphosis,  less  often  some  other  deformity,  and  the  head  gen- 
erally becomes  more  and  more  bent  forward  upon  the  sternum.  As  a  result,  the 
patient  grows  decidedly  shorter,  and  this  very  shortening  may  be  an  important 
45 


706 


DISEASES    OF    THE    OEGAXS    OE   LOCOMOTIOiT 


factor  in  diagnosis.  The  sick  woman  is  apt  to  remark  it,  because  she  has  to  keep 
shortening  her  gown  in  front.  The  thorax,  also,  is  apt  to  be  much  distorted  in: 
severe  cases.  It  is  compressed  laterally,  while  the  sternum  becomes  very  promi- 
nent, and  is  sharply  bent.    The  change  in  the  shape  of  the  pelvis  in  osteomalacia 

is  less  obvious  externally,  but  it  can  be  detected  on 
internal  examination.  It  is,  of  course,  of  great 
importance  from  an  obstetrical  point  of  view.  The 
pelvis,  like  the  chest,  is  compressed  laterally,  while- 
the  symphysis  is  made  to  project  forward  like  a 
beak.  The  sacrum  and  its  promontory  are  also 
pushed  forward,  and  the  superior  strait  thus  ac- 
quires somewhat  of  a  heart  shape.  This  change- 
in  the  pelvis  is  apt  to  appear  very  early.  It  is 
probably  the  chief  cause  of  the  peculiar  gait  (vider 
supra). 

The  extremities  are  less  often  distorted,  par- 
ticularly if  the  patient  becomes  bed-ridden  at  an 
early  period.  Manifold  changes  are,  however, 
possible.  Sometimes  there  is  also  fracture.  In  a 
few  reported  cases  the  softness  of  the  bones  of 
the  extremities  was  so  extreme  that  one  could  bend 
the  limbs  at  will,  like  wax,  and  give  them  the  most 
extraordinary  jjositions.  In  cases  so  far  advanced 
as  these,  the  pain  in  the  bones  seems  finally  to 
cease.  The  bones  of  the  head  and  face  seldom  un- 
dergo noticeable  change,  but  we  often  find  that  the 
teeth  are  carious  or  lost.  In  the  muscles,  several 
observers  have  noticed  trembling  and  fibrillary 
contractions,  also  paresis  and  complete  paralysis. 
It  is  also  said  that  sometimes  even  a  slight  irrita- 
tation  of  the  skin  sufiices  to  excite  painful  con- 
tractions of  the  underlying  muscles.  These  phe- 
nomena have  not  yet  been  thoroughly  investi- 
gated. 

The  general  condition  of  the  patient  is  often 
unimpaired  for  a  long  while,  except  for  the  pain 
and  the  impairment  of  motion.  The  internal 
organs  perform  their  functions  in  a  normal  man- 
ner, and  the  appetite  is  good.  Eever  is  observed 
only  when  the  disease  is  undergoing  some  tem- 
porary exacerbation.  With  regard  to  changes 
in  the  urine,  there  have  been  a  good  many 
statements  made,  but  their  significance  is  extremely  doubtful.  It  is  said  that 
the  amount  of  phosphoric  acid  excreted  is  diminished.  With  regard  to  the- 
amount  of  lime,  no  definite  statement  can  be  made.  Lactic  acid  has  been 
repeatedly  detected  in  the  urine,  as  has  also  albumen.  Concretions  of  lime  have- 
been  found  in  the  bladder  and  the  kidneys. 

The  disease  runs  a  chronic  course,  occupying  seldom  less  than  two  or  three 
years,  and  sometimes  even  five  to  ten  or  even  longer.  Apparent  improvement  is 
not  infrequently  observed,  but  this  is  followed  by  fresh  exacerbations,  especially 
after  confinement.  The  most  frequent  termination  is  in  death.  This  results 
either  from  general  debility,  or,  more  often  still,  from  the  dyspnoea  caused  by  the 
compression  of  the  lungs,  or  by  some  such  disease  as  lobular  pneumonia.  In  milder 
cases,  however,  particularly  if  they  receive  prompt  and  suitable  attention,  there 


Fig.  78.  —Puerperal  osteomalacia. 
(Erlangen  Medical  Clinique.) 


OSTEOMALACIA  TOY 

may  be  comiilete  recovery ;  or  in  severe  cases,  even  if  deformity  has  occurred,  there 
may  be,  at  any  rate,  a  permanent  cessation  of  the  disease. 

Diagnosis. — In  well-developed  cases  it  is  not  difficult  to  recognize  the  disease, 
but  at  first  a  correct  diagnosis  is  often  impossible,  unless  the  endemic  frequency 
of  osteomalacia  suggests  it.  In  the  onset  of  the  disease  we  may  often  be  led  to  the 
false  belief  that  there  is  incipient  disease  of  the  cord  or  the  vertebrse.  We  our- 
selves, as  well  as  other  observers,  have  repeatedly  seen  cases  in  which  women  as  a 
sequel  to  pregnancy,  or  even  apparently  spontaneously,  have  developed  paresis  in 
the  lower  extremities,  particularly  in  the  psoas  and  iliacus  muscles,  associated  with 
pain  and  exaggerated  tendon  reflex,  and  in  which  diagnosis  at  first  was  very  difli- 
cult.  Not  very  infrequently  the  complaint  of  the  patient  at  the  start  was  re- 
garded as  hysterical.  Later,  the  peculiar  hobbling  and  waddling  gait  ("  like  a 
duck")  would  suggest  the  possibility  of  osteomalacia,  and  this  diagnosis  would 
be  established  by  the  results  of  a  careful  examination  of  the  pelvis.  At  any  rate, 
it  is  important  to  know  that  even  before  there  are  demonstrable  changes  in  the 
bones,  there  may  be  paralysis,  probably  referable  to  an  early  involvement  of  the 
muscles  in  the  morbid  process.  As  the  disease  is  almost  entirely  confined  to 
adults,  we  are  seldom  in  danger  of  confounding  it  with  rachitis.  Besides,  osteo- 
malacia does  not  produce  swelling  of  the  epiphyses,  nor  changes  in  the  bones  of 
the  skull.  It  is  said  that  osteomalacia  is  occasionally  confounded  with  diffuse 
carcinosis  of  the  bones,  as  this  may  produce  similar  symptoms  and  deformities. 

Treatment. — As  has  been  already  implied,  therapeutic  efforts  have  thus  far 
proved  in  severe  cases  almost  unavailing  in  this  disease.  In  the  onset  of  the  dis- 
ease we  can  obtain  a  distinct  improvement  by  the  use  of  hygienic  remedies,  good 
air,  proper  food,  etc.  Internally  we  give  cod-liver  oil  and  also  iron.  Many  pa- 
tients praise  warm  baths,  with  or  without  salt.  The  exhibition  of  lime  seems  to  be 
of  no  special  use.  On  the  other  hand,  personal  experience  leads  us  earnestly  to 
recommend  a  trial  of  small  doses  of  phosphorus,  either  in  the  form  of  phosphorized 
cod-liver  oil  (vide  supra),  or  in  pills  of  one  sixtieth  of  a  grain  (gramme  0.001) 
several  times  a  day.  Particularly  in  the  above-mentioned  forms  of  incipient 
osteomalacia  with  paresis  of  the  legs,  and  even  also  in  cases  with  distinct  changes 
in  the  pelvis  already  developed,  we  have  seen,  repeatedly,  striking  benefit  from 
treatment  with  phosphorus.  Yet  sometimes  even  this  remedy  proves  disap- 
pointing. 

The  changes  in  the  bony  pelvis  produced  by  osteomalacia  may  eventually 
demand  obstetrical  interference,  but  we  need  not  discuss  such  procedures  here. 
We  should  invariably  warn  women  who  suffer  from  the  disease  of  the  dangers  of 
becoming  pregnant.  Recently,  therefore,  castration  has  been  repeatedly  per- 
formed in  cases  in  which  an  aggravation  of  the  disease  was  invariably  associated 
with  fresh  pregnancies.  Under  these  circumstances,  it  has  been  shown  that  the 
removal  of  the  ovaries  has  resulted  in  a  remarkably  rapid  recovery  from  the  dis- 
ease, a  fact  which  suggests  an  intimate  connection  between  the  processes  in  the 
ovaries  and  the  symptoms  of  osteomalacia  (vide  supra).  Certainly,  these  rela- 
tions should  receive  the  greatest  consideration  in  the  future. 


DISEASES   AFFECTING   THE   BLOOD   AND 
TISSUE-METAMORPHOSIS 

{CONSTITUTIONAL  DISEASES) 


CHAPTER   I 

ANEMIA    AND    CHLOROSIS 


1.  General  Preliminary  Remarks  as  to  the  Classification  and  etiology  of 
the  Various  Forms  of  Anaemia. — The  word  "  ansemia  "  (or,  more  strictly,  oli- 
gsemia)  might  properly  be  taken  to  signify  diminution  of  the  total  volume  of  the 
blood,  such  as,  for  example,  is  directly  brought  about  by  a  severe  haemorrhage. 
Usually,  however,  the  word  is  employed  to  signify  not  so  much  diminution  in 
quantity  as  deterioration  in  quality.  The  total  volume  of  the  blood  is  not  liable 
to  nearly  so  great  variations  as  is  the  number  of  its  most  important  constituents 
— the  red  corpuscles — inasmuch  as  the  total  volume  is  dependent  merely  upon  the 
amount  of  watery  constituents,  and  even  after  large  haemorrhages  the  water  is 
quite  rapidly  replaced  by  absorption.  This  is  undoubtedly  the  case  in  most  in- 
stances of  sudden  loss  of  blood.  Even  in  chronic  anasmia  there  is  usually  no  rea- 
son to  assume  that  the  total  amount  of  blood  is  diminished,  although  it  may  be 
when  there  is  general  emaciation,  or  diminished  supply  of  liquids  (persistent 
vomiting,  dysphagia),  or  large  watery  discharges  (as  in  cholera).  The  essential 
element  in  anaemia  is,  therefore,  a  diminution  in  the  number  of  the  red  blood- 
corpuscles,  or  so-called  oligocythaamia.  Changes  in  the  character  of  the  red 
blood-corpuscles  are  not  taken  into  consideration  here.  On  the  other  hand,  how- 
ever, we  shall  see  later  that,  even  in  spite  of  a  normal  number  of  red  blood-cor- 
puscles, their  abnormal  condition,  particularly  their  poverty  in  haemoglobin,  may 
lead  to  well-marked  "  anaemic  "  conditions. 

The  circumstances  under  which  anaemia  is  observed  are  manifold.  They 
admit,  however,  of  our  distinguishing  two  great  classes  of  anaemia — primary 
and  secondary.  Primary  anaemia  is  developed  as  an  apparently  primary  and 
idiopathic  disease  in  persons  previously  healthy,  while  secondary  anaemia  is 
merely  a  symptom  of  some  already  existing  disease.  However  simple  this  theoret- 
ical distinction,  yet  in  actual  practice  it  is  often  quite  difficult  to  determine 
whether  the  particular  case  before  us  should  be  regarded  as  primary  or  secondary. 
A  secondary  anaemia  may  occur  where  the  true  primary  cause  can  not  be  at  all 
readily  determined.  There  are,  nevertheless,  quite  a  large  number  of  cases  which 
would  seem  to  deserve  the  name  of  primary  or  essential,  in  which  we  feel  com- 
pelled to  assume  that  some  pathogenic  influence  acts  directly  upon  the  blood  and 
the  haematopoietic  processes. 
708 


ANAEMIA   AND    CHLOEOSIS  709 

In  the  first  place,  we  would  class  as  primary,  cases  which  may  best  be  described 
as  "  simple  constitutional  anaemia."  These  often  stand  close  to  the  borderland 
between  health  and  disease.  There"  are  not  a  few  individuals  who  present  a  strik- 
ing- pallor  for  a  large  part,  if  not  all,  of  their  lives.  These  persons  may  feel  so 
well  and  vigorous  that  we  scarcely  have  a  right  to  regard  the  existent  anaemia 
(usually  moderate)  as  an  actual  disease.  Sometimes,  however,  such  individuals 
do  betray  some  diminution  of  energy,  are  easily  fatigued,  and  are  subject  to  head- 
ache. We  may  then  regard  the  conditions  as  certainly  pathological.  In  many 
instances  the  cause  of  this  simple  anaemia  is  found  in  the  general  hygienic  sur- 
roundings of  the  patient,  for  such  cases  are  most  often  met  with  among  the  poorer 
classes.  Deficient  nutrition,  bad  air,  unhealthy  occupation  in  factories  or  the 
like,  not  only  affect  the  general  health,  but  more  especially  interfere  with  the 
processes  of  normal  blood-making.  Other  cases  of  constitutional  anaemia,  appar- 
ently primary,  occur  in  individuals  who  are  entirely  beyond  the  reach  of  such 
influences  as  have  just  been  mentioned,  in  whom  the  anaemia  has  developed  and 
persists  despite  the  best  of  food  and  air.  Here  we  are  forced  to  the  conclusion 
that  the  organs  engaged  in  the  manufacture  of  the  blood  are  in  some  way  pre- 
vented from  performing  their  proper  functions.  The  trouble  often  seems  to  be 
congenital,  for  such  individuals  may  present  the  symptoms  of  anaemia  in  their 
earliest  infancy.  There  are  persons  who  have  always  been  pale  and  feeble.  Or, 
again,  anaemia  does  not  develop  until  later  on,  in  which  case  it  not  infrequently 
associates  itself  with  certain  phases  of  physiological  development,  as  when  growth 
is  particiilarly  rapid,  or  when  adolescence  occurs.  Virchow  has  directed  atten- 
tion to  another  factor,  which  he  regards  as  potent  in  many  of  these  cases  of  con- 
genital anaemia.  He  has  found  that  the  arteries  may  be  congenitally  small,  or 
that  the  whole  arterial  system  may  be  imperfectly  developed.  The  condition  may 
be  associated  with  a  congenitally  weak  and  small  heart.  The  importance  of  this 
factor  has  not  yet  been  fully  determined.  Possibly  the  condition  of  the  circula- 
tory system  just  mentioned  may  be  the  result  rather  than  the  cause  of  the  anaemia. 

A  second  division  of  primary  aniemia  includes  cases  which  present  a  far  more 
definite  and  distinct  group  of  symptoms.  They  quite  often  appear  in  persons  pre- 
viously healthy,  last  for  a  certain  length  of  time,  and  then  end  in  complete  recov- 
ery. The  typical  form  of  this  variety  is  chlorosis  (x^(op6s  =  greenish  yellow),  or 
"  green  sickness."  This  well-known  disease  is  especially  frequent  in  young  girls 
fourteen  to  twenty  years  of  age — that  is,  at  puberty.  It  often  comes  on  quite  rap- 
idly without  any  ascertainable  cause.  There  are  not  infrequently  predisposing 
influences  in  the  outward  circumstances  of  the  patient.  Thus  it  is  promoted  by 
an  unhealthy  sedentary  mode  of  life,  as  in  seamstresses ;  bad  air,  as  in  factory 
operatives;  mental  and  physical  over-exertion,  as  in  teachers,  governesses,  and 
students;  and,  finally,  by  mental  influences  (excitement,  etc.).  It  is,  neverthe- 
less, true  that  chlorosis  also  appears  in  girls  who  have  lived  under  the  most  favor- 
able hygienic  conditions  possible.  Sometimes  the  disease  seems  to  be  merely  a 
temporary  exacerbation  of  a  simple  constitutional  anaemia  which  has  existed  a 
long  time ;  but  it  may  also  appear  in  j-oung  women  who  have  been  previously 
healthy,  and  even  robust. 

The  true  cause  of  chlorosis  is  unknown.  Perhaps  the  interesting  investiga- 
tions of  Bunge  with  reg-ard  to  the  amount  of  iron  in  milk  and  in  new-born  ani- 
mals afford  at  least  a  starting-point  for  some  future  theory  as  to  chlorosis.  Bunge 
found  that  the  constituents  of  the  ash  of  milk,  and  the  constituents  of  the  total 
ashes  of  young  suckling  animals,  correspond  precisely  in  their  proportions.  The 
suckling  animal,  therefore,  receives  with  his  mother's  milk  all  the  salts  that  are 
needed  for  his  body,  in  a  proper  amount — the  single  exception  being  the  iron 
compounds.  The  amount  of  iron  in  milk  is  A'^ery  small  compared  with  the  amount 
of  iron  in  the  suckling.    Indeed,  the  proportion  of  iron  in  the  new-born  animal  is 


TIO  CONSTITUTIONAL   DISEASES 

decidedly  large,  but  it  diminishes  gradually  as  the  creature  develops.  This  in- 
dicates that  the  animal  comes  into  the  world  with  a  supply  of  iron,  which  can 
originate  only  in  the  maternal  organism;  and  in  the  first  part  of  his  life,  so 
long  as  he  has  milk  for  his  exclusive  nourishment,  he  draws  upon  this  supply. 
If,  therefore,  we  consider  that  it  is  a  function  of  the  female  organism  in  some 
way  to  store  up  iron  for  the  next  generation,  there  might  be  some  disturbance 
of  this  function,  either  an  imperfect  assimilation  or  an  abnormal  conversion  of 
the  assimilated  iron,  and  this  might  very  likely  rob  the  blood  of  hsemoglobine. 
It  must  be  confessed  that  as  yet  we  have  no  thorough  understanding  at  all  of 
the  internal  processes  of  metabolism  which  relate  to  the  matter.  Still,  the 
facts  and  conditions  which  we  have  mentioned  explain  to  a  certain  degree  the 
fact  that  genuine  chlorosis  is  found  exclusively  in  the  female  sex  and,  indeed, 
precisely  at  the  time  of  puberty — i.  e.,  the  time  of  preparation  for  the  sexual  life. 
Perhaps,  also,  the  fact  that  disturbances  of  menstruation  are  so  frequent  in  asso- 
ciation with  chlorosis  is  connected  with  the  conditions  above  mentioned,  but  it 
is  also  possible  that  the  menstrual  disturbances  may  be  a  result  of  chlorosis. 

A  third  form  of  primary  essential  ansemia  is  the  so-called  pernicious  anaemia. 
This,  likewise,  appears  independently  of  other  diseases,  and  is  characterized  by 
its  steady  progress,  as  a  rule  leading  finally  to  death.  We  do  not  regard  pernicious 
anaemia  as  a  very  severe  form  of  chlorosis,  but  as  an  entirely  separate  disease. 
It  is  distinguished  from  chlorosis  not  merely  by  the  much  more  definite  morpho- 
logical changes  in  the  blood,  but  still  more  by  the  circumstance  that  it  is  not  con- 
fined to  women,  but  appears  also  in  men,  both  in  early  and  advanced  life.  Cases 
of  "  severe  essential  ansemia  "  also  have  many  points  in  common  with  certain  other 
diseases,  such  as  pseudo-leuksemia  and  splenic  ansemia.  These  will  be  discussed 
later. 

The  forms  of  secondary  anasmia  offer  a  contrast  to  the  forms  of  primary  or 
essential  anaemia  just  described  in  the  much  greater  number  of  their  causes. 
Under  this  head  come  cases  of  ansemia  which  do  not  occur  idiopathically,  but  as 
a  result  of  other  abnormal  processes.  The  simplest  variety  is  ansemia  from 
haemorrhage.  This  is  produced  by  profuse  loss  of  blood,  whether  from  the  stom- 
ach, lungs,  uterus,  intestines,  kidneys,  or  some  wound.  Repeated  small  hsemor- 
rhages  finally  produce  the  same  result  as  a  single  large  one.  Thus  the  most  pro- 
found ansemia  may  be  observed  where  there  is  a  very  frequent  epistaxis  (hsemor- 
rhagic  diathesis,  contracted  kidney),  or  where  cancer  of  the  womb  gives  rise  to  a 
constant  oozing  of  blood. 

Other  cases  of  secondary  ansemia  may  be  divided  into  two  great  groups.  In 
one  class  the  ansemia  is  a  symptom  of  impaired  nutrition.  This  is  seen  in  almost 
every  severe  disease,  acute  or  chronic,  and  is  usually  associated  with  more  or  less 
emaciation  and  loss  of  strength.  The  bad  appetite,  the  lack  of  fresh  air  and  exer- 
cise, and  perhaps  an  impairment  of  digestion,  or  fever,  or  some  abnormal  drain 
upon  the  system,  as  in  suppuration — these  injure  the  entire  body.  It  is  not  sur- 
prising that  the  blood  shares  in  the  universal  misfortune.  This  is  why  most 
chronic  invalids  seem  pale,  particularly  if  they  suffer  from  disease  of  the  stomach, 
kidneys,  chest,  or  nervous  system.  In  the  second  class,  the  ansemia  is  secondary 
to  some  other  disease,  but  assumes  especial  prominence  as  a  symptom,  independ- 
ently of  any  general  impairment  of  nutrition.  Of  course,  it  is  often  associated 
with  emaciation,  but  nevertheless  its  extraordinary  intensity  offers  a  striking  con- 
trast to  the  condition  of  the  rest  of  the  body.  This  "  specific  secondary  ansemia  " 
must,  like  essential  ansemia,  be  due  to  a  special  lesion  of  the  blood  itself,  and  is, 
therefore,  to  be  regarded  as  in  a  certain  sense  a  special  complication  or  localiza- 
tion of  the  primary  disease.  General  malnutrition  never  produces  anaemia  of 
this  grade  directly.  This  fact  is  illustrated  in  stenosis  of  the  (psophagus.  Here 
the  ingestion  of  food  is  very  greatly,  if  not  completely,  hindered,  and  there  is 


ANEMIA   A^^D    CHLOEOSIS  711 

the  greatest  emaciation,  with  a  subnormal  temperature  and  slow  pulse.  Of  course, 
such  a  patient  appears  pale  and  wretched,  but  he  does  not  present  that  peculiar 
waxy  pallor  which  is  the  sign  of  genuine  anaemia. 

The  exact  mode  of  origin  of  specific  secondary  anaemia  is  often  obscure.  We 
liave  already  reported,  in  a  preceding  chapter,  a  very  instructive  exami^le.  In 
cancer  of  the  stomach  we  find  usually  emaciation  and  pallor.  This  is  natural 
enough;  but  sometimes  the  carcinoma  is  complicated  by  an  extraordinarily  pro- 
iound  anaemia,  comparable  only  to  the  pernicious  variety.  In  one  such  case  we 
found,  at  the  autopsy,  an  extensive  secondary  carcinosis  of  the  bone-marrow. 
JSere,  therefore,  the  anaemia  certainly  was  not  the  result  merely  of  the  general  im- 
pairment of  nutrition  occasioned  by  the  gastric  carcinoma,  but  of  the  disease  of 
the  marrow,  which  tissue  undoubtedly  plays  an  important  part  in  the  manufac- 
ture of  the  blood. 

Some  cases  of  specific  secondary  anaemia  deserve  special  mention,  although  it 
is  seldom  possible  to  demonstrate  their  precise  cause.  In  the  first  place  come  such 
^ases  as  develop  after  certain  acute  diseases,  usually  of  an  infectious  character. 
For  example,  there  may  be  great  anaemia  after  typhoid  fever,  or  less  often  after 
.acute  articular  rheumatism.  A  peculiar  form  of  anaemia  is  often  observed  during 
the  secondary  stage  of  syphilis,  although  nutrition  seems  to  be  otherwise  well 
maintained.  This  is  known  as  "  syphilitic  chlorosis."  Tuberculosis,  chronic 
malarial  poisoning,  chronic  septic  infection,  and  other  forms  of  chronic  poisoning 
(lead),  as  well  as  amyloid  disease,  renal  disease,  etc.,  may  also  be  attended  by 
anaemia  of  such  intensity  as  to  justify  the  conclusion  that  there  is  some  special 
■disturbance  of  secondary  origin  affecting  the  manufacture  of  the  blood  or  the  blood 
itself.  Of  great  importance  is  the  striking  anaemia  which  occurs  in  association 
with  many  intestinal  parasites  (vide  supra,  page  512  et  seq.),  sometimes  as  a  re- 
sult of  actual  loss  of  blood,  but  probably  more  often  because  of  the  action  upon 
the  blood  of  certain  poisons  generated  by  the  entozoa. 

[Chronic  arsenical  poisoning  from  wall  papers,  dress  fabrics,  furniture  cover- 
ing, and  the  like,  is  a  not  infrequent  cause  of  anaemia  and  debility,  which  resists 
treatment  as  long  as  the  exposure  to  the  toxic  influence  lasts.  The  classical 
symptoms  of  chronic  arsenical  poisoning  are  not  necessarily  present.  The  num- 
ber of  cases  in  which  prompt  recovery  has  taken  place  after  the  removal  of  the 
poison  which  was  proved  to  exist  in  the  surroundings  as  well  as  in  the  urine  of  the 
patient  is  too  large  and  too  striking  to  explain  by  simple  coincidence.  Recovery 
may,  howevei%  be  slow  in  those  whose  toleration  of  arsenic  is  slight,  or  in  whom 
the  cause  of  the  symptoms  has  remained  long  undetected.] 

We  shall  now  proceed  to  describe  the  symptoms  directly  dependent  upon  the 
anaemia,  and  therefore  common  to  all  its  forms.  Upon  this  will  follow  a  sketch  of 
chlorosis.  A  special  chapter  is  assigned  to  the  grave  form  of  essential  anaemia 
known  as  progressive  pernicious  anemia ;  and  in  the  same  connection  will  be  set 
forth  the  little  that  is  known  with  regard  to  the  relations  of  anaemia  to  patho- 
logical changes  in  the  haematopoietic  organs. 

2.  Symptomatology  of  Anaemia. — The  first  symptom  which  attracts  the  at- 
tention of  the  physician  in  any  case  of  anaemia  is  the  altered  appearance,  the 
pallor  of  the  skin  and  visible  mucous  membranes.  This  is  especially  striking  in 
the  face,  but  it  is  sufiiciently  evident  everywhere.  Special  value  is  usually  as- 
sig-ned  to  pallor  of  the  mucous  membranes,  for  example,  of  the  lips  and  conjunc- 
tiv£e,  inasmuch  as  their  color  is  not  liable  to  be  interfered  with  by  pigmentation 
or  opacity  of  the  epidermis.  The  degree  of  pallor,  of  course,  varies  greatly.  The 
whole  body  may  present  a  waxy  appearance.  A  pallor  of  this  kind  implies,  of 
course,  a  very  considerable  diminution  in  the  amount  of  coloring  matter  in  the 
blood — that  is,  of  haemoglobino.  The  diminution  of  hn^moglobine  in  simple  anae- 
mia is  usually  a  direct  result  of  diminution  in  the  number  of  red  blood-coi-puscles. 


T12  CONSTITUTIONAL   DISEASES 

each  one  remaining  normal ;  but  the  red  corpuscles  themselves  may  show  a  dimi- 
nution in  the  amount  of  hsemoglobine,  although  their  number  is  normal.  In  order 
to  determine  these  important  facts  we  must  in  every  case  of  decided  anaemia  find 
out  not  merely  the  relative  number  of  blood-corpuscles — i.  e.,  the  number  of  blood- 
corpuscles  in  a  cubic  millimetre  of  blood — but  also  the  proportion  of  hsemoglobine 
in  the  blood  (the  simplest  way  being  by  the  well-known  methods  of  Gowers  and 
Eleischl),  and  compare  the  two. 

Besides  the  alteration  in  complexion,  there  is  always  a  group  of  symptoms  ref- 
erable ultimately  to  an  impairment  of  the  normal  processes  of  innervation  result- 
ing from  a  lack  of  arterial  blood.  Eirst  among  these  phenomena  comes  general 
weakness  of  the  motor  system.  The  voluntary  muscles  are  easily  fatigued,  and 
the  patient  suffers  from  constant  languor.  When  the  angemia  is  very  great,  as 
after  severe  haemorrhage,  this  weakness  may  be  so  pronounced  that  the  patient 
can  neither  walk  nor  stand;  but  even  in  moderate  anaemia  there  is  more  or  less 
impairment  of  strength. 

This  diminished  nervous  energy  is  shown  also  by  the  mental  condition.  There 
is  no  intellectual  vigor.  The  patient  is  incapable  of  any  great  mental  exertion, 
and  experiences  a  constant  feeling  of  weariness  and  sleepiness.  In  cases  of  severe 
anaemia  there  is  not  infrequently  a  decided  tendency  to  faintness,  or  actual  syn- 
cope, as  the  result  of  cerebral  anaemia. — It  is  very  common  to  have  such  subjective 
symptoms  as  impaired  vision,  specks  before  the  eyes,  and  pain  in  the  eyes.  In 
occasional  instances,  particularly  after  a  great  loss  of  blood  (for  example,  after 
haematemesis),  total  amaurosis  develops.  Examination  with  the  ophthalmoscope 
shows  nothing  abnormal,  beyond  the  anaemia  of  the  retina. — Impairment  of  hear- 
ing is  exceptional ;  on  the  other  hand,  there  is  often  great  annoyance  from  marked 
tinnitus  aurium,  which  of  course  is  due  to  the  irritated  condition  of  the  auditory 
nerve,  or  perhaps  also  of  the  auditory  center. 

The  processes  of  secretion  are  much  less  affected.  It  is  true  that  there  is  often 
dryness  of  the  tongue  and  mouth,  but  this  is  mainly  subsequent  to  the  loss  of 
large  amounts  of  blood,  and  probably,  therefore,  is  occasioned  less  by  a  diminution 
in  the  activity  of  the  mucous  and  salivary  glands  than  by  the  desiccation  of  the 
tissues.  As  relates  to  other  secretory  functions,  the  only  one  which  has  been  care- 
fully investigated  is  the  formation  of  gastric  juice.  The  earlier  experiments  on 
animals  caused  the  opinion  to  be  held  for  a  long  while  that  in  anaemia  the  propor- 
tion of  hydrochloric  acid  in  the  gastric  juice  was  diminished.  Numerous  more 
recent  experiments,  however,  have  shown  that  this  assumption  is  subject  to  excep- 
tions. Although  ,the  amount  of  hydrochloric  acid  in  the  gastric  juice  may  be 
small  in  anaemia  and  chlorosis,  and  although  there  may  be  complete  absence  of  free 
hydrochloric  acid  in  the  gastric  juice;  yet,  on  the  other  hand,  it  is  a  very  fre- 
quent experience  to  find  a  fully  normal  or  even  excessive  amount  of  hydrochloric 
acid ;  nor  are  the  motor  functions  of  the  stomach,  as  a  rule,  disturbed ;  but  it  may 
be  that  the  constipation  which  is  so  often  present  in  anaemia  is,  at  least  in  part, 
connected  with  an  impairment  of  the  energy  of  intestinal  peristalsis. 

The  symptoms  thus  far  described  are  referable  partly  to  diminished  functional 
activity.  On  the  other  hand,  anaemia  gives  rise  to  certain  symptoms  of  irritation 
in  the  nervous  system.  These  are,  in  all  probability,  expressive  of  the  irritation 
excited  in  certain  portions  of  the  nervous  system  by  the  products  of  abnormal 
metabolism,  perhaps  due  to  incomplete  oxidation.  Some  of  these  symptoms,  such 
as  the  annoying  tinnitus,  the  specks  before  the  eyes,  and  the  vertigo,  have  been 
already  mentioned.  We  should  also  note  especially  eructations  and  vomiting  as 
anaemic  symptoms ;  these  are  in  most  cases  of  central  origin,  and  in  severe  anae- 
mia they  may  be  very  annoying.  In  the  same  way  may  be  explained  the  occasional 
occurrence  of  annoying  hiccough,  the  frequent  spasmodic  yawning,  and  similar 
symptoms.    Anaemic  headache  may  be  very  severe.    It  is  usually  referred  either 


ANiEMIA   AND   CHLOEOSIS  713 

to  the  entire  head  or  to  the  forehead ;  there  is  a  painful  feeling  of  pressure,  which 
may  attain  great  severity. 

Other  important  evidences  of  irritation  are  to  be  found  in  the  behavior  of  the 
pulse  and  the  respiration.  The  changes  here  are  apparently  in  part  of  a  compen- 
satory character.  The  pulse  is  accelerated  in  most  cases  of  any  severity,  reaching 
80  to  100  beats  per  minute,  or  even  more.  It  is  also  very  excitable,  so  that  com- 
paratively slight  external  influences  suffice  to  increase  its  rapidity  for  the  time 
being.  This  increase  in  frequency  would  not,  of  course,  necessitate  an  increase  of 
intra-vascular  tension,  or  of  the  rapidity  of  the  circulation;  but  it  may  exert  a 
favorable  influence  in  this  direction,  and  so  be  compensatory.  Respiration  also  is 
usually  accelerated  in  ansemia.  In  cases  of  great  severity  the  breathing  may  be  so 
deep  and  noisy  as  to  justify  the  term  "  anaemic  dyspnoea."  This  is  the  direct  ex- 
pression of  the  body's  hunger  for  oxygen.  It  is  obvious  that  this  increase  in  the 
number  of  respirations  favors,  to  a  certain  extent,  the  absorption  of  that  gas. 

There  are  still  other  symptoms  referable  to  the  circulatory  system.  It  has 
been  already  stated  that  the  total  volume  of  the  blood  is  not  diminished  in  ansemia 
unless,  of  course,  there  has  just  been  an  actual  haemorrhage.  This  explains  why 
the  pulse  in  ansemia  is  often  comparatively  full  and  strong.  Quite  frequently 
there  is  a  peculiar  quickness  of  the  pulse.  This  seems  to  be  due  to  a  vigorous 
cardiac  systole,  in  conjunction  with  a  low  intra-arterial  tension.  Akin  to  these 
phenomena  is  the  fact  that  in  severe  ansemia  it  is  not  exceptional  to  hear  a  dis- 
tinct pistol-shot  sound  in  the  femoral  artery,  or,  in  rare  cases,  even  a  distinct 
double  sound,  just  as  in  aortic  insufficiency. 

It  has  long  been  known  that  ansemia  may  produce  functional  cardiac  mur- 
murs, often  called  "  ansemic  murmurs."  Their  mode  of  origin  is  not  yet  fully 
explained.  They  are  usually  heard  loudest  over  the  base  of  the  heart,  in  the 
neighborhood  of  the  pulmonary  valves,  and  at  the  apex  of  the  heart.  As  a  rule, 
they  are  purely  systolic  in  time,  but  we  certainly  heard  in  one  case  of  pernicious 
ansemia  a  loud  diastolic  murmur  of  anaemic  origin.  The  murmurs  are  of  a  blow- 
ing character.  Sometimes  they  are  so  rough  as  to  simulate  pericardial  friction- 
murmurs  ;  it  has  therefore  been  suggested  that  many  anaemic  murmurs  are  ac- 
tually due  to  the  rubbing  upon  each  other  of  the  abnormally  dry  folds  of  the  peri- 
cardial sac.  Another  explanation  of  their  occurrence  is,  that  the  movements  of  the 
cardiac  valves  are  interfered  with,  as  a  result,  perhaps,  of  fatty  degeneration  of  the 
myocardium  (vide  infra).  It  is  also  possible  that  there  may  be  sometimes  relative 
insufficiency  of  the  valves — e.  g.,  due  to  dilatation  of  the  heart  or  to  imperfect 
action  of  the  papillary  muscles.  Still,  the  question  has  not  yet  been  settled 
whether  genuine  dilatation  of  the  heart  is  at  all  frequent  in  ansemia.  Increase  in 
the  cardiac  dullness  is  observed,  but  it  is  due  mainly  to  retraction  of  the  lungs. 

Murmurs  in  the  large  veins  of  the  neck  are  very  often  heard  in  ansemia,  either 
with  or  without  cardiac  murmurs.  They  are  often  called  hruit  de  diable.  No 
less  an  authority  than  A.  Weil  has  maintained  that  murmurs  in  the  jugular  veins 
are  just  as  frequent  in  healthy  persons  as  in  the  ansemic;  but  our  experience 
compels  us  to  diff^er  from  this  view.  We  believe  that  the  loud  venous  murmurs  are 
more  frequent  in  the  anaemic  than  in  other  persons,  so  that  they  possess  a  certain 
diagnostic  value. 

The  processes  of  metabolism  in  profound  anffimia  are  of  great  interest,  but,  un- 
fortunately, they  have  not  yet  been  thoroughly  investigated.  A  priori,  we  should 
expect  that  the  absorption  of  oxygen  would  be  diminished  in  severe  ansemia ;  but 
it  has  not  yet  been  possible  to  confirm  this  surmise,  at  least  in  the  cases  of  medium 
severity,  doubtless  because  the  compensatory  acceleration  of  the  respiration  and 
pulse  {vide  supra)  equalizes  matters.  Whether,  even  in  severe  ansemia,  there 
is  any  diminution  in  the  absorption  of  oxygen,  has  not  yet  been  proved;  yet  many 
facts  seem  to  faA'^or  this  idea.     One  is  that  in  severe  ansemia  there  is  usually  a 


"714  CONSTITUTIOIsTAL   DISEASES 

somewliat  increased  destruction  of  albumen,  as  compared  with,  the  amount  of  nour- 
ishment ingested.  This  can  be  recognized  by  the  increase  in  the  excretion  of  nitro- 
gen in  the  urine.  This  circumstance,  which  accords  with  the  results  of  experi- 
ments as  to  the  consequences  of  a  diminution  in  the  supply  of  oxygen,  assumes  the 
more  importance  if  we  associate  it  with  certain  anatomical  results  of  antemia, 
there  being  almost  always  a  marked  fatty  degeneration  of  many  organs,  particu- 
larly the  heart  and  kidneys.  This  fatty  degeneration  is  the  direct  result  of  the 
abnormal  destruction  of  albuminoid  structures.  The  fat  represents  the  non-nitro- 
^•enous  remnants  of  the  decomposed  albuminoids.  The  reason  the  fat  itself  does 
not  undergo  oxidation  is  the  lack  of  oxygen.  It  is  perhaps  for  the  same  reason 
that  the  panniculus  adiposus  is  for  a  long  while  preserved  in  many  cases  of 
anaemia. 

It  is  evident  that  the  fatty  degeneration  once  produced  must,  in  its  turn,  lead 
to  unfavorable  results.  It  has  already  been  suggested  that  the  fatty  degeneration 
of  the  heart  may  be  the  cause  of  certain  irregularities  in  its  functional  activity; 
but  it  should  be  said  that  this  is  not  invariably  the  case,  for  often  the  heart 
exhibits  a  surprising  energy  despite  marked  fatty  degeneration  of  its  muscular 
tissue.  The  corresponding  changes  in  the  walls  of  the  blood-vessels  are,  how- 
ever, of  great  importance,  as  they  frequently  occasion  disturbance,  above  all  by 
haemorrhage.  In  many  instances  (for  example,  in  leukaemia,  vide  infra)  an 
actual  hsemorrhagic  diathesis  is  developed;  but  we  shall  find  later  (see  the  chapter 
on  pernicious  anaemia)  that  other  factors  may  also  play  a  part  in  producing  capil- 
lary haemorrhages  in  severe  anaemia.  There  is  strong  evidence  in  many  cases  of 
an  abnormal  permeability  of  the  vascular  walls.  Erom  this  results  the  mild  grade 
of  oedema  frequently  seen  in  anaemic  patients,  although  in  some  few  cases  this 
cedema  may  be  ascribed  to  passive  congestion,  resulting  from  the  cardiac  debility 
(vide  supra).  The  increased  permeability  of  the  renal  blood-vessels  is  sometimes 
shown  by  polyuria. 

The  urine  is  usually  rather  light-colored,  if  the  anaemia  be  at  all  marked.  It  is 
evident  that  there  is  a  diminished  production  of  urinary  pigment,  the  material  for 
which  is  the  coloring  matter  of  the  blood.  Another  reason  for  the  light  color  of 
the  secretion  is  the  polyuria  above  mentioned.  There  may  be  fifty  to  seventy 
ounces  (1,500-2,000  cubic  centimetres),  or  more,  secreted  in  twenty-four  hours. 
The  specific  gravity  may  nevertheless  be  comparatively  high,  and  higher  than  one 
would  expect  from  the  appearance  of  the  urine,  not  infrequently  ranging  between 
1015  and  1021.  This  indicates,  of  course,  that  the  amount  of  solid  constituents  is 
comparatively  large ;  and  in  fact  we  find  a  corresponding  amount  of  urea,  perhaps 
four  or  five  hundred  grains  (grammes  25-32)  in  twenty-four  hours.  This  is  a  large 
figure  when  we  consider  the  amount  of  ingesta.  As  to  the  other  constituents  of  the 
urine,  we  possess  as  yet  little  definite  knowledge.  The  amount  of  phosphoric 
acid  is  sometimes  surprisingly  small,  compared  with  the  amount  of  nitrogen. 
Albuminuria  is  exceptional  in  cases  of  simple  anaemia. 

The  bodily  temperature  is  very  often  affected  in  anaemia.  An  "  anaemic 
fever  "  is  very  frequently  associated  with  pernicious  anfemia,  and  even  with  cases 
of  profound  secondary  anaemia,  as  after  a  large  haemorrhage  from  the  stomach. 
There  are  irregular  elevations  of  temperature,  usually  occurring  in  the  evening, 
and  attaining  101°-102°  (38.5°-39°  C),  or  even  still  higher  figures.  This  fever 
is  not  due  to  inflammatory  organic  changes,  but,  in  all  probability,  is  rather  the 
result  of  the  presence  in  the  blood  of  matter  due  to  the  disintegration  of  the  blood- 
globules  (perhaps  fibrine  ferment). 

Clinical  History  of  Chlorosis. — Chlorosis,  or  "  green  sickness,"  is  a  definite 
form  of  primary  essential  anaemia,  which  appears  exclusively  in  the  female  sex 
and  in  the  years  of  adolescence,  mainly  from  the  fifteenth  to  about  the  twentieth 
year  of  life.    The  disease  either  may  appear  quite  suddenly  in  a  previously  healthy 


AN.EMIA   AND   CHLOEOSIS  715 

girl,  and  in  such  a  case  may  completely  disappear  again  after  a  few  weeks  or 
months ;  or  the  entire  course  may  be  a  chronic  one  without  sharp  limits,  so  that  the 
condition  approaches  more  nearly  to  a  constitutional  anaemia.  In  many  cases, 
also,  it  would  be  proper  to  say  that  there  are  recurrences  of  chlorosis,  for  severe  at- 
tacks of  the  disease  may  be  seen  more  than  once  in  the  same  girl.  As  a  rule,  there 
is  no  definite  cause  to  be  found  for  the  appearance  of  chlorosis,  except  that  some- 
times it  seems  to  be  promoted  by  an  unhygienic  mode  of  life,  too  many  social 
demands,  or  long-continued  mental  excitement. 

The  various  symptoms  of  chlorosis  are  almost  all  direct  results  of  the  anaemia, 
so  that  they  have  already  been  described.  Their  intensity  and  variety  are,  how- 
ever, very  different  in  different  cases.  There  are  mild  cases  where  the  patient 
can  hardly  be  called  ill.  She  feels  perfectly  well,  but  is  "  a  little  pale."  From 
these  cases  there  is  a  gradual  and  unbroken  transition  to  the  other  extreme  of 
severity. 

A  constant  and  essential  symptom  is  the  greater  or  less  pallor  of  the  face  as 
well  as  of  the  rest  of  the  surface  of  the  body,  and  of  the  mucous  membranes  so 
far  as  visible.  This  pallor  sometimes  really  has  a  greenish  tint.  There  is  almost 
invariably  general  languor;  the  patient  is  easily  fatigued,  and  has  neither  the 
desire  nor  the  ability  to  make  any  great  bodily  or  mental  exertion.  There  is  also 
a  tendency  to  headache  and  vertigo.  Chlorotic  patients  often  complain  of  dys- 
pepsia. The  appetite  is  usually  diminished,  and  there  is  often  a  sense  of  pressTire 
in  the  epigastrium  after  meals.  There  may  be  severe  cardialgia.  It  is  not 
always  easy  to  determine  its  cause,  often  it  seems  to  be  purely  nervous.  Some- 
times there  may  be  myalgia.  Moreover,  chlorosis  may  be  associated  with  a  genu- 
ine ulcer  of  the  stomach,  as  has  been  already  mentioned.  We  believe,  however, 
that  this  combination  is  much  less  frequent  than  is  commonly  supposed,  for  many 
physicians  make  a  diagnosis  of  gastric  ulcer  upon  insufficient  data.  The  earlier 
assumption  that  the  dyspeptic  symptoms  of  chlorosis  are  associated  with  a  lack 
of  hydrochloric  acid  in  the  gastric  juice  is  entirely  incorrect.  If  we  make  a  care- 
ful investigation  of  the  gastric  functions  in  chlorotic  girls,  we  shall  find  that  the 
amount  of  hydrochloric  acid  in  the  gastric  juice  is  normal  or  even  excessive.  That 
gastroptosis  may  often  be  found  in  conjunction  with  chlorosis  is  not  surprising 
{vide  supra,  page  462).  An  attempt  has  even  been  made  to  regard  chlorosis  as  a 
result  of  gastroptosis,  although  of  course  this  is  entirely  incorrect.  The  bowels 
are  usually  constipated  in  chlorosis,  which  is  explained  by  the  impaired  appetite 
and  the  sluggish  intestinal  peristalsis. 

Over  the  cervical  veins  we  often  hear  a  loud  murmur,  which  has  been  above 
mentioned  as  the  hruit  de  diahle.  Examination  of  the  heart  often  shows  a  slight 
increase  in  the  area  of  cardiac  dullness,  although  this  does  not  seem  due  in  most 
■cases  to  an  actual  dilatation  of  the  heart,  but  merely  to  a  retraction  of  the  borders 
of  the  lung.  Anaemic  cardiac  murmurs  are  often  heard,  the  pulse  is  accelerated 
and  easily  excited.  Otherwise  physical  examination  does  not  reveal  any  abnormal 
<3ondition  of  the  internal  organs.  It  is  a  very  great  exception  to  find  any  indica- 
tions of  disturbance  in  the  spleen  or  lymph-glands,  or  the  bone-marrow.  Fever  is 
rare  in  mild  cases  of  chlorosis,  but  in  severe  cases  we  sometimes  see,  especially  at 
night,  a  slight  rise  of  temperature,  up  to  101°  F.  (38.5°  C).  The  urine  is  usually 
pale,  but  seldom  differs  greatly,  either  in  amount  or  constituents,  from  the  normal 
character.  It  is  noteworthy  that  chlorotic  girls  are  very  apt  to  suffer  from  disor- 
ders of  menstruation.  The  menses  may  not  appear  until  late,  or  they  are  very 
•scanty.  Even  complete  and  long-continued  amenorrhoea  is  often  seen  in  chlorosis. 
All  these  disturbances  seem  to  point  to  an  essential  relation  between  the  appear- 
ance of  chlorosis  and  the  phenomena  of  sexual  life.  It  is  only  in  exceptional  in- 
stances that  chlorotic  patients  have  menorrhagia. 

Examinations  of  the  blood  have  been  made,  in  the  hope  of  gaining  a  clearer 


716  CONSTITUTIONAL   DISEASES 

insig-ht  into  the  true  character  of  chlorosis.  The  blood  is  usually  pale.  Upon 
microscopic  examination,  we  notice  that  the  red  blood-corpuscles  do  not  tend  to 
form  rouleaux  so  much  as  normally,  and  sometimes  we  can  perceive  that  the  glob- 
ules are  comparatively  light-colored,  and  are  not  all  of  the  same  size.  Some 
are  of  the  normal  dimensions,  others  are  notably  small  (microcytes),  while  there 
are  a  few  which  are  unusually  large  (macrocytes).  Irregularities  in  the  shape 
(poikilocytosis)  are  also  seen,  particularly  in  severe  cases.  In  mild  chlorosis  all 
these  changes  in  the  form  of  the  red  blood-corpuscles  are  slight,  or  scarcely  appre- 
ciable. The  white  blood-corpuscles  are  present  in  normal  amount,  or  sometimes 
somewhat  above  normal,  so  that  there  is  a  slight  leucocytosis.  In  occasional 
instances  there  are  considerable  numbers  of  "  granular  bodies "  in  the  blood. 
These  are, usually  regarded  as  products  of  the  disintegration  of  white  blood-cor- 
puscles. 

Malassez,  Hayem,  Thoma,  and  others  have  endeavored  to  determine  the  num- 
ber of  blood-corpuscles  in  chlorosis  and  allied  diseases  by  means  of  special  meth- 
ods of  counting.  In  general,  we  may  say  that  in  many  cases  of  severe  chlorosis 
the  number  of  red  blood-corpuscles  is  decidedly  diminished.  In  a  cubic  milli- 
metre of  blood  we  find  perhaps  only  3,000,000  to  3,500,000  red  blood-corpuscles, 
instead  of  the  normal  number  of  5,000,000.  The  diminution  may  be  even  greater 
than  this.  On  the  other  hand,  it  should  be  noted  that  Duncan,  Hayem,  and 
Laache  have  met  with  cases  where  the  number  of  corpuscles  was  not  diminished ; 
but  the  amount  of  hsemoglobine  in  the  blood-corpuscles  was  diminished.  JSTot  in- 
frequently, when  the  number  of  red  blood-corpuscles  is  but  slightly  diminished, 
perhaps  the  amount  of  hsemoglobine  in  the  blood  is  much  reduced,  to  thirty  or 
forty  per  cent,  of  normal.  This  justifies  the  conclusion  that  in  chlorosis  the  num- 
ber of  red  corpuscles  is  less  affected  than  is  their  constitution,  particularly  the 
proportion  of  hsemoglobine  contained  in  them.  How  this  lack  of  hgemoglobine  in 
the  red  corpuscles  comes  about  we  do  not  yet  know. 

We  have  already  intimated  that  there  is  great  variety  in  the  general  course  of 
chlorosis.  Many  cases  which  seem  severe  at  first  terminate  in  complete  recovery 
by  the  end  of  four  to  six  weeks,  or  within  a  few  months.  Other  cases  are  much 
more  obstinate,  resist  all  modes  of  treatment,  and  undergo  frequent  relapses;  so 
that  with  its  manifold  variations,  improvements,  and  exacerbations,  the  disease 
may  occupy  one  or  two  years  or  more.  The  prognosis  may  be  regarded  as  favor- 
able on  the  whole,  but  it  should  always  be  given  with  a  certain  degree  of  reserve. 
It  is  true  that  ordinary  chlorosis  never  involves  direct  danger  to  life.  We  shall, 
however,  find  that,  so  far  as  symptoms  go,  there  is  no  sharp  dividing-line  between 
"  simple  chlorosis  "  and  "  pernicious  ansemia  " ;  and  in  any  individual  case  it 
may  not  at  first  be  possible  to  decide  which  variety  of  ansemia  is  before  us. 

There  are  hardly  any  true  complications  of  chlorosis.  If  other  organic  diseases, 
such  as  pulmonary  tuberculosis  or  gastric  ulcer,  exist  along  with  chlorosis,  one 
should  always  consider  that  the  ansemia  may  have  developed  secondarily,  or  that 
the  diseases  inay  be  present  from  mere  coincidence.  All  the  varieties  of  nervous- 
ness and  hysteria  are  frequently  found  in  association  with  chlorosis,  and  yet  it 
can  not  be  assumed  in  every  case  that  there  is  an  essential  causative  relation 
between  them. 

Diagnosis. — The  diagnosis  of  chlorosis  is,  in  a  certain  sense,  easy,  for  the  char- 
acteristic symptoms,  the  pallor,  and  the  ordinary  phenomena  consequent  on  consti- 
tutional ansemia,  are  always  easy  to  appreciate ;  but,  on  the  other  hand,  the  diag- 
nosis is  not  perfectly  simple,  for  the  ansemia  must  be  actually  a  primary  essential 
ansemia  in  order  to  justify  the  name  chlorosis.  We  therefore  have  no  right  to 
declare  the  diagnosis  of  chlorosis  until  we  have  made  a  careful  and  thorough  phys- 
ical examination,  and  have  found  that  no  factors  are  present  which  might  pro- 
duce a  secondary  ansemia.    We  should,  above  all,  bear  in  mind  the  possibility  of 


ANEMIA   AND    CHLOROSIS  TlY 

incipient  tuberculosis,  and  examine  the  lungs,  the  expectoration,  and  the  general 
condition  of  the  patient,  and  also  consider  hereditary  and  other  predisposing  in- 
fluences. We  should  bear  in  mind  the  possibility  of  some  organic  disease  of  the 
stomach,  such  as  ulcer,  catarrh,  or  dilatation,  or  chronic  renal  disease,  or  possibly 
constitutional  syphilis,  giving  rise  to  the  syphilitic  chlorosis  before  mentioned. 
In  many  cases  it  is  easy  to  exclude  all  these  secondary  forms  of  anaemia,  but  occa- 
sionally the  task  is  a  very  difiicult  one.  In  making  a  diagnosis  of  chlorosis  it  is 
very  important,  also,  to  consider  the  entire  course  of  the  disease,  particularly  the 
rapid  onset  of  the  anaemia  at  the  time  of  adolescence  in  young  girls,  and  the 
greater  or  less  disturbance  of  menstruation. 

Treatment  of  Anaemia  and  Chlorosis. — The  first  indication  in  treating  chlo- 
rosis, as  well  as  every  other  form  of  anasmia,  is  to  promote  the  regeneration  of  the 
blood.  There  are  two  ways  in  which  we  can  endeavor  to  fulfill  this  indication: 
first,  by  general  hygienic  and  dietetic  measures,  and,  secondly,  by  employing 
certain  internal  remedies. 

First  among  general  measures  comes  a  care  for  pure  air,  sunlight,  and  proper 
food.  Many  a  pale  city  girl  regains  her  ruddy  cheeks  after  a  few  weeks  spent 
either  in  the  country,  or  on  the  mountains,  or  at  the  seashore.  The  choice  of  a 
place  must,  of  course,  depend  mainly  upon  the  circumstances  of  the  patient.  In 
many  instances,  boarding  in  any  suitable  country  place  answers  as  well  as  a  long 
and  expensive  journey.  If  the  seashore  be  chosen,  some  bathing  resort  on  the 
North  Sea  will  usually  be  preferable.  There  are  other  places,  where  the  patient 
can  combine  the  advantages  of  pure  forest  air  and  ferruginous  mineral  water; 
these  will  be  mentioned  below. 

The  diet  of  anaemic  patients  should  be  easily  digestible  and  rich  in  albumen; 
carbohydrates  and  fat  should  be  given  in  but  limited  amounts  to  patients  in 
whom  the  panniculus  adiposus  is  already  well  developed.  Lean  patients,  on  the 
other  hand,  require  such  ingredients  in  their  diet,  and  should  be  recommended  to 
take  simple  puddings,  extract  of  malt,  butter,  and  cod-liver  oil.  Milk,  if  well 
borne,  is  certainly  not  an  unsuitable  food  for  anaemic  patients,  but  we  do  not 
ascribe  any  special  value  to  the  drinking  of  large  amounts  of  milk  as  a  cure 
for  chlorosis.  In  the  first  place,  milk  contains  an  extremely  small  amount  of  iron, 
and  secondly,  it  is  very  apt  to  cause  troublesome  constipation.  Formerly  it  was 
not  uncommon  to  order  "  milk-cures,"  but  we  regard  this  as  decidedly  unsuitable. 
On  the  other  hand,  we  would  especially  advise  the  use  of  the  yolks  of  eggs,  pro- 
vided eggs  are  well  borne  by  the  patient,  and  are  not  the  object  of  strong  aversion. 
The  yolk  of  egg  is  comparatively  rich  in  haematogen,  which  is  a  nucleine-like  com- 
pound of  iron  from  which  it  is  probable  that  haemoglobine  is  formed;  emphasis 
should  likewise  be  laid  upon  the  use  of  an  abundance  of  green  vegetables,  such  as 
spinach,  for  these  all  contain  a  large  amount  of  iron.  Some  authors  ascribe  an 
exaggerated  value  to  alcoholic  beverages.  They  may  be  allowed  in  moderate 
amount  if  the  patient  asks  for  them  and  finds  the  appetite  improve  under  their 
use.  The  best  to  choose  for  an  emaciated  patient  are  porter  and  other  varieties  of 
beer  rich  in  extractive  principles,  but  wine  is  often  ill  borne  by  chlorotic  girls, 
being  apt  to  cause  palpitation,  etc. 

Many  physicians  also  insist  upon  "  abundant  exercise  in  the  open  air."  This 
can,  however,  be  carried  too  far.  A  chlorotic  girl  is  often  made  to  take  long 
walks  in  spite  of  her  own  reluctance  to  do  so,  with  the  result  of  becoming  more 
languid  and  exhausted  than  she  was  before.  We  even  believe  that  a  case  of  pro- 
found anaemia  will  be  benefited  by  a  certain  degree  of  bodily  rest.  Thus  any 
needless  tax  upon  the  muscles  is  avoided.  The  most  brilliant  results  we  have 
ever  observed  in  the  treatment  of  chlorosis  have  been  within  the  hospital.  The 
patients,  who  are  usually  factory  operatives  and  servant  girls,  are  often  kept  in 
bed  for  the  first  two  or  three  weeks.    We  admit  that  pure  country  air  may  be  very 


Y18  COIn^STITTJTIOIsTAL   DISEASES 

beneficial,  but  we  would  strongly  advise  moderation  in  bodily  exercise.  If  the 
patient  begins  to  feel  more  vigorous,  she  will  of  herself  take  more  exercise. 

Of  internal  remedies,  the  preparations  of  iron  have  long  occupied  the  first 
place  in  the  treatment  of  all  varieties  of  anaemia.  How  these  exert  their  influence 
is  at  present  quite  uncertain,  for  the  body  needs  so  small  an  amount  of  iron  that 
the  iron  contained  in  ordinary  food  seems  to  be  quite  sufiicient  for  the  demands 
of  the  system;  still,  the  therapeutic  efiiciency  of  iron,  particularly  in  chlorosis,  has 
been  established  by  so  many  instances  that  there  is  scarcely  room  for  doubt.  On 
the  other  hand,  in  simple  constitutional  ansemia  the  efficacy  of  preparations  of 
iron  is  much  more  uncertain  and  doubtful. 

The  number  of  iron  preparations  that  are  recommended  and  are  used  is  very 
large,  and  is  continually  being  increased  by  the  commercial  manufacturers  of 
drugs,  although  there  is  no  actual  need  of  such  increase.  Almost  every  physician 
has  his  favorite  prescription,  to  which  he  ascribes  the  greatest  efficiency.  We 
ourselves  employ  most  frequently  in  chlorosis  the  long-  and  well-known  Blaud's 
pills.  We  can  assure  the  reader  that  they  are  almost  always  well  borne,  and  often 
cause  a  surprisingly  rapid  and  decided  improvement  in  chlorosis.  We  usually  pre- 
scribe them  in  the  following  form  :  Dried  sulphate  of  iron,  pure  carbonate  of  potas- 
sium, each  one  hundred  and  fifty  to  two  hundred  and  twenty-five  grains  (grammes 
10-15)  ;  tragacanth,  q.  s.  This  makes  one  hundred  pills,  of  which  two  to  four  are  to 
be  given  three  times  a  day  after  meals.  Other  ferruginous  remedies  which  are 
likewise  often  useful  are  reduced  iron,  which  is  absolutely  pure  iron  in  a  very 
finely  divided  powder,  and  is  prescribed  as  such  or  in  pills,  from  one  to  three 
grains  (grammes  0.05  or  0.2),  to  be  given  several  times  a  day;  two  prepara- 
tions, ferri  carbonas  saccharata  (U.  S.  P.),  and  ferrum  oxydatum  saccharatum 
solubile  (Ph.  G.),  are  prescribed  as  loose  powders,  of  which  one  half  to  one  tea- 
spoonful  may  be  given  in  water  three  times  a  day.  The  last  named  has  a  special 
advantage  in  that  it  does  not  blacken  the  teeth.  Another  good  preparation  of  iron 
is  the  lactate,  which  may  be  given  in  powders  and  pills,  in  the  dose  of  five  to  twelve 
grains  (gramrae  0.3-0.75).  The  tinctures  of  iron  are,  in  general,  scarcely  to  be 
recommended,  and  are  usually  employed  only  for  children.  The  liquor  ferri  albu- 
minati  (Ph.  G.)  deserves  praise;  a  teaspoonful  of  it  is  given  three  times  a  day. 
It  often  has  a  good  effect  upon  the  appetite.  Of  late  there  have  been  repeated  trials 
of  the  internal  administration  of  organic  compounds  of  iron.  First,  haemoglobine 
itself  was  tried  (Pfeufer's  haemoglobine  tablets  or  hsemoglobine  extract)  ;  also 
Schmiedeberg's  "ferratine";  hsemagallol,  which  was  recommended  by  Kobert; 
haematogen,  hsemalbmnen,  and  many  others.  All  these  preparations  have  found 
their  champions,  but  it  is  by  no  means  certain  that  they  act  better  than  the  old 
approved  inorganic  forms  of  iron.  Often  iron  is  given  in  combination  with  other 
remedies,  of  which  quinine  is  chief.  This  is  said  not  only  to  increase  the  tonic 
action,  but  to  lessen  the  headaches  to  which  ansemic  patients  are  subject.  Sto- 
machic tonics,  such  as  gentian,  or  laxatives,  such  as  aloes,  are  also  combined  with 
iron. 

Exceptionally  iron  is  not  well  borne,  and  causes  digestive  disturbances  or  diar- 
rhoea. We  must  then  try  another  preparation  or  diminish  the  dose.  It  is  usual 
to  forbid  the  ingestion  of  sour  articles  of  diet  while  taking  iron,  but  the  injunc- 
tion is  due  mainly  to  prejudice. 

The  use  of  mineral  waters  containing  iron  is  quite  common,  although  the 
amount  of  iron  thus  introduced  into  the  system  is  so  small  that  it  is  hard  to  under- 
stand their  therapeutic  value.  Of  those  artificially  produced,  that  which  contains 
the  pyrophosphate  of  iron  is  the  best,  and  seldom  irritates  even  a  delicate  stom- 
ach. The  natural  chalybeate  waters  are  also  bottled  and  sent  to  distant  places. 
They  are  often  more  effective  if  drunk  upon  the  spot,  but  merely  because,  in  that 
case,  the  general  hygienic  surroundings  of  the  patient  are  better  than  they  would 


PKOGEESSIVE   PEENICIOUS   ANEMIA  71D 

be  at  home.  The  best-known  and  most  popular  ferruginous  springs  in  Germany 
and  Switzerland  are  situated  at  Cudowa,  Eippoldsau,  Elster,  Schwalbach,  Pyr- 
mont,  Steben,  Kohlgrub,  Driburg,  Liebenstein,  and  St.  Moritz.  "  Steel-baths  "  are 
also  much  employed ;  but  the  effect  is  due  not  to  the  iron  contained  in  the  water, 
but  to  the  temperature  of  the  water  and  the  carbonic-acid  gas  it  contains.  Baths 
generally  seem  to  be  of  decided  service  in  chlorosis,  and  hence  we  often  prescribe 
simple  baths  or  salt-baths,  giving  a  bath  of  fifteen  or  twenty  minutes'  duration,  at 
a  temperature  of  90°-95°  F.,  two  or  three  times  a  week,  adding  five  or  six  pounds 
of  salt  to  the  bath. 

Some  other  remedies  besides  iron  are  occasionally  employed  in  chlorosis.  Of 
these,  the  chief  is  arsenic.  Its  effects  are  often  very  beneficial,  and  it  deserves  a 
trial,  especially  in  severe  cases.  It  may  be  given  alone  or  in  combination  with 
iron.  We  have  repeatedly  seen  cases  of  chlorosis  which  showed  no  improvement 
after  the  use  of  iron,  in  which  the  combination  of  iron  with  small  amounts  of 
arsenic,  a  thirtieth  to  a  fifteenth  of  a  grain  (gramme  0.002-0.004)  three  times  a 
day,  had  a  strikingly  beneficial  effect.  Scholz  and  Striibing  recommend  the  ad- 
ministration of  sulphur  in  chlorosis — ^purified  sulphur,  ten  parts;  sugar  of  milk, 
twenty  parts ;  dose,  as  much  as  can  be  lifted  on  the  point  of  a  knife,  three  times  a 
day.  Other  physicians  extol  manganese.  ISTo  especial  advantage,  however,  has 
been  shown  to  pertain  to  these  remedies. 

Although  the  constitutional  treatment  is  always  the  main  consideration,  yet 
sometimes  special  symptoms  demand  attention.  Violent  headache  may  be  re- 
lieved by  antipyrine,  or  similar  remedies;  dyspeptic  symptoms  are  to  be  treated 
chiefly  by  careful  injunctions  as  to  diet.  The  patient  should  avoid  pressure  from 
without  upon  the  region  of  the  stomach,  and  should  have  easily  digested  food. 
The  internal  administration  of  hydrochloric  acid  is  proper  only  when  the  examina- 
tion of  the  gastric  juice  has  shown  that  there  is  a  diminution  in  hydrochloric  acid ; 
as  a  rule,  there  is  an  abundance  of  hydrochloric  acid  secreted  {vide  supra),  and 
if  so,  alkalies  are  preferable. 

If  there  be  constipation,  it  is  desirable  to  remedy  it  rather  by  suitable  diet  than 
by  laxatives.  Thus  we  may  prescribe  fruit,  Graham  bread,  and  other  foods  which 
promote  peristaltic  action  by  the  mechanical  irritation  which  they  exert ;  also 
gentle  massage  of  the  abdomen,  and  only  when  these  fail,  injections  or  mild 
laxatives. 


CHAPTEE   11 


PROGRESSIVE    PERNICIOUS    ANJEMIA 

(Grave  Form  of  Essential  Ancemia) 

Definition  and  .Sltiology. — We  apply  the  term  pernicious  antemia  to  a  severe 
and  rare  form  of  anemia  which  is  usually  fatal,  and  which  develops  as  a  primary 
disease,  without  demonstrable  cause,  in  both  men  and  women.  We  must  hold 
fast  to  this  conception  of  the  disease,  especially  as  the  attempt  has  been  repeatedly 
made  of  late  to  degrade  pernicious  anaemia  from  the  rank  of  an  idiopathic  dis- 
ease, and  regard  it  as  merely  a  grave  form  of  secondary  anaemia  which  may  result 
from  any  one  of  the  most  various  causes. 

Of  course,  the  diagnosis  of  primary  anaemia  may  be  wrongly  made  in  cases 
where  a  more  careful  search  will  detect  some  special  cause  for  the  condition. 
Such  a  mistake  may  become  evident  at  the  autopsy.  Thus,  in  repeated  instances, 
cases  which  have  been  during  life  regarded  as  "  pernicious  anaemia  "  have  been 
shown  to  be  cancer  of  the  stomach  (vide  page  448).    In  other  cases,  however,  it  is 


720  CONSTITUTIONAL   DISEASES 

more  difficult  to  discover  the  primary  cause  of  the  anaemia.  Thus  the  profound 
anaemia  which  attacked  the  men  at  work  upon  the  St.  Gothard  Tunnel  was 
at  first  regarded  as  idiopathic,  but  more  careful  investigation  showed  that  the  dis- 
ease was  really  due  to  anchylostoma  (vide  page  578),  the  ravages  of  which  parasite 
have  in  other  cases  also  been  confounded  with  the  symptoms  of  pernicious  anae- 
mia. Reyher  and  Runeberg  have  lately  called  attention  to  the  fact  that  the  pres- 
ence of  bothriocephalus  latus  in  the  intestine  may  produce  an  affection  resem- 
bling severe  and  apparently  primary  anaemia.  Of  late  there  have  been  a  number 
of  cases  reported  where  the  post-mortem  examination  showed  that  the  progressive 
marasmus  and  anaemia  of  the  patient  had  resulted  from  an  extensive  atrophy  of 
the  coats  of  the  stomach  and — what  is  more  important — of  the  intestine,  associ- 
ated in  some  instances  with  well-marked  lesions  of  the  sympathetic  plexus.  These 
cases  are  very  interesting,  but  have  nothing  whatever  to  do  with  pernicious  anae- 
mia. Often  the  symptoms  even  during  life  differ  not  a  little  from  those  of  per- 
nicious anaemia,  so  that  we  can  not  think  it  right  to  establish  what  is  called  a 
"  gastro-intestinal  variety  of  pernicious  anaemia."  It  is  proper  to  group  and 
classify  the  forms  of  secondary  anaemia  according  to  their  various  causes,  but 
not  the  cases  of  primary  idiopathic  anaemia,  which  are  all  due  to  some  trouble  with 
the  manufacture  of  the  blood,  or  with  the  blood  itself,  and  form  a  distinct  clin- 
ical group. 

The  credit  of  having  been  the  first  to  study  pernicious  anaemia  as  a  special 
form  of  disease  belongs  to  Biermer  (1868),  although  occasional  instances  of  the 
disease  had  long  before  been  noticed.  Its  occurrence  during  pregnancy  was  first 
pointed  out  by  Gusserow.  [The  puerperal  form  of  pernicious  anaemia  was  de- 
scribed by  Walter  Channing  in  1842.] 

With  regard  to  the  special  aetiology  of  progressive  pernicious  anaemia,  it  must 
be  confessed  that  we  have  as  little  definite  information  as  about  the  aetiology  of 
chlorosis.  Often  it  has  been  thought  that  the  disease  might  be  infectious,  but  the 
discoveries  thus  far  reported  of  specific  micro-organisms  in  the  blood — for  instance, 
the  so-called  cercomonads  of  Klebs  and  Frankenhauser — lack  confirmation.  There 
do  not  usually  seem  to  be  any  special  exciting  causes.  It  has  been  maintained 
that  unfavorable  hygienic  surroundings  and  insufficient  nourishment  promote  the 
development  of  the  disease;  and  this  would  apply  perhaps  to  some  cases,  but 
certainly  it  does  not  to  all.  We  are  inclined  to  regard  it  as  characteristic  of  this 
disease,  as  well  as  of  chlorosis,  that  the  anaemia  may  develop  despite  the  most 
favorable  outward  circumstances.  There  is,  however,  one  factor  which  seems  to 
have  a  decided  infiuence,  and  that  is  the  condition  associated  with  pregnancy  and 
childbirth.  These  are  comparatively  often  the  occasion  of  the  development  of  the 
first  symptoms  of  the  disease  in  women.  Still,  pernicious  anaemia  has  this  essen- 
tial difference  from  chlorosis,  that,  as  we  have  already  said,  it  is  not  confined  to 
women.  Most  cases  occur  in  middle  life,  from  about  twenty-five  to  forty  years  of 
age.  It  is  a  very  interesting  but  somewhat  puzzling  fact,  that  the  disease  may 
appear  as  a  sequel  to  a  great  loss  of  blood,  whether  from  one  or  several  haemor- 
rhages. It  seems  as  if  the  body  were  sometimes  unable  to  recover  from  the  effects 
of  large  haemorrhages  of  this  sort,  so  that  the  acute  merges  into  a  chronic  and 
progressive  anaemia,  which,  despite  nursing  and  treatment,'  advances  to  a  fatal 
termination.  It  is  quite  doubtful,  however,  whether  such  cases  should  be  classed 
as  genuine  pernicious  anaemia. 

Pathology. — Pernicious  anaemia  so  often  terminates  fatally  that  there  has  been 
abundant  opportunity  to  make  accurate  anatomical  investigations  of  the  lesions 
it  produces.  We  shall  not  here  discuss  the  changes  in  the  blood  itself,  inasmuch 
as  they  will  more  properly  be  described  among  the  clinical  phenomena.  The 
changes  in  the  internal  organs  are  divisible  into  two  groups :  First,  such  as  are 
secondary  and  the  result  of  the  anaemia;  and,  secondly,  such  as  may  perhaps  be 


PEOGEESSIVE   PEENICIOUS    AI^^MIA  Y21 

primary  and  characteristic.  All  the  internal  organs  are,  of  course, .  anaemic.  An- 
other striking  change  is  fatty  degeneration.  This  is  usually  best  marked  in  the 
heart,  but  it  also  affects  the  kidneys,  the  liver,  and  the  walls  of  the  stomach  and 
intestines,  as  well  as  the  intima  of  the  blood-vessels.  We  have  already  pointed 
out  that  this  fatty  change  is  to  be  regarded  as  the  direct  result  of  the  anaemia, 
probably  because  of  the  diminished  supply  of  oxygen  in  the  tissues. 

The  second  important  lesion  of  pernicious  anaemia  is  the  haemorrhages,  usually 
small,  but  occasionally  large;  these  are  usually  numerous,  and  are  found  in  all 
sorts  of  locations.  The  most  important  of  these  haemorrhages  are  into  the  retina, 
because  they  can  be  demonstrated  by  means  of  the  ophthalmoscope  during  life. 
They  are  very  frequent.  We  may  also  find  minute  haemorrhages  in  the  serous 
membranes,  such  as  the  pleura  or  pericardium,  in  the  brain  and  in  the  mucous 
membranes.  Cutaneous  ecchymoses  are  also  occasionally  found.  We  shall  revert 
later  to  the  aetiology  of  these  haemorrhages. 

Still  another  secondary  symptom  is  an  abundant  deposit  of  iron  in  the  cells  of 
many  organs.  This  can  usually  be  determined  only  by  the  aid  of  the  microscope 
■or  micro-chemical  tests.  It  is  most  abundant  in  the  peripheral  zone  of  the  hepatic 
lobules,  but  it  also  occurs  in  the  kidneys,  pancreas,  and  other  organs.  Quincke 
has  studied  this  point  very  carefully,  and  finds  that  the  total  amount  of  iron  con- 
tained in  the  liver  in  pernicious  anaemia  is  much  larger  than  normal.  The  most 
natural  and  most  ]probable  interpretation  of  this  fact  is  that  the  iron  originates 
from  the  destruction  of  large  numbers  of  red  blood-corpuscles. 

The  changes  thus  far  described  are  undoubtedly  the  result  of  anaemia,  and 
hence  are  the  same  in  all  severe  anaemias,  whatever  their  cause.  On  the  other 
hand,  search  has  been  made  for  specific  changes  which  could  be  regarded  as  the 
primary  disease,  and  thus,  of  course,  our  attention  has  been  especially  directed  to 
the  organs  engaged  in  the  formation  of  the  blood.  The  lymph-glands  do  not  usu- 
ally present  any  special  changes  in  pernicious  anaemia.  If  they  are  much  altered, 
it  is  probable  that  the  disease  is  a  different  one,  which  we  shall  later  have  an  oppor- 
tunity to  study  (vide  pseudo-leukaemia).  The  spleen  is  in  many  cases  normal. 
In  exceptional  instances,  however,  it  is  decidedly  enlarged,  although  never  enor- 
m.ous.  Even  when  the  organ  is  enlarged  there  are  no  important  histological 
changes  to  be  detected.  Cases  of  pernicious  anaemia  with  marked  splenic  tumor 
are  often  termed  splenic  anaemia  (vide  infra),  but  we  do  not  ourselves  see  how 
such  cases  differ  essentially  from  others  in  which  the  spleen  is  not  enlarged.  The 
changes  in  the  bone-marrow  are  by  far  the  most  constant.  This  structure  plays 
an  important  part  in  the  formation  of  the  blood.  C.  Wood,  and  after  him  Cohn- 
heim,  called  attention  to  the  fact  that  the  bone-marrow  is  almost  invariably 
affected  in  pernicious  anaemia.  Instead  of  its  normal  yellow  color,  it  has  a  dark- 
red  color,  like  raspberry  jelly.  This  is  due  mainly  to  the  fact  that  the  numerous 
fat-cells  of  the  marrow  are  all,  or  nearly  all,  destroyed.  This  is  the  more  surpris- 
ing as  the  fatty  tissues  in  other  parts  of  the  body  are  often  very  little  affected  in 
pernicious  anaemia.  The  specific  cellular  elements  of  the  marrow  also  exhibit  cer- 
tain changes.  There  is  a  decided  hyperplasia,  and,  as  a  rule,,  there  are  found  large 
numbers  of  nucleated  red  blood-corpuscles.  Cohnheim  is  inclined  to  regard  the 
disease  of  the  bone-marrow  as  specific  and  primary,  but  it  must  be  confessed  that 
there  are  many  reasons  which  strongly  oppose  this  view,  and  suggest  the  possibility 
of  this  change  in  the  marrow  being  merely  a  secondary  phenomenon,  a  sign  of  the 
extremely  active  formation  and  regeneration  of  the  red  blood-corpuscles.  Neu- 
mann's investigations  would  lead  to  the  belief  that  the  nucleated  red  blood-cor- 
puscles are  young  blood-cells  in  the  process  of  development.  Furthermore,  these 
vigorous  processes  of  regeneration,  and  the  corresponding  changes  in  the  bone- 
marrow,  are  often  found  in  cases  of  profound  anaemia  which  are  beyond  a  doubt 
of  secondary  origin. 
46 


T22  CONSTITUTIONAL  DISEASES 

We  can  not,  therefore,  feel  certain  tliat  the  lesion  of  the  bone-marrow  is  the 
primary  anatomical  disturbance,  and  hence  we  are  obliged  to  assume  that  essen- 
tial anasmia  may  be  a  disease  of  the  blood  itself — that  is,  some  specific  but  un- 
known process  which  does  direct  injury  to  the  red  blood-corpuscles. 

Symptoms. — As  already  stated,  the  symptoms  of  pernicious  anaemia  usually 
begin,  independently  of  any  demonstrable  cause,  in  individuals  previously  healthy,, 
and  develop  so  slowly  and  gradually  that  it  is  hardly  ever  possible  to  determine 
the  precise  date  of  the  commencement  of  the  disease.  This  is  still  more  likely  to 
be  the  case  if  the  trouble  occurs,  as  indeed  it  may,  in  individuals  who  were  pre- 
viously feeble  and  pale  without  being  actually  ill.  Occasionally  a  more  acute 
onset  is  observed  in  pregnant  women. 

The  first  symptoms  are  almost  invariably  traceable  to  the  incipient  anaemia. 
They  include  the  subjective  disturbances  and  the  objective  changes  which  are  seen 
in  any  ordinary  anaemia.  The  patient  feels  languid  and  is  easily  fatigued,  is 
liable  to  headache,  vertigo,  palpitation,  and  tinnitus  aurium;  there  are  anorexia,, 
frequent  nausea,  and,  above  all,  a  striking  pallor  of  the  skin  and  mucous  mem- 
branes, but  while  these  symptoms  in  ordinary  anaemia  and  chlorosis  are  moderate, 
in  the  severe  forms  of  essential  anaemia  they  are  extreme. 

In  every  well-marked  case  of  pernicious  anaemia  the  weakness  of  the  patient 
is  so  great  that  he  is  permanently  confined  to  bed,  and  standing  or  sitting  for  any 
length  of  time  is  impossible.  Usually  the  patient  lies  upon  his  back,  with  his 
head  rather  low,  and  presents  a  countenance  of  waxy  pallor.  Yery  frequently  a 
slight  but  distinct  yellowish  hue  may  be  detected.  Occasionally  there  are  cutane- 
ous ecchymoses,  but  these  are  exceptional.  The  mucous  membrane  of  the  lips, 
the  gums,  and  the  conjunctivae  are  likewise  pale  and  colorless.  The  intellect  is 
unimpaired,  but  all  answers  to  questions  are  slow,  apathetic,  and  delivered  in  a 
low  and  feeble  tone  of  voice.  The  patient  is  usually  incapable  of  any  great  men- 
tal exertion.  He  is  sleepy,  and  often  yawns.  If  the  body  be  moved,  and  especially 
if  an  upright  position  be  substituted  for  a  horizontal  one,  there  is  great  liability 
to  syncope.  This  may  result  from  any  slight  physical  exertion,  and  is  often  ac- 
companied by  a  peculiar  spasmodic  rigidity  of  the  body.  The  main  subjective 
symptoms  are  weakness,  and  more  especially  intense  headache ;  this  often  assumes 
a  pulsating  character,  and  is  located  mainly  in  the  temples  or  forehead.  There  is 
also  an  annoying  ringing  in  the  ears,  described  as  a  singing,  rushing,  or  roaring 
sound.  There  are  certain  other  subjective  sensations,  namely,  nausea,  a  sense  of 
thoracic  oppression,  and  pain  in  the  bones,  which  will  be  considered  later  on. 

If  we  now  proceed  to  a  systematic  physical  examination,  we  are  struck,  in  the 
first  place,  by  the  condition  of  the  eyes.  The  pupils  are  often  somewhat  enlarged, 
but  react  in  a  normal  manner.  Vision  is  often  disturbed  by  spots  before  the  eyes. 
The  anaemic  amaurosis  seen  after  a  sudden  large  haemorrhage  has  not  yet  been 
observed  in  pernicious  anaemia.  The  ophthalmoscopic  examination  of  the  fundus 
has  very  great  diagnostic  importance.  We  find  in  a  majority  of  cases,  although 
not  in  all,  retinal  haemorrhage.  There  may  be  either  one  or  many  haemorrhages. 
If  they  are  extensive  enough  to  involve  the  macula  lutea  or  the  disk,  they  may 
disturb  vision  greatly.  Retinal  haemorrhages  invariably  signify  that  the  anaemia 
is  profound,  and  are,  with  considerable  justice,  regarded  as  distinguishing  perni- 
cious from  simple  anaemia. 

Respiratory  Symptoms. — Breathing  is  usually  accelerated,  and,  in  the  most 
advanced  cases,  is  often  remarkably  deep  and  noisy  (anaemic  dyspnoea,  vide  supra). 
Sometimes  there  is  a  very  annoying  and  almost  painful  sense  of  thoracic  oppres- 
sion, which  is  evidently  connected  with  the  dyspnoea.  There  is  a  "  hunger  for  air.'* 
Physical  examination  of  the  lungs  gives  negative  results.  Sometimes  there  is  a 
little  cough,  and  there  may  be  sufficient  haemorrhage  into  the  mucous  membrane 
of  the  air-passages  to  give  rise  to  a  slight  haemoptysis.    Even  in  this  case  no  ana- 


PEOGEESSIVE   PEENICIOUS    ANJEMIA  Y23 

tomical  changes  can  be  detected  during  life.  We  may  also  mention  in  this  con- 
nection that  epistaxis  is  not  very  infrequent. 

Phenomena  referable  to  the  circulatory  system  are  of  still  greater  clinical 
importance.  The  area  of  cardiac  dullness  is  usually  normal,  although  sometimes 
slightly  increased.  Upon  palpation,  we  often  find  that  the  heart's  action  is  exag- 
gerated, and  that  its  beat  is  felt  over  a  larger  area  than  normal.  The  pulse  is  usu- 
ally decidedly  rapid  (100-120),  but  it  is  regular,  and  sometimes,  but  by  no  means 
invariably,  small.  It  is  often  surprisingly  strong.  The  loud  "  anaemic  murmurs  " 
are  very  characteristic.  They  can  be  appreciated  at  the  apex  of  the  heart,  but  are 
usually  heard  still  better  at  its  base.  We  generally  hear  a  loud  hruit  de  diable  in 
the  veins  of  the  neck. 

Digestive  Organs. — The  tongue  is  usually  pale,  smooth,  and  dry.  The  appe- 
tite is  often  very  poor.  The  most  prominent  disturbances,  however,  are  not  due 
directly  to  the  condition  of  the  stomach,  but  they  result  from  the  cerebral  ansemia 
— that  is,  they  are  symptoms  of  the  irritation  of  the  nervous  centers.  We  refer  to 
eructations  and  vomiting,  which  may  be  very  frequent  and  distressing.  There  is 
generally  a  tendency  to  constipation.    Occasionally  there  is  diarrhoea. 

The  liver  is  usually  normal;  as  is  also  the  spleen  in  many  instances,  while  in 
others  it  is  shown  by  percussion  and  palpation  to  be  enlarged.  It  is  sometimes 
possible,  as  we  can  ourselves  bear  witness,  to  observe  an  enlargement  of  the  spleen 
increasing  as  the  ansemia  grows  more  profound,  and  again  decreasing  if  improve- 
ment occurs  (vide  infra).  On  ordinary  examination,  the  urine  does  not  usually 
differ  essentially  from  normal.  With  few  exceptions  it  is  free  from  albumen, 
and  it  never  contains  sugar.  As  already  set  forth,  however,  accurate  quantitative 
analysis  often  furnishes  important  evidence  of  changes  in  tissue-metamorphosis 
resultant  upon  the  ansemia  (cf.  page  714).  We  will  merely  mention  once  more 
the  comparative  increase  in  the  amount  of  urea  excreted,  and  the  occasional 
excess  of  uric  acid.    Sometimes  the  urine  gives  a  vivid  reaction  for  indican. 

In  regard  to  what  has  already  been  said  about  the  marrow  of  the  bones,  it  is  an 
interesting  fact  that  they  are  very  sensitive  to  pressure  in  many  cases  of  perni- 
cious ansemia.  The  sternum  in  particular  is  painful  upon  light  percussion;  and 
sometimes  pressure  will  cause  pain  in  the  bones  of  the  extremities.  In  rare  in- 
stances swelling  of  the  knee  and  other  joints  has  been  observed.  A  series  of  very 
interesting  observations  have  been  recently  made  by  Lichtheim,  Minnich,  and 
others,  which  show  that  persons  with  primary  or  even  secondary  pernicious  ansemia 
(e.  g.,  ansemia  due  to  the  bothriocephalus)  may  quite  suddenly  develop  well-marked 
nervous  symptoms.  These  consist  chiefly  in  pargesthesise  in  the  hands  and  legs,  in 
slight  disturbances  of  sensation,  unsteadiness  and  ataxia  of  the  legs,  weakness  or 
complete  abolition  of  the  tendon  reflexes,  etc. — in  brief,  a  group  of  symptoms  re- 
sembling tabes.  The  pupils  have  been  observed  to  become  irresponsive  to  light. 
Upon  the  post-mortem  examination  of  such  cases,  there  is  found,  particularly  in 
the  posterior  columns  of  the  spinal  cord,  a  well-marked  disease  which  consists  for 
the  most  part  in  small  scattered  foci  of  degeneration,  and  in  a  more  systemic  (sec- 
ondary) degeneration  of  the  columns  of  Goll.  Sometimes  small  capillary  haemor- 
rhages are  also  found.  Slight  changes  of  this  sort  may  be  observed  in  the  spinal 
column,  even  when  no  special  spinal  symptoms  had  been  present.  Probably  these 
conditions  are  due  to  toxic  action. 

The  blood  has  been  made  the  subject  of  numerous  and  careful  investigations; 
nevertheless,  no  characteristic  change  has  been  discovered.  The  changes  presented 
in  pernicious  ansemia  likewise  occur  in  cases  of  profound  secondary  ansemia. 
This  seems  the  more  readily  intelligible  to  us  because  of  the  view  which  we  have 
already  expressed  on  page  YlO  with  regard  to  the  origin  of  secondary  ansemia. 
To  the  naked  eye  the  blood  seems  extremely  pale  and  watery.  The  number  of 
red  blood-corpuscles  is  sometimes  so  diminished  that  it  seems  incredible  that  life 


724:  COjS^STITUTIOXAL   DISEASES 

should  persist.  It  is  not  at  all  unusual,  in  the  worst  stages  of  the  disease,  to  find 
only  600,000  to  1,000,000  red  blood-corpuscles  per  cubic  millimetre,  or  even 
250,000— that  is,  even  less  than  one  tenth  of  the  normal  amount.  The  proportion 
of  hsemoglobine  in  the  blood  is  consequently  much  diminished,  but  comparative 
,  determinations  of  the  number  of  blood- 

corpuscles  and  the  amount  of  hsemoglo- 

j  I    (g) 1      l^ine  seem  to  indicate  that  the  individual 

(5  I  blood-corpuscles    have    not    lost    any    of 

^   ' — ^J)    A.  ^  O  their  coloring  matter.     The   red  blood- 

Q-^  O  corpuscles  are  found  to  present  striking 

(P^^    r\  *^'   O «     varieties  in  size  and  form  (ricZe  Eig.  79). 

\o]/P  (^  /)  Q'^N  While   some   corpuscles   have   a   normal 

p,  [J  v^Q    ^~.  appearance,  others  may  be  of  an  unusu- 

Q^  Oo  0(0        o c      ally    large    size     (macrocytes).       These 

'^         (S^   /p"^    Q       ly  "  giant    corpuscles "    appear   normal   es- 

W     (3   rn     yO^    &  S  ^^P*  ^^^  dimensions,  and  some  observers 

^,,0    \  /)  ,0° ^       (Laache)   have  thought  that  they  were 

^..--'^        j  ^  ^  even  possessed  of  an  unusual  amount  of 

^  /      /— \  °  hsemoglobine.     It  is  therefore  feurmised 

/       ^-^  that  they  represent  an  effort  on  the  part 

'  ,  of  nature  toward  compensation.    In  con- 

^,    ^      .    ^^       ^  v.,    J  ,     •       trast  with  these  large  cells  are  found  a 

Fig.  79.— Changes  in  the  red  blood-corpuscles  in  .  ,  „       .  ^        ^^        £ 

pernicious  anaemia.   (From  Quincke.)    a.  Nor-       varying  number  01  mmute  red  celis  01  a 

?r"ol,?iL°'-rrof^Uocytt.'''^''°'^^'''"    " '''■     spherical    shape:  these    were    first    de- 

scribed  by  Yanlair  and  Masius,  and 
called  microcytes.  Finally,  there  are  numerous  red  blood-corpuscles  of  abnormal 
shape.  These  Quincke  was  the  first  to  notice.  They  present  remarkable  forms, 
being  biscuit-shaped,  hammer-shaped,  or  anvil-shaped,  and  so  on,  as  illustrated  in 
the  accompanying  cut.  These  "  poikiiocytes  "  are  found  in  perfectly  fresh  undi- 
luted blood,  so  that  there  is  no  reason  to  suppose  that  they  are  artificial  products. 
Both  the  microcytes  and  the  poikiiocytes  are  regarded  as  degenerative  forms  of 
the  blood-corpuscles.  They  are  the  products  of  the  division  and  constriction  of  old 
blood-corpuscles.  Careful  histological  examination  discloses  several  definite  and 
histologically  distinct  forms  of  degeneration  in  the  red  blood-corpuscles.  We  have 
already  pointed  out  that  the  microcytes  and  poikiiocytes  are  not  essentially  char- 
acteristic of  pernicious  anaemia,  but  occur  in  other  severe  forms  of  anemia; 
but  besides  these  products  of  degeneration,  we  find  in  the  blood,  also,  indications 
of  an  increase  in  the  formation  of  new  elements.  We  refer  to  the  nucleated 
blood-corpuscles.  Ehrlich,  to  whom  we  are  indebted  for  the  best  investigations 
with  regard  to  this  matter,  distinguishes  the  so-called  normoblasts  and  megalo- 
blasts.  The  normoblasts  are  nucleated  red  blood-corpuscles  of  ordinary  size,  which 
correspond  to  the  youthful  forms  of  red  blood-corpuscles  normally  present.  The 
megaloblasts,  on  the  other  hand,  are  nucleated  structures  which  exceed  the  ordi- 
nary red  blood-disks  in  size,  two  to  four  fold.  Megaloblasts  are  found  normally  in 
the  embryo  alone,  so  that  Ehrlich  conceives  the  appearance  of  megaloblasts  to  be 
a  sort  of  reversion  to  the  embryonic  state.  The  appearance  of  megaloblasts  in  the 
blood  is  very  characteristic  of  pernicious  ansemia.  The  white  blood-corpuscles  are 
not  usually  increased  in  number;  in  occasional  instances,  however,  a  temporary 
leucocytosis  has  been  found.  "  Granule-masses  "  are  often  found  in  considerable 
abundance.  Chemical  examination  of  the  blood  has  not  as  yet  brovight  to  light 
any  facts  of  great  importance.  It  has  been  already  stated  that  there  is  a  great 
diminution  in  the  total  amount  of  hsemoglobine.  The  amount  of  albumen  in  the 
blood-serum  remains  nearly  normal. 

We  observe  in  pernicious  anaemia  the  tendency  to  fever  common  to  all  varie- 


PEOGEESSIVE   PEENICIOUS    AX^MIA  725 

ties  of  profound  ana3mia.  In  many  cases  the  evening  temperature  will  for  weeks 
reach  100°-101°  (38°-38.5°  C),  or  even  higher.  Previous  to  death,  however,  the 
temperature  may  become  subnonnal,  falling  to  86°  (30°  C),  or  even  lower. 

As  to  the  origin  of  all  these  symptoms  we  must,  as  we  have  said,  regard  the 
impairment  of  the  blood,  especially  its  poverty  in  red  blood-corpuscles,  as  the 
essential  morbid  process.  How  this  impairment  is  produced,  whether  by  injury 
to  the  blood-coriDuscles  themselves  or  to  the  organs  where  they  are  formed,  we  do 
not  know.  A  large  part  of  the  other  morbid  symptoms — the  pallor  of  the  skin, 
the  weakness,  the  "  anaemic  cerebral  symptoms,"  tinnitus,  vertigo,  nausea,  f  aint- 
ness,  etc.,  are  due  directly  to  the  anaemia.  In  regard  to  certain  other  important 
symptoms,  however,  another  factor  is  probably  of  great  significance,  namely,  an 
auto-intoxication  of  the  body  with  fibrine  ferment  or  some  similar  substance. 

By  the  destruction  of  many  red  blood-corpuscles,  probably  a  certain  amount 
of  haemoglobine  is  always  set  free,  and  enters  the  blood  plasma.  There  is  then 
a  hsemoglobinsemia.  From  many  experiments,  however  (Dorpat  school  of  Alex- 
ander Schmidt,  Ponfick,  Silbermann,  etc.),  we  know  that  hsemoglobine  dissolved 
in  the  blood  destroys  the  white  blood-corpuscles,  and  in  some  way  produces  from 
them  fibrine  ferment.  Chronic  "  ferment  intoxication  "  of  the  body  causes  certain 
symptoms,  which  are  almost  never  absent  in  pernicious  anaemia — capillary  haemor- 
rhages and  fever.  The  haemorrhages  are  usually  associated  with  embolism  of  the 
smaller  vessels,  seldom  with  local  thrombi.  Many  severe  nervous  symptoms  (vide 
supra)  may  perhaps  also  be  referred  to  this  intoxication. 

General  Course,  Duration,  and  Prognosis. — As  the  very  name  "  pernicious  " 
indicates,  the  disease  generally  terminates  unfavorably.  Death  usually  seems  to 
be  the  direct  result  of  the  extreme  anaemia ;  special  complications  are  exceptional. 
The  disease  often  maintains  a  slow  but  gradual  progress  to  the  end.  Its  dura- 
tion, reckoning  from  the  appearance  of  the  first  symptoms,  may  not  exceed  three 
to  six  months.  It  may  even  run  its  course  in  a  still  shorter  time.  It  seldom  lasts 
more  than  a  year.  Sometimes  its  course  is  interrupted;  there  may  be  an  arrest 
of  the  process,  or  improvement,  or  even  apparent  recovery.  Usually,  however, 
there  are  fresh  relapses.  In  a  certain  class  of  cases  the  disease  lasts  two  or  three 
years,  and  is  marked  by  a  number  of  "  attacks  of  anaemia  "  so  intense  that  the 
subsequent  improvement  of  the  patient  seems  simply  marvelous.  It  is  in  cases 
of  this  sort  that  splenic  tumor  has  been  made  out  at  the  time  the  anaemia  was  at 
its  height ;  yet  we  do  not  perceive  the  necessity  of  establishing  "  splenic  anaemia  " 
as  an  affection  essentially  different  from  progressive  pernicious  anaemia.  It  is 
merely  a  clinical  variety  of  the  disease  under  discussion.  Apparently,  it  likewise 
has  an  invariably  fatal  termination. 

Permanent  recovery  may  occur  in  cases  of  idiopathic  anaemia  so  profound  that 
we  are  at  first  inclined  to  regard  them  as  pernicioiis.  These  cases  are  unfortu- 
nately very  rare,  and  even  when  there  is  a  marked  improvement  the  danger  of  a 
relapse  is  to  be  borne  in  mind.  The  prognosis  is  therefore  always  very  grave, 
if  not  absolutely  unfavorable.  Of  course,  general  hygienic  surroundings  and 
good  care  may  exert  some  influence  upon  the  course  of  the  disease.  It  is  note- 
worthy that  if  pregnancy  be  complicated  by  profound  antemia  there  is  a  great 
liability  to  premature  delivery,  after  which  there  is  often  a  rapid  change  for  the 
worse.    There  are  exceptions  to  this  rule. 

Diagnosis. — It  is  seldom  difficult  to  make  out  the  existence  of  a  profound 
anaemia,  or  to  determine  the  degree  of  danger  which  the  consequent  symptoms 
indicate.  "We  have,  however,  the  same  difficulty  here  as  in  chlorosis  in  proving 
that  the  anaemia  is  primary  and  idiopathic.  The  factors  essential  to  this  diagnosis 
have  been  already  indicated.  We  should  bear  in  mind  the  possibility  of  insidious 
tuberculosis,  organic  diseases  of  the  stomach,  or  such  parasites  as  the  anchylos- 
toma  and  bothriocephalus. 


726  CONSTITUTIONAL   DISEASES 

Treatment. — For  treating  progressive  pernicious  anaemia  we  have  only  the 
same  remedies  as  for  the  benign  variety  of  anaemia.  We  must  provide  the  patient 
with  nourishing  and  digestible  food,  and  regulate  all  other  hygienic  matters ;  and 
in  the  way  of  medicine  the  greatest  prospect  of  benefit  lies  in  arsenic,  while  the 
efficiency  of  ferruginous  preparations  in  pernicious  anaemia  is  dubious.  We  may, 
however,  try  a  combination  of  iron  with  arsenic.  The  best  form  in  which  to  ad- 
minister the  arsenic  is  pills,  but  subcutaneous  injections,  also,  may  be  tried,  in 
the  manner  which  will  be  fully  described  in  the  following  chapter.  Besides 
arsenic,  some  physicians  recommend  phosphorus. 

If  the  case  be  not  too  far  advanced,  baths  may  prove  useful  adjuvants  to  the 
internal  treatment.  Salt  baths  or  artificial  carbonic-acid  baths  may  be  employed. 
Symptomatic  treatment  is  often  indicated:  the  dyspepsia  may  call  for  dilute 
hydrochloric  acid,  or  the  troublesome  vomiting  may  require  bits  of  ice,  bromide 
of  potassium,  or  opium. 

The  transfusion  of  blood  has  been  employed  in  pernicious  anaemia.  Some- 
times the  effect  seems  to  be  favorable.  Experience  thus  far,  however,  would  not 
lead  one  to  expect  very  great  benefit  from  it.  Von  Ziemssen  has  lately  recom- 
mended in  all  severe  forms  of  anaemia  the  subcutaneous  injection  of  blood.  It  is 
done  by  injecting  under  the  skin,  by  thoroughly  disinfected  instruments,  fifty 
cubic  centimetres  of  defibrinated  human  blood,  divided  into  two  parts,  twenty-five 
cubic  centimetres  being  injected  into  each  thigh.  The  point  of  injection  is  vigor- 
ously rubbed,  and  thus  the  injected  blood  is  forced  into  the  lymph-channels.  In 
severe  cases  this  procedure  should  be  frequently  repeated.  Experience  of  this 
method  has  thus  far  been  very  favorable.  Not  only  the  subjective  symptoms,  but 
the  objective  condition  of  the  blood,  the  number  of  red  blood-corpuscles,  some- 
times show  a  striking  improvement  after  the  injection, 

[In  the  experience  of  American  and  English  clinicians,  arsenic,  long  continued 
and  in  as  large  doses  as  are  tolerated,  is  of  far  greater  value  than  iron. 

The  inhalation  of  oxygen  is  expensive,  but  seems  to  be  of  distinct  service  in 
some  cases  of  grave  anaemia  of  all  forms.] 


CHAPTEE   III 

LETJKJEMIA 

( LeucocythcBinia ) 

Definition  and  .ffitiology. — Virchow,  in  1845,  was  the  first  to  obtain  an  insight 
into  the  disease  leukaemia  ("white  blood").  He  detected  the  great  increase  of 
white  corpuscles  occasioned  by  it,  and  from  this  time  these  constituents  of  the 
blood  were  subjected  to  observation  in  all  sorts  of  diseases.  It  was  soon  found 
that  there  may  be  a  temporary  increase  of  the  white  corpuscles  in  various  primary 
diseases,  and  that  in  certain  instances  this  increase  may  actually  constitute  the 
essential  symptom.  In  this  latter  case  the  increase  is  due  to  a  depraved  condition 
of  certain  internal  organs.  In  the  temporary  cases,  in  which  the  increase  of  white 
blood-corpuscles  is  usually  not  very  great,  we  find  one  white  corpuscle  to  one 
hundred  red,  or  even  one  to  fifty — the  normal  ratio  being  one  to  six  hundred  or 
more.  This  is  usually  termed  leucocytosis,  in  distinction  from  leukaemia  proper 
If  we  take  for  normal  a  count  of  about  6,000  to  10,000  leucocytes  in  a  cubic  milli- 
metre of  blood,  the  term  leucocytosis  is  applied  to  conditions  in  which  the  number 
of  leucocytes  rises  to  15,000  or  20,000,  or  even  still  higher  up  to  and  beyond 
40,000.    A  leucocytosis  of  this  sort  is  found,  under  normal  conditions,  at  the  time 


LEUKEMIA  ^^27 

of  digestion,  also  in  pregnant  women  and  in  tlie  new-born;  under  pathological 
conditions,  chiefly  in  certain  acute  febrile  diseases,  particularly  croupous  pneu- 
monia, erysipelas,  and  sepsis. 

Genuine  leukaemia  is  a  rather  rare  disease.  Its  characteristics  are  well  marked 
in  most  cases,  but  of  its  true  nature  we  remain  entirely  ignorant.  In  a  majority 
of  the  cases  the  change  in  the  blood  is  associated  with  marked  changes  in  the 
spleen  and  the  bone-marrow,  and  often  also  in  the  lymph-glands.  The  organs 
just  enumerated  being  concerned  in  the  manufacture  of  the  blood,  and  particularly 
of  the  white  corpuscles,  it  is  very  reasonable  to  suppose  that  leukaemia  is  a  disease 
which  primarily  affects  these  organs,  and  that  the  increase  in  white  corpuscles  re- 
sults from  the  disturbance  thus  occasioned.  The  cause  of  the  disease  in  the  organs 
mentioned  is  as  yet  unknown.  Various  authors  have  suggested  that  there  may 
be  some  specific  infection,  but  they  have  not  been  able  thus  far  to  produce 
any  evidence  of  the  truth  of  their  surmise.  In  few  cases  can  we  discover  even  any 
exciting  cause.  The  illness  seems  to  develop  spontaneously  in  perfectly  healthy 
persons.  In  some  cases,  on  the  other  hand,  leukaemia  does  seem  to  be  a  sequel  of 
some  other  disease.  Thus  it  occasionally  follows  a  tedious  attack  of  intermittent 
fever.  It  has  also  been  asserted  that  syphilis  and  other  infectious  diseases,  such  as 
typhoid  fever,  may  give  rise  to  leukaemia,  but  this  is  not  very  probable.  Finally, 
trauma  of  the  spleen  or  bones  has  in  repeated  instances  been  regarded  as  the  occa- 
sion of  the  disease.  The  hygienic  surroundings  of  the  patient  have  also  been  re- 
garded as  a  cause  of  leukaemia.  The  disease  is  somewhat  more  frequent  among 
the  poorer  classes  than  among  the  wealthy ;  but  there  are  numerous  exceptions  to 
this  rule.  Etiological  importance  has  also  been  ascribed  to  anxiety,  trouble,  and 
mental  depression  in  general.  Still,  all  these  apparent  exciting  causes  are 
scarcely  ever  of  real  importance,  and  in  most  cases  of  leukaemia  there  is,  as  we 
have  said,  no  evidence  of  any  of  them. 

Leukaemia  is  most  common  in  middle  life,  between  thirty  and  forty-five  years 
of  age,  but  well-marked  cases  have  been  observed  repeatedly  even  in  childhood, 
as  also,  though  less  frequently,  in  old  age.  Men  are  somewhat  more  liable  to 
the  disease  than  women.  It  has  been  repeatedly  stated  that  in  female  patients 
the  disease  is  sometimes  referable  to  sexual  derangement,  but  apparently  this  was 
mistaking  effect  for  cause. 

Pathological  Anatomy. — The  essential  change  in  leukaemia  is  a  great  increase 
in  the  number  of  white  blood-corpuscles.  The  characteristics  of  the  blood  can  be 
studied  during  the  life  of  the  patient,  and  upon  them  the  diagnosis  is  mainly 
based.  They  will  therefore  be  discussed  under  symptomatology,  while  we  shall 
here  confine  ourselves  to  the  lesions  presented  by  the  spleen,  bone-marrow,  and 
lymph-glands. 

Of  the  organs  just  enumerated,  the  spleen  is  the  one  most  frequently  affected 
(splenic  leukaemia).  It  is  often  greatly  increased  in  size,  and  may  attain  a  weight 
of  six  to  eleven  pounds  (3-5  kilogrammes)  and  a  length  of  a  foot  (30  centimetres). 
There  is  a  true  hyperplasia  of  the  whole  organ:  all  the  histological  constituents 
are  increased.  The  cut  surface  is  usually  a  rather  vivid  red  in  early  cases,  but 
later  on  it  often  has  a  lighter,  yellowish  color.  The  consistency  is  usually  dimin- 
ished, but  in  the  later  stages  it  may  be  greater  than  normal.  Upon  microscopic 
examination,  we  find  enlargement  of  the  blood-vessels  and  a  great  increase  in 
the  cells  of  the  pulp  and  of  the  follicles.  Sometimes  the  hyperplasia  of  the  folli- 
cles predominates,  giving  the  spleen  a  spotted  appearance,  like  marble.  In  such 
cases  the  pulp  usually  presents  retrograde  metamorphosis,  with  atrophy  and  fatty 
degeneration  of  its  cells  and  deposits  of  pigment.  In  advanced  cases  a  consider- 
able amount  of  firm  connective  tissue  may  be  present.  There  are  often  haemor- 
Thagic  infarctions,  presenting  the  appearance  of  circumscribed  spots,  dark  red,  or 
in  the  later  stages  brownish  yellow,  in  color. 


Y28  CONSTITUTIOIv'AL   DISEASES 

Lesions  of  the  bone-marrow  are  next  in  frequency  to  those  of  the  spleen  (med- 
ullary or  myelogenous  variety  of  leuksemia).  Neumann  and  a  few  other  au- 
thorities regard  changes  in  the  bone-marrow  as  an  essential  lesion,  and  hold  that 
they  can  be  demonstrated  in  every  case  of  leukemia.  There  would  certainly 
seem  to  be  exceptions  to  this  last  rule,  but  nevertheless  in  a  majority  of  cases  the 
marrow  does  present  a  peculiar  yellowish  or  almost  puriform  appearance.  By 
means  of  the  microscope  we  can  detect  a  great  increase  in  the  lymphoid  cells  of 
the  marrow  and  the  presence  of  a  considerable  number  of  nucleated  red  blood- 
corpuscles. 

In  many  eases  the  lymph-glands  remain  perfectly  normal;  but  in  others  they 
become  considerably  enlarged,  and  form  actual  tumors  in  various  parts  of  the- 
body,  such  as  the  axilla,  neck,  and  groin,  and  sometimes  the  internal  lymph-glands.. 
Such  cases  are  examples  of  lymphatic  leukaemia.  Histologically,  the  change  here- 
is  simple  hyperplasia  of  the  glandular  tissue. 

These  three  forms  of  leukaemia — splenic,  myelogenous,  and  lymphatic— can  not 
be  regarded  as  distinct  diseases,  inasmuch  as  cases  occur  which  present  all  sorts  of 
combinations  of  these  different  lesions.  Purely  myelogenous  cases  are  very  rare,  if 
they  occur  at  all;  and  we  rarely  meet  with  cases  which  are  purely  splenic  or 
purely  lymphatic.  Most  cases  present  lesions  of  the  spleen  and  marrow  con- 
jointly. In  less  frequent  instances  splenic  disease  is  associated  with  that  of  the 
lymphatic  glands.  The  fact  that  these  combinations  exist  indicates  that  there  i& 
one  common  cause  for  the  disease,  which  assails  sometimes  one,  sometimes  two,  or 
sometimes  all  three  of  the  organs  named. 

Just  what  the  connection  is  between  the  changes  in  the  blood  and  the  lesions- 
of  these  various  organs  is  an  unanswered  question.  The  view  which  seems  to  us 
most  plausible  regards  the  disturbance  in  the  spleen,  marrow,  or  lymph-glands, 
as  the  case  may  be,  as  the  primary  one,  and  the  alteration  in  the  blood  as  a  result 
of  this  primary  disturbance;  there  is  an  increase  in  the  number  of  colorless  cor- 
puscles formed,  and  a  consequent  increase  in  the  number  of  them  introduced  into- 
the  circulatory  fluid.  It  is  true,  however,  that  the  number  of  red  blood-corpuscles 
is  usually  diminished  in  leukaemia.  This  diminution  in  number  might  be  ascribed 
either  to  scantiness  of  supply  or  to  increase  in  the  processes  of  destruction,  but 
which  factor  is  in  reality  the  important  one  must  remain  undetermined. 

Changes  in  Other  Organs. — Leukaemia  sometimes  causes  new  growths  of  a 
lymphatic  character  in  certain  organs  other  than  those  already  mentioned.  The 
growths  may  either  be  diffuse  or  circumscribed.  They  are  observed  in  the  tonsils,, 
Peyer's  patches,  and  the  intestinal  follicles.  They  are  also  found  very  frequently 
in  the  liver,  kidneys,  and  retina,  and  more  rarely  in  the  lungs  and  the  pleura.. 
These  various  lesions  may  be  regarded  as  in  a  certain  sense  analogous  to  the- 
metastatic  tumors  of  cancer  or  sarcoma,  and  suggest  the  possibility  of  the  diffu- 
sion of  the  pathogenic  poison  throughout  the  whole  body.  In  one  or  two  cases 
a  well-marked  leukaemia  has  been  found  independent  of  any  demonstrable  organic 
lesions.  It  is  impossible,  at  present,  to  explain  such  occurrences.  Leube  and 
Fleischer  have  reported  a  case  of  this  sort,  and  are  inclined  to  believe  that  the 
blood  itself  was  diseased. 

There  is  little  known  as  yet  as  to  changes  in  the  chemical  composition  of  the 
blood  and  viscera  in  leukaemia.  Glutine,  xanthine,  and  hypoxanthine  have  been 
found  in  the  blood,  as  have  also  lactic  acid  and  formic  acid.  It  is  also  interesting- 
that  nucleo-albumen  is  found  in  the  blood  serum  of  leukfemic  patients,  for  this 
fact  points  directly  to  destruction  of  the  blood-corpuscles  (Matthes). 

It  is  noteworthy  that  octahedral  crystals  are  often  found  after  death  in 
the  blood,  spleen,  and  marrow,  and  in  otlier  parts.  These  are  known  as  Charcot's 
crystals,  and  have  already  been  described  as  occurring  in  the  sputum  in  bronchial 
asthma  (see  page  184). 


LEUKEMIA 


;29 


Symptoms. — The  clinical  phenomena  of  leukaemia  are  in  many  respects  similar 
to  those  of  progressive  pernicious,  anaemia,  and  need  not  be  enumerated  again 
here.  In  leuksemia,  however,  we  have,  in  addition,  symptoms  referable  to  the 
spleen,  lymph-glands  or  bone-marrow  (as  the  case  may  be),  and  also  the  char- 
acteristic alterations  in  the  blood.  The  blood-changes,  being  pathognomonic, 
demand  a  full  description. 

The  pallor  and  watery  character  of  the  blood  in  leuksemia  are  noticeable  even 
to  the  naked  eye  in  advanced  stages  of  the  disease.  They  can  not,  however,  be 
distinguished  without  the  aid  of  the  microscope  from  the  changes  present  in  grave 
anaemia  (vide  Fig.  80).  In  this  way  it  is  often  possible  to  determine  by  the  first 
glance  that  there  is  an  enormous  increase 
in  the  white  corpuscles,  their  number 
seeming  of  more  significance  because  the 
number  of  red  globules  is  apt  to  be  con- 
siderably diminished.  If  an  accurate  count 
is  made  we  find  in  a  cubic  millimetre  of 
blood  about  2,500,000  to  3,500,000  of  red 
blood-corpuscles  and  about  300,000  to  500,- 
000,  or  even  700,000  leucocytes.  The 
proportion  of  white  to  red  blood-corpus- 
cles is  one  to  twelve,  or  even  one  to  eight 
and  one  to  seven.  The  earlier  reports  of 
ratios  of  one  to  two  and  one  to  one  are 
probably  due  to  inaccurate  counting. 
Still  more  interesting  than  these  ratios 
are  the  special  forms  of  leucocytes ;  even  in 
the  fresh  unstained  preparation  it  is  easy 
to  appreciate  that  there  are  decided  dif- 
ferences in  the  size  and  character  of  the  individual  leucocytes;  but  all  these 
differences  become  far  more  distinct  in  the  stained  preparation*  (Fig.  81).  In 
this  we  see  that  a  very  large  proportion  of  the  leucocytes  consists  of  the  ordi- 
nary polynuclear  cells,  but  we  also  find  small  mononuclear  cells,  called  lympho- 
cytes, which  probably  originate  in  the  lymph-glands,  so  that  an  increase  in  the 
number  of  them  is  regarded  as  especially  characteristic  of  the  lymphatic  form  of 
leuksemia.  We  also  see  in  most  cases  numerous  large  mononuclear  cells,  almost 
twice  as  large  as  a  white  blood-corpuscle,  so  that  they  can  be  distinctly  recog- 
nized even  in  the  fresh  unstained  specimen.  These  cells  are  at  present  usually 
termed  marrow-cells,  or  myelocytes,  because  they  are  found  in  large  numbers  in 
the  bone-marrow,  both  in  normal  conditions  and  particularly  also  in  leuksemic 
subjects,  so  that  it  is  regarded  as  probable  that  the  myelocytes  which  are  present 
in  leuksemic  blood  originate  in  the  bone-marrow.  Finally,  we  ordinarily  find  in 
every  microscopic  field  several  so-called  eosinophilous  cells — that  is,  cells  whose 
marked  granulation  is  noticeable  even  in  the  fresh  specimen,  but  becomes  still 
more  striking  when  the  granules  are  stained  red  with  eosine.  As  to  the  origin 
(bone-marrow?)  and  the  significance  of  eosinophiles,  we  have  as  yet  no  certain 
knowledge,  nor  can  we  make  absolute  statements  as  to  the  source  of  the  lympho- 
cytes and  myelocytes.  Many  investigators  regard  the  mononuclear,  small 
leucocytes,  or  lymphocytes,  as  merely  the  immature  form  of  the  polynuclear  and 
large  nucleated  cells,  into  which  they  are  supposed  to  develop.  The  red  blood- 
corpuscles  in  leukaemia  often  undergo  certain  changes  in  size  and  shape  (poikilo- 
cytosis),  but  seldom  to  such  a  degree  as  in  grave  essential  anaemia.     We  should 


Leuksemic  blood.    (From  Fdnke.) 


*  For  particulars  with  regard  to  the  various  methods  of  staining  the  blood  (which  are  chiefly  due 
to  P.  Ehrlich),  the  reader  is  referred  to  text-books  on  methods  of  clinical  examination. 


730 


CONSTITUTIONAL   DISEASES 


Fig.  81. — Mixed  leukgemia  fmyelaemia). 
(From  RiEDER.) 


mention,  however,  that  in  leukaemia  we  almost  invariably  find  nucleated  red  blood- 
corpuscles,  and  these  are  exclusively  normoblasts  (see  the  preceding  chapter). 
Granular  masses  are  usually  present  in  leuksemic  blood  in  large  numbers. 

Splenic  tumor  is  the  most  frequent  and  important  of  the  organic  lesions  pro- 
duced by  leukaemia.     It  is  rarely  possible  to  observe  its  development.     In  most 

instances  the  spleen  is  already  large 
when  the  patient  first  comes  under  ob- 
servation. It  projects  from  under  the 
ribs  as  a  firm,  hard  mass,  the  lower  and 
anterior  extremity  of  which  often  ex- 
tends to  the  median  line  of  the  body. 
The  inner  edge  of  the  tumor  is  some- 
what characteristic;  it  is  rather  sharp, 
and  presents  one  or  two  notches.  At 
first  there  is  little  subjective  disturb- 
ance or  pain  referred  to  the  spleen. 
When  the  enlargement  is  very  great, 
there  is  often  an  annoying  or  even  dis- 
tressing feeling  of  distention  and  full- 
ness in  the  abdomen.  Respiration  may 
also  be  interfered  with  by  the  crowding 
up  of  the  diaphragm. 

The  lesion  of  the  bone-marrow  can 
be  determined  during  life  mainly  if  at 
all  by  the  myelocytes  (vide  supra). 
The  only  direct  symptom  which  renders  its  existence  probable  is  pain  in  the  bones, 
but  even  this  is  not  an  infallible  symptom.  There  is  seldom  pain  except  upon 
pressure.  It  is  usually  brought  out  by  percussion  of  the  sternum,  but  there  may 
be  well-marked  disease  of  the  marrow  without  this  "  sternal  pain." 

As  already  stated,  the  lymph-glands  often  remain  perfectly  normal.  If  they 
also  are  affected,  the  disturbance  is  betrayed  by  their  increase  in  size.  Not  only 
may  the  glands  in  the  neck,  axilla,  and  groin  be  enlarged,  but  occasionally  also 
those  of  the  mesentery  and  retroperitoneum,  as  can  be  demonstrated  upon  palpa- 
tion of  the  abdomen.  The  enlarged  lymph-glands  rarely  cause  severe  pain,  if  any 
at  all.  If  the  blood  were  found  to  contain  large  numbers  of  small  mononuclear 
lymphocytes,  this  would  suggest,  as  has  already  been  said,  involvement  of  the 
lymph-glands.  Unfortunately,  however,  our  knowledge  as  to  the  significance  of 
all  the  various  forms  of  leucocytes  is  too  imperfect  as  yet  to  justify  absolute  diag- 
nostic conclusions. 

We  have  already  referred  to  leukaemic  new  growths  in  other  internal  organs. 
These  possess,  for  the  most  part,  merely  a  scientific  interest,  as  they  cause  no  spe- 
cial symptoms.  Sometimes  hepatic  enlargement  occurs,  as  the  result  of  a  diffuse 
leuksemic  infiltration.  The  changes  in  the  retina  associated  with  leukaemia  are  of 
importance,  as  they  can  be  detected  by  means  of  the  ophthalmoscope.  The  retina 
presents  white  spots  or  stripes  running  parallel  with  the  blood-vessels.  They  are 
due  to  collections  of  lymphoid  cells,  or  to  actual  lymphoid  growths.  These  lesions 
have  been  inappropriately  called  leukaemic  retinitis.  Retinal  haemorrhages  occur 
also  in  leukaemia,  as  in  grave  cases  of  idiopathic  anaemia. 

All  the  other  clinical  phenomena  of  leukaemia  result  from  the  abnormal  con- 
dition of  the  blood,  meaning  thereby  the  anaemia.  The  ability  of  the  blood  to. 
perform  its  normal  functions  is  impaired  mainly  through  the  loss  of  red  blood- 
corpuscles;  the  resulting  symptoms  are  therefore  precisely  the  same  as  in  essen- 
tial anaemia,  and  we  do  not  need  to  describe  them  again.  They  usually  are  the 
most  prominent  symptoms  of  the  disease,  and  include  noticeable  pallor  of  the 


LETJKiEMIA  Y31 

skin,  equal  to  that  seen  in  pernicious  anaemia;  anaemic  murmurs  over  the  heart 
and  the  veins  of  the  neck;  general  debility;  anorexia,  and  digestive  disturbances; 
palpitation  and  dyspnoea ;  and,  finally,  the  whole  group  of  the  "  cerebral  symptoms 
of  anaemia,"  that  is,  headache,  vertigo,  syncope,  and  tinnitus  aurium.  Sometimes 
there  is  a  troublesome  pruritus.  Provided  he  has  no  great  anaemia,  the  general 
condition  of  a  leuksemic  patient  may  be  fairly  good.  A  symptom  that  is  observed 
remarkably  often  in  men  suffering  from  leukaemia  is  persistent  priapism.  This 
symptom  may,  as  we  ourselves  have  known,  be  the  first  one  noticed  by  the  patient. 
Its  cause  is  to  be  sought  not  in  conditions  of  nervous  irritation,  but  in  the  forma- 
tion of  white  thrombi,  rich  in  leucocytes,  in  the  corpora  cavernosa  (Kast). — In  a 
few  cases  paralysis  of  the  cranial  nerves  has  been  observed,  such  as  the  facial, 
hypoglossal,  and  acoustic.  This  paralysis  is  due  sometimes  to  small  haemorrhages, 
and  sometimes  to  degenerative  changes  in  the  medulla  oblongata. 

We  would  also  call  attention  once  more  to  the  frequent  haemorrhages.  These 
must  be  due  to  impaired  nutrition  of  the  vascular  walls,  and  sometimes  they 
justify  our  speaking  of  a  "  haemorrhagic  diathesis."  Obstinate  epistaxis  is  par- 
ticularly frequent.  Less  often  we  have  haemorrhage  from  the  intestine,  stomach, 
kidneys,  or  into  the  skin  or  muscles,  etc.  We  may  have  cerebral  hemorrhage, 
with  hemiplegia,  or  sometimes  immediate  death,  consequent  upon  it.  Severe 
cases  may  present  a  slight  oedema  of  the  skin  and  serous  effusions  into  the  vari- 
ous cavities  of  the  body. 

The  urine  in  leukaemia  is  essentially  like  that  excreted  in  pernicious  ansemia. 
Fleischer  and  Penzoldt  have  shown  that  in  leukaemia  as  well  as  in  pernicious 
anaemia  there  is  increased  destruction  of  albuminoids,  and  a  consequent  relative 
increase  in  the  excretion  of  nitrogen.  There  is  often  also  a  considerable  increase 
of  uric  acid.    These  rules,  however,  do  not  seem  to  be  without  exceptions. 

The  temperature  is  apt  to  undergo  slight  elevations,  as  in  severe  cases  of  anae- 
mia. In  advanced  stages  there  may  be  quite  high  fever  of  an  intermittent  char- 
acter, reaching  103°-104°  (39.5°^0°  C).  The  fever  is  sometimes  accompanied 
by  chills,  and  when  the  temperature  falls  there  is  often  a  profuse  and  debilitating 
perspiration. 

Complications  are,  on  the  whole,  rare.  Sometimes  we  observe  pulmonary  tu- 
berculosis, or  some  acute  intercurrent  disease  such  as  pneumonia.  We  saw  one 
case  end  in  death  from  haemorrhagic  angina  and  oedema  of  the  glottis. 

Clinical  History. — Leukaemia  is  almost  always  chronic  in  its  course.  The  dis- 
ease begins  insidiously  and  progresses  gradually ;  the  patient  grows  pale,  feels  lan- 
guid, and  has  slight  and  apparently  insignificant  symptoms,  which  gradually 
give  place  to  alarming  phenomena.  The  patient  may  himself  notice  the  organic 
lesions  incident  to  the  disease.  If  the  leukaemia  be  of  the  lymphatic  type,  he  is  apt 
to  be  struck  by  the  swelling  of  the  lymph-glands,  while  in  splenic  leukemia  his 
attention  is  attracted  by  the  feeling  of  tension  and  pressure  in  the  abdomen,  the 
increasing  prominence  of  the  left  side,  and  the  unusual  sense  of  resistance  present 
in  that  part  of  the  abdomen.  Sometimes  it  is  obstinate  epistaxis,  or  haemorrhage 
from  some  other  source,  which  first  attracts  attention  and  leads  to  a  careful  exam- 
ination of  the  blood  and  spleen. 

The  entire  duration  of  the  disease  is  usually  one  or  two  years  or  perhaps  more. 
Many  cases  pursue  a  rather  benign  and  slow  course,  while  in  others  there  is  a  more 
rapid  advance  of  all  the  symptoms,  even  justifying  the  term  of  acute  leukaemia. 
Attention  has  been  particularly  directed  to  such  cases  by  Ebstein.  In  them  the 
changes  in  the  spleen  and  lymph-glands  may  be  only  moderate.  Usually,  however, 
there  is  a  distinct  splenic  tumor.  The  lymph-glands  are  almost  invariably  in- 
volved, as  is  found  at  the  autopsy,  if  not  before.  The  constitutional  symptoms  are 
very  severe  and  grow  rapidly  worse,  and,  in  particular,  there  is  apt  to  develop  an 
acute  haemorrhagic  diathesis,  with  hemorrhages  into  the  skin  and  the  internal 


732  co:n'Stitutional  diseases 

organs,  including  the  brain.  Often  the  temperature  rises  to  104°  (40°  C).  Al- 
though there  may  be  many  fluctuations  in  the  course  of  the  disease,  it  leads, 
apparently  invariably,  in  a  few  weeks  to  death.  For  diagnosis  a  microscopic 
examination  of  the  blood  is  essential.  It  is  characteristic  of  acute  leukgemia,  as 
A.  Frankel  has  pointed  out,  that  the  leucocytes  in  the  blood  are,  in  an- overwhelm- 
ing proportion,  the  small  mononuclear  lymphocytes  (immature  form,  vide  supra). 
These  cases  of  acute  leukaemia  give  one  the  decided  impression  of  an  acute  infec- 
tious disease. 

In  ordinary  cases  of  leukaemia  we  see  frequently  an  apparent  arrest  of  the  dis- 
ease, or  temporary  improvement,  and  fresh  relapses.  The  final  termination  is,  how- 
ever, almost  invariably  unfavorable.  Recovery  from  leukaemia  is  not  absolutely 
impossible ;  still,  it  is  very  rare,  and  at  the  most  can  be  hoped  for  only  during  the 
early  period  of  the  disease.  In  almost  all  the  advanced  cases  the  prognosis  must 
be  described  as  absolutely  unfavorable.  Death  usually  takes  place  with  symptoms 
of  profound  anaemia,  and  progressive  bodily  weakness.  Sometimes  the  end  is 
hastened  by  the  occurrence  of  dangerous  haemorrhage  from  the  nose  or  into  the 
brain,  or  by  some  intercurrent  disease. 

Diagnosis. — Leukaemia  can  be  easily  and  unmistakably  recognized  by  a  micro- 
scopic examination  of  the  blood.  In  a  very  early  stage  of  the  disease  the  increase 
of  white  blood-corpuscles  may  be  so  slight  that  a  definite  decision  can  not  be  made ; 
but  the  later  developments  will  afford  absolute  certainty  in  any  typical  case. 

We  can  not  fail  to  recognise  a  case  of  leukaemia  if  the  blood  be  examined. 
Such  an  examination  is  therefore  demanded  in  every  case  of  obstinate  anaemia, 
and,  above  all,  in  such  patients  as  have  a  chronic  enlargement  of  the  spleen,  or 
swelling  of  the  lymph-glands  in  various  parts  of  the  body.  The  enlarged  lymph- 
glands  are  readily  recognizable.  The  splenic  tumor  can  usually  be  diagnosticated 
from  its  characteristic  position  and  shape,  and  especially  from  its  inner,  rather 
sharp  edge,  usually  notched.  It  may  be  simulated  by  hydronephrosis  and  other 
diseases  causing  enlargement  of  the  kidneys,  and  in  women  by  ovarian  tumors. 
In  cases  of  doubt  the  blood  should  be  examined,  and  if  the  result  be  a  positive  one, 
we  may  feel  certain  of  our  diagnosis.  If  there  is  a  chronic  enlargement  of  the 
spleen  without  a  leukaemic  change  in  the  blood,  we  must  consider  all  the  possible 
causes  of  such  an  enlargement;  thus  there  may  be  a  passive  congestion  of  the 
spleen,  with  enlargement,  as  the  result  of  hepatic  disease,  portal  thrombosis,  or 
disease  of  the  heart,  or  a  splenic  tumor  from  malarial  poisoning.  Again,  there  are 
cases  where  we  have  the  signs  of  a  gradually  progressive  anaemia,  apparently  idio- 
pathic, and  a  chronic  enlargement  of  the  spleen,  or  still  more  frequently  enlarge- 
ment of  the  lymph-glands  in  various  parts  of  the  body,  without  increase  in  the 
number  of  white  blood-corpuscles.  Such  cases  are  termed  pseudo-leukaemia,  or 
splenic  anaemia,  and  are  described  in  the  next  chapter. 

Treatment. — Nearly  the  same  remedies  are  employed  in  leukaemia  as  in  idio- 
pathic anaemia.  Of  course  the  greatest  attention  should  be  paid  to  the  general 
condition.  The  patient  should  be  well  nourished,  and  perhaps  he  may  be  sent  into 
the  country  or  to  some  health-resort.  Of  internal  remedies,  the  preparations  of 
iron  have  been  mainly  employed.  They  seldom  produce  any  brilliant  or  permanent 
effects.  We  have  much  more  confidence  in  the  administration  of  arsenic,  and  this 
remedy  should  certainly  be  tried  in  large  doses.  It  may  be  given  either  in  the 
shape  of  pills,  or,  with  still  more  advantage,  subcutaneously.  Ziemssen  recom- 
mends that  fifteen  grains  (gramme  1)  of  arsenious  acid  should  be  boiled  with 
seventy-five  minims  (5  cubic  centimetres)  of  a  fifteen-per-cent.  solution  of  sodic 
hydrate,  and  the  solution  then  diluted  to  make  three  ounces  and  a  third  (grammes 
100).  Of  this  one-per-cent.  solution  of  arsenate  of  soda,  at  first  one  quarter,  then 
one  half,  and,  finally,  an  entire  Pravaz's  syringeful,  is  injected  once  or  twice  a 
day.     [A  Pravaz's  syringe  holds  about  thirteen  minims. — V.]     Of  course,  the  only 


PSEUDO-LEUKEMIA  733 

hope  of  permanent  benefit  from  this  treatment  would  be  in  incipient  cases.  We 
have  seen  repeatedly,  however,  most  satisfactory  although  temporary  improve- 
ment follow  the  persistent  use  of  arsenic  in  leuksemia. 

What  are  called  "  splenic  remedies  "  have  been  often  employed,  but  they  do  not 
seem  very  effectual  in  leukaemia.  Mosler  obtained  good  results  from  the  long- 
continued  use  of  quinine  (5-8  grains  =  0.30-0.50  gramme,  or  more,  in  twenty-four 
hours).    He  also  recommends  a  trial  of  piperine  and  oil  of  eucalyptus: 

^  Olei  eucalypti gtt.  100; 

Piperini, 

Cerse  albas aa  5j   (gramme  4.0) ; 

Pulv.  altheas 3ij   (gramme  Y.5). 

M.  et  fiant  pilulas  no.  c. 

S.  Three  to  five  pills  three  times  a  day. 

Local  treatment  of  the  spleen  has  been  attempted.  If  an  ice-bag  be  constantly 
kept  on  the  splenic  region,  it  will  sometimes  diminish  the  size  of  the  tumor,  and 
it  may  also  relieve  pain.  Botkin  has  recommended  faradization  of  the  spleen, 
but  we  can  scarcely  expect  any  great  benefit  from  such  a  procedure.  Injections 
of  quinine,  arsenic,  and  other  remedies,  have  been  made  into  the  substance  of  the 
spleen.  We  do  not  believe  that  this  is  advisable,  because  it  may  cause  dangerous 
haemorrhage.  The  splenic  tumor  of  leucaemia  has  actually  been  extirpated  surgi- 
cally; but  the  proceeding  is  so  ineffectual  and  so  fatal  that  it  is  now  universally 
abandoned.  The  transfusion  of  healthy  human  blood  has  also  been  tried,  but 
without  satisfactory  results.  Subcutaneous  injections  of  blood  (vide  supra)  have 
been  tried  in  only  a  few  cases,  but  they  may,  perhaps,  have  good  results.  In  some 
recent  cases  inhalations  of  oxygen  are  said  to  have  improved  the  symptoms. 


CHAPTER   IV 

PSEUDO-LEUKEMIA 

(HodghMs  Disease.     Adenia.     Malicjnant  Lymplio-sarcoma.     Pseudo-leucocythaimia) 

It  was  mentioned  in  the  preceding  chapter  that  there  are  cases  in  which  the 
organic  lesions  are  apparently  the  same  as  in  genuine  leuksemia,  and  yet  there  is 
little  if  any  increase  in  the  number  of  white  corpuscles  in  the  blood.  There  is 
generally,  however,  a  diminution  in  the  number  of  red  corpuscles.  These  cases 
"usually  receive  the  name  which  Cohnheim  gave  them  of  pseudo-leukaemia.  It  is 
nevertheless  doubtful  whether  they  are  to  be  regarded  as  a  special  form  of  dis- 
ease, and  there  are  various  facts  which  indicate  that  they  are  at  least  very  closely 
allied  to  genuine  leukaemia.  There  is  a  great  similarity  in  most  of  the  symptoms 
of  the  two  diseases  and  in  their  general  course,  as  well  as  in  the  organic  changes 
they  produce.  Furthermore,  a  case  of  pseudo-leukaemia  may  finally  assume  the 
character  of  genuine  leukaemia,  with  its  characteristic  blood  changes. 

The  purely  splenic  type  of  pseudo-leukaemia  is  the  least  frequent  one.  As  yet 
very  few  such  cases  have  been  reported.  There  is  a  gradually  increasing  anaemia 
with  the  usual  symptoms,  and  associated  with  these  increasing  enlargement  of 
the  spleen.  It  is  impossible  to  draw  any  sharp  dividing  line  between  such  cases 
and  cases  of  pernicious  anaemia  attended  with  moderate  enlargement  of  the  same 
organ  (splenic  anaemia).  It  may  be  said  to  be  a  matter  of  taste  which  name  the 
physician  shall  give  to  a  case  of  this  sort.  The  bone-marrow  seems  to  present  the 
same  characteristics  in  splenic  pseudo-leuka?mia  as  in  pernicious  anaemia. 


734  CONSTITUTIOTiTAL   DISEASES 

Pseudo-leukaemia  Lymphatiea. — Pseudo-leuksemia  of  a  lymphatic  type  is  a 
much  more  frequent  and  well-defined  disease.  It  was  first  described  in  1832  by  the 
Englishman  Hodgkin,  and  is  sometimes  called  Hodgkin's  disease.  Wunderlich 
was  the  first  in  Germany  to  study  the  disease  thoroughly;  he  described  it  in  1858 
under  the  name  of  "  progressive  multiple  hypertrophy  of  the  lymph-glands  " ;  and 
later  Billroth  termed  it  "  multiple  malignant  lymphoma."  Trousseau  gave  it  the 
name  of  "  adenia." 

Little  is  known  about  the  aetiology  of  lymphatic  pseudo-leuksemia.  The  tend- 
ency of  late  is  to  assign  adenia  to  the  group  of  infectious  tumors,  although  the 
reasons  for  this  belief  are  as  yet  purely  theoretical.  Many  cases  seem  to  be  directly 
referable  to  tuberculosis,  in  the  form  of  tubercular  adenitis  without  other  tuber- 
cular disease.  Whether  this  is  true  as  regards  all  cases  of  pseudo-leuksemia  is  as 
yet  very  doubtful,  but  this  point  should  receive  especial  attention  in  the  future. 
Pseudo-leuksemia  is  most  common  in  young  and  middle-aged  persons,  and  is  ap- 
parently rather  more  frequent  in  men  than  in  women. 

Pathological  Anatomy. — The  hyperplasia  of  the  lymph-glands  may  be  very 
great,  producing  large  tumors  of  varying  consistency.  These  have  been  called 
lymphoma,  lymphadenoma,  and  lymphosarcoma.  On  section,  the  tumors  dis- 
play a  white  or  grayish-red  surface,  and  are  seen  to  be  made  up  of  a  number 
of  swollen  glands  fused  into  nodular  masses.  Upon  microscopic  examination,  we 
find  a  very  abundant  proliferation  of  lymph-cells,  sufficient  to  obscure  the  reticu- 
lum of  the  gland  completely.  The  new  growth  may  even  escape  beyond  the 
capsule  of  the  gland  and  invade  surrounding  structures.  Inflammatory  adhesions 
often  take  place  between  the  tumor  and  the  overlying  skin.  There  does  not  seem 
to  be  any  essential  difference  between  the  harder  and  the  softer  varieties  of  these 
tumors. 

These  changes  in  the  lymph-glands  are  often,  though  not  invariably,  associated 
with  a  swelling  of  the  spleen.  Its  increase  in  size  is  usually  slight.  Lymphomata 
may  also  develop  in  the  tonsils,  the  intestinal  lymphatics,  liver,  kidneys,  and  other 
organs.  Whether  there  are  changes  in  the  bone-marrow  has  not  yet  been  deter- 
mined. 

The  symptoms  are  very  gradually  developed.  It  is  almost  invariably  the 
swelling  of  the  lymph-glands  which  first  attracts  the  attention  of  the  patient  or 
his  physician.  The  glands  upon  one  or  both  sides  of  the  neck  are  usually  the 
first  to  be  enlarged,  and  they  may  finally  grow  to  tumors  the  size  of  the  fist,  or 
even  larger,  producing  great  disfigurement.  To  the  changes  in  the  neck  succeed 
swelling  of  the  axillary,  inguinal,  and  perhaps  also  the  internal  lymph-glands. 
The  changes  are  gradual,  and  vary  in  their  rapidity  and  extent. 

At  first  the  general  health  is  hardly  at  all  affected,  but  as  the  disease  pro- 
gresses its  constitutional  effects  become  more  and  more  marked.  The  patient 
grows  pale  and  languid,  and  finally  presents  all  the  symptoms  of  profound  ane- 
mia. We  may  also  have  certain  symptoms  due  to  mechanical  compression  occa- 
sioned by  the  growth  of  the  lymphomata.  The  tumors  in  the  neck  may  cause 
dysphagia,  from  compression  of  the  pharynx  and  oesophagus ;  dyspnoea,  from  com- 
pression of  the  larynx  and  trachea;  and  perhaps  alarming  cardiac  disturbance, 
from  interference  with  the  vagus.  Hypertrophy  of  the  bronchial  glands  some- 
times occasions  great  difficulty  in  respiration;  enlargement  of  the  abdominal 
glands  may  produce  ascites  or  jaundice;  and  enlargement  of  the  glands  in  the 
groin  may  give  rise  to  oedema  in  the  lower  extremities.  In  advanced  stages  we 
may  have  "  cerebral  symptoms  of  ansemia  "  precisely  similar  to  those  seen  in 
genuine  leucsemia  or  in  pernicious  ansemia.  There  may  be  a  tendency  to  haemor- 
rhage, pruritus,  and  occasionally  prurigo,  and  the  urinary  secretion  and  tempera- 
ture may  be  abnormal.  For  particulars  the  reader  is  referred  to  the  preceding 
chapters  on  leucsemia  and  pernicious  ansemia. 


PSEUDO-LEUE^MIA  735 

Upon  examination  of  the  blood,  there  are  usually  found  the  changes  charac- 
teristic of  ordinary  anaemia,  without  increase  in  the  number  of  white  blood-cor- 
puscles. Sometimes,  however,  there  may  be  a  slight  leucocytosis ;  and  sometimes, 
as  already  said,  lymphatic  pseudo-leukaemia  may  merge  into  genuine  leukaemia. 
The  examination  of  the  blood  must  therefore  be  repeated  from  time  to  time.  The 
spleen  should  also  be  examined.  It  is  usually  somewhat  enlarged,  and  in  some 
cases  the  enlargement  may  be  considerable.  Such  cases  might  be  properly  de- 
nominated splenic-lymphatic  pseudo-leukaemia.  We  may  also  discover  a  tender- 
ness of  the  sternum  or  other  bones. 

The  disease  often  lasts  but  a  few  months ;  it  may,  in  rare  instances,  extend 
over  two  or  three  years  or  more.  Recovery  is  not  completely  impossible  in  the 
early  stages  of  the  disease  (vide  infra),  but  at  a  later  period  the  prognosis  is  abso- 
lutely unfavorable.  The  fatal  termination  results  either  from  increasing  debility 
and  anaemia,  or  from  the  effects  of  mechanical  compression,  or  from  haemorrhage, 
or  from  some  intercurrent  disease. 

A  peculiar  form  of  pseudo-leukaemia  has  lately  been  described  by  Ebstein  and 
Pel.  In  this  there  are,  at  intervals  of  about  ten  to  fourteen  days,  periods  of 
marked  fever,  which  last,  also,  about  the  same  length  of  time.  The  condition  has 
received  the  name  chronic  relapsing  fever.  Death  occurs  with  symptoms  of  anae- 
mia; and  the  autopsy  shows  firm  swelling  of  the  liver,  spleen,  and  the  retro- 
peritoneal, mesenteric,  and  bronchial  lymph-glands.  Less  often  the  external 
lymph-glands  also  are  swollen,  so  that  they  can  be  felt  during  the  life  of  the 
patient.  The  character  of  the  blood  is  not  leukaemic,  so  that  these  cases  must  be 
provisionally  regarded  as  pseudo-leukaemia. 

The  diagnosis  of  pseudo-leukaemia  is  usually  easy.  It  is  to  be  based  upon  the 
objective  signs  and  the  condition  of  the  blood.  The  disease  is  most  apt  to  be 
confounded  with  swelling  of  the  lymph-glands  occasioned  by  tubercular  infec- 
tion; but  in  this  latter  case  the  changes  are  seldom  seen  in  so  many  parts  of 
the  body,  and  the  patient  usually  presents  other  indubitable  evidences  of  tubercu- 
losis.    (See  also  under  aetiology.) 

Treatment. — "We  possess  only  one  remedy  capable  of  promoting  absorption  of 
the  lymphomata,  namely,  arsenic.  We  have  ourselves,  in  common  with  a  great 
number  of  observers,  had  the  most  convincing  evidence  of  the  favorable  influence 
of  arsenic.  It  must,  however,  be  given  in  sufficient  doses  :  for  example,  a  pill  con- 
taining one  fifteenth  of  a  grain  (gramme  0.004),  or  even  a  larger  amount  of 
arsenious  acid,  three  times  a  day;  and  its  use  must  be  persisted  in  for  a  long  time. 
Still  more  efficient  are  subcutaneous  injections  of  the  solution  of  arseniate  of  soda 
which  we  have  described  quite  fully  in  the  preceding  chapter.  We  have  also  seen 
apparent  benefit  from  associating  with  the  arsenic  inunctions  of  iodoform  (iodo- 
form one  part,  vaseline  fifteen  parts)  over  the  tumors. 

In  the  early  stages  decided  benefit  may  be  expected  from  this  mode  of  treat- 
ment. At  a  later  period  we  may  obtain  a  decrease  in  the  size  of  the  tumors,  but 
we  can  hardly  hope  for  any  permanent  improvement.  Operative  interference  is 
out  of  the  question,  except  at  the  very  beginning  of  the  disease.  Later  on,  it 
would  be  perfectly  useless,  and  it  could  seldom  be  carried  out. 

Other  suggestions  with  regard  to  treatment  may  be  obtained  from  the  chapters 
on  anaemia  and  leukaemia. 


736  COISTSTITUTIOATAL   DISEASES 

CHAPTEE   V 
H^MOGLOBINJEMIA    AND    HJEMOGLOBINURIA 

Definition  and  General  etiological  Considerations. — If  any  cause  produces  a 
solution  of  the  red  blood-corpuscles  in  the  blood-serum,  hsemoglobine  is  excreted 
through  the  kidneys.  The  hseraoglobineemia — the  presence  of  free  hsemoglobine 
in  solution  in  the  blood — excites  hsemoglobinuria,  i.  e.,  the  excretion  of  h^rao- 
globine  in  the  urine.  The  causes  of  hsemoglobinsemia  and  its  correlative  hsemo- 
globinuria are  manifold.  In  the  first  place,  there  is  a  whole  series  of  poisons 
which,  if  introduced  into  the  blood  in  sufficient  amount,  exercise  a  directly  de- 
structive influence  upon  the  red  blood-corpuscles,  and  thus  excite  hsemoglobinu- 
ria. To  this  list  belong  chlorate  of  potash  (Marchand),  pyrogallic  acid  and  naph- 
thol  (ISTeisser),  sulphuric  acid,  glycerine,  toluylendiamine,  and  many  other  sub- 
stances. Distilled  water  is  also  in  this  sense  a  poison.  Bostrom  has  discovered  a 
fact  of  practical  importance  which  deserves  mention  in  this  connection.  It  is, 
that  a  certain  kind  of  mushroom  (Helvetia  esculenta) ,  when  fresh,  contains  a  poi- 
son which  is  capable  of  producing  intense  hsemoglobinuria,  and  such  grave  symp- 
toms as  jaundice,  delirium,  drowsiness,  and  tetanic  convulsions,  with  perhaps  a 
fatal  termination.  This  poison  is,  however,  so  evanescent  and  so  readily  soluble 
in  hot  water  that  the  mushroom  becomes  perfectly  harmless  if  thoroughly  soaked 
and  then  boiled,  or  if  it  has  been  dried. 

Secondly,  hsemoglobinuria  may  be  developed  in  connection  with  infectious 
diseases.  In  this  case,  also,  it  is  probably  referable  to  the  action  of  poisons  cre- 
ated within  the  system.  Thus  hsemoglobinuria  has  been  observed  in  the  course  of 
a  severe  attack  of  scarlet  fever  or  typhoid  fever.  Possibly  malarial  poisoning  and 
syphilis  may  give  rise  to  paroxysmal  hsemoglobinuria.  This  question  will  be  dis- 
cussed later  on. 

There  is  a  third  mode  of  origin  which  also  possesses  practical  importance.  If 
blood  from  one  animal  be  injected  into  another  of  a  different  species,  hsemoglo- 
binuria is  almost  sure  to  result.  Not  only  do  the  injected  blood-corpuscles  undergo 
solution,  but  also  the  injected  serum  acts  as  a  poison  upon  the  original  blood-cor- 
puscles, destroying  and  dissolving  them.  This  transfusion-hsemoglobinuria  has 
been  described  by  Prevost,  Dumas,  Ponfick,  and  Landois.  It  can  be  produced  in 
human  beings,  as  there  was  only  too  good  opportunity  to  observe  during  the  brief 
period  when  the  transfusion  of  lamb's  blood  Avas  in  vogue.  The  practical  deduc- 
tion is  evident,  that  we  should  not  use  for  injection  into  the  circulatory  system 
of  a  patient  anything  but  an  unirritating  salt  solution,  or  human  blood. 

A  fourth  and  very  important  setiological  factor  is  exposure  to  extremes  of 
temperature.  Hsemoglobinuria  follows  extensive  burns.  The  blood-corpuscles  in 
that  region  of  the  periphery  exposed  to  the  heat  are  destroyed.  Cold  is  capable 
of  producing  precisely  analogous  results.  This  is  particularly  evident  in  the  cases 
of  so-called  paroxysmal  hsemoglobinuria  described  by  Wickham  Legg,  Lichtheim, 
Murri,  and  Kiissner.  [Raynaud's  disease  (see  page  900)  and  hsemoglobinuria 
are  associated  in  a  sufficiently  large  proportion  of  cases  to  show  some  relation- 
ship between  the  two.] 

Pathology  and  Symptoms  of  Hsemoglobinsemia,  particularly  the  Parox- 
ysmal Variety. — In  most  of  the  cases  above  enumerated,  hsemoglobinuria  is  the 
result  of  an  obvious  or  easily  demonstrable  cause.  There  is,  however,  another 
variety  which  appears  paroxysmally  in  individuals  who  are  otherwise  perfectly 
well.  Its  symptoms  are  extremely  characteristic.  Although  not  a  very  frequent 
disease,  there  has  been  abundant  opportunity  to  study  it. 

As  just  intimated,  the  disease  is  paroxysmal.    Very  often  an  attack  is  ushered 


H^MOGLOBIlsTiEMIA   AI^D   HiEMOGLOBINUEIA  Y3T 

in  by  frequent  and  persistent  yawning-.  To  this  symptom  are  soon  added  pain  in 
the  limbs,  headache,  nausea,  vomiting,  and  coolness  of  the  periphery.  The  tem- 
perature speedily  rises  to  102°  (39°  C.)  or  more.  With  this  is  often  associated  a 
decided  chill.  Sometimes  there  is  a  violent  pain  in  the  hepatic  region.  There  is 
a  distinct  enlargement  of  the  spleen.  Then  the  temperature  falls  again,  perspira- 
tion appears,  and  the  patient,  although  languid  and  depressed,  soon  recovers. 
A  slig'ht  icteric  hue  can  almost  invariably  be  detected  toward  the  end  of  the  at- 
tack, the  ordinary  duration  of  which  is  from  two  to  twelve  hours.  An  eruption  of 
urticaria  has  been  repeatedly  seen  in  connection  with  the  attacks. 

The  most  interesting-  phenomenon  of  all  remains  to  be  described.  We  refer  to 
the  condition  of  the  urine  during-  and  directly  after  the  paroxysm.  This  secretion 
presents  a  dark  brownish-red  color  resembling  blood;  it  may  even  appear  almost 
black.  Its  reaction  is  almost  invariably  acid;  its  specific  gravity  is  usually 
rather  low,  say  1008-1012.  On  boiling  the  urine,  the  haemoglobine  is  decomposed 
and  a  brown  coagulum  of  albumen  formed.  If  the  fresh  urine  be  examined 
through  a  spectroscope,  we  find  the  bands  characteristic  of  hsemoglobine,  and 
sometimes  also  the  narrow  bands  indicative  of  methsemoglobine.  It  is  therefore 
impossible  to  doubt  the  existence  of  hsemoglobine  in  the  urine;  and  yet,  upon 
microscopic  examination,  we  find  no  red  blood-corpuscles  in  the  urine,  or,  in 
other  words,  no  "  hsematuria."  Frequently  there  are  large  numbers  of  opaque 
red  granules  in  the  urine,  the  shape  of  which  is  extremely  irreg-ular.  These  are, 
doubtless,  granules  of  hsemoglobine.  Some  of  them  are  free  in  the  urine,  some 
are  attached  to  casts.  Of  the  latter,  we  find  hyaline  and  a  few  epithelial  casts 
present.  Sometimes  masses  of  ha3moglobine  assume  the  appearance  of  casts.  The 
sediment  may  also  contain  a  few  cells  of  renal  epithelium.  The  presence  of  this 
and  of  hyaline  casts  indicates  that  the  kidneys  have  been  slig-htly  irritated  by  the 
excretion  of  hsemoglobine.  Hence,  we  sometimes  observe  a  persistence  of  slig'ht 
albuminuria  after  the  hsemoglobinuria  has  ceased.  In  mild  attacks,  also,  there 
may  be  merely  albuminuria,  without  hsemoglobinuria. 

If  now  we  examine  the  blood  during  a  paroxysm,  we  shall  find  that  h^emoglo- 
binsemia  is  associated  with  hsemoglobinuria  of  the  paroxysmal  type,  as  well  as 
with  that  occasioned  by  the  action  of  various  poisons.  Kiissner  obtained  blood 
from  a  patient  during  a  paroxysm,  and  found  that  its  serum  had  a  naby-red  color, 
and  contained  hsemoglobine  in  solution.  This  proves  that  the  destruction  of  blood- 
corpuscles  takes  place  within  the  circulatory  system.  Indubitable  tokens  of  this 
destructive  process  are  to  be  seen  upon  microscopic  examination  of  the  blood 
during  a  paroxysm,  especially  when  the  paroxysm  has  been  produced  artificially 
in  the  manner  described  below.  The  red  blood-corpuscles  have  little  tendency  to 
form  rouleaux.  They  are  pale,  and  many  of  them  are  irregular  in  shape  (poikilo- 
cytes).  Irregularly  shaped  flakes  of  hsemoglobine  are  also  present,  and  often  large 
numbers  of  decolorized  red  blood-corpuscles  are  to  be  seen.  To  these  latter  Pon- 
fick  has  given  the  name  of  "  shadows."  The  exciting  cause  of  the  individual 
attacks  of  paroxysmal  hsemoglobinuria  is,  in  most  instances,  catching  cold.  A 
paroxysm  is  usually  due  to  being  outdoors  in  a  cold  storm,  and  perhaps  being  wet 
through.  In  summer  the  attacks  cease  completely  in  patients  of  this  sort ;  still, 
as  Eosenbach  showed  by  experiment,  an  attack  may  even  then  be  artificially  ex- 
cited at  any  time  by  exposing  the  patient's  skin  on  purpose  to  a  decided  chill — e.  g., 
by  causing  the  patient  to  take  an  ice-cold  foot-bath,  or  the  like.  In  order  to  show 
that  there  is  merely  a  local  action  of  cold  in  these  cases,  Ehrlich  and  Boas  (each 
independently)  arranged  the  experiment  in  the  following  manner:  They  tied  an 
elastic  ligature  firmly  arovmd  the  finger  of  a  subject,  and  had  him  immerse  it  for  a 
quarter  of  an  hour  in  ice-water.  In  every  sample  of  blood  taken  from  the  finger 
the  above-described  changes  could  be  most  distinctly  demonstrated,  while  blood 
taken  from  other  parts  of  the  patient's  body  showed  scarcely  any  abnormality. 
47 


T38  CONSTITTJTIONAL  DISEASES 

The  influence  of  cold  is  not  the  only  exciting  cause  for  such  attacks,  although 
it  is  the  most  frequent  one.  Paroxysms  of  ha3moglobinuria  have  been  seen  after 
great  bodily  exertion,  particularly  after  a  rather  long  walk ;  in  women  sometimes 
at  the  menstrual  period;  and  also  after  mental  excitement,  and  the  like.  'No 
explanation  has  as  yet  been  given  why  some  few  human  beings  have  this  remark- 
able sensitiveness  of  their  red  blood-corpuscles,  while  most  persons  undergo  the 
same  influences  without  similar  consequences.  In  this  regard  should  be  noted 
the  statement  of  Murri,  that  paroxysmal  hsemoglobinuria  is  particularly  apt  to 
appear  in  persons  who  have  a  syphilitic  taint. 

Finally,  with  regard  to  the  origin  of  the  other  symptoms  of  the  hsemoglobin- 
uric  attack,  such  as  fever,  at  first  it  was  thought  that  there  was  a  sort  of  ursemic 
condition,  inasmuch  as  the  urinary  tubules  are  often  so  choked  with  granules  of 
haemoglobine  that  the  excretion  of  urine  might  well  be  hindered.  Probably, 
however,  another  circumstance  is  still  more  important — ^viz.,  the  toxic  infliience  of 
the  fibrine  ferment  which  is  formed  because  of  the  hsemoglobinuria.  The  hsemo- 
globine,  as  it  is  set  free,  destroys  numerous  white  blood-corpuscles,  and  in  this 
way  fibrine  ferment  is  produced,  as  we  have  already  mentioned  (see  page  725). 

Another  important  point  is  that  it  is  not  the  kidneys  alone  which  serve  for 
the  reception  of  the  constituents  of  the  disintegrated  and  dissolved  blood-corpus- 
cles. Ponfick  has  been  led  by  the  result  of  certain  experiments  to  believe  that 
the  spleen  and  liver  are  also  affected.  The  spleen  appropriates  the  undissolved 
remnants  of  the  corpuscles,  and,  as  a  consequence,  it  may  undergo  considerable 
enlargement.  The  liver  absorbs  a  large  part  of  that  portion  of  the  hsemoglobine 
which  has  undergone  solution,  and  converts  it  into  bile.  As  a  result  there  seems 
to  be  an  increased  secretion  of  bile.  Jaundice  is  probably  due  to  local  biliary 
stasis  and  biliary  absorption  in  the  liver  itself  ("  hsemo-hepatogenous  jaundice  " 
of  Afanassiew).  No  proof  has  been  furnished  that  a  part  of  the  hsemoglobine  dis- 
solved in  the  blood  can  be  changed  into  bile  pigment  (true  "  hsematogenous 
jaundice  ")• 

Prognosis. — When  hsemoglobinuria  is  merely  a  symptom  of  other  abnormal 
processes  caused  by  poisoning  or  by  some  specific  infection,  the  future  of  the 
patient  depends  entirely  upon  the  severity  of  the  primary  disease.  An  attack  of 
paroxysmal  hsemoglobinuria  would  not  seem  to  involve  any  direct  danger  to  life. 
Eecurrence  of  the  paroxysms  is  always  to  be  feared  if  the  patient  be  exposed  to 
those  influences  which  produce  it.  There  are  no  certain  means  of  decreasing  the 
patient's  liability  to  attacks.  In  a  few  cases,  however,  where  there  had  been 
syphilis,  the  paroxysms  are  said  to  have  been  permanently  banished  by  mercurial 
inunctions.    Likewise,  if  we  suspect  malarial  influences,  quinine  should  be  tried. 

No  special  treatment  is  required  during  the  paroxysm  itself.  The  patient 
must  escape  as  soon  as  possible  from  the  exciting  cause ;  it  is  then  advisable  for 
him  to  lie  quietly  in  bed,  and  to  drink  a  large  amount  of  fluid,  so  as  to  wash  out 
the  masses  of  haemoglobin  from  the  kidneys. 


CHAPTER   VI 
SCURVY 

{Scorhutv.s) 

Prefatory  Remarks. — Scurvy  is  one  of  a  group  of  diseases  which  may  be 
termed  "  hsemorrhagic."  They  all  have  one  predominant  sjonptom,  namely,  a 
decided  hsemorrhagic  diathesis,  respectively  associated  in  the  different  diseases 


SCTJEVY  739 

with  various  other  more  or  less  pronounced  disturbances.  This  tendency  to  spon- 
taneous haemorrhage  is  in  many  cases,  particularly  the  milder  ones,  confined 
more  or  less  exclusively  to  the  skin,  but  in  numerous  other  instances  hsemorrhage 
also  takes  place  into  the  underlying  tissues,  such  as  the  muscles  or  joints,  as  well 
as  into  the  mucolis  membranes. 

The  distinctions  between  these  various  diseases  are  founded  upon  the  manner 
in  which  the  haemorrhages  occur  and  the  symptoms  which  attend  them.  We 
may  mention  scorbutus,  purpura  simplex,  purpura  hsemorrhagica,  and  peliosis. 
It  should,  however,  be  stated  that,  although  it  is  possible  to  distinguish  several 
varieties  of  disease,  each  one  of  which  presents  a  tolerably  characteristic  picture, 
there  are  innumerable  transitional  forms.  It  may,  indeed,  be  almost  a  matter  of 
taste  in  any  particular  case  what  name  shall  be  applied  to  it.  The  existence  of  so 
many  intermediate  forms  renders  it  evident  that  the  various  members  of  this 
group  of  diseases  are  at  least  closely  related  if  not  actually  identical.  We  shall 
even  find,  upon  careful  consideration,  that  certain  other  diseases  not  usually 
regarded  as  hsemorrhagic  are  nearly  akin  to  the  group  now  under  consideration. 
We  refer  to  certain  skin  diseases,  which  are  characterized  mainly  by  inflamma- 
tory and  exudative  lesions  of  the  skin.  Chief  among  these  should  be  mentioned 
erythema  exsudativum  multiforme,  which  not  very  infrequently  exhibits  some 
tendency  to  haemorrhages,  and  thus  presents  external  appearances  closely  simu- 
lating the  forms  of  purpura.  In  the  last-mentioned  forms  of  disease,  however, 
there  appears  still  another  clinical  relationship — viz.,  to  the  ordinary  acute  articu- 
lar rheumatism  (q.v.).  All  of  the  hsemorrhagic  diseases  are  distinguished  by 
a  frequent  involvement  of  the  joints,  while,  on  the  other  hand,  acute  articular 
rheumatism  is  sometimes  associated  with  haemorrhagic  lesions  in  the  skin. 

In  order  to  understand  the  underlying  connection  between  these  various  dis- 
orders, a  precise  knowledge  of  their  aetiology  is  requisite.  Already  considerable 
evidence  has  been  gathered  pointing  to  the  importance  of  infectious  influences  in 
their  production  (vide  infra),  but  no  absolute  proof  has  yet  been  obtained.  Still, 
it  must  be  said  that  various  observations  already  made  indicate  that  we  are  likely 
to  find  some  aetiological  relations  between  the  haemorrhagic  and  the  septic  dis- 
eases. In  the  meanwhile,  we  must  be  guided  mainly  by  the  purely  clinical  phe- 
nomena. These,  again,  indicate  that  sharp  distinctions  between  the  various  haem- 
orrhagic diseases  would  be  purely  artificial.  In  this  and  the  following  chapters  we 
shall  discuss  the  two  main  types  of  haemorrhagic  disease. 

.etiology  of  Scurvy. — Scurvy  is  sometimes  sporadic,  and  sometimes  epidemic 
and  endemic  in  its  occurrence.  There  were  formerly  very  extensive  and  fatal 
epidemics  of  the  disease,  at  a  time  when  the  laws  of  health  with  regard  to  large 
aggregations  of  human  beings  were  little  regarded.  The  disease  was  prone  to 
attack  armies,  or  the  inhabitants  of  besieged  cities,  or,  especially,  seamen.  It 
was,  and  to  a  certain  extent  is  still,  one  of  the  diseases  most  dreaded  by  the 
mariner.  It  has  often  swept  away  an  entire  ship's  crew.  To-day  endemics  of 
scurvy  are  by  no  means  infrequent,  although  not  so  extensive  as  formerly.  They 
are  most  apt  to  occur  in  prisons  and  similar  institutions,  and  in  barracks. 

These  facts,  under  the  light  of  our  present  views  in  regard  to  such  matters, 
would  almost  force  us  to  seek  some  organic  infectious  poison  as  the  origin  of  the 
disease.  Formerly  men  were  inclined  to  direct  their  sole  attention  to  such  cir- 
cumstances as  the  character  of  the  food,  the  dwelling,  the  climate,  and  similar 
conditions ;  nor  can  it  indeed  be  denied  that  these  hygienic  factors  do  exert  a 
decided  influence  upon  the  spread  of  the  disease.  It  is,  however,  evident  that  they 
can  not  be  its  proper  cause,  for,  beyond  a  doubt,  scurvy  may  occur  independently 
of  any  of  the  factors  usually  regarded  as  essential  to  its  development.  These 
causes  must  therefore  be  regarded  as  simply  predisposing  influences. 

Great  aetiological  importance  has  long  been  ascribed  to  certain  errors  in  diet. 


74:0  CONSTITUTIONAL  DISEASES 

These  include  the  use  of  bad  or  insufficient  food,  the  undue  predominance  of 
certain  kinds  of  food,  and  in  particular  of  the  salt  meats  so  much  employed  on 
shipboard;  or,  again,  the  deficiency  of  certain  varieties  of  food,  in  particular  the 
lack  of  vegetable  food,  and  still  more  of  fresh  vegetables.  Much  industry  and 
acuteness  have  been  expended  in  defending  the  theory  that  the  lack  of  vegetable 
food  is  injurious  because  of  the  deficient  supply  of  potassium  salts  under  such 
circumstances  (Garrod).  Nevertheless,  this  view  does  not  reach  the  heart  of  the 
matter,  for  in  numerous  epidemics  of  scurvy  there  has  been  no  such  lack  of  vege- 
table nourishment;  and  in  some  instances  the  diet  employed  has  contained  an 
unusual  abundance  of  potassium  compounds. 

A  like  predisposing  but  not  specific  influence  is  exerted  by  the  other  factors  to 
which  setiologieal  importance  has  been  assigned.  They  are  indeed  often  present 
in  epidemic  as  well  as  in  sporadic  cases,  but,  as  previously  stated,  they  may  not 
exist  at  all.  To  this  class  belong  damp  and  unfavorable  quarters,  cold,  moisture, 
persistent  heat,  and  excessive  muscular  exertion. 

Age  and  sex  exert  no  great  influence  upon  the  disease.  Weakly  persons  seem 
to  be  somewhat  more  liable  to  be  attacked  than  are  the  vigorous.  The  possibil- 
ity of  contagion  has  been  maintained  repeatedly,  but  contagion  has  not  been 
proved  to  exist,  and  unprejudiced  observation  would  incline  one  strongly  to  doubt 
its  existence. 

[It  seems  probable  that  the  dietetic  causes  of  scurvy  lie  rather  in  a  want  of 
variety  in  the  food  than  in  the  absence  of  any  one  class  or  order  of  foods.  Wales 
says  (Pepper,  System  of  Medicine)  :  "  No  single  natural  order  contains  plants 
that  supply  all  the  elements  essential  to  the  nutrition  of  the  body  and  the  right 
composition  of  the  blood.  The  graminaceous  and  leguminous  articles  of  food,  for 
instance,  are  numerous  but  not  various;  they  all  afford  the  same  or  analogous 
albuminous  elements,  which  have  about  the  same  nutrient  value  as  the  corre- 
sponding substances  in  animal  food,  and  hence  health  and  vigor  can  not  be  sus- 
tained on  a  diet  of  flesh  combined  with  wheat,  rice,  and  oatmeal,  or  with  beans 
and  peas,  or  with  all  of  them  together.  Outbreaks  of  scurvy  have  occurred  on 
shipboard  where  the  ration  is  made  up  principally  of  these  articles — as  in  Anson's 
ship  when  supplied  with  an  abundance  of  fresh  animal,  farinaceous,  and  legumi- 
nous foods.  It  is  clear,  therefore,  that,  in  order  to  obtain  a  variety  of  materials 
required  in  nutrition,  we  must  resort  to  several  of  the  natural  groups,  those  par- 
ticularly which  comprise  the  succulent  vegetables  and  fruits." 

It  is  certain  that  scurvy  is  a  disease  which  we  can  produce  artificially,  and  that 
it  is  preventable  in  the  vast  majority  of  cases.  It  is  now  as  rare  among  seamen  as 
it  was  formerly  common — a  change  which  is  the  result  chiefly  of  care  to  vary  the 
diet,  especially  on  long  voyages.  The  United  States  law  requires  that  lime-  or 
lemon-juice,  sugar,  and  vinegar  shall  be  carried  by  all  sailing  vessels  bound  on 
ocean  voyages  or  engaged  in  the  fisheries,  specifies  the  circumstances  and  mini- 
mum doses  under  which  the  antiscorbutics  are  to  be  given,  and  provides  penalties 
for  violation  or  neglect.] 

Clinical  History. — The  disease  does  not  usually  begin  suddenly.  There  is  a 
gradual  onset,  marked  by  certain  constitutional  symptoms.  The  chief  of  these 
are  languor  and  debility,  a  sense  of  thoracic  oppression,  palpitation,  and  usually 
a  "  rheumatic,  dragging  pain  "  in  the  loins  and  extremities,  especially  in  the  lower 
extremities.  The  patient  is  obliged  to  take  to  his  bed  if  the  case  be  at  all  severe ; 
he  is  very  sensitive  to  cold,  and  often  is  drowsy  and  apathetic.  These  somewhat 
indefinite  premonitory  symptoms  last  for  a  few  days  or  a  week,  when  other  and 
more  characteristic  phenomena  appear. 

Among  these  new  appearances  are  spontaneous  hsemorrhages,  occurring  chiefly 
in  the  lower  extremities.  There  are  cutaneous  haemorrhages,  producing  dark-red 
macules  of  varying  size,  most  of  them  with  a  hair-follicle  in  their  center,  and 


SCUEVY  Ul 

there  are  almost  invariably  hsemorrhages  into  tlie  deeper  tissues  also.  The  sub- 
cutaneous connective  tissue  and  muscles,  and  sometimes  the  periosteum,  are 
affected.  These  deeper  extravasations  are  a  peculiarity  of  scurvy.  They  can 
sometimes  be  felt  as  hard,  painful  swelling-s  in  the  parts  affected,  and  are  some- 
times discernible  from  the  discoloration  of  the  skin,  which  soon  results  from  the 
solution  and  diffusion  of  the  blood-pigment.  The  patches  present  a  diffuse  bluish 
color,  merg-ing  into  greenish  or  yellowish  at  the  periphery,  and  they  are  often 
quite  large.  They  have  a  precisely  similar  appearance  to  "  black-and-blue  "  spots 
resulting  from  injury.  Of  course,  the  more  abundant  and  the  more  superficial 
the  extravasation,  the  more  extensive  and  darker  is  the  macule.  Similar  appear- 
ances may  sometimes  be  observed  in  the  upper  extremities  and  trunk,  mainly  in 
severe  cases.    The  face  and  scalp  rarely  present  ecchymoses. 

Sometimes  a  htemorrhage  results  in  the  necrosis  and  sloughing  away  of  a  por- 
tion of  the  skin.  The  necrosis  is  succeeded  by  ulceration  ("scorbutic  ulcers"). 
Under  unfavorable  hygienic  influences  this  process  may  assume  a  grave  signifi- 
cance. It  should  also  be  stated  that  we  may  observe  other  cutaneous  disturbances, 
such  as  erythema,  wheals,  vesicles  (the  contents  of  which  may  be  tinged  with 
blood—"  scorbutic  pemphigus  "),  papules,  and  pustules.  These  eruptions  are  more 
frequent  in  some  epidemics  than  in  others ;  they  may  either  be  associated  with  or 
replace  the  cutaneous  ecchymoses. 

In  the  ordinary  sporadic  cases  of  scurvy  which  occur  among  us,  haemorrhages 
into  the  mucous  membrane,  except  of  the  gums,  are  very  rarely  seen.  The  same 
is  true  of  hsemorrhages  from  the  stomach  and  other  internal  organs.  In  severe 
cases,  during  epidemics  and  under  bad  hygienic  surroundings,  it  is  otherwise; 
hsemorrhage  may  take  place  from  the  nose,  stomach,  intestines,  bronchi,  and  kid- 
neys, and  blood  may  be  effused  into  the  serous  membranes. 

ISText  in  importance  to  haemorrhage  is  another  peculiar  symptom,  presented  by 
the  mucous  membrane  of  the  mouth,  and  particularly  that  of  the  gums.  In  order 
to  establish  a  diagnosis  of  scurvy  in  sporadic  cases,  we  must  demonstrate  the 
existence  of  these  two  main  symptoms — namely,  the  hsemorrhage  into  the  skin 
or  muscles,  and  the  changes  in  the  gums  now  to  be  described. 

The  scorbutic  changes  in  the  gums  usually  appear  quite  early  in  the  course  of 
the  disease,  being  in  many  cases  simultaneous  with  the  haemorrhages,  although 
they  may  either  precede  or  follow  the  latter.  The  gums  assume  a  bluish  hue, 
become  swollen  and  spongy,  are  painful,  and  have  a  tendency  to  bleed.  The 
changes  are  usually  most  pronounced  in  the  salient  parts  of  the  gums  between 
the  teeth.  It  is  a  remarkable  fact  that  they  are  hardly  visible  at  all  at  places 
where  there  are  no  teeth;  and  the  gums  of  very  young  children  and  of  aged 
patients  remain  almost  intact.  In  severe  cases  the  gums  are  not  only  swollen  but 
necrosed;  the  change  is  at  first  a  superficial  one,  but  it  may  extend  inward  and 
produce  dirty-looking  ulcers.  Other  parts  of  the  mouth  are  liable  to  become 
involved  in  the  ulceration,  producing  a  diffuse  ulcerative  stomatitis,  and  giving 
the  breath  a  most  offensive  odor. 

Certain  other  local  and  constitutional  phenomena  are  not  infrequent,  though 
less  characteristic  than  the  haemorrhages  and  the  alterations  in  the  gums.  Chief 
among  the  general  disturbances  is  scorbutic  anaemia.  This  is  often  referable  in 
part  to  the  unfavorable  hygienic  influences  surrounding  the  patient,  but  the  dis- 
ease itself  seems  to  impair  the  general  nutrition.  The  patient  looks  pale,  has  a 
dry  skin,  and  loses  flesh  rapidly.  The  temperature  is  often  normal.  Sometimes 
there  may  be  an  occasional  rise  of  temperature,  either  in  the  beginning  or  in  the 
further  course  of  the  disease.  If  complications  occur,  they  are  not  infrequently 
accompanied  by  considerable  fever. 

Among  more  localized  symptoms  should  be  mentioned  the  premonitory  sore 
throat  which  sometimes  occurs.     It  is  usually  of  the  ordinary  catarrhal  variety, 


742  CONSTITUTIONAL   DISEASES 

but  it  may  assume  a  liasmorrhagic  character.  Broncliitis  also  may  occur.  Lobular 
pneumonia  and  genuine  lobar  pneumonia  have  been  repeatedly  seen  in  severe 
cases.  Pleurisy,  pericarditis,  and  inflamniations  of  other  serous  membranes  occa- 
sionally complicate  the  disease.  They  may  likewise  display  a  hsemorrhagic  tend- 
ency in  the  exudations  to  which  they  give  rise.  Disturbances  in  the  joints  are 
sometimes  seen,  and  are  characterized  by  an  effusion  of  liquid  into  the  articular 
cavities,  which  effusion  may  be  either  serous  or  hasmorrhagic.  This  is  a  favor- 
able opportunity  to  call  attention  to  a  peculiarity  common  to  all  the  hsemorrhagic 
diseases  and  allied  affections  (vide  supra) — they  are  apt  to  be  associated  with 
articular  swelling. 

The  pulse  may  be  somewhat  accelerated,  or  may  be  slower  than  normal.  It  is 
usually  small  and  compressible.  Endocarditis  may  occur,  but  it  is  very  excep- 
tional. The  blood  does  not  present  any  constant  and  characteristic  alterations  in 
scurvy.  The  spleen  may  be  decidedly  enlarged,  particularly  in  severe  cases. 
Albuminuria  has  been  repeatedly  observed,  but  it  is  almost  wholly  confined  to 
severe  cases,  in  which,  indeed,  a  typical  acute  nephritis  may  be  developed. 

Course  of  the  Disease.  Varieties  of  Scurvy.  Prognosis. — The  sporadic  cases 
usually  met  with  in  this  region  almost  invariably  pursue  a  favorable  course.  The 
symptoms  are  confined  mainly  to  constitutional  disturbance,  ecchymoses  in 
the  lower  extremities,  and  the  affection  of  the  gums,  the  grave  complications 
above  mentioned  being  rarely  met  with.  The  average  duration  of  the  disease  is, 
nevertheless,  some  weeks.  Recovery  is  deferred  in  proportion  as  the  hygienic 
surroundings  are  bad,  but  even  then  the  termination  is  almost  sure  to  be 
favorable.  Scurvy  has,  however,  a  noteworthy  tendency  to  relapse,  so  that  the 
course  of  the  disease  may  be  very  much  prolonged.  Even  when  the  illness  has 
terminated  in  recovery,  there  remains  behind  a  certain  liability  to  fresh  attacks 
of  scurvy,  just  as  acute  articular  rheumatism  is  apt  to  recur.  We  are  acquainted 
with  a  patient  who  has  been  severely  ill  with  scurvy  some  five  or  six  times  within 
the  last  few  years,  and  this  without  any  demonstrable  cause. 

The  prognosis  in  grave  cases,  occurring  under  unfavorable  hygienic  influences, 
and  aggravated  by  the  lack  of  proper  food  and  attention,  is  far  otherwise.  Here 
death  is  not  infrequent,  sometimes  as  a  result  of  progressive  cachexia,  some- 
times because  of  pneumonia,  pericarditis,  cerebral  haemorrhage,  or  a  similar 
intercurrent  disease. 

Anomalous  or  rudimentary  cases  of  scorbutus  may  occur.  They  are  most  apt 
to  be  seen  when  the  disease  is  epidemic  or  endemic.  As  a  rule,  the  symptoms  are 
mild.  We  find,  for  example,  a  scorbutic  gingivitis  and  stomatitis  without  haem- 
orrhage, or,  on  the  other  hand,  haemorrhages  into  the  skin  and  mucous  membranes 
unattended  by  alteration  in  the  gums.  There  have  even  been  cases  reported  of 
simple  scorbutic  anaemia  without  any  local  sjnnptoms. 

[The  experience  of  army  surgeons  during  our  civil  war  deserves  mention 
in  this  connection.  Hammond,  Woodward,  and  others  state  that  many  cases 
classed  in  the  sick  reports  as  "  general  debility  "  were  cases  of  incipient  or  imper- 
fectly developed  scurvy,  haemorrhage  from  mucous  membranes  or  into  the  skin 
being  absent.] 

Biagnosis. — The  diagnosis  of  scorbutus  is  almost  self-evident  when  the  two 
chief  symptoms  of  haemorrhage  and  alteration  in  the  gums  are  both  present.  If, 
however,  one  or  the  other  of  these  symptoms  is  suppressed  or  imperfectly  devel- 
oped, it  may  be  difficult  to  determine  what  disease  we  have  before  us,  or  to  exclude 
ordinary  stomatitis,  rheumatic  peliosis,  and  similar  diseases.  One  characteristic 
sign  should  be  emphasized  again  in  this  connection.  The  haemorrhage  of  scurvy 
is  scarcely  ever  confined  to  the  skin,  but  almost  invariably  there  are  large  extrava- 
sations deeper  in,  in  the  muscles  and  fasciae.  These  occasion,  secondarily,  the 
characteristic  bruise-like  bluish-yellow  spots  seen  through  the  skin. 


BARLOW'S   DISEASE  T43 

Treatment. — The  essential  requisites  in  the  treatment  of  scurvy  are  proper 
hygiene  and  diet.  Eresh  air,  suitable  nourishment,  and  good  nursing,  if  promptly 
supplied,  are  usually  of  themselves  sufficient  to  induce  recovery,  while  the  physi- 
cian possesses  no  remedies  which  compensate  for  their  absence. 

The  belief  that  a  main  cause  of  scurvy  lies  in  a  deficiency  of  fresh  vegetables 
has  given  rise  to  a  practice,  still  in  vogue,  of  prescribing  a  great  abundance  of 
fresh  vegetables,  such  as  lettuce,  spinach,  and  sorrel,  fruit,  lemonade,  and  other 
drinks  prepared  from  fruit  syrups.  There  is  no  reason  to  deviate  from  a  course 
to  which  experience  has  given  its  sanction,  although  we  have  repeatedly  had 
opportunity  to  see  that  the  administration  of  fresh  vegetables  is  by  no  means 
essential  to  rapid  recovery.  Patients  supplied  with  any  other  proper  nourishment 
thrive  equally  well.  Certain  varieties  of  plants  have  attained  a  special  reputa- 
tion as  "  antiscorbutics,"  such  as  the  spoonwort  (Cochlearia  officinalis),  so  fre- 
quently mentioned  in  accounts  of  early  polar  expeditions.  None  of  these  plants, 
however,  possess  the  specific  properties  assigned  to  them.  The  administration 
of  vegetable  acids  and  the  salts  of  potassium  (bitartrate  and  nitrate  of  potas- 
sium), in  a  chemically  pure  form,  has  also  been  repeatedly  tried,  but  it  has  not 
gained  popularity. 

The  drugs  most  employed  are  the  bitters  and  tonics.  They  have  no  specific 
value,  but  are  perhaps  as  good  remedies  to  prescribe  as  any.  We  may  give  a 
decoction  of  cinchona,  to  which  may  be  added  a  small  amount  of  dilute  sulphuric 
acid  and  syrup,  or  some  preparation  of  gentian  or  a  similar  bitter.  It  was  once 
believed  that  the  internal  administration  of  the  mineral  acids  exerted  a  specially 
favorable  influence  upon  the  hsemorrhagic  diathesis;  but  this  is  very  doubtful. 

Certain  symptoms  may  demand  attention;  in  particular,  the  affection  of  the 
mouth  and  gums.  It  is  of  great  importance  to  cleanse  the  mouth  frequently  with 
disinfectants  and  mild  astringents,  such  as  chlorate  of  potassium  or  sage  tea.  It 
is  also  advisable  to  paint  the  inflamed  and  spongy  gums  at  short  intervals  with 
tincture  of  myrrh  or  tincture  of  rhatany.  The  absorption  of  the  ecchymoses  in 
the  lower  extremities  will  be  promoted  by  cautious  massage.  Inunctions  of  lini- 
mentum  chloroform!  and  the  like  give  relief  from  the  pain  caused  by  the  extrava- 
sations into  the  deeper  tissues.  In  severe  cases  stimulants  are  often  demanded, 
such  as  camphor,  ether,  and  alcohol.  Such  complications  as  appear  may  also 
demand  special  treatment. 

Convalescence  is  promoted  by  continued  attention  to  diet,  bathing,  and  the 
administration  of  iron  and  quinine. 


APPENDIX 

barlow's  disease 

In  this  connection  we  desire  to  mention  briefly  a  peculiar  symptom-complex 
which  has  been  associated  with  scurvy,  in  regard  to  the  real  nature  of  which  we 
do  not  yet  possess  any  definite  knowledge.  The  disease  is,  therefore,  usually 
named  after  the  person  who  discovered  it  (1883),  as  Barlow's  disease. 

The  disease  has  been  seen  thus  far  in  children  alone,  and  most  often  between 
the  ages  of  six  and  eighteen  months;  almost  all  the  children  had  previously 
shown  definite  signs  of  rickets.  There  is  little,  if  any,  fever,  but  an  extremely 
painful  swelling  of  the  bones,  particularly  of  the  epiphyses  of  the  long  bones, 
though  the  lower  jaw,  cranium,  and  other  parts  may  be  involved.  The  epiphyses 
may  become  loosened,  but  the  joints  themselves  are  not  affected.  Upon  careful 
examination  it  is  found  that  the  swelling  is  due  to  subperiosteal  haemorrhages. 
In  association  with  these  there  may  be  other  indications  of  a  hsemorrhagic  diath- 


T44  CONSTITUTION'AL   DISEASES 

esis,  such  as  liseinorrliage  into  the  skin,  and  into  the  serous  membranes,  and 
hematuria.  In  mild  cases  the  haemorrhages  along  the  bones  are  absorbed  and  do 
not  recur.  In  severe  cases,  however,  the  haemorrhages  are  constantly  repeated, 
and  the  child  may  finally  die  of  exhaustion. 

The  prognosis  is  consequently  to  be  expressed  with  some  reserve.  Treatment 
consists  chiefly  in  suitable  regulation  of  the  diet.  If  the  hgemorrhages  are  quite 
large  it  is  advantageous  to  make  a  surgical  incision,  and  allow  the  blood  to  escape. 


CHAPTER   VII 
PURPTJEA.      MORBUS    MACULOSUS    WERLHOPII.      PELIOSIS 

As  already  stated  in  the  preceding  chapter,  the  various  "hemorrhagic  dis- 
eases "  are  so  intimately  related  to  one  another  that  it  is  quite  impossible  to  make 
a  rigid  categorical  division  of  them.  The  numerous  names  which  have  been 
introduced  into  the  literature  of  this  subject  certainly  contribute  more  to  obscure 
than  to  elucidate  the  attendant  phenomena. 

From  a  clinical  standpoint  this  fact  is  the  all-important  one — namely,  that 
there  are  cases  in  which  the  foremost  symptom  is  the  spontaneous  occurrence  of 
hemorrhage.  There  are  cutaneous  ecchymoses,  and  there  may  be  at  the  same 
time  haemorrhages  in  the  internal  organs  and  into  the  mucous  membranes.  In 
the  milder  cases  of  this  sort  these  haemorrhages  constitute  almost  the  only  symp- 
tom of  disease;  but  they  may  be  associated  with  considerable  general  disturb- 
ance, indicated  by  fever  and  weakness,  or  with  certain  local  complications.  The 
true  cause  of  these  diseases  has  not  yet  been  discovered.  There  is  seldom  any 
evidence  of  an  exciting  cause,  and  the  disorder  may  attack  either  the  well-nour- 
ished or  the  poorly  nourished,  the  old  or  the  young,  men  or  women.  There  is, 
however,  an  indisputable  relationship  between  these  diseases  and  certain  others — 
namely,  scurvy,  erythema  exsudativum,  and  perhaps  acute  rheumatism  and  endo- 
carditis. This  similarity  indicates  that  the  process  is  of  an  infectious,  or  toxic, 
character.  Such  an  assumption  promotes  greatly  a  proper  understanding  of  the 
phenomena  under  consideration.  It  is  also  said  that  subcutaneous  injections  of 
blood  from  patients  with  morbus  maculosus  may  cause  a  like  affection  in  rabbits 
(Petrone  and  others).  In  some  few  cases  the  weight  of  evidence  would  seem, 
however,  to  point  to  an  antecedent  impairment  of  nutrition  in  the  walls  of  the 
blood-vessels.  A  good  example  of  this  is  seen  where  cutaneous  ecchymoses  occur 
in  old  and  marantic  individuals  (peliosis  senilis).  There  is  some  doubt  whether 
these  exceptional  cases  belong  with  the  others. 

The  mildest  forms  of  the  diseases  under  discussion  are  termed  purpura.  The 
haemorrhages  are  seen  mainly  in  the  skin  of  the  lower  extremities,  and  are  apt  to 
take  place  in  the  follicles.  There  may  also  be  ecchymoses  upon  the  trunk  and 
upper  extremities,  but  the  mucous  membranes  and  the  deeper  tissues  repiain 
intact.  A  means  of  distinguishing  purpura  from  scorbutus  lies  in  the  fact  that  in 
purpura  there  are  no  haemorrhages  into  the  muscles  and  no  lesions  of  the  gums, 
although  it  should  be  confessed  that  transitional  forms  between  the  two  occur. 
The  disorder  is  called  purpura  simplex  if  the  cutaneous  ecchymoses  constitute 
the  only  sjnnptom,  or,  at  any  rate,  the  only  important  one.  These  cases  almost 
invariably  terminate  in  recovery,  and  are  over  at  the  end  of  ten  days  or  three 
weeks.  Sometimes  elevations  of  the  skin  are  formed  resembling  wheals,  and 
haemorrhages  take  place  here  and  there  into  them.  This  subvariety  has  been 
called  by  some  purpura  urticans.    It  forms  a  connecting  link  between  purpura 


PUEPUEA.    MOEBUS    MACULOSUS   WEELHOFII.     PELIOSIS  745 

simplex  and  those  cases  of  erythema  exsudativum  which  are  associated  with  haem- 
orrhage.    Further  particulars  may  be  found  in  special  works  upon  dermatology. 

Quite  often  the  haemorrhages  are  attended  by  "  dragging  rheumatic  pains  "  ; 
such  cases  are  termed  purpura  rheumatica  or  rheumatic  peliosis  (Schonlein). 
There  may  also  be  constitutional  disturbance,  slight  fever,  anorexia,  and  indis- 
position to  either  bodily  or  mental  exertion.  There  may  sometimes  be  actual 
arthritis,  with  an  inflammatory  effusion  into  the  joints.  The  knee  and  other 
joints  of  the  lower  extremities  are  most  apt  to  suffer  in  this  way.  The  gums  are 
usually  normal ;  nor  is  there,  as  a  rule,  hsemorrhage  into  the  mucous  membranes 
or  the  viscera.  These  cases  may  last  but  two  or  three  weeks.  Often,  however, 
they  are  more  tedious,  being  marked  by  the  recurrence  of  the  ecchymoses  and 
articular  pain.    Most  of  them  get  well  at  last. 

'No  sharp  dividing  line  can  be  drawn  between  the  forms  of  purpura  thus  far 
described  and  certain  graver  cases.  These  latter  are  most  of  them  grouped  under 
the  name  of  purpura  hcemorrhagica,  or  its  preferable  because  more  distinctive 
synonym — every  purpura  being  hasmorrhagic — morbus  maculosus  Werlhofii. 
The  cutaneous  ecchymoses  in  this  class  of  cases  are  usually  extensive ;  and,  fur- 
thermore, we  have  haemorrhages  into  the  mucous  membranes  of  the  nose,  mouth, 
soft  palate,  stomach,  and  intestinal  canal,  as  well  as  into  internal  organs  (the 
brain  and  kidneys),  and  also  into  the  serous  membranes.  The  constitutional 
disturbance  is  apt  to  be  severe.  The  condition  may  be  distinctly  "  typhoidal." 
Pever  may  be  entirely  absent,  even  in  grave  cases,  although  sometimes  there  is 
a  considerable  rise  in  temperature. 

There  are  usually  no  local  symptoms  beyond  those  already  mentioned.  In 
typical  cases  the  gums  remain  intact.  Swelling  of  one  or  more  joints  has  been 
repeatedly  observed,  as  have  also  endocarditis  and  acute  haemorrhagic  nephritis. 
If  marked  cerebral  symptoms  are  developed,  suggesting  an  apoplectic  shock,  we 
may  surmise  that  a  cerebral  haemorrhage  has  taken  place.  It  should  also  be  stated 
that  marked  gastro-intestinal  disturbance  may  occur.  Cases  of  this  sort  have 
been  observed  by  Henoch  in  children.  They  may  also  occur  in  adults.  In  rare  in- 
stances there  may  be  intestinal  ulceration,  with  perforation  and  consequent  peri- 
tonitis.   The  spleen  may  undergo  acute  enlargement. 

All  the  symptoms  which  have  been  enumerated  render  distinct  the  similarity 
of  the  clinical  picture,  in  severe  cases  of  morbus  maculosus  Werlhofii,  to  that  of 
severe  septic  infection.  In  fact,  it  is  not  impossible  that  continued  investigation 
will  deprive  morbus  maculosus  of  its  individuality  as  a  specific  fonn  of  disease, 
and  show  that  it  is  merely  a  special  form  of  profound  sepsis. 

The  prognosis  in  purpura  hsemorrhagica  should  always  be  a  guarded  one ;  the 
patient  is  in  danger  both  from  the  general  depression  and  anaemia,  and  from 
certain  special  lesions.  Even  a  severe  case  may,  however,  recover.  The  disease 
sometimes  proves  very  tedious ;  it  may  occupy  several  months. 

Treatment. — The  general  regimen  to  be  prescribed  is  similar  to  that  directed 
in  scurvy.  The  physician  must  strive  to  siipport  his  patient's  strength  by 
proper  nourishment.  A  great  many  internal  remedies  have  been  recommended, 
most  of  them  on  purely  theoretic  grounds.  It  is  diflicult  to  say  whether  they 
actually  exert  a  favorable  influence  upon  the  course  of  the  disease.  The  follow- 
ing drugs  are  chiefly  employed:  Ergotine,  perchloride  of  iron,  dilute  sulphuric 
acid,  and  cinchona.  If  there  be  swelling  of  the  joints  or  endocarditis,  we  should 
advise  a  trial  of  salicylic  acid  or  antipyrine.  Such  special  symptoms  as  demand 
attention,  particularly  heart-failure,  should  be  treated  according  to  general 
principles. 


U6  CONSTITUTIONAL   DISEASES 

GHAPTEE  VIII 
HEMOPHILIA 

Definition  and  etiology. — Haemophilia  is  the  term  used  to  denote  a  peculiar 
constitutional  anomaly,  exhibited  in  a  remarkable  tendency  to  spontaneous  and 
traumatic  hsemorrhage.  The  condition  is  probably  in  every  instance  congenital, 
and  is  usually  hereditary;  the  existence  of  families  of  "  bleeders  "  has  long  been 
known.  Generation  after  generation  displays  frequent  cases  of  hsemophilia,  both 
among  the  direct  descendants  and  the  lateral  branches.  Bleeders  are  very  apt  to 
have  a  numerous  progeny.  Not  all  of  the  children,  however,  fall  victims  to  the 
disease.  Grandidier  has  pointed  out  two  facts  which  are  of  interest  in  this 
connection,  as  they  might  aid  in  deciding  as  to  the  marriageability  of  certain 
persons. 

If  a  man  belonging  to  a  family  of  bleeders  marries  a  healthy  woman,  neither  a 
bleeder  herself  nor  inheriting  a  predisposition  to  haemophilia,  his  children  are 
almost  certain  to  be  healthy,  even  though  the  father  himself  be  a  bleeder.  On  the 
other  hand,  a  woman  belonging  to  a  family  of  bleeders,  even  though  she  herself 
be  healthy,  will  almost  always  have  some  children  who  are  subject  to  haemophilia. 
In  other  words,  hereditary  predisposition  is  transmitted  much  oftener  through 
the  female  than  through  the  male  members  of  the  family.  Haemophilia  itself  is, 
on  the  contrary,  much  more  frequent  in  the  male  sex  than  in  the  female;  at  least 
this  is  true  of  the  pronounced  cases.  Hossli,  who  has  lately  published  a  very 
careful  family  tree  of  bleeders  of  Tenna  (Canton  Graubiinden),  comes  to  the  fol- 
lowing conclusions :  "  The  inheritance  of  haemophilia  is  often  from  the  father, 
through  the  daughter,  to  the  grandson,  also  from  the  mother,  through  the  daugh- 
ter, to  the  grandson,  and  most  rarely  directly  from  the  father  to  the  son."  It  is 
doubtful  whether  race  and  place  of  residence  are  of  aetiological  importance.  So 
far  as  is  known,  haemophilia  appears  to  occur  in  all  countries,  although  it  is  for- 
tunately rare  everywhere. 

[A  similar  transmission  through  the  females,  who  themselves  usually  escape, 
is  seen  in  color-blindness  and  in  pseudo-hypertrophic  paralysis.] 

The  real  causes  of  haemophilia  are  entirely  luiknown  to  us.  We  can  make  one 
or  two  steps  toward  finding  the  source  of  the  haemorrhage,  but  we  are  unable  to 
proceed  further.  It  would  seem  that  the  bleeding  must  depend,  in  the  first  place, 
upon  an  abnormal  delicacy  of  the  walls  of  the  vessels  predisposing  them  to  rup- 
ture, and,  secondly,  upon  deficient  coagulability  of  the  blood.  This  latter  abnor- 
mality is  evident  from  the  fact  that  in  haemophilia  it  is  difficult  to  check  even  the 
most  insignificant  haemorrhage.  Thus  far  all  attempts  to  discover  any  anatom- 
ical or  chemical  explanation  of  this  imperfect  coagulability  have  been  vain.  It  has 
not  been  possible  to  detect  any  variation  in  the  saline  constituents  of  the  blood, 
or  in  the  amount  of  albuminoids,  such  as  fibrinogen,  that  it  contains,  or  in  its 
morphological  elements.  And  likewise  no  anatomical  change  in  the  vascular  walls 
or  the  heart  has  yet  been  reported  which  throws  light  upon  the  character  of  the 
disease.  Various  authorities  have  laid  stress  upon  the  small  diameter  of  the 
arteries  and  the  thinness  of  the  intima,  but  these  conditions  may  occur  independ- 
ently of  haemophilia.  Fatty  degeneration  of  the  intima  is,  to  be  sure,  often  found 
in  connection  with  this  disease,  but  it  is  doubtless  rather  a  result  of  the  coinci- 
dent anaemia  than  the  cause  of  the  haemophilia.  The  observations  with  regard  to 
the  heart  are  very  contradictory;  sometimes  it  is  found  to  be  very  small,  some- 
times of  normal  size,  and  again  actually  hypertrophied. 

The  subjects  of  haemophilia  do  not  present  any  distinctive  constitutional  pe- 
culiarities.   It  has  been  stated  that  they  are  very  apt  to  be  blondes  with  a  delicate 


HEMOPHILIA  ■  U7 

white  skin,  and  superficial  and  abnormally  distended  cutaneous  veins;  but  the 
exceptions  to  this  rule  are  not  a  few. 

Clinical  History. — Hsemophiliadoes  not  display  equal  malignity  in  all  cases. 
If  we  have  opportunity  to  obtain  thorough  information  with  regard  to  families  of 
bleeders,  we  shall  find  that  quite  often  rudimentary  varieties  occur  side  by  side 
with  typical  and  severe  cases.  There  is,  to  be  sure,  a  striking  tendency  to  ha3mor- 
rhage  even  in  them;  but  the  hsemorrhage  never  assumes  threatening  proportions. 
By  perseverance  and  industry  it  is  possible  to  collect  an  almost  unbroken  series 
of  cases,  varying  in  degree  from  extreme  mildness  to  extreme  severity.  The  fol- 
lowing sketch  applies  mainly  to  typical  and  severe  cases. 

That  hasmophilia  is  a  hereditary  constitutional  disease  is  shown  by  the  fact 
that  it  sometimes  appears  in  earliest  infancy.  Many  cases  of  umbilical  hsemor- 
rhage in  the  new-born  are  referable  to  hasmophilia.  Of  course  this  does  not 
apply  to  all  cases.  In  Jewish  children  the  disease  may  betray  itself  for  the  first 
time  when  the  rite  of  circumcision  is  performed.  In  many  cases  the  disease  is 
not  recognized  at  so  early  a  period;  but  this  is  no  proof  that  the  disease  is  not 
already  developed,  inasmuch  as  the  young  child  is  not  much  exposed  to  trauma- 
tism and  other  causes  which  naturally  occasion  hsemorrhage. 

The  most  striking  symptom  in  a  fully  developed  case  of  hsemophilia  is  the 
occurrence  of  severe  hsemorrhage  as  a  result  of  the  most  insignificant  causes.  A 
slight  blow  produces  a  "  black-and-blue  spot  "  such  as  is  ordinarily  seen  only  after 
a  very  violent  injury.  The  prick  of  a  pin,  a  slight  cut  on  the  finger,  or  the  extrac- 
tion of  a  tooth,  may  give  rise  in  hsemophilia  to  an  obstinate  and  alarming  haemor- 
rhage. Epistaxis  may  be  caused  by  blowing  the  nose,  hsemorrhage  from  the 
gums  by  brushing  the  teeth,  and  so  on.  Whether  there  is  ever  a  perfectly  spon- 
taneous hsemorrhage  is  uncertain.  It  is  true  that  in  severe  cases  haemorrhages 
take  place  independently  of  any  visible  cause.  This  may  be  seen  in  the  skin  and 
mucous  membranes  (nose  and  gums) ;  and  in  rare  instances  we  may  even  have 
free  haemorrhage  from  the  stomach,  intestines,  or  urinary  passages.  Yet  it  may 
be  doubted  whether  these  occurrences  are  not  the  result  of  comparatively  insig- 
nificant mechanical  injuries  which  escape  our  notice.  At  any  rate,  we  scarcely 
ever  find  hsemorrhage  taking  place  into  the  parenchyma  of  the  viscera,  in  places 
where  injury  from  external  sources  is  entirely  out  of  the  question.  This  fact  con- 
stitutes an  important  point  of  distinction  between  haemophilia  and  the  acquired 
hsemorrhagic  diathesis. 

The  second  important  symptom  of  haemophilia  has  been  already  referred  to : 
it  is  extremely  difficult,  and  may  even  be  impossible,  to  check  by  artificial  means 
any  free  hsemorrhage  which  may  occur.  It  is  this  which  makes  the  disease  so 
dangerous,  and  prevents  most  patients  from  reaching  old  age.  It  has  frequently 
happened  that  an  apparently  trifling  wound  of  the  skin,  some  insignificant 
operation,  or  a  leech-bite,  or  in  women  childbirth,  has  started  up  a  haemorrhage, 
which  eventually  became  fatal.  In  other  cases  the  hsemorrhage  is  finally  checked, 
but  not  until  it  has  caused  profound  anaemia.  Bleeders  are  apt  to  recover  with 
remarkable  rapidity  from  the  effects  of  excessive  ha3morrhage;  yet  continually 
repeated  haemorrhages  may  lead  to  a  persistent  and  profound  anaemia,  attended 
by  all  the  symptoms  described  in  the  preceding  chapters. 

We  see,  therefore,  that  the  general  condition  in  haemophilia  varies  with  the 
severity  of  the  individual  case,  and  with  the  more  or  less  fortuitous  circumstances 
which  develop  its  dormant  characteristics.  If  no  special  accident  occurs,  the 
patient  may  maintain  the  appearance  of  perfect  health  for  years.  In  the  worst 
cases,  however,  such  a  state  is  very  temporary,  if  it  exists  at  all,  because  the  haem- 
orrhages can  be  so  easily  excited.  As  a  consequence,  the  skin  almost  always  pre- 
sents a  greater  or  less  number  of  ecehyraoses,  while  haemorrhages  from  the  inter- 
nal organs  contribute  from  time  to  time  to  the  general  debility  and  anaemia. 


748  co:ntstitutional  diseases 

Certain  complications  may  occur  in  hasmophilia,  but  they  are  little  cliaracteristic. 
There  is  a  noticeable  tendency  to  "  rheumatic  "  inflammation  of  the  muscles  and 
swelling  of  the  joints,  wherein  is  seen  a  striking  analogy  to  the  "  hasmorrhagic 
diseases."  Often  there  is  an  actual  effusion  of  blood  into  the  joints.  This  may 
cause  considerable  functional  disturbance  of  the  joints,  and  eventuate  in  anchy- 
losis. Various  writers  have  also  called  attention  to  the  comparative  frequency  of 
neuralgia,  especially  in  the  trigeminus. 

Prognosis. — In  only  too  many  instances  the  victims  of  haemophilia  die  in 
childhood;  in  other  cases  the  patient  attains  an  advanced  age.  A  fact  of  great 
practical  importance  is  that  often,  although  not  invariably,  haemophilia  grows 
gradually  milder  with  advancing  years.  If,  therefore,  the  patient  have  survived 
the  period  of  adolescence,  we  may  believe  that  his  prospects  are  gradually  improv- 
ing. The  prognosis  of  hemophilia  is  obvious.  The  amount  of  danger  at  any 
given  time  depends  upon  the  severity  of  the  haemorrhage  and  the  consequent 
anaemia.  The  comparative  severity  of  the  case  must  be  judged  from  its  previous 
history;  as  has  just  been  said,  the  prognosis  g^rows  more  favorable  as  the  patient 
grows  older. 

Treatment. — Prophylaxis  assumes  a  very  important  place  in  the  treatment  of 
haemophilia.  First,  children  who  inherit  a  tendency  to  the  disease,  or  who  have 
given  evidence  of  its  existence,  should  be  treated  with  a  view  to  improve  their 
general  constitutional  condition,  so  as  to  check  the  development  of  the  disease  as 
far  as  possible.  The  means  to  this  end  need  not  be  described  at  length.  They 
comprise  good  nourishment,  fresh  air,  cautious  endeavors  to  harden  the  system, 
baths,  and  tonics.  Secondly,  when  haemophilia  already  exists,  the  patient  should 
be  guarded  as  much  as  possible  from  any  mechanical  injury,  such  as  might  excite 
haemorrhage.  Thus  caution  is  demanded  in  performing  vaccination  and  other 
apparently  trifling  operations. 

As  regards  direct  treatment  of  the  disease,  no  effectual  remedy  is  known.  The 
general  tonic  treatment  already  referred  to  should  not  be  neglected;  but  the 
administration  of  ergotine,  acetate  of  lead,  and  similar  drugs  is  indicated,  if  at 
all,  only  when  haemorrhage  is  actually  taking  place,  and  even  then  it  is  very  apt  to 
fail.  The  only  way  to  stop  the  haemorrhage  is  by  surgical  methods,  and  these 
need  not  be  described  here.  They  do  not  differ  essentially  from  those  employed 
when  haemorrhage  occurs  independently  of  haemophilia.  If  mechanical  efforts 
to  check  the  bleeding  fail,  we  can  expect  nothing  from  the  remedies  above  men- 
tioned, nor  from  sulphate  of  sodium  and  the  other  laxatives  which  have  been 
recommended.  Eor  the  symptomatic  treatment  of  the  anaemia  and  of  its  results, 
we  may  refer  to  the  first  chapter  of  this  section. 


CHAPTEE   IX 
DIABETES    MELLITTJS 

Definition  and  .ZEtiology. — Under  normal  circumstances  the  blood  always  eon- 
tains  a  slight  amount  of  sugar ;  but  this  ingredient  does  not  usually  pass  over  in 
appreciable  quantities  into  the  urinary  excretion.  If,  however,  the  amount  of 
sugar  in  the  blood  exceeds  certain  limits — that  is,  if  there  exists  an  abnormal 
"  glycaemia  " — then  sugar  is  excreted  in  the  urine,  and  we  have  glycosuria.  This 
is  seen  as  a  more  or  less  temporary  phenomenon  under  the  most  varied  conditions. 
The  amount  of  sugar  in  the  urine  is  usually  comparatively  slight,  and  it  soon  dis- 
appears again.     Its  presence  does  not  imply  any  persistent  abnormal  condition. 


DIABETES   MELLITUS  ^749 

This  phenomenon  has  been  termed  glycosuria  or  melituria,  in  contrast  with  the 
peculiar  disease  which  has  for  its  jchief  symptom  a  persistence  of  sugar  in  the 
urine,  and  has  therefore  received  the  name  of  diabetes  mellitus.  It  is  not  neces- 
sary in  this  connection  to  enumerate  all  the  causes  of  glycosuria,  i.  e.,  of  a  tem- 
porary appearance  of  sugar  in  the  urine.  It  may  be  briefly  mentioned,  however, 
that  glycosuria  is  observed  even  in  healthy  persons  after  excessive  indulgence  in 
sugar.  If  a  healthy  person  takes  at  one  time  about  seven  ounces  (grammes  200) 
or  more  of  grape-sugar  dissolved  in  water,  there  will  probably  be  after  an  hour  or 
two  a  demonstrable,  although  not  a  very  great,  amount  of  sugar  in  the  urine. 
This  is  the  so-called  alimentary  glycosuria.  In  this  case  the  blood  is  so  over- 
burdened with  sugar  that  the  sugar  can  not  be  oxygenated  fast  enough.  A 
portion  of  the  sugar,  therefore,  escapes  change  and  is  excreted  with  the  urine. 
If  the  same  amount  of  sugar  is  given  in  divided  doses  at  intervals,  there  will  be 
no  glycosuria.  If  glycosuria  appears  upon  the  administration  of  small  amounts 
of  sugar  (two  to  three  ounces,  grammes  50-100)  we  are  justified  in  speaking  of  a 
morbid  alimentary  glycosuria,  the  power  of  the  body  to  assimilate  sugar  being 
subnormal.  An  abnormal  glycosuria  of  this  sort  is  observed,  for  example,  not  in- 
frequently in  obese  beer-drinkers,  and  in  patients  with  severe  traumatic  neuroses, 
or  with  exophthalmic  goitre.  Temporary  glycosuria  is  also  observed  not  infre- 
quently in  certain  kinds  of  poisoning,  particularly  after  severe  poisoning  with  car- 
bonic oxide,  morphine,  hydrocyanic  acid,  mercury,  nitrite  of  amyl,  and  curare.  Von 
Mehring  has  lately  discovered  in  phloridzine,  a  glucoside  in  the  bark  of  the  rDots 
of  apple  and  cherry  trees,  a  substance  which  causes  a  very  large  amount  of  sugar 
in  the  urine  if  given  to  dogs,  rabbits,  etc.  A  marked  glycosuria  may  be  iDroduced 
in  m.an  also  by  giving  phloridzine,  without  other  disturbances  of  the  general  con- 
dition. It  is  not  improbable  that  the  phloridzine-glycosuria  is  different  from  the 
other  toxic  glycosurias,  in  that  it  depends  upon  a  change  in  the  renal  epithelium, 
as  a  consequence  of  which  the  cells  become  permeable  to  the  sugar  which  is  cir- 
culating in  the  blood.  Temporary  glycosuria  has  also  been  seen  occasionally  in 
connection  with  the  acute  infectious  diseases — for  example,  malignant  pustule, 
cholera,  typhus  or  typhoid  fever,  scarlet  fever,  diphtheria,  and  malarial  poison- 
ing. A  far  more  frequent  cause  is  disturbance  of  the  nervous  system.  Thus, 
glycosuria  may  result  from  severe  concussion  of  the  brain,  fracture  of  the  skull, 
cerebral  haemorrhage,  cerebro-spinal  meningitis,  and  after  epileptic  fits.  It  is 
especially  apt  to  occur  when  there  is  disease  of  the  medulla ;  and  we  need  hardly 
point  out  how  close  is  the  connection  between  this  clinical  fact  and  the  famous 
discovery  of  Claude  Bernard,  who  found  by  experiment  that,  when  certain  in- 
juries are  inflicted  upon  the  floor  of  the  fourth  ventricle,  glycosuria  inevitably 
follows.  This  glycosuria  is  explained  by  assuming  that,  as  a  resiilt  of  nervous 
influences,  the  liver  discharges  its  supply  of  glycogen  into  the  blood  in  the  form 
of  grape  sugar.  The  blood  is  overwhelmed  with  the  sugar,  and  a  portion  escapes 
into  the  urine. 

In  some  other  oganic  diseases,  also,  there  may  be  a  temporary  and  symp- 
tomatic glycosuria.  Formerly,  special  attention  in  this  regard  was  directed  to 
hepatic  diseases,  but  it  is  to  be  noted  that,  as  a  rule,  even  when  there  is  extensive 
disease  of  the  liver — for  example,  in  hepatic  cirrhosis — no  glycosuria  is  observed, 
even  if  the  patient  is  given  large  amounts  of  sugar  in  his  dietary.  On  the  other 
hand,  the  combination  of  persistent  diabetes  mellitus  and  hepatic  cirrhosis  is  not 
very  exceptional.  As  we  shall  point  out  again  later  on,  we  regard  both  diseases  in 
these  cases  as  co-ordinate  effects  of  the  same  cause,  chronic  alcoholism.  We  shall 
likewise  refer  again  to  the  relation  between  diabetes  and  renal  disease.  Espe- 
cially great  interest  attaches  to  the  question  of  the  relation  between  glycoeuria 
and  diseases  of  the  pancreas,  since  Minkowski  and  Von  Mehring  made  the  impor- 
tant discovery  that  we  can  excite  severe  diabetes  in  dogs  by  extirpation  of  the 


750  constitutio:n'al  diseases 

pancreas.  The  ligation  of  the  excretory  duct  of  the  gland,  or  the  diversion  of  the 
pancreatic  juice  into  a  fistula  leading  to  the  surface  of  the  body,  does  not  excite 
diabetes,  nor  does  the  diabetes  occur  if  the  pancreas  is  partially  and  not  wholly 
extirpated.  Pancreatic  diabetes,  therefore,  implies  a  disturbance  of  a  special 
function  of  the  pancreas,  of  which  we  have  as  yet  no  intimate  knowledge,  but  the 
abolition  of  which  prevents  the  complete  splitting  up  or  oxidation  of  sugar  in  the 
normal  organism.  Diseases  of  the  pancreas  in  man  (carcinoma;  pancreatic  cal- 
culi, with  secondary  atrophy  of  the  gland)  occasion  glycosuria  sometimes,  but  by 
no  means  invariably.  The  atrophy  of  the  pancreas  observed  in  many  cases  of 
genuine  diabetes  will  be  discussed  later  on.  We  should  mention  in  this  connec- 
tion, also,  the  glycosuria  which  sometimes  appears  in  association  with  exoph- 
thalmic goitre,  and  finally  the  interesting  and  frequent  combination  of  acro- 
megaly (q.  v.),  and  the  persistent  excretion  of  sugar  in  the  urine. 

In  contrast  with  the  temporary  phenomenon  of  glycosuria,  we  apply  the  name 
diabetes  mellitus  to  a  chronic  morbid  state,  in  which  a  permanent  disturbance  in 
the  metabolism  of  the  carbohydrates  is  indicated  by  a  persistent  excretion  of 
sugar  in  the  urine,  and  in  which  this  anomaly  of  metabolism  is  the  main  symptom 
of  the  disease.  If  the  excretion  of  sugar  in  this  disease  is  not  absolutely  per- 
sistent, at  least  it  is  sure  to  occur  under  certain  conditions  of  nutrition.  It  is 
doubtful  whether  diabetes  mellitus  is  to  be  regarded  from  an  setiological  stand- 
point as  a  single,  distinct  disease.  With  regard  to  most  of  the  "  pure  "  cases,  par- 
ticularly the  severe  form  of  diabetes  which  usually  occurs  in  youthful  individuals 
without  any  demonstrable  cause  and  also  without  any  primary  organic  lesion, 
there  is  great  probability  in  the  assumption  that  the  morbid  process  is  a  single 
and  definite  one,  although  we  are  as  yet  entirely  unacquainted  with  its  real 
nature.  On  the  other  hand,  with  regard  to  the  so-called  milder  forms  of  diabetes 
mellitus,  particularly  those  which  occur  in  middle  and  advanced  life,  there  are 
probably  various  causes  which  may  excite  the  disease.  Still,  it  must  be  emphat- 
ically stated  that  no  sharp  dividing  line  can  be  drawn  between  the  "  severe  " 
and  the  "  milder  "  forms  of  diabetes.  The  physician  is,  therefore,  bound  in  every 
individual  case  to  search  for  certain  causative  factors  and  harmful  influences, 
which  sometimes,  at  least,  play  a  part  in  the  development  of  the  disease.  These 
causative  factors  are  the  following :  First,  heredity :  diabetes  has  been  repeatedly 
observed  to  occur  in  several  generations  of  the  same  family,  or  in  several  brothers 
and  sisters.  It  is  noteworthy  that  the  disease  may  also  occur  in  families  where 
there  is  a  hereditary  predisposition  to  nervous  diseases.  Eor  example,  we  ob- 
served once  in  the  same  patient  the  remarkable  combination  of  diabetes  and 
progressive  muscular  atrophy  of  spinal  origin.  Second,  improper  mode  of  life : 
by  this  is  meant  chiefly  unsuitable  diet,  especially  the  persistent  overindulgence 
in  starchy  foods  and  sugar;  sedentary  habits  are  also  considered  harmful,  espe- 
cially if  associated  with  overeating.  This  is  said  to  be  the  reason  why  diabetes  is 
more  frequent  among  the  wealthy  classes,  and  why  it  is  comparatively  common 
in  corpulent  persons  (vide  infra).  Our  personal  observations  lead  us  to  ascribe 
to  long-continued  and  excessive  beer-drinking  (four  or  flve  litres  and  more  per 
day)  an  influence  upon  the  development  of  diabetes.  In  such  cases  it  may  be  that 
we  have  a  combined  action  of  the  excessive  ingestion  of  carbohydrates  in  a  state 
of  solution,  and  of  chronic  alcoholism.  It  can,  in  our  opinion,  be  no  mere  coin- 
cidence that  diabetes  so  often  attacks  brewers,  inn-keepers,  and  the  like,  in  Ba- 
varia. Furthermore,  the  complication  of  diabetes  with  other  results  of  chronic 
alcoholism,  such  as  hepatic  cirrhosis,  chronic  nephritis,  and  alcoholic  neuritis, 
is  an  argument  for  the  correctness  of  our  supposition.  The  "  diabetes  of  obes- 
ity "  has  been  long  recognized,  but  in  many  cases  it  is  really  a  "  beer  diabetes." 
Third,  taking  cold  and  getting  wet  are  said,  in  occasional  rare  instances,  to  deter- 
mine the  appearance  of  diabetes.    The  author  has  never  seen  a  clear  case  of  this 


DIABETES   MELLITUS  T51 

sort.  Fourth.,  emotional  disturbances,  excessive  mental  exertion,  anxiety,  and 
passion,  are  sometimes  thought  to  occasion  the  disease;  and  apparently  with 
some  reason.  Fifth,  it  is  very  remarkable  that  sometimes  the  same  factors  which 
we  have  already  seen  to  be  possible  causes  of  temporary  glycosuria,  may  also  occa- 
sion a  chronic  diabetes  mellitus;  thus,  cases  of  diabetes  have  been  known  to 
follow  injuries  to  the  head,  and  such  acute  infectious  diseases  as  typhus,  typhoid, 
and  scarlet  fevers,  cholera,  and  malarial  poisoning.  Sixth,  a  few  authors  (Schmitz 
and  others)  have  hinted  at  the  possibility  of  the  disease  being  transferred  by  con- 
tagion— for  example,  in  the  case  of  married  people.  This  interpretation  of  the 
scattered  instances  which  have  been  reported  is,  however,  at  least  open  to  doubt. 
Seventh,  a  very  important  matter  is  the  occurrence  of  diabetes  in  association 
with,  or  as  a  sequel  to,  certain  other  constitutional  diseases.  In  this  category  be- 
long the  above-mentioned  diabetes  of  the  obese ;  also  the  simultaneous  appearance 
of  diabetes  and  genuine  gout  (g.  v.)  ;  and  finally,  the  extremely  important  com- 
bination of  diabetes  with  general  arterio-sclerosis.  That  all  these  combinations  do 
frequently  occur  can  not  be  doubted,  but  it  is  very  difficult  to  explain  the  connec- 
tion between  them ;  often  both  conditions  may  be  the  simultaneous  effect  of  the 
same  cause — for  instance,  congenital  anomalies  of  constitution,  unhygienic  modes 
of  life,  and  alcoholism. 

If  we  survey  all  the  facts  thus  far  known  with  regard  to  the  aetiology  of 
diabetes,  we  feel  obliged  to  conclude  just  as  in  almost  all  other  constitutional 
diseases,  that  in  regard  to  the  development  of  diabetes  we  must  distinguish 
endogenous  and  exogenous  factors.  The  endogenous  relate  to  the  constitutional 
tendencies  which  the  patient  possesses,  perhaps  by  inheritance;  and  the  exoge- 
nous to  harmful  influences  from  without,  such  as  trauma,  infection,  and  intoxi- 
cation. The  severe  cases  of  diabetes  which  seem  to  occur  absolutely  spontane- 
ously in  young  persons,  are  mainly  of  an  endogenous  character;  while  in  the 
milder  forms  of  later  years  the  above-mentioned  exogenous  influences  often  play 
an  important  part,  although  even  in  them  the  endogenous  factor  can  not  be 
entirely  disregarded,  for  the  same  noxious  influence  does  not  produce,  by  any 
means,  the  same  effect  upon  all  persons. 

Diabetes  occurs  everywhere,  but  certain  countries  and  districts  seem  to  be 
particularly  liable  to  it — for  example,  India,  Ceylon,  and  Italy.  In  Germany, 
Wiirtemberg  and  Thiiringen  are  said  to  present  the  largest  relative  number  of 
cases.  Jews  are  very  liable  to  the  disease.  Most  cases  occur  in  patients  between 
thirty-five  and  fifty  years  of  age.  ISTest  in  liability  to  the  disease  come  younger 
individuals,  under  thirty-five  and  over  twenty  years  old.  After  the  fiftieth  year 
diabetes  is  not  exceptional,  but,  in  the  other  direction,  children  under  ten  are 
very  seldom  attacked  by  it,  although  they  are  not  absolutely  exempt.  With 
regard  to  sex,  males  are  much  more  often  attacked  than  females. 

Clinical  History. — With  few  exceptions,  the  symptoms  of  diabetes  mellitus 
come  on  slowly  and  gradually.  Sometimes  the  symptoms  are  merely  general  and 
indefinite,  such  as  languor,  emaciation,  weakness,  and  deficient  endurance. 
Sometimes  we  have  mild  nervous  disturbances,  including  headache,  mental  de- 
pression, wakefulness,  and  neuralgia,  and  in  still  other  cases  gastro-intestinal 
symptoms,  including  nausea,  eructations,  and  irregularity  of  the  bowels.  At  last 
the  patient's  attention  is  called  to  the  altered  character  of  the  urine,  and  particu- 
larly to  its  increased  amount.  He  also  notices  that  he  is  very  thirsty,  and  that, 
in  spite  of  his  enormous  appetite,  he  is  constantly  growing  weaker.  Sometimes 
quite  different  symptoms  first  arouse  suspicion  of  the  existence  of  diabetes ;  these 
will  be  mentioned  later.  In  order  to  make  a  diagnosis  of  diabetes  mellitus,  a 
knowledge  of  the  abnormal  character  of  the  urine  is  indispensable,  so  that  it  is 
proper  to  begin  our  consideration  of  the  symptoms  of  diabetes  with  a  description 
of  diabetic  urine. 


T52  COI^STITUTIOIsTAL   DISEASES 

1.  Character  of  the  TJrixe.  Demonstration  of  Sugar. — Usually  tlie  first 
point  that  attracts  attention  is  the  increased  amount  of  urine.  There  are  often  a 
hundred  to  a  hundred  and  fifty  ounces  (three  to  five  quarts,  3,000-5,000  cubic 
centimetres)  excreted  in  twenty-four  hours,  and  sometimes  the  amount  equals  or 
exceeds  ten  or  twelve  quarts  (8,000-12,000  cubic  centimetres).  Under  suitable 
treatment  and  with  proper  diet  the  amount  may,  of  course,  be  much  smaller. 
In  not  very  exceptional  cases,  mostly  of  the  milder  varieties  (vide  infra),  there 
is  slight,  if  any,  increase  in  the  amount  of  urine  (diabetes  decipiens) ;  and  in 
severe  cases  with  initial  polyuria  we  may  often  observe  that  during-  intercurrent 
diseases,  and  likewise  in  the  last  days  before  the  fatal  termination  of  the  disease, 
the  daily  amount  of  urine  diminishes. 

In  color  the  urine  is  light  yellow,  corresponding  to  its  amount.  It  often  has 
something  of  a  greenish  hue,  but  a  small  quantity  of  it  may  seem  almost  as  color- 
less as  water.  Ordinarily  the  urine  is  clear  and  without  sediment;  but  after  it 
has  stood  for  some  time  it  may  become  cloudy,  usually  as  a  result  of  the  abundant 
development  of  fermentation  spores. 

The  odor  may  be  somewhat  aromatic,  suggesting  acetone  (vide  infra).  Its 
taste  is  said  sometimes  to  be  distinctly  sweetish.  The  reaction  is  acid,  and  the 
acidity  of  the  urine  may  increase  on  standing,  because  of  the  alcoholic  and  lactic- 
acid  fermentation  processes  which  the  sugar  undergoes. 

The  specific  gravity  is  almost  invariably  greatly  increased,  as  a  result  of  the 
large  amount  of  sugar.  If  a  pale  urine  is  found  to  have  a  specific  gravity  of  more 
than  1025,  we  may  feel  almost  certain  that  it  contains  sugar.  Specimens  often 
have  a  specific  gravity  of  1030-1045,  and  even  higher.  In  exceptional  instances 
the  specific  gravity  may  fall  below  1020.  A  specific  gravity  below  1020  is  excep- 
tional, but  one  should  never  be  kept  from  making  an .  examination  for  sugar 
because  of  the  low  specific  gravity  of  the  specimen.  We  have  ourselves  demon- 
strated sugar  by  means  of  the  fermentation  test  in  urine  which  had  a  specific 
gravity  of  1007. 

The  diagnosis  requires  that  sugar  be  detected  in  the  urine.  The  sugar  found 
in  both  the  blood  and  the  urine  of  diabetic  patients  is  grape-sugar  (glucose,  dex- 
trose). The  amount  of  sugar  secreted  in  twenty-four  hours  often  reaches  half  a 
pound  to  a  pound  (grammes  200-500).  Of  course  the  amount  varies  greatly  ac- 
cording to  the  diet,  mode  of  life,  and  treatment  of  the  patient.  The  greatest 
amount  ever  known  to  be  produced  in  twenty-four  hours  was  more  than  two  and 
one  fifth  pounds  (grammes  1,000).  The  percentage  of  sugar  in  the  urine  varies 
between  0.5-1  per  cent,  at  the  lowest  extreme,  and  8-10  per  cent,  as  the  maxi- 
mum; usually  it  is  about  2-4  per  cent.  It  is  noteworthy  that  in  the  last  weeks, 
or  just  before  death,  the  sugar  in  the  urine  may  become  greatly  diminished  in 
amount,  or  may  absolutely  disappear. 

The  most  important  tests  for  sugar  in  the  urine  are  :  First,  Trommer's  test :  To 
urine  in  a  test-tube  sufficient  potassic  or  sodic  hydrate  is  added  (say  one  part  to 
three  or  four  of  urine)  to  make  the  reaction  strongly  alkaline ;  then  a  solution  of 
sulphate  of  copper  (about  one  part  of  the  salt  to  ten  of  water)  is  added,  drop  by 
drop.  If  the  urine  contain  sugar,  the  hydrated  cupric  oxide,  which  is  at  first 
formed,  is  largely  dissolved,  and  usuallj^  the  fluid  assumes  a  beautiful  deep-blue 
color.  We  ought,  properly,  to  go  on  adding  the  sulphate  of  copper  until  the 
hydrated  cupric  oxide  ceases  to  be  dissolved.  The  urine  is  then  heated,  where- 
upon the  cupric  oxide  is  reduced  and  a  yellow,  or  reddish-yellow,  precipitate  of 
cuprous  oxide,  or  hydrated  cuprous  oxide,  is  formed.  The  application  of  heat 
should  not  be  continued  long  after  the  precipitation  begins  to  take  place,  lest 
the  test  be  obscured;  the  reduction  will  go  on  even  without  heat.  If  the  urine 
contains  more  than  0.5-1  per  cent.,  this  test  is  perfectly  reliable.  If  the  reaction 
be  a  doubtful  one — that  is,  if  there  be  no  precipitate  of  cuprous  oxide,  although 


DIABETES   MELLITUS  753 

the  urine  becomes  yellow;  or  if  cuprous  oxide  be  finally  precipitated  when  the 
urine  cools — we  should  be  cautious  in  making  a  diagnosis,  as  the  urine  may  con- 
tain substances  other  than  sugar  capable  of  reducing  the  copper,  such  as  uric 
acid,  kreatinine,  mucine,  etc.  Second,  the  bismuth  test  (Bottger's) :  Sodic 
hydrate  or  sodic  carbonate  is  added  to  the  urine,  and  then  a  small  pinch  of  sub- 
nitrate  of  bismuth.  Upon  boiling,  the  urine,  if  it  contains  sugar,  quickly  assumes 
a  perfectly  black  color,  the  oxide  being  reduced  to  the  metallic  state.  It  is  much 
more  convenient,  and  consequently  universally  customary  at  present,  to  make  the 
bismuth  test  by  adding  to  the  urine  about  one  tenth  of  its  volume  of  the  follow- 
ing solution  (JSTylander)  :  two  parts  subnitrate  of  bismuth,  four  parts  Eochelle 
salts,  one  hundred  parts  of  an  eight-per-eent.  solution  of  sodic  hydrate.  After 
one  or  two  minutes'  boiling  the  fluid  turns  black.  Errors  with  this  test  are  most 
apt  to  occur  if  the  patient  has  taken  certain  drugs,  such  as  antipyrine,  salicylic 
acid,  or  rhubarb.  Third,  the  potassium  test  (Moore's)  :  Potassic  hydrate  is  added 
to  the  urine  in  the  test-tube  and  the  uppermost  layer  cautiously  heated ;  if  it  con- 
tains sugar,  the  urine  quickly  assumes  a  deep-brown  color,  as  a  result  of  the 
action  of  the  potassium  on  the  sugar;  and  this  upper  dark-colored  layer  contrasts 
strongly  with  the  clear  urine  below. 

[Eehling's  test  is  justly  a  favorite  in  this  country,  and  has  the  advantage  of 
being  applicable  to  the  quantitative  as  well  as  to  the  qualitative  analysis.  The 
difficulty  of  its  not  keeping  well  can  be  met  by  having  separate  bottles  for  the 
copper  and  tartrate  solutions,  and  making  the  mixture  at  the  time  of  using  the 
test.  The  Fehling's-test  pellets  put  up  by  chemists  are  convenient  for  the  quali- 
tative analysis,  but,  on  the  whole,  they  are  inferior  to  the  solution.] 

If  the  above-described  tests  leave  us  still  in  doubt,  there  can  be  only  a  small 
amount  of  sugar,  if  any,  present.  We  may,  however,  attain  certainty  by  employ- 
ing the  fermentation  test  (which  causes  a  decomposition  of  the  sugar  into  alcohol 
and  carbonic  dioxide),  or  circumpolarization  (deflection  of  the  plane  of  polariza- 
tion to  the  right  by  the  grape-sugar).  Certainly  in  no  doubtful  case  should  we 
omit  to  perform  the  fermentation  test,  for  it  is  easy  and  gives  absolutely  unam- 
biguous results.  Further  particulars  in  regard  to  these  and  other  tests,  and  also 
in  regard  to  the  quantitative  estimation  of  sugar,  may  be  found  in  works  on 
medical  chemistry. 

Diabetic  urine  sometimes  contains  other  varieties  of  sugar  in  small  amounts 
— namely,  levulose,  which  deflects  the  plane  of  polarization  toward  the  left,  and 
inosite ;  these  are,  however,  of  no  practical  importance. 

The  amount  of  urea  is  usually  somewhat  increased  (vide  infra).  In  the  main, 
this  is  doubtless  connected  with  the  increased  ingestion  of  albumen,  but  in  severe 
cases  it  may  be  that  the  carbohydrates  are  so  imperfectly  appropriated  that  the 
albumen  of  the  body  is  broken  up  and  consequently  contributes  to  an  increase  in 
the  excretion  of  nitrogen.  Uric  acid  is  usually  excreted  in  approximately  nor- 
mal amounts.  In  exceptional  cases  it  also  seems  to  be  excreted  in  excess.  The 
amount  of  kreatinine  is  apt  to  be  increased  (Senator).  The  amount  of  phos- 
phoric acid  and  sulphuric  acid  usually  corresponds  to  the  amount  of  urea,  or,  in 
other  words,  to  the  decomposition  of  albuminoids.  Occasionally,  according  to 
Teissier,  the  amount  of  phosphates  is  surprisingly  great,  and  it  may  either  corre- 
spond with  the  amount  of  sugar  simultaneously  excreted,  or  replace  the  sugar  in 
the  urine.  This  subject  has  not  yet  been  fully  investigated.  The  amount  of  sodic 
chloride  excreted  depends,  as  in  health,  merely  upon  the  amount  ingested. 

Hallervorden  has  discovered  an  important  fact  in  regard  to  the  excretion  of 
ammonia.  In  many  cases  of  diabetes,  although  not  in  all,  it  is  much  increased: 
forty-five  to  ninety  grains  (grammes  3-6).  or  even  more,  may  be  excreted  in 
twenty-four  hours.  Despite  this,  diabetic  urine  has  an  acid  reaction;  and,  as 
Stadelmann  has  shown,  the  basic  elements  are  considerably  out  of  proportion  to 
48 


'Toi  CON'STITUTIOE'AL   DISEASES 

the  acids  known  to  us.  It  is,  therefore,  evident  that  diabetic  urine,  since  it 
contains  a  large  amount  of  ammonium  and  yet  has  an  acid  reaction,  must  hare 
among  its  constituents  some  unusual  acid.  The  later  investigations  of  Minkow- 
sky and  Kiilz  have  shown  that  the  acid  is  mainly  oxybutyric  acid,  or,  more  accu- 
rately, beta-oxj'butyric,  although  sometimes  still  other  acids  are  found  in  the 
urine,  particularly  volatile  fatty  acids  and  lactic  acid  (Eumpf).  The  oxybutyric 
acid  is  often  excreted  in  large  amounts,  up  to  two  or  three  ounces  (grammes  50— 
100)  daily.  It  is  traced  to  the  destruction  of  albumen,  and  usually  does  not 
appear  in  the  urine  until  the  patient  is  obliged,  because  of  the  imperfect  appro- 
priation of  carbohydrates,  to  use  the  albumen  of  the  body  instead  to  satisfy  the 
needs  of  the  economy.  The  appearance  of  oxybutyric  acid  in  the  urine  is,  there- 
fore, unfavorable  from  a  prognostic  point  of  view,  and  in  particular  it  indicates 
that  there  is  danger  of  diabetic  coma  (vide  infra). 

Oxybutyric  acid  is  probably  the  substance  from  which  are  derived  two  other 
organic  bodies  which  are  not  infrequently  found  in  the  urine  of  diabetes — ^viz., 
acetone  and  acet-acetic  acid.  These  substances  also  arise  from  the  destruction  of 
albumen — that  is,  the  body  albumen — so  that  they  are  seen  especially  in  severe 
cases  with  impaired  nutrition  (Van  Noorden).  Acetone  is  probably  developed 
from  acet-acetic  acid.  The  latter  is  the  cause  of  the  reaction  which  was  first 
demonstrated  by  Gerhardt,  which  consists  in  the  appearance  of  a  Burgundy-red 
color  on  the  addition  of  chloride  of  iron,  and  which  is  not  infrequently  to  be 
observed  in  diabetic  urine.  Acetone  is  shown  by  Legal's  test :  a  few  drops  of 
fresh  solution  of  nitro-prusside  of  sodium  are  mixed  with  the  urine,  and  then 
sodic  hydrate  is  added.  If  acetone  is  present  a  purple-red  color  appears,  [and 
persists,  even  if  acetic  acid  is  added  (excluding  kreatinine). — V.]. 

The  not  infrequent  occurrence  of  albumen  in  diabetic  urine  will  be  mentioned 
below,  when  considering  the  renal  complications. 

2.  Metabolism  in  Diabetes.  Sources  of  the  Sugar  and  Variations  in  its 
Amount  occasioned  by  External  Influences. — Inasmuch  as  the  presence  of  sugar 
in  the  urine  is  the  most  prominent  symptom  in  diabetes,  the  question  of  its 
origin  is  all-important.  One  fact  is  indubitable — namely,  that  the  secretion  of 
sugar  depends  in  large  part  upon  the  amount  of  potential  sugar  ingested — that  is, 
upon  the  proportion  of  starches  in  the  food.  The  amount  of  sugar  excreted  with 
the  urine  increases  and  diminishes  with  the  amount  of  starchy  food  eaten.  If 
a  diabetic  patient  abstains  totally  for  any  length  of  time  from  such  articles  of 
food  as  contain  starch,  sugar  will,  in  many  instances,  entirely  disappear  from  the 
urine.  In  other  words,  the  system  of  a  diabetic  patient  is  almost,  if  not  quite, 
incapable  of  oxidizing  sugar  into  carbonic-dioxide  gas  and  water.  Although, 
therefore,  in  a  diabetic  patient  the  absorption  of  oxygen  from  the  atmosphere 
goes  on  as  usual,  yet  there  always  remains  a  deficit  in  the  excretion  of  carbonic- 
dioxide  gas  and  water,  corresponding  to  that  portion  of  the  ingested  carbo- 
hydrates which  is  not  oxidized. 

The  oxidation  of  sugar  is  not  absolutely  nil  in  diabetes.  Kiilz  has  proved  by 
numerous  experiments  that  not  all  the  starch  is  excreted  in  the  form  of  sugar. 
In  severe  cases  of  diabetes  the  largest  part  of  the  ingested  sugar  is  excreted  as 
such,  unoxidized,  with  the  urine,  but  in  mild  cases  only  a  small  portion  is  thus 
excreted.  It  is,  therefore,  necessary  to  determine  the  degree  of  tolerance  for 
carbohydrates  in  every  individual  case  of  diabetes ;  even  in  the  same  patient  this 
tolerance  is  not  the  same  at  all  times.  Another  very  interesting  fact  was  dem- 
onstrated by  Kiilz.  The  diabetic  patient  has  lost  only  the  power  of  oxidizing 
that  kind  of  sugar  which  turns  the  plane  of  polarization  toward  the  ri^^;.  The 
sugar  which  turns  it  toward  the  left  (levulose),  inuline,  and  also  certain  other 
carbohydrates,  such  as  mannite  and  inosite,  are  broken  up  even  in  diabetic 
patients  in  very  large  part,  if  not  completely,  so  that  the  amount  of  sugar  ex- 


DIABETES   MELLITUS  ^55 

cieted  in  the  urine  is  but  little,  if  any,  increased  by  the  ingestion  of  these  sub- 
stances. 

Yet  the  carbohydrates  are  not  the  only  source  of  the  sugar  excreted  by  dia- 
betic patients.  In  many  cases,  although  not  in  all,  sugar  persists  in  the  urine 
even  when  the  patient  receives  a  dietary  absolutely  free  from  carbohydrates. 
In  such  instances,  there  can  be  no  doubt  that  the  glycogen,  or  the  sugar  which 
is  formed  out  of  it,  is  referable  to  the  albumen  of  the  food.  In  general,  we  may 
say  that  it  is  always  a  sign  of  a  severe  variety  of  diabetes  to  have  a  part  of  the 
sugar  which  is  formed  out  of  albumen,  when  carbohydrates  are  absolutely  ex- 
cluded from  the  diet,  excreted  unoxidized ;  while  it  is  a  proof  that  the  variety  is  a 
milder  one,  to  have  the  sugar  vanish  from  the  urine  when  the  patient  is  put  upon 
a  diet  which  contains  little,  if  any,  carbohydrates. 

Muscular  exertion  is  one  of  the  external  influences  which  modify  the  excre- 
tion of  sugar  in  diabetes.  According  to  our  present  views,  muscular  activity 
consumes  mainly  non-nitrogenous  substances,  and,  accordingly,  we  find  in  dia- 
betes that  an  increase  of  muscular  exertion,  other  things  being  equal,  diminishes 
the  amount  of  sugar  excreted. 

Emotional  excitement  is  said  to  increase  the  amount  of  sugar  excreted. 

Intercurrent  acute  febrile  diseases  may  cause  a  great  diminution  in  the 
amount  of  sugar,  but  sometimes  there  is  no  essential  change.  Probably  the 
altered  diet  of  the  patient  plays  an  important  part  in  this  connection,  although 
the  modifications  of  metabolism  occasioned  by  the  high  temperature  or  by  the  dis- 
ease itself  also  exert  some  influence.  Just  before  death  the  urine  may  become 
entirely  free  of  sugar. 

3.  Constitutional  Symptoms  in  Diabetes  Mellitus. — In  many  of  the  milder 
cases  there  is  for  a  long  time  little  apparent  disturbance  of  the  general  healths 
The  patient  is  well  nourished,  and  suffers  little  discomfort,  except  that  he  is 
rather  easily  fatigued,  and  somewhat  inconvenienced  by  the  polyuria  and  the 
polydipsia.  In  severer  cases  the  system  is  deeply  affected  by  the  drain  upon  it. 
The  patient  becomes  emaciated,  weak,  and  easily  exhausted,  and  at  length  there 
may  be  profound  marasmus.  Mentally,  the  patient  is  apt  to  be  depressed  and 
irritable.  The  intellectual  powers  are  not  impaired,  but  there  is  indisposition  to 
mental  effort.  The  temperature  is  normal  or  subnormal.  Fever  invariably  indi- 
cates some  complication. 

4.  Symptoms  referable  to  the  Digestive  Organs. — We  have  already  men- 
tioned the  excessive  thirst  experienced  in  diabetes.  This  may  be  a  source  of  great 
discomfort,  obliging  the  patient  to  drink  at  short  intervals,  even  through  the 
night.  The  interdependence  of  polyuria  and  polydipsia  is  not  yet  fully  under- 
stood. The  most  natural  view  seems  to  be  that  the  increased  excretion  of  water 
by  the  kidneys  is  the  primary  factor,  and  the  increased  thirst  secondary  thereto. 
One  cause  of  the  polyuria  is  the  excretion  of  sugar,  in  order  to  dissolve  which  a 
large  amount  of  water  is  necessary,  but  certain  nervous  factors  would  also  seem 
to  be  implicated.  That  they  exert  some  influence  is  rendered  probable  by  the  fact 
that  the  amount  of  urine  does  not  always  correspond  to  the  amount  of  sugar 
excreted.  A  very  large  amount  of  urine  may  be  excreted  containing  little  or  no 
sugar ;  and,  on  the  other  hand,  there  are  genuine  cases  of  diabetes  mellitus  where 
the  amount  of  urine  is  normal,  and  the  patient  feels  no  unusual  thirst  (diabetes 
decipiens).  It  has  also  been  suggested  that  the  sugar  may  irritate  the  nerves  of 
the  mouth  and  throat,  and  thus  cause  thirst.  According  to  this  idea,  the  polyuria 
would  be  partly  the  result  of  the  excessive  ingestion  of  liquids.  The  abnor- 
mally great  appetite  in  diabetes  seems  to  be  due  to  defective  assimilation  of  the 
food.  Many  patients  are  never  able  to  eat  enough.  They  have  a  longing,  in 
many  cases,  for  carbohydrates.  Occasionally  the  hunger  becomes  ravenous,  and 
is  associated  with  headache  and  a  general  sense  of  weakness,  all  these  symptoms 


756  COI^STITUTIO]!^AL   DISEASES 

being  alleviated  when  food  is  taken.  This  rule  has  rare  exceptions  in  which  the 
appetite  is  not  unusually  great,  even  though  the  case  be  severe. 

The  tongue  is  frequently  dry ;  it  is  broad  and  thick,  with  an  irregular  and  fis- 
sured surface,  sometimes  coated  and  sometimes  red.  The  gums  may  be  spongy, 
and  may  exhibit  a  tendency  to  bleed.  A  very  characteristic  condition  is  necrosis 
along  the  free  borders  of  the  gums,  probably  due  to  an  enfeeblement  of  the  resist- 
ing power  of  the  tissues.  This  is  particularly  apt  to  lead  to  a  gradual  loosening 
of  the  incisors,  so  that  at  last  they  drop  out.  The  teeth  frequently  decay  rapidly. 
The  saliva  is  invariably  found  to  give  an  acid  reaction.  This  is  true  of  the  isolated 
secretion  of  the  parotid  gland  also,  and  is  said  to  be  due  to  the  presence  of  lactic 
acid.  It  is  only  in  exceptional  instances  that  sugar  can  be  demonstrated  in  the 
saliva.    In  severe  cases  thrush  sometimes  forms  upon  the  soft  palate. 

Special  gastric  symptoms  are  usually  absent.  There  may  be  a  dilatation  of 
the  stomach,  due  to  the  great  quantity  of  food  ingested,  but  this  has  no  practical 
importance.  If  disease  of  the  stomach  does  develop  (e.  g.,  chronic  gastritis)  the 
complication  is  an  unfavorable  one.  There  is  usually  constipation,  but  some- 
times there  is  a  severe,  though  temporary,  diarrhoea.  The  liver  and  spleen  are 
seldom  much  affected;  the  liver  rarely  is  somewhat  enlarged.  Jaundice  is  fre- 
quently observed,  but  it  is  always  referable  to  some  complication.  As  a  rule, 
the  secretion  of  the  bile  goes  on  as  in  health.  After  death,  we  may  find  atrophy 
of  the  pancreas  (vide  infra). 

5.  Symptoms  referable  to  the  Respiratory  Organs. — ^In  many  cases  the  or- 
gans of  respiration  are  unimpaired  for  a  long  while.  It  may  be  mentioned  that 
often  patients  have  a  decidedly  fruity  odor  to  the  breath  (acetone  odor).  In  the 
later  stages  of  the  disease  pulmonary  complications  are  very  frequent.  First  in 
importance  is  tuberculosis  of  the  lungs.  This  is  particularly  apt  to  occur  in  the 
severe  forms  of  diabetes  in  youth,  and  it  may  pursue  a  rapid  and  fatal  course. 
The  diagnosis  can  be  settled  by  the  discovery  of  tubercle  bacilli  in  the  sputum. 
Next  in  point  of  frequency  is  pulmonary  gangrene.  Sometimes  there  is  a  diifuse 
gangrenous  process,  and  sometimes  there  are  isolated  foci  of  necrosis,  which  be- 
come liquid,  and  have  an  acid  reaction,  but  they  often  have  comparatively  little 
odor.  The  expectoration  in  these  cases  may  be  odorless.  Croupous  pneumonia 
may  also  occur.  It  often  terminates  unfavorably,  and  may,  as  we  have  ourselves 
observed,  result  in  gangrene. 

6.  Symptoms  referable  to  the  Circulatory  System. — In  many  instances  the 
circulatory  apparatus  presents  no  special  lesions.  The  pulse  is  either  of  a  nor- 
mal rate  or  a  trifle  slow.  It  is  usually  soft,  although  exceptionally  it  may  exhibit 
increased  tension.  There  is  often  distinct  evidence  of  cardiac  weakness 
(Schmitz) ;  the  pulse  is  small,  intermittent,  sometimes  very  slow  (50  or  even  40 
beats  per  minute),  and  sometimes  accelerated  (100  to  120  beats  per  minute). 
There  are  shortness  of  breath,  faintness,  nausea,  and  the  like.  Sometimes  sudden 
and  profound  cardiac  disturbance  occurs,  and  this  may  occasion  speedy  death 
(vide  infra,  coma).  N'ot  infrequently,  diabetes  is  combined  with  general  arterio- 
sclerosis (vide  infra). 

7.  Genito-urinary  Symptoms. — Despite  the  great  demands  made  upon  them, 
the  kidneys  often  maintain  a  normal  condition.  As  we  shall  see  when  we  come 
to  the  pathological  anatomy  of  diabetes,  the  kidneys  are  often  very  large.  Some- 
times a  chronic  nephritis  is  developed  as  a  complication,  usually  in  the  later 
stages  of  the  disease.  The  urine  contains  albumen,  and  there  are  oedema  and 
other  symptoms  of  renal  disorder.  The  cause  of  albuminuria  in  diabetes  does  not 
seem  to  be  the  same  in  every  case;  sometimes  it  is  due  to  changes  in  the  kidneys 
resulting  from  the  persistent  excretion  of  abnormal  urinary  constituents.  In 
this  connection  we  must  think,  not  only  of  the  sugar,  but  also  of  the  other  sub- 
stances— such   as   acetone,   diacetic   acid,   and   oxybutyric   acid — which,   as   they 


DIABETES   MELLITUS  757 

traverse  the  kidneys,  damage  the  renal  epithelium.  In  other  cases,  diabetes  and 
nephritis  seem  to  be  simultaneous  and  co-ordinate  results  of  the  same  cause,  such, 
as  arterio-sclerosis  or  alcoholism.  Finally,  it  must  not  be  forgotten  that  other 
complications  of  diabetes — e.  g.,  pulmonary  tuberculosis — may  promote  the  devel- 
opment of  nephritis.  It  is  an  interesting  fact  that  in  diabetes,  glycosuria  and 
albuminuria  may  to  a  certain  extent  alternate  with  each  other.  If  the  amount 
of  albumen  in  the  urine  becomes  considerable,  the  excretion  of  sugar  usually 
undergoes  marked  diminution.  Many  physicians  therefore  consider  the  transi- 
tion of  diabetes  into  chronic  renal  disease  (contracted  kidney)  as  a  comparatively 
favorable  symptom. 

Saccharine  urine  is  apt,  as  it  decomposes,  to  cause  irritation  of  the  skin  (de- 
velopment of  fungi).  This  is  the  explanation  of  the  troublesome  pruritus  pudendi, 
•which  is  especially  marked  in  women.  It  may,  indeed,  be  this  symptom  which 
first  directs  attention  to  the  disease.  Sometimes  the  external  genitals  are  at- 
tacked by  eczema  or  furunculosis.  Men  often  suffer  from  balanitis,  with  inflam- 
matory phimosis,  or  paraphimosis.  A  frequent  and  important  symptom  in  men  is 
impotence.  This  sometimes  occurs  very  early  in  the  disease,  but  it  may  afterward 
undergo  improvement.  The  origin  of  it  is  probably  referable  to  degenerative 
changes  in  the  nervous  system  (vide  infra).  Some  authorities  state  that  diabetes 
is  apt  to  occasion  atrophy  of  the  testicles. 

8.  Disturbances  op  the  Organs  of  Special  Sense. — An  important  and  not 
infrequent  result  of  diabetes  is  cataract.  This  may  occasion  almost  total  blind- 
ness. The  cause  of  cataract  in  diabetes  is  not  known.  It  was  formerly  supposed 
that  the  sugar  in  the  blood  absorbed  water  from  the  crystalline  lens,  and  thus 
occasioned  its  opacity;  but  this  has  not  been  confirmed.  Diabetic  patients  are 
subject  to  disturbances  of  accommodation.  Eetinitis  and  atrophy  of  the  optic 
nerve  may  occur,  but  they  are  very  rare.  Purulent  choroiditis,  if  it  develops, 
is  probably  merely  a  chance  complication. 

l^one  of  the  other  special  senses  is  peculiarly  affected  in  diabetes. 

9.  Cutaneous  Affections. — In  most  cases  the  skin  is  remarkably  dry  and 
rough.  There  may,  however,  be  abundant  perspiration.  Several  authorities  claim 
to  have  found  sugar  in  the  perspiration,  but  this  statement  has  not  been  confirmed 
by  later  investigators.  Sometimes  there  is  a  troublesome  pruritus.  We  often  see 
a  rapid  loss  of  hair  and  a  shedding  of  the  nails.  In  many  cases  there  is  a  great 
tendency  to  furunculosis.  This  may  be  the  first  symptom  to  suggest  the  existence 
of  diabetes.  In  the  later  stages  there  are  sometimes  extensive  carbuncles,  and 
multiple  phlegmonous  abscesses  in  the  subcutaneous  cellular  tissue,  which  may 
prove  fatal.  Bacteriological  examinations  of  all  these  processes  have  not  yet  been 
made,  so  far  as  we  know.  Probably  they  are  complications,  like  the  frequent 
occurrence  of  pulmonary  tuberculosis  in  diabetes.  Occasionally  we  have  seen 
a  pemphigus-like  eruption  on  the  skin.  This,  in  one  case,  developed  into  a  local- 
ized gangrene.  Gangrenous  processes  have  been  repeatedly  observed,  in  par- 
ticular necrosis  of  one  or  more  toes,  which  may  take  the  form  of  perforating 
ulcer  (mal  perforani),  or  rarely  of  an  entire  extremity.  This  gangrene  often 
seems  to  be  due  to  arterial  sclerosis;  in  other  cases  its  cause  is  obscure.  The 
gangrene  of  the  toes  may  be  apparently  the  first  symptom  of  the  disease,  and  it 
may  be  very  slight.  It  is  not  until  all  therapeutic  and  operative  procedures  prove 
unavailing  that  suspicion  is  aroused,  leading  to  the  discovery  of  diabetes.  We 
have  often  seen  cases  of  this  sort,  which  usually  turn  out  badly,  in  obese  drinkers. 

(Edema  of  the  subcutaneous  cellular  tissue  may  occur  independently  of  nephri- 
tis.   It  is  then  probably  occasioned  by  the  cardiac  weakness. 

10.  Symptoms  referable  to  the  Nervous  System. — It  has  already  been  men- 
tioned that  there  is  frequently  in  diabetes  a  moderate  disturbance  of  the  whole 
nervous  system,  as  indicated  by  headache,  physical  and  mental  hebetude,  and 


T58  CONSTITUTIONAL   DISEASES 

depression  of  spirits.  There  are,  besides,  a  number  of  nervous  complications  which 
are  probably  referable  to  the  irritative  or  degenerative  effects  upon  certain  nerve 
areas  of  the  abnormal  products  of  metabolism  formed  in  diabetes.  This  is  the 
explanation  of  the  comparatively  frequent  appearance  of  neuralgia,  most  often 
in  the  form  of  sciatica.  This  is  probably  due  to  neuritis  of  the  nerve.  Bilateral 
sciatica  may  be  one  of  the  first  symptoms  of  the  disease,  and  a  very  obstinate  one. 
We  also  meet  with  occipital  neuralgia,  facial  neuralgia,  and  pain  resembling 
hemicrania.  Sometimes,  also,  we  observe  localized  anaesthesia  of  the  skin  and  pe- 
ripheral palsies.  These  are  probably  due  to  degenerative  changes  in  the  peripheral 
nerves.  We  have  ourselves  seen,  in  one  case,  paralysis  of  the  peroneal  nerve,  due 
to  peripheral  neuritis.  Another  Symptom  which  should  be  grouped  with  those 
just  considered,  is  one  which  was  first  pointed  out  by  Bouchardat — viz.,  the  com- 
paratively frequent  abolition  of  the  patellar  reflex  in  diabetes.  It  should  be  said, 
however,  that  we  have  repeatedly  seen  cases,  of  the  most  severe  form,  in  which  the 
knee-jerk  remained  perfectly  normal.  If  the  reader  will  imagine  a  case  in  which 
absence  of  the  knee-jerk  is  associated  with  neuritic  pains  in  the  legs,  he  will 
understand  the  reason  for  the  term  "  diabetic  pseudo-tabes."  The  pathological 
basis  of  the  symptoms  just  enumerated  has  been  repeatedly  shown  to  be  neuritic 
degeneration.  In  some  few  cases  there  may  even  be  slight  changes  in  the  poste- 
rior columns  of  the  spinal  cord,  perhaps  of  toxic  origin. 

The  most  important  nervous  symptom  of  all  is  a  peculiar  disturbance  which 
occurs  in  a  considerable  proportion  of  all  cases  with  more  or  less  suddenness,  and 
usually  terminates  in  a  surprisingly  speedy  death.  This  strange  phenomenon 
was  first  thoroughly  investigated  by  Kussmaul,  although  known  long  before.  It 
is  termed  diabetic  coma.  The  condition  sometimes  develops  without  any  evident 
cause.  In  other  instances  it  is  apparently  brought  on  by  violent  muscular  exer- 
tion, mental  excitement,  or  some  trifling  illness,  such  as  gastric  catarrh,  bron- 
chitis, or  sore  throat. 

Frequently  certain  mild  prodromata  herald  its  onset.  There  may  be  nausea, 
headache,  a  sense  of  thoracic  oppression,  and  general  uneasiness.  Soon  the  con- 
dition becomes  aggravated.  The  patient  is  seized  with  a  feeling  of  great  anxiety, 
and  becomes  delirious,  sometimes  jumping  out  of  bed  and  growing  uncontrol- 
lable. Gradually,  however,  the  excitement  gives  place  to  an  ever-increasing 
drowsiness,  usually  terminating  in  the  most  profound  coma.  One  of  the  most 
frequent  and  striking  symptoms  attending  this  condition  is  the  peculiar  alteration 
in  respiration.  The  breathing  becomes  remarkably  deep  and  noisy.  Its  rate  may 
remain  nearly  normal;  or  it  may  be  considerably  increased,  so  as  to  justify  the 
term  "  diabetic  dyspnoea."  The  patient  is  sometimes  cyanotic.  The  pulse  is  usu- 
ally very  rapid  and  small.  The  temperature  gradually  sinks,  and  has  in  repeated 
instances  fallen  to  86°  (30°  C),  or  even  lower.  In  most  instances,  also,  the 
breath  has  a  very  noticeable  odor,  resembling  fruit  or  chloroform,  which  may  be 
perceived  on  entering  the  room.  Even  the  urine  may  have  this  same  odor;  and 
it  almost  invariably  becomes  dark  red  on  the  addition  of  ferric  chloride,  and 
gives  a  distinct  acetone  reaction  (vide  supra). 

Diabetic  coma  does  not  pursue  the  same  course  in  all  cases;  sometimes  the 
patient  lingers  on  for  several  days  before  death,  while  in  other  instances  the 
change  is  extremely  rapid  and  death  speedy.  The  early  stage  of  excitement 
may  be  wanting.  The  patient  becomes  somnolent  and  then  speedily  comatose, 
and  never  regains  consciousness.  Temporary  improvement,  and  even  complete 
cessation  of  the  threatening  symptoms,  are  not  impossible,  but  they  are. very 
exceptional. 

As  to  the  cause  of  diabetic  coma,  the  results  of  recent  investigations  are  in- 
teresting, although  they  do  not  explain  everything.  Of  course  the  cases  where 
an  autopsy  discloses  some  marked  organic  lesion,  such  as  cerebral  haemorrhage. 


DIABETES   MELLITUS  T59 

capable  of  producing  the  nervous  symptoms,  are  not  true  diabetic  coma.  !N'or 
do  the  cases  of  sudden  death  reported  by  Ererichs  deserve  to  be  classed  as  diabetic 
coma,  where  death  occurred  with  the  symptoms  of  acute  cardiac  failure — ^namely, 
collapse,  coolness  of  the  extremities,  small  and  rapid  pulse,  and  unconsciousness. 
Besides,  these  patients  never  have  the  acetone  odor,  the  exaggerated  respiration, 
nor  the  ferric-chloride  reaction,  and  usually  the  myocardium  is  found  to  be  in 
an  advanced  state  of  degeneration. 

In  genuine  diabetic  coma,  on  the  other  hand,  everything  seems  to  indicate 
that  the  system  has  been  poisoned  by  some  noxious  product  of  abnormal  metabo- 
lism. Great  effort  has  been  made  to  discover  what  this  product  is,  but  with  im- 
perfect success.  Kussmaul  regarded  acetone  as  the  injurious  substance,  and 
therefore  called  diabetic  coma  "  acetonaemia."  Other  investigators  believe  that 
acet-acetic  acid  (Jaksch)  is  the  cause  of  the  phenomenon  in  question,,  or  at  least 
regard  the  coma  as  a  result  of  poisoning  from  some  of  the  unusual  acids  present 
in  diabetes  (Stadelmann,  vide  supra).  JSTo  one  view  has  obtained  general  accept- 
ance, nor  has  it  been  possible  to  produce  diabetic  coma  in  animals  by  the  employ- 
ment of  acetone,  acet-acetic  acid,  crotonic  acid,  or  similar  substances  (Brieger 
and  others).  It  is,  nevertheless,  extremely  probable  that  these  substances  do  have 
some  close  connection  with  "  diabetic  intoxication  "  (Ererichs).  Ear  more  proba- 
bility attaches  to  the  theory  which  was  advocated  first  by  Stadelmann  and  then  by 
Minkowsky,  according  to  which  diabetic  coma  is  the  result  of  an  "  acid  intoxi- 
cation." There  is  no  doubt  that,  as  we  have  already  stated,  in  diabetes  there 
is  a  formation  of  abnormal  acids,  particularly  oxybutyric  acid.  If  these  acids 
accumulate  in  the  blood,  they  neutralize  its  alkalies,  so  that  it  loses  its  capacity 
of  combining  with  the  carbonic  acid  formed  in  the  tissues,  and  carrying  it  away. 
Certainly  the  symptoms  of  diabetic  coma  bear  a  great  resemblance  to  the  phe- 
nomena which  have  been  observed  in  animals  when  poisoned  by  acids — viz., 
stupor,  dyspnoea,  diminution  of  the  amount  of  carbonic  dioxide  in  the  blood,  and 
increase  in  the  excretion  of  ammonium  in  the  urine  (vide  supra).  The  blood  of 
patients  who  die  in  diabetic  coma  contains  large  amounts  of  oxybutyric  and 
sarcolactic  acids. 

11.  Changes  in  the  Lymph-glands. — There  may  be  extensive  and  distinct 
swelling  of  the  lymph-glands,  particularly  in  severe  cases  of  diabetes.  The  glands 
are  hard  and  insensitive. 

Pathological  Anatomy  and  Histochemistry  of  Diabetes  Mellitus. — If  we  ex- 
clude the  organic  diseases,  such  as  pulmonary  tuberculosis  and  nephritis,  which 
are  merely  complications,  the  pathological  changes  in  diabetes  are  trifling.  Ber- 
nard's  discovery,  that  an  injury  inflicted  in  a  certain  spot  on  the  floor  of  the 
fourth  ventricle  produces  glycosuria  in  animals,  has  directed  the  attention  of  in- 
vestigators to  the  condition  of  the  nervous  system  in  this  disease.  In  some  in- 
stances, tumors,  sclerosis,  or  similar  troubles  have  been  found  in  the  medulla  and 
cerebellum;  but  in  these  cases  there  was  evidently  a  symptomatic  glycosuria  and 
not  an  idiopathic  diabetes  (vide  supra).  In  idiopathic  cases  the  central  nervous 
system  presents  no  striking  macroscopic  changes.  By  means  of  the  microscope, 
Ererichs  has  found  lesions  of  the  medulla  oblongata  in  frequent  instances.  The 
minute  blood-vessels  are  widely  dilated;  there  are  small  capillary  hfemorrhages, 
some  of  a  more  recent  and  others  of  a  more  remote  date;  and  occasionally  there 
are  microscopic  foci  of  myelitis.  The  nervous  elements  proper,  the  nerve-fibers 
and  ganglion  cells,  betray  no  alteration ;  and  as  the  changes  enumerated  are  not 
invariably  present,  their  significance  is  dubious. 

The  stomach  and  intestines  present  no  constant  alterations  of  importance. 

The  liver  has  naturally  been  the  object  of  repeated  and  careful  examinations, 
because  of  its  well-known  part  in  the  manufacture  of  glycogen.  Yet  this  organ 
seldom  presents  any  special  abnormality.    It  is  usually  of  the  natural  size,  and 


760  CO:t^STITUTIOXAL   DISEASES 

it  may  contain  either  considerable  or  very  little  blood.  The  amount  of  glycogen  in 
the  hepatic  cells  can  be  demonstrated  with  iodine  by  a  micro-chemical  reaction. 
It  appears  that,  other  things  being  equal,  there  is  less  glycogen  present  than 
normal.  It  is  usually  found  only  in  the  cells  situated  upon  the  periphery  of  the 
lobules,  and  in  small  quantities.  In  an  extremely  advanced  case  of  diabetes 
Ehrlich  obtained,  by  means  of  a  hollow  needle,  small  amounts  of  the  hepatic 
parenchyma  for  examination  during  life,  and  found  that  glycogen  was  almost 
completely  absent.  In  other  cases  the  liver  has  been  examined  as  early  as  possi- 
ble after  death,  and,  with  rare  exceptions,  has  presented  no  trace  of  glycogen. 

The  spleen  is  usually  of  normal  size.  Occasionallj^  it  is  atrophied,  or,  on  the 
other  hand,  slightly  enlarged.    'No  other  changes  in  it  have  been  observed. 

Wot  a  few  cases  have  presented  a  striking  atrophy  of  the  pancreas  (Bouchar- 
dat),  a  fact  which  has  acquired  great  significance  from  Minkowsky's  discovery, 
already  mentioned,  that  glycosuria  may  come  on  after  extirpation  of  the  pancreas. 
It  is  uncertain  whether  the  coeliac  plexus  may  also  sometimes  share  in  the 
atrophy  of  the  pancreas.  We  must  also  state,  however,  that  atrophy  of  the  pan- 
creas is  not  at  all  a  constant  lesion  in  diabetes,  so  that  it  is  not  proper  to  regard 
the  disease  of  the  pancreas  as  the  special  cause  of  diabetes  in  all  cases.  Lately  in 
repeated  instances  the  pancreas  has  been  found  perfectly  normal,  even  upon  the 
most  careful  microscopic  examination. 

The  kidneys  are  usually  enlarged,  from  functional  hypertrophy.  Ehrlich  dis- 
covered in  them  a  glycogenic  degeneration  of  the  loops  of  Henle.  The  epithelial 
cells  in  the  loops  are  enlarged,  and  the  protoplasm  in  these  cells,  although  appar- 
ently homogeneous,  is  found,  by  the  addition  of  a  solution  of  iodine  in  mucilage, 
to  contain  glycogen,  in  flakes  and  clumps  of  varying  size.  How  important  this 
glycogenic  degeneration  of  the  kidneys  may  be  has  not  yet  been  determined. 
Perhaps  the  glycogen  represents  sugar  which  has  been  absorbed  by  the  cells. 
That  chronic  nephritis  may  complicate  diabetes  has  already  been  mentioned. 

No  thorough  investigation  of  the  chemical  composition  of  the  blood  in  diabetes 
has  yet  been  made.  One  fundamental  and  constant  characteristic  is  the  greatly 
increased  proportion  of  sugar  in  the  blood.  There  is  usually  somewhere  between 
0.2  and  0.45  per  cent,  of  sugar,  while  in  health  the  blood  rarely  contains  over  0.1 
per  cent.  The  lymph,  and  such  serous  effusions  as  are  found,  contain  sugar,  but 
the  saliva,  perspiration,  bile,  gastric  juice,  and  other  secretions  rarely  furnish  evi- 
dence of  its  existence. 

Varieties,  Course,  and  Prognosis  of  the  Disease. — The  study  of  a  large  num- 
ber of  cases  of  diabetes  will  show  great  variations  in  the  course  and  duration  of 
the  disease.  As  already  stated,  we  may  in  practice  distinguish  between  mild 
and  severe  forms  of  diabetes.  Following  Seegen's  suggestion,  this  division  is 
usually  based  upon  the  relation  between  the  sugar  excreted  and  the  character 
and  amount  of  the  food  eaten.  Those  cases  are  regarded  as  belonging  to  the  mild 
form  in  which  the  sugar  disappears  from  the  urine  when  the  patient  takes  food 
containing  no  carbohydrates.  Some  patients  with  this  milder  form  may  ingest 
small  amounts  of  the  amylacea,  particularly  if  they  take  a  proper  amount  of 
physical  exercise  (vide  infra),  without  bringing  on  glycosuria.  In  the  severe 
form  of  diabetes,  on  the  other  hand,  the  excretion  of  sugar  in  the  urine  persists 
even  on  a  purely  meat  diet,  and  if  any  carbohydrates  are  taken,  there  will  be  a 
corresponding  and  large  increase  in  the  amount  of  sugar  in  the  urine,  as  soon  as 
half  an  hour  to  an  hour  thereafter.  Of  almost  gTcater  practical  importance  are 
the  clinical  signs  which  sometimes  indicate,  at  the  first  glance,  that  an  individual 
suffers  from  the  mild  or  the  severe  form,  as  the  case  may  be.  The  severe  cases 
usually  attack  youthful  individuals ;  the  patient  loses  flesh  rapidly,  his  face 
becomes  narrow,  and  is  apt  to  assume  a  peculiar  expression  of  quiet  melancholy; 
he  is  languid  and  feeble,  and  the  urine  presents  all  the  indications  of  diabetes  in 


DIABETES   MELLITUS  Y61 

an  extreme  degree.  The  milder  cases,  on  the  other  hand,  are  more  apt  to  occur  in 
later  life,  the  patient  has  only  moderate  discomfort,  and  usually  retains  consid- 
erable strength  and  energy;  he  is' but  little,  if  at  all,  emaciated,  and  even  the 
changes  in  the  urine  are  so  slight  that  they  are  not  recognized  until  the  attention 
is  especially  directed  to  them.  It  must  be  noted,  however,  that  an  apparently 
mild  case  of  diabetes  may  become  severe.  Sometimes,  also,  the  behavior  of  the 
case  as  to  the  excretion  of  sugar  remains  like  that  of  the  mild  variety,  and  still, 
fatal  complications  occur  at  last,  such  as  coma,  necrotic  processes,  and  pulmonary 
tuberculosis. 

In  general,  the  clinical  course  of  diabetes  presents  great  variations.  In  a  few 
instances  the  disease  occupies  only  a  few  weeks,  and  it  may  almost  be  termed 
"  acute  diabetes."  Other  cases  last  one  or  two  years,  and  still  others  ten  or 
twenty  years.  The  patient's  condition  may  vary  from  time  to  time.  We  have 
repeatedly  seen  the  sugar  disappear  temporarily  from  the  urine,  and  the  patient 
apparently  completely  recover;  but  sooner  or  later  the  disease  breaks  out  again. 
These  cases,  which  are  commoner  in  old  people,  have  been  called  "  intermittent 
diabetes."  The  relapse  is  often  brought  about  by  emotional  excitement  or  some 
grave  error  in  diet.  Again,  the  disease  may  become  apparently  stationary  and 
the  patient  enjoj^  comparative  comfort  for  years. 

Different  cases  also  differ  in  the  relative  severity  of  particular  symptoms. 
Thus,  the  clinical  picture  presented  by  diabetes  may  be  modified  by  the  general 
constitution  of  the  patient — for  instance,  his  corpulence  or  emaciation;  by  such 
complications  as  diseases  of  the  lungs,  kidneys,  or  brain,  or  syphilis  and  gout; 
and  by  many  other  conditions.  In  practice,  especially  in  practice  among  the 
better  classes,  it  is  very  im^portant  to  have  a  knowledge  of  the  milder  forms  of 
diabetes,  in  which  sugar  is  present  in  the  urine  only  at  times,  and  not  in  very 
large  amount.  The  more  we  are  accustomed  to  examine  every  urine  for  sugar 
the  oftener  we  find  such  cases,  as  to  the  significance  of  which  our  knowledge  is 
still  very  slight.  The  glycosuria  of  the  corpulent  is  worthy  of  special  considera- 
tion. It  is,  as  we  have  said,  particularly  apt  to  occur  in  obese  beer-drinkers,  and 
it  is  not  uncommon  in  patients  who  have  formerly  suffered  from  true  gout.  The 
tendency  to  the  formation  of  furuncles  and  cataract  is  noteworthy.  We  must  also 
mention  the  cases  of  diabetes  in  neurasthenics — that  is,  cases  where  there  is 
sugar  in  the  urine,  and  where  the  chief  complaint  is  of  general  nervous  symptoms, 
pressure  in  the  head,  anxiety,  a  dull  feeling,  incapacity  for  mental  work,  neural- 
gic pains,  etc.  In  such  cases  glycosuria  has  not  at  all  the  serious  significance  that 
it  has  in  genuine  and  severe  diabetes.  Finally,  we  would  point  out  an  especial 
clinical  form  of  diabetes,  in  which  glycosuria  occurs  in  patients  with  severe  gen- 
eral arterio-sclerosis ;  usually  the  patients  are  men  in  middle  or  advanced  life. 
l^ot  infrequently  the  condition  seems  referable  to  long-continued  mental  excite- 
ment or  exertion.  The  amount  of  sugar  in  the  urine  is  not  large,  and  the  sugar 
usually  entirely  disappears  with  appropriate  diet ;  still,  this  form  can  not  be  un- 
qualifiedly regarded  as  mild,  for  we  must  bear  in  mind,  also,  the  serious  results  of 
arterio-sclerosis.  There  are  particularly  apt  to  be  cardiac  symptoms  referable  to 
arterio-sclerosis  of  the  coronary  arteries.  In  all  these  "  mild  "  varieties  of  dia- 
betes there  may  be  no  polyuria  or  thirst,  so  that  an  error  in  diagnosis  is  easy 
unless  a  careful  examination  of  the  urine  is  made. 

We  should  also  mention  the  interesting  fact,  of  which  Frerichs  reports  some 
striking  examples,  that  diabetes  mellitus  in  a  few  exceptional  cases  may  gradu- 
ally change  into  diabetes  insipidus  (see  the  following  chapter).  The  reverse 
change  is  also  said  to  occur. 

The  usual  termination  of  diabetes  is  death.  We  have  already  seen  how  great 
a  difference  there  may  be  in  the  length  of  time  preceding  the  fatal  termination, 
and  in  what  various  ways  it  may  be  brought  about.    The  most  frequent  immediate 


762  CONSTITUTIOl^AL  DISEASES 

causes  of  death  are  marasmus,  diabetic  coma,  pulmonary  consumption,  nepliritis, 
furunculosis,  or  tlie  development  of  carbuncles. 

There  is  no  doubt  that  complete  recovery  may  occur ;  but  this  is  rare,  and  is 
possible  only  in  the  milder  cases.  It  should  also  be  borne  in  mind  that,  as  we 
have  said,  apparent  recovery  does  not  exclude  the  possibility  of  a  fresh  outbreak 
of  the  disease. 

Theoretical  Discussion  of  the  Nature  of  Diabetes. — ^We  have  endeavored  to 
give  an  approximately  complete  summary  of  the  facts  pertaining  to  diabetes.  We 
trust  we  shall  be  excused  from  detailing  all  the  theories  and  hypotheses  which 
have  been  devised  to  explain  the  peculiar  phenomena  of  the  disease,  particularly 
the  glycosuria.  It  is  a  better  way  simply  to  confess  that  the  true  nature  of  dia- 
betes mellitus  as  yet  remains  very  obscure.  We  shall  confine  ourselves  to  a  few 
remarks  upon  the  present  state  of  the  question. 

The  essential  fact  which  demands  explanation  is  the  excess  of  sugar  in  the 
blood.  The  blood  of  a  healthy  man  does  not  contain  over  0.15  per  cent,  of  sugar, 
while  that  of  a  diabetic  has  0.22-0.44  per  cent.  The  source  of  this  sugar  is  prob- 
ably the  same  as  of  the  sugar  normally  contained  in  the  blood.  The  largest  part 
of  the  sugar  probably  comes  from  the  carbohydrates  ingested  as  food.  These 
are,  for  the  most  part,  converted  in  the  primas  vise,  into  sugar,  which  sugar 
thereupon  enters  the  portal  system.  It  may  also  be  assumed  that  glycogen,  so 
widely  diffused  throughout  the  system,  is  another  source  of  sugar.  The  liver  is 
the  main  seat  of  the  manufacture  of  glycogen;  but  it  is  produced  in  other  parts 
as  well,  and  in  particular  in  the  muscles.  The  question  next  arises,  From  what 
is  the  glycogen  formed?  A  part  of  it  is  manufactured  from  the  carbohydrates 
contained  in  the  food,  but  another  part  is  certainly  due  to  the  ingested  albu- 
minoids. Thus,  Yon  Mehring  found  that  in  fasting  animals,  who  have  no 
more  glycogen  stored  up  in  the  body,  diabetes  may  be  produced  by  giving  phlorid- 
zine  (vide  supra).  The  sugar  excreted  can  therefore  come  only  from  the  de- 
struction of  albumen  in  the  body.  Again,  the  transformation  of  glycogen  into 
sugar  is  not  confined  to  the  liver,  but  it  may  take  place  wherever  glycogen  is  pro- 
duced. How  it  takes  place  is  unknown.  It  is  usually  assumed  that  there  is  some 
"  saccharific  ferment." 

It  would  seem,  therefore,  that  the  sources  of  sugar  are  the  same  in  diabetes  as 
in  health.  We  have  next  to  seek  for  the  reason  of  its  excessive  accumulation  in 
the  blood.  Under  normal  circumstances,  the  sugar  present  in  that  fluid  rapidly 
undergoes  decomposition  into  other  substances.  In  health  there  is  no  great 
excess  of  sugar  in  the  blood,  even  upon  a  diet  extremely  rich  in  starch;  and  it  is 
possible  to  eat  large  amounts  of  sugar  without  any  glycosuria.  That  changes  in 
the  secretory  action  of  the  kidneys  are  not  the  cause  of  the  excretion  of  the  sugar, 
is  evident  from  the  fact  that  in  diabetes  insipidus  no  glycosuria  occurs  even  if  a 
large  amount  of  sugar  is  ingested  (Frerichs).  We  see,  therefore,  that  diabetes 
can  not  be  explained  by  assuming  that  there  is  an  increased  production  of  sugar, 
nor  in  fact  is  there  such  an  increase,  except  as  corresponds  to  the  increased 
amount  of  ingesta.  On  the  other  hand,  everything  points  toward  the  conclusion 
that  in  diabetes  the  ordinary  processes  effecting  the  decomposition  and  destruction 
of  sugar  are  suspended.  The  sugar  is  excreted  by  the  kidneys  unaltered,  for  the 
reason  that  it  is  not  destroyed.  It  is  difficult  to  conjecture  what  the  circum- 
stances may  be  which  thus  interfere  with  the  decomposition  of  the  sugar.  Per- 
haps it  is  some  special  nervous  influence,  or  perhaps  some  ferment  may  be  want- 
ing in  diabetes  which  in  health  promotes  the  metamorphosis  of  the  sugar.  This 
latter  supposition  is  rendered  the  more  probable  by  the  above-mentioned  experi- 
ments of  Von  Mehring  and  Minkowsky.  Lepine  also,  having  repeated  these  ex- 
periments, has  reached  the  conclusion  that  the  blood,  under  normal  conditions, 
receives  directly  from  the  pancreas  a  "  glycolytic  "  ferment  which  decomposes 


DIABETES   MELLITUS  763 

sugar.  In  a  diabetic  subject  this  glycolytic  function  of  the  blood  is  supposed  to  be 
much  impaired,  because  the  blood  is  deprived  of  this  ferment,  and  as  a  conse- 
quence sugar  is  excreted  unchanged;  but  this  explanation  has  been  disputed, 
so  that  really  the  question  as  to  the  true  cause  of  diabetes  remains  absolutely 
unsettled. 

Diagnosis. — For  the  diagnosis  of  diabetes  mellitus  it  is  indispensable  that 
sugar  should  be  demonstrated  in  the  urine.  We  have  also  to  decide  whether  the 
condition  be  a  temporary  or  a  permanent  one,  or,  in  other  words,  whether  we 
have  to  deal  with  mere  glycosuria  (vide  supra)  or  genuine  diabetes  mellitus. 
This  point  is  to  be  determined  by  means  of  the  symptoms  and  general  course  of 
the  disease. 

Diabetes  often  exists  for  some  time  unsuspected  even  by  the  physician.  It 
may  therefore  be  well  to  name  over  the  symptoms  which  may  be  the  first  to 
attract  the  patient's  attention,  and  which  should  therefore  always  suggest  to  a 
physician  the  possibility  of  the  existence  of  diabetes.  They  are :  1,  languor  and 
debility;  2,  f urunculosis ;  3,  pruritus  pudendi  in  women,  balanitis  in  men;  4, 
cataract;  5,  sciatica,  especially  if  bilateral;  6,  impotence.  We  should  be  in  the 
habit  of  examining  the  urine  for  sugar  in  all  cases  when  complaint  is  made  of 
indefinite  symptoms,  which  can  not  be  explained  without  further  evidence,  espe- 
cially if  the  patient  is  fat  or  nervous,  and  also  if  he  is  elderly  and  shows  signs  of 
arterio-sclerosis. 

If  symptoms  similar  to  those  just  enumerated  lead  to  an  examination  of  the 
urine,  and  the  result  of  this  is  ambiguous,  it  is  advisable  to  have  the  patient  par- 
take of  a  meal  rich  in  starchy  elements,  and  to  examine  the  urine  thereafter,  pref- 
erably by  means  of  the  fermentation  test.  If  even  then  no  sugar  is  found,  dia- 
betes does  not  exist. 

Treatment. — Medical  science  does  not  possess  the  power  to  cure  the  disease, 
but  it  can  greatly  benefit  the  patient,  both  by  alleviating  his  symptoms  and  by 
shielding  him,  at  least  for  the  time,  from  many  of  the  secondary  effects. 

The  first  requisite  is  to  institute  a  proper  regimen.  All  the  hygienic  circum- 
stances of  the  patient  should  be  regulated.  This  is  more  important  than  any  sort 
of  medicinal  treatment.  We  must  consider  that  the  increased  amount  of  sugar 
in  the  blood  is  not  without  influence  upon  the  tissues  of  the  body,  that  as  a  con- 
sequence of  the  imperfect  conversion  of  the  carbohydrates  there  may  be  other 
injurious  substances  formed  in  the  blood,  and  that  the  presence  of  sugar  in  the 
urine  may  lead  to  certain  disagreeable  symptoms  (pruritus,  balanitis) ;  and  con- 
sequently we  must  aim  by  our  dietetic  treatment  to  prevent  any  excessive  accu- 
mulation of  sugar  in  the  blood,  and  at  the  same  time  to  furnish  the  body  with  a 
substitute  for  the  carbohydrates  which  can  no  longer  be  employed  as  food. 

It  would  be  erroneous  to  conclude  that  this  last  point  is  the  only  essential  one, 
and  that  we  accomplish  our  whole  duty  by  reducing  the  amount  of  sugar  con- 
tained in  the  urine  to  a  minimum.  The  general  condition  of  the  patient  should 
invariably  be  considered.  There  can  be  no  doubt  that  a  diabetic  patient  whose 
strength  is  well  maintained  is  better  off,  even  if  there  is  considerable  sugar  in  his 
urine,  than  one  whose  urine  contains  less  sugar,  but  who  yet  is  daily  growing 
weaker.  In  managing  the  dietary  of  a  diabetic  patient,  we  must  first  determine 
what  tolerance  for  carbohydrates  there  may  be  in  each  particular  case.  The  prin- 
ciple of  dietetic  treatment  of  diabetes  does  not  consist  in  the  simple  withdrawal 
of  all  carbohydrates,  but  rather  in  allowing  each  patient  as  much  of  such  sub- 
stances as  his  body  is  in  a  condition  to  appropriate.  This  amount  varies  greatly 
in  different  cases,  and  also  in  the  same  patient  at  different  times.  We  must  first 
determine  whether  the  case  belongs  to  the  severe  or  the  mild  type,  as  above  de- 
fined— that  is,  whether  sugar  entirely  disappears  from  the  urine  if  no  carbo- 
hydrates whatever  are  allowed.    If  it  does — that  is,  if  we  are  dealing  with  the 


764:  CONSTITUTIONAL  DISEASES 

milder  form  of  diabetes — ^we  then  proceed,  after  the  -urine  has  been  freed  from 
sugar,  to  give  gradually  increasing  amounts  of  carbohydrates,  at  the  same  time 
examining  the  urine  every  day  in  order  to  see  whether  the  starch  ingested  is  com- 
pletely oxidized  in  the  blood.  The  more  carbohydrates  that  can  be  allowed  with- 
out the  appearance  of  sugar  in  the  urine,  the  more  favorable  the  case.  When  we 
have  in  this  manner  measured  the  ability  of  the  system  to  utilize  carbohydrates, 
the  patient  is  kept  for  a  considerable  time  upon  such  food  as  his  system  can 
manage  completely  to  appropriate.  The  experience  of  physicians  has  shown  that 
this  sort  of  limitation  of  the  carbohydrates  may  have  a  permanent  beneficial  in- 
fluence, inasmuch  as  after  the  patient  has  adhered  for  a  considerable  time  to  a 
diet  which  keeps  the  urine  free  from  sugar,  the  tolerance  of  the  system  for  carbo- 
hydrates increases.  We  may,  therefore,  try  gradually  to  make  some  increase  in 
the  amount  of  carbohydrates,  and  Ave  shall  not  infrequently  find  that  after  per- 
sistence in  such  a  diet  for  a  considerable  time,  the  patient  will  bear  more  car- 
bohydrates without  the  return  of  glycosuria.  Thus,  guided  by  constant  examina- 
tions of  the  urine,  we  can  easily  prescribe  the  correct  diet  for  the  individual 
patient. 

If  we  are  dealing  with  the  severe  form  of  diabetes — that  is,  if  sugar  is  still 
excreted  in  the  urine,  even  when  the  diet  consists  exclusively  of  meat  and  fat — 
we  may  try  the  effect  of  withdrawing  all  carbohydrates  completely  for  a  consid- 
erable time.  Many  physicians  (Cantani,  Naunyn,  and  others)  have  observed  that 
an  absolutely  strict  diet  of  this  sort,  excluding  all  carbohydrates,  may  have  a  very 
favorable  therapeutic  eifect,  so  that  finally  the  patient  will  regain  a  certain  tol- 
erance for  carbohydrates;  but  it  is  precisely  in  these  severe  cases  that,  in  our 
opinion,  it  is  improper  to  be  guided  too  much  by  general  rules.  We  should  con- 
sider not  only  the  character  of  the  urine,  but  the  condition  of  the  individual  in 
other  respects — ^his  subjective  sensations,  his  weight,  and  his  strength.  Many  of 
these  severe  cases  undoubtedly  feel  better  when  they  are  allowed  a  moderate 
amount  of  carbohydrates  than  when  they  are  on  a  purely  nitrogenous  and  fatty 
diet,  despite  the  somewhat  greater  amount  of  sugar  excreted.  Particularly  when 
the  appearance  of  acetone,  acet-acetic  acid,  butyric  acid,  and  the  like  in  the  urine, 
suggests  a  considerable  destruction  of  the  albuminoids  of  the  body,  and  perhaps 
an  impending  diabetic  coma,  practical  experience  has  shown  that  we  should  not 
insist  too  strictly  upon  a  purely  nitrogenous  diet,  but  should  try,  by  the  cautious 
administration  of  carbohydrates,  to  improve  the  general  condition  and  avert  the 
danger  of  coma. 

As  we  have  already  mentioned,  it  is  decidedly  advantageous  to  make  up  for  the 
diminution  in  carbohydrates  by  giving  other  food  which  does  not  contain  nitrogen. 
The  most  natural  thing,  certainly,  is  to  allow  an  abundance  of  fat  as  a  substitute 
for  the  carbohydrates;  and  practical  experience  is,  as  regards  this  matter,  in 
entire  unison  with  theory.  Fat  is  well  borne  by  most  diabetics,  and  it  may  be 
allowed  in  the  form  of  butter,  cream,  salad  oil,  and  the  like.  It  should  be  particu- 
larly recommended  to  emaciated  patients,  if  they  can  digest  it.  Sometimes  cod- 
liver  oil  may  be  prescribed  for  a  time.  Beside  the  fats,  the  use  of  alcohol  as  a 
preventive  of  waste  might  be  considered;  in  small  amounts  brandy  and  claret 
may  be  allowed  to  some  patients.  We  would  earnestly  advise  against  the  use  of 
larger  amounts,  for  the  toxic  effect  of  alcohol  might  injure  the  vitality  of  the 
cells  (vide  supra). 

With  a  view  of  aiding  the  physician  in  preparing  a  bill  of  fare  for  his  indi- 
vidual cases,  we  append  a  list  of  the  separate  foods  which  are  available  for  the 
nourishment  of  diabetic  patients:  1.  A  diet  which  contains  almost  no  carbo- 
hydrates would  be  as  follows :  On  waking,  tea  or  coffee  with  cream,  but  no  sugar; 
for  breakfast,  eggs,  ham,  cold  meat;  at  noon,  broth,  not  thickened,  fish  with 
butter,  meat  with  greens  or  salad;  for  supper,  tea,  eggs,  cold  meat,  cheese;  in 


DIABETES   MELLITUS  T65 

addition  the  patient  may  drink  water  or  a  moderate  amount  of  claret.  The  fol- 
lowing articles  are  almost  absolutely  devoid  of  carbohydrates :  all  sorts  of  meat, 
ham,  smoked  meat,  tongue,  all  sorts  of  fish,  crabs,  caviare,  oysters,  sardines,  eggs, 
green-colored  vegetables,  lettuce,  endives,  cress,  asparagus,  cauliflower,  spinach, 
cucumbers,  red  and  white  cabbage,  string  beans  when  young,  soi-rel.  Of  course, 
if  these  are  boiled,  only  butter  can  be  added,  or  meat,  but  no  cereal.  Other  arti- 
cles of  this  class  are  all  sorts  of  cheese ;  such  fatty  foods  as  butter,  olive-oil,  and 
cream;  meat  broths,  artificial  meat-peptone,  meat  extract,  somatose,  mineral 
waters,  and  light  claret.  2.  Articles  which  contain  a  small  amount  of  carbo- 
hydrates, and  which,  therefore,  may  be  allowed  in  moderate  amounts  if  there  is 
a  certain  degree  of  tolerance  for  carbohydrates  (vide  supra)  :  rusks,  rye  bread, 
milk,  cocoa,  turnips,  kohl  rabi,  radishes,  nuts,  sour  fruits — such  as  apples,  cur- 
rants, and  cherries.  3.  Articles  which  contain  a  large  amount  of  carbohydrates,  • 
and  are  therefore  to  be  prohibited  or  allowed  sparingly,  according  to  individual 
circumstances :  all  sweet  dishes,  cake,  honey,  potatoes,  oatmeal,  rice,  peas,  beans, 
lentils,  sago,  sweet  fruits,  sweet  wines,  and  beer. 

The  hardest  thing  for  diabetics  to  do  without  is  bread.  Every  physician  who 
has  had  much  experience  with  diabetic  patients  can  relate  experiences  of  the  cun- 
ning of  patients  in  satisfying  their  unconquerable  longing  for  this  forbidden 
article  by  the  employment  of  underhand  m.eans.  Hence,  many  attempts  have 
been  made  to  furnish  special  sorts  of  bread  for  diabetic  patients,  containing  a 
minimum  proportion  of  carbohydrates.  Most  of  these  preparations,  however, 
the  patients  do  not  like.  Chiefly  to  be  recommended  are  gluten  bread  and  aleu- 
ronat  bread.  Finally,  it  is  well  to  employ  saccharine  to  sweeten  food  and  drink, 
particularly  tea  and  coffee,  provided  the  saccharine  does  not  produce  dyspepsia 
and  also  proves  agreeable  to  the  patient. 

[The  dietetic  treatment  of  diabetes  is  so  important  that  it  is  desirable  to  go 
more  into  detail. 

There  is  some  discrepancy  between  the  authorities  on  this  point,  a  more  strict 
diet  being  laid  down  by  some  than  by  others.  Ralfe's  list  is  as  rigid  as  any,  and 
is  as  follows : 

To  avoid :  Milk  (except  very  small  quantities  for  cooking  purposes) .  The  liver 
of  all  animals  (as  the  liver  of  oysters  and  all  mollusca  is  large,  and  abounds  in 
glycogen,  these  animals  must  be  forbidden),  so  also  the  interior  of  crabs,  lobsters, 
etc.  Bread,  biscuits,  rusks,  toast,  farinaceous  vegetables,  such  as  potatoes,  Jeru- 
salem artichokes,  rice,  oatmeal,  corn-flour,  sago,  tapioca,  arrowroot,  etc.  Saccha- 
rine vegetables,  turnips,  carrots,  parsnips,  green  peas,  French  beans,  beet-root, 
asparagus,  tomatoes.  Blanched  vegetables  of  every  sort,  as  celery,  sea-kale, 
endive,  radishes;  also  the  stalks  and  white  parts  of  such  vegetables  as  cabbage, 
lettuce,  broccoli,  etc.  Fruits  of  all  kinds.  Jams,  syrups,  sugars.  Certain  condi- 
ments, such  as  chutney  and  sweet  pickles,  cocoa,  chocolate,  liqueurs,  sweet  wines. 

May  take :  Meat,  fish,  poultry,  game,  bacon,  ham,  eggs.  Bread  and  biscuits 
made  with  prepared  gluten,  bran,  or  almond-flour.  Green  vegetables,  summer 
cabbage,  turnip-tops,  spinach,  broccoli-tops,  water-cresses,  mustard  and  cress, 
laver,  sauerkraut,  the  green  parts  of  lettuce,  sorrel,  mushrooms.  ISTuts  of  various 
kinds  (except  chestnuts).     Cheese. 

Flint's  list  is  more  lenient,  allowing  oysters  and  a  much  larger  choice  of  vege- 
tables, such  as  asparagus,  string  beans,  artichokes,  cauliflower,  tomatoes,  etc. 
("Journal  of  the  American  Medical  Association,"  July  12,  1884;  also  "Pepper's 
System  of  Medicine,"  vol.  ii,  page  221). 

Donkin's  treatment  by  skim  milk  exclusively  is  highly  approved  by  Tyson. 

Bhenish  and  similar  wines,  moderate  quantities  of  spirits,  or  a  malt  liquor  in 
which  the  sugar  has  been  entirely  converted  into  carbonic  acid  and  alcohol  (Bass's 
ale,  for  instance),  are  permitted. 


T66  CONSTITUTIONAL  DISEASES 

In  the  opinion  of  the  writer,  it  is  always  well  to  begin  treatment  with  a  very 
stringent  dietary,  which  may  be  relaxed  gradually  as  circumstances  dictate.  The 
severity  of  the  case  is  to  be  regarded  rather  than  the  name  of  the  disease.  The 
gluten  and  other  diabetic  flours  are  unreliable;  and  I  agree  with  Flint  that,  if 
bread  be  allowed,  it  is  better  to  give  the  crust  of  a  French  roll,  the  ingredients  of 
which  are  known.  Saccharine  may  be  used  to  sweeten  tea  and  coffee,  jellies,  ice 
cream,  and  the  like.] 

Certain  other  general  directions  are  important.  The  patient  should  take  suffi- 
cient exercise.  Kiilz  has  determined  by  means  of  accurate  experiments  that, 
other  things  being  equal,  the  assimilation  of  sugar  is  increased  by  muscular 
activity,  with  a  consequent  diminution  in  the  excretion  of  sugar.  Practical 
experience  also  shows  that  regular  exercise  is  extremely  beneficial.  A  proper 
discretion  should  be  employed,  however;  nothing  would  be  more  injudicious  than 
to  force  a  feeble  patient  to  exhausting  efforts ;  but  if  the  patient  be  vigorous  and 
well  nourished,  he  should  be  strongly  urged  to  take  a  walking-trip  in  the  moun- 
tains, or  to  try  horseback  riding  and  the  like.  Methodical  massage  of  the  muscles 
sometimes  has  a  good  effect. 

Proper  care  of  the  skin  is  indispensable.  Baths,  cold  sponging,  and  douching 
may  be  employed.  Strict  attention  should  also  be  given  to  the  teeth,  lest  they  be- 
come carious.    Thorough  ventilation  should  be  maintained,  both  day  and  night. 

Of  internal  remedies,  opium  should  be  named  first.  One  good  effect  of  this 
drug  is  that  it  lessens  the  annoying  thirst.  It  sometimes  also  causes  decided 
diminution  in  the  amount  of  urine  and  sugar  excreted.  It  is  further  indicated 
when  there  is  general  restlessness  or  sleeplessness.  It  is  often  well  borne  by 
diabetic  patients,  even  in  large  doses.  A  patient  sometimes  can  take  four  to 
eight  grains  (gramme  0.25-0.5),  or  even  more,  of  opium  in  twenty-four  hours 
without  any  bad  effects.  We  have  repeatedly  administered  to  patients  with  a 
severe  form  of  diabetes,  for  weeks  at  a  time,  from  sixty  to  one  hundred  drops  of 
laudanum,  divided  into  three  doses  daily,  with  apparently  the  best  results.  It 
should  be  especially  noted  that  the  bowels  were  not  at  all  disturbed  by  the  drug. 
It  is  deserving  of  mention  that  the  alkaloids  of  opium,  such  as  morphine  and 
codeine,  possess  much  less  value  than  opium  itself. 

[The  inhalation  of  oxygen  is  worthy  of  mention  as  a  remedial  measure. 

Purdy  seems  to  show  that  diabetes  attains  its  highest  mortality  in  those 
States  which  combine  relatively  high  altitudes  with  low  temperature.  A  resi- 
dence in  the  Gulf  States  or  Southern  California  may  therefore  be  curative  or  pro- 
long life.] 

The  alkalies,  and  still  more  the  alkaline  mineral  waters,  enjoy  a  reputation 
second  only  to  that  of  opium.  Hundreds  of  patients  visit  Carlsbad,  Neuenahr, 
and  Vichy  every  year,  to  return  much  benefited.  Of  course  it  must  not  be  for- 
gotten that  it  is  not  merely  the  waters  which  produce  these  beneficial  changes. 
Other  factors  are  also  important,  in  particular  the  strict  diet,  exercise,  fresh  air, 
and  freedom  from  the  cares  of  the  household  and  business.  Why  the  alkalies 
should  act  favorably  we  do  not  know.  Perhaps  it  is  because  they  neutralize  the 
abnormal  acids  in  the  organism,  Griesinger,  and  later  Klilz,  as  well  as  others, 
have  made  careful  comparisons  of  the  amounts  of  sugar  excreted  under  like  cir- 
cumstances, with  and  without  the  ingestion  of  bicarbonate  of  soda  or  of  Carlsbad 
water  and  similar  substances,  and  for  the  most  part  have  not  been  able  to  per- 
ceive any  benefit  from  these  remedies.  Practical  experience,  however,  shows  the 
value  of  these  alkaline  waters ;  and  their  use  is  to  be  recommended,  provided  the 
patient  is  comparatively  vigorous  and  fit  for  travel,  although  his  expectations 
should  not  be  raised  to  too  high  a  pitch. 

From  a  theoretical  point  of  view,  there  is  interest  in  the  fact  that  certain 
remedies  which  are  antagonistic  to  fermentation  have  been  shown  by  Ebstein  and 


DIABETES   mSIPIDIJS  767 

Miiller  to  diminish  the  excretion  of  sugar  in  many  cases  of  diabetes.  Chief 
among  these  are  carbolic  acid  and  salicylate  of  sodium.  Carbolic  acid  is 
given  in  the  amount  of  ten  to  twenty  grains  (gramme  0.5-1.5)  per  diem.  The 
amount  of  salicylate  of  sodium  is  one  to  two  and  a  half  drachms  (grammes  5-10) 
daily.  There  is  no  doubt  that  these  drugs  possess  the  property  ascribed  to  them; 
but  they  are  not  advantageous  to  the  patient,  inasmuch  as  the  general  condition 
is  seldom  improved  by  their  use.  On  the  contrary,  very  unpleasant  effects  are 
sometimes  observed. 

We  need  not  enumerate  all  the  remedies  which  have  been  recommended  in 
diabetes.  We  have  already  mentioned  those  that  possess  any  extended  repu- 
tation. We  may  therefore  merely  refer  to  certain  drugs  which  have  been  lately 
introduced. 

Cantani  has  suggested  the  employment  of  lactic  acid  in  the  amount  of  one  to 
two  and  a  half  drachms  (grammes  5-10)  per  diem,  dissolved  in  half  a  pint  of 
water.  This  drug  may  perhaps  serve  as  a  physiological  substitute  for  sugar,  as 
glycerine  is  supposed  to  do  (vide  supra),  but  it  has  no  specific  virtues.  Cer- 
tain salts  of  ammonia,  such  as  the  carbonate  and  acetate,  are  said  to  diminish 
the  excretion  of  sugar,  and  have  therefore  long  been  employed  in  diabetes. 
Good  results  can  not,  however,  be  claimed  for  them,  nor  for  iodoform  (3-7  grains, 
gramme  0.2-0.4,  daily),  nor  for  the  lately  much-lauded  jambul.  The  trials  of 
pancreatic  juice,  also,  have  led  to  no  definite  results. 

It  is  evident,  in  brief,  that  the  best  mode  of  treating  diabetes,  at  least  accord- 
ing to  our  present  knowledge,  is  by  regulating  the  diet,  and  that  it  is  well,  in 
addition,  to  recommend  the  employment  for  a  time  of  the  above-mentioned  min- 
eral waters,  with  opium  and  other  internal  remedies  to  combat  special  symptoms. 
The  treatment  of  such  complications  as  phthisis  or  cutaneous  eruptions  need  not 
be  described  here. 

In  diabetic  coma,  camphor  or  ether,  subcutaneously,  should  be  employed, 
together  with  lukewarm  baths  and  douching.  In  consideration  of  the  possibility 
that  diabetic  coma  is  connected  with  an  acid  intoxication  (vide  supra),  we  should 
always  try  the  administration  of  large  doses  of  carbonate  of  soda,  either  by  the 
mouth  or  in  an  enema,  or  by  the  subcutaneous  or  intravenous  injection  of  a  three- 
to  five-per-cent.  solution.  The  results  thus  far,  it  must  be  confessed,  are  not  very 
favorable ;  still,  sometimes  this  mode  of  treatment  has  been  decidedly  beneficial. 
A  more  important  matter  seems  to  be,  as  !N^aunyn  pointed  out,  the  administra- 
tion of  two  to  five  drachms  (grammes  10-20)  of  the  bicarbonate  of  soda,  daily, 
for  a  long  time,  to  any  diabetic  patient  whose  urine  gives  a  positive  ferric  chlo- 
ride reaction  (vide  supra),  thus  justifying  suspicion  that  an  acid  intoxication  is 
beginning. 


CHAPTEE   X 
DIABETES    INSIPIDUS 

Definition  and  etiology. — In  the  preceding  chapter  a  distinction  was  drawn 
between  diabetes  mellitus  and  the  symptomatic  condition  termed  glycosuria. 
There  is  a  similar  distinction  to  be  made  between  diabetes  insipidus  and  polyuria. 
Polyuria  is  an  increase  in  the  volume  of  urine,  and  mainly  in  the  amount  of 
water  excreted  by  the  kidneys.  It  is  a  symptom  which  may  be  produced  in  many 
different  ways.  In  the  first  place,  it  is  a  natural  consequence  of  the  ingestion  of 
large  amounts  of  water,  or  of  the  absorption  of  serous  effusions ;  it  also  occurs  in 
certain  diseases  of  the  nervous  system,  especially  of  the  medulla  and  cerebellum ; 


768  CONSTITUTIONAL   DISEASES 

it  is  occasionally  seen,  as  we  have  had  opportunity  to  ohserve,  in  chronic 
hydrocephalus,  and  is  a  not  very  infrequent  phenomenon  in  hysteria.  Large 
amounts  of  urine  are  also  secreted  in  certain  renal  diseases  (interstitial  ne- 
phritis and  amyloid  degeneration),  and  often  during  convalescence  from  acute 
diseases,  such  as  typhoid  fever,  or  after  the  ingestion  of  certain  drugs,  called 
diuretics. 

Diabetes  insipidus,  on  the  other  hand,  is  a  disease  which  may  develop  idio- 
pathicaily  in  persons  otherwise  perfectly  healthy.  Its  setiology  is  unknown.  It 
occasionally  seems  to  be  excited  by  emotional  disturbance,  concussion  or  other 
injury  of  the  brain,  or  some  previous  acute  disease,  such  as  typhoid  or  typhus 
fever,  malarial  poisoning,  and  cerebro-spinal  meningitis.  The  disease  sometimes 
appears  in  the  syphilitic,  and  it  may,  therefore,  in  many  instances,  be  due  to  syphi- 
lis. Patients  frequently  state  that  their  symptoms  began  immediately  after 
drinking  a  very  large  amount  of  some  fluid,  as  on  a  very  hot  day  or  after  a  long 
march.  Einally,  there  are  cases  in  which  the  disease  appears  to  be  hereditary,  or 
to  attack  members  of  the  same  family.  A  distinction  should  be  made  between 
genuine  diabetes  insipidus  and  those  cases  in  which  the  primary  symptom  is  not 
polyuria,  but  an  abnormal  thirst,  polydipsia,  so  that  the  polyuria  is  merely  a 
result  of  drinking  so  much  water.  In  many  of  these  cases  the  polydipsia  is  un- 
doubtedly a  hysterical  symptom  (see  the  chapter  on  hysteria). 

The  true  nature  of  diabetes  insipidus  is  entirely  unknown  to  us.  The 
view  which  seems  most  probable  of  any  is,  that  some  nervous  disturbance  is 
its  direct  cause.  In  support  of  this,  we  have  the  appearance  of  a  "  symptomatic 
diabetes  insipidus  "  in  connection  with  organic  disease  of  the  brain  (vide  supra), 
and  the  fact  that  polyuria  may  be  artificially  excited  by  injury  to  a  definite  spot 
in  the  floor  of  the  fourth  ventricle  or  by  section  of  the  vagus  nerve.  Diabetes 
insipidus  presents  a  most  striki;ng  analogy  with  diabetes  mellitus.  This  is  shown 
both  by  the  similarity  in  setiology  and  symptomatology,  and  still  more  by  the  fact 
that  occasionally  one  disease  merges  into  the  other. 

Diabetes  insipidus  is  a  disease  of  very  infrequent  occurrence,  and  is  decidedly 
less  often  seen  than  diabetes  mellitus.  Most  patients  are  youthful  or  middle- 
aged.  Genuine  diabetes  insipidus  has  also  been  observed  in  children,  perhaps  in 
connection  with  hereditary  syphilis.  The  male  sex  is  somewhat  more  liable  to 
the  disease  than  the  female. 

Clinical  History. — Diabetes  insipidus  may  be  developed  gradually  or  with  con- 
siderable abruptness;  the  latter  case  is  especially  frequent  when  there  is  some 
definite  cause,  such  as  the  ingestion  of  a  large  amount  of  liquid,  or  traumatism. 

The  essential  and  characteristic  symptom  is  an  increase  in  the  volume  of 
urine.  This  is  usually  very  considerable.  Often  eight  or  ten  quarts  (8,000  to 
10,000  cubic  centimetres)  are  excreted  in  twenty-four  hours,  and  cases  have  even 
been  reported  where  the  amount  reached  the  almost  incredible  volume  of  thirty 
to  forty  quarts  (litres).  If  a  healthy  person  and  a  sufferer  from  diabetes  insipidus 
are  each  given  the  same  amount  of  water  in  food  and  drink,  the  sick  man  will 
excrete  more  urine  than  the  healthy.  In  color  the  urine  is  very  pale,  and  some- 
times almost  like  water.  The  specific  gravity  is  very  low,  being  usually  1004  to 
1002,  or  even  1001.    The  reaction  is  slightly  acid,  sometimes  almost  neutral. 

The  percentage  of  solid  constituents  in  the  urine  is,  of  course,  trifling.  The 
total  amount  of  solids,  however,  corresponds  perfectly  with  the  ingesta,  or  indeed 
is  even  somewhat  above  normal.  The  amount  of  urea,  in  particular,  seems  to  be 
increased,  but  it  has  also  been  stated  that  other  constituents  of  the  urine  have 
been  excreted  in  abnormally  large  amounts — namely,  phosphoric  acid,  sulphuric 
acid,  lime,  and  kreatinine.  Inosite  has  been  foimd  in  the  urine  by  Strauss  and 
other  observers,  so  that  it  has  even  been  proposed  to  give  diabetes  insipidus  the 
name  of  "diabetes  inositus,"  in  distinction  from  diabetes  mellitus.     Inosite  is 


DIABETES   INSIPIDUS  '      T69 

not  invariably  present,  however,  in  the  urine  of  diabetes  insipidus.     In  cases  of 
true  diabetes  insipidus,  albuminuria  is  extremely  exceptional. 

Another  important  symptom  is  the  excessive  thirst.  To  make  up  for  the 
loss  of  vpater  by  way  of  the  kidneys  the  patient  is  obliged  to  drink  great  quantities 
of  liquid,  and,  indeed,  it  is  always  found  that  the  amount  of  water  ingested,  in  the 
way  of  drink  and  solid  food,  somewhat  exceeds  the  total  volume  of  urine  excreted. 
Despite  this,  the  tongue  is  usually  dry,  as  is  also  the  skin,  the  insensible  perspira- 
tion being  considerably  below  the  normal  amount.  The  furunculosis  seen  in  dia- 
betes mellitus  is  exceptional  in  diabetes  insipidus.  The  same  is  true  of  pruritus, 
balanitis,  etc.  Occasionally  profuse  salivation  has  been  associated  with  the 
disease. 

Symptoms  referable  to  the  various  internal  organs  are  few.  Cataract  has  been 
■occasionally  observed,  but  it  is  much  less  frequent  than  in  diabetes  mellitus.  The 
same  may  be  said  of  pulmonary  tuberculosis.  In  most  cases  the  appetite  is  not 
excessive.  The  bowels  are  regular  or  slightly  constipated.  There  is  seldom  much 
^astro-intestinal  disturbance,  unless  from  some  chance  complication.  The  sexual 
functions  are  usually  unimpaired. 

The  general  health  is  considerably  affected  in  cases  of  any  severity.  The 
patient  becomes  emaciated,  languid,  and  feeble,  and  has  no  inclination  to  mental 
or  physical  exertion.  Sleep  is  often  disturbed,  the  mind  depressed.  The  tempera- 
ture is  normal,  or  even  a  trifle  below  normal,  probably  as  a  result  of  the  large 
amount  of  cold  water  drunk. 

Diabetes  insipidus  is  a  very  chronic  disease.  If  there  is  no  serious  complica- 
tion it  may  last  for  decades,  yet  there  are  cases  that  run  a  more  rapid  and  unfa- 
vorable course.  Sometimes  there  are  considerable  vicissitudes  in  the  condition  of 
the  patient,  in  part  dependent  upon  external  circumstances  and  in  part  appar- 
ently spontaneous.  In  case  some  intercurrent  acute  disease  develops  there  may 
be,  during  its  continuance,  a  considerable  diminution  in  the  amount  of  urine 
excreted. 

The  termination  is  usually  unfavorable.  Recovery  is  extremely  rare.  In  the 
more  fortunate  cases  the  condition  finally  becomes  stationary,  and  the  patient 
attains  to  advanced  years.  Sometimes,  however,  death  occurs  more  prematurely, 
being  usually  hastened  by  phthisis  or  some  similar  complication. 

Weil  has  lately  contributed  to  our  knowledge  of  this  disease  the  results  of  an 
accurate  study  of  its  hereditary  and  apparently  congenital  variety.  Weil  narrates 
the  history  of  a  family  in  which  marked  polyuria  and  corresponding  polydipsia 
appeared  in  numerous  raembers  for  several  generations.  These  persons  all  en- 
joyed excellent  health,  with  this  exception;  and  most  of  them  attained  old  age. 
We  hardly  need  to  emphasize  the  fact  that  this  form  of  the  disease  is  radically 
different  from  the  ordinary  acquired  variety.  Perhaps  its  true  cause  is  an  abnor- 
mal congenital  permeability  of  the  glomeruli,  but  we  have  no  certain  information 
in  regard  to  it. 

Post-mortem  Appearances. — Such  lesions  as  have  been  found  in  diabetes  in- 
sipidus are  usually  the  result  of  fortuitous  complications,  such  as  tuberculosis, 
carcinoma,  and  pneumonia.  There  are  but  very  few  changes  referable  directly  to 
the  disease  itself :  among  these  are  enlargement  of  the  kidneys  and  dilatation  of 
the  ureters.  In  rare  instances  a  possible  cause  for  the  symptoms  has  been  found 
in  some  lesion  of  the  central  nervous  system,  but  these  were  cases  of  symptomatic 
polyuria  and  not  of  genuine  diabetes  insipidus.  Instances  of  this  sort  are  seen  in 
connection  with  tumors  or  inflammatory  changes  in  the  medulla  or  cerebellum, 
and  exostoses  at  the  base  of  the  skull. 

Diagnosis. — The  characteristic  urinaiy  phenomena  usually  render  the  diagno- 
sis of  diabetes  insipidus  an  easy  matter.    It  is  of  course  necessary  to  exclude  such 
diseases  as  might  occasion  symptomatic  polyuria  (vide  supra)  ;  but  this  is  seldom 
49 


,Y7o  co:nstitftion'al  diseases 

difficult  if  we  make  a  careful  physical  examination  and  duly  consider  all  the 
attendant  symptoms.  The  differential  diagnosis  between  diabetes  insipidus  and 
diabetes  mellitus  can  almost  invariably  be  made  by  means  of  the  urinometer.  If 
the  specific  gravity  is  below  normal,  it  is  scarcely  necessary  to  test  for  sugar,, 
although  in  doubtful  cases  this  is  the  sole  criterion.*  [The  early  stage  of  con- 
tracted kidney  has  repeatedly  been  mistaken  for  diabetes  insipidus. — V.] 

Treatment. — No  special  injunctions  with  regard  to  diet  are  required.  It 
would  of  course  be  a  mistake  to  forbid  the  patient  to  assuage  his  excessive  thirst ; 
but  we  may  possibly  lessen  the  amount  of  water  drunk  by  prescribing  bits  of  ice, 
or  lemonade  and  other  acid  drinks.  Opium  sometimes  lessens  both  the  thirst  and 
the  amount  of  urine  excreted.  Rather  large  doses  should  be  prescribed,  say 
fifteen  to  twenty  drops  of  laudanum,  several  times  a  day.  It  is  also  important  that 
the  skin  should  be  well  cared  for  by  means  of  baths  and  friction,  and  every  effort, 
should  be  made  to  promote  the  general  vigor  of  the  patient.  He  should  have 
nourishing  food  and  good  air. 

There  have  been  a  great  number  of  internal  remedies  recommended  as  spe- 
cifics, but,  in  general,  we  can  expect  no  great  results  from  them.  Most  employed 
are  valerian,  of  which  one  to  one  and  a  half  drachms  (grammes  5-10)  are  given 
daily  in  powder,  or  infusion ;  and  erg-otine,  of  which  one  and  a  half  to  eight  grains, 
(gramme  0.1-0.5)  are  given  several  times  a  day.  Other  remedies  which  are  said 
to  have  been  sometimes  tried  with  benefit  are  carbolic  acid,  atropine,  and  the 
bromides ;  also,  galvanization  of  the  cervical  cord. 

Occasionally  we  may  find  an  apparent  cause  for  the  disease  and  endeavor  to 
remove  it.  If  there  is  a  suspicion  of  syphilis,  mercurial  inunctions  should  be 
tried,  perhaps  in  combination  with  iodide  of  potassium  or  sodium.  Sometimes,, 
as  we  can  confirm  by  our  own  experience,  they  have  an  excellent  effect.  Of  course, 
where  there  is  symptomatic  polyuria,  the  primary  disease,  such  as  hysteria,  de- 
mands treatment.  [Da  Costa  and  others  report  very  good  results  as  following  the 
administration  of  ergot.] 


CHAPTER   XI 

GOUT 

(Podagra) 

.ffitiology. — Thomas  Sydenham  was  the  first  to  write  a  careful  clinical  descrip- 
tion of  gout.  He  himself  suffered  from  the  disease  for  about  forty  years,  and  he 
has  given  a  detailed  description  of  his  own  case  in  the  treatise  which  he  published 
in  1683,  under  the  title  "  Tractatus  de  podagra  et  hydrope."  It  was,  however.  Wol- 
laston  who,  in  1797,  threw  the  first  light  upon  the  peculiar  anomaly  of  metabolism 
which  exists  in  this  disease.  He  demonstrated  that  the  gouty  deposits  found  in 
the  joints  and  other  parts  of  the  body  are  mainly  uric  acid.  From  his  time  an  all- 
important  point  with  regard  to  the  nature  of  the  disease  has  been  the  relation 
between  the  symptoms  of  gout  and  disturbances  in  the  manufacture  and  excretion 
of  uric  acid.  In  1848  Garrod  showed  that  in  gout  the  blood  contains  an  excess 
of  uric  acid,  and  that  the  excretion  of  uric  acid  by  the  kidneys  is  diminished. 
He  was  thus  in  a  position  to  frame  a  theory  consistent  with  all  the  clinical  facts. 
Numerous  investigations  have  been  undertaken  since  his  day;  but  we  still  re- 
main with  regard  to  gout  in  a  position  analogous  to  that  which  we  hold  toward 
diabetes.    We  are,  it  is  true,  in  the  possession  of  a  considerable  number  of  well- 

*  [Compare,  however,  the  author's  statements  on  page  752. — Trans.] 


GOUT  771 

established  facts  relating  to  it,  but  we  do  not  know  why  the  normal  chemical  pro- 
cesses are  disturbed,  and  we  are  unable  to  explain  the  connection  between  the 
various  phenomena  observed. 

Clinical  experience  has  taught  us  certain  remote  causes  of  gout,  first  of  which 
comes  heredity.  About  fifty  per  cent,  of  all  cases  occur  in  patients  whose  families 
have  already  suffered  from  the  disease,  or  have  given  other  indications  of  the 
uric-acid  diathesis — such  as  renal  calculi;  and  it  is  sometimes  possible  to  trace 
this  transmitted  taint  through  many  generations.  It  is  decidedly  more  apt  to 
pass  down  through  the  male  members  of  the  family  than  through  the  female. 

Next  in  importance  to  hereditary  influences  is  the  mode  of  life.  From  time 
immemorial  this  has  been  regarded  as  an  exciting  cause  of  the  disease.  It  has 
been  a  matter  of  universal  belief  that  over-feeding,  and  especially  the  ingestion  of 
too  large  a  quantity  of  albuminoids,  is  strongly  provocative  of  the  disease.  The 
same  opinion  has  been  held  with  regard  to  persistent  over-indulgence  in  alco- 
holic beverages.  Seneca  relates  that  at  the  time  of  the  decay  of  the  Roman 
Empire  women  practiced  such  excesses  that  they  were  as  subject  to  gout  as  the 
men,  and  an  old  verse  runs :  "  Wine  is  the  father  of  gout,  feasting  is  its  mother, 
and  Venus  is  the  midwife."  That  this  old  view  of  gout  as  a  rich  man's  disease 
has  much  truth  in  it  can  not  be  denied.  The  not  infrequent  cases  of  genuine 
gout  which  we  observe  every  year  in  Erlangen  attack  mainly  great  beer  drinkers, 
who  for  years  have  imbibed  three  or  four  litres  of  beer  a  day;  but,  on  the 
other  hand,  it  would  be  going  too  far  to  refer  all  cases  of  genuine  gout  to  an  im- 
proper mode  of  life,  and  excessive  indulgence  in  alcohol.  Sometimes  genuine 
gouty  arthritis  is  seen  in  individuals  who  have  always  lived  moderately,  or  who 
have  even  been  in  needy  circumstances. 

Besides  alcohol,  there  is  another  well-known  poison  which  is  capable,  by  its 
chronic  action,  of  producing  that  change  in  metabolism  which  forms  the  founda- 
tion of  gout ;  we  refer  to  lead.  We  are  absolutely  certain  that  persons  who  have 
much  to  do  with  lead,  such  as  compositors  and  house-painters,  suffer  with  com- 
parative frequency  from  genuine  gout,  with  deposits  of  uric  acid  in  the  joints. 
We  have  repeatedly  seen  cases  of  this  sort  in  Leipsic  and  Erlangen.  In  a  sur- 
prising number  of  patients  lead-poisoning  is  associated  with  contracted  kidney. 
We  have  repeatedly  observed  that  the  combination  of  chronic  alcoholism  and 
chronic  lead-poisoning  is  especially  provocative  of  gout. 

With  regard  to  all  other  alleged  aetiological  factors,  confirmatory  evidence  is 
lacking.  Possibly,  however,  when  the  foundation  for  the  disease  is  already  laid, 
an  attack  may  be  excited  by  certain  determining  causes — namely,  trauma,  taking 
cold,  errors  in  diet,  or  mental  emotion. 

The  geographical  distribution  of  gout  is  remarkably  unequal.  The  disease  is 
more  frequent  in  England  than  in  Germany,  although  in  the  latter  country 
certain  regions  appear  to  be  more  affected  by  it  than  others.  In  Leipsic  gout 
seemed  to  us  to  be  rather  rare-,  but  in  Bavaria  it  is  more  common. 

Gout  is  rarely  seen  in  childhood  and  youth.  It  is  a  disease  of  middle  or 
advanced  life.     Men  are  much  more  often  attacked  than  women. 

Clinical  History. — Gout  may  produce  symptoms  in  many  different  organs ; 
but  its  effect  upon  the  joints  is  so  characteristic  that  the  arthritic  disturbance 
has  long  been  termed  "  normal  or  regular  gout,"  in  contradistinction  from  "  atypi- 
cal, internal  gout."  This  distinction  is  of  course  an  artificial  one,  for  the  various 
phenomena  of  gout  present  the  most  manifold  gradations  and  transitions.  It  will, 
however,  be  advantageous,  in  attempting  to  gain  a  practical  insight  into  the  vari- 
ous symptoms  of  the  disease,  if  we  first  discuss  the  so-called  "  typical  attack  of 
gout,"  subsequently  appending  a  description  of  the  other  manifestations  of  the 
disease.  Furthermore,  the  regular  attack  of  gout  is,  in  at  least  a  majority  of 
cases  (vide  infra),  the  first  and  earliest  symptom  of  the  disease. 


7Y2  CONSTITUTIOISTAL   DISEASES 

1.  The  typical  attack  of  gout  (primary  articular  gout)  is  sometimes  abrupt; 
but  it  is  often  preceded  for  a  longer  or  shorter  period  by  certain  premonitory 
symptoms,  the  meaning  of  which,  though  not  evident  to  one  who  is  about  to  suffer 
from  his  first  attack,  is  sufiiciently  clear  to  more  experienced  patients,  particu- 
larly as  each  individual  case  is  apt  to  present  a  marked  similarity  in  the  prodrom- 
ata  of  the  separate  paroxysms.  These  premonitoiy  symptoms  vary  in  different 
individuals.  Sometimes  they  consist  of  dyspeptic  disturbances;  sometimes  of  a 
feeling  of  languor  and  mental  depression;  very  often  of  dragging,  muscular 
pains  or  cramjDS  in  the  calves  of  the  legs ;  or  again  of  slight  f everishness,  with 
chilliness,  sense  of  heat,  and  perspiration.  These  prodromes  occur  a  longer  or 
shorter  time  before  the  true  attack  of  gout.  On  the  other  hand,  it  must  be  con- 
fessed that  a  patient  may  feel  unusually  well  just  before  an  attack. 

The  attack  is  noticeably  apt  to  begin  in  the  night-time,  or  very  early  in  the 
morning-.  The  patient  is  awakened  by  a  sudden  and  very  violent  pain  in  the 
metatarso-phalangeal  joint  of  one  of  the  great  toes  ("podagra")-  The  joint 
becomes  swollen,  the  skin  over  it  red,  hot,  and  tense,  the  veins  in  the  neighbor- 
hood distended.  At  the  same  time  there  is  chilliness  and  moderate  fever  (101°— 
102°;  38.5°-39°  C).  This  condition  persists  till  morning.  Then  the  pain  is 
almost  sure  to  abate,  the  fever  to  remit  at  the  same  time  that  sweating  begins, 
and  the  patient  to  feel  tolerably  well  during  the  day.  The  joint,  however,  re- 
mains swollen,  with  inflammation  and  oedema.  The  next  night  the  pain  begins 
again,  and  there  is  a  fresh  fever ;  and  these  alternations  are  repeated,  as  a  rule, 
for  three  to  seven  days.  Usually  there  are  not  many  other  symptoms  present; 
the  appetite  is  impaired,  but  ordinarily  there  are  no  marked  gastric  disturbances, 
such  as  eructations  and  vomiting,  or  intestinal  symptoms.  There  may  be  a 
slight  bronchitis.  Even  when  the  attack  is  more  persistent  than  this,  the  pain 
is  usually  much  less  severe  after  the  first  two  or  three  nights.  After  that  time 
it  gradually  abates ;  and  it  is  commonly  said  that  an  attack  is  brief  in  propor- 
tion to  the  violence  of  its  first  symptoms.  When  the  pain  ceases,  swelling  soon 
disappears,  the  skin  undergoes  a  slight  desquamation  and  resumes  its  normal 
appearance,  the  general  health  of  the  patient  rapidly  improves,  and  he  is  often 
found  to  be  better  after  an  attack  than  he  was  before. 

For  theoretical  purposes  (vide  infra)  it  would  be  very  advantageous  to  possess 
a  more  accurate  knowledge  of  the  condition  of  the  urine,  and  in  particular  of  the 
excretion  of  uric  acid  during  the  attack  and  at  other  times.  As  yet,  however, 
there  have  been  but  few  careful  investigations  made,  and  these  have  led  to  some- 
what contradictory  conclusions.  Garrod  has  made  a  very  important  observation; 
it  is,  that  the  amount  of  uric  acid  excreted  diminishes  several  days  before  the 
commencement  of  an  attack,  and  remains  diminished  during  the  attack.  Subse- 
quently to  the  attack  the  excretion  of  uric  acid  is  said  to  be  above  normal.  In 
contrast  with  the  excretion  of  uric  acid  in  the  urine,  the  amount  of  uric  acid  in 
the  blood  is  increased  during  the  attack.  This  is  an  important  fact  which  was 
discovered  by  Garrod,  and  which  has  been  confirmed  by  others,  including  Salo- 
mon, Klemperer,  and  others. 

If  there  has  been  one  attack  of  gout,  there  are  almost  sure  to  be  others.  They 
come  sooner  or  later,  at  regular  or  irregular  intervals,  and  separated  by  weeks, 
months,  or  even  years.  The  attacks  recur  at  long  intervals  in  mild  cases,  more 
frequently  and  at  gradually  diminishing  intervals  in  the  severe.  Spring  and 
autumn  are  regarded  as  the  time  when  attacks  of  gout  are  most  apt  to  occur.  In 
these  subsequent  attacks  the  great  toe  still  remains  the  part  most  constantly  and 
severely  affected;  but  other  joints  may  also  suffer — for  example,  the  wrist,  the 
small  joints  of  the  fingers  (see  Fig.  82),  the  knee,  or  the  shoulder.  In  all  these 
joints  there  appears  an  acute  and  very  painful  inflammation,  with  considerable 
swelling  of  the  affected  parts.     Sometimes  traumatism  apparently  determines  the 


GOUT 


Y73 


localization  of  the  gouty  disturbance.  In  each  attack,  the  trouble  is  usually  con- 
fined to  a  single  joint.  It  is  only  in  exceptional  or  advanced  cases  that  several 
joints  are  simultaneously  invaded. 

The  longer  the  disease  has  lasted,  the  less  typical  are  the  separate  attacks. 
There  may  now  be  less  suffering  at  the  time  of  an  attack;  but  the   articular 


Fig.  82.— Acute. attack  of  gout  in  the  joints  of  the  fingers.    (Personal  observation.) 

changes  are  more  persistent.  The  joints  gradually  become  deformed.  There  are 
symptoms  referable  to  other  parts  of  the  body;  and  the  gout  gradually  passes  into 
its  second  chronic  stage.  Occasionally  the  disease  is  irregular  and  atypical  from 
its  incipiency;  and  the  first  manifestations  may  not  be  arthritic,  but  referable 
to  the  kidneys  (vide  infra)  or  other  organs. 

2.  Chronic  Gout  and  the  Gouty  Diseases  of  Various  Organs. — As  a  rule,  the 
most  striking  results  of  chronic  gout  are  the  changes  in  the  joints.  There  is  a 
gradual  development  of  marked  deformity,  particularly  in  the  small  joints  of  the 
fingers,  the  joints  of  the  great  toe,  and  less  often  the  other  joints.  The  fingers 
(see  Fig.  83)  are  deflected  toward  the  ulnar  side,  at  the  metacarpo-phalangeal 
joints,  as  in  arthritis  deformans,  and  at  the  same  time  the  fingers,  as  a  whole,  are 
thickened,  particularly  at  the  joints.  Almost  always  the  small  finger-joints  early 
undergo  firm  anchylosis.  The  great  toes  are  often  bent  out  of  shape.  ISTot  infre- 
quently there  are  formed  around  some  of  the  joints  which  are  often  attacked, 
particularly  the  metatarso-phalangeal  joint  of  the  great  toe,  soft  fluctuating 
masses,  which  are  very  painful.    If  these  burst  spontaneously,  or  if  they  are  in- 


T74 


CONS'TITUTIONAL   DISEASES 


cised,  they  are  found  to  contain  little,  if  any,  pus,  but  much  detritus,  and  numer- 
ous crystals  of  uric-acid  salts,  mainly  the  urates  of  sodium  and  calcium.  When 
these  nodes  break  open  they  may  develop  into  tedious  ulcers ;  similar  gouty  nodes 
(arthritic  tophi)  may  develop  in  other  portions  of  the  skin,  particularly  in  the 
lobe  of  the  ear,  and  sometimes  also  in  the  tendons  and  muscles. 


Fig.  83. — Changes  in  the  joints  of  the  Angers  in  genuine  chronic  gout.    (Personal  observation. 


Gout  may  affect  the  mucous  membranes.  A  gouty  dyspepsia  is  very  frequent. 
Its  symptoms  are  more  or  less  severe.  The  gouty  are  also  subject  to  intestinal 
catarrh  of  varying  severity,  and  to  bronchitis  and  conjunctivitis,  as  well  as  to 
catarrh  of  the  urinary  organs.  Ebstein  regards  "  gouty  gonorrhoea  "  as  essen- 
tially a  catarrh  of  the  excretory  ducts  of  the  prostate  gland.  It  is  not  an  easy 
matter  to  explain  why  these  various  forms  of  catarrh  should  occur  in  gout. 
Some  of  them  may  be  complications.  In  other  cases  they  are  doubtless  the 
result  of  passive  congestion,  due  to  cardiac  failure  (vide  infra)  ;  but  in  still  other 
instances  it  must  be  confessed  that  they  are  apparently  due  to  the  toxic  influence 
of  the  accumulated  uric  acid  or  other  noxious  products  of  abnormal  metabolism. 

[My  experience,  though  far  more  limited  than  that  of  Draper,  nevertheless 
leads  me  to  believe,  as  he  does,  that  the  irregular  forms  of  gout  are  by  no  means 
uncommon  in  women  as  an  inheritance  from  a  previous  generation.  The  mani- 
festations in  soihe  of  these  cases  are  so  ill-defined  that  a  diagnosis  may  be  diffi- 
cult without  a  knowledge  of  the  family  history;  in  other  cases,  more  or  less  de- 
formity of  the  smaller  joints,  or  slight  recurrent  swellings  of  those  parts,  thi'ow 
much  light  on  the  condition  underlying  the  symptoms.] 

Inflammation  of  serous  membranes — for  example,  of  the  i^leura — also  occurs ; 


GOUT  775 

and  there  may  be  pneumonia.  The  skin  not  infrequently  suffers  from  acute  or 
chronic  eczema,  which  sometimes  appears  to  be  referable  directly  to  the  gout. 
Keratitis,  iritis,  and  other  inflammatory  disturbances  of  the  eye  are  also  said  to 
be  caused  directly  by  gout.  Cirrhosis  of  the  liver  has  been  repeatedly  found,  and 
is  probably  to  be  referred  chiefly,  in  our  opinion,  to  chronic  alcoholism. 

By  far  the  most  important  of  all  these  gouty  manifestations  are  referable  to 
the  kidneys  and  to  the  circulatory  system.  The  disorder  of  the  latter  is  some- 
times symptomatic  of  the  renal  trouble,  but  in  other  instances  it  occurs  inde- 
pendently of  it.  There  may  be  severe  gouty  arthritis  for  years  w^ithout  any  lesion 
of  the  kidneys ;  but  this  is  exceptional.  In  severe  cases  of  gout  it  is  the  rule  that, 
sooner  or  later,  symptoms  of  renal  disorder  present  themselves.  The  so-called 
"  gouty  kidney  "  is  a  form  of  chronic  interstitial  nephritis.  Hovpever  important 
this  comiDlication,  its  symptoms  do  not  need  to  be  discussed  here,  as  they  are  pre- 
cisely similar  to  those  seen  in  ordinary  cases  of  contracted  kidney  (vide  page  628 
et  seq.).  The  distinctive  symptom  of  this  disturbance  is  albuminuria;  and  the 
g-radually  developing  secondary  hypertrophy  of  the  left  ventricle  is  the  pivot  on 
v^hich  turns  the  whole  future  course  of  the  disease.  So  long  as  the  heart  remains 
capable  of  performing  its  functions,  the  condition  of  the  patient  will  probably 
remain  endurable  if  not  actually  comfortable.  Finally,  however,  compensation 
is  sure  to  become  impaired;  and  then  appear  oedema,  dyspnoea,  debility,  and 
emaciation — in  short,  all  the  familiar  symptoms  of  cardiac  failure.  A  speedy 
end  may  be  brought  about  by  uraemia,  cerebral  embolism,  or  cerebral  haemorrhage ; 
but  in  other  cases  the  patient  suffers  for  years,  both  from  the  heart  disease  and 
from  fresh  arthritic  attacks. 

The  cardiac  hypertrophy  just  mentioned  is  the  result  of  the  contracted  kidney. 
Other  disturbances  of  the  circulatory  system  appear  to  be  referable  directly  to  the 
gout  itself.  Among  these  are  chronic  endocarditis  or  myocarditis,  and  perhaps 
■certain  "  functional "  symptoms,  such  as  palpitation  and  angina.  An  important 
symptom  is  chronic  endarteritis  or  arterio-sclerosis.  This  is  often  seen  in  gouty 
subjects,  and  in  many  instances  seems  to  be  connected  with  the  gout.  Some- 
times, also,  there  are  gouty  lesions  of  the  veins,  such  as  varicosities  or  throm- 
l)osis.  Of  course,  these  changes  in  the  blood-vessels  may,  in  their  turn,  give  rise 
to  various  disorders. 

In  a  few  very  rare  instances  gout  seems  to  attack  the  brain  and  spinal  cord. 
Usually,  however,  the  nervous  disturbances  seen  in  gout  are,  as  already  stated, 
symptoms  of  uraemia,  or  of  circulatory  disturbance,  arterio-sclerosis  of  the  cere- 
laral  arteries,  and  the  like.  The  patient  may  also  have  certain  functional  nervous 
troubles,  such  as  neixralgia  or  migraine.  The  direct  cause  of  these  is  seldom 
evident. 

Complications  of  Gout. — Apart  from  chance  complications  there  are  sevei'al 
morbid  conditions  which  undoubtedly  may  stand  in  close  relation  to  gout. 
Among  these  is,  first,  the  formation  of  renal  calculi,  or  gravel  (q.  v.).  This 
has  often  been  observed  in  gouty  persons.  Another  not  very  infrequent  combina- 
tion is  gout  and  diabetes  mellitus;  ordinarily,  attacks  of  gout  appear  first,  and 
later  glycosuria  develops.  Often  gout  and  diabetes  seem  to  alternate.  The  con- 
nection between  the  two  affections  seems  to  us  to  be  that  both  diseases  result 
from  the  same  cause  (chronic  alcoholism,  less  often  heredity),  so  that  they  de- 
velop together,  or  one  after  the  other.  Equally  obvious  is  the  explanation  of  the 
frequent  association  of  gout  with  obesity,  arterio-sclerosis,  etc. 

Anatomical  Changes  in  Gout.  Theory  of  its  Nature. — The  essential  ana- 
tomical lesion  in  gout  consists  in  an  abundant  deposit  of  crystalline  urates  in  the 
tissues.  This  is  most  evident  in  the  affected  joints,  the  cartilaginous  surfaces  of 
which  are  often  completely  covered  with  white,  chalk-like  material.  In  severe 
■cases  the  same  appearance  may  also  be  presented  by  the  articular  ligaments,  ten- 


TT6  CONSTITUTIO^TAL  DISEASES 

dons,  and  bursse,  while  there  are  at  the  same  time  numerous  concretions  of  urates 
here  and  there  beneath  the  skin.  These  deposits  are  composed  mainly  of  acid 
sodic  urate,  with  traces  of  calcic  urate,  calcic  phosphate,  and  sodic  chloride. 
However  certain  it  is  that  these  abnormal  deposits  of  uric  acid  should  be  regarded 
as  the  pathognomonic  sign  of  gout,  we  are  absolutely  without  knowledge  as  to 
their  origin  and  intrinsic  importance.  One  question  in  particular  remains  un- 
solved— whether  the  deposits  of  uric  acid  excite  the  inflammatory  symptoms,  or 
whether,  conversely,  the  deposits  of  uric  acid  are  secondary  and  are  formed  in  tis- 
sues already  attacked  by  the  disease.  Ebstein  believes  that  the  process  of  the  pre- 
cipitation of  uric  acid  is  invariably  preceded  by  a  tissue  necrosis.  The  uric  acid 
while  still  in  solution  acts  as  a  chemical  irritant  upon  the  cartilage  here  and  there, 
and  thus  produces  necrosis,  whereupon  the  urates  are  crystallized  out  and  depos- 
ited ;  but  this  view  has  not  escaped  contradiction,  and  possibly  the  primary  damage 
in  gout  is  due  not  to  the  uric  acid  itself,  but  to  some  other  noxious  substance. 

The  nephritis  of  gout  corresponds  in  its  pathological  appearances  to  that  of  the 
true  contracted  kidney,  with  one  exception;  the  organs  usually  present  deposits- 
of  uric  acid  or  urates,  in  stripes,  both  in  the  lumen  of  the  urinary  tubules  and  also 
in  the  epithelial  cells  and  the  interstitial  tissue.  In  the  connective  tissue  it  is 
probable  that  some  lesion  precedes  the  deposit. 

The  lesions  presented  by  the  heart,  blood-vessels,  and  remaining  parts  of  the 
body  are  not  especially  characteristic  of  the  disease.  The  blood  of  gouty  subjects, 
as  Garrod  demonstrated,  contains  an  excess  of  uric  acid. 

With  regard  to  the  true  nature  of  gout  our  knowledge  is  still  more  limited  and 
unreliable  than  in  the  case  of  diabetes.  The  earlier  view  was  that  in  g-out  an 
excessive  formation  of  uric  acid  took  place  because  of  the  incomplete  oxidation 
of  uric  acid  into  urea.  This  view  has  been  losing  ground,  because  of  late  it  is- 
assumed  that  uric  acid  is  not  at  all  an  end-product  of  the  ordinary  metamorphosis 
of  albumen,  but  that  it  is  the  specific  product  of  the  metamorphosis  of  nucleine, 
which  is  the  special  form  of  albumen  contained  in  the  cell  nuclei ;  thus  uric  acid 
resembles  the  alloxur  bases — that  is,  xanthine,  hypoxanthine,  etc.  Upon  the  in- 
gestion of  ordinary  albumen  the  uric  acid  is  not  increased,  but  it  is  increased  by 
food  rich  in  nucleine — for  example,  liver  or  sweetbread.  The  formation  of  uric 
acid  seems,  however,  to  be  particularly  favored  by  the  destruction  of  the  nucleines 
already  organized  in  the  body,  and  especially  the  nvicleated  white  corpuscles,  but 
whether  there  is  in  gout  an  actual  increase  in  the  amount  of  uric  acid,  or  whether 
merely  a  normal  amount  is  formed  and  its  excretion  through  the  kidneys  is  hin- 
dered, we  are  entirely  unable  to  say.  Many  authors  have  assumed  that  the  blood 
is  less  alkaline  than  normal,  and  consequently  uric  acid  is  deposited  in  the  tis- 
sues ;  but  the  most  reliable  investigations  do  not  indicate  any  marked  change  in 
the  alkalinity  of  the  blood.  In  brief,  the  true  riddle  of  gout,  the  special  role 
which  uric  acid  plays  in  this  disease,  is  as  yet  unsolved. 

Diagnosis. — It  is  usually  easy  to  recognize  an  acute  attack  of  gout.  The  sud- 
den onset  of  the  pain  and  its  localization  in  one  of  the  great  toes  are  very  char- 
acteristic symptoms,  and  render  it  easy  to  distinguish  between  it  and  other  acute 
affections  of  the  joints.  When  an  acute  attack  of  gout  affects  other  joints, 
we  have  a  sudden  develo]Dment  of  marked  swelling  and  tenderness  in  one  single 
place,  and  a  comparatively  rapid  abatement  of  the  inflammation,  while  in  acute 
articular  rheumatism  the  disease  attacks  several  joints,  and  moves  quickly  from 
one  to  another;  so  that  usually  the  two  diseases  can  be  readily  distinguished. 
The  diagnosis  is  more  difficult  in  advanced  stages  of  the  disease,  in  which  the 
symptoms  are  more  obscure,  but  in  such  cases  we  can  usually  obtain,  by  careful 
questioning,  an  account  of  the  previous  occurrence  of  typical  gouty  paroxysms 
and  the  existence  of  certain  setiological  factors,  such  as  heredity,  mode  of  life, 
or  chronic  poisoning  from  alcohol  or  lead,  which  are  of  considerable  diagnostic 


GOUT  777 

importance.  In  chronic  articular  gout  the  main  question  is  its  diagnosis  from 
ordinary  arthi-itis  deformans.  The  external  appearance  of  the  diseased  joints 
is  not  of  itself  decisive,  although  the  gouty  arthritis  leads  to  greater  and  more 
diffuse  enlargement,  especially  in  the  fingers,  and  much  oftener  occasions  com- 
plete anchylosis  in  individual  joints  than  does  arthritis  deformans.  The  most  im- 
portant means  of  diagnosis,  however,  in  every  case,  are  a  careful  inquiry  into  the 
previous  history  with  regard  to  typical  attacks  of  gout,  and  a  consideration  of  the 
characteristic  gouty  changes — such  as  tophi  breaking  open.  We  should  also  bear  in 
mind,  with  regard  to  differential  diagnosis,  the  chronic  arthritis  of  gonorrhoea. 

If  there  is  chronic  nephritis  of  gouty  origin,  its  source  can  be  recognized  only 
from  its  association  with  other  indubitable  symptoms  of  gout,  particularly  typi- 
cal gouty  paroxysms,  unless  possibly  the  knowledge  of  certain  setiological  factors, 
such  as  a  history  of  gout  in  the  family  or  of  chronic  lead-poisoning,  should  put  us 
upon  the  right  track.  Ebstein  has  reported  cases  of  "  primary  renal  gout  "  where 
there  was  no  arthritis  during  the  whole  course  of  the  disease.  Such  cases  can 
seldom  be  correctly  diagnosticated  during  life. 

Brief  mention  should  here  be  made  of  an  experiment  performed  by  Garrod, 
which  may  be  employed  to  demonstrate  the  existence  of  uric  acid  in  the  blood,  for 
diagnostic  purposes.  A  drachm  or  two  of  blood-serum,  or  of  the  serum  obtained 
from  a  fly-blister,  is  put  into  a  shallow  watch-glass,  and  six  or  eight. drops  of  a 
thirty-per-cent.  solution  of  acetic  acid  are  added  to  it.  A  linen  thread  is  then 
laid  in  the  fluid,  and  the  whole  allowed  to  remain  at  a  moderate  temperature  for 
about  a  day.  If  the  proportion  of  uric  acid  in  the  fluid  is  sufficiently  large,  crystals 
of  that  acid  will  now  be  found  on  the  thread  and  may  be  recognized  by  their  shape 
and  chemical  reaction.  This  "  thread  test "  of  Garrod's  is  not  extensively  used, 
because  it  does  not  succeed  unless  there  is  a  comparatively  large  amount  of  uric 
acid  in  the  blood,  and,  furthermore,  uric  acid  may  exist  in  the  blood  in  health,  or 
in  other  diseases  than  gout. 

Prognosis. — However  favorable  the  prognosis  may  be  with  regard  to  the  sin- 
gle gouty  attack,  yet  a  permanent  release  from  the  disease  is  rarely  to  be  hoped 
for.  Only  such  patients  as,  from  the  first  appearance  of  gout,  pursue  most  care- 
fully all  the  requisite  prophylactic  and  dietetic  measures,  can  expect  that  future 
attacks  will  be  rare  and  comparatively  mild,  and  that  severe  lesions  of  the  internal 
organs  will  not  occur.  So  long  as  the  kidneys  and  other  viscera  are  intact,  there 
is  no  immediate  danger  to  life,  and  the  patient  may  attain  advanced  years 
despite  his  gout.  The  gradual  and  chronic  alterations  in  the  joints  may,  how- 
ever, impede  locomotion  as  well  as  all  other  movements  of  the  body.  Except  for 
this,  the  general  condition  of  the  patient  in  the  intervals  between  the  attacks  is 
often  one  of  tolerable  comfort.  Indeed,  it  is  frequently  the  case  that  the  patient 
will  feel  at  his  very  best  directly  after  a  severe  paroxysm,  while  rudimentary  or 
atypical  attacks  are  often  regarded  as  an  ill  omen.  Really,  however,  there  is  no 
serious  danger  until  chronic  nephritis  has  developed.  The  prognosis  then  be- 
comes as  unfavorable  as  in  the  other  forms  of  contracted  kidney  (q.v.),  and 
involves  the  same  possibilities. 

Treatment. — All  authorities  agree  that  the  first  essential  in  treating  gout  is  a 
proper  regimen.  Unless  the  patient  has  energy  enough  to  yield  the  most  implicit 
obedience  to  the  injunctions  regarding  diet  and  mode  of  life  in  general,  from  the 
first  appearance  of  his  disease,  no  great  benefit  can  be  obtained  from  treatment. 

Various  authorities  have,  of  late,  prescribed  special  diets  for  the  gouty.  The 
various  and  almost  contradictory  theories  as  to  the  nature  of  gout  have  led  to 
extremely  diverse  dietetic  injunctions.  If  we  cling  to  simple  practical  experi- 
ence, the  general  conclusion  for  centuries  has  been  that  we  should  enjoin  upon 
gouty  subjects  moderation  in  everything,  most  of  all  in  alcoholic  beverages,  and 
in  meat. 


778  co:n"stitutional  diseases 

We  should  advise,  therefore,  that  the  total  amount  of  meat  eaten  should  be 
limited,  and  that  so-called  "  white  "  meat  (veal,  mutton,  fowl,  fish)  should,  on  the 
whole,  be  preferred  to  "  red"  meat  (beef  and  game).  The  cellular  organs  (liver, 
kidneys,  sweetbread,  brain)  are  now  usually  forbidden,  out  of  regard  to  the  above- 
mentioned  views  as  to  the  formation  of  uric  acid.  Milk  and  eggs  may  be  allowed, 
fat  and  carbohydrates  are  to  be  given  freely,  or  to  be  limited,  according  to  the 
general  nutrition  of  the  patient.  Gouty  subjects  who  are  obese  should  have  less 
of  such  articles  of  diet,  while  emaciated  patients  should  be  encouraged  to  par- 
take of  them.  Green  vegetables  that  are  easily  digested,  such  as  spinach,  salad, 
kohl  rabi,  cauliflower,  Brussels  sprouts,  and  asparagus,  have  long  been  regarded  as 
especially  suitable.  The  most  appropriate  beverages  are  water,  milk,  tea,  and 
coffee,  also  the  ordinary  mineral  waters,  Seltzer,  Giesshiibler,  and  lemonade. 
Emits,  especially  when  cooked,  are  usually  permissible  and  to  be  recommended. 
Such  alcoholic  beverages  as  beer  and  wine  are  to  be  allowed  in  very  small  quan- 
tities, if  at  all.  In  general,  we  should  not  be  schematic  and  theoretical  in  our 
dietetic  prescriptions,  but  should  consider  the  individual.  The  quality  of  the 
articles  of  food  eaten  is,  on  the  whole,  usually  less  important  than  the  total 
quantity. 

[Many  gouty  persons,  especially  those  suffering  from  the  irregular  form  of  the 
disease  and-  acid  dyspepsia,  are  more  comfortable  and  seem  to  do  better  on  a  diet 
which  is  largely  nitrogenous,  the  starches  and  sugars  being  greatly  limited  in 
amount.  The  diet,  in  fact,  should  be  similar  to  that  laid  down  for  diabetes  melli- 
tus,  though  not  so  strictly  carried  out.  In  chronic  and  irregular  cases  it  is  often 
■desirable  to  prescribe  a  stimulant,  for  a  time  at  least;  brandy,  whisky,  or  gin, 
well  diluted  with  water,  is  perhaps  the  best  form.] 

By  thus  limiting  the  amount  of  food  taken,  we  shall  avoid  any  excessive  for- 
mation of  uric  acid,  and  perhaps  other  harmful  substances ;  but  a  direct  means 
of  promoting  metabolism  is  rauscular  exercise.  If  a  corpulent  patient  is  still 
vigorous  and  is  not  threatened  by  any  serious  internal  disease,  he  should  be  urged 
to  take  a  large  amount  of  exercise  in  mountain-climbing,  gymnastics,  gardening, 
or  similar  pursuits.  This  same  indication  of  accelerating  tissue-metamorphosis 
is  fulfilled  also  by  bathing.  In  early  stages  cool  baths  and  sponging  are  useful, 
as  are  also  baths  containing  common  salt,  or  perhaps  even  sea-bathing  cautiously 
employed.  In  more  advanced  cases,  particularly  if  the  joints  present  permanent 
lesions,  the  warmer  baths  are  more  desirable,  such  as  are  found  in  Wiesbaden, 
Baden-Baden,  Teplitz,  Ems,  and  Aix. 

The  internal  administration  of  alkalies  is  an  efficient  adjuvant  to  the  dietetic 
and  hygienic  prescriptions  above  enumerated.  Although  there  may  be  doubt 
about  the  correctness  of  the  ordinary  theoretical  basis  for  this  prescription — viz., 
that  alkalies  prevent  the  deposit  of  uric  acid  in  the  tissues — yet  simple  practical 
experience  justifies  the  employment  of  suitable  mineral  waters.  These  waters 
stimulate  the  conversion  of  the  albuminoids,  increase  the  activity  of  the  kidneys, 
benefit  gastric  catarrh,  and  overcome  constipation,  and  in  all  these  ways  combine 
to  produce  a  favorable  effect  upon  the  patient's  health.  Still  another  factor  is  the 
judicious  diet  and  mode  of  life  at  such  health-resorts.  The  waters  of  Carlsbad 
and  Yichy  have  gained  the  greatest  repute  in  gout,  although  the  waters  of  Ems 
and  Neuenahr  have  an  analogous  composition,  and  doubtless  they  would  produce 
similar  effects.  The  same  is  true  of  Kronenquelle  and  Fachinger-water.  Most  of 
these  waters  can  be  taken  very  well  in  the  patient's  own  home.  The  salts  of 
lithium  especially  promote  the  solution  of  uric  acid,  and  the  waters  which  contain 
lithium  have  been  strongly  recommended.  The  natural  springs  of  this  sort,  such 
as  the  Crown  Spring  in  Obersalzbrunn,  and  those  of  Assmannshausen  and  Salz- 
chlirf,  contain  comparatively  insignificant  amounts  of  lithium;  and  it  might  be 
a  better  way  to  use  the  artificial  lithium  waters,  such  as  are  made  by  Struve  or 


OBESITY  Y79 

Ewich.  Another  way  is  to  prescribe  carbonate  of  lithium,  in  powders  containing 
two  or  three  grains  each  (gramme  0.10-0.20),  one  powder  two  or  three  times  a  day, 
in  a  glass  of  Seltzer  or  Biliner  water. 

As  to  the  treatment  of  the  acute  attack,  it  has  ceased  to  be  customary  to  em- 
ploy any  potent  remedies.  The  patient  must,  of  course,  keep  his  bed.  The 
affected  joint  should  be  wrapped  up  in  cotton  wool,  the  whole  leg  elevated,  and  a 
proper  diet  strictly  enjoined.  Free  movement  of  the  bowels  should  be  maintained 
by  means  of  enemata.  If  there  is  considerable  gastric  disturbance,  bicarbonate 
of  sodium,  magiiesia,  or  some  bitter  may  be  prescribed.  The  most  certain  remedy 
for  severe  pain  is  a  subcutaneous  injection  of  morphine.  Less  efficient  are  nar- 
cotics locally  applied,  and  warm  compresses.  Whether  any  internal  remedies  are 
calculated  to  abbreviate  the  attack  is  doubtful.  Formerly  colchicum  (twenty  or 
thirty  drops  of  vinum  colchici  seminis  three  or  four  times  a  day)  was  the  favorite 
medicine,  but  it  seems  to  be  going  out  of  use.  Salicylic  acid  and  salicylate  of 
sodium  may  be  administered  in  the  same  way  as  in  acute  articular  rheumatism, 
and  sometimes,  although  not  always,  they  are  followed  by  improvement.  Anti- 
pyrine,  salipyrine,  salol,  and  similar  remedies  sometimes  succeed  in  allaying  the 
pain  in  the  joints.  Some  physicians  recommend  subcutaneous  injections  of  anti- 
pyrine  in  the  neighborhood  of  the  joint,  but  we  have  no  personal  experience  on 
this  point.  On  the  basis  of  dubious  theoretical  assumptions,  a  number  of  drugs 
have  been  recommended  recently  which  possess  the  power  of  dissolving  large 
amounts  of  uric  acid.  Prominent  among  these  are  piperazine,  of  which  about 
eight  grains  (gramme  0.5)  are  given  daily  in  soda-water;  and  lysidine,  fi.fteen  to 
seventy-five  minims  (cubic  centimetres  1-5)  of  a  fi^fty-per-cent.  solution  daily. 
Many  physicians  report  favorable  results  with  these  remedies ;  others,  on  the  con- 
trary, have  found  no  virtue  in  them. 

[One  reason  why  colchicum  has  fallen  into  relative  disuse  is  that  the  relief 
obtained  from  it  is  often  so  prompt  and  complete  that  patients  are  tempted  into 
continued  indulgence  in  a  faulty  manner  of  life.  It  is  also  supposed  by  some 
that  the  drug  interferes  with  the  effort  of  nature  to  eliminate  the  poison,  which 
hecomes  generally  diffused,  and  sets  up  changes  in  the  vessels  and  internal 
organs.  Precisely  how  colchicum  acts  we  do  not  know,  but  that  it  does  act,  and 
sometimes  with  marvelous  success,  there  can  be  no  question.] 

The  chronic  affections  of  the  joints  in  gout  are  treated  as  are  other  varieties 
of  chronic  arthritis.  The  most  efficient  remedies  are  cautious  massage  and  baths, 
including  hot  sulphur  baths  and  mud-and-sulphur  baths.  The  internal  adminis- 
tration of  the  alkalies,  lithium,  and  similar  drugs,  to  combat  the  general  gouty 
•diathesis,  should  be  associated  with  these  external  remedies.  Some  physicians 
report  that  iodide  of  potassium  favors  the  absorption  of  the  gouty  deposits. 

The  treatment  of  the  nephritis  and  other  complications  need  not  be  discussed 
at  length.  The  gout  itself  should  always  be  the  main  object  of  our  therapeutic 
•efforts,  and  beyond  this  we  may  be  guided  by  general  principles. 


CHAPTER   XII 

OBESITY 

{Corpulence.     Poly-mrvia  adiposa) 

Definition  and  2Etiologj. — The  amount  of  adipose  tissue  in  the  body  is  sub- 
ject to  considerable  variation,  and  it  is  not  possible  to  state  absolutely  what 
should  be  considered  as  normal  and  what  as  abnormal.    For  practical  purposes  we 


780  CONSTITUTIOITAL  DISEASES 

may  draw  the  line  where  the  increased  size  grows  burdensome  to  the  individual. 
After  a  certain  point,  any  further  addition  to  the  amount  of  fatty  tissue  is  almost 
sure  to  work  serious  injury,  and  is  therefore  to  be  regarded  as  an  actual  disease, 
and  not  merely  an  inconvenience.  It  should  be  said,  however,  that  in  such  cases 
the  symptoms  of  obesity  are  very  frequently  confounded  with  those  springing 
from  other  disorders — these  latter  possessing,  indeed,  the  same  aetiology  as  obes- 
ity, but  distinct  from  it. 

The  most  frequent  and  important  cause  of  obesity  is  the  habitual  ingestion  of 
too  large  an  amount  of  food.  By  "  too  large  "  is  meant  an  amount  sufficient  to 
occasion  a  continual  increase  of  the  adipose  tissue  of  the  body,  when  this  is 
already  fairly  well  developed.  It  is  a  matter  of  indifference  whether  the  excess  is 
composed  mainly  of  albuminoids,  carbohydrates,  or  fats ;  for  in  either  case,  if 
the  quantity  be  sufficient,  an  increase  of  adipose  tissue  may  take  place.  We 
shall  soon  see,  however,  that  the  excess  is  usually  in  fat  and  carbohydrates.  Inas- 
much as  this  overfeeding  is  almost  certain  to  be  habitual,  the  excess  at  any  one 
time  need  not  be  at  all  large.  We  often  hear  a  corpulent  person  express  his  sur- 
prise that  he  grows  heavier  every  day,  although  he  "  does  not  eat  any  more  than 
others  who  are  lean."  The  explanation  is  easy  if  we  consider  that  a  daily  in- 
crease of  five  grammes  of  fat  (one  and  one  fourth  drachm)  suffices  to  increase 
the  weight  in  ten  years — for  example,  between  the  thirty-fifth  and  forty-fifth 
years — forty  pounds  avoirdupois.  In  reality  the  daily  increase  is  sometimes 
greater  than  this. 

The  basis  for  a  detailed  consideration  of  the  causes  which  lead  to  the  deposit 
of  fat  will  be  gained  by  a  consideration  of  the  physiological  laws  relating  to  nutri- 
tion discovered  by  Yoit,  Pettenkofer,  and  their  pupils.  It  has  been  shown  that 
both  the  albuminoids  and  the  carbohydrates  of  the  food  may  be  a  source  of  fat,, 
formed  within  the  economy,  and  also  that  the  fat  contained  in  the  food  may  be  to 
a  large  extent  directly  deposited  in  the  fat-cells  of  the  body.  One  product  of  the 
decomposition  of  albuminoid  substances  is  invariably  fat.  This  usually  under- 
goes further  oxidation,  but  it  is  sometimes  retained  unaltered  in  the  system.  It 
would  even  seem  that  the  albuminoids  give  rise  to  much  more  of  the  fatty  tissues 
of  the  body  than  are  produced  from  the  carbohydrates  ingested,  although  there  is. 
no  doubt  that  these  latter  may  also  yield  fat.  Carbohydrates  do  promote  obesity,, 
but  less  because  they  are  a  direct  source  of  fat  than  because  they  are  easily  de- 
composed, and  so  shield  both  the  ingested  fat  and  that  which  is  formed  out  of 
the  albuminoids  from  oxidation.  In  this  indirect  way  they  do  greatly  favor  a 
tendency  to  corpulence. 

We  thus  perceive  that  various  diets  may,  each  one  of  them,  permit  of  an 
increase  of  adipose  tissue.  In  actual  life,  of  course,  the  most  frequent  conditions 
are  such  as  result  from  the  customs  and  habits  of  the  population  in  general.  The 
diet  is  almost  invariably  a  "  mixed  "  one — that  is,  it  contains  albumen,  fat,  and 
carbohydrates — and  in  most  instances  the  obesity  is  due  to  an  excessive  amount 
of  all  three  elements,  or  at  least  of  the  fat  and  carbohydrates.  A  person  may,, 
however,  become  corpulent  who  eats  very  little  fat,  provided  he  consumes  a  large 
quantity  of  albuminoids  and  carbohydrates;  or  if  he  eats  very  little  starchy  food, 
provided  he  consumes  a  large  amount  of  meat  and  fat.  Perhaps  these  facts  may 
be  made  clearer  by  giving  a  concrete  example.  Voit  tells  us  that  a  vigorous 
man  who  requires  daily  118  grammes  of  albumen  and  259  grammes  of  fat  to 
maintain  a  physiological  equilibrium  as  regards  fat  and  albumen  will,  other 
things  being  equal,  begin  to  store  up  fat  if  there  is  any  further  increase  in  the 
amount  of  fat  in  his  diet.  The  same  result  will  also  take  place  if,  instead  of  the 
rations  previously  stated,  he  ingests  more  than  118  grammes  of  albumen  and 
600  grammes  of  starch,  or  more  than  664  grammes  of  albumen  alone,  or,  finally, 
more  than  118  grammes  of  albumen,  100  grammes  of  fat,  and  368  grammes  of 


OBESITY  Y81 

starch.*  It  is  obvious  that  this  last  diet,  which  closely  resembles  the  average 
diet  of  an  adult  f  in  good  circumstances,  whose  weight  is  neither  increasing  nor 
diminishing,  is  the  one  most  likely  to  be  exceeded;  whereupon  there  must  take 
place  a  deposition  within  the  system  of  the  superfluous  fat. 

Among-  the  various  kinds  of  food  is  one  group  which  deserves  mention,  as 
being  an  important  factor  in  many  cases  of  obesity;  we  refer  to  alcoholic  bever- 
ages. There  can  be  no  doubt  that  intemperance  in  this  regard  plays  a  prominent 
part  in  many  instances.  Sufficient  illustration  is  furnished  by  brewers,  hotel- 
keepers,  and  the  inhabitants  of  countries  like  Bavaria,  where  beer-drinking  is 
prevalent.  In  this  particular  it  is  evident  that  beer  works  more  harm  than  does 
wine  or  strong  liquor ;  for  beer  contains,  in  addition  to  the  alcohol,  an  appreciable 
amount  of  starchy  material,  making  the  sum  total  from  the  beer  drunk  during 
the  entire  day  a  considerable  one.  Many  persons  who  would  be  extremely  indig- 
nant if  called  "  tipplers,"  habitually  take  five  or  six  glasses  of  beer  a  day,  equiva- 
lent to  150  grammes  of  starch,  or,  in  other  words,  to  one  half  the  total  amount  of 
starch  required  by  the  system.  Even  this  quantity  is  frequently  exceeded.  Of 
course,  the  three  or  four  per  cent,  of  alcohol  which  the  beer  contains  also  pro- 
motes the  deposition  of  fat.  Alcohol  is  readily  oxidizable,  and  it  thus  shields  to  a 
considerable  extent  the  fat  already  present  in  the  body ;  and  it  also,  in  all  proba- 
bility, works  such  injury  to  the  tissues  as  to  diminish  their  power  of  effecting 
decomposition.  We  must  also  remember  that  most  beer  drinkers  take  little  exer- 
cise. The  long  sitting  at  the  beer  table,  and  the  mental  and  physical  sluggishness 
which  immoderate  indulgence  in  beer  always  causes,  and  finally  the  increasing 
corpulence  itself,  explain  why  most  beer  drinkers  dislike  protracted  exercise. 

We  have  thus  seen  that  in  by  far  the  larger  number  of  cases  obesity  is  mainly 
due  to  the  ingestion  of  too  much  food.  'No  weight  need  be  attached  to  the  usual 
statement  of  corpulent  persons,  that  they  eat  no  more  than  others.  Few  of  them 
have  any  idea  how  much  nourishment  they  do  consume.  Others,  having  already 
become  corpulent,  eat  less,  to  be  sure,  than  they  used  to,  but  nevertheless  an 
amount  sufficient  to  maintain  the  acquired  weight. 

Other  factors  may  no  doubt  exert  an  influence  upon  the  increase  of  adipose 
tissue  by  diminishing  the  consumption  of  fat  in  the  system.  The  most  important 
factor  of  this  class  is  physical  inactivity.  Muscular  contractions  lead  to  the  de- 
composition of  a  large  amount  of  fat.  This  explains  why  people  of  sedentary 
habits,  and  those  who  sleep  long  and  exercise  little,  are  more  apt  to  become  corpu- 
lent than  are  manual  laborers.  Again,  there  are  certain  diseases  which  seem  to 
promote  corpulence.  In  anaemia  there  is  sometimes  a  striking  tendency  to  obesity, 
due  in  part  to  the  diminished  supply  of  oxygen  and  in  part  to  diminished  muscu- 
lar activity.  This  same  inactivity  is  probably  the  main  cause  of  corpulence  in 
paralysis  (hemiplegia).  It  may  be,  however,  that  disturbances  of  the  nervous 
system  may  directly  afl^ect  metamorphosis.  Thus,  idiots  and  other  subjects  of 
congenital  defects  of  the  brain  are  liable  to  obesity.  Disturbances  of  the  circu- 
latory system  seem  to  favor  the  production  of  corpulence  by  impairing  oxidation. 
This  is  seen  in  many  young  persons  with  cardiac  disease,  although  it  is  not  easy 
to  exclude  in  this  case  the  influence  of  still  other  factors,  such  as  a  sedentary  life. 

Finally,  some  cases  of  obesity  seem  to  result  from  a  constitutional  and  inborn 

*  This  statement  is  founded  upon  an  important  discovery  of  Rubncr,  tliat,  as  far  as  the  storinfr  up 
of  fat  is  concerned,  the  measure  of  value  for  different  foods  is  the  amount  of  lieat  given  oflt'  l>y  them 
when  they  underfro  oxidation  into  carbonic-dioxide  f(as  and  water.  Measured  in  this  way,  100  grm. 
fat  =  'Jll  grm.  albumen  —  232  grm.  starch  =  234  grm.  cane-sugar  =  256  grm.  grape-sugar. 

+  Probably  tlie  amount  of  fat  contained  in  the  food  is  often  less  than  tlie  above,  and  the  amounts 
of  albumen  and  starch  somewhat  larger.  Voit  estimates  the  diet  of  a  well-to-do  person  at  127  grm. 
albumen,  89  grm.  fat,  and  362  grm.  starch  ;  and  that  for  a  vigorous  laborer  at  118  grm.  albumen,  56 
grm.  fat,  and  500  grm.  starch.     Of  course,  these  figures  are  merely  approximate. 


782  CONSTITUTIONAL   DISEASES 

predisposition.  Young-  children  sometimes  suffer  from  obesity;  and  the  condi- 
tion seems  in  many  cases  to  be  hereditary.  Many  races  and  nations  exhibit  an 
especial  tendency  to  corpulence — for  example,  the  Jews.  Age  and  sex  have  some 
importance  in  this  regard :  extreme  obesity  is  seldom  seen  previously  to  the  thir- 
tieth year;  and  women  appear  to  be  somewhat  more  subject  to  the  disease  than 
men.  The  importance  of  a  "  tendency  "  to  obesity  should  not  be  overrated.  Upon 
careful  investigation,  we  shall  almost  invariably  find  in  the  habits  of  the  indi- 
vidual, as  regards  food  and  exercise,  a  satisfactory  explanation  of  his  obesity. 
Still,  it  may  be  possible  that  upon  accurate  examinations  into  metabolism  it 
would  be  found  that  the  power  of  fat-combustion  is  subnormal  in  many  persons,, 
analogous  to  the  impaired  combustion  of  carbohydrates  in  diabetics.  This  dimi- 
nution of  the  oxidizing  function  might  be  due  to  congenital  or  acquired  anoma- 
lies. If  our  supposition  prove  correct,  it  might  explain  the  not  infrequent  com- 
bination of  obesity  and  diabetes  {q.  v.),  or  obesity  and  gout.  Strictly  speak- 
ing, the  condition  can  not  be  regarded  as  a  disease  unless  the  habits  as  to  diet 
and  exercise  fail  to  account  for  it. 

Pathology. — After  corpulence  has  passed  a  certain  point  the  condition  is  evi- 
dent at  the  first  glance.  The  subcutaneous  cellular  tissue  is  one  of  the  chief 
places  in  which  the  fat  is  deposited.  Consequently,  the  panniculus  adiposus  soon 
attains  considerable  thickness.  The  countenance  grows  more  round  and  plump; 
beneath  the  chin  is  formed  a  second  prominence  known  as  the  "  double  chin  " ;  the 
chest  appears  broadened;  the  waist  enlarg-es;  and,  particularly  in  women,  the 
breasts  are  changed  to  great  shapeless  masses,  over  which  the  skin  is  so  tightly 
stretched  as  to  present  linese  albicantes.  The  abdominal  walls  are  greatly  altered. 
The  belly  projects  more  and  more  until  it  becomes  actually  pendulous,  and  its 
lower  surface  touches  the  interior  surface  of  the  thighs.  Intertrigo  is  apt  to 
occur  in  the  groins,  below  the  breasts,  and  between  the  buttocks.  The  skin  every- 
where has  a  fatty  feel,  due  to  the  increased  secretion  of  the  sebaceous  glands. 
This  hyperplasia  of  the  fatty  tissue  in  the  panniculus  adiposus  is  associated  with 
a  deposit  of  fat  in  many  parts  of  the  interior  of  the  body,  including  the  mesen- 
tery, mediastinum,  pericardium,  and  the  capsules  of  the  kidneys.  Some  of  these 
will  be  mentioned  again  further  on. 

Of  course,  the  circumference  and  weight  of  the  body  become  greatly  increased. 
As  an  approximate  measure  it  may  be  stated  that  for  men  of  middle  height  a 
weight  exceeding  ninety  kilogrammes  (200  pounds),  and  for  women  seventy-five 
kilogrammes  (165  pounds),  may  be  regarded  as  abnormal.*  This  increase  in  bulk 
is  the  first  cause  of  subjective  symptoms.  An  obese  person  has  to  exert  a  greater 
effort  in  making  any  motion  than  do  other  people,  and  as  a  necessary  consequence 
he  gets  easily  tired,  and  seeks  as  far  as  possible  to  avoid  exertion.  The  increased 
demand  upon  the  muscles  explains  the  familiar  fact  that  corpulent  persons  per- 
spire readily. 

The  graver  symptoms  of  obesity,  and  properly  the  first  pathological  phe- 
nomena of  the  condition,  relate  to  the  respiration  and  the  circulation.  The 
patient  begins  to  complain  of  shortness  of  breath,  and  is  subject  to  marked  dysp- 
noea upon  running  or  climbing  stairs.  There  may  be,  at  the  same  time,  cardiac 
disturbance,  indicated  by  a  rapid  pulse,  palpitation,  intermission  of  the  pulse,  or 
other  slight  irregularities  in  cardiac  action.  All  these  symptoms  grow  gradually 
worse ;  and  to  them  are  added  symptoms  of  cardiac  failure  and  consequent  passive 
congestion.  There  is  a  tendency  to  bronchitis  and  other  catarrhal  troubles.  The 
appetite  and  digestion  are  affected,  and  oedema  appears. 

A  careful  analysis  of  all  these  symptoms  shows  that  many  causes  combine  to 
produce  them,  all  having  a  common  tendency  to  impede  respiration,  and,  still 

*  A  weight  of  even  150  kilogrammes  (330  pounds)  lias  been  repeatedly  observed. 


OBESITY  783 

more,  circulation.  One  source  of  disturbance  is  the  increased  deposit  of  fat  upon 
the  framework  of  the  body.  It  is  probable  that  the  excess  of  adipose  tissue  cover- 
ing the  thorax  exerts  a  direct  influence  in  obstructing  the  respiratory  motion  of 
the  thoracic  walls,  and  renders  the  respiration  more  superficial.  In  this  way  the 
return  of  venous  blood  to  the  heart  and  the  pulmonary  circulation  are  both  im- 
peded, because  the  negative  pressure  in  the  chest  is  less  than  normal.  Likewise 
the  diminished  amount  of  bodily  exercise  affects  the  circulation  unfavorably. 
Brauner  has  shown  how  numerous  are  the  arrangements  connected  with  the 
fasciae  for  promoting  the  venous  currents,  by  means  of  the  negative  pressure 
resulting  from  the  movements  of  the  body.  Whether  the  fat  deposited  around 
the  heart  directly  obstructs  the  cardiac  movements  is  somewhat  doubtful,  though 
this  view  is  held  by  many.  The  fatty  infiltration  of  the  myocardium  is  of  more 
importance:  the  fat  is  deposited  in  the  intermuscular  connective  tissue.  Still, 
it  is  doubtful  whether  this  condition,  which  is  not  so  very  frequent,  after  all, 
occurs  as  a  primary  change,  or  whether  it  is  not  rather  a  result  of  previous, 
atrophy  of  the  myocardium  (compare  the  chapter  on  fatty  heart). 

There  is  no  doubt  that,  in  almost  all  cases  where  the  corpulence  actually  in- 
duces grave  disturbance,  the  cardiac  symptoms  are  of  prime  importance.  These 
are  due,  as  has  just  been  indicated,  in  part  to  the  increased  amount  of  adipose 
tissue,  and  in  still  greater  part  to  complications,  most  of  which  are  excited  by  the 
same  causes  as  is  the  obesity  itself.  The  abundant  adipose  tissue  may  obstruct 
the  circulation  in  the  smaller  blood-vessels  and  capillaries  inclosed  within  it. 
Furthermore,  the  excessive  development  of  fatty  tissue  probably  leads  to  the 
growth  of  new  blood-vessels,  and,  as  a  consequence,  to  an  increase  in  the  total  vol- 
ume of  the  blood.  This  is  one  way  in  which  the  demands  made  upon  the  heart 
are  rendered  greater  than  normal,  and  explains  why  the  corpulent  frequently 
exhibit  cardiac  hypertrophy.  Other  influences  are  also  at  work  to  produce  this 
same  result:  they  are,  in  the  first  place,  the  same  factor  which  occasions  the 
obesity  itself,  namely,  the  ingestion  of  increased  amounts  of  food  and  drink  (see 
the  chapter  on  cardiac  hypertrophy),  and,  secondly,  certain  other  lesions  which 
are  frequently  associated  with  obesity  and  are  referable  to  the  same  causes  as  it 
is.  Chief  among  this  latter  class  is  general  arterio-sclerosis.  If  this  involve  the 
coronary  arteries,  it  may  in  turn  occasion  still  further  damage — for  example,  de- 
generative myocarditis  (compare  page  341).  Chronic  interstitial  nephritis  is  an- 
other not  infrequent  complication.  This  is  referable  in  part  to  the  same  causes 
as  is  the  obesity.    Gout  and  diabetes  are  less  frequent. 

We  thus  see  that  obesity  is  often  merely  one  of  many  injurious  results  occa- 
sioned by  an  improper  mode  of  life.  It  is,  in  a  certain  sense,  the  first  danger- 
signal,  warning  the  patient  and  his  physician  to  avoid  the  graver  disturbances 
which  threaten.  This  is  a  point  of  great  practical  importance;  for,  when  once 
we  have  a  combination  of  obesity  with  cardiac  hypertrophy,  fatty  infiltration  of 
the  heart,  arterio-sclerosis,  or  interstitial  nephritis,  the  various  causes  and  effects 
act  and  react  upon  one  another  in  a  way  most  perilous  to  health,  and  even  to  life. 
There  is  no  need  of  describing  the  grave  disturbances  which  invariably  develop 
at  the  close  of  the  scene.  They  are  the  result  of  chronic  cardiac  insufficiency,  and 
have  been  fully  described  under  cardiac  disease. 

In  every  case  of  obesity  the  physician  should  examine  the  heart,  lungs,  vascu- 
lar system,  and  kidneys,  particularly  if  there  be  already  subjective  disturbances. 
The  examination  of  the  heart  may  present  considerable  difficulties,  because  the 
results  of  palpation  and  percussion  are  so  much  obscured  by  the  thick  cushion  of 
fat  which  covers  the  thorax.  We  can,  however,  have  recourse  to  auscultation, 
and  can  feel  the  pulse.  The  pulse  may  be  either  rapid,  slow,  or  irregular. 
We  need  not  mention  any  minute  particulars  as  to  the  examination.  It  may 
be  stated,  however,  that  a  hepatic  enlargement  is  often  found,  but  it  is  much 


784  CONSTITUTIONAL   DISEASES 

less  often  the  result  of  fatty  infiltration  than  of  simple  hypertrophy  or  passive 
congestion. 

We  have  thus  seen  that  corpulence  may  sometimes  be  associated  with  grave 
and  dangerous  lesions ;  but,  on  the  other  hand,  it  should  be  stated  that  this  unfor- 
tunate condition  by  no  means  invariably  exists.  Not  infrequently  the  corpulence 
remains  moderate,  in  which  case  it  is  not  really  dangerous,  however  incon- 
venient. This  is  true  of  a  proportion  of  those  cases  which  are  due  to  the  in- 
gestion of  a  large  araount  of  nourishment,  associated  with  defective  oxidation, 
and  where  there  are  no  other  unfavorable  influences  at  work.  The  obesity  of 
hard  drinkers  is  almost  always  a  more  or  less  dangerous  condition,  while  that 
seen  in  many  elderly  persons  and  in  women  is  often  comparatively  free  from 
peril.  These  latter  individuals  are,  to  be  sure,  discommoded  by  their  great 
weight,  they  can  accomplish  less  than  they  used  to,  they  are  easily  put  out  of 
breath,  and  have  a  certain  tendency  to  catarrhal  inflammations  and  rheumatic 
difficulties;  but  they  escape  the  severer  lesions  above  enumerated.  Even  these 
apparently  harmless  conditions  should  not  be  disregarded  by  the  physician,  as  he 
can  never  be  absolutely  certain  that  grave  complications  may  not  be  developed 
eventually. 

Treatment  of  Obesity. — To  cause  the  disappearance  of  the  accumulated  fat,  it 
is  necessary  to  promote  its  oxidation  in  the  system  and  to  prevent  the  ingestion 
of  new  supplies  of  fat.  To  accomplish  this  purpose  we  possess  only  two  means — 
first,  a  limitation  of  the  ingestion  of  such  kinds  of  food  as  may  lead  to  the  forma- 
tion of  fat  in  the  system,  and,  secondly,  stimulation  of  muscular  activity  and 
other  factors  which  occasion  the  destruction  of  the  fat  already  present.  All  the 
various  methods  of  treating  obesity,  without  exception,  aim  either  to  diminish 
the  supply  or  to  increase  the  destruction  of  fat. 

The  methods  vary  greatly.  It  must  be  borne  in  mind  that  the  diminution  of 
the  adipose  tissue  must  not  involve  injury  to  the  body  itself.  The  treatment 
should  not  weaken  the  constitution,  but  should  invigorate  the  patient,  or  at  least 
be  innocuous. 

It  is  of  prime  importance,  in  every  method  of  treatment,  that  the  total  quan- 
tity of  ingested  food  should  be  diminished.  It  is  a  mistake  to  forbid  the  patient 
some  particular  kind  of  food — for  instance,  the  carbohydrates  or  the  fats — ^with 
the  idea  that  they  alone  do  harm,  or  to  allow  him  unlimited  quantities  of  other 
kinds  of  food,  in  the  belief  that  they  are  harmless.  Any  person  can  eat  albu- 
minoids, fat,  and  starch  at  every  meal,  and  yet  not  grow  fat ;  while,  on  the  other 
hand,  too  much  of  any  one  of  these  may  lead  to  an  increase  of  adipose  tissue. 
The  amount  of  food  which  a  person  can  take  without  increasing  the  amount  of 
adipose  tissue  varies  with  the  individual.  It  depends  upon  the  amount  of  mate- 
vial  already  present  in  the  body,  and  upon  the  various  demands  made  upon  the 
system,  as  well  as  other  factors.  This  renders  it  difficult  to  draw  up  a  universal 
dietary  for  the  obese.  We  can  best  judge  of  the  value  of  any  course  of  treatment 
by  its  results,  and  these  are  best  measured  by  the  weight  and  the  subjective  con- 
dition of  the  individual  patient. 

Of  the  various  elements  of  food,  the  albuminoids  should  be  diminished  least 
of  any,  because  it  would  be  sure  to  work  injury  to  the  system  if  they  were  sup- 
plied in  too  small  an  amount.  Of  course,  the  albuminoids  must  not  be  eaten  to 
such  an  extent  that  the  fat  into  which  they  decompose  remains  intact  in  the  body. 
An  increase  in  the  amount  of  nitrogenous  tissue  is,  however,  desirable,  because 
this  promotes  the  vigor  of  the  muscles  and  the  heart,  and  so  leads  to  the  oxidation  , 
of  larger  quantities  of  the  non-nitrogenous  tissues. 

The  amount  of  fat  and  starch  must  be  much  more  limited.  The  fats  and 
starches  are  more  potent  in  increasing  adipose  tissue  and  in  shielding  from  oxida- 
tion the  fat  already  stored  up  in  the  body  than  is  nitrogenous  food.     It  would 


OBESITY  785 

2iot  be  at  all  advisable  to  forbid  the  use  of  either  one  of  these  two  constituents  of 
a  mixed  diet,  allowing  the  other  alone  to  be  eaten.  A  varied  diet  is  extremely 
-desirable,  even  for  one  who  is  corpulent;  and  we  should  exclude  neither  fat  nor 
starch  wholly  from  the  dietary,  but  we  should  merely  limit  the  amounts  to  be 
taken.  As  already  indicated,  the  amount  of  albuminoid  food  remaining  un- 
•changed,  a  person  can  eat  double  the  quantity  of  starchy  food  that  he  can  of  fat, 
without  increasing  his  adipose  tissue.  It  is  therefore  irrational  to  allow  the  cor- 
jpulent  fat  in  larger  proportions  than  starchy  foods.  The  diet  which  Ebstein  has 
recently  proposed  for  the  treatment  of  obesity  does  prove  successful,  but  the  ex- 
planation of  its  success  lies  in  the  comparatively  small  amounts  of  meat  and  fat 
ingested.  Precisely  the  same  results  would  be  attained  if  a  corresponding 
.amount  of  starch  were  substituted  for  all  or  a  portion  of  the  fat ;  and  in  practice 
it  is  desirable,  at  least  in  most  eases,  to  allow  the  patient  both  starches  and  fats. 
Of  course,  the  likings  and  experience  of  the  individual  should  be  considered  in 
-each  separate  case.  The  Banting  treatment,  introduced  in  1864,  enjoyed  for  a 
time  a  great  reputation.  Its  inventor  applied  it  first  of  all  to  his  own  case,  and 
with  success.  It  rests  upon  a  rational  basis,  inasmuch  as  the  albuminoids  are 
allowed  in  abundance,  and  the  ingestion  of  fat  and  starch  is  limited.  It  lays 
too  much  stress,  however,  upon  the  exclusion  of  fat  as  compared  with  starch.  Of 
.great  practical  importance  in  many  cases  is  the  strict  prohibition  of  beer  drink- 
ing. Many  cases  of  obesity  are  due  merely  to  the  excessive  amount  of  carbo- 
iydrates  contained  in  the  unreasonable  quantity  of  beer  drunk  daily.  If  corpu- 
lent beer  drinkers  of  this  sort  change  their  mode  of  life  in  this  single  particular, 
and  drink  no  beer  whatever  for  from  three  to  six  months,  they  are  almost  sure  to 
lose  a  great  deal  of  weight. 

The  physician  who  bears  in  mind  the  principles  just  expounded  can  lay  down 
lis  own  rules  for  the  diet  of  his  patient.  As  already  stated,  it  is  impossible  to 
.^ive  figures  which  will  apply  to  every  case.  If  we  take  as  a  basis  the  average 
diet  for  an  adult — that  is,  about  125  grammes  of  albumen,  80  grammes  of  fat,  and 
■350  grammes  of  starch — we  might  say  that  most  cases  of  obesity  would  be  sure  to 
undergo  improvement  upon  a  diet  containing  125  grammes  albumen  (or  possibly 
■even  more  than  this),  40  grammes  fat,  and  150  grammes  starch.  The  amounts  of 
fat  and  starch  could  be  even  more  diminished,  but  it  is  usually  best  not  to  be  too 
precipitate.  A  gradual  diminution  of  two  or  three  pounds  a  week,  exteiiding 
-over  a  long  period  without  interruption,  is  to  be  preferred  to  the  rapid  treatment 
-common  at  many  health-resorts.  Of  course,  the  loss  of  fat  is  greater  at  the  com- 
mencement of  treatment  than  later  on,  when  the  amount  of  adipose  tissue  has 
already  approached  more  nearly  to  normal,  and  the  diet  must  undergo  a  gradual 
and  corresponding  change.  It  is  of  particular  importance  to  increase  the  amount 
of  non-nitrogenous  foods  in  the  later  stages  of  treatment,  lest  the  albuminoid 
tissues  of  the  body  become  wasted. 

The  following  dietary  may  be  taken  as  an  illustration  of  what  would  be  suit- 
able for  a  patient  in  the  beginning  of  treatment :  For  breakfast,  a  cup  of  coffee 
with  milk,  and  about  75  grammes  of  bread.  At  noon,  a  plate  of  soup,  150  to  175 
^grammes  of  lean  meat  or  fish,  lettuce,  green  vegetables,  and  about  25  grammes  of 
bread.  For  dessert,  about  75  grammes  of  boiled  rice,  or  some  simple  pudding,  or 
100  grammes  of  fruit.  To  quench  the  thirst,  water,  or  half  a  pint  of  light  wine. 
In  the  afternoon,  a  cup  of  coffee,  and  with  it  not  more  than  20  to  30  grammes  of 
bread.  For  supper,  two  eggs,  or  100  to  120  grammes  of  meat,  with  30  grammes  of 
bread,  a  little  fruit,  lettuce,  half  a  pint  of  wine,  or  one  or  two  cups  of  tea,  not  much 
sweetened.  Butter  should  be  entirely  proscribed  at  first;  later  on  it  may  be  used 
in  small  amounts. 

Some  approach  to  this  bill  of  fare  must  be  enforced  not  merely  for  a  few  weeks, 
but  for  months.  It  is  absolutely  necessaiy  that  the  patient  should  be  weighed 
50 


Y86  CONSTITUTIOI^AL   DISEASES 

every  two  or  three  weeks.  If  the  weight  diminishes  slowly  and  gradually,  with- 
out any  subjective  disturbance,  we  have  the  best  proof  that  the  diet  is  a  suitable 
one.  If  the  weight  does  not  diminish,  then  the  amount  of  ingesta  must  undergo 
further  reduction.  If  more  food  can  be  taken  without  the  weight  increasing 
again,  a  larger  amount  may  be  unhesitatingly  permitted,  and  indeed  may  even 
be  advisable  if  the  patient  be  languid.  The  increase  should  at  first,  however, 
be  m.ainly  in  the  amount  of  albuminous  food,  the  amount  of  starches  and  fats- 
not  being  much  increased.  The  "  cure  "  can  not  be  regarded  as  complete  until 
the  weight  has  been  brought  down  to  that  of  the  average  individual  of  the 
given  age  and  sex.  This  goal  having  been  reached,  greater  freedom  in  diet  is 
permissible. 

The  object  of  the  treatment  just  suggested  is  exclusively  the  limitation  of  the 
production  of  fat.  We  may  also  promote  the  destruction  of  the  fat  already  stored 
up  in  the  system.  A  chief  means  to  this  end  is  muscular  exercise,  which  undoubt- 
edly increases  the  oxidation  of  the  adipose  tissues.  Carried  out  in  a  proper  man- 
ner, it  is  therefore  a  most  valuable  adjuvant  to  treatment.  Oertel  has  recently 
pointed  out  that  muscular  exertion  does  good  in  still  another  way — namely,  by 
promoting  cardiac  activity  and  inducing  deep  respiratory  efforts.  Thus  the  heart 
is  strengthened  and  circulation  promoted.  Mountain-climbing  is  one  of  the  best 
modes  in  which  to  take  the  desired  exercise.  We  need  hardly  say  that  the 
increased  muscular  activity  makes  it  possible  for  the  patient  to  take  an  increased 
amount  of  food  without  injury.  In  dealing  with  cases  of  obesity  in  which  the 
condition  is  due  less  to  overfeeding  than  to  lack  of  muscular  exercise,  it  might 
be  decidedly  advisable  to  lay  the  most  stress  upon  the  increase  in  muscular  activ- 
ity; for  certainly  it  is  more  advantageous  for  the  organism  to  get  rid  of  its  excess 
of  fat  by  means  of  lively  metabolism,  while  nutrition  is  well  maintained,  than 
to  be  more  or  less  starved  by  an  excessive  limitation  of  diet.  We  should  not  rest 
satisfied  with  a  single  mountain  tour,  but  should  insist  upon  a  persistent  and 
considerable  employment  of  the  muscles  in  gymnastics,  walking,  and  the  like. 

Baths  also  promote  oxidation,  but  they  are  far  less  potent  than  is  muscular 
exercise.  Cold  baths,  brine  baths,  or  baths  containing  carbonic-acid  gas,  may  be 
employed.  One  way  in  which  they  do  good  is  by  stimulating  the  nervous  system, 
Oertel  regards  it  of  great  importance  to  diminish  the  amount  of  water  in  the  sys- 
tem, a  point  which  has  until  very  lately  received  little  attention.  The  diminution 
in  the  amount  of  fluids  may  ameliorate  any  circulatory  disturbance  (vide  supra) 
and  relieve  venous  congestion,  and  it  undoubtedly  has  some  value  in  the  treat- 
ment of  obesity.  Oertel  has  shown  that  a  simple  diminution  in  the  amount  o£ 
fluids  ingested,  when  there  is  no  other  change  in  the  diet  or  mode  of  life,  will 
effect  a  diminution  of  the  adipose  tissues.  This  result  is  probably  due  mainly  to 
the  diminished  strain  upon  the  heart  and  the  consequent  increase  of  oxidation; 
but  the  chief  cause  of  the  rapid  loss  of  weight,  which  we  actually  see  in  the  cor- 
pulent as  a  result  of  the  deprivation  of  fluid,  is  to  be  found  not  in  the  loss  of  fat, 
but  in  the  marked  loss  of  water  contained  in  the  body.  "  Desiccation  "  may  fur- 
ther be  promoted  by  stimulating  the  perspiration  by  bodily  exercise  or  by  steam 
baths.  This  withdrawal  of  liquid  from  the  system,  however,  is  advisable  only  in 
cases  where  there  is  already  incipient  cardiac  failure. 

It  is  evident  that  numerous  excellent  methods  are  at  our  disposal  for  the  treat- 
ment of  obesity ;  but  their  application  to  any  particular  case  should  be  the  result 
of  a  careful  consideration  of  the  special  circumstances  presented.  A  very  essen- 
tial point  is  that  the  injunctions  of  the  physician  should  not  merely  be  made,  but 
be  carried  out ;  and  it  is  precisely  here  that  the  treatment  of  many  cases  suffers 
shipwreck.  We  may  be  baffled  by  the  patient's  lack  of  energy  and  persistence, 
or  by  the  importunate  demands  which  his  profession  or  social  position  make  upon 
him.    Indeed,  it  is  sometimes  absolutely  impossible  to  prosecute  the  treatment  at 


SCEOFULA  T8Y 

home,  in  which  case  bathing-  and  health-resorts  are  to  be  urgently  recommended. 
There  alone  can  the  patient  muster  up  the  resolution  necessary  for  carrying  out 
the  desired  changes  in  his  mode  of  life.  The  incontestable  success  of  treatment  at 
Carlsbad,  Marienbad,  Kissingen,  Tarasp,  and  similar  resorts  is  doubtless  only  to  a 
very  small  extent  the  result  of  their  specific  medicinal  influence,  but  it  is  mainly 
due  to  a  strict  observance  of  the  above-described  diet  and  regimen.  The  internal 
use  of  mineral  waters  is  not  entirely  without  a  beneficial  effect.  Their  laxative 
qualities  diminish  the  absorption  of  food  from  the  intestinal  canal.  It  should  be 
said,  however,  that  the  patient  is  at  the  same  time  exposed  to  the  danger  of  a 
waste  of  his  nitrogenous  tissues.  This  is  why  patients  frequently  complain  of  the 
debilitating  effect  of  these  mineral  springs;  to  avoid  which,  it  would  be  well  to 
increase  the  amount  of  albuminoids  in  the  diet.  We  must  also  consider  the  need 
of  guarding  against  too  great  a  supply  of  fluid,  with  regard  to  what  was  said 
above  as  to  the  occasional  service  of  "  desiccation  "  of  the  body. 


CHAPTER   XIII 
SCROFULA 

Definition  and  Symptoms  of  what  is  called  Scrofula. — We  desire  to  present, 
at  the  close  of  this  section,  a  brief  description  of  scrofula,  but  merely  from  a  prac- 
tical standpoint.  From  a  scientific  point  of  view  scrofula  is  not  to  be  regarded  as 
any  special  variety  of  disease.  The  term  is  applied  to  a  group  of  symptoms  seen 
most  frequently  in  childhood,  the  essential  features  of  which  consist  in  the  ap- 
pearance of  chronic  enlargements  of  the  lymph-glands,  and  in  certain  diseases  of 
the  skin  and  mucous  membranes.  The  simultaneous  appearance  of  these  various 
phenomena  does  really  produce  a  somewhat  characteristic  picture,  which  can  fre- 
quently be  recognized  at  the  first  glance. 

Most  scrofulous  children  appear  pale,  with  a  flabby  skin  and  soft  muscles. 
The  panniculus  adiposus  may  nevertheless  be  tolerably  well  developed.  Xot 
infrequently  the  face  is  puffy,  with  prominent  lips.  This  is  called  the  "  torpid 
habitus."  In  other  cases  the  child  has  small  features  and  a  remarkably  delicate 
white  skin,  which  but  partly  conceals  the  superficial  veins,  and  is  readily  suf- 
fused with  blushes.  To  these  the  name  "  erethitic  habitus  "  is  applied.  Enlarged 
lymph-glands  are  to  be  felt  in  the  throat,  at  the  angles  of  the  lower  jaw,  and  in 
the  back  of  the  neck,  and  occasionally  in  other  parts  of  the  body.  These  glands 
may  remain  indolent  for  a  long  while,  or  they  may  suppurate  and  break  exter- 
nally. Chronic  cutaneous  eruptions  are  often  seen  in  various  places.  The  most 
common  of  these  is  a  scaly  or  impetiginous  eczema,  affecting  the  face,  scalp,  or 
extremities.  More  severe  affections  are  lupus  ("  lupus  scrophulosorum  "),  pru- 
rigo, and  lichen  scrophulosorum. 

Of  the  mucous  membranes,  the  conjunctiva  and  the  lining  membrane  of  the 
nostrils  are  most  frequently  affected.  Conjunctivitis  in  various  forms  is  a  char- 
acteristic symptom  of  scrofula;  as  are  also  blepharitis  ciliaris,  keratitis,  and 
chronic  rhinitis,  which  last  often  terminates  in  a  pronounced  ozaena  (q.  v.). 
Chronic  diseases  of  the  ear  are  also  frequent,  such  as  otitis  media,  with  perfora- 
tion of  the  tympanum,  and  occasionally  caries  of  the  mastoid  cells  and  its  unfor- 
tunate results. 

Of  the  deeper-lying  tissues,  the  bones  and  joints  are  most  apt  to  suffer.  The 
affections  located  here  are  almost  exclusively  "  fungous " — namely,  fungous 
ostitis  and  periostitis,  white  swelling,  and  caries.     Formerly  there  was  frequent 


Y88  CONSTITTJTIOITAL   DISEASES 

use  of  such  terms  as  "  scrofulous  inflammation  of  the  knee-joint,"  or  "  scrofulous 
caries  of  the  ribs."^ 

If  we  inquire  into  the  nature  of  this  strange  group  of  symptoms  thus  briefly 
enumerated,  we  shall  find  that  by  far  the  greater  number  of  cases  of  well-marked 
scrofula  are  examples  of  tuberculosis.  Tubercle  bacilli  have  been  demonstrated 
in  connection  with  most  of  the  fungous  or  "  scrofulous  "  diseases  of  the  bones  and 
joints.  Ozsena  is  often  a  tubercular  disease  of  the  nose,  lupus  is  a  tuberculosis  of 
the  skin,  and  many  forms  of  otorrhcea  are  really  tuberculosis  of  the  ear.  The 
aetiology  of  "  scrofula  "  is  therefore  in  the  main  identical  with  that  of  tuberculosis 
(g.  v.),  and  this  explains  why  the  old  physicians  habitually  insisted  upon  the  inti- 
mate relationship  between  the  two  diseases.  It  was  formerly  thought  that  scrof- 
ula often  terminated  in  tuberculosis — that  is,  a  scrofulous  child  is  apt  to  suffer 
eventually  from  tuberculosis  of  the  lungs,  intestine,  or  brain.  To-day  we  know 
that  most  scrofulous  children  do  not  become,  but  that  they  are  already,  tuberculous. 

It  must,  however,  be  borne  in  mind  that  in  practice  many  diseases  are  termed 
scrofulous  which  have  nothing  to  do  with  tuberculosis.  Many  cases  of  perfectly 
innocent  eczema  of  the  face  and  scalp  lead  to  swelling  of  the  glands  in  the  throat, 
and  are  therefore  termed  scrofulous  eczema.  These  cases  are  probably  most  of 
them  secondary,  and  the  result  of  external  irritation  and  the  like.  Again,  many  en- 
larged glands  in  the  neck  are  the  result  of  pharyngeal  trouble,  as  after  scarlet  fever, 
and  are  equally  devoid  of  a  tubercular  taint,  Pseudo-leuka3mic  lymphomata  may 
also  occur  in  children ;  and  it  should  be  borne  in  mind  that  hereditary  or  acquired 
syphilis  may  produce  in  children  lesions  closely  resembling  those  of  scrofula. 

It  is  therefore  the  duty  of  the  physician  in  every  case  of  "  scrofula  "  to  analyze 
the  etiology  and  symptoms  carefully,  in  order  to  determine  with  what  he  has  to 
deal.  "  Scrofula  "  should  be  regarded  merely  as  a  short  way  of  naming  a  certain 
group  of  symptoms.  It  is  convenient  to  retain  the  term  as  being  less  likely  to 
startle  the  friends  of  the  child  than  would  the  true  name  of  the  disease. 

Treatment.- — In  the  treatment  of  scrofula  we  have  first  to  attack  the  various 
local  diseases,  and,  second,  to  invigorate  the  general  health.  We  can  not  here 
enter  into  all  the  details  of  local  treatment,  but  we  must  refer  the  reader  to  the 
special  descriptions  already  given  of  the  various  local  affections.  We  may,  how- 
ever, briefly  mention  a  few  facts  with  regard  to  the  treatment  of  scrofulous  swell- 
ing of  the  lymph-glands.  Painting  the  overlying  skin  with  tincture  of  iodine  is 
a  very  common  practice,  but  it  seldom  does  much  good.  We  have  obtained  more 
satisfactory  results  from  iodoform  ointment,  or  from  the  repeated  inunction  of 
sapo  viridis.  For  particulars  as  to  the  opening  of  abscesses,  or  the  extirpation  of 
glands,  we  must  refer  to  Avorks  on  surgery. 

Second,  in  the  general  treatment  of  scrofula  every  possible  means  is  to  be 
employed  to  invigorate  the  system.  Abundant  nourishment  and  fresh  air  are 
essential.  The  child  may  be  taken  either  to  the  country,  the  mountains,  or  the 
seashore.  Cod-liver  oil  is  regarded  by  some  as  a  specific  in  scrofula;  but  its  un- 
doubted value  really  lies  in  the  fact  that  it  is  an  easily  digested  fat.  Some  children 
can  take  a  considerably  larger  dose  than  others  without  its  disturbing  the  stomach. 
Usually  we  prescribe  two  or  three  tablespoonfuls  per  diem.  Salt  baths  enjoy  a  great 
reputation  as  a  remedy  in  scrofula.  If  circumstances  permit,  the  best  way  is  to 
visit  some  place  where  there  are  brine  baths,  such  as  Kosen,  Suiza,  Salzungen, 
Arnstadt,  Kreuznach,  Miinster  am  Stein,  Rehme,  Eeichenhall,  Ischl,  or  Colberg. 

Treatment  at  these  resorts  is  preferable  to  the  use  of  artificial  baths  at  home, 
because  it  is  under  more  favorable  hygienic  surroundings. 

The  chief  internal  remedies  are  iron,  iodine,  and  arsenic.  A  favorite  prescrip- 
tion is  syrup  of  the  iodide  of  iron.  Arsenic  may  have  a  slight  specific  influence 
upon  the  tuberculous  adenitis  and  bone  diseases,  as  also  upon  lupus,  but  beyond 
this  we  can  not  expect  anj'  great  benefit  from  internal  remedies. 


DISEASES   OF   THE   NERVOUS   SYSTEM 


I.— THE    DISEASES   OF   THE   PERIPHERAL   NERVES 

SECTION  I 

Diseases  of  the  Sensory  Nerves 

CHAPTEK   I 
GENERAL    REMARKS    UPON    THE    DISTURBANCES    OF    SENSIBILITY 

The  disturbances  of  sensibility,  like  all  otlier  functions  of  the  nerves,  are  mani- 
fested in  two  directions.  Under  pathological  conditions  we  observe  either  an 
abnormal  diminution  or  a  complete  absence  of  sensibility — anaesthesia — or  a  mor- 
bid increase — hypergesthesia.  While,  in  anaesthesia,  the  ordinary  or  even  the 
strongest  irritations  which  excite  the  sensory  nerves  produce  only  a  weak  and  in- 
significant sensation,  or  even  no  corresponding  sensation  at  all,  in  hypersesthesia 
very  severe  and  painful  sensations  are  caused  by  weak  irritations.  The  "  symp- 
toms of  sensory  irritation  "  are  to  be  distinguished  from  hypersesthesia,  although 
they  are  often  present  along  with  it.  By  this  term  we  mean  sensations  which  cause 
internal  irritation,  not  from  without,  but  from  certain  abnormal  morbid  condi- 
tions in  the  nerve  itself.  In  the  region  of  cutaneous  sensibility,  with  which  we 
shall  chiefly  concern  ourselves  in  what  follows,  these  symptoms  of  sensory  irrita- 
tion show  themselves  partly  as  actual  pain  and  partly  as  the  so-called  parses- 
thesiee — that  is,  abnormal  sensations  in  the  skin,  which  are  termed  "  formication  " 
(the  crawling  of  ants),  "prickling,"  "numbness,"  "a  furry  feeling,"  "hot  and 
cold  feelings,"  etc. 

The  Different  Varieties  of  Cutaneous  Sensibility  and  the  Methods  of  testing 
them. — As  is  known  from  physiology,  the  irritation  of  the  sensory  cutaneous 
nerves  produces  in  us  a  number  of  sensations,  differing  in  quality  according  to 
the  manner  in  which  the  irritation  acts.  If,  therefore,  we  would  obtain  an  accu- 
rate estimate  of  the  condition  of  the  patient's  ciitaneous  sensibility,  we  must 
make  a  special  test  of  all  the  different  forms  of  sensation ;  for  we  often  see  that 
the  disturbances  of  sensibility  do  not  involve  all  the  forms  mentioned  alike,  but 
that  one  kind  of  irritation  is  followed  by  perfectly  normal  sensation,  while  there  is 
more  or  less  complete  anaesthesia  for  another  kind.  We  term  such  partial  anaes- 
thesias of  the  skin,  which  are  manifest  toward  only  one  or  more  forms  of  irrita- 
tion, "  dissociated  "  or  "  partial  anaesthesias."  The  study  of  these  partial  anaes- 
thesias is  the  more  interesting,  since,  according  to  recent  physiological  theories 
(Blix,  Goldscheider,  etc.),  the  different  qualities  of  cutaneous  sensibility  are 
transmitted  to  the  consciousness  by  special  nerve-fibers,  so  that  there  are  probably 
in  the  skin  different  terminal  nervous  organs  for  the  perception  of  sensations  of 
pressure,  cold,  heat,  etc.  Such  a  condition  recalls  the  well-known  specific  energy 
of  the  different  fibers  of  the  optic  nerve  to  colors,  assumed  by  many  physiologists. 

789 


790  DISEASES    OF    THE   Is^ERVOUS    SYSTEM 

The  separate  varieties  of  cutaneous  sensibility,  and  the  chief  practical  methods  of 
testing  them,  are  as  follows  : 

1.  Sensibility  to  Contact. — The  examination  of  the  sensibility  of  the  skin 
to  simple  contact  is  usually  performed  by  repeatedly  touching  or  stroking  the 
part  of  the  skin  to  be  tested  with  the  finger,  a  fine  brush,  or  some  other  blunt 
object  (not  of  metal,  in  order  to  exclude  sensations  of  cold)  while  the  patient's 
eyes  are  shut,  and  asking  the  patient  to  say  whether  he  has  felt  the  touch  or  not. 
When  it  is  necessary  to  call  the  patient's  attention  to  the  investigation,  it  is 
always  best  to  do  so  afresh  by  asking  "  Xow  ? "  and  then  either  really  to  touch 
the  skin  or  else  to  ask  the  question  when  only  pretending  to  touch  it.  In  this  way 
we  are  safest  from  the  error,  Avhich  otherwise  may  readily  arise,  from  a  lack  of 
attention  or  of  practice  on  the  part  of  the  patient.  We  may  often  make  the  patient 
close  his  eyes  and  then  count  the  number  of  times  we  touch  the  skin,  or  we  touch 
the  skin  alike  in  different  parts  of  the  body  (alternating  on  the  two  legs,  etc.),  and 
then  ask  him  to  tell  merely  the  place  Avhere  he  is  touched  (vide  infra).  The  degree 
of  correctness  of  his  answer  of  course  shows  the  condition  of  the  sense  of  contact. 
The  comparison  of  the  sensibility  in  symmetrical  parts  of  the  body  is  of  impor- 
tance, especially  in  unilateral  disturbances. 

In  a  good  many  cases  the  patients  feel  the  slightest  touch,  but  nevertheless 
they  say  that  the  touch  on  the  affected  part  is  "  more  indistinct,"  "  duller,"  in 
short,  "  different "  from  that  on  the  normal  part  of  the  skin. 

2.  Sense  of  Locality  {Localization  of  Sensation). — Under  normal  conditions, 
as  we  know,  not  only  do  we  feel  the  touch  of  an  object,  but  we  can  tell  with  a 
good  deal  of  accuracy  the  place  on  our  skin  which  was  touched.  This  power  we 
term  the  ability  to  localize  our  sensation.  In  nervous  patients  we  often  see  that, 
while  cutaneous  sensibility  is  still  present  (we  refer  not  only  to  tactile  sensibility 
but  also  to  the  other  forms),  it  is  localized  more  poorly  and  with  less  accuracy 
than  is  the  case  under  normal  conditions. 

In  the  simple  test  of  the  sense  of  contact  we  may  also  examine,  at  least  rough- 
ly, the  power  of  localization  if  we  ask  the  patient  also  to  state  where  the  touch 
is  felt,  or  if  we  ask  him  to  designate  with  his  hand  as  accurately  as  possible  the 
part  of  the  skin  touched.  A  more  accurate  method  was  proposed  by  E.  H.  Weber. 
It  consists  in  determining  the  smallest  distance  which  must  separate  two  simulta- 
neous cutaneous  irritants  from  each  other,  in  order  that  they  may  be  perceived 
as  two  locally  distinct  sensations.  Weber  has  found  that  this  distance  differs 
very  much  in  different  parts  of  the  body,  and  from  this  he  has  divided  the  whole 
surface  of  the  sjfin  into  so-called  tactile  circles.  As  data  for  the  examination  of 
patients,  some  of  the  figures  obtained  by  Weber  in  healthy  individuals  may  here 
be  given :  The  smallest  distance  at  Avhich  the  two  points  of  a  pair  of  compasses  * 
applied  at  the  same  time  to  the  skin  may  plainly  be  distinguished  from  each  other 
is  11  to  15  millimetres  on  the  cheeks,  6  millimetres  at  the  tip  of  the  nose,  22  milli- 
metres on  the  forehead,  1.2  millimetre  at  the  tip  of  the  tongue,  4  to  5  millimetres 
at  the  back  of  the  tongue  and  on  the  lips,  34  millimetres  on  the  neck,  77  milli- 
metres on  the  upper  arm,  40  millimetres  on  the  forearm,  31  millimetres  on  the 
backs  of  the  hands,  11  to  16  millimetres  on  the  backs  of  the  fingers,  2  to  3  milli- 
metres at  the  tips  of  the  fingers,  55  to  77  millimetres  on  the  back,  45  millimetres 
on  the  chest,  77  millimetres  on  the  thigh,  40  millimetres  on  the  leg,  40  milli- 
metres on  the  instep;  but  these  figures  show  certain  variations  in  different  indi- 
viduals, so  that  they  are  to  be  regarded  as  only  average  values. 

Testing  the  sense  of  locality  by  Weber's  method  has  no  great  practical  impor- 
tance; it  also  takes  very  much  time  and  demands  intelligence,  patience,  and 
good  will  on  the  part  of  the  patient.     The  influence  of  practice  is  manifested 

*  There  are  special  "  tactile  compasses  "  with  lilunt  ivory  points  and  graduated  quadrants. 


EEMAEKS    UPO^T   THE   DISTUKBANCES    OF    SENSIBILITY   791 

in  a  very  remarkable  way,  since  tlie  perceptible  difference  becomes  considerably 
less  if  the  examinations  are  often  repeated.  On  the  other  hand,  a  single  exami- 
nation, as  in  testing-  any  form  of  sensibility,  must  not  be  too  long  protracted,  for 
otherwise  the  patient  may  easily  become  fatigued,  and  the  data  obtained  will  be 
entirely  contradictory.  If  we  test  the  sense  of  locality  by  bringing  down  the  two 
points  not  at  the  same  time  but  one  after  the  other,  and  vaiy  it  by  touching  the 
same  place  twice,  or  a  diiferent  place  each  time,  we  obtain  from  the  outset,  as  we 
have  repeatedly  proved,  smaller  numbers  than  if  we  touch  the  skin  with  the  two 
points  of  the  compasses  at  the  same  time.  We  also  obtain  somewhat  different  val- 
ues for  the  fineness  of  the  sense  of  locality  if  we  test  the  so-called  sensations  of 
motion  (Leube) — that  is,  the  distinction  between  a  simple  circumscribed  touch  of 
the  skin,  and  a  very  short  line  drawn  with  a  stick  on  the  skin.  In  this  way  we 
can  also  determine  whether  the  patient  can  distinguish  accurately  the  direction 
of  transverse  and  longitudinal  lines. 

We  may  also  mention  here  two  peculiar  anomalies  of  sensibility,  polycesthesia 
(G.  Fischer)  and  allochiria  (Obersteiner).  Polysesthesia  is  a  symptom  shown  by 
certain  patients  (especially  patients  with  tabes),  who,  when  the  skin  is  touched 
with  only  one  point  of  the  compasses,  have  a  sensation  as  if  they  felt  two  or  even 
more  points.  The  cause  of  this  remarkable  anomaly  of  sensation  is  not  yet  ade- 
quately explained.  In  allochiria  a  stimulation  of  the  skin  (touch,  pain)  is  felt 
not  on  the  part  touched,  but  on  the  corresponding  point  on  the  other  half  of  the 
body.  This  remarkable  symptom  has  been  observed  a  few  times  in  cerebral  hemi- 
plegia, tabes,  etc. 

3.  Sense  op  Pressure. — The  healthy  man  distinguishes  with  ease  whether  an 
object  merely  touches  the  skin  or  exerts  pressure  upon  it.  In  the  perception  of 
pressure  we  must  consider  not  merely  the  sensibility  of  the  skin,  but  probably 
even  more  the  sensibility  of  the  deep  parts  below  the  skin  (fasciae,  muscles,  peri- 
osteum). If  a  fold  of  the  skin  be  raised,  differences  of  pressure  are  felt  much  less 
plainly  than  when  pressure  is  at  the  same  time  exerted  on  the  deeper  parts.  Since 
E.  H.  Weber's  investigations  we  know  that  we  estimate  the  difference  in  the  in- 
tensity of  our  sensations  of  pressure,  not  according  to  the  absolute,  but  according 
to  the  relative  increase  in  the  pressure.  If,  for  example,  a  part  of  the  skin  has 
a  weight  of  nineteen  grammes  on  it,  and  we  perceive  the  first  manifest  increase 
in  our  sensation  of  pressure  when  a  weight  of  one  gramme  is  added  to  it;  when 
the  skin  has  a  weight  of  one  hundred  and  ninety  grammes  on  it,  we  first  perceive 
the  increase  of  pressure  not  when  one  gramme  is  added,  but  when  we  add  ten 
grammes.  If  this  law,  on  more  accurate  testing,  has  not  proved  so  simple  as  it 
would  seem  according  to  the  results  of  Weber's  first  investigations,  still  it  is  gen- 
erally a  fact  that  under  normal  conditions  an  increase  of  pressure  of  about  one 
twentieth  to  one  thirtieth  of  the  original  pressure  may  be  plainly  perceived  in  the 
different  parts  of  the  body. 

Different  methods  and  instruments,  such  as  Eulenburg's  "  barsesthesiometer," 
have  been  devised  for  testing  accurately  the  sense  of  pressure  in  patients,  but  they 
have  entered  but  little  into  practice  on  account  of  their  elaborate  character.  We 
usually  content  ourselves  with  testing  the  sense  of  pressure  by  applying  different 
weights,  or  coins.  We  must  mention  here  that  the  part  of  the  body  to  be  tested 
must  be  fully  supported,  that  we  must  also  exclude  sensations  of  temperature  at 
the  same  time  by  putting  some  non-conductor  beneath  the  weights,  and  that  we 
must  apply  the  separate  weights  to  the  same  place  on  the  skin  at  equal  intervals  of 
time,  which  must  not  be  too  long  after  one  another.  For  the  ordinary  needs  of 
practice  it  is  wholly  sufficient  to  test  the  pressure  sense  simply  with  the  finger  or 
any  blunt  object.  By  pressing  with  the  finger  we  can  vary  the  pressure,  make  it 
weaker  or  stronger,  and  thus  learn  whether  the  patient  is  able  correctly  to  state 
all  these  differences. 


792  DISEASES    OF   THE   NEEVOUS    SYSTEM 

We  should  never  fail  to  test  tlie  pressure  sense  in  patients  with  nervous  dis- 
ease, since  anaesthesia  of  the  pressure  sense,  or  at  least  a  diminution,  is  by  no 
means  rare.  We  find  quite  often,  especially  in  spinal  diseases  (tabes,  myelitis,, 
compression),  that  the  patient  feels  a  light  touch  on  the  skin,  but  that  he  can  not 
distinguish  a  marked  pressure  at  all,  or  only  obscurely.  On  the  other  hand,  the- 
sense  of  pressure  is  sometimes  well  preserved  when  the  other  forms  of  cutaneous 
sensibility  are  much  impaired  (as  in  syringomyelia). 

4.  Sense  of  Temperature. — As  we  have  already  said  (p.  789),  we  have  lately 
been  led  by  physiological  investigations  (Goldscheider,  etc.)  to  believe  more  and 
more  strongly  that  sensations  of  heat  and  cold  are  to  be  regarded  as  due  to  two 
wholly  distinct  functions  of  the  cutaneous  nerves.  These  functions  are  probably 
performed  by  special  nerve  terminations  and  nerve-fibers.  If  we  test  the  sensi- 
bility of  the  skin  for  heat  and  cold  with  a  pointed  metal  rod,  heated  or  cooled,, 
we  can  easily  be  convinced  that  the  hot  rod  excites  a  sensation  of  warmth  only  on 
definite  parts  of  the  skin,  and  that  the  cold  rod  excites  a  sensation  of  cold  only  on 
other  definite  points  ("warm  points,"  "cold  points"),  but  on  the  intervening 
points  these  rods  excite  no  sensation  of  temperature.  Erom  repeated  personal 
observation  we  can  state  that  pathological  symptoms  agree  completely  with  this 
theory  of  the  existence  of  special  nerve  conduction  for  sensations  of  heat  and  cold, 
for  we  see  that  changes  in  the  temperature  sense  in  the  skin  by  no  means  affect 
the  heat  sense  and  the  cold  sense  equally.  It  is  therefore  always  necessary  to  test 
both  forms  of  the  temperature  sense  separately.  We  often  find  that  while  one 
form  of  temperature  sense  is  in  normal  activity,  the  other  is  much  altered — a 
pronounced  partial  anaesthesia  to  heat  or  cold.  The  affected  sense  may  be  wholly 
lost  or  merely  blunted,  so  that  hot  water  is  felt  merely  as  tepid,  or  ice  as  cool. 
If  the  temperature  sense  be  lost,  the  application  of  a  hot  or  cold  object  will  cause- 
only  a  sensation  of  touch,  and  not  of  temperature.  Extreme  temperatures,  espe- 
cially extreme  heat,  excite,  as  is  well  known,  a  sensation  of  pain.  This  may,  of 
course,  remain  normal;  but  if  there  is  also  analgesia  (vide  infra),  it  disappears. 

If  anassthesia  to  cold  be  present,  patients  often  speak  of  having  a  distinct 
sensation  of  warmth  when  the  skin  is  touched  with  a  bit  of  ice.  This  symptom, 
which  we  discovered  and  called  "  perverted  temperature  sense,"  may  perhaps  be- 
explained  by  supposing  that  the  heat  nerves  are  excited  by  the  severe  irritation 
from  cold.  The  contrary  symptom,  that  heat  excites  a  distinct  sensation  of  cold,, 
is  very  much  less  common. 

Besides  the  sensations  of  temperature  we  usually  test  also  the  patient's  ca- 
pacity to  distinguish  differences  of  temperature.  Within  the  moderate  degrees  of 
temperature,  80°  to  100°  (25°-35°  C),  differences  of  a  degree  Fahrenheit  (0.5° 
C.)  are  easily  distinguishable  under  normal  conditions,  and  even  half  a  deg-ree 
(0.2°  C.)  can  be  distinguished  on  the  face  and  fingers,  but  only  about  two  degrees- 
(1°  C.)  on  the  back. 

Variations  in  the  temperature  sense  are  very  common.  We  often  find  them 
(especially  in  spinal  disease)  in  those  cases  where  the  simple  sensibility  to  touch 
is  fully  retained.  The  test  of  the  sensibility  to  heat  and  cold  should  therefore 
never  be  omitted  in  testing  the  sensibility.  It  can  be  done  with  sufficient  accu- 
racy for  all  practical  diagnostic  purposes  simply  by  touching  the  skin  with  large 
test-tubes  filled  with  ice  or  hot  water.  The  various  thermsesthesiometers  that 
have  been  devised  are  too  complicated  for  practical  purposes.  For  a  hasty  test 
it  is  sometimes  quite  serviceable  to  try  whether  the  patient  can  distinguish  warm' 
breathing  upon  a  given  portion  of  the  skin  from  cool  blowing  upon  it. 

5.  Sensation  of  Pain. — The  sensibility  to  pain,  also,  can  not  be  excited  in  all 
parts  of  the  skin  by  circumscribed  irritation,  such  as  a  pin-prick.  We  find  "  pain 
points"  and  parts  insensible  to  pain.  From  this  fact  and  for  other  reasons, 
which  can  not  be  detailed  here,  von  Frey  has  concluded  that  there  are  special 


EEMAEKS   UPOl^   THE   DISTUEBANCES    OF    SENSIBILITY    79^ 

pain  nerves,  whose  terminal  apparatus  is  to  be  found  in  the  free  intra-epithelial 
nerve  endings.  It  is  a  fact  that  the  sensibility  of  the  skin  for  touch  and  that 
for  pain  are  not  always  parallel  under  pathological  conditions.  We  sometimes  see 
that  a  patient  does  not  feel  a  simple  touch  on  the  skin,  when  sticking  a  needle 
into  it  is  immediately  painful ;  while,  on  the  other  hand,  we  still  more  frequently 
find  that  a  patient  feels  quite  a  light  touch  on  the  skin,  but  that  the  most  marked 
irritation,  such  as  pinching  or  pricking  it,  does  not  excite  the  slightest  pain,  but  is 
felt  only  as  a  simple  touch,  or  at  most  as  a  slight  pressure.  This  latter  con- 
dition of  sensibility,  the  loss  of  cutaneous  sensibility  to  pain  with  retained  tactile 
sensibility,  is  termed  analgesia.  Both  in  peripheral  and  in  central  nervous  dis- 
eases analgesia  is  a  symptom  that  may  be  quite  frequently  observed. 

The  test  of  sensibility  to  pain  may  be  best  performed  by  pricking  with  the 
point  of  a  pin,  and  also  by  pinching  a  fold  of  the  skin  with  considerable  force. 
The  simple  test,  whether  a  patient  is  able  to  distinguish  between  the  head  and  the 
point  of  a  pin,  is  much  employed.  We  thus  obtain  information  at  the  same  time 
of  the  sensibility  to  pressure  or  touch;  for  a  prick  with  the  point  of  a  pin  nor- 
mally excites  a  slight  pain,  while  the  application  of  the  pin-head  causes  a  sensa- 
tion of  simple  touch  or  slight  pressure.  In  testing  the  sensibility  to  pain  we  must 
be  careful  to  prick  deep  enough  (penetrating  the  epidermis),  but  at  first  we  must 
employ  only  brief  pin-pricks.  Only  when  these  are  not  felt  as  painful  should  we 
use  long-continued  pin-pricks.  Very  often  by  summation  of  the  irritation  (vide 
infra)  a  lively  sensation  of  pain  is  produced.  If  there  be  marked  analgesia  we 
can  of  course  stick  a  pin  deep  into  the  skin  or  push  it  through  a  fold  of  skin  with- 
out causing  pain. 

It  is  well  known  that  various  kinds  of  irritation  may  produce  pain :  severe 
pressure,  extreme  temperature,  strong  electrical  currents,  etc.,  as  well  as  wounds 
of  the  skin  (for  pin-pricks  are  to  be  regarded  as  such).  It  is  always  some  irrita- 
tion which  acts  on  the  deeper  layers  of  the  skin. 

6.  Electro-cutaneous  Sensibility. — The  test  of  cutaneous  sensibility  by 
means  of  the  electric  current  has  been  proposed  by  various  observers.  The 
advantage  of  it  is  that  in  this  way  the  intensity  of  the  irritation  can  be  very 
easily  and  accurately  graded  and  expressed  in  numbers,  by  the  position  of  the 
coil  in  using  the  faradic  current,  or  by  the  galvanometer  in  using  the  con- 
stant current.  The  faradic  current  is  usually  sufficient  in  testing  the  sensibility, 
and  we  desig-nate  it  by  the  position  of  the  coil  when  the  first  sensation  is  felt 
and  the  position  when  the  first  pain  is  felt.  In  general,  the  differences  of  the 
farado-cutaneous  sensibility  are  not  very  marked.  Pathological  deviations  are 
given  by  comparison  with  normal  portions  of  the  skin  (testing,  if  possible,  sym- 
metrical parts)  or  with  healthy  people.  The  galvanic  current  is  also  used  to  test 
sensibility,  noting  the  occurrence  of  a  burning  sensation  at  the  cathode.  For 
practical  purposes,  the  test  of  electro-cutaneous  sensibility  is  unnecessary,  since 
its  results  are  the  same  as  in  testing  the  sensibility  to  touch  and  to  pain. 

7.  Delay  of  Sensation  (so-called  Delayed  Conduction),  Summation  of  Irri- 
tation AND  After-sensations. — Quite  frequently  in  diseases  of  the  spinal  cord, 
especially  in  compression  paralysis  and  tabes  (q.  v.),  and  not  infrequently  in 
peripheral  nerve  disease  (neuritis),  we  see  a  marked  delay  in  sensation  after  the 
action  of  an  irritant.  This  symptom  affects  chiefly  the  sensibility  to  pain.  If 
in  such  a  case  we  stick  a  pin  into  the  sole  of  a  patient's  foot,  several  seconds 
elapse,  even  ten  or  twenty,  it  is  said,  before  the  pain  is  felt.  As  was  first  observed 
by  ISTaunyn  and  E.  Eemak  in  tabes,  and  as  has  often  been  confirmed  since,  after 
sticking  a  pin  into  the  foot  there  is  in  such  cases  first  a  simple  sensation  of  slight 
pressure,  and  some  seconds  later  the  peculiar  sensation  of  pain,  so  that  the 
patient  at  once  responds  to  the  prick  with  "  Now,"  and  a  little  later  with  "  Ow !  "' 
as  an  expression  of  pain. 


794  DISEASES    OF   THE   NEKVOUS    SYSTEM 

On  analyzing  this  symptom  somewhat  more  closely  we  will  have  to  distinguish 
between  single  brief  and  continuous  irritations  (pin-pricks).  If  we  make,  for 
example,  a  single  short  prick  in  the  skin,  it  may  happen  that  the  pain  thus  caused 
appears  comparatively  late.  This  symptom  depends  perhaps  upon  a  "  delay  of 
conduction,"  although  it  is  still  undetermined,  of  course,  whether  this  delay  takes 
place  actually  in  the  peripheral-nerve  fiber  or  in  the  interpolated  ganglion  cells. 
The  conditions  in  permanent  painful  excitation  (continued  pin-prick)  are  dif- 
ferent. In  these  cases  we  notice  very  often  that  immediately  after  the  insertion 
of  the  pin  the  patient  feels  nothing  or  only  a  simple  touch.  If  the  prick  be  con- 
tinued, however,  there  is  felt  a  lively  sensation  of  pain,  often  only  after  a  few 
seconds.  This  phenomenon  is  apparently  due,  not  to  a  delay  of  conduction,  but 
to  a  summation  of  the  irritant  action,  which  thus  gradually  attains  sufficient 
intensity  finally  to  break  through  the  existing  resistance  and  to  reach  the  con- 
sciousness in  full  strength.  At  the  same  time  with  the  sensation  of  pain  there  is 
usually  a  reflex  twitching,  and  the  same  conditions  are  therefore  to  be  considered 
in  testing  the  cutaneous  reflexes  (vide  infra). 

In  this  connection,  it  is  well  to  mention  briefly  the  after-sensations,  which 
we  have  noted  in  the  most  striking  fashion,  especially  in  cases  of  tabes.  After  a 
single  short  prick  these  after-sensations  appear  as  a  burning  feeling  in  the  skin, 
which  lasts  a  strikingly  long  time,  or  else  the  first  sensation  soon  ceases  after  the 
prick,  and  then,  in  the  same  spot  on  the  skin,  new  sudden  sensations  of  pain  are 
felt  several  times,  just  as  if  the  patient  had  been  pricked  anew. 

8.  The  Sensibility  of  the  Muscles  and  Joints. — A  number  of  sensations  are 
classed  together  under  the  names  of  "  muscular  sense  "  or  "  muscular  sensibil- 
ity." They  are  not  all  wholly  of  the  same  value,  and,  under  pathological  condi- 
tions, they  must  be  tested  separately. 

Ordinarily  we  call  our  power  to  be  informed  of  the  position  of  any  of  our 
limbs  without  the  help  of  our  eyes,  and  of  the  extent  of  any  motion  made  by  them, 
the  "  muscular  sense."  If  we  put  a  healthy  person's  arm  into  a  given  position 
when  his  eyes  are  closed,  and  tell  him  to  put  the  other  arm  into  the  same  position, 
he  can  do  it  with  considerable  accuracy.  If  we  make  passive  movements  in  any  of 
the  joints  of  the  extremities,  a  healthy  person  whose  eyes  are  closed  can  easily 
and  correctly  state  the  form  and  direction  of  these  movements.  In  nervous  pa- 
tients, however,  this  power  may  be  diminished  or  lost,  and  we  often  speak  of  "  dis- 
turbances of  the  muscular  sense  "  ;  but  we  must  note  that  the  judgment  as  to  the 
position  of  the  limbs  and  the  passive  movements  executed  with  them  is  not  chiefly, 
much  less  exclusively,  due  to  the  sensibility  of  the  muscles.  In  all  probability  it 
depends  much  more  upon  the  sensibility  of  the  articular  surfaces,  the  ligaments 
and  tendons,  and  in  part  even  of  the  skin,  all  of  which  tissues  are  relaxed  or  made 
tense  in  the  different  movements.  It  would  therefore  be  more  correct  to  speak 
of  sense  of  position  (the  sensation  of  position  of  the  limbs)  and  sense  of  motion 
(sensation  of  passive  movements)  instead  of  the  "  muscular  sense."  The  sensi- 
bility to  movement  is  tested  simply  by  making  the  patient  close  his  eyes,  by  tak- 
ing an  arm  or  a  leg  flrmly  in  both  hands,  and  then  by  making  passive  movements 
up  and  down,  right  and  left,  at  first  extensive  and  then  gradually  less.  The  pa- 
tient should  state  the  direction  of  the  movement  made.  We  may  also  describe 
with  the  extremities  different  letters  or  figures  in  the  air,  which  the  patient  should 
recognize  with  his  eyes  closed.  If  the  test  is  to  be  absolutely  accurate,  passive 
movements  must  be  tested  in  all  the  joints  individually  (shoulder,  elbow,  hip, 
knee,  etc.),  but  as  a  rule  we  can  judge  correctly  if  we  test  the  passive  movements 
for  the  whole  extremity  at  the  shoulder  or  hip.  By  control  experiments  on  healthy 
persons  we  can  readily  convince  ourselves  how  uncommonly  sharp  and  accurate 
the  sensation  of  passive  motion  is  under  normal  conditions. 

The  sensation  of  the  position  of  the  limbs  is  tested  by  putting  one  extremity  , 


EEMAEKS   UPON   THE   DISTUEBAITCES    OF    SENSIBILITY    795 

passively  into  a  given  position  and  then  asking  the  patient  to  put  the  other  cor- 
responding extremity  into  the  same  position,  as  nearly  as  possible.  It  is  still  bet- 
ter to  have  the  patient  make  some  definite  movement,  especially  pointing  to  or 
seizing  some  object,  at  first  with  the  eyes  open ;  then  to  let  him  close  his  eyes  and 
repeat  the  movement  as  well  as  he  can. 

The  sensation  of  the  strength  of  voluntary  muscular  contraction,  the  so- 
called  "  sense  of  power,"  is  quite  different  from  the  sensations  just  described. 
Besides  the  peripheral  sensations  in  the  muscles  and  tendons  we  perhaps  have  to 
do  with  special  sensations  of  innervation.  In  raising  weights  we  can  distinguish 
with  considerable  accuracy  the  lighter  from  the  heavier,  when  the  pressure  on  the 
skin  is  excluded  as  far  as  possible.  In  such  cases,  also,  we  do  not  deal  with  the 
absolute,  but  with  the  relative  differences  in  weight;  we  can  usually  tell  quite 
plainly  when  one  fortieth  of  the  original  weight  has  been  added  or  taken  away. 
The  sense  of  power,  then,  is  somewhat  finer  than  the  sense  of  pressure.  In  order 
to  exclude  the  latter  in  the  test  we  have  the  patient  lift  the  weight,  suspended  in 
a  towel,  with  his  hand  or  foot,  but  in  the  lower  extremities  it  is  scarcely  possible 
to  exclude  entirely  the  co-existing  sensations  of  pressure. 

We  must  mention,  in  conclusion,  that  muscular  contraction  is  in  itself  ac- 
companied by  a  sensation,  as  may  be  proved,  for  example,  in  irritating  the  mus- 
cles by  faradism — electro-muscular  sensibility.  In  certain  forms  of  spasm  the 
muscular  contraction  becomes  so  strong  that  it  causes  a  decided  pain,  which 
is  probably  due  to  irritation  of  the  sensory  muscular  nerves  discovered  by  C. 
Sachs. 

Tests  of  the  sense  of  power  and  of  the  electro-muscular  sensibility  have  thus 
far  been  but  little  employed  in  nervous  diseases.  They  also  have  no  great  prac- 
tical significance,  but  the  test  of  the  sensations  of  position  and  motion  are  often 
of  great  importance.  Marked  disturbances  in  these  functions  are  often  found  in 
advanced  cases  of  tabes  and  sometimes  in  other  spinal  diseases  and  in  cerebral 
(especially  cortical)  paralyses.  Complete  loss  of  "  muscular  sense  "  is  also  found 
quite  frequently  in  severe  hysterical  affections,  usually  associated  with  other 
hysterical  anaesthesias  and  hysterical  paralysis. 

9.  The  Special  Sensibility  to  Touch  (Stereognostic  Sense,  Active  Touch). — 
The  highest  and  most  valuable  function  of  the  skin  as  a  sensory  organ  is  the  judg- 
ment we  can  often  make  of  the  size,  form,  hardness,  and  consistency  of  objects 
solely  by  feeling  of  them — in  short,  the  recognition  of  them.  This  function,  the 
special  sense  of  touch,  is  apparently  a  complicated  estimate  of  all  the  separate 
sensations  derived  from  the  different  cutaneous  nerves,  to  which  are  always  added 
at  the  same  time  a  large  number  of  sensations  of  movement.  For  "  touch  "  and 
"  feeling  "  always  imply  a  movement  of  the  parts  which  touch.  We  see,  therefore, 
that  a  patient  whose  hand  is  completely  paralyzed  can  recognize  objects  either 
with  difficulty  or  not  at  all  by  the  touch,  although  the  cutaneous  sensibility  is 
retained.  If  there  be  actual  anaesthesia  of  the  skin  it  is,  of  course,  also  impossible 
to  recognize  objects  by  the  sense  of  touch,  although  mobility  is  retained.  There 
are,  however,  also  cases  where  the  hand  can  be  moved  well  enough  and  where  the 
sensibility  of  the  skin  and  muscles  for  the  different  qualities  of  sensation  is  re- 
tained, but  nevertheless  the  recognition  of  objects  by  the  sense  of  touch  is  mark- 
edly impaired.  In  such  cases  there  is  probably  always  some  cerebral  (cortical) 
disturbance,  which  may  be  regarded  as  analogous  to  cortical  blindness  and  corti- 
cal deafness — that  is,  the  normal  mental  estimate,  the  "  understanding  "  of  the 
various  cutaneous  sensations  received.  The  author  has  seen  such  conditions, 
especially  in  cerebral  infantile  paralysis ;  the  intelligent  child  feels  every  touch 
on  the  skin  perfectly  well,  but,  when  his  eyes  are  closed,  he  can  not  recognize  by 
feeling  of  them  with  the  affected  hand  the  most  familiar  objects  (key,  knife,  ring, 
money,  etc.).     At  any  rate  it  is  very  important,  especially  in  cerebral  diseases, 


796 


DISEASES  OF  THE  K'EEVOUS  SYSTEM 


not  to  neglect  this  mode  of  investigating  the  special  "  sense  of  touch."'  If  we 
choose  for  our  tests  simple  stereometric  figures  (sphere,  cube,  cone,  octahedron), 
"we  may  also  speak  of  a  "  stereognostic  sense." 


CHAPTEE   n 


THE    SENSORY    CONDUCTION    TRACTS    AND    ANESTHESIA    OF 

THE    SKIN 

1.  Course  of  the  Sensory  Conduction  Tracts. — In  every  tract  of  the  conduct- 
ing path,  which  runs  from  the  terminal  apparatus  of  the  sensory  cutaneous 
nerves  to  the  centers  for  the  perception  of  sensation  in  the  cerebral  cortex,  we 

may  have,  under  pathological  conditions, 
a  break  in  the  conduction,  and,  as  a  result 
of  it,  a  complete  or  partial  anaesthesia  of 
the  corresponding  part  of  the  skin.  We 
speak  of  a  peripheral,  spinal,  or  cerebral 
anassthesia,  according  to  the  place  where 
this  break  in  the  conduction  occurs.  The 
anatomical  course  of  the  sensory  fibers 
(Fig.  84)  is,  however,  not  yet  known  as- 
accurately  as  we  could  desire ;  the  course 
of  the  sensory  tract  is  also  apparently  far 
more  complicated  than  that  of  the  chief 
motor  tract  (vide  infra,  Section  II).  This 
is  dependent  partly  upon  the  different 
qualities  of  sensation,  and  partly  on  the 
fact  that  the  sensory  tracts  enter  into 
many  combinations  with  motor  cells  for 
the  excitation  of  reflex  movements  or  for 
the  purpose  of  co-ordination  of  motion. 

We  must  regard  the  sensory  nerve- 
fiber,  like  every  fiber  in  the  nervous  sys- 
tem, as  the  direct  process  of  a  nerve-cell 
(ganglion-cell).  This  sensory  fiber  receives 
the  external  impressions  made  upon  its 
peripheral  terminal  organs  in  the  skin. 
We  now  know  definitely  that  all  peripheral 
sensory  nerve-fibers  come  from  the  cells 
of  the  spinal  ganglia  (intervertebral  gan- 
glia). All,  or  at  least  most  of  these  cells, 
have  a  short  process  which  soon  divides 
into  two  offshoots  from  the  cell:  one 
long  one,  going  to  the  surface  of  the  body 
(the  peripheral  sensory  nerve),  and  a 
shorter  one,  which  enters  the  posterior 
root  of  the  spinal  cord  and  is  intended 
Fig.  84.  (From  Edisger.)  —  Diaprram  of  the  for  the  further  conduction  of  sensory  im- 
fn''^'!s%n'^%^rfTJrr^!ZL'oZnf.fl  pressions.  Almost  all  the  fibers  of  the 
Vorder  SeiteyMp:  =  AnteTo-\a.tera.\  columns,     posterior  roots  accordiuglv  come  from  the 

Klemhirn.  Seiten.  B.  —  Lateral  cererjellar      •'.  ..  „         ^    .        , 

tract.  spinal  ganglia ;  during  foetal  development 


A^^STHESIA   OF   THE    SKIN 


r9Y 


■they  grow  from  their  cells  of  origin  into  the  spinal  cord.  The  spinal  gan- 
glion cell  with  its  processes  forms  the  first  (peripheral)  sensory  neurone.  The 
posterior  root-fibers,  entering  the  spinal  cord  with  their  branches  (collaterals, 
vide  infra),  take  very  different  courses,  apparently  according  to  their  different 
functions  (see  Figs.  8i  and  85).     A  part  of  them  (Fig.  85,  4)  go  to  the  anterior 


Pig.  85.— (From  Edixger.)  Diagram  of  a  transverse  section  of  the  spinal  cord  with  especial  regard  to  the 
course  of  the  posterior  root-fibers  :  1.  Fibers  in  the  posterior  column.  2.  Fibers  to  the  cells  of  Clarke's 
column,  whose  processes  enter  the  lateral  cerebellar  tract.  3  Direct  fibers  in  the  "lateral  limiting 
layer""  of  the  lateral  column  (not  mentioned  in  the  text).  4.  Fibers  to  the  motor  cells  of  the  anterior 
horn  (reflex  fibers).  5.  Fibers  in  the  posterior  horn  splitting  up  about  its  cells.  Balm,  tract  ;  Grenz- 
schicht.  limiting  layer  ;  Grund-Biindel,  ground  bundle  ;  Kleinhirn,  cerebellum  ;  Pyramiden,  pyramid  ; 
Seitenstrang,  lateral  column  ;  Vorderstrang ,  anterior  column  ;  Strangzellen,  cells  to  columns. 

h.orns  and  break  up  about  their  motor  ganglion  cells ;  these  are  apparently  tracts 
for  the  reflex  movements.  Another  part  go  to  the  cells  of  Clarke's  columns,  from 
which  arise  fibers  for  the  lateral  cerebellar  tract  (see  Fig.  84  and  Fig.  85  in  the 
right  half  of  the  figure)  ;  these  fibers  seem  to  serve  for  the  maintenance  of  the 
hodily  equilibrium  and  perhaps  for  the  co-ordination  of  movements.  The  special 
sensory  fibers,  however,  divide  into  two  main  groups  (Figs.  84-86)  ;  a  part  of 
them,  chiefly  the  median  root-fibers,  enter  directly  into  the  posterior  column  of 
the  same  side.  Soon  after  their  entrance  the  fibers  divide  again  into  a  short 
•descending  and  a  long  ascending  branch.  The  short  descending  branches  serve, 
as  I  suspect,  for  reflex  processes,  while  the  ascending  fibers  in  the  posterior  col- 
umns form  the  special  continuation  of  the  centripetal  tract.  That  portion  of  the 
posterior  columns,  into  which  these  root-fibers  enter,  is  called  the  "  posterior  root- 
zone,"  or  "  root  entrance  zone  " ;  in  the  lumbar  cord  it  lies  in  the  middle  part  of  the 
posterior  columns,  in  the  dorsal  and  cervical  cord  in  the  lateral  parts  (columns  of 
3urdaeh).  Since  new  root-fibers  are  constantly  entering  the  cord  as  we  go  up- 
ward, the  fibers  coming  from  the  lower  portions,  and  especially  from  the  lumbar 
•cord,  are  gradually  pressed  toward  the  median  line  by  the  new  fibers  that  enter. 


Y98 


DISEASES    OF   THE   NERVOUS    SYSTEM 


Fig.  86.— Diagram  of  the  course  of  the  sensory  conduction  tracts  :  A.  En- 
trance of  the  posterior  sensory  root-fibers  in  the  lumbar  cord;  gi^  in- 
tervertebral ganglion;  ?-p,  posterior  root.  A  part  of  the  fibers  that 
enter  end  in  the  posterior  horns,  from  whose  cells  new  fibers  arise 
and  enter  the  lateral  columns,  partly  crossed,  partly  uncrossed.  An- 
other part  of  the  fibers  from  the  posterior  roots  pass  upward  in  the 
posterior  columns  and  form  in  B  the  so-called  columns  of  Goll  ((?). 
B.  Cervical  cord.  Lettering  as  in  A.  B.  Columns  of  Burdach.  C. 
Medulla  oblongata.  Region  of  the  decussation  of  the  lemniscus. 
The  fibers  from  the  posterior  columns  end  in  the  nuclei  of  GoU's 
and  Burdach's  columns  (G  and  B).  New  fibers  arise  from  the  cells 
of  these  nuclei,  which  form  the  decussation  of  the  lemniscus.  Py. 
Motor  pyramids.  D.  L,  sensory  lemniscus  ;  oZ,  olivary  body  ;  cr,  cor- 
pus restiforme.  E.  Section  through  the  pons.  L,  lemniscus  ;  6,  su- 
perior cerebellar  peduncle  ;  iv,  fourth  ventricle.  F.  Frontal  section 
through  the  region  of  the  corpora  quadrigemina  ;  i,  lemniscus  ;  m\ 
red  nucleus  ;  Py,  pyramidal  tract  in  the  crusta  of  the  cms  cerebri ; 
nL,  lenticular  nucleus  ;  Th,  optic  thalamus  (interruption  of  the  sen- 
sory tract  ?  Beginning  of  a  third  sensory  neurone  ?)  ;  cqa,  anterior 
corpora  quadrigemina  :  ii,  corpus  geniculatum  externum  and  optic 
nerve  ;  cc,  corpus  callosum. 


Thus  it  happens  that  the 
fibers  from  the  lumbar 
and  the  lower  dorsal 
cords  are  in  quite  a  me- 
dian position  in  the  cer- 
vical cord,  in  the  region 
of  the  so-called  columns 
of  Goll.  All  these  fibers 
end  in  the  nuclei  of 
Goll's  and  Burdach's  col- 
umns in  the  beginning 
of  the  medulla  oblonga- 
ta. From  the  cells  of 
these  nuclei  come  the 
secondary  sensory  neu- 
rones, whose  fibers  de- 
cussate in  the  medulla 
oblongata  (fibrffi  arcua- 
tfe  interna,  or  sensory 
decussation  in  the  lem- 
niscus. Fig.  86),  and  in 
their  further  course 
form  the  so-called  lem- 
niscus, which  passes 
through  the  medulla, 
pons,  and  tegmentum  of 
the  crus  to  the  cere- 
brum. 

A  second  (lateral) 
portion  of  the  fibers  of 
the  posterior  roots  enter 
at  once  the  gray  matter 
of  the  posterior  horn. 
These  fibers  also  divide 
into  an  ascending  and  a 
descending  branch.  A 
number  of  especially  fine 
fibers  remain  in  the 
periphery  of  the  poste- 
rior horn  {zona  termi- 
nalis,  Fig.  85,  also  called 
Lissauer's  zone).  The 
fine  collaterals  of  these 
fibers  probably  enter  the 
posterior  horn  through 
the  zona  spongiosa,  and 
enter  into  similar  rela- 
tions with  the  ganglion- 
cells  as  the  other  coarser 
fibers  of  this  portion  of 
the  posterior  root-fibers, 
which  enter  the  pos- 
terior horns  directly- 
through    the    substantia. 


ANESTHESIA   OF   THE    SKIN  799 

gelatinosa,  and  after  a  short  course  split  up  iu  so-called  terminal  arborization 
about  the  ganglion-cells  there.  With  these  cells  begin  the  second  sensory  neu- 
rones for  this  part  of  the  sensory  tract;  the  processes  (fibers)  of  these  cells  at 
once  enter  the  lateral  column  of  the  opposite  side  through  the  anterior  commis- 
sure, decussate  therefore  in  the  anterior  commissure  of  the  cord,  ascend  in  the 
anterior  and  middle  portions  of  the  antero-lateral  columns  (anterior  and  internal 
to  the  motor  pyramidal  lateral  tract),  reach  the  medulla  oblongata  also  in  the  lem- 
niscus, and  unite  here  with  the  above-described  fibers  from  the  cells  of  Goll's  and 
Burdach's  nuclei.  The  diagram  on  the  opposite  page  (Fig.  86,  the  red  portion,  L, 
signifying  the  lemniscus)  gives  an  idea  of  the  position  of  the  lemniscus — that  is, 
of  the  chief  sensory  tract — farther  upward  in  the  pons  and  tegmentum.  Higher 
still,  in  the  internal  capsule,  the  sensory  tract  lies  in  the  posterior  limb  behind  the 
motor  pyramidal  tract  {vide  infra.  Fig.  95).  There  is  still  considerable  obscurity 
as  to  its  further  course.  A  part  of  the  lemniscus  fibers  probably  end  in  the  optic 
thalamus,  from  whose  cells,  to  all  appearances,  a  third  sensory  neurone  arises, 
sending  its  fibers  to  the  cerebral  cortex.  Another  part  of  the  lemniscus  fibers, 
however,  pass  directly  to  the  cerebral  cortex  without  interruption.  The  sensory 
fibers  from  the  posterior  columns  probably  end  in  the  cerebral  cortex  in  the  cen- 
tral convolutions,  especially  in  the  posterior  central  convolution  and  in  the  neigh- 
boring portion  of  the  parietal  lobe,  and  perhaps  also  of  the  frontal  lobe.  It  is  ex- 
tremely interesting  physiologically  that  the  central  terminal  region  of  the  sensory 
fibers  in  part  quite  coincides  in  its  localization  with  the  motor  centers  {vide 
infra). 

It  would  be  extremely  valuable  if  we  knew  the  centripetal  conduction  tracts 
to  the  cerebrum  for  the  different  kinds  of  cutaneous  and  muscular  sensibility 
(see  the  preceding  chapter).  Unfortunately,  our  knowledge  in  this  regard  is  still 
extremely  defective  and  uncertain.  The  hypothesis,  which  seems  relatively  the 
most  certain,  is  that  the  sensory  fibers  entering  directly  into  the  gray  posterior 
horns  serve  chiefiy  for  the  conduction  of  sensations  of  pain  and  temperature. 
This  is  supported  especially  by  the  observations  on  syringomyelia  {vide  infra). 
It  has  also  long  been  claimed  by  the  physiologists  (Schiff)  that  section  of  the 
posterior  gray  matter  causes  analgesia.  The  posterior  root-fibers,  which  ascend 
in  the  posterior  columns,  seem  to  serve  especially  for  the  conduction  of  muscular 
sensations  and  the  co-ordination  of  motion  {vide  infra).  Many  ways  seem  to  be 
open  for  the  conduction  of  simple  sensations  of  contact :  it  is  striking  how  rarely 
total  anaesthesia  of  the  skin  occurs  in  organic  diseases  of  the  spinal  cord,  and  it 
almost  never  occurs  in  organic  diseases  of  the  brain. 

2.  The  General  Causes  of  Cutaneous  Anaesthesia. — Eegarding  the  separate 
causes  of  anaesthesia,  we  see,  in  the  first  place,  peripheral  anaesthesia  under  con- 
ditions where  the  terminal  organs  of  the  sensory  cutaneous  nerves  have  lost  their 
direct  irritability.  After  chilling  the  skin,  after  the  local  action  of  ether  and 
similar  substances,  after  the  corrosive  action  of  acids  and  alkalies,  carbolic  acid, 
etc.,  as  well  as  after  the  use  of  certain  narcotics,  such  as  cocaine,  we  see  an 
anaesthesia  of  the  skin,  which  is  due  to  injury  of  the  terminal  sensory  organs. 
We  may  probably  put  the  frequent  anaesthesia  of  washerwomen  in  this  class,  for 
their  hands  and  forearms  are  exposed  all  day  to  the  action  of  cold,  lye,  etc.  The 
anaesthesias  which  develop  in  circulatory  disturbances  of  the  skin  also  have  the 
same  peripheral  origin,  especially  the  "  spastic  anaemia  "  which  sometimes  comes 
in  the  hands  and  is  due  to  a  spasm  of  the  small  arteries. 

We  distinguish  the  peripheral  anaesthesia  of  conduction,  which  may  be  pro- 
duced by  all  forms  of  lesion  of  the  nerve-trunks,  from  the  peripheral  anaesthesias 
in  the  strict  sense  of  the  term.  Traumatic  influences,  compression  from  new 
growths,  and  inflammation  and  degeneration  of  the  peripheral  nerves,  as  in  neu- 
ritis, are  the  most  frequent  causes  of  this  form  of  anaesthesia,  which  is  often  lim- 


800  DISEASES    OF   THE   NEEVOUS    SYSTEM 

ited  to  the  region  of  distribution  of  one  or  more  individual  nerves.  The  circum- 
scribed anaesthesias  which  often  come  on  after  acute  diseases  (typhoid  fever, 
diphtheria),  and  in  some  chronic  diseases  (diabetes),  are  usually  peripheral 
(neuritic)  anaesthesias. 

Spinal  ansesthesia  is  very  often  seen  in  the  different  diseases  of  the  spinal 
■cord,  most  frequently  in  tabes,  because  this,  as  we  shall  see  later,  is  a  direct  dis- 
ease of  the  peripheral  sensory  neurone;  but  spinal  anesthesia  is  not  infrequent 
in  diffuse  acute  and  chronic  inflammation  of  the  cord  and  in  compression  and 
new  growths,  and  especially  in  syringomyelia.  As  a  rule,  it  is  bilateral  para-an- 
sKSthesia,  but  in  unilateral  lesion  of  the  cord  it  may  also  be  unilateral,  the  anaes- 
thesia being  found  on  the  half  of  the  body  opposite  to  the  affected  half  of 
the  cord,  owing  to  the  decussation  of  the  sensory  fibers  in  the  gray  matter  {vide 
supra). 

Cerebral  anaesthesia  is  seen  especially  in  haemorrhages,  foci  of  softening,  and 
tumors,  which  affect  any  part  of  the  lemniscus  tract  or  the  posterior  portion  of 
the  internal  capsule.  Such  anaesthesias  affect  the  half  of  the  body  opposite  to  the 
lesion,  and  are  called  hemianaesthesia.  As  a  rule,  experience  shows  that  cerebral 
anaesthesia  of  organic  origin  is  seldom  very  intense.  Hysterical  anaesthesias, 
however,  may  attain  an  extreme  degree;  they  are  due  to  a  disturbance  of  the 
perception  of  sensory  impressions  by  the  consciousness. 

3.  The  Symptoms  of  Cutaneous  Anaesthesia. — In  many  cases  the  patient 
himself  notices  the  existence  of  anaesthesia.  He  finds  that  in  certain  parts  of 
"the  body  he  no  longer  feels  the  pressure  of  his  clothing  or  the  bed-clothes  in  the 
usual  way.  Anaesthesia  of  the  hands  is  soonest  noticed,  because  this  affects  the 
patient's  occupation  in  diverse  ways,  so  that,  for  example,  he  is  apt  to  let  fine 
objects,  such  as  needles,  drop  from  his  hands.  In  other  cases,  of  course,  the 
anaesthesia  is  first  found  on  a  physical  examination.  It  is  worthy  of  note  that 
hysterical  anaesthesia  especially,  even  if  it  be  very  marked  and  extensive,  may 
often  be  wholly  overlooked  by  the  patients  themselves. 

Anaesthesia  is  very  often  combined  with  abnormal  subjective  sensations,  par- 
Eesthesiae,  in  the  affected  portions  of  the  skin.  The  patient  has  a  feeling  there  of 
"  numbness,"  or  a  "  furry  feeling,"  or  complains  of  prickling  or  formication.  The 
anaesthetic  parts  may  even  be  the  seat  of  very  decided  pain  (ancesthesia  dolorosa), 
if  there  is  abnormal  irritation  of  the  sensory  nerves  from  the  break  in  the  con- 
duction toward  the  center.  The  most  diverse  forms  of  anomalies  of  motility  and 
of  the  reflexes,  and  vaso-motor  disturbances,  may  of  course  be  present  in  addition 
to  the  anaesthesia.  Special  mention  must  be  made  of  the  so-called  trophic  dis- 
turbances (inflammation,  ulceration,  bed-sores,  etc.)  which  are  often  seen  in  an- 
aesthetic regions.  Whether  in  these  cases  we  actually  have  to  do  in  part  with 
direct  injury  of  the  tissues  from  the  failure  of  normal  "  tropho-neurotic  "  influ- 
ences is  at  present  wholly  undetermined.  The  majority  of  the  ordinary  so-called 
■*'  trophic  "  disturbances  are  without  doubt  due  to  external  injuries  (slight  wounds 
with  consequent  pui-ulent  infection).  When  there  is  anaesthesia,  or  especially 
analgesia,  of  the  patient's  skin,  these  injuries  do  not  receive  sufficient  attention, 
and  therefore  they  are  neither  avoided  nor  thoroughly  treated  (compare  especially 
the  chapter  on  syringomyelia).  Greater  external  injuries — bums,  bed-sores,  etc. 
— are  often  not  noticed  at  all  when  on  anaesthetic  parts,  and  therefore  they  may 
attain  an  extraordinary  size  and  become  very  bad. 

Voluntary  motion,  if  we  may  draw  conclusions  from  existing  clinical  observa- 
tions, is  not  disturbed  by  anaesthesia  in  itself,  of  however  great  a  degree,  as  long 
as  the  motions  can  be  controlled  by  the  eyes,  but  finer  movements  are  often  con- 
siderably impaired  by  cutaneous  anaesthesia ;  thus  patients  with  diminished  sen- 
sibility in  the  fingers  can  usually  no  longer  sew,  because  they  lose  the  needle  every 
minute.     With  the  eyes  shut,  however,  the  motions  of  the  anaesthetic  parts  be- 


ANiESTHESIA   OE   THE   SKIIT 


801 


come  very  uncertain,  botli  in  ansestliesia  of  the  skin  and  of  the  deeper  parts,  the 
muscles  and  joints;  since  then  the  patient  loses,  to  a  great  degree,  his  power  of 
judging  of  the  extent  and  of  the  precise  direction  of  his  movements.  Very  ex- 
tensive anaesthesia  of  the  skin,  associated  at  the  same  time  with  anaesthesia  of 
the  organs  of  special  sense,  is  sometimes  not  without  influence  upon  conscious- 
ness. We  have  had  under  observation  a  very  remarkable  case  of  total  anaes- 
thesia of  the  whole  body  associated  with  unilateral  blindness  and  deafness.    If 

we  entirely  excluded  this 
patient  from  all  external 
impressions  of  sense  by 
closing  his  still  service- 
able eye  and  ear,  we  could 
at  once  in  this  way  put 
him  into  a  deep  sleep! 
It  must,  of  course,  be  said 
in  this  connection  that 
such  extensive  anaesthe- 
sias have  thus  far  been  ob- 
served almost  exclusively 
in   hysteria    (vide    infra), 

^j  I  rvpii  \\/v  \   \ 


Fig.  87.  Fig.  88.  .  Fig.  89. 

Figs.  87  and  88.*— Distribution  of  the  sensory  cutaneous  nerves  in  the  trunk  and  upper  extremities: 
Fig.  87.  Posterior  aspect.  Fig.  88.  Anterior  aspect.  The  shaded  portion  in  Fig.  87  de.signates  the 
territory  supplied  by  the  radial  nerve.  (From  Henle.)  sc.  Supraclavicular  nerves  (from  the  cervical 
plexus),  ax.  Cutaneous  branch  of  the  axillary  nerve,  cps  and  cpi.  Superior  and  inferior  posterior 
cutaneous  nerves  from  the  radial  (ra).  cmd,  cm,  and  cl.  Median  cutaneous,  median,  and  lateral  nerves. 
me.  Median  nerve,  u.  Ulnar  nerve,  du.  Second  dorsal  nerve,  dxii.  Twelfth  dorsal  nerve,  ih.  Ileo- 
hypogastric  nerve,  ii.  Ilio-inguinal  nerve,  il.  Lateral  perforating  branches,  and  m,  anterior  per- 
forating branches  of  the  intercostal  nerves. 

Fig.  89.— Detailed  distribution  of  the  nerves  to  the  dorsal  surface  of  the  fingers.  (From  Krause.)  r.  Radial 
nerve,    m.  Median  nerve,    u.  Ulnar  nerve. 

and  that  therefore  special  psychical  factors  have  perhaps  been  of  influence  in 
the  phenomenon  just  mentioned. 

We  can  not  here  go  into  details  of  the  different  forms  and  varieties  in  the 
course  of  anaesthesia,  since  they  will  be  spoken  of  under  the  different  diseases 
which  lie  at  the  basis  of  the  anaesthesia.  The  regions  of  distribution  of  the 
peripheral  sensory  nerves  of  the  skin  are  given  diagrammatically  in  the  accom- 
panying cuts  (Eigs.  87  to  91).  Experience  shows,  however,  that  complete  section 
of  a  peripheral  sensory  (or  mixed)  nerve  almost  never  causes  total  anaesthesia 
in  the  corresponding  cutaneous  region,  probably  because  there  are  many  anasto- 
moses of  the  terminal  branches  of  the  sensory  nerves. 


[*  Henle's  nomenclature  of  the  peripheral  nerves  has  been  adopted. — Trans.J 
51 


802 


DISEASES    OF   THE   NERVOUS    SYSTEM 


X 


cl 


li 


cl 


^P 


cr 


mt 


Ansestliesia  in  the  region  of  tiie  trigeminus  demands   a  brief  special  de- 
scription. 

4.  Anaesthesia  of  the  trigeminus  is  observed  in  tumors,  syphilitic  new 
growths,  chronic  inflammations,  and  analogous  processes  at  the  base  of  the  skull, 
which  compress  the  trunk,  the  Gasserian  ganglion,  or  one  of  the  three  branches  of 
the  trigeminus,  or  directly  involve  the  nerves.  Traumatic  lesions  of  the  tri- 
geminus also  are  not  very  uncommon.  The  distribution  of  the  ansesthesia,  ac- 
cording as  the  affection  involves  the  whole  trigeminus,  or. only  one  branch  of  it, 
may  be  seen  in  Eigs.  92  and  93,  but  individual  variations  occur.  In  total  anaes- 
thesia of  the  trigeminus,  the  conjunctiva 
and  cornea,  the  mucous  membrane  of  the 
nose,  the  cavity  of  the  mouth,  the  tongue 
up  to  the  foramen  caecum,  and  the  soft 
palate  are  ansesthetie  on  the  affected  side. 
Hence  we  often  find  ulcers  on  the  tongue 
and  the  mucous  membrane,  which  come 
from  being  bitten.  The  "  neuro-paralytic 
ophthalmia,"  not  infrequently  seen  in  an- 
aesthesia of  the  trigeminus  is  of  special  in- 
terest, and  it  has  been  much  studied  by 
physicians  and  physiologists.  This  is  an 
ulcerative  keratitis,  almost  always  begin- 
ning in  the  lower  segment  of  the  cornea, 
and  sometimes  passing  over  into  a  purulent 
inflammation  of  the  whole  eyeball.  This 
affection  is  regarded  in  many  quarters  as 
an  immediate  result  of  the  disturbance  of 
special  ''  trophic "  functions,  but,  after 
careful  experiments,  it  seems  certain  that 
external  traumatic  influences  always  occa- 
sion the  first  trouble,  and  render  the  in- 
trusion of  inflammatory  agents  possible. 
As  a  result  of  the  anaesthesia  of  the  eye 
the  patient  does  not  notice  the  inflamma- 
tory symptoms,  which  therefore  often  at- 
tain an  extremely  high  degree.  It  is  still 
uncertain,  but  not  wholly  improbable,  that 
we  must  also  assume  a  specially  dimin- 
ished power  of  resistance  on  the  part  of 
the  tissues  and  a  limitation  of  all  com- 
pensating functions  as  a  result  of  the 
nervous  lesion. 

The  skin  of  the  face  is  often  somewhat 
bloated  and  reddened  in  anaesthesia  of 
the  trigeminus,  and  it  is  sometimes 
warmer,  but  often  colder,  than  normal. 
The  reflexes  are  lost  in  peripheral  anass- 
thesia,  and  the  lachrymal  secretion  ceases. 
The  taste  is  almost  always  decidedly  dimin- 
ished on  the  anterior  two  thirds  of  the  tongue  on  the  affected  side,  the  territory 
supplied  by  the  lingual  nerve.  According  to  the  investigations  of  Krause  on 
patients  in  whom  the  Gasserian  ganglion  has  been  extirpated  i^vide  infra),  the 
trigeminus  contains  fibers  which  conduct  sensations  of  taste  for  sweet,  sour,  and 
salt  from  the  tip  of  the  tongue  and  the  anterior  two  thirds  of  its  lateral  border; 


'V 


/ 


we{\  SSL 


ctij 


Fig.  91. 


Fig.  90. 

Figs.  90  and  91.— Distribution  of  the  sensory  cu- 
taneous nerves  to  the  lower  extremities.  Fig. 
90.  Posterior  aspect.  Fir.  91.  Anterior  as- 
pect. (From  Henle.)  ii.  Ilio  inguinal  nerve. 
li.  Lumbo-ing:ufnal  nerve,  se.  External  sper- 
matic, cp.  Posterior  cutaneous,  cl.  Lateral 
cutaneous,  cr.  Crural,  obt.  Obturator,  sa. 
Saphenous,  cpe.  Peroneal  communicating- 
nerve,  cti.  Tibial  communicating  nerve. 
jyer'.  Superficial  branch  of  the  peroneal 
nerve,  per".  Deep  peroneal  nerve,  cjwi. 
Posterior  median  cutaneous  nerve,  cpp.  Cu- 
taneous plantar  nerve. 

or  at  least  is  persistently  diminished. 


ANESTHESIA   OF   THE    SKIN 


803 


"but  individual  variations  seem  to  occur.  The  secretion  of  saliva  as  a  rule  suffers 
no  perceptible  change,  but  we  sometimes  see  a  diminished  secretion  of  mucus  in 
the  nasal  cavity  on  the  affected  side. 

Besides  the  peripheral  anaesthesias  just  described,  other  anaesthesias  occur, 
especially  in  syringomyelia,  and  more  rarely  in  other  diseases  of  the  medulla 
oblongata,  which  are  due  to  a  lesion  in  the  region  of  the  trigeminal  nucleus  (nu- 
clear aneesthesia).    In  those  cases  a  remarkable  condition  is  manifest — namely, 
that,  in  diseases  which  extend  from  below  upward,  the  ansesthesia  first  appears 
in  the  upper  part  of  the  forehead  next  to  the  hairy  scalp  (and  usually  on  the  lat- 
eral portion  before  the  median),  and  that  the  sensory  disturbance  extends  in  a 
curve   downward   and 
inward    to    the    eye- 
brows,   then    to    the 
outer   portion   of   the 
eyelids,    then   to    the 
median  portion  of  the 
lids,  and  finally  to  the 
skin  of  the  alse  nasi 
and  the  bridge  of  the 
nose.       The     frontal 
portion    of    the    first 
branch  of  the  trigem- 
inus, therefore,  seems 
to    derive    its    fibers 
from    the    most    dis- 
tal   (lowest)    nuclear 
groups,     next     above 
come   the   nuclei    for 
the       third       branch 
(temporal        region), 
and  then  for  the  sec- 
ond  branch    and   the 
nasal  portion  of  the 
first  branch   (see  the 
anatomical  description  in  the  section  on  diseases  of  the  medulla  oblongata). 
The  disturbances  of  sensibility  in  the  mucous  membrane  of  the  mouth  are  usually 
seen  first  in  the  posterior  portion  of  the  miicous  membrane  of  the  cheeks,  then  in 
the  hard  palate,  and  finally  in  the  region  of  the  soft  palate  and  the  tonsils.    The 
mucous  membrane  of  the  oral  cavity,  therefore,  derives  its  sensory  fibers  from  the 
distal  portion  of  the  trigeminus  nuclei  (Schlesinger). 

5.  Treatment  of  Cutaneous  Ansesthesia. — Since  ansesthesia  in  most  cases  is 
only  a  symptom,  treatment,  of  course,  must  always  first  be  directed  against  the 
underlying  disease.  Therefore  we  will  mention  here  only  those  measures  which 
are  to  be  used  symptomatically  against  ansesthesia. 

The  chief  remedy  is  the  electric  current.  We  treat  the  anaesthetic  part  of  the 
skin  with  the  faradic  current,  using  ordinary  electrodes,  or,  better  still,  the  wire 
brush,  or  with  the  galvanic  current,  stroking  the  skin  slowly  back  and  forth  with 
the  cathode  for  three  or  four  minutes.  Sometimes  we  can  see  a  result  imme- 
diately after  the  sitting.  Hysterical  ansesthesia  may  often  be  removed  in  this 
way  in  a  very  short  time. 

Besides  electricity  we  prescribe  embrocations,  such  as  spirit  of  camphor, 
formic  acid,  spirit  of  thyme,  etc.,  and  also  baths,  and  cold  or  hot  local  douches, 
combined  with  rubbing  the  skin.  The  action  of  internal  remedies,  such  as  strych- 
nine, is  extremely  doubtful. 


Fig.  92.  Fio-  93. 

FiG3.  92  and  93.— Distribution  of  the  sensory  cutaneous  nerves  in  the  head  : 
uma  and  omi.  Occipitalis  major  and  minor,  am.  Auricularis  magnus. 
c.s  Superficial  cervical.  Fj.  Fj.  F3.  First,  second,  and  third  branches 
of  the  fifth  (F).  so.  Supraorbital,  sf.  Supratrochlear,  if.  Infratroch- 
lear.  e.  Ethmoidal.  I.  Lachrymal,  sm.  Subcutaneus  malae,  or  zygo- 
matic, at.  Auriculotemporal.'  b.  Buccinator,  m.  Mental.  B.  Poste- 
rior branches  of  the  third  cervical. 


804  DISEASES    OE   THE   l^EEVOUS    SYSTEM 

It  is  very  important  to  protect  the  aneesthetic  part  against  external  injuries. 
In  anaesthesia  of  the  trigeminus,  particularly,  we  guard  the  eye  as  far  as  possible 
from  the  development  of  a  neuro-paralytic  keratitis,  by  a  carefully  applied  oc- 
clusive bandage,  and  treat  even  the  slightest  inflammation  with  the  greatest  care. 
We  can  thus  almost  certainly  avoid  bad  results. 


CHAPTEE   in 
NEURALGIA    IN    GENERAL 

Concept  and  .Sltiolog^. — Although  every  pain  is,  of  course,  excited  by  abnor- 
mal irritation  of  the  nerves,  still  we  are  justified  in  giving  a  certain  special  vari- 
ety of  pain  the  name  of  neuralgia.  By  that  name  we  understand  pain  due  to  a 
disease  of  a  definite  sensory  nerve  (or  perhaps  sometimes  of  its  central  con- 
tinuation). The  name  neuralgia  has  therefore  both  a  symptomatica!  and  an  ana- 
tomical significance.  Symptomatically  most  neuralgias  are  characterized  by  the 
following  peculiarities :  1,  the  pain  is  felt  exactly  in  the  course  or  in  the  distribu- 
tion of  one  or  more  special  nerve-trunks  or  nerve-branches;  2,  it  is  usually 
of  very  considerable  intensity;  and,  3,  as  a  rule,  it  is  not  present  continuously, 
but  it  shows  manifest  variations.  Many  neuralgias  come  on  in  pronounced  parox- 
ysms of  pain,  which  are  interrupted  by  wholly  painless  intervals.  Anatomically, 
neuralgia  is  not  one  single  disease.  Every  severe  affection  of  a  sensory  nerve 
leads  to  neuralgic  pain.  The  trouble  is  often  merely  one  symptom  of  another 
more  extensive  morbid  process  (symptomatic  neuralgia).  In  other  cases  the 
affection  of  the  sensory  nerve  is  an  independent  disease  by  itself  (idiopathic, 
primary  neuralgia).  In  many  idiopathic  neuralgias  we  may  with  great  probabil- 
ity assume  an  inflammatory  affection  of  the  nerve  or  the  nerve-sheath,  as  in  sci- 
atica, but  in  other  eases,  and  indeed  in  most  typical  neuralgias,  as  in  severe 
trigeminal  neuralgia,  this  theory  is  improbable.  In  these  cases  the  special  nature 
of  the  "  neuralgic  disease "  is  still  entirely  obscure.  At  times,  in  separate  at- 
tacks and  without  any  known  cause,  extremely  active  irritative  processes  occur 
in  the  special  nerve  territory,  causing  the  most  intense  pain.  Trousseau  has 
compared  these  paroxysms  of  sensory  irritation  to  the  motor  discharges  of  the 
epileptic  attack,  and  hence  has  spoken  of  "  epileptiform  neuralgia." 

In  regard  to  the  general  occurrence  of  neuralgia,  age  has  thus  far  an  influ- 
ence that  most  cases  occur  in  middle  life,  but  neuralgia  also  occurs  in  older  peo- 
ple and  much  less  frequently  in  children.  Sex  exerts  an  influence  so  far  that 
certain  forms,  such  as  sciatica  and  brachial  neuralgia,  are  more  common  in 
men.  On  the  other  hand,  certain  phases  of  the  female  sexual  life,  such  as 
puberty,  pregnancy,  childbed,  and  the  climacteric,  favor  the  disposition  to  neu- 
ralgia. The  general  neuropathic  predisposition,  which  is  hereditary  in  the  ma- 
jority of  cases,  is  of  great  significance.  Neuralgia  often  appears  in  people  who 
suffer  from  other  neuroses,  or  in  whose  families  other  nervous  diseases,  such  as 
the  psychoses,  epilepsy,  hysteria,  or  neurasthenia,  have  repeatedly  occurred.  The 
physical  constitution  also  seems  to  be  of  influence.  We  often  see  neuralgia  in 
anaemic  people,  or  in  those  whose  constitution  has  been  impaired  by  physical  and 
mental  strain,  by  imprudent  living,  or  by  mental  excitement. 

We  may  mention,  as  exciting  or  at  least  as  favoring  causes  of  neuralgia :  1. 
Cold,  the  action  of  draughts,  wind,  or  wet — the  so-called  "  rheumatic  neuralgias." 
It  is  not  perfectly  clear  how  the  cold  acts  in  such  cases.  We  usually  assume  that 
by  its  action  slight  anatomical  (inflammatory?)  changes  arise  directly  or  in  a 


NEUEALGIA   IN   GENERAL  805 

reflex  manner  in  the  nerves  themselves.  2.  Mechanical  and  traumatic  action. 
Among  these  are,  first,  wounds  and  contusions  which  directly  involve  the  nerves. 
Thus,  for  example,  extremely  severe  neuralgia  sometimes  arises  from  the  pres- 
sure of  foreign  bodies,  such  as  splinters  of  wood  or  of  bones  in  wounds,  on  the 
branch  of  a  nerve.  We  may  also  mention  here  the  very  severe  neuralgia  some- 
times met  with  after  amputations.  These  cases  are  probably  due  less  to  the  so- 
called  amputation  neuromata  than  to  the  pulling  and  stretching  of  the  nerve- 
trunks  in  the  amputation  cicatrix,  giving  rise  to  the  pain.  To  this  class,  too, 
belong  many  diseases  in  the  neighborhood  of  nerves.  Diseases  of  the  bones  or 
periosteum,  by  pressure  and  mechanical  irritation,  and  often  perhaps  by  the  ac- 
companying inflammation,  may  lead  to  neuralgia  in  those  nerves  which  run 
through  bony  canals  or  grooves.  Lastly,  tumors,  aneurisms,  hemise,  or  the  gravid 
uterus,  may  lead  to  neuralgia  by  pressure  on  the  neighboring  nerves;  but  we 
must  call  to  mind  that  every  pressure  on  a  nerve  does  not  lead  to  neuralgia  in 
the  same  way,  so  that  we  must  assume  a  special  consequent  change  in  the  nerve 
in  "  neuralgia  from  compression."  3.  The  relation  which  certain  infections  and 
poisons  have  to  the  development  of  neuralgia  is  very  important.  In  the  first 
place,  it  is  not  impossible  that  many  of  the  appalrently  "  idiopathic  "  neuralgias 
are  to  be  referred  to  infectious  causes — an  assumption  which  may  be  made,  for 
instance,  in  intercostal  neuralgia  associated  with  an  eruption  of  zoster  {q.  v.),  or 
in  many  acute  trigeminal  neuralgias.  Many  neuralgias,  however,  also  have  a 
definite  relation  to  other  infectious  diseases.  We  may  mention  in  particular 
the  malarial  neuralgias,  which  are  directly  dependent  upon  the  malarial  infec- 
tion, often  come  on  at  regular  intervals,  and  are  cured  by  specific  treatment — 
namely,  quinine.  Neuralgia  is  often  seen  during  the  course,  or  as  a  result,  of 
typhoid  fever,  small-pox,  and  similar  acute  infectious  diseases,  and  in  the  second- 
ary stage  of  syphilis.  Among  toxic  substances  we  may  mention  especially  alcohol, 
lead,  arsenic,  mercury,  and  perhaps  nicotine,  as  those  which  have  a  relation  to  the 
development  of  neuralgia.  Yet  in  these  cases  it  is  usually  not  neuralgia  but  pain 
of  some  other  kind — the  arthralgia  of  lead  poisoning,  the  polyneuritic  pains  of 
alcoholic  subjects,  etc.  4.  Symptomatic  neuralgia  is  also  found  in  many  con- 
stitutional diseases,  in  gout,  and  very  often  in  diabetes  mellitus.  It  is  supposed 
that  in  such  cases  abnormal  chemical  influences  act  on  the  sensory  nerves.  5. 
Finally,  there  was  formerly  much  said  about  "  reflex  neuralgia,"  where,  for  exam- 
ple, disease  of  the  sexual  organs  was  thought  to  cause  neuralgia  in  distant  nerves. 
Such  observations,  however,  can  not  endure  strict  criticism.  Most  of  these  cases 
are  hysterical. 

[Although  the  reflex  origin  of  neuralgia  and  other  nervous  disturbances  is 
very  doubtful,  it  is  well  known  that  pain  due  to  disease  of  a  given  organ  may  be 
referred  to  another  part  of  the  body.    A  familiar  example  is  the  reference  of  the 
pain  from  hip  disease  to  the  knee.     This  reference  of  pain  to  distant  parts  is 
probably  dependent  upon  the  anatomical  distribution  of  the  nerves.     Head  has 
made  an  exhaustive  study  of  the  distribution  of  the  visceral  nerves  in  the  spinal 
cord,  and  has  found  that,  in  disease  of  the  internal  organs,  the  pain  is  apt  to  be 
referred  to  certain  areas  of  the  skin  whose  sensory  nerves  go  to  the  correspond- 
ing spinal  segments.     The  internal  organs  are  represented  in  the  spinal  cord  as 
follows :  Heart,  1-3  D ;  *  lungs,  1-5  D ;  stomach,  6-9  D   (cardiac  end,  6-7  D 
pylorus,  9  D)  ;  intestines,  9-12  D ;  rectum,  2-4  S ;  liver  and  gall-bladder,  7-10 
D ;  kidney  and  ureter,  10-12  D ;  bladder,  mucous  membrane,  and  neck,  1— i  S 
over-distention  of  bladder,  11  D-1  L;  prostate,  10-12  D;  1-3  S;  5  L;  epididymis 
11  D-1  L;  testicle  and  ovary,  10  D;  appendages,  11  D-1  L;  uterus,  in  contraction 
10  D-1  L;  03  uteri,  1-4  S.    For  the  cutaneous  areas  corresponding  to  these  seg- 

*  D,  dorsal  segment:  L,  lumbar;  S,  sacral. 


806  DISEASES    OE   THE   NEEVOUS    SYSTEM 

ments  of  the  cord  see  the  colored  plate  (page  924).  Disease  of  the  internal  organs 
may  also  cause  referred  pains  in  the  head,  perhaps  through  the  connections  of  the 
vagus  nerve.  Disease  of  the  lungs  causes  referred  pain  in  the  fronto-nasal,  mid- 
orbital,  and  fronto-temporal  areas;  of  the  heart  in  the  mid-orbital,  fronto-tem- 
poral,  and  temporal  areas;  of  the  stomach  and  intestines  in  the  temporal,  verti- 
cal, and  parietal  areas;  of  the  liver  in  the  vertical  and  occipital  areas;  and  of 
the  ovaries  and  testicles  in  the  occipital  area.  Diseases  of  the  uterus.  Fallopian 
tubes,  and  bladder  do  not  give  rise  to  referred  pain  in  the  head.  Affections  in  the 
head  itself  also  give  rise  to  referred  pains  in  the  head.  Refraction  errors  cause 
pain  in  the  mid-orbital  region ;  disease  of  the  cornea  or  anterior  chamber  of  the 
eye,pain  in  the  fronto-nasal  area;  of  the  iris,  in  the  temporal  area;  farther  back  in 
the  eye,  in  the  temporal,  fronto-temporal,  and  maxillary  areas ;  of  the  membrana 
tympani  and  middle  ear,  in  the  hyoid  area;  elevation  of  tension  in  the  middle  ear, 
in  the  vertical  and  parietal  areas;  disease  of  the  tongue,  in  the  mental,  hyoid, 
and  superior  laryngeal  areas.  Dana  had  previously  represented  the  regions  of 
referred  pain  in  visceral  disturbances  in  much  the  same  way.] 

General  Symptomatology  of  Neuralgia. — The  neuralgic  paroxysm  begins 
either  quite  suddenly,  or,  more  frequently,  after  certain  prodromata,  such  as  cold 
feelings,  prickling,  slight  painful  sensations,  etc.,  have  preceded  it  for  some  time. 
The  pain  during  the  attack  is  usually  of  the  greatest  severity,  and  is  described 
as  either  burning  and  boring,  or  as  shooting  and  tearing  like  lightning.  There  are 
frequently  short  temporary  remissions  of  the  pain.  The  location  of  the  pain  usu- 
ally corresponds  precisely  to  the  distribution  of  the  affected  nerve,  so  that  the 
patient  can  often  point  out  quite  definitely  the  anatomical  course  of  the  nerve. 
At  the  height  of  the  attack  there  is  often  an  "  irradiation  "  or  shooting  of  the  pain 
into  the  territory  of  neighboring  nerves.  External  irritants,  such  as  cold  air, 
mental  excitement,  and  especially  movements  of  the  affected  part,  often  produce 
an  increase  of  the  pain. 

On  physical  examination,  we  notice,  first,  certain  disturbances  of  sensibility. 
The  skin  in  the  neuralgic  part  often  shows  more  or  less  anaesthesia,  which  is  most 
apparent  in  the  intervals  between  the  separate  attacks  and  immediately  after 
them.  Much  more  frequently,  however,  both  during  the  attack  and  during  the 
time  when  the  patient  is  free  from  pain,  there  is  hypersesthesia  of  the  skin  and 
the  parts  beneath.  There  are  certain  definite  points  which  are  often  very  sensi- 
tive and  tender  even  to  light  pressure.  These  are  called  painful  points  (points 
douloureux).  They  were  first  fully  described  for  the  different  forms  of  neuralgia 
by  Valleix,  in  1841,  although  in  much  too  schematic  a  way,  but  they  have  con- 
siderable diagnostic  importance,  since  they  may  often  be  found,  not  only  during 
the  attack  itself,  but  also  during  the  free  intervals,  although  then  they  are  less 
marked.  The  painful  points  always  correspond  to  certain  places  in  the  course  of 
the  trunk  or  the  larger  branches  of  the  affected  nerve,  and  are  found  especially 
where,  in  marked  and  deep  pressure  on  the  nerve,  we  can  press  on  some  firm  part 
beneath.  They  are  probably  always  due  to  an  abnormal  sensitiveness  to  pressure 
in  the  affected  nerve  itself.  In  many  cases  of  neuralgia  they  may  of  course  be 
wholly  wanting. 

Motor  symptoms  as  well  as  sensory  are  not  infrequent  in  neuralgia.  Co-exist- 
ing symptoms  of  paralysis  must  always  be  regarded  as  a  complication  caused  by 
some  coarse  lesion  of  the  motor  nerves ;  hence  in  pure  idiopathic  neuralgia  they 
are  entirely  absent.  The  co-existing  symptoms  of  motor  irritation,  which  are 
often  seen,  are  usually  directly  dependent  upon  the  neuralgia,  however,  and 
hence  are  to  be  regarded  chiefly  as  reflex  contractions,  due  to  the  great  irritation 
of  the  sensory  nerves. 

Vaso-motor  symptoms  are  often  seen  in  neuralgia.  In  the  face  especially,  in 
trigeminal  neuralg-ia,  we  often  see  a  marked  pallor  or  a  decided  reddening  of  the 


K^EUKALGIA   IX   GEXEEAL  807 

skin  and  conjunctiva.  Abnormal  secretions,  of  tears  or  sweat,  may  also  be  seen 
during  the  attack  or  at  the  end  of  it.  We  do  not  know  whether  all  these  symp- 
toms arise  from  direct  or  reflex  nervous  irritation.  Trophic  disturbances  are 
noticed  in  various  ways.  During  the  attack  we  see  eruptions  of  urticaria,  or  still 
more  frequently  of  herpes  vesicles,  along  the  course  of  the  affected  nerves,  as  in 
herpes  zoster.  In  severe  and  protracted  neuralgias  permanent  changes  in  the 
tissues  have  been  repeatedly  seen  in  the  parts  supplied  by  the  affected  nerves. 
Among  these  are  a  falling  out  or  a  whitening  of  the  hair,  or  more  rarely  an 
abnormally  great  growth  of  hair,  thickening  or  atrophy  of  the  skin,  staining  or 
pigmentation  of  the  skin,  atrophy  of  the  deeper  parts,  etc.  Lastly  we  may  men- 
tion that  during  the  neuralgic  attack  we  sometimes  find  a  diminished  frequency 
of  the  pulse. 

The  general  nutrition  of  the  body  often  does  not  suffer  at  all  in  neuralgia,  but 
in  many  cases,  especially  when  sleeping  and  eating  are  constantly  disturbed  by 
the  attacks  of  pain,  the  disease  gradually  has  a  noticeable  action  on  the  whole 
constitution.  The  patient  becomes  pale  and  emaciated,  and  often  the  persistent 
and  distressing  pain  is  not  without  influence  on  his  mental  condition.  He  be- 
comes irritable  and  inclined  to  melancholy.  Patients  have,  in  repeated  instances, 
even  committed  suicide  as  a  result  of  severe  and  incurable  neuralgia. 

The  whole  course  of  neuralgia  shows  the  greatest  diversity.  As  has  been  said 
repeatedly,  the  onset  of  the  disease  in  separate  attacks  is  the  chief  characteristic 
feature.  The  precise  pathogenesis  of  these  attacks  is,  of  course,  entirely  unknown 
to  us.  These  attacks  usually  come  on  every  day  or  several  times  a  day,  or  some- 
times at  longer  regular  or  irregular  intervals.  They  may  last  only  a  few  minutes 
or  several  hours.  During  the  period  between  the  attacks  many  patients  feel  quite 
well,  but  some  have  still  a  certain  sensitiveness  of  the  skin.  The  disease  as  a 
whole  sometimes  lasts  only  a  few  days  or  weeks,  but  sometimes  it  persists  with 
manifold  variations  for  years  and  years,  and,  in  a  word,  is  not  capable  of  im- 
provement ;  although,  on  the  other  hand,  there  are  recoveries  after  the  disease 
has  lasted  for  years.  In  many  cases,  of  course,  the  disease  depends  upon  the  pres- 
ence of  some  definite  anatomical  cause,  such  as  a  tumor,  a  disease  of  the  bone,  or 
an  aneurism. 

Many  details  will  be  spoken  of  in  the  following  chapter. 

General  Treatment  of  Neuralgia. — ^Prophylaxis  of  neuralgia  is  possible  in 
this  way,  that  certain  constitutional  anomalies,  such  as  anaemia  or  a  general  nerv- 
ous predisposition,  favor  its  appearance,  as  we  have  seen;  and  in  attacking  these 
conditions,  we  may  recognize  a  factor  which  can  prevent  to  a  certain  degree  any 
subsequent  development  of  neuralgia.  It  is  still  more  important,  in  people  who 
have  already  suffered  from  neuralgia,  to  prevent  the  return  of  the  affection  if  we 
can.  For  this  object  we  must  first  consider  the  strengthening  of  the  whole  body, 
in  order  to  make  it  better  resist  the  action  of  any  causes  of  disease.  The  meas- 
ures to  be  chiefly  employed  for  this  purpose  are  proper  food,  good  air,  baths,  sea- 
bathing, cold  bathing,  gymnastics,  etc.  Of  course,  we  must  also  particularly 
guard  the  part  of  the  body  that  has  once  been  attacked  from  any  irritation,  such 
as  cold,  mechanical  and  toxic  irritants,  or  over-exertion. 

In  treating  neuralgia  itself  we  must  always  look  first  with  great  care  for  some 
causal  factor,  which  may  be  accessible  to  treatment.  This  fulfillment  of  the 
causal  indication  is  often  possible  in  neuralgias  which  are  due  to  mechanical 
causes.  The  extirpation  of  tumors,  the  excision  of  cicatrices,  the  removal  of  for- 
eign bodies,  the  treatment  of  inflammatory  new  growths,  of  syphilitic  affections, 
of  aneurisms,  etc.,  is  in  many  cases  attended  by  brilliant  success,  but,  of  course,  in 
many  other  cases  the  underlying  disease  is  unfortunately  not  amenable  to  suc- 
cessful treatment.  "We  should  also  carry  out  a  causal  treatment  in  the  neuralgias 
which  are  to  be  referred  to  general  aneemia,  to  a  general  neuropathic  constitution. 


808  DISEASES    OF   THE   NERVOUS    SYSTEM 

to  hysteria,  etc.  In  such  cases  we  must  always  ascribe  great  value  to  the  general 
treatment,  such  as  diet,  manner  of  life,  psychical  treatment,  baths,  iron,  and 
nervines,  as  well  as  to  the  special  treatment  directed  against  the  neuralgia;  and 
the  same  holds  true,  of  course,  in  the  neuralgias  occurring  in  diabetes,  gout,  and 
syphilis.  We  must  always  bear  particularly  in  mind  the  possibility  of  syphilitic 
neuralgia,  since  in  such  cases  iodide  of  potassium  may  often  have  a  marked 
curative  acticfn.  We  may  also  fulfill  the  causal  indication  in  the  malarial  neu- 
ralgias. If  neuralgia  comes  on  at  approximately  regular  intervals  in  persons 
who  come  from  a  malarial  district,  and  who  perhaps  have  already  suffered  from 
other  malarial  affections,  the  exhibition  of  quinine  in  large  doses,  twenty  to  forty- 
five  grains  (granmaes  1.5-3.0)  at  once,  will  usually  speedily  cut  short  the  attack. 
In  obstinate  cases  in  which  quinine  does  no  good,  we  should  try  arsenic,  in  the 
form  of  Fowler's  solution.  In  many  apparently  toxic  neuralgias,  too,  from  lead, 
mercury,  or  alcohol,  our  first  endeavor  in  treatment  should  be  to  remove  the  cause 
of  the  disease. 

In  all  cases  where  the  causal  treatment  can  not  be  carried  out,  or  where  it 
alone  is  not  sufficient,  we  must  consider  those  numerous  remedies  and  methods  of 
treatment  which  correspond  to  the  indicatio  morbi  and  to  the  symptomatic  indica- 
tions. Starting  with  the  hypothesis  of  an  inflammatory  condition  of  the  nerve, 
we  have  often  tried  to  exert  a  favorable  influence  on  the  disease  by  local  deriva- 
tives, mustard  plasters,  irritating  embrocations,  such  as  spirit  of  mustard,  vera- 
trine  ointment  (two  and  a  half  per  cent.),  or  tincture  of  iodine,  or  by  blisters,  or 
even  by  the  cautery.  The  remedies  first  mentioned  are  used  only  in  mild  cases. 
Vesicatories,  placed  along  the  course  of  the  affected  nerve,  or  behind  the  ear  in 
facial  neuralgia,  sometimes  act  very  well  in  fresh  cases,  especially  in  fresh 
"  rheumatic  "  cases  of  sciatica.  We  resort  to  the  hot  iron  chiefly  in  old  and  very 
severe  cases,  in  which,  indeed,  especially  in  sciatica,  some  very  favorable  results 
have  been  thus  obtained. 

The  local  electrical  treatment  of  neuralgia  is  sometimes  of  undoubted  benefit. 
We  many  times  secure  an  improvement  in  the  symptoms,  which  is  of  course 
temporary,  even  in  those  cases  where  the  special  cause  of  the  disease  is  not  influ- 
enced by  the  electricity,  although  in  idiopathic  neuralgias  in  fresh,  and  some- 
times even  in  old  cases,  we  can  often  obtain  a  complete  cure.  There  are  no  gen- 
eral rules  with  regard  to  the  methods  to  be  employed,  since  different  specialists 
have  their  own  favorite  methods.  The  following  forms  of  application  are  most  in 
use  and  are  most  to  be  recommended :  1.  Stabile  action  of  the  anode  of  a  constant 
current  on  the  affected  nerve-trunk  over  as  great  an  extent  as  possible,  especially 
on  any  painful  points.  We  must  entirely  avoid  any  great  variations  in  the  cur- 
rent or  interruptions  of  it.  We  gradually  increase  the  intensity  of  the  current 
up  to  medium  strength.  The  sittings  should  last  three  to  six  minutes,  and  some- 
times even  longer,  and  they  must  be  repeated  daily.  2.  In  neuralgia  of  the  larger 
nerves  we  should  use  a  stabile  descending  (sometimes  ascending)  constant  cur- 
rent, in  which  the  anode  is  placed  on  the  most  central  point  of  the  nerve-trunk 
available,  or  on  the  vertebral  column,  and  the  cathode  on  different  peripheral 
points.  3.  The  faradic  current  also  frequently  acts  very  well.  We  faradize  the 
nerve  either  with  a  moderately  strong  "  increasing  "  current,  or  we  apply  the  wire 
brush  to  the  skin  over  the  affected  nerves.  The  latter  method  is  very  painful, 
but  it  is  often  attended  with  excellent  results.  4.  Some  electro-therapeutists, 
like  Moritz  Meyer,  lay  stress  upon  the  stabile  application  of  the  anode  of  the 
constant  current  to  any  painful  points  on  the  vertebral  column,  such  as  have  been 
found  in  many  cases  of  neuralgia  by  Trousseau. 

As  a  general  rule,  it  is  always  well  to  begin  with  a  mild  and  very  cautious  use 
of  electricity,  and  not  to  go  on  to  the  stronger  currents  until  later.  Electricity 
often  acts  brilliantly  at  once,  during  the  attack  of  pain,  but  sometimes  no  im- 


NEUEALGIA   IN   GENEEAL  809 

provement  is  seen  until  after  several  sittings.  If,  after  two  or  three  weeks,  we 
obtain  no  result  at  all,  after  employing-  different  methods  of  applying  electri- 
city, it  is  the  best  plan  to  give  up  electrical  treatment  entirely  as  not  suited  to 
the  ease. 

In  the  treatment  of  neuralgia  we  must  consider  a  number  of  internal  rem- 
edies, as  well  as  electricity;  some  of  these  act  symptomatically,  like  the  narcotics, 
while  others  have  obtained  the  reputation  of  having  a  specific  action.  Among  the 
latter,  quinine  has  decidedly  the  greatest  value.  In  severe  cases  quinine  may 
do  excellent  service,  not  only  in  malarial  neuralgias,  although  most  surely  in 
those,  but  also  in  "  idiopathic  "  neuralgias.  It  is  in  these  cases  that  the  remedy 
is  given  in  large  doses.  We  begin  with  fifteen  to  thirty  grains  (grammes  1-2)  a 
day,  best  given  in  one  dose,  and  in  severe  cases  we  may  increase  to  sixty  or  sev- 
enty-five grains  (grammes  4—5)  or  more.  We  see  the  best  results  from  quinine  in 
trigeminal  neuralgia,  while  in  other  forms,  as  in  sciatica,  it  is  much  less  efficient. 
Beside  quinine,  salicylate  of  sodium  is  sometimes  beneficial,  especially  in  the 
rheumatic  forms  of  neuralgia.  Antipyrine,  in  fifteen-  to  thirty-grain  (grammes 
1-2)  doses,  antifebrine,  in  three-  to  seven-grain  (gramme  0.25-0.5)  doses,  phe- 
nacetine,  in  seven-  to  fifteen-grain  (gramme  0.5-1)  doses,  salipyrine,  in  twenty- 
to  thirty-grain  doses  (grammes  1.5-2.0),  and  similar  remedies,  have  lately  been 
very  often  used,  l^ext  in  rank,  for  continued  use,  come  arsenic  and  bromide  of 
potassium.  The  former  is  given  in  pill  form  or  as  Fowler's  solution,  five  drops 
three  times  a  day,  increasing  gradually.  Bromide  of  potassium  acts  only  in  large 
doses,  forty-five  to  seventy-five  or  a  hundred  and  fiity  grains  a  day  (grammes  3-5— 
10).  Among  the  many  other  remedies  which  have  been  recommended  in  the  past, 
but  which  at  present  are  seldom  used,  we  may  mention  here  ergotine,  internally 
and  subeutaneously,  oil  of  turpentine,  oxide  of  zinc,  valerianate  of  zinc,  tincture 
of  gelsemium,  aconitine,  phosphorus,  subcutaneous  injections  of  osmic  acid,  ten  to 
fifteen  minims  (gramme  0.5-1)  of  a  one-per-cent.  solution,  etc. 

In  all  severe  neuralgias  the  use  of  narcotics,  especially  of  morphine,  is  un- 
avoidable. Morphine  is  used  almost  exclusively  during  the  attack,  and  is  best 
given  as  a  subcutaneous  injection  of  one  twelfth  to  one  sixth  of  a  grain  (gramme 
0.005-0.01)  in  the  vicinity  of  the  painful  part.  The  anodyne  effect  almost  invari- 
ably follows,  but  in  obstinate  and  protracted  cases  the  patient  gradually  becomes 
accustomed  to  the  remedy.  We  must  then  resort  to  still  larger  doses,  and  these, 
too,  finally  fail  in  their  effect.  Among  the  victims  of  the  morphine  habit  we  find 
many  patients  who  have  suffered  or  who  still  suffer  from  severe  neuralgia,  so  that 
we  must  always  be  very  cautious  and  conservative  in  the  protracted  use  of  mor- 
phine. We  should  be  especially  cautious  before  deciding  to  put  the  hypodermic 
syringe  into  the  patient's  own  hand.  Many  physicians  ascribe  not  only  a  pallia- 
tive but  a  permanent  benefit  to  injections  of  morphine  in  neuralgia.  We  some- 
times see,  in  fact,  that  mild  neuralgias  recover  under  the  exclusive  use  of  mor- 
phine injections;  but  these  are  probably  cases  of  spontaneous  recovery.  The 
internal  use  of  morphine  and  opium  preparations  is  decidedly  inferior  to  the  stib- 
cutaneous  administration  in  certainty  and  rapidity  of  action.  The  external  appli- 
cation of  narcotic  ointments,  or  embrocations,  is  much  employed  in  practice,  but 
it  appears  to  be  of  advantage  only  in  milder  cases.  We  prescribe  ointments  with 
extract  of  opium  (one  to  ten),  extract  of  belladonna  (two  to  ten),  extract  of 
opium  and  veratrine  (one  part  of  each  to  twenty  of  simple  ointment),  etc.  We 
may  also  use  chloroform,  by  applying  blotting-paper  wet  with  chloroform,  or 
embrocations  of  chloroform  oil,  and  ether  as  a  spray.  Chloral  and  also  paralde- 
hyde are  often  prescribed  in  chronic  neuralgias  for  their  hypnotic  effect.  Croton 
chloral  has  been  especially  recommended  in  neuralgia.  Other  hypnotics,  sul- 
phonal,  etc.,  are  also  used.  Finally,  we  must  add  that  some  physicians  have 
praised  the  anodyne  effect  of  subcutaneous  injections  of  atropine,  grain  120   to 


810       ■  DISEASES    OE   THE   NEEYOUS    SYSTEM 

-^V  to  ^V  !  (grammes  0.0005-0.001-0.003  !)  at  a  dose,  sometimes  even  in  cases  where 
morphine  does  not  act. 

In  severe  cases  the  surgical  treatment  of  neuralgia  is  often  of  great  impor- 
tance—the section  of  nerves,  neurotomy,  or  the  excision  of  a  portion  of  the  nerve, 
neurectomy — in  order  to  prevent  the  union  of  the  divided  nerve,  or,  finally,  the 
drawing  out  of  the  nerve — so-called  exairesis.  A  detailed  account  of  the  meth- 
ods of  operation  is  to  be  found  in  the  text-books  of  surgery.  We  may  state  here 
merely  that  the  surgical  treatment  of  neuralgia,  especially  of  severe  trigeminal 
neuralgia,  often  has  excellent  results.  The  explanation  of  this  success,  however, 
is  by  no  means  easy.  There  is  probably  not  only  a  break  in  conduction  from  the 
pain-exciting  spot  to  the  center,  but  an  immediate  or  secondary  change  in  the 
whole  sensory  neurone,  by  which  the  neuralgic  change  is  made  to  cease.  Of 
course  a  cure  is  not  obtained  in  all  cases.  In  any  event,  we  should  advise  an 
operation  only  in  severe  cases,  where  all  other  remedies  have  been  tried  in  vain, 
and  the  patient  may  be  promised  the  possibility,  or  even  the  probability,  of  suc- 
cess, but  never  the  certainty  of  it.  Besides  section  of  the  nerves,  nerve  stretch- 
ing has  lately  been  frequently  tried  in  neuralgia.  We  will  return  to  this  method 
of  treatment  in  speaking  of  sciatica. 

The  chief  question  as  to  the  use  of  baths  arises  only  in  the  treatment  of  neu- 
ralgias in  the  domain  of  the  nerves  of  the  extremities,  especially  in  sciatica,  and 
therefore  these  and  massage  will  be  spoken  of  more  in  detail  in  connection  with 
the  separate  forms  of  neuralgia. 

We  see,  then,  that  a  large  number  of  remedies  are  at  our  command  in  the  treat- 
ment of  neuralgia,  and  that  the  choice  among  them  is  not  always  easy.  In  any 
given  case  we  look  for  the  causal  indication,  and  try  to  fulfill  it  if  possible.  In 
the  many  cases,  however,  where  we  fail  to  find  this,  we  must  first  of  all  try  to 
alleviate  the  pain,  for  which  purpose,  if  external  derivatives  do  not  suffice,  our 
most  effective  remedy  is  morphine.  We  must  then  lay  out  a  special  plan  of  treat- 
ment. We  try  electricity,  or,  if  this  be  not  practicable,  one  of  the  other  remedies 
mentioned  above.  We  put  most  trust  in  quinine  and  antipyrine,  especially  in 
fresh  cases;  among  other  remedies,  in  anaemic  persons,  arsenic,  and,  in  more 
robust  persons,  bromide  of  potassium  are  of  service.  If  all  these  and  similar  rem- 
edies give  no  aid,  in  proper  cases  we  may  still  hope  for  success  from  operative  in- 
terference, or  else  we  must  confine  ourselves  simply  to  a  purely  symptomatic 
treatment  with  narcotics. 


CHAPTEK   lY 

THE    INDIVIDUAL    FORMS    OF    NEURALGIA 

1.  Neuralgia  of  the  Trigeminus 

(Prosopalgia.     Tic  douloureux.     FotliergiWs  Face-aclu) 

.Etiology. — Trigeminal  neuralgia  is  one  of  the  commonest  and  most  impor- 
tant neuralgias.  In  its  origin  many  causes  and  predisposing  factors  of  all  sorts 
play  a  part,  as  was  stated  in  detail  in  the  preceding  chapter.  Many  mild  forms, 
especially  neuralgia  in  the  first  branch,  apparently  are  of  acute  origin  and  have 
no  discoverable  cause.  In  such  cases  some  unknoAvn  infectious  or  auto-toxic 
influences  may  play  a  part.  ISTot  infrequently,  especially  in  mild  neuralgias  of  the 
first  branch,  we  can  not  overlook  the  influence  of  exposure  to  cold  (wind,  wet) 
as  a  possible  cause.  ITeuralgias  after  acute  infectious  diseases  (influenza, 
typhoid),  and  especially  malarial  neuralgias,  are  situated  most  frequently  in  the 


THE   INDIVIDUAL   FOEMS    OF   NEUKALGIA  811 

first  branch  of  the  trigeminus,  more  rarely  in  the  second,  and  only  exceptionally 
in  the  third.  Trigeminal  neuralgia  may  also  be  due  to  diseases  of  the  cranial 
bones  and  periosteum,  very  often  to"  diseases  of  the  teeth  (caries,  exostoses,  anom- 
alies of  development  and  position  of  the  teeth),  and  also  to  diseases  of  the  nasal 
and  frontal  cavities  and  diseases  of  the  middle  ear  and  of  the  eye  (inflammation 
and  also  strain  of  the  eyes).  Eomberg  found  an  aneurism  of  the  internal  carotid, 
pressing  on  the  Gasserian  ganglion,  as  the  cause  in  a  severe  and  incurable  case. 
We  have  seen  a  precisely  analogous  case.  Finally,  the  severe  trigeminal  neural- 
gias, which  last  for  years,  are  of  very  great  practical  importance ;  for  these  we  can 
usually  find  no  cause  at  all,  or  at  most  a  general  nervous  predisposition.  This 
form,  which  is  the  prototype  of  the  genuine,  severe,  idiopathic  neuralgias,  comes 
on  usually  in  somewhat  advanced  life,  and  is  perhaps  somewhat  more  frequent  in 
women  than  in  men.  The  special  form  of  disease  of  the  nerve  in  these  cases  is 
still  wholly  obscure.  The  few  anatomical  reports  as  to  resected  nerve  branches 
and  extirpated  Gasserian  ganglions  (vide  infra)  are  contradictory  and  capable 
of  no  positive  interpretation,  [Dana,  Putnam,  and  others  have  found  degenera- 
tive neuritis  in  the  peripheral  fibers  of  the  excised  nerve  in  these  severe  cases, 
sometimes  associated  with  obliterating  endarteritis  in  the  blood-vessels  supplying 
the  nerves.  Spiller  has  found  extensive  degenerative  changes  in  the  nerve-cells  of 
the  Gasserian  ganglion,  but  these  may  be  secondary  to  the  changes  in  the  nerve- 
fibers. — K.] 

Symptoms  and  Course. — The  attacks  of  pain  in  neuralgia  of  the  fifth  pair  are 
usually  quite  intense,  and  in  severe  cases  they  may  attain  a  most  distressing  and 
terrible  severity.  They  arise  either  entirely  without  cause,  or  from  some  slight 
influence,  such  as  washing  the  face  [making  the  slightest  movement  of  the  face  in 
eating  or  talking. — K.],  taking  physical  exercise,  or  mental  excitement.  They 
often  come  on  quite  regularly  at  definite  hours,  especially  in  the  forenoon,  but  in 
other  cases  they  follow  no  rule.  There  are  sometimes  long,  painless  intervals 
between  the  separate  attacks,  and  sometimes  the  attacks  follow  one  another  in 
an  almost  uninterrupted  series.  The  lightning-like,  cutting  pains  extend  to  the 
distribution  of  the  affected  branch  of  the  trigeminus,  but  they  sometimes  shoot 
into  the  occiput,  the  back  of  the  neck,  the  shoulders,  etc.  We  can  often  perceive 
reflex  twitchings  in  the  face,  especially  blepharospasm,  and  twitching  of  the 
corners  of  the  mouth.  The  vaso-motor  disturbances  are  noticed  at  first  as  abnor- 
mal pallor,  but  later  usually  as  quite  an  abnormal  redness  of  the  face  and  con- 
junctiva. In  neuralgia  of  the  upper  two  branches  we  often  see,  during  the  attack, 
an  unusually  great  secretion  of  tears.  An  excessive  flow  of  saliva  and  an  in- 
creased secretion  from  the  nasal  mucous  membrane  are  more  rare.  Sometimes, 
but  still  quite  rarely,  we  see  herpetic  eruptions  in  the  course  of  the  affected 
nerve,  zoster  frontalis,  herpes  of  the  conjunctiva,  etc.  In  some  cases,  too,  more 
severe  diseases  of  the  eyes,  belonging  to  the  category  of  neuroparalytic  ophthalmia, 
have  been  observed,  and  also  paralysis  of  the  ocular  muscles.  Such  complications 
always  point  to  some  gross  organic  lesion  of  the  trigeminus  and  its  neighborhood. 
In  neuralgias  that  have  lasted  longer,  we  often  see  still  further  trophic  disturb- 
ances :  changes  (thickening  or  atrophy)  in  the  skin  and  subcutaneous  cellular  tis- 
sue, the  hair  turning  gray  or  falling  out  in  the  frontal  region,  etc. 

Most  trigeminal  neuralgias  are  situated,  not  in  the  whole  distribution  of  the 
nerve,  but  only  in  one  or  more  of  its  branches  (see  Figs.  92  and  93,  page  803). 
We  accordingly  distinguish:  1.  Neuralgia  of  the  first  branch  (ophthalmic  neural- 
gia) which  is  especially  frequent  as  supra-orbital  or  frontal  neuralgia.  The  pain 
shoots  chiefly  from  the  supra-orbital  foramen  upward  into  the  forehead,  and 
sometimes  to  the  region  of  the  internal  angle  of  the  eye  and  the  bridge  of  the 
nose  (ethmoidal  nerve)  or  into  the  zygomatic  region  (lachrymal  nerve).  In  this 
we  find,  as  a  rule,  that  pressure  on  the  point  of  exit  of  the  nerve  at  the  supra- 


812  DISEASES    OF   THE  NEEVOUS    SYSTEM 

orbital  foramen  is  more  or  less  painful.  More  rarely  we  find  painful  points  also 
on  the  nose,  at  the  inner  angle  of  the  eye,  or  the  parietal  eminence,  etc.  2. 
Neuralgia  of  the  second  branch  (supra-maxillary  neuralgia)  is  most  frequent  in 
the  distribution  of  the  infra-orbital  nerve  (infra-orbital  neuralgia),  with  the  chief 
painful  point  at  the  infra-orbital  foramen,  and  others  on  the  zygoma,  on  the 
upper  lid,  etc.  The  chief  pain  usually  starts  from  the  infra-orbital  foramen,  and 
is  situated  in  the  lower  eyelid,  the  cheek,  the  upper  jaw,  the  upper  lip,  and  in  part 
also  in  the  temporal  region.  During  the  attack  of  pain  tears  are  often  seen  in 
the  eye.  3.  Neuralgia  of  the  third  branch  (infra-maxillary  neuralgia)  is  situ- 
ated chiefly  in  the  branches  of  the  mandibular  nerve  (inferior  alveolar  and  men- 
tal nerves).  The  pain  affects  the  region  of  the  lower  jaw  and  the  chin;  but  some- 
times the  pain  occurs  in  the  temporal  region,  in  the  auriculo-temporal  nerve,  and 
in  some  cases  it  is  especially  distressing  in  the  tongue,  in  the  lingual  nerve.  The 
chief  painful  points  are  at  the  mental  foramen  and  the  lower  temporal  region. 

The  general  course  of  neuralgia  of  the  fifth  pair  differs  very  much  in  different 
cases.  We  see  all  forms,  from  the  mildest,  which  rapidly  passes  off,  to  the  sever- 
est and  incurable  types,  which  may  drive  the  patient  to  despair.  In  general, 
neuralgia  of  the  first  branch  usually  belongs  to  the  relatively  milder  forms ;  neu- 
ralgia of  the  second,  and  especially  of  the  third  branch  to  the  severer  forms. 
The  above-mentioned  *^  epileptiform  "  neuralgia  (the  true  tic  douloureux)  may 
last  for  years  with  slight  interruptions;  this  occurs  chiefly  in  the  second  and 
third  branches. 

Diagnosis. — The  diagnosis  of  trigeminal  neuralgia  is  in  general  not  difficult 
if  only  we  consider  the  character  and  distribution  of  the  pain,  its  occurrence  in 
separate  paroxysms,  and  the  presence  of  any  painful  pressure  points.  Of  course  a 
careful  local  examination  is  always  necessary  to  exclude  the  existence  of  inflam- 
matory or  other  diseases  of  the  bones,  periosteum,  and  teeth.  Neuralgia  of  the 
first  branch  may  be  confounded  with  other  forms  of  headache,  and  especially  with 
true  migraine  (vide  infra),  since  in  the  latter  the  pain  is  often  located  in  the  re- 
gion of  the  supra-orbital  nerve.  Only  by  a  careful  consideration  of  accompanying 
symptoms  (scotoma,  vomiting)  can  we  avoid  a  mistake.  In  the  severe  neuralgias 
of  the  second  and  third  branches  the  reflex  muscular  twitchings  are  very  marked, 
so  that,  on  very  superficial  observation,  trigeminal  neuralgia  may  be  mistaken  for 
clonic  facial  spasm  ("tic  douloureux"  for  "tie  eonvulsif  ")• 

Prognosis. — The  prognosis  is  never  to  be  made  with  complete  certainty.  It  is 
most  favorable  in  fresh  cases  of  supra-orbital  neuralgia  which  have  a  manifest 
cause,  which  may  be  removed,  as  a  basis ;  but  if  the  affection  is  due  to  a  coarse 
anatomical  cause  which  can  not  be  removed,  or  if  we  are  dealing  with  chronic 
cases,  especially  of  the  second  or  third  branch,  the  prognosis,  unfortunately,  is 
often  very  doubtful  or  utterly  unfavorable. 

Treatment. — The  treatment  of  trigeminal  neuralgia  rests  entirely  upon  the 
principles  given  in  the  preceding  chapter.  In  searching  for  the  causal  indications 
we  must  look  chiefly,  in  neuralgia  of  the  second  and  third  branches,  for  diseased 
teeth,  and  also  in  all  cases  for  any  affections  of  the  nose,  of  the  frontal  sinuses,  or 
of  the  middle  ear.  If  such  affections  exist  they  should  be  treated  in  the  appro- 
priate way.  Carious  teeth,  which  are  painful  and  which  seem  to  have  any  relation 
to  the  neuralgia,  should  always  be  removed;  but  we  must  warn  patients  against 
permitting  in  their  despair  all  their  sound  teeth  to  be  extracted  by  unskillful 
dentists  without  any  benefit — a  thing  which  we  have  frequently  known  to  happen. 
If  there  be  a  suspicion  of  syphilis  or  malaria,  we  should  prescribe  iodide  of  potas- 
sium or  quinine.  [Even  in  non-syphilitic  cases  of  the  severer  type  large  doses 
of  iodide  of  potassium  (grammes  2.0-6.0,  grain  30-90,  thrice  daily)  combined 
with  mercury  may  act  very  beneficially.  Aconitine  is  of  some  benefit.  The 
application  of  the  positive  pole  of  the  galvanic  battery,  wet  with  a  ten-  to  twenty- 


THE   INDIVIDUAL   FOEMS    OF   NEUEALGIA  813 

per-cent.  solution  of  cocaine,  may  give  temporary  relief  (electrical  cataplioresis). 
Dana  has  obtained  good  results  from  absolute  rest  in  bed  and  daily  injections  of 
strychnine  (grammes  0.001-0.004,  grain  rh~Tt)  fo^"  several  weeks. — K.] 

In  addition,  in  fresh  "  rheumatic  "  neuralgias,  we  should  first  try  quinine,  in 
doses  of  fifteen  to  forty-five  grains  (grammes  1.0-3.0)  or  more,  or  one  of  the  many 
new  "  nervines  " — antipyrine,  antif  ebrine,  phenacetine,  salipyrine,  exalgine,  etc. 
They  sometimes  act  very  favorably,  but  in  other  cases  the  action  is  uncertain. 
Mixtures  of  the  above-mentioned  drugs  (antipyrine  with  phenacetine,  etc.)  often 
act  better  than  a  single  drug.  Many  other  remedies,  which  were  formerly  often 
used  in  neuralgia,  are  at  present  only  rarely  prescribed;  as,  for  example,  butyl 
(croton)  chloral,  tincture  of  gelsemium,  aconitine,  etc.  Arsenic  is  more  fre- 
quently prescribed  at  present,  with  somewhat  more  prospect  of  benefit. 

Besides  internal  remedies,  electricity  is  also  to  be  considered.  It  is  best  given 
by  applying  the  anode  to  the  painful  points  of  exit  of  the  affected  nerve  and  to  any 
other  painful  points,  while  the  cathode  is  held  on  the  back  of  the  neck.  We 
should  use  weak  currents  and  avoid  any  sudden  variations  in  the  current.  Other 
methods  (faradic  brush)  may  also  be  tried.  Massage  has  also  been  recommended 
for  trigeminal  neuralgia;  but  in  really  severe  cases  neither  massage  nor  electric- 
ity is  of  any  permanent  benefit. 

If  a  severe  neuralgia  persists  in  spite  of  rational  treatment  by  electricity  or 
drugs,  we  should  not  delay  too  long  in  proposing  to  the  patient  operative  treat- 
ment if  possible.  In  frontal  and  infra-orbital  neuralgia  especially  neurectomy  is 
a  comparatively  slight  operation,  which  has  many  excellent  results  to  show. 
Even  in  the  severe  and  otherwise  incurable  neuralgias  of  the  third  branch  neurec- 
tomy is  sometimes  attended  with  the  best  results.  The  full  description  of  the 
technicalities  of  the  operation,  as  well  as  the  description  of  nerve-stretching 
(which  is  much  less  to  be  recommended),  must  be  left  to  the  text-books  on  sur- 
gery. We  may  add  that  Krause  and  others  in  very  severe  cases  have  extirpated 
the  Gasserian  ganglion  successfully  and  with  benefit. 

If  we  have  to  limit  ourselves  to  a  purely  symptomatic  treatment,  injections  of 
morphine  become  unavoidable  in  severe  cases,  but  we  should  restrict  their  use 
as  much  as  possible.  The  above-mentioned  nervines  have  sometimes  a  symptom- 
atic action.  We  can  sometimes  lessen  or  shorten  the  paroxysm  of  pain  by  pres- 
sure on  the  nerve  or  by  compression  of  the  carotid. 

2.  Occipital  IN'euralgia 

Of  the  neuralgias  involving  the  sensory  region  of  the  upper  four  cervical 
nerves,  neuralgia  of  the  occipitalis  major  (Figs.  92,  93)  is  relatively  the  most 
frequent  and  practically  the  most  important.  Besides  the  factors  to  be  considered 
in  all  neuralgias,  we  must  pay  particular  attention,  in  regard  to  setiology,  to  dis- 
eases of  the  upper  cervical  vertebrae — caries  and  new  growths.  The  painful  par- 
oxysms may  attain  the  greatest  severity.  They  are  usually  located  in  the  two 
occipital  nerves  at  once,  although  often  more  severe  on  one  side  than  on  the 
other.  Painful  points  are  most  frequently  found  midway  between  the  mastoid 
process  and  the  upper  cervical  vertebrae.  Vaso-motor  disturbances,  falling  out  of 
the  hair,  etc.,  have  been  often  observed. 

The  prognosis  depends  upon  the  variety  of  the  disease.  In  primary  neuralgic 
affections  it  is  generally  favorable.  In  such  cases,  if  fresh,  a  rapid  recovery  may 
often  be  brought  about  by  salicylate  of  sodium,  antipyrine,  the  constant  current, 
or  sometimes  by  strong  cutaneous  irritants  to  the  back  of  the  neck  (blisters).  In 
other  cases,  of  course,  which  are  due  to  some  severe  disease  (vertebral  caries, 
tumors,  etc.),  the  prognosis  is  often  utterly  unfavorable,  and  treatment  can  be 
only  symptomatic  (morphine,  etc.). 

Other  neuralgias  in  the  distribution  of  the  cervical  plexus  are  rare.     They 


814  DISEASES    OF   THE   NERVOUS    SYSTEM 

occur  in  tlie  distribution  of  the  occipitalis  minor,  when,  according  to  Seeligmiil- 
ler,  they  are  quite  frequently  due  to  syphilis,  and  are  easily  cured  by  iodide  of 
potassium,  and  in  the  distribution  of  the  great  auricular  and  the  supra-clavicular 
nerves.  A  phrenic  neuralgia  even  has  been  described,  in  which  the  pain  extends 
along  the  course  of  the  phrenic  nerve  to  the  insertion  of  the  diaphragm ;  but  this 
is  at  all  events  very  rare.  In  these  cases,  as  in  many  of  the  so-called  visceral 
neuralgias,  we  probably  mistake  quite  different  forms  of  disease  or  hysterical 
symptoms  for  neuralgia.  ^ 

3.  Neuralgia  in  the  Region  of  the  Brachial  Plexus  i  ' 

(  Cervico-lrachial  Neuralgia) 

Brachial  neuralgia  is,  on  the  whole,  rare,  and  it  is  hardly  ever  limited  strictly 
to  the  distribution  of  a  single  nerve.  In  general,  the  radial  and  ulnar  nerves  are 
rather  more  frequently  affected  than  the  median.  We  also  see  at  times  neuralgia 
of  the  internal  cutaneous  nerve  and  other  cutaneous  branches,  and  neuralgia  of 
the  sensory  branches  of  the  axillary  (circumflex)  nerve.  In  regard  to  aetiology, 
we  have  to  mention  first  wounds  and  contusions  of  the  nerves,  and  also  cicatrices 
and  foreign  bodies.  The  amputation  neuralgias  also  belong  to  this  class.  Severe 
neuralgia  in  which  the  pain  may  extend  over  a  greater  part  of  the  whole  arm  is 
sometimes  seen  after  injury  of  the  fingers  (crushing,  cuts,  etc.).  In  some  of 
these  eases  we  may  have  to  do  with  an  ascending  neuritis,  starting  from  injury 
of  a  small  nerve  branch ;  in  other  cases  there  are  probably  cicatricial  contractions, 
thickenings  of  the  neurilemma,  or  small  neuromata  developing  after  the  injury, 
which  excite  the  pains.  The  "  amputation  neuralgias,"  which  are  often  very 
severe  in  amputation  stumps,  are  due  to  neuromata  which  form  on  the  cut  ends 
of  nerves.  Severe  neuralgia  often  arises  from  pressure  on  the  brachial  nerves, 
as  in  cases  of  tumors  in  the  axilla  or  neck  (cancer,  etc.),  aneurisms  of  the  aorta, 
etc.  Double  brachial  neuralgia  should  always  excite  suspicion  of  disease  in  the 
neighborhood  of  the  upper  posterior  nerve-roots,  especially  of  cervical  pachy- 
meningitis, spondylitis  of  the  lower  cervical  vertebrae,  etc. 

If  we  except  the  neuralgias  secondary  to  trauma  and  compression  already 
described,  true  primary  neuralgia  in  the  region  of  the  brachial  nerves  is  very 
rare.  We  may  sometimes,  and  most  frequently,  speak  of  neuralgia  coming  on 
after  exposure  to  cold,  although  the  distinction  between  this  form  of  neuralgia 
and  true  neuritis  {q.  t;.)  is  often  very  slight.  If  we  hold  less  strictly  to  the  con- 
ception of  neuralgia  and  include  also  the  "  nervous  "  pains  not  limited  to  the 
region  of  one  special  nerve  and  not  due  to  any  other  discoverable  local  disease, 
we  may  find  such  "  brachialgias  "  more  frequently.  They  come  on  chiefly  as  one 
symptom  of  hysteria  or  neurasthenia  in  persons  with  a  nervous  predisposition, 
and  are  often  very  obstinate  and  apparently  severe.  We  must  also  pay  especial 
attention  to  the  patient's  calling  and  occupation.  In  seamstresses,  piano-players, 
persons  who  write  much  or  do  much  other  work  with  the  arms  supported,  etc., 
we  sometimes  see  quite  severe  brachialgia  for  which  we  can  find  no  other  cause — 
the  so-called  "  occupation  neuralgias."  A  general  nervous  predisposition  also 
comes  into  play  not  infrequently  in  such  cases. 

We  must  mention  finally  those  brachialgias  which  are  dependent  upon  arterio- 
sclerosis. In  the  true  stenocardiac  attack  {vide  page  343)  the  pain  often  shoots 
into  the  left  arm.  Many  brachialgias,  apparently  associated  with  gout  or  diabetes 
mellitus,  may  also  be  dependent  upon  such  vascular  changes  and  the  disturb- 
ances of  nutrition  caused  by  them  in  the  peripheral  nerves. 

We  hfive  little  to  add  concerning  the  special  symptomatology  of  brachifil  neu- 
ralgia. The  pain,  as  we  have  stated,  is  usually  ascribed  to  the  whole  course  of  the 
nerves  without  being  very  exactly  localized.    It  is  greater  either  in  the  upper  arm 


THE  INDIVIDUAL  FORMS    OF  ITEURALGIA  815 

or  in  the  forearm  and  fingers.  Painful  points  are  sometimes  found  over  the  bra- 
chial plexus,  over  the  radial  nerve  on  the  external  surface  of  the  upper  arm,  over 
the  ulnar  nerve  in  the  sulcus  at  the  internal  condyle,  over  the  median  nerve  at  the 
inner  border  of  the  biceps,  and  where  the  cutaneous  nerves  emerge  from  the  f ascise. 
Vaso-motor  and  trophic  disturbances,  such  as  "  glossy  fingers,"  a  peculiar,  shiny, 
atrophic  condition  of  the  skin  of  the  fingers,  eruptions  of  herpes,  etc.,  are  often 
seen  in  true  organic  neuralgias,  and  sometimes  we  also  see  a  pronounced  atrophy 
of  the  whole  arm.  The  diagnosis  of  neuralgia  as  such  is  usually  easy;  we  must 
bear  in  mind  only  the  risk  of  confusion  with  articular  affections,  and  especially 
with  beginning  arthritis  deformans.  It  is  sometimes  much  harder  to  determine 
the  cause  of  the  neuralgia.  This  always  requires  a  careful  general  investigation 
and  close  attention  to  all  the  conditions  which  may  be  involved. 

The  treatment  of  brachial  neuralgia  is  often  no  easy  task,  since  we  frequently 
have  to  do  with  protracted  and  obstinate  diseases.  The  causal  indications  should 
be  met  if  possible ;  besides  these  we  should  make  use  chiefly  of  electricity  (the  de- 
scending galvanic  current  along  the  affected  nerves).  To  relieve  the  pain  we  may 
also  use  salicylate  of  sodium,  antipyrine,  phenacetine,  etc.,  and  finally  local 
warm  packs,  peat-baths,  sand-baths,  etc.  We  should  be  very  guarded  in  using 
narcotics  (morphine).  If  the  brachialgia  be  associated  with  neurasthenia  or 
hysteria,  we  can  obtain  success  only  by  an  appropriate  general  treatment  with  a 
psychical  suggestive  influence.  In  some  severe  cases  of  true  neuralgia  we  must 
consider  the  possibility  of  surgical  interference,  such  as  nerve-stretching,  the 
extirpation  of  cicatrices,  etc. 

4.  Intercostal  Neuralgia 

{Dor so-intercostal  Neuralgia) 

The  neuralgias  of  this  class  are  almost  always  pure  intercostal  neuralgias, 
since  the  posterior  dorsal  branches  of  the  thoracic  nerves  are  only  exceptionally 
involved.  The  middle  intercostal  nerves,  from  the  flfth  to  the  ninth,  are  usually 
affected,  one  or  more  of  them  being  attacked  at  the  same  time.  The  affection  is 
much  more  frequent  on  the  left  side  than  on  the  right. 

In  regard  to  aetiology,  it  is  important  to  remember  that  obstinate  intercostal 
neuralgias  are  often  a  symptom,  and  for  a  long  time  the  only  symptom,  of  severe 
organic  disease,  especially  affections  of  the  ribs;  diseases  of  the  vertebrae,  such 
as  caries,  carcinoma,  and  actinomycosis ;  diseases  of  the  cord,  such  as  tabes,  me- 
ningeal tumors,  syphilis,  and  aneurism  of  the  aorta.  Genuine  idiopathic  inter- 
costal neuralgia,  however,  is  also  met  with,  as  well  as  these  symptomatic  forms, 
but,  according  to  our  own  experience,  less  often  than  we  might  imagine  from 
many  of  the  statements.  Intercostal  neuralgia  has  been  reported,  especially  in 
anaemic  and  nervous  women,  both  in  youth  and  middle  age.  Traumatic  lesions 
of  the  intercostal  nerves  and  taking  cold  also  play  a  part  in  the  aetiology. 

The  pain  in  intercostal  neuralgia  may  attain  a  remarkable  severity,  and  it  is 
usually  increased  by  any  considerable  movement  of  the  thorax.  Hence  the  pa- 
tient avoids  deep  inspirations,  coughing,  loud  talking,  etc.,  as  much  as  possible. 
We  usually  find  three  painful  points — one  near  the  vertebral  column,  one  some- 
where in  the  middle  of  the  nerve,  and  a  third  near  the  sternum  or  over  the  rectus 
abdominis.  We  may  mention,  among  the  trophic  disturbances,  the  comparatively 
frequent  occurrence  of  herpes  zoster.  In  such  cases  we  probably  always  have  an 
actual  neuritis  of  one  or  more  nerves.  The  pain  precedes  the  eruption  of  zoster, 
or  comes  on  at  the  same  time  with  it.  It  often  lasts  for  a  long  time  after  the 
cutaneous  affection  has  healed.  The  special  method  of  origin  of  the  zoster  ves- 
icles is  still  obscure.  Recent  careful  anatomical  investigations  (A.  Dubler) 
favor  the  hypothesis  that  the  formation  of  vesicles  arises  simply  from  a  direct 


816  DISEASES    OE   THE   l^EEYOUS    SYSTEM 

extension  of  the  inflanxmatory  process  from  the  terminal  branches  of  the  nerves 
to  the  skin.  The  hypothesis  of  special  trophic  disturbances  would  therefore  be 
unnecessary.  It  is  worthy  of  note  that  the  attacks  of  zoster  often  exhibit  a  cer- 
tain epidemic  and  sometimes  even  an  endemic  distribution,  so  as  to  suggest  an 
infectious  agency.  The  almost  constant  swelling  of  the  neighboring  lymph- 
glands,  in  the  axillse,  at  the  lower  border  of  the  pectoral  muscle,  etc.,  also  favors 
the  theory  of  the  existence  of  a  true  inflammatory  neuritis  in  herpes  zoster.  We 
can  often  find  a  slight  diminution  of  sensibility  on  the  skin  between  the  individ- 
ual vesicles. 

The  course  of  intercostal  neuralgia  depends  chiefly  upon  the  setiology  of  the 
affection.  Primary  neuralgias  are  often  quite  obstinate,  but  on  the  whole  they 
usually  give  a  favorable  prognosis.  This  is  especially  true  of  the  intercostal  neu- 
ritis associated  with  herpes  zoster.  The  differential  diagnosis  between  genuine 
intercostal  neuralgia  and  rheumatic  affections  of  the  muscles,  incipient  pleurisy, 
etc.,  is  not  always  easy.  In  these  eases  a  careful  physical  examination,  a  con- 
sideration of  the  localization  of  the  pain,  of  the  presence  of  painful  points,  and  of 
the  whole  course  of  the  disease,  are  needed  to  protect  us  from  errors.  Steno- 
cardiac  attacks  (see  page  343)  are  sometimes  falsely  regarded  as  intercostal  neu- 
ralgia, and  we  must  also  remember  that  severe  diseases  of  the  vertebrae  or  the 
spinal  meninges  may  at  first  assume  the  aspect  of  intercostal  neuralgia. 

The  treatment  is  governed  by  the  general  rules  given  in  the  previous  chapter. 
Cutaneous  irritants,  mustard  plasters,  or  blisters  often  act  very  well  in  fresh 
cases.  Local  anaesthesia  (chloroform,  ether),  especially  a  spray  of  methyl  or 
ethyl  chloride,  may  occasionally  be  of  benefit.  Electricity  is  given  by  the  f aradic 
brush  or  the  constant  current ;  with  the  latter,  the  cathode  is  placed  on  the  verte- 
bral column,  and  the  anode  on  the  lateral  and  anterior  painful  points,  using  quite 
a  strong  stabile  current.  All  the  usual  anti-neuralgics  (antipyrine,  phenacetine, 
exalgine,  etc.)  may  be  used  internally.  In  severe  eases  we  can  not  avoid  injec- 
tions of  morphine.  Herpes  zoster  heals  by  simple  treatment  with  lanoline  or  by 
dusting  on  powders,  such  as  one  part  of  zinc  oxide  to  two  of  starch. 

Mastodynia  {Neuralgia  of  the  Mammary  Gland). — Mastodynia  ("irritable 
breast "  of  Astley  Cooper)  is  to  be  considered  as  a  special  form  of  nerve  pain 
in  the  distribution  of  the  intercostal  nerves.  It  occurs  almost  solely  in  women, 
after  the  age  of  puberty,  although  it  may  occur  in  men,  and  is  a  very  painful, 
distressing,  and  obstinate  affection.  The  pain  is  either  continuous,  or  it  comes  on 
in  separate  paroxysms,  sometimes  accompanied  by  vomiting.  The  whole  breast, 
or  more  frequently  different  parts  of  it,  is  extremely  sensitive  to  the  touch.  We 
know  little  that  is  definite  as  to  its  aetiology.  Anaemia,  hysteria,  and  traumatic 
action  seem  to  have  some  influence  on  it.  We  sometimes  feel  little  nodules  in  the 
breast,  which  are  very  painful  {tuhercula  dolorosa,  neuromata?),  and  which  may 
sometimes  give  rise  to  the  suspicion  that  a  carcinoma  is  developing. 

The  disease  may  last  for  years.  Treatment  is  difficult.  Warm  packs  to  the 
breast,  bandaging  the  breast,  and  especially  narcotics,  may  afford  relief.  Elec- 
tricity may  be  of  decided  service.  In  the  worst  cases  operative  interference  has 
been  attempted — amputation  of  the  breast,  or  extirpation  of  the  painful  nodules 
— but  its  results  are  uncertain.  ISTageli  highly  recommends  stretching  of  the 
whole  breast  en  masse :  the  breast  is  seized  with  both  hands  and  stretched  and 
extended  for  several  minutes  with  special  regard  to  the  tenderest  points. 

5.  ISTeuralgia  in  the  Region  of  the  Lumbar  Plexus 
As  the  neuralgias  of  this  class  are  rare,  and  show  few  peculiarities,  we  will 

content  ourselves  with  a  brief  account  of  the  most  important  forms. 

Lumbo-abdominal  neuralgia  causes  pain  in  the  lumbar  region,  which  shoots 

into  the  buttocks,  the  hypogastrium,  and  the  genitals.    Crural  neuralgia  is  seated. 


THE   INDIVIDUAL   TOEMS    OF   NEUEALGIA  817 

in  part,  in  the  region  of  the  external  anterior  cutaneous  nerve  of  the  thigh,  and  in 
part  in  the  region  of  the  cutaneous  branches  of  the  crural  nerve,  the  internal  and 
middle  cutaneous.  Its  distribution  over  the  cutaneous  distribution  of  the  great 
saphenous  nerve,  the  inner  portion  of  the  calves,  and  the  inner  border  of  the  foot, 
is  especially  characteristic.  In  obturator  neuralgia  the  pain  extends  along  the 
inside  of  the  thigh,  down  to  the  vicinity  of  the  knee-joint  (see  Figs.  90  and  91, 
page  802). 

In  their  individual  characteristics,  all  these  neuralgias  agree  with  what  has 
been  said  in  the  previous  chapter.  The  diagnosis  is  not  always  easy,  and  we  must 
pay  special  attention  to  avoid  confusing  them  with  affections  of  the  bones  and 
joints,  with  lumbago,  renal  colic,  etc. 

We  must  mention  here  a  special  symptom-complex,  meralgia  parcesthetica 
(Bernhardt,  Eoth),  the  chief  symptoms  of  which  are  pain,  pareesthesia,  and  par- 
tial anassthesia  on  the  outer  side  of  one  or  both  thighs — that  is,  in  the  territory 
of  the  external  cutaneous  femoral  nerve.  Mechanical  factors  in  particular  (long- 
continued  walking,  the  pressure  of  articles  of  clothing,  hard  work),  or  in  some 
cases  exposure  to  cold  or  acute  infectious  diseases,  seem  to  excite  this  trouble, 
which  is  sometimes  very  persistent.  The  treatment  consists  of  embrocations, 
electricity,  baths,  etc. 

6.  Sciatica 

{Ischiatic  Heuralgia.     Ischialgia.     Malum  Cotunnii) 

.^itiology. — l^ext  to  trigeminal  neuralgia,  sciatica  is  by  far  the  most  fre- 
quent, and  practically  the  most  important  form  of  neuralgia.  The  anatomical 
course  of  the  sciatic  nerve  renders  it  especially  exposed  to  mechanical  injuries 
and  the  influence  of  cold.  Many  cases  of  sciatica  are  certainly  due  to  such 
causes  as  over-exertion  of  the  leg  in  hard  work,  sitting  for  a  long  time  on  an 
uncomfortable  seat,  exposure  to  wet  and  cold,  etc. ;  and  this  is  why  sciatica  is  in 
general  far  commoner  in  men  than  in  women,  and  also  much  commoner  in  the 
laboring  classes  than  in  the  higher  classes.  Certain  setiological  conditions  may 
of  course  provoke  sciatica  in  women  also,  especially  the  pressure  of  the  gravid 
uterus  on  the  sacral  plexus  or  mechanical  injury  of  the  plexus  in  difficult  labor 
(forceps,  etc.).  Venous  stasis  in  the  pelvic  veins  (haemorrhoids)  and  habitual 
constipation  more  rarely  seem  to  give  rise  to  the  development  of  sciatica. 

The  relations  of  sciatica  to  certain  constitutional  and  toxic  general  diseases 
are  of  practical  importance.  Thus  a  simple  or  even  a  double  sciatica  is  not  very 
rare  in  diabetes  mellitus,  and  it  is  sometimes  seen  in  true  gout  (arthritis  urica), 
in  articular  rheumatism,  following  syphilis  or  gonorrhoea,  in  alcoholic  subjects, 
etc.  We  must  also  bear  in  mind  the  occurrence  of  apparently  pure  sciatic  pain 
in  tabes  dorsalis. 

Symptomatic  neuralgia  in  the  region  of  the  sciatic  nerve  is  also  seen  in  pelvic 
tumors,  caries  of  the  sacrum,  and  similar  diseases. 

Symptoms  and  Course. — Sciatica  takes  a  somewhat  different  position  from 
the  other  forms  of  neuralgia,  since  the  sciatic  pain  does  not  usually  show  the 
special  characteristics  of  true  neuralgia  in  a  fully  pronounced  fashion.  In  par- 
ticular, the  individual  paroxysms  of  pain  are  rarely  so  pronounced  and  so  inter- 
rupted by  free  intervals  in  sciatica  as  is  the  case,  for  example,  in  many  trigem- 
inal neuralgias.  Although  an  increase  or  a  diminution  of  the  pain  is  common  in 
sciatica,  the  pain  on  the  whole  gives  us  more  definitely  the  impression  of  a  per- 
sistent neuritic  pain,  and  we  can  therefore  scarcely  be  mistaken  if  we  consider 
the  anatomical  cause  of  most  cases  of  ordinary  sciatica  to  be  an  actual  sciatic 
neuritis. 

The  pain  usually  begins  in  the  lumbar  and  sacral  regions  and  then  gradually 
passes  downward,  following  the  course  of  the  sciatic  nerve,  through  the  gluteal 
52 


818 


DISEASES    OE   THE   IsTekVOUS    SYSTEM 


region  and  the  posterior  surface  of  the  thigh  to  the  hollow  of  the  knee,  and  then 
down  to  the  peroneal  region  (outer  part  of  the  leg,  outer  edge  of  the  foot,  and 
back  of  the  foot),  or  more  rarely  to  the  tibial  region  (sole  of  the  foot).  The 
accuracy  with  which  many  patients  point  out  with  the  finger  the  distribution  of 
the  pain,  corresponding  accurately  to  the  anatomical  course  of  the  nerve,  is  a  most 
characteristic  feature  for  the  diagnosis  of  sciatica.  Individual  cases,  however, 
differ  considerably,  since  at  times  the  pain  is  felt  to  a  marked  degree  only  in  the 
upper  portion  and  hardly  extends  at  all  to  the  lower  leg,  while  in  other  cases  the 
severest  pain  is  felt  below  the  knee.  This  is  probably  due  to  the  fact  that  the 
neuritis,  which  is  the  cause  of  the  pain,  affects  one  or  another  part  of  the  nerve,, 
being  chiefly  either  in  the  upper  root  portion  or  in  the  terminal  branches.  The 
pains  themselves  are  rarely  described  by  the  patients  as  "  darting,"  but  more  com- 
monly as  "  burning,"  "  boring,"  etc.  The  pain  is 
often  worse  at  night  than  during  the  day.  It  is  in- 
creased by  different  movements  of  the  leg,  by  an 
uncomfortable  position,  by  pressure,  by  cold,  etc. 
Patients  with  severe  sciatica  are  therefore  almost 
completely  bedridden,  and  they  can  take  a  few  un- 
aided steps  only  with  the  greatest  pain.  If  we  make 
the  patient  stand,  there  is  often,  but  of  course  not 
always,  a  very  characteristic  way  of  holding  the 
body.  In  order  to  take  the  weight  of  the  body  off 
the  affected,  tender  leg,  the  trunk  is  bent  over  to 
the  opposite  side,  and  the  spine  thus  becomes 
scoliotic,  the  convexity  being  usually  toward  the 
healthy  side  (sciatic  scoliosis,  see  Fig.  94). 

If  we  examine  the  affected  leg  more  closely, 
we  shall  notice  first  the  sensitiveness  of  the  sciatic 
nerve  to  direct  pressure.  This  is  often  not  so  great 
as  we  might  expect,  probably  because  the  upper  part 
of  the  nerve,  which  is  not  so  easily  accessible  to 
pressure,  is  chiefly  affected;  but  we  frequently  find 
the  nerve  itself  quite  sensitive  to  pressure  in  the 
middle  of  the  gluteus  or  at  its  lower  border,  in  the 
hollow  of  the  knee,  or  at  the  head  of  the  fibula  and 
elsewhere.  If  the  patient  be  in  a  lying  or  sitting 
position  and  the  thigh  be  strongly  flexed,  passively, 
on  the  trunk,  while  the  lower  leg  is  at  the  same 
time  kept  extended,  the  procedure  gives  rise  to  a 
gluteal  pain  which  is  characteristic.  By  this  ma- 
neuver the  sciatic  nerve  is  apparently  irritated  by 
being  stretched  so  much.  Among  the  other  nervous 
disturbances  we  may  mention  an  actual  paresis  of 
the  muscles  supplied  by  the  sciatic  nerve  (for  ex- 
ample, the  flexors  of  the  lower  leg)  ;  this  is  rare, 
and,  as  a  rule,  indicates  more  deeply-seated  disease. 
The  muscular  hypertonicity  (in  part  of  reflex  ori- 
gin) is  more  striking;  it  sometimes  takes  the  form 
of  actual  tremor  or  twitching  of  the  painful  leg.  A  peculiar  muscle-wave  (the 
so-called  "  myokymia  ")  is  also  seen  in  sciatica.  The  patellar  reflex  is  usually 
unchanged;  but  in  severe  sciatica  we  have  quite  frequently,  although,  of  course, 
not  always,  seen  the  gastrocnemius  reflex,  obtained  by  striking  the  Achilles  ten- 
don, absent  on  the  affected  side ;  this  is  of  value  in  diagnosis.  [The  patellar  reflex 
is  often  somewhat  exaggerated  on  the  affected  side  in  the  early  stages  of  sciatica. 


Fig.  94. — Sciatic  scoliosis  in  severe 
sciatica.    (Personal  observation.) 


THE   INDIVIDUAL   FOEMS    OF   NEUEALGIA  819 

and  diminished  in  the  later  stages. — K.]  On  careful  examination  we  sometimes 
find  a  slight  disturbance  of  sensibility,  but  it  is  very  rarely  marked.  In  long-con- 
tinued cases  there  is  almost  always-  a  very  noticeable  atrophy  of  the  affected  leg. 
The  circumference  of  both  the  thigh  and  calf  is  usually  several  centimetres  less 
on  the  affected  side  than  on  the  healthy  side.  This  atrophy  is  possibly  connected 
with  vaso-motor  disturbances,  for  the  skin  of  the  affected  leg  often  feels  decidedly 
cooler  than  that  of  the  healthy  side.  The  atrophy,  however,  is  due  mainly  to  the 
inactivity  of  the  painful  leg.  [In  a  considerable  number  of  cases  quantitative 
or  qualitative  changes  in  the  electrical  reactions  are  found  on  the  affected  side. 
This  would  indicate  that  the  atrophy  was  degenerative  in  character,  due  to  neu- 
ritic  changes  in  the  nerve. — K.] 

Sciatica  rarely  lasts  less  than  several  weeks,  and  in  many  cases  months  or 
even  years  may  elapse  before  the  pain  entirely  disappears  and  the  leg  completely 
regains  its  normal  usefulness.  The  course,  however,  often  shows  very  marked 
variations.  In  simple  sciatica  (not  due  to  some  other  underlying  disease)  the 
final  outcome  is  usually  favorable.  We  must  bear  in  mind,  however,  that  the 
disease  has  a  marked  tendency  to  recur,  so  that  any  one  who  has  once  had  sciatica 
must  avoid  with  special  care  all  exposure  which  may  cause  a  return  of  the  suffer- 
ing. The  general  course  of  symptomatic  sciatica  is  of  course  dependent  mainly 
upon  the  nature  of  the  underlying  disease. 

Diagnosis. — The  diagnosis  of  sciatica  is  easy  in  the  majority  of  typical  cases, 
but  it  may  sometimes  be  quite  difficult.  It  is  chiefly  confused  with  lumbago,  an 
acute  coxitis, , nervous  coxalgia  (vide  infra),  and  psoas  abscess.  Even  when  the 
diagnosis  of  sciatica  as  such  is  definite,  we  must  always  consider  with  care  the 
patient's  general  condition  to  determine  whether  we  are  dealing  with  a  simple 
primary  sciatica  (primary  sciatic  neuritis)  or  with  a  symptomatic  sciatica  fol- 
lowing some  other  underlying  disease.  In  the  section  on  aetiology  above  we 
have  mentioned  the  possibilities  which  the  physician  must  especially  bear  in  mind. 
In  cases  where  there  is  a  suspicion  of  simulation  (as  in  accident  cases),  we  must 
note  the  accurate  localization  of  the  pain  and  the  tender  points,  and  especially 
the  objective  symptoms,  the  almost  invariable  wasting  of  the  affected  leg,  and  the 
frequent  absence  of  the  Achilles  tendon  reflex. 

Treatment. — In  ordinary  primary  sciatica  and  in  fresh  cases  we  usually  begin 
with  "  anti-rheumatic  "  treatment.  The  patient  should  be  put  to  bed  and  kept 
warm.  We  ourselves  have  treated  many  cases  of  sciatica  with  very  good  results 
by  methodical  sweating  (hot-packs,  hot-air  baths).  Internally,  we  would  first 
prescribe  salicylate  of  sodium,  antipyrine,  salipyrine,  or  phenacetine,  from  which 
we  often  obtain  at  least  an  improvement  in  the  symptoms.  We  have  never  seen 
any  good  effect  from  oil  of  turpentine,  which  is  often  used  in  England.  We  have 
as  little  faith  in  the  injections  of  osmic  acid  which  are  recommended  (vide  page 
809).  "Local  derivatives,"  especially  blisters  along  the  nerve,  are  at  present 
somewhat  out  of  fashion,  but  we  have  often  seen  decided  benefit  from  blisters, 
and  we  therefore  use  them  quite  frequently  in  obstinate  cases.  Warm  fomenta- 
tions, a  Priessnitz's  bandage  about  the  entire  leg,  etc.,  usually  give  relief,  and 
also  embrocations  with  chloroform  oil,  a  spray  of  chloride  of  methyl,  etc.  If  the 
pain  is  very  severe,  so  that  sleep  is  constantly  disturbed,  we  must  use  narcotics, 
especially  subcutaneous  injections  of  morphine.  The  author  has  not  been  able  to 
bring  himself  to  employ  methodical  treatment  by  morphine  injections,  as  has  been 
recommended  from  many  sides. 

Of  other  methods  of  treatment,  besides  those  already  mentioned,  we  may  con- 
sider electricity,  massage,  nerve-stretching,  and  baths. 

In  electrical  treatment  we  usually  employ  quite  strong  descending  currents, 
with  large  electrodes,  which  we  let  act  on  the  nerve  for  five  or  ten  minutes  a  day, 
while  we  include  one  portion  of  the  nerve  after  another  in  the  current.     Where 


820  DISEASES    OF   THE   NERVOUS    SYSTEM 

there  is  much  stiffness  in  the  leg,  we  open  and  close  the  current  a  few  times,  in 
order  to  excite  muscular  contraction.  Many  cases  are  suitable  for  the  use  of  the 
faradic  current,  especially  for  the  wire  brush.  Besides  electricity,  massage  has 
often  given  excellent  results  in  sciatica.  Details  of  the  technique  to  be  employed 
may  be  found  in  the  special  treatises  on  this  important  method  of  treatment.* 

Baths  (douches,  rubbing)  are  beneficial  in  most  cases  of  persistent  sciatica. 
The  regular  use  of  simple  warm  baths  (half  an  hour  daily  at  a  temperature  of 
27°-28°  E.  [93°-95°  F.])  is  of  benefit,  especially  when  combined  with  massage 
or  electrical  treatment.  We  see  still  more  favorable  results  at  certain  bath  cures, 
especially  in  Wiesbaden  and  also  in  Wildbad,  Teplitz,  etc.  Peat-baths,  and  espe- 
cially hot  sand-baths  (Kostritz,  Blasewitz),  may  have  a  good  effect. 

Operative  nerve-stretching  may  be  tried  only  in  very  old  and  very  obstinate 
cases.  In  some  eases  it  has  been  attended  by  benefit.  We  have  repeatedly  em- 
ployed bloodless  nerve-stretching  with  satisfactory  results.  This  is  done  by  put- 
ting the  patient  on  the  back  and  then  passively  flexing  the  thigh  against  the  trunk 
as  much  as  possible,  and  keeping  it  there  for  two  or  three  minutes  each  day. 
[This  may  be  done,  if  necessary,  under  ether.  If  the  lower  leg  be  kept  extended 
the  stretching  is  greater. — K.] 

It  is  very  important  always  to  pay  attention  to  the  general  as  well  as  the 
local  treatment,  in  order  to  remove  any  active  causative  conditions.  A  change 
in  the  mode  of  life,  avoidance  of  rheumatic,  toxic,  and  mechanical  injuries,  regu- 
lation of  the  bowels,  etc.,  are  sometimes  attended  by  visible  results.  Any  under- 
lying diseases  must  of  course  be  especially  treated  (iodide  of  potassium  in  syphi- 
lis, anti-diabetic  treatment,  etc.). 

[Mention  should  be  made  here  of  a  method  of  treatment  advocated  by  Weir 
Mitchell,  which  is  occasionally  useful  in  other  forms  of  neuralgia  as  well  as  in 
sciatica.  It  consists  in  absolute  rest  of  the  affected  limb  by  application  of  a  splint. 
With  this  he  combines  the  application  of  cold,  by  an  ice-bag  over  the  length  of  the 
nerve,  which  may  be  continued  for  a  number  of  hours. — K.] 

7.  ISTeuralgia  of  the  Genitals  and  the  Eectal  Region 

Neuralgic  affections  of  the  parts  named  are  not  frequent,  but  still  a  number  of 
cases  have  been  described  by  different  observers.  Of  course  most  of  these  obser- 
vations are  of  ancient  date  and  many  of  them  are  at  present  perhaps  to  be  ex- 
plained in  some  other  way. 

The  pain  in  these  cases  has  its  seat  either  in  the  external  genitals,  or  in  the 
urethra,  or  in  the  anal  and  perineal  region.  The  most  frequent  form  is  spermatic 
neuralgia  ("  irritable  testis  "  of  Astley  Cooper),  in  which  there  is  the  most  in- 
tense pain  in  the  spermatic  cord  and  the  testicles,  which  is  almost  always  asso- 
ciated with  an  extreme  hypersesthesia  of  the  affected  parts.  The  treatment  of 
this  form  of  neuralgia  by  narcotics  and  electricity  is  often  unsuccessful,  so  that 
in  severe  cases  resort  has  sometimes  been  had  even  to  castration.  In  women, 
genuine  uterine  and  ovarian  neuralgia  does  occur,  but  most  cases  are  either  symp- 
tomatic neuralgia  or  a  manifestation  of  hysteria. 

Coccygodynia  is  the  name  of  a  form  of  severe  pain  in  the  coccygeal  region, 
seen  usually  in  women,  which  is  much  inci'eased  by  walking,  defecation,  etc.  The 
affection  is  so  distressing  that  operations  have  been  repeatedly  performed  on  ac- 

*  Busch,  "  Allgemeine  Orthopadie,  Gymnastik  u.  Massage,"  Leipsic,  Vogel,  1882;  Schreiber, 
"Praktische  Anleitung  zur  Behandlung  durch  Massage,"  Vienna,  1883  [translated  by  Mendelson, 
Philadelphia,  1887] ;  Keibmayr,  "Die  Massage  und  ihre  Verwerthung  in  der  pralct.  Medicin,"  Vienna, 
1883;  Hunerfauth,  "  Handbuch  der  Massage,"  Leipsic,  1887,  etc.  [Graham,  "A  Treatise  on  Massage," 
New  York,  1890  ;  Eccles,  "  The  Practice  of  Massage,"  London,  1895  ;  Kleen,  "  Handbook  of  Massage  " 
(translated  byjiartwell),  Philadelphia,  1892]. 


THE   INDIVIDUAL   EOEMS    OF   NEUEALGIA  821 

count  of  it  to  remove  or  to  cut  around  the  coccyx.    We  have  twice  seen  this  same 
symptom  as  a  complication  of  tabes. 

8.   ACHILLODYNIA.       TALALGIA.      TARSALGIA.      MeTATARSALGIA 

For  practical  reasons  we  will  mention  briefly  here  a  number  of  peculiar  and 
often  very  painful  aflfections  of  the  feet. 

Achillodynia  is  the  name  given  to  a  pain  at  the  insertion  of  the  Achilles 
tendon,  which  is  often  very  obstinate  and  a  hindrance  to  walking.  The  trouble 
often  seems  to  be  connected  with  gonorrhoea,  in  other  cases  with  gout,  injury, 
over-exertion,  hysteria,  etc.  We  can  sometimes  make  out  a  slight  local  swelling, 
but  often  there  is  no  objective  change.  The  treatment  consists  of  rest,  inunction 
of  mercurial  ointment,  warm  baths  and  packs,  attention  to  any  existing  under- 
lying disease,  etc. 

Pain  in  the  heel  is  called  talalgia  or  tarsalgia.  Mechanical  causes  (long- 
continued  standing  or  walking,  the  pressure  of  boots,  etc.)  often  seem  to  be  of 
significance,  but  sometimes  we  can  not  discover  any  cause.  We  must  of  course 
always  consider  inflammatory  changes,  flat-foot,  etc.  Baths,  massage,  and  gal- 
vanism are  most  to  be  recommended. 

Metatarsalgia  (nevralgie  metatarsienne,  Morton's  disease)  is  an  extremely 
distressing  and  severe  pain,  chiefly  in  the  neighborhood  of  the  fourth  and  fifth 
metatarso-phalangeal  joints.  The  trouble  is  observed  especially  in  women  in  mid- 
dle life,  and  it  may  be  sometimes  connected  with  wearing  ill-fitting  shoes.  In 
other  cases  injury,  gout,  etc.,  are  regarded  as  causes.  [It  is  often  due  to  the  pres- 
sure upon  the  nerve  between  the  two  phalangeal  ends  of  the  metatarsal  bones,  and 
it  may  be  relieved  by  pressure  upon  the  tarsal  ends,  which  causes  the  phalangeal 
ends  to  separate. — K.]  The  treatment  consists  of  prescribing  proper  shoes,  rest, 
local  fomentations,  baths,  etc.  In  some  severe  cases  the  painful  bones  have  been 
resected  with  success. 

There  are  also  other  forms  of  pain  in  the  feet  besides  these  mentioned,  which 
are  usually  hard  to  explain.  Hysterical  conditions  certainly  play  a  part  in  some 
cases,  and  are  to  be  taken  into  account  in  treatment,  but  in  other  cases  we  often 
have  to  deal  with  mechanical  and  inflammatory  conditions  which  are  hard  to 


9.  The  so-called  Articular  Neuralgias  (Articular  Neuroses) 

Neuralgia  of  the  joints,  first  described  by  the  English  physician  Brodie,  was 
first  generally  known  in  Germany  after  Esmarch  proved,  by  publishing  many 
observations,  that  apparently  severe  and  very  painful  diseases  of  the  joints  are 
often  found,  which  are  due  to  no  discoverable  anatomical  disease  of  the  joint,  and 
which  we  are  therefore  justified  in  regarding  as  nervous  affections.  Since  the 
localized  pain  in  the  joint  is  the  chief  symptom  in  most  of  the  cases  of  this  class, 
the  somewhat  unfit  term  "  neuralgia  of  the  joints  "  has  been  chosen,  although  we 
do  not  find  here,  as  a  rule,  such  typical  and  paroxysmal  attacks  of  pain  as  in  gen- 
uine neuralgia,  and  although,  too,  a  number  of  other  symptoms  are  usually  pres- 
ent, which  do  not  occur  in  genuine  neuralgia. 

We  see  neuralgia  of  the  joints  chiefiy  in  nervous  persons  disposed  to  hysteria, 
and  therefore  more  frequently  in  women  and  girls  than  in  men,  but  it  is  also  quite 
common  in  children.  We  can  very  often  make  out  a  psychical  cause  for  the 
origin  of  the  disease.  The  affection  is  often  caused  by  injuries  which  affect  the 
joint,  and  which  would  be  in  themselves  without  significance,  if  they  were  not 
associated  with  a  decided  fright,  and  did  not  direct  the  patient's  thoughts  to  the 
affected  limb.  Articular  neuralgias  do  not,  therefore,  belong  to  the  pure  neural- 
gias, but  are  symptoms  of  hysteria  (traumatic  hysteria). 


822  DISEASES    OF   THE   XEEVOUS    SYSTEM 

Either  immediately  after  such  an  occurrence,  or  often  only  some  weeks  later, 
the  patient  begins  to  complain  of  pain.  The  knee-  or  hip-joint  is  almost  always 
affected,  only  rarely  the  joints  of  the  upper  extremity.  The  pain  is  continuous, 
but  it  is  more  severe  at  times,  especially  on  motion,  or  mental  excitement.  At 
other  times,  especially  if  the  patient's  attention  be  diverted  from  the  trouble,  it 
seems  to  diminish  to  a  considerable  extent.  It  is  localized  mainly  in  the  joint,  but 
the  whole  leg  is  often  painful.  The  patient  is  usually  very  sensitive  to  pressure  or 
jarring,  and  sometimes  we  may  even  discover  some  painful  points  on  pressure 
over  the  joints.  The  patient  can  not  walk  at  all,  or  at  least  walking  is  very  pain- 
ful, and  she  limps  badly.  In  severe  cases,  especially  if  the  excessive  sympathy  of 
those  about  her  reduces  the  patient's  power  to  resist  her  suffering,  she  becomes 
completely  bedridden  for  weeks  or  months.  There  is  usually  a  decided  weakness 
in  the  affected  leg,  which  is  almost  always  associated  with  great  muscular  rigidity 
and  tension.  The  leg  is  extended,  or  flexed,  and  rotated  inward,  in  just  the  same 
way  as  in  genuine  coxitis. 

The  diagnosis  of  articular  neurosis  is  often  quite  difficult,  but  it  is  almost 
always  possible,  with  long  observation  of  the  case.  At  first,  of  course,  the  disease 
often  seems  to  be  a  severe  affection  of  the  joint,  on  account  of  the  great  pain,  the 
rigid  position,  and  the  complete  inability  to  use  the  leg.  The  experienced  physi- 
cian, however,  is  usually  struck  by  the  absence  of  any  definite  physical  changes  in 
the  joint,  especially  of  swelling,  and  also  by  the  changes  in  the  intensity  of  the 
complaint,  by  the  influence  of  mental  emotion  on  the  suffering,  and  finally  by  the 
general  impression  he  gets  from  the  patients,  the  way  they  behave,  and  the  con- 
trast between  their  evidently  exaggerated  complaint  and  their  usual  (though,  of 
course,  not  invariable)  good  appearance,  appetite,  and  undisturbed  sleep.  If  the 
patient's  attention  be  diverted,  the  same  pressure  on  the  joint,  which  before  was 
unendurable,  is  not  even  felt.  In  doubtful  cases  an  examination  under  chloro- 
form is  very  advisable.  With  this,  contractures  apparently  the  most  severe  van- 
ish, and  the  normal  character  and  mobility  of  the  joint  become  plainly  manifest. 

As  soon  as  the  diagnosis  of  an  articular  neurosis  is  made  the  treatment  has 
quite  definite  indications.  All  embrocations,  poultices,  bandages,  etc.,  are  to  be 
laid  aside.  The  patient  is  to  be  brought  to  the  conviction  that  the  pain  is  de- 
pendent only  upon  the  morbid  anxiety,  and  that  walking  is  indeed  quite  possible  if 
she  will  only  first  learn  to  will  to  walk  again.  We  therefore  make  the  patient 
practice  walking  methodically;  these  attempts  at  first  prove  very  poor  and  appar- 
ently distressing  to  the  patient,  but  they  often  lead  very  speedily  to  better  results. 
These  exercises  are  very  much  aided  by  electrical  treatment  of  the  joint,  passing  a 
strong  current  through  it  or  using  the  faradic  brush,  and  also  by  local  cold 
douches  and  massage.  Under  some  circumstances  the  use  of  internal  remedies 
may  be  indicated,  in  many  cases  with  regard  only  to  the  mental  condition.  We 
give  iron  to  ansemic  patients,  and  also  the  nervines.  (See  the  chapters  on  hys- 
teria and  traumatic  neuroses.) 

10.  Acroparesthesia 

Certain  symptoms  of  sensory  irritation,  to  which  F.  Schultze  has  given  the 
name  of  "  acroparsesthesia,"  have  only  of  late  years  aroused  general  attention 
(Laquer  and  others),  although  they  have  long  been  familiar  to  all  experienced 
physicians  and  have  been  repeatedly  described  in  medical  literature.  It  is,  in  fact, 
quite  a  common  complaint,  the  chief  symptom  of  which  consists  of  an  unpleasant 
and  often  even  very  painful  sensation  at  the  tips  (aKpa)  of  the  extremities, 
especially  in  the  hands,  finger-tips,  feet,  and  toes.  This  sensation  is  almost 
constant,  or  at  least  it  recurs  very  frequently. 

The  trouble  usually  appears  in  middle  life,  and  it  is  said  to  be  somewhat  more 
frequent  in  women  than  in  men.    In  many  cases  we  can  find  no  special  cause,  but 


THE   IXDIVIDUAL   FOEMS    OF   NEUEALGIA  823 

Sometimes  we  can  discover  certain  injurious  influences  which  have  affected  the 
hands  or  feet,  such  as  past  exposure  to  cold,  freezing,  much  washing  in  cold 
water,  fatiguing  mechanical  occupations,  chemical  irritants,  etc. 

The  abnormal  sensations  are  usually  described  as  darting,  prickling,  tearing, 
etc.  Their  chief  seat  is,  as  has  been  said,  in  the  fingers  and  finger-tips.  Both 
hands  are  usually  affected,  but  the  trouble  is  often  more  pronounced  upon  one 
side  than  upon  the  other,  and  certain  fingers  of  the  same  hand  are  sometimes 
more  painful  than  others.  The  feet  (toes)  are  more  rarely  affected  than  the 
hands ;  in  such  cases  venous  stasis  (varicose  veins)  seems  to  us  to  have  a  certain 
significance  in  the  aetiology.  We  must  also  consider  arterio-sclerotic  changes  in 
the  vessels  (see  page  373).  The  pain  is  not  equally  severe  at  all  times;  it  is 
often  worse  at  night  and  toward  morning,  ceasing  during  the  day. 

If  we  examine  the  hands  or  feet  closely  we  can  sometimes  detect  no  objective 
abnormality,  but  in  many  cases  certain  "  vaso-motor  "  phenomena  are  first  of  all 
manifest.  The  painful  parts  are  cooler  and  more  cyanotic  than  under  normal 
conditions,  but  we  have  also  seen  very  obstinate  cases  in  which  the  hands  usually 
felt  hot  and  sweated  constantly  and  profusely.  The  sensibility  is  normal,  or  there 
may  be  in  some  parts  a  very  slight  blunting  of  tactile  sensibility,  or  more  rarely 
a  marked  hj^^eraesthesia  to  touch.  ]!kIotion,  as  a  rule,  is  undisturbed,  but  many 
patients  complain  of  a  certain  stiffness  of  the  hands.  In  general,  however,  it  is 
the  pain,  often  very  severe,  which  limits  the  usefulness  of  the  hands,  and  often 
greatly  disturbs  the  patient's  work.  There  are  no  special  changes  in  the  reflexes. 
In  some  cases  we  have  seen  very  marked  trophic  changes,  especially  a  manifest 
smallness  and  tapering  of  the  terminal  phalanges,  marked  curving  of  the  nails, 
a  shininess  of  the  skin  (glossy  skin),  etc.  A  short  time  ago  in  a  very  obstinate 
case,  which  had  lasted  for  years,  we  saw  torpid  ulcers  develop  on  the  toes  without 
any  external  cause ;  thej"  were  very  painful  and  showed  no  tendency  at  all  to  heal. 

The  course  of  the  disease  is  in  some  cases  benign,  recovery  taking  place  after 
several  months ;  but  in  many  other  eases  acropartesthesia  is  a  very  obstinate, 
chronic  condition,  lasting  for  years,  and,  in  spite  of  its  lack  of  danger,  causing 
the  patient  great  discomfort  and  distress. 

Xothing  definite  is  known  as  yet  as  to  the  nature  and  special  origin  of  the 
■disease.  It  is  generally  assumed  that  it  is  an  irritative  condition  of  the  sensory 
terminal  nerve-fibers  and  terminal  apparatus — that  is,  that  it  is  a  purely  periph- 
eral trouble ;  but  it  is  still  uncertain  whether  we  have  to  do  with  a  primary  dis- 
ease of  the  nerves  themselves  or  with  a  disease  of  the  smallest  terminal  arteries 
and  consequent  circulatory  disturbances  with  their  sequels. 

The  diagnosis  of  acroparsesthesia  is  in  general  easy,  since  the  picture  of  the 
disease  is  in  fact  very  characteristic ;  but  we  must  always  bear  in  mind  that  such 
parsesthesise  sometimes  occur  as  symptoms  or  precursors  of  organic  central  dis- 
eases (for  example,  as  precursors  of  apoplexy,  in  other  brain  diseases,  in  tabes, 
diabetes,  etc.). 

SjTnptomatic  treatment  is  all  that  is  possible,  and  in  this  regard  the  local  use 
of  electricity,  especially  the  faradic  brush,  seems  to  give  the  best  results;  but  the 
constant  current,  electrical  hand-baths,  etc.,  are  sometimes  of  benefit.  Experi- 
ence must  decide  in  the  individual  case  as  to  the  influence  of  thermic  procedures 
(warm  and  cold  hand-baths,  cold  douches,  the  Scotch  douche,  etc.).  Besides  local 
treatment,  we  must  also  pay  attention  to  the  patient's  general  condition  (iron, 
quinine,  arsenic  in  anaemia,  etc.).  [Drugs  which  act  upon  the  blood-vessels,  such 
as  ergot,  nitroglycerine,  or  the  nitrites,  are  sometimes  of  service. — K.] 


824  DISEASES    OF   THE   NEEVOUS    SYSTEM 


CHAPTEE   Y 

HABITUAL    HEADACHE 

( CephaUea.      Cephalalgia) 

In  addition  to  the  neuralgias,  we  must  speak  here  of  habitual  or  "  nervous  " 
headache,  an  affection  which  is  very  often  met  with  in  practice,  but  in  regard  to 
whose  precise  causes  or  whose  special  nature  our  knowledge  is  still  in  many  re- 
spects very  unsatisfactory. 

We  do  not  term  the  symptomatic  headaches,  so  often  observed,  "  nervous  head- 
aches." The  former  come  on  in  acute  febrile  infectious  diseases,  in  pronounced 
general  ansemia,  in  the  different  anatomical  diseases  of  the  brain  and  its  mem- 
branes, of  the  skull,  the  frontal  sinuses,  etc.  Just  as  little  ought  we  to  confuse 
habitual  headache  with  other  painful  and  well-characterized  affections,  especially 
typical  neuralgia  in  the  frontal  branch  of  the  trigeminus,  or  in  the  occipital 
nerves,  or  with  genuine  migraine  or  hemicrania  {vide  infra).  The  cases  whicK 
belong  to  this  class  are  rather  those  in  which  the  headache  forms  to  a  certain  de- 
gree a  disease  in  itself,  and  is  the  sole,  or  at  least  the  chief,  symptom  of  which 
the  patient  complains,  and  for  which  he  seeks  aid.  We  know  no  definite  ana- 
tomical basis  for  them.  We  usually  assume  disturbances  of  circulation  and  of 
the  fine  nutrition  as  the  special  causes  of  headache;  but  the  nature  of  these 
changes  is  still  wholly  unknown.  We  can  also  state  little  that  is  definite  as  to 
the  special  place  where  these  pains  arise.  We  do  not  know  positively  whether 
painful  irritations  may  arise  in  the  brain-substance  itself.  In  case  pain  should 
be  produced  by  irritation  of  the  sensory  parts  of  the  brain,  it  would  probably  not 
be  felt  in  the  head,  but  it  would  be  projected  toward  the  periphery  of  the  body. 
The  cerebral  meninges,  however,  especially  the  dura  mater,  are  decidedly  sensi- 
tive, and  hence  they  may  usually  be  regarded  as  the  special  seat  of  headache. 

The  manifold  character  of  the  circumstances  under  which  headaches  arise 
renders  it  probable  that  the  causes  of  headache  are  very  different  in  different 
cases.  We  have  to  do  either  with  persons  who  seem  perfectly  healthy  in  other  re- 
spects, or  with  weak  and  ansemic  people,  or  again  with  robust,  very  well  nour- 
ished, "  full-blooded  "  persons  with  red  faces.  Hence  we  look  for  the  cause  of  the 
pain,  according  to  the  general  constitution  of  the  patient,  either  in  an  abnormal 
hyperemia  or  in  an  ansemia  of  the  brain  and  its  membranes — ^hypersemic  or  anas- 
mic  cephalalgia.  We  very  often  find  headache,  too,  as  the  chief  symptom  in  nerv- 
ous, neurasthenic  people — neurasthenic  cephalalgia.  To  this  class  belong  espe- 
cially people  who  are  overworked  physically  and  mentally — scholars,  officials,, 
students  before  an  examination,  etc.  If  we  believe  that  we  can  make  out  "  rheu- 
matic "  influences,  such  as  taking  cold,  or  toxic  influences,  such  as  alcohol,  nico- 
tine, or  chronic  lead  poisoning,  we  speak  of  a  rheumatic  or  a  toxic  cephalalgia; 
but,  strictly  speaking,  "  rheumatic  "  headache  is  probably  not  a  nervous  headache 
at  all,  since  it  seems  to  be  in  many  cases,  at  least,  a  slight  rheumatic  inflammation 
of  the  external  soft  parts  of  the  head.  Patients  with  habitual  headache  often 
suffer  at  the  same  time  from  chronic  gastric  disturbances  or  habitual  constipa- 
tion, so  that  the  latter  disorders,  in  many  cases,  stand  perhaps  in  a  causal  rela- 
tion (toxic  influences  ?)  to  the  headaches.  Finally,  it  is  a  very  important  point 
that  headache  is  sometimes  associated  with  chronic  diseases  of  neighboring 
organs,  especially  of  the  nose,  the  naso-pharynx,  and  the  ear.  In  very  many 
cases,  however,  we  can  find  no  definite  cause  at  all  for  the  affection,  so  that  we 
have  to  do  with  a  genuine  idiopathic  disease.  Habitual  headache,  existing  from 
childhood,  is  certainly  in  most  cases  the  expression  of  a  general  "  nervous  con- 
stitution," which  is  due  to  congenital  conditions  which  of  course  are  still  wholly 


HABITUAL  HEADACHE  825 

unknown  in  their  details.  Habitual  headache,  therefore,  is  often  an  hereditary- 
disease.  [One  of  the  frequent  causes  of  persistent  headache  is  eye-strain,  due 
to  the  persistent  unconscious  effort  of  the  muscles  of  accommodation  to  over- 
come some  error  of  refraction,  such  as  astigmatism  or  hypermetropia.  The  pain, 
is  often  referred  to  the  frontal  region,  and  it  is  brought  on  or  made  worse  by 
using  the  eyes  for  near  work.  In  some  cases  this  eye-strain  may  be  associated 
with  insufficiency  of  some  of  the  external  muscles  of  the  eye.  This  condition  may 
be  associated  with  normal  visual  power,  so  that  the  patient  often  maintains  that 
there  can  be  no  trouble  with  the  eyes ;  this  is  especially  true  where  the  refractive 
error  is  slight,  less  than  one  dioptric.  It  is  therefore  essential,  in  every  case  of 
persistent  headache,  to  have  a  thorough  examination  of  the  eyes,  in  order  to 
determine  whether  there  is  astigmatism  or  hypermetropia.  The  adjustment  of 
proper  glasses,  or,  in  rare  cases,  tenotomy  of  some  of  the  external  muscles,  will 
often  give  marked  relief,  although  even  in  these  cases  attention  must  also  be 
paid  to  the  general  condition.  In  many  cases  the  error  of  refraction  is  but  one 
out  of  many  causes  which  give  rise  to  the  headache,  so  that  we  should  never  be  too 
confident  in  our  prognosis  of  cure,  and  we  should  also  never  be  content  with  find- 
ing a  single  cause,  but  we  should  search  for  all  possible  causes.  Referred  pains  in 
the  head  from  disease  elsewhere  have  been  spoken  of  on  page  806. — K.] 

Habitual  headache  is  always  a  chronic  disease.  It  may  last  for  months  or 
years,  or  even  through  the  whole  life,  either  being  present  continually,  or,  what 
is  more  frequent,  coming  on  in  separate  attacks  and  lasting  several  hours  or  days. 
These  attacks  sometimes  come  without  any  evident  cause,  but  they  may  often 
be  referred  to  definite  influences,  to  mental  excitement,  physical  exertion,  errors 
of  diet,  etc.  The  pain  is  felt  either  in  the  forehead  or  in  the  occiput,  or  some- 
times over  the  whole  head.  It  is  sometimes  limited  to  a  definite  and  quite  sharply 
defined  part  of  the  head.  The  precise  form  of  the  pain  is  described  in  different 
ways,  either  as  boring,  or  tearing,  or  as  if  the  head  were  pressed  together  from 
without,  or  as  if  it  would  split  open.  In  many  cases  the  intensity  of  the  pain  is 
not  great ;  there  is  merely  a  dizziness  and  a  feeling  of  "  pressure  "  in  the  head, 
but  in  other  cases  the  pain  is  very  severe.  In  such  cases  there  is  also  at  times  a 
pronounced  hypersesthesia  of  the  skin  of  the  head,  so  that  it  may  cause  pain  even 
to  touch  the  hair. 

The  general  health  is  almost  always  disturbed  in  headache.  The  patient  can 
not  work,  he  is  often  ill-tempered  and  irritable,  and  he  loses  his  appetite.  We 
sometimes  see  more  marked  gastric  symptoms,  especially  nausea  and  vomiting 
(transition  forms  to  migraine,  q.  v.),  and  sometimes  copious  perspiration.  Severe 
cases  of  the  disease  are  of  great  importance,  since  by  an  attack  the  patient  is 
rendered  almost  wholly  unable  to  attend  to  his  business.  For  many  women,  espe- 
cially, habitual  headache  is  a  factor  which  dominates  their  whole  life  as  a  re- 
straint and  disturbance. 

The  treatment  of  headache  is  a  very  difficult  and  usually  a  thankless  task.  In 
the  first  place,  of  course,  we  should  try  to  adapt  our  treatment  to  the  setiology  of 
the  disease  if  it  is  evident.  We  should  therefore  never  neglect  to  make  a  thor- 
ough examination  of  all  the  organs  which  are  to  be  considered  (nose,  ear,  stom- 
ach, heart,  kidneys,  [eyes],  etc.),  and  pay  especial  attention  to  any  existing  under- 
lying diseases  (syphilis,  gout,  alcoholism,  organic  nei-vous  disease,  etc.).  The 
general  physical  constitution  also  requires  the  greatest  attention.  For  anfemic 
patients  we  prescribe  iron,  arsenic,  a  country  residence,  strengthening  diet,  etc. 
We  order  full-blooded  persons,  especially  if  they  also  suffer  from  indigestion,  to 
follow  a  restricted  diet,  to  have  gymnastic  treatment,  or  to  drink  bitter  waters, 
or  we  send  them  to  such  health-resorts  as  Marienbad  or  Carlsbad.  Nervous  head- 
aches in  hysterical  and  nei^rasthenic  patients  require,  above  all,  a  rational  gen- 
eral treatment :  mental  treatment,  a  regulation  of  their  mode  of  life,  cold-water 


826  DISEASES    OF   THE   NERVOUS    SYSTEM 

cures,  electricity,  general  faradization,  galvanism  to  the  head  or  to  the  sympa- 
thetic, etc.  For  persons  who  suffer  from  nervous  headache  in  consequence  of 
excessive  mental  strain  and  excitement,  we  most  urgently  advise  complete  physi- 
cal and  mental  rest  for  a  long  time.  We  send  them  to  the  country  or  make  a  trial 
of  sea-bathing. 

The  number  of  symptomatic  remedies  recommended  to  relieve  headache  is 
very  considerable.  In  most  of  the  tedious  cases  the  patient  himself  has  learned 
to  know  his  disease  perfectly  well.  Many  know  that  there  is  no  remedy  for 
"  their  old  headaches,"  and  they  merely  desire  to  rest,  waiting  until  the  pain 
ceases  of  itself.  Others  have  become  accustomed  to  employ  certain  domestic 
remedies :  they  put  poultices  on  the  head,  take  a  cold  or  a  hot  foot-bath,  put  a 
mustard  plaster  to  the  back  of  the  neck,  bathe  the  forehead  with  cologne-water, 
use  a  menthol  pencil,  bind  a  towel  tightly  about  the  head,  drink  strong  tea, 
smell  ammonia  or  "  smelling-salts,"  etc.  We  sometimes  see  good  results,  although 
frequently  we  do  not,  from  the  internal  remedies.  These  may  be  used,  either 
during  the  attack  or  for  a  longer  period,  to  prevent  the  return  of  the  pain.  A  new 
remedy  often  works  well,  but  the  benefit  is  not  lasting.  There  are  no  special 
indications  for  the  different  remedies,  so  that  we  must  try  to  see  which  one  is 
the  most  efficacious.  Antipyrine  is  most  used  of  late  in  doses  of  seven  to  twenty 
grains  (gramme  0.5-1.5).  Its  efficacy  in  migraine  is  undoubted,  but  it  sometimes 
gives  distinct  relief  in  other  forms  of  headache.  We  may  also  use  antifebrine,  in 
doses  of  three  to  seven  grains  (gramme  0.25-0.5),  phenacetine,  seven  to  fifteen 
grains  (gramme  0.5-1),  and  quinine,  five  to  twelve  grains  (gramme  0.3-0.75).  In 
"  rheumatic "  headaches  which  come  on  after  exposure  to  cold,  draughts,  etc., 
we  may  try  sodic  salicylate,  half  a  drachm  to  a  drachm  (grammes  2-4).  It  is  of 
practical  importance  that  a  mixture  of  these  remedies  (for  instance,  equal  parts  of 
antipyrine  and  phenacetine)  is  often  more  efficient  than  a  single  remedy  by  itself. 
Of  other  drugs  we  may  mention  paullinia  serbilis  (guarana,  which  contains  caf- 
feine), in  seven-  to  thirty-grain  powders  (grammes  0.5-2),  three  to  six  one-grain 
ergotine  pills  (gramme  0.05)  a  day  in  hyper^mic  headache,  potassic  bromide  half 
a  drachm  to  a  drachm  (grammes  2-4),  arsenic,  [cannabis  indica,  caffeine],  etc. 

Electrical  treatment  (vide  supra)  has  given  decidedly  good  results  in  many 
cases,  although  the  mental  factor  perhaps  plays  the  chief  part  here.  We  must 
always  begin  electrical  treatment  with  great  caution,  and  try  first  what  method 
is  best  borne.  Cold-water  cures,  too,  are  sometimes  beneficial,  as  we  have  said 
above,  or  residence  in  the  country,  at  the  seashore,  or  in  the  mountains. 

We  can  sometimes  do  the  patient  good  service  with  the  remedies  mentioned, 
but  in  other  cases  the  evil  obstinately  defies  all  attempts  at  cure.  Then,  however, 
the  patient  has  still  the  encouragement  left  that  the  disease  often  ceases  at  last 
spontaneously  in  advanced  age,  after  lasting  years  and  years. 


CHAPTER   VI 
ANOMALIES    OP    THE    SENSE    OF    SMELL 

Anomalies  of  smell,  which  depend  upon  a  disease  of  the  olfactory  nerve  itself, 
of  its  terminal  apparatus,  or  of  its  central  termination,  are  not  infrequently 
observed,  but  they  have  no  great  practical  interest.  It  is  well  known  that  only 
the  upper  two  turbinated  bones  and  the  upper  part  of  the  septum  of  the  nares,  the 
olfactory  region,  are  supplied  by  fibers  of  the  olfactory  nerve.  The  odors  excite 
the  special  olfactory  cells  which  lie  between  the  epithelial  cells.     The  processes 


ANOMALIES    OF   THE    SENSE    OF   TASTE  82Y 

of  these  cells — that  is,  the  olfactory  nerves — pass  through  the  openings  of  the 
lamina  cribrosa  to  the  olfactory  bulhs  in  which  they  split  up.  The  ganglion  cells 
of  the  bulb  form  neurones  of  the  second  order  for  the  olfactory  tract.  Their 
nerve-fibers  pass  through  the  olfactory  tract  to  the  brain.  The  fibers  for  smell 
either  enter  into  relation  with  the  optic  thalamus  or  terminate  in  the  cortex  of 
the  uncinate  gyrus  and  the  cornu  Ammonis.  A  part  of  the  olfactory  fibers,  how- 
ever, undergo  a  decussation  in  the  anterior  commissure.  The  fornix  and  the 
corpora  albicantia  have  also  relations  with  the  olfactory  apparatus,  which  in 
man  is  only  a  poorly  developed  organ,  while  in  many  animals  it  has  a  very  de- 
cided morphological  development. 

In  testing  the  sense  of  smell,  we  use  substances  which  do  not  at  the  same  time 
irritate  the  sensory  fibers  of  the  trigeminus  in  the  nasal  cavity.  The  best  sub- 
stances to  use  are  cologne-water,  ethereal  oils,  such  as  oil  of  cloves  or  oil  of  berga- 
mot,  oil  of  turpentine,  camphor,  musk,  valerian,  asafoetida,  etc. 

ITypersesthesia  of  the  sense  of  smell  (hyperosmia)  makes  itself  manifest  either 
by  a  remarkably  fine  perception  of  odors,  or  by  an  abnormal  sensitiveness  to 
them.  The  latter  symptom  is  often  noticed,  especially  in  the  hysterical.  Patients 
have  headaches,  or  attacks  of  fainting,  from  slight  odors,  which  healthy  persons 
notice  but  little.  Subjective  sensations  of  smell  (hallucinations  of  smell)  are 
quite  frequent  among  the  insane,  and  sometimes  during  the  aura  of  an  epi- 
leptic attack. 

A  diminution  of  the  power  of  smell  (olfactory  anaesthesia,  anosmia)  is  not 
infrequently  seen  in  the  different  diseases  of  the  nose — coryza,  severe  inflamma- 
tion, etc. ;  also  in  affections  of  the  base  of  the  skull,  such  as  tumors,  and  acute 
and  chronic  meningitis,  which  involve  the  trunk  of  the  olfactory  sympathetically, 
and  also  in  cerebral  disease,  tumors,  etc.  In  right  hemiplegia  and  aphasia,  for 
example,  co-existing  anosmia  of  the  left  nasal  cavity  has  sometimes  been  ob- 
served. In  far-advanced  tabes  dorsalis  we  have  sometimes  found  pronounced 
anosmia,  dependent,  perhaps,  upon  an  atrophy  of  the  olfactory  nerve.  Complete 
or  unilateral  anosmia,  however,  is  most  frequently  observed  in  the  hysterical 
(hysterical  hemiansesthesia,  traumatic  hysteria,  etc.).  It  is  important  to  state 
that  in  every  marked  enf eeblement  of  the  smell  the  "  taste  "  for  many  forms  of 
food  suffers,  since  it  is  well  known  that  their  "  aroma,"  as  in  roast  meats,  wines, 
and  the  different  sorts  of  cheese,  is  due  chiefly  to  the  co-existing  sensations 
of  smell. 

The  treatment  of  anomalies  of  smell  almost  always  coincides  with  the  treat- 
ment of  the  primary  disease.  In  case  the  disturbance  of  smell  makes  special 
interference  desirable,  we  can  try  electrization  of  the  nasal  mucous  membrane, 
or  painting  it  with  very  irritating  or  very  odorous  solutions. 


CHAPTER   VII 
ANOMALIES    OF    THE    SENSE    OE    TASTE 

Sensations  of  taste  are  obtained  from  two  nerves — the  glosso-pharyngeal,  and 
the  lingual  nerve  from  the  third  branch  of  the  trigeminus.  The  glosso-pharyn- 
geal is  the  nerve  of  taste  for  the  posterior  third  of  the  tongue  and  the  palate,  the 
lingual  for  the  anterior  two  thirds  of  the  tongue.  The  gustatory  fibers  of  the  lin- 
gual, all,  or  at  least  a  great  part  of  them,  pass  over  to  the  chorda  tympani,  and 
reach  with  this  the  trunk  of  the  facial;  they  do  not  remain  in  the  facial,  how- 
ever, as  many  pathological  observations  have  most  plainly  shown,  but  they  finally 


828  DISEASES    OE   THE   NEEVOUS    SYSTEM 

come  back  to  the  trigemimis,  and,  as  has  been  believed  up  to  the  present  time,, 
probably  chiefly  by  the  great  superficial  petrosal  nerve  and  the  Vidian  nerve  to 
the  spheno-palatine  ganglion,  in  this  way  passing  to  the  second  branch  of  the 
trigeminus;  or,  as  is  rendered  probable  by  more  recent  investigations,  they  pass 
by  means  of  the  otic  ganglion  to  the  third  branch  of  the  trigeminus  and  to  the 
Gasserian  ganglion  (vide  page  802).  We  know  nothing  definite  as  to  their 
further  course  and  their  central  termination. 

Hypersesthesia  of  taste  is  rare,  and  it  has  been  seen  almost  exclusively  in  the 
hysterical.  Parsesthesia  of  taste  is  sometimes  found  in  patients  with  facial 
paralysis,  who  complain  of  an  abnormal  taste  in  their  mouths.  In  the  insane^ 
too,  subjective  sensations  of  taste  (hallucinations  of  taste)  may  occur.  Anaes- 
thesia of  the  gustatory  nerves  (gustatory  anaesthesia,  ageusia)  is,  however,  quite 
frequent.  As  follows  from  what  has  gone  before,  this  may  be  seen :  (1)  In  affec- 
tions of  the  peripheral  terminal  organs  of  the  gustatory  nerves,  as  in  disease  of 
the  mucous  membrane  of  the  tongue ;  (2)  in  affections  of  the  glosso-pharyngeal, 
such  as  compression;  (3)  in  affections  of  the  lingual  nerve,  and  of  the  trigem- 
inus within  the  cranial  cavity;  (4)  in  affections  of  the  chorda  tympani,  from 
diseases  of  the  middle  ear;  (5)  in  affections  of  the  facial  nerve  between  the 
entrance  of  the  chorda  tympani  and  the  geniculate  ganglion ;  but  we  know  from 
experience  that  any  obstacle  to  conduction  in  this  nerve,  above  or  below  the  points 
named,  causes  no  disturbance  of  the  sense  of  taste.  Central  disturbances  of 
taste  are  said  to  have  been  observed  in  affections  of  the  posterior  portion  of  the 
internal  capsule.  Disturbances  of  taste  are  very  common  in  hysteria  and  allied 
conditions  (traumatic  neuroses,  etc.). 

The  test  of  the  sense  of  taste  must  be  made  separately  for  all  the  different 
varieties  of  the  sensation  of  taste,  since  partial  paralyses  of  taste  are  not  infre- 
quent. The  test  is  performed  by  putting  small  amounts  of  the  substance  to  be- 
tasted  in  solution  on  the  tongue  with  a  glass  rod  or  a  brush.  The  anterior  and 
posterior  parts  are  to  be  tested  separately.  A  solution  of  quinine  or  tincture  of 
nux  vomica  serves  as  a  test  for  bitter,  a  solution  of  sugar  for  sweet,  vinegar  or 
dilute  muriatic  acid  for  sour,  and  a  solution  of  common  salt  for  salt.  We  may 
also  use  as  a  test  for  taste  the  well-known  galvanic  taste,  which  is  strongest  at 
the  anode,  but  is  also  detected  at  the  cathode  in  even  very  weak  currents,  and 
hence  is  so  often  noticed  from  by-currents  in  galvanizing  the  head,  neck,  etc. 

An  accurate  diagnosis  as  to  the  seat  and  cause  of  disturbances  of  taste  can  be- 
made  only  by  considering  the  other  symptoms  which  are  also  present.  Direct- 
treatment  may  best  be  employed  by  the  aid  of  electricity. 


EEMAEKS    UPON   THE   DISTUEBANCES    OF   MOTILITY      829 


u 


SECTION  II 

Diseases   of  the  Motor   Nerves 

CHAPTEE   I 

GENERAL    REMARKS    UPON    THE    DISTURBANCES    OF    MOTILITY 

1,  Paralysis 

General  Classification  of  Paralyses. — By  "  paralysis  "  we  mean  the  loss  of  vol- 
"untary  motion  in  the  muscles  of  the  body  controlled  by  the  will.  We  usually  dis- 
tinguish between  the  complete  loss  of  the  power  of  active  motion  (paralysis)  and 
the  mere  weakening  of  it  (paresis).  In  complete  paralysis  of  any  part  of  the 
hody,  or  of  a  single  muscle,  the  slightest  voluntary  motion  can  not  be  produced 
in  it;  while  in  paresis  of  a  diseased  part  certain 
movements  are  still  possible,  but  they  are  more 
or  less  below  the  normal  in  strength,  extent,  and 
duration. 

In  every  portion  of  the  tract  that  leads  from  the 
motor  portions  of  the  cortical  gray  matter  of  the 
brain  to  the  muscles — that  is,  in  every  part  of  the 
so-called  great  "  cortico-muscular  conduction- 
path  "  or  "  pyramidal  tract  " — disease  may  lead  to 
paralysis  if  it  takes  away  from  the  part  affected  its 
power  to  conduct  voluntary  motor  excitations. 
Every  destruction  or  inhibition  of  function  of  the 
motor  centers  in  the  cerebral  cortex,  with  whose 
integrity  the  initiation  of  voluntary  innervation 
is  associated,  must  also  lead  to  a  paralysis  in  the 
corresponding  muscular  region.  Finally,  diseases 
of  the  muscles  even  may  cause  paralysis,  since 
the  muscles  may  either  have  their  contractile 
substance  injured,  or  lose  their  power  to  respond 
by  a  contraction  to  any  nervous  excitation  that 
reaches  them  ("myopathic  paralyses"). 

If  we  represent  to  ourselves  briefly  the  precise 
course  of  the  chief  tract  for  exciting  voluntary 
movements,  so  far  as  it  is  now  known,  we  must  put 
the  beginning  of  this  tract,  according  to  all  recent 
■experiments,  in  the  region  of  the  central  convolu- 
tions of  the  cerebrum  and  of  the  paracentral  lobule. 
Here  we  find  the  so-called  psycho-motor  centers 
(see  the  details  in  the  chapter  on  cerebral  localiza- 
tion), from  which  the  motor  fibers  in  the  corona 
radiata  converge  and  pass  downward.  The  lat- 
ter, after  they  have  united  into  quite  a  compact 
bundle,  enter  the  internal  capsule,  which  they  traverse  obliquely.  As  we  see  in  a 
horizontal  section  through  the  cerebral  hemispheres  (see  Fig.  95),  the  internal 
capsule  consists  of  two  limbs — an  anterior,  between  the  lenticular  and  the  caudate 
nuclei,  and  a  posterior,  between  the  lenticular  nucleus  and  the  optic  thalamus. 
The  two  limbs  form  an  obtuse  angle,  opening  outward,  whose  top — that  is,  the 
junction  of  the  anterior  and  posterior  limbs  of  the  internal  capsule — is  termed 
the  "  knee  of  the  capsule."    The  motor  tract  {,Py)  lies  in  the  posterior  limb  of  the 


kkii^ 


Fig.  95.— Horizontal  section  through 
the  right  cerebral  hemisphere. 
NC.  Caudate  nucleus.  Th.  Optic 
thalamus.  LK.  Lenticular  nu- 
cleus (first,  second,  and  third  di- 
visions). vS.  Anterior  limb  of 
the  internal  capsule.  hS.  Poste- 
rior limb  of  the  internal  capsule. 
Fa.  Fibers  belonging  to  the  facial 
nerve.  Py.  Pyramidal  tract  (mo- 
tor). S.  Sensory  tract  (probably 
cutaneous  nerves  and  those  of 
special  sense).   0.  Occipital  lobe. 


830 


DISEASES    OF   THE   NEEVOUS    SYSTEM 


Fig.  96. — Transverse  section  through  the  crura 
cerebri  in  secondary  degeneration  of  the 
right  pyramidal  tract.  (From  Charcot.) 
sn.  Substantia  nigra,  p.  The  degenerated 
and  therefore  translucent  pyramidal  tract. 
III.  Oculo-motor  nerve.  AS.  Aqueduct  of 
Sylvius. 


ryK 


internal  capsule  about  the  posterior  end  of  its  middle  third.     The  fibers  for  the 
cranial  motor  nerves  (facial,  hypoglossus)  lie  farther  forward  than  the  fibers  for 

the  extremities.  The  tract  runs  downward 
rather  obliquely,  so  that  in  the  upper  part 
of  the  internal  capsule  it  lies  somewhat 
farther  forward  than  in  the  lower.  From 
the  internal  capsule  the  pyramidal  tract 
enters  the  crusta.  It  lies  first  in  the  third 
quarter,  counting  from  the  inside,  then 
farther  down  in  the  middle  third  of  the 
crusta  (see  Fig.  96).  The  fibers  for  the 
cranial  motor  nerves  here  lie  nearer  the 
median  line  than  the  fibers  for  the  extrem- 
ities. Farther  downward  the  tract  passes 
into  the  anterior  half  of  the  pons.  In 
the  pons  the  fibers  of  the  pyramidal 
tract  are  somewhat  separated,  but  they 
come  together  below  it  into  the  compact 
bundle  of  the  pyramids  on  the  anterior 
surface  of  the  medulla.  In  this  course 
from  the  internal  capsule  to  the  medulla 
oblongata  all  the  nerve  tracts  for  the  muscles  of  the  head  branch  off  laterally, 
and,  after  they  have  decussated  in  the  median  line,  they  go  to  the  nuclei  of  their 

respective  nerves  (oculo-motor  nuclei 
under  the  aqueduct  of  Sylvius,  facial  nu- 
clei in  the  pons,  hj^oglossal  nuclei  in  the 
medulla,  etc.).  The  motor  fibers  for  the 
trunk  and  extremities  remain  in  the 
pyramids,  at  the  lower  end  of  which  the 
decussation  of  these  fibers  (motor  decus- 
sation of  the  pyramids,  decussatio  pyram- 
idum),  takes  place.  The  fibers  of  each 
pyramid  pass  over,  for  the  most  part,  into 
the  lateral  column  of  the  opposite  half 
of  the  spinal  cord,  and  here  from  the  dis- 
tinct bundle  of  the  lateral  pyramidal 
tract  {Py8,  see  Figs.  97  and  98),  A  small 
part  of  the  pyramids,  which  sometimes 
seems  to  be  entirely  wanting,  remains  uncrossed,  and  passes  downward  as  the 
so-called  anterior  pyramidal  tract    {PyV,  Fig.   97)    in  the   anterior  column  of 

the  cord  on  the  same  side.  From  the  lat- 
eral column,  or  the  anterior  column  of  the 
cord,  the  motor  fibers  pass  into  the  ante- 
rior gray  columns  of  the  cord,  and  are 
here  connected  with  the  large  motor  gan- 
glion-cells of  the  anterior  cornua.  We 
now  know  that  this  connection  does  not 
take  place  in  the  sense  of  a  direct  pas- 
sage of  the  lateral  tract  fibers  into  the 
cells  of  the  anterior  cornua,  but  that  each 
fiber  breaks  up  into  a  "  nervous  terminal 
Fig.  98.-Transverse  section  through  the  lumbar     arborization,"  which  surrounds  the  proto- 

enlargement.  PyS  Lateral  pyramidal  tract,      plasmic  prOCCSSeS  of  a  ganglion-cell  of  the 
(The  anterior  tract  is  no  longer  present  m      -"^  .      -^  ,    .        ,  . 

the  lumbar  portion  of  the  cord.)  anterior  horn  and  m  this  way  enters  into 


Fig.  97.— Transverse  section  through  the  cervi- 
cal enlargement  of  the  spinal  cord.  PyS. 
Lateral  pyramidal  tract.  PyV.  Anterior 
pyramidal  tract  (in  this  case  present  only  on 
one  side). 


EEMAEKS    UPON   THE   DISTUEBANCES    OF   MOTILITY      831 

the  closest  relation  with  it.  From  the  ganglion-cell  of  the  anterior  horn  its  axis- 
cylinder  process  passes  off  directly  as  the  anterior  root-fiber,  and  the  anterior 
spinal  roots  are  further  continued  ^s  the  peripheral  motor  nerves.  In  the  muscle, 
as  we  know,  the  nerve-fiber  again  breaks  up  into  a  terminal  arborization  ("  motor 
end  plate"),  which  finally  transmits  the  irritation  coming  from  the  cerebrum  to 
the  contractile  muscular  fiber. 

The  long  motor  tract,  just  described,  the  cortico-muscular  path  or  the  pyram- 
idal tract,  whose  course  has  been  quite  accurately  determined  in  its  details  by 
the  results  of  pathological  observations  (Tiirck,  Charcot)  and  investigations  into 
the  history  of  its  development  (Flechsig),  is  composed  of  two  neurones  connected 
with  each  other:  the  first  (central)  motor  neurone  extends  from  the  cell  of  origin 
in  the  cerebral  cortex  to  the  terminal  arborization  of  the  fiber  in  the  motor  nuclei 
(nuclei  of  the  cranial  motor  nerves,  motor  ganglion  cells  in  the  anterior  cornua)  ; 
the  second  (peripheral  neurone)  extends  from  the  above-mentioned  ganglion  cells 
to  the  muscles,  and  is  accordingly  formed  essentially  by  the  ganglion  cell  and  the 
peripheral  nerve-fiber.  It  forms,  at  all  events,  the  chief  path  for  the  conduction 
of  voluntary  innervation.  It  is  possible  that  there  are  other  motor  paths  of  con- 
duction besides  this  tract,  but  we  know  nothing  definite  concerning  them. 

If  we  pay  attention  to  the  course  of  the  motor  tracts  described,  we  shall  easily 
understand  certain  peculiarities  in  the  distribution  of  motor  paralyses,  which  are 
of  great  importance  in  diagnosis.  Since  the  motor  centers  for  separate  parts  of 
the  body,  such  as  the  face,  the  arm,  or  the  leg,  are  separated  from  one  another  in 
the  cerebral  cortex,  and  are  distributed  over  a  comparatively  large  surface,  as  we 
shall  see  more  fully  later  on,  it  is  easily  explained  why  affections  of  the  cortex,  if 
they  are  not  very  extensive,  may  lead  to  paralysis  of  only  a  single  part  of  the 
body.  We  call  such  an  isolated  paralysis  of  one  part  of  the  body  monoplegia,  and 
thus  we  speak  of  a  cortical  facial  or  brachial  monoplegia.  Farther  downward  in 
the  brain,  in  the  internal  capsule  and  the  crus  cerebri,  however,  as  we  have  seen, 
all  the  motor  fibers  are  collected  into  one  bundle,  whose  diameter  takes  up  com- 
paratively little  space.  Hence  we  perceive  that  any  disease  of  the  brain,  which 
is  situated  in  this  part  of  the  motor  tract,  may  easily  make  this  tract  incapable 
of  conduction  throughout  its  whole  extent,  or  at  least  throughout  the  great- 
est part  of  it.  The  result  must  be,  then,  a  more  or  less  complete  paralysis  of  the 
facial  muscles,  the  arm,  and  the  leg  at  the  same  time — ^that  is,  of  the  entire  half 
of  the  body — a  form  of  paralysis  which  is  termed  hemiplegia  or  unilateral  paraly- 
sis. We  may  note  here  that,  as  a  result  of  the  passage  of  the  motor  fibers  to 
the  other  half  of  the  cord  in  the  decussation  of  the  pyramids,  the  paralysis  must 
develop  on  the  side  of  the  body  opposite  to  the  focus  of  disease  in  the  brain. 
Farther  down  in  the  medulla  and  the  cord  the  fibers  coming  from  both  hemi- 
spheres, and  belonging  to  the  two  sides  of  the  body,  lie  quite  near  each  other.  Since 
many  diseases  of  the  cord  have  a  tendency  to  affect  the  two  halves  of  the  cord  at 
once,  or  gradually  to  extend  over  the  whole  transverse  section  of  the  cord,  a  simul- 
taneous paralysis  of  the  corresponding  portion  of  the  two  sides  of  the  body  will 
be  apt  to  arise  as  a  result  of  this.  This  form  of  paralysis  we  call  paraplegia.  Dis- 
eases in  the  cervical  cord  may  have  as  a  result  a  paralysis  of  all  four  extremities 
or  of  the  two  arms — cervical,  brachial,  or  superior  paraplegia;  diseases  in  the 
dorsal  and  lumbar  cord  a  paraplegia  of  the  two  legs — inferior  paraplegia,  often 
called  simply  "  paraplegia,"  without  further  prefix.  In  diseases  of  the  peripheral 
nerves  we  have,  of  course,  again  a  limitation  of  the  paralysis  to  the  region  of  the 
affected  nerve.  The  paralysis  may  be  quite  extensive  in  diseases  of  a  nervous 
plexus — paralysis  of  a  peripheral  plexus;  or  it  may  confine  itself  wholly  to  the 
region  of  a  single  nerve,  or  even  of  a  single  branch  of  the  nerve — paralysis  of  a 
peripheral  nerve. 

We  will  have  to  add  many  more  details  to  what  has  just  been  said,  but  as  a 


832  DISEASES    OF   THE   ITEEYOUS    SYSTEM 

fundamental  principle  we  may  now  note  tliat  hemiplegia  is  the  chief  form  of 
<;erebral  paralysis,  while  paraplegia  is  the  chief  form  of  spinal  paralysis.  Mono- 
plegias are  usually  either  cortical  cerebral  paralyses,  or  peripheral  paralyses. 

General  2Etiologj  of  Paralysis. — The  kind  of  lesion  which  leads  to  paralysis 
may,  in  the  different  cases,  be  very  diverse.  Erom  easily  understood  reasons  we 
can  very  rarely  decide  as  to  the  kind  of  lesion  from  the  intensity  and  extent  of 
the  paralysis,  but  only  from  the  manifest  setiological  factors,  from  the  develop- 
ment and  course  of  the  paralysis,  from  other  morbid  symptoms  that  are  also 
present,  etc.  In  general,  we  may  divide  the  paralyses  into  two  groups,  according 
to  the  nature  of  their  cause:  into  paralyses  from  causes  that  can  be  discovered 
anatomically,  and  into  the  so-called  functional  paralyses,  in  which  no  anatomical 
cause  for  the  paralysis  can  be  found ;  but  since  our  anatomical,  and  especially  our 
histological,  methods  of  investigation  have  become  better  developed  and  are  more 
employed,  the  domain  of  functional  paralyses  has  become  gradually  more  and 
more  restricted,  and  a  definite  anatomical  cause  has  now  been  found  for  many 
paralyses  which  were  once  regarded  as  functional. 

All  the  diseases  of  the  nervous  system  may  be  anatomical  causes  of  paralysis, 
if  they  lie  in  a  spot  where  they  damage  or  destroy  the  paths  of  motor  conduction. 
Inflammation,  degeneration,  new  growths,  haemorrhages,  and  severe  disturbances 
of  circulation,  with  their  results,  especially  embolic  and  thrombotic  softening,  are 
found  in  the  brain,  the  cord,  and  the  peripheral  nerves,  and  under  some  circum- 
stances give  rise  to  the  phenomenon  of  paralysis.  Mechanical  lesions  of  the  nerv- 
ous system  also  play  a  great  part  in  the  pathogenesis  of  paralysis,  especially  in- 
juries, and  compression  of  the  brain,  the  cord,  and  the  peripheral  nerves  by  swell- 
ings, new  growths,  and  other  diseases  in  their  vicinity. 

We  also  know  certain  toxic  substances  which  cause  direct  injury  (degenera- 
tion) of  the  motor-nerve  territory  (chiefly  the  peripheral  motor  nerves),  and  con- 
sequent paralysis.  Of  these  toxic  paralyses,  alcoholic  paralysis  (vide  infra)  and 
lead  paralysis  (vide  infra)  are  the  most  important  in  their  clinical  relations ;  but 
other  poisonous  substances,  such  as  copper,  arsenic,  and  certain  vegetable  alka- 
loids, may  also  cause  paralysis. 

We  may  group  a  large  number  of  paralyses  together  under  the  term  of  "  paraly- 
sis after  acute  diseases."  Since  in  these  cases  we  always  have  to  do  with  acute 
infectious  diseases,  we  may  assume,  as  their  most  probable  cause,  certain  changes 
in  the  nervous  system,  sometimes  in  the  brain  or  cord,  but  much  more  frequently 
in  the  peripheral  nerves,  which  stand  in  direct  relation  to  the  specific  infectious 
material.  There  seem  to  be  chemical  poisons  ("  ptomaines  ")  which  form  in  the 
body  in  infectious  disease,  and  cause  degeneration  of  certain  nerve-fibers,  in  the 
same  way,  for  example,  as  lead.  We  most  frequently  see  paralysis  appear  after 
diphtheria,  diphtheritic  paralysis  (vide  infra),  or  more  rarely  after  typhoid  fever, 
small-pox,  dysentery,  the  acute  exanthemata,  etc.  The  paralyses  which  may 
arise  in  certain  chronic  infectious  diseases,  especially  in  syphilis  and  tubercu- 
losis, usually  have  another  origin.  Here  we  usually  have  to  do  with  the  specific 
morbid  product  itself  (gumma,  tubercle),  which  may  invade  various  parts  of  the 
nervous  system,  but,  on  the  other  hand,  we  must  under  some  circumstances  con- 
sider the  action  of  toxines  even  in  paralyses  in  sj^hilis  and  tuberculosis.  Final- 
ly, certain  paralyses  which  occur  in  certain  general  constitutional  diseases,  such 
as  diabetes  and  gout,  are  also  due  probably  to  toxic  infiuences. 

Those  paralyses  which  come  on  most  manifestly  because  of  exposure  to  cold 
are  termed  paralyses  from  exposure  to  cold,  or  "  refrigeratory,"  or  frequently 
"  rheumatic  "  paralyses.  Although  many  spinal  diseases,  such  as  myelitis,  may 
perhaps  be  referred  to  exposure  to  wet  or  cold,  we  usually  reckon  among  rheu- 
matic paralyses  only  certain  peripheral  paralyses,  such  as  that  in  the  domain  of 
the  facial  nerve.    The  functional  disturbance  of  the  nerves  in  these  cases  probably 


EEMAUKS   UPO:^r   THE   DISTUEBANCES    OF   MOTILITY      833 

depends  upon  mild  inflammatory  changes  in  them  produced  by  cold,  and  is  accord- 
ingly of  an  anatomical  and  not  merely  of  a  functional  nature. 

There  are,  however,  quite  a  comprehensive  group  of  paralyses  which  we  must 
to-day  still  term  functional  paralyses.  To  this  class  belong  the  hysterical  paraly- 
ses, the  paralyses  from  psychical  causes,  such  as  paralysis  from  fright,  the  "  pa- 
ralyses from  imagination,"  etc.  We  shall  learn  to  recognize  these  more  fully  in 
the  chapter  on  hysteria. 

In  conclusion,  we  must  bear  in  mind  the  so-called  "  reflex  paralyses,"  whose 
aetiology  is  not  yet  fully  explained — that  is,  paralyses  which  may  come  on  in  the 
course  of  diseases  of  certain  internal  organs,  especially  of  the  intestine,  and  of 
the  urinary  and  sexual  organs,  as  a  result  of  centripetal  irritations  acting  reflexly. 
An  attempt  has  been  made  to  explain  their  origin,  from  analogy  with  well-known 
physiological  experiments,  by  the  idea  that  a  "  reflex  inhibition  "  is  excited  in 
certain  motor  regions  by  a  sensory  irritation  arising  in  the  diseased  organs,  a 
theory  which  has  not  yet  been  fully  confirmed.  Leyden's  hypothesis  is  scarcely 
more  probable,  and  it  is  by  no  means  proved.  According  to  it  the  paralyses  of  this 
class  are  explained  by  an  ascending  neuritis,  arising  from  the  organs  originally 
affected  (see  the  chapter  on  neuritis).  Generally  speaking,  the  whole  conception 
of  "  reflex  paralyses  "  is  still  far  from  clear,  and  we  will  do  well  to  be  extremely 
guarded  in  their  diagnosis.  Many  cases  which  were  formerly  regarded  as  reflex 
paralyses  are  to  be  classed  as  hysteria,  especially  as  traumatic  hysteria  (q.v.). 
Lepine  has  also  regarded  the  paralysis  of  the  arm  of  the  affected  side,  seen  in 
some  cases  of  empyema,  especially  after  operative  interference,  as  a  "  reflex  pa- 
ralysis," an  explanation  which  may  be  proper  in  some  cases,  but  in  regard  to 
which  we  should  be  the  more  cautious,  as  metastatic  abscesses  of  the  brain  are 
not  very  infrequently  found  in  empyema  (see  the  chapters  on  purulent  menin- 
gitis and  cerebral  abscess). 

General  Symptomatology  of  Paralyses. — We  can  recognize  the  existence  of  a 
paralysis,  independently  of  the  patient's  statements  as  to  the  impossibility  of  per- 
forming certain  motions  and  functions,  only  by  a  careful  and  thorough  physical 
examination  of  the  power  of  voluntary  motion.  This  examination  in  patients 
with  nervous  disease  must  extend  to  all  parts  of  the  body,  and  demands  an  accu- 
rate knowledge  of  all  the  movements  that  can  normally  be  executed  by  the  differ- 
ent joints,  and  of  the  muscles  and  nerves  requisite  to  produce  them  (see  the  tables 
at  the  end  of  this  chapter). 

In  each  individual  case  of  paralysis  some  other  symptoms  must  be  considered 
besides  immobility — first  the  condition  of  the  paralyzed  muscles,  and  then  certain 
accompanying  symptoms  that  are  often  present  with  the  paralysis. 

In  regard  to  the  first  point,  the  trophic  condition  of  the  paralyzed  muscle  is  of 
the  greatest  diagnostic  and  practical  importance.  In  comparing  a  large  number 
of  paralyses,  a  very  evident  difference  in  this  respect  strikes  us  at  once.  We  see 
on  the  one  hand  paralyses  where  the  paralyzed  muscles  retain  their  normal  vol- 
ume for  a  comparatively  long  time  and  only  gradually  waste  as  a  consequence  of 
disease  and  the  lack  of  the  normal  influences  of  innervation,  although  this  atro- 
phy never  goes  beyond  a  certain  degree.  On  the  other  hand,  however,  we  also  see 
cases  in  which  there  is  a  considerable  atrophy  in  the  paralyzed  muscles  in  a  few 
weeks  or  months,  finally  progressing  to  an  almost  complete  disappearance  of  the 
muscles.  This  distinction  is  so  comprehensive  that  all  the  last-named  paralyses 
have  been  classed  together  under  the  name  of  "  atrophic  paralyses." 

If  we  once  more  represent  to  ourselves  the  whole  course  of  the  motor  tracts, 
from  the  cerebral  cortex  to  the  voluntary  muscles,  we  shall  remember  that  these 
tracts  are  composed  of  two  connected  yet  independent  neurones.  The  peripheral 
neurone  directly  innervating  the  muscle  has  its  ganglion-cell  in  the  anterior 
cornua  of  the  spinal  cord.  Clinical  and  anatomical  experience  teaches  us  that, 
53 


834  DISEASES    OF   THE   NEEVOUS    SYSTEM 

in  all  those  paralyses  where  the  cause — that  is,  the  break  in  conduction  of  the 
motor  fibers — lies  in  the  first  (central)  neurone  from  the  cortex  up  to,  but  exclud- 
ing the  cells  in  the  anterior  cornua,  there  is,  as  a  rule,  only  a  slow  and  relatively 
slight  amount  of  atrophy  in  the  paralyzed  muscles,  while  in  those  paralyses  where 
the  cause  is  situated  in  the  second  (peripheral)  neurone — that  is,  in  these  gan- 
glion-cells themselves,  or  in  the  motor  nerves  peripheral  to  them — a  pronounced 
muscular  atrophy  rapidly  develops.  The  only  possible  interpretation  of  this  fact 
is,  that  the  large  motor  ganglion-cells  of  the  anterior  cornua  have,  as  we  express 
it,  a  trophic  influence  on  the  muscles  innervated  by  them.  As  we  have  seen  above, 
the  peripheral  motor-nerve  fiber  is  nothing  but  the  direct,  long  cellular  process 
of  a  motor  ganglion-cell  in  the  anterior  horn.  It  is  therefore  easy  to  under- 
stand that  this  process  atrophies  when  it  is  separated  from  the  cell-body  and  its 
cell  nucleus,  or  when  the  cell  itself  is  destroyed.  If,  however,  the  motor  nerve 
degenerates,  the  muscle  belonging  to  it  is  entirely  separated  from  all  influences  of 
innervation;  neither  voluntary  nor  reflex  nerve  irritations  can  act  upon  it  any 
longer.  This  lack  of  innervation  apparently  causes  such  a  change  in  the  trophic 
conditions  of  the  paralyzed  muscle  that  its  fibers  disappear  one  after  the  other, 
until  finally,  in  long-continued  paralyses,  only  a  slight  trace  of  muscular  tissue  is 
left.  We  can  therefore  consider  the  peripheral  motor  neurone  and  the  muscular 
fiber  as,  in  a  certain  degree,  a  trophic  unit. 

It  has  been  generally  believed  that  the  anatomico-histological  processes  in  the 
rapidly  atrophying  muscles  were  also  different  in  diseases  of  the  peripheral  motor 
neurones  from  the  processes  of  slow  and  slighter  atrophy  in  paralyses  from  dis- 
ease of  the  central  motor  neurones.  In  the  first  case  we  were  dealing  with  a 
so-called  "  degenerative  "  atrophy  of  the  fibers — that  is,  with  an  atrophy  asso- 
ciated with  granular  and  fatty  destruction  of  the  fibers — and  in  the  second  case 
only  with  a  "  simple  "  atrophy.  Such  a  histological  difference,  however,  can  not 
be  strictly  maintained.  We  are  always  dealing,  essentially,  with  a  diminution  in 
the  size  of  the  fibers,  where,  however,  the  transverse  striation  of  the  muscle  re- 
mains plainly  visible.  We  also  find  a  great  increase  in  the  nuclei  of  the  muscle, 
and,  finally,  we  often  see  an  increase  of  the  interstitial  connective  and  fatty 
tissue. 

We  observe  a  further  distinction  in  the  condition  of  the  paralyzed  muscles  if 
we  perform  passive  motion  in  the  paralyzed  parts.  There  are  paralyses  where  we 
can  perform  passive  motion  of  the  paralyzed  parts  at  any  joint  with  perfect  ease 
and  freedom,  and  without  perceiving  the  slightest  resistance.  We  term  such 
paralyses  "  flaccid  paralyses,"  but  there  are  also  paralyses  where  passive  motion 
meets  with  considerable  muscular  resistance,  so  that  it  can  be  performed  only  with 
a  certain  greater  or  less  amount  of  exertion,  or  not  at  all,  or  only  within  certain 
limits :  spastic  paralyses.  This  distinction  is  dependent  upon  the  state  of  mus- 
cular tonus  in  the  paralyzed  muscles.  If  this  tonus  be  increased  (hypertonia  of 
the  muscles)  and  the  muscles  be  found  in  a  state  of  marked  and  permanent  con- 
traction, the  paralyzed  parts  show  a  peculiar  stiffness,  or  even  an  almost  com- 
plete spastic  rigidity.  If  the  muscular  tonus  be  diminished  or  wholly  lost  (hypo- 
tonia of  the  muscles),  the  paralyzed  limbs  are  flaccid  and  sometimes  even  "flap- 
ping." Since  the  muscular  tonus  is  in  all  probability  of  reflex  origin,  it  is  not 
remarkable  that  spastic  paralyses  are  usually  associated  with  an  increase,  and 
flaccid  paralyses  often  with  a  loss  of  the  reflexes,  especially  the  tendon  reflexes 
(vide  infra).  States  of  marked  permanent  shortening  of  the  muscles,  whereby 
certain  parts  are  fixed  in  an  abnormal  position,  are  called  muscular  contractures. 
The  cause  of  their  development  will  be  spoken  of  later. 

Finally,  in  every  case  of  paralysis,  we  must  consider  the  other  nervous  symp- 
toms which  accompany  it,  since  these  may  also  be  of  great  importance  in  judging 
of  the  cause  of  the  paralysis.    We  must  first  of  all  investigate  the  condition  of 


EEMAEKS   UPON   THE  DISTUKBANCES   OF  MOTILITY      835 

the  reflexes  (vide  infra)  in  tlie  paralyzed  parts,  already  mentioned,  from  which 
many  conclusions  can  be  drawn  as  to  the  seat  of  the  lesion  which  causes  the 
paralysis.  We  must  also  test  the  &tate  of  the  sensibility,  both  in  the  skin  and  in 
the  muscles  themselves.  Certain  attendant  trophic  and  vaso-motor  symptoms 
are  also  to  be  regarded.  The  skin  over  the  paralyzed  parts  sometimes  appears 
cyanotic,  or  marble-like ;  it  feels  cool,  is  oedematous,  and  sometimes  is  peculiarly 
dry,  hard,  and  scaly.  The  examination  of  the  electrical  excitability  of  the 
paralyzed  nerves  and  muscles  is  of  especial  importance.  The  phenomena  oc- 
curring in  these  conditions  will  be  particularly  described  below. 

2.  Symptoms  of  Motor  Irritation 

As  we  have  termed  the  symptoms  of  motor  deficiency  "paralysis,"  we  group 
the  symptoms  of  motor  irritation  in  general  together  under  the  name  of  "  spasm." 
We  mean  by  this  all  the  morbid  movements  occurring  in  the  muscles  involunta- 
rily and  even  against  the  will.  Although  we  may  find  spasm  in  the  smooth  mus- 
cles, which  generally  are  not  controlled  by  the  will,  as  in  spasm  of  the  bronchial 
muscles,  spasm  of  the  vessels,  etc.,  we  will  concern  ourselves  here  only  with  the 
spasmodic  movements  in  the  voluntary  muscles.  We  must  look  for  the  cause  of 
these  in  abnormal  irritation  exerted  in  some  way  on  the  motor  tracts,  but  we 
know  very  little  of  the  precise  nature  and  character  of  this  irritation  in  most 
cases.  The  abnormal  irritation  often  acts  directly  on  the  motor  nervous  region, 
especially  in  the  frequent  spasms  in  affections  in  the  neighborhood  of  the  cortical 
motor  centers;  but  the  motor  irritations  often  seem  to  be  excited  secondarily 
through  some  reflex  channel — reflex  spasms. 

For  a  long  time  two  kinds  of  spasm  have  been  distinguished  symptomatically. 
We  term  those  spasms  clonic  where  the  abnormal  muscular  contraction  lasts 
only  a  short  time,  and  then  is  interrupted  by  a  short  period  of  relaxation,  to  come 
on  again  afresh.  The  affected  parts  of  the  body  are  thus  put  in  a  constant  con- 
vulsive motion.  In  distinction  from  this  we  term  those  abnormal  muscular  con- 
tractions tonic  spasms  where  the  muscle  remains  spasmodically  contracted  for  a 
longer  time — minutes,  hours,  or  days.  The  affected  part  of  the  body  is  thus  kept 
motionless  in  some  abnormal  position.  Both  forms  of  spasm,  however,  show 
many  transitions  and  combinations,  so  that  we  must  often  speak  of  "  tonic-clonic  " 
spasms. 

A  more  careful  examination  of  the  symptoms  of  motor  irritation,  however, 
gives  a  still  greater  number  of  different  forms.  We  will  here  group  together  the 
most  important  varieties  of  morbid  involuntary  movements. 

1.  Epileptiform  convulsions  are  severe,  and  usually  clonic  spasms,  at  times 
tonic-clonic,  either  involving  the  whole  body,  and  then  always  associated  with  dis- 
turbances of  consciousness,  or  limited  to  one  half  or  one  portion  of  the  body.  By 
them  the  whole  body  or  the  affected  part  is  put  into  violent  motion,  usually 
thrashing  and  shaking  movements.  The  pure  epileptic  spasm  in  epilepsy  is  the 
type  of  this  form  of  spasm,  but  precisely  analogous  spasms,  "epileptiform" 
spasms,  are  seen  in  organic  diseases  of  the  brain,  in  uraemia,  etc. 

2.  Persistent  rhythmical  contractions  in  single  groups  of  muscles  are  some- 
times seen  in  certain  cerebral  diseases,  such  as  apoplexy  and  sclerosis,  and  also, 
as  we  have  observed,  after  acute  myelitis.  In  these  the  part  of  the  body  affected 
is  put  in  motion  by  continuous,  separate,  weaker  or  stronger  thrusts,  which  follow 
one  another  in  a  regular  rhythm.  Ehythmical  contractions  are  also  seen  as  pre- 
cursors or  at  the  end  of  epileptiform  spasms. 

3.  Tremlling  motions,  or  tremor,  as  we  say  in  ordinary  parlance,  are  moderate 
motions,  rapidly  following  one  another,  with  a  not  very  marked  excursion.  If  the 
tremor  is  more  pronounced,  we  term  it  "  shaking."  Tremor  is  an  important  symp- 
tom, almost  pathognomonic  in  many  nervous  diseases,  such  as  paralysis  agitans. 


836  DISEASES    OF   THE   NEKVOUS    SYSTEM 

but  we  know  almost  nothing  in  regard  to  the  more  intimate  manner  of  its  origin. 
We  often  see  pronounced  tremor,  especially  in  the  hands,  in  exophthalmic  goitre. 
We  know  that'  tremor  is  often  present  in  old  people — senile  tremor ;  and  in  alco- 
holic subjects — alcoholic  tremor.  Tremor  sometimes  appears  in  muscles  at  rest, 
that  is,  not  innervated  by  the  will,  and  sometimes  only  in  those  which  are  moved 
voluntarily.  This  latter  form  of  tremor,  which  is  seen  most  frequently  in  multi- 
ple sclerosis  (vide  infra),  is  termed  "  intention  tremor."  Very  marked  intention 
tremor,  which  is  increased  by  any  mental  excitement,  is  also  seen  as  a  symptom 
of  chronic  mercurial  poisoning  (mercurial  tremor),  particularly  in  mirror-mak- 
ers, etc. 

We  may  mention  here  the  so-called  essential  tremor,  that  is,  a  condition  where 
the  tremor,  which  is  most  marked  in  the  hands,  is  the  only  morbid  symptom  and 
can  be  referred  to  no  known  cause.  On  energetic  voluntary  innervation  of  the 
muscles  the  tremor,  as  a  rule,  ceases.  This  form  of  tremor  is  sometimes  seen  in 
comparatively  young  people,  and  even  in  children.  A  distinct  hereditary  pre- 
disposition is  often  present,  so  that  several  "  tremblers  "  are  found  in  the  same 
family  (hereditary  tremor). 

We  very  often  find  trembling  in  "  nervous  "  persons,  which  is  at  once  increased 
by  any  emotion  (nervous,  neurasthenic  tremor).  Marked  tremor  is  also  frequent 
in  hysteria,  especially  in  traumatic  hysteria. 

4.  Single  contractions,  either  sudden  twitchings,  or  in  the  form  of  a  slow  con- 
traction of  the  muscle,  are  seen  with  especial  frequency  in  diseases  of  the  cord. 
They  are  either  single,  or  frequent  and  persistent.  Their  mode  of  origin  is  not 
always  plain.  They  may  depend  on  direct  motor  irritation  or  they  may  have  a 
reflex  origin.  In  the  latter  case  each  twitching  is  sometimes  associated  with  a 
sudden  feeling  of  pain  (symptoms  of  irritation  of  the  posterior  roots?). 

5.  Fascicular  and  fibrillary  muscular  contractions  are  little  contractions  in  the 
separate  muscular  bundles,  which  may  be  seen  on  a  close  examination  of  the  mus- 
cles, but  which  do  not  have  any  special  influence  on  motion.  If  the  fibrillary  con- 
tractions in  a  muscle  are  very  pronounced,  there  may  develop  an  actual  "  wave  " 
in  the  muscular  substance.  We  see  this  symptom  especially  in  atrophied  muscles, 
particularly  in  spinal  progressive  muscular  atrophy  {vide  infra)  and  other  spinal 
amyotrophies,  but  there  also  seem  to  be  independent  forms  of  diseases  of  the 
muscles,  in  which  we  may  see  for  a  long  time  a  persistent  and  extensive  muscular 
wave,  associated  with  pain,  profuse  sweating,  etc. — ^the  so-called  myokymia  of 
E.  Schultze. 

6.  Choreic  movements  are  either  slight  contractions  or  quite  complicated  and 
extensive,  but  brief  and  involuntary  movements,  which  usually  appear  in  the  face, 
in  one  limb,  or  sometimes  over  the  whole  body,  without  regard  to  rule.  In  severe 
cases  they  are  almost  continuous,  but  in  milder  cases  they  are  interrupted  by 
shorter  or  longer  pauses.  They  form  the  chief  symptom  of  chorea  proper,  but  they 
are  also  present  in  other  cerebral  affections,  such  as  symptomatic  chorea,  post- 
heiniplegic  chorea,  etc. 

7.  Movements  of  athetosis  is  the  name  we  give  to  peculiar  involuntary  and 
usually  quite  slow  movements,  which  are  seen  especially  in  the  arms  and  hands, 
but  also  in  the  head,  trunk,  etc.  The  fingers  make  slow  but  often  very  exten- 
sive movements,  are  extended,  spread  apart,  flexed,  and  moved  over  and  around 
one  another  in  the  most  remarkable  way.  This  form  of  motor  irritation  occurs  as 
a  special  disease,  "  athetosis,'"  or  as  a  symptom  in  certain  central  nervous  diseases, 
especially  the  cerebral  paralysis  of  children  (vide  infra). 

8.  Constant  or  co-ordinated  spasms  are  symptoms  of  motor  irritation  in  which 
the  patient  performs  complicated  movements  by  compulsion — forced  movements. 
Among  these  are  classed  the  compulsory  going  forward  or  moving  in  a  circle,  the 
turning  about  the  axis  of  the  body  (forced  attitudes),  and  also  certain  peculiar 


EEMAEKS   UP0:N   THE   DISTUEBANCES    OF   MOTILITY      837 

complicated  forms  of  spasm,  such  as  spasms  of  jmnping,  laughing,  screaming, 
with  all  sorts  of  spasms  of  the  respiratory,  pharyngeal,  and  laryngeal  muscles, 
associated  with  hiccoughing  and  belching  sounds,  etc.  They  are  seen  most  fre- 
quently in  severe  cases  of  hysteria,  but  epilepsy  may  also  occur  exceptionally  in 
the  form  of  co-ordinated  spasms.  The  forced  movements  and  attitudes  men- 
tioned above  are  seen  chiefly  in  affections  of  the  cerebellum  and  the  cerebellar 
peduncles. 

9.  Tonic  spasm,  as  has  been  said,  is  the  name  for  all  morbid  muscular  contrac- 
tions that  continue  for  a  long  time.  Tonic  spasm  in  the  muscles  of  mastication, 
the  masseters,  is  termed  trismus.  Tonic  spasm  in  the  muscles  of  the  back  and 
neck,  by  which  the  whole  body  is  drawn  backward,  and  the  vertebral  column  is 
bent  into  an  arch  with  the  convexity  in  front,  is  called  opisthotonos.  Tonic 
rigidity  of  the  whole  body  is  termed  tetanus.  Tonic  spasms  are  seen  not  infre- 
quently as  an  idiopathic  condition,  but  also  in  tetanus,  tetany,  hysteria,  etc. 

10.  Cataleptic  rigidity  is  the  name  of  that  tonic  condition  of  the  muscles  in 
which  the  limbs  are  deprived  of  the  influence  of  the  will,  but  are  held  in  position 
by  the  muscles  in  any  position  given  to  them  passively.  It  is  seen  chiefly  in  cer- 
tain cases  of  hysteria,  but  cataleptic  states  are  also  present  in  other  cerebral  dis- 
eases, especially  if  associated  with  general  mental  stupor,  such  as  tumors,  menin- 
gitis, etc.  (see  the  chapter  on  catalepsy). 

11.  Associated  movements  are  abnormal  movements  which  appear,  while  mak- 
ing voluntary  movements,  in  muscles  which  have  no  connection  with  the  move- 
ment willed.  Thus  in  hemiplegia  associated  movements  sometimes  take  place 
in  the  arm  when  ilie  patient  wills  to  move  the  leg  alone.  In  spinal  cases  the 
movement  of  one  leg  is  sometimes  accompanied  also  by  an  unintentional  move- 
ment of  the  other' leg.  Associated  movements  are  commonest  in  the  muscles  of 
the  same  limb.  Thus  we  often  see  in  hemiplegia  or  in  spastic  spinal  paralysis 
that  patients  can  not  flex  the  leg  up  toward  the  body  without  at  the  same  time  pro- 
ducing a  marked  dorsal  extension  of  the  foot  as  an  associated  movement.  In 
old  peripheral  facial  paralysis  (q.  v.)  we  very  often  see  associated  movements  in 
the  facial  muscles. 

Besides  the  conditions  of  motor  irritation,  other  attendant  nervous  symptoms 
often  occur  at  the  same  time.  Symptoms  of  motor  paralysis  and  irritation  are 
very  often  combined  with  each  other,  since  the  different  forms  of  spasm  may 
appear  not  only  in  groups  of  muscles  whose  motion  is  otherwise  normal,  but  also 
in  paretic  or  paralyzed  muscles.  In  general  convulsions  the  state  of  the  con- 
sciousness deserves  special  attention.  Genuine  general  epileptic  attacks  are  asso- 
ciated with  complete  loss  of  consciousness,  hysterical  attacks  are  often  associated 
with  clouding  of  consciousness,  but  in  most  of  the  other  forms  of  spasm  the  con- 
sciousness is  unaffected.  Finally,  it  is  worthy  of  mention  that  tonic  spasms  espe- 
cially are  attended  by  a  feeling  of  decided  pain,  which  is  probably  due  to  an  irrita- 
tion of  the  intra-muscular  sensory  nerves.  Such  painful  tonic  muscular  contrac- 
tions are  termed  cramps.  Among  them  are  the  well-known  painful  spasms  in  the 
calves,  etc. 

3.  Ataxia 

In  executing  all  normal  complicated  movements  we  need  the  simultaneous 
action  of  several  muscles.  Consider  the  numerous  muscles  which  must  be  put  in 
activity  in  walking,  in  grasping,  and  in  all  the  manifold  employments  of  the 
hands.  Hence,  in  order  to  perform  such  movements  correctly,  it  is  not  only 
necessary  that  all  the  muscles  concerned  should  be  innervated  by  the  will — that 
is,  that  they  be  not  paralyzed — but  that  we  should  also  be  able  so  to  modify  the 
innervation  of  each  individual  muscle  that  its  contraction  corresponds  precisely 
to  the  special  part  of  the  work  belonging  to  it.     A  prescribed  voluntary  motion 


838  DISEASES    OF   THE   NEKVOUS    SYSTEM 

can  take  place  only  when,  first,  all  the  muscles  requisite  for  it  come  into  no  less 
but  also  no  greater  action ;  second,  when  each  individual  muscle  contracts  only  so 
far  and  so  much  as  its  special  task  requires ;  and,  third,  when  the  conditions  in 
the  time  of  innervation  take  their  normal  course — that  is,  when  all  the  muscles 
involved  contract  at  the  same  time  or  in  the  proper  order  one  after  another.  A 
movement  which  is  executed  in  such  a  prescribed  manner  we  call  a  co-ordinated 
movement,  and  the  process  of  modifying-  properly  the  innervation  of  the  different 
muscles  necessary  for  a  complicated  movement  we  call  the  co-ordination  of  motion. 
We  must  especially  bear  in  mind  that  the  simultaneous  action  of  several  muscles 
is  so  far  necessary,  even  for  what  seem  to  be  the  simplest  movements,  that  muscles 
antagonistic  to  those  moved  must  also  come  into  activity.  Only  by  the  aid  of  the 
ever-ready  antagonistic  muscles  can  we  grade  our  movements  as  finely,  or  check 
or  hasten  them  as  rapidly,  as  is  demanded  for  the  execution  of  almost  all  compli- 
cated movements. 

!N"ervous  pathology  is  rich  in  facts  which  can  make  the  idea  and  the  necessity 
of  the  co-ordination  of  motion  clear  to  us.  We  often  see  disturbances  of  motility 
which  make  the  patient  incapable  of  any  fine  motor  acts,  and  yet  which  do  not 
depend  at  all  upon  any  motor  weakness  or  paralysis,  but  only  upon  a  disturbance 
in  the  co-ordination  of  motion.  Such  a  disturbance  we  call  ataxia,  and  we  speak 
of  an  ataxia  of  the  arms,  of  the  legs,  etc.,  when  the  parts  named  can  perform  all 
the  motions  and  often  even  retain  their  full  strength,  but  these  movements  show, 
usually  at  once,  a  striking,  disordered,  uncertain  "  ataxic  "  character. 

Many  theories  have  been  advanced  as  to  the  precise  cause  of  ataxia.  In  gen- 
eral, however,  there  can  be  hardly  a  doubt  that  ataxia  depends  upon  a  disturbance 
of  centripetal  influences.  We  must  suppose  that  our  movements  are  constantly 
kept  in  order  and  control  (co-ordinated)  by  centripetal  excitations  coming  from 
the  skin,  muscles,  and  joints,  although  they  are  not  all  by  any  means  consciously 
perceived.  By  such  excitations  the  child  learns  gradually  to  change  his  original 
uncontrolled  and  unregulated  movements  into  orderly  movements.  In  the  adult 
most  movements  have  already  been  so  long  practiced  as  to  be  sure  and  steady. 
The  learning  of  a  new  movement,  a  new  dexterity,  however,  takes  place  in  pre- 
cisely the  same  way.  Even  a  long-practiced  movement  (walking,  grasping) 
needs  the  constant  control  and  regulation  exerted  by  centripetal  excitations. 
If  these  controlling  influences  are  lacking  by  reason  of  any  disease  of  their 
corresponding  centripetal  tracts,  ataxia  is  the  necessary  result.  Ataxia  may  occur 
both  in  peripheral  nervous  diseases  and  also  in  diseases  of  the  spinal  cord,  cere- 
bellum, and  cerebrum.  It  is  therefore  evident  that  the  special  circumstances 
which  give  rise  to  ataxia  may  be  very  diverse.  We  will  return  to  this  point  in 
the  description  of  the  individual  diseases  which  lead  to  ataxia.  (See  especially 
the  chapters  on  tabes  dorsalis,  multiple  neuritis,  and  affections  of  the  cerebellum.) 

4.  General  Remarks  upon  testing  the  Reflexes  and  upon  the  Condition 

OF   THEM 

In  testing  the  reflexes,  which  should  never  be  omitted  in  any  case  of  nervous 
disease  on  account  of  its  frequent  great  diagnostic  importance,  we  must  distin- 
guish the  two  chief  groups  of  reflexes  from  each  other:  the  cutaneous  reflexes, 
and  the  "  tendon  reflexes." 

Cutaneous  Reflexes. — We  term  the  muscular  contractions,  excited  reflexly  by 
irritation  of  the  sensory  centripetal  cutaneous  nerves,  cutaneous  reflexes.  These 
are  usually  present  only  to  a  slight  degree  in  the  upper  extremities;  but  we  can 
sometimes  excite  reflexes  even  here  by  pricking  or  pinching  the  skin,  especially 
the  skin  of  the  fingers.  The  very  marked  reflex  in  many  people  caused  by  tickling 
the  axilla  is  well  known.  The  test  of  the  cutaneous  reflexes  in  the  lower  extrem- 
ities is  much  more  important.    The  soles  of  the  feet  are  the  most  sensitive  parts 


EEMAEKS   UPON   THE   DISTUKBANCES    OF   MOTILITY      839 

for  exciting  a  reflex,  whose  arc  lies  in  the  first  and  second  sacral  segments  of 
the  spinal  cord.  Simply  tickling  the  soles  with  the  finger  is  a  sufficient  irritation 
(the  tickling  reflex),  and  so  is  the  prick  of  a  pin  (the  prick  reflex),  or  stroking 
the  skin  hard  with  a  blunt  object,  usually  the  handle  of  a  percussion-hammer  (the 
stroking  reflex).  Thermal  irritants  are  also  very  suitable  for  exciting  a  reflex, 
especially  bits  of  ice  held  to  the  skin  (cold  reflex).  It  is  often  advisable  to  try  all 
these  methods,  since  with  diminished  reflex  irritability  a  reflex  contraction  in  the 
leg  can  often  be  excited  by  some  one  of  them,  alone.  We  should  also  examine  the 
reflex  irritability  of  the  rest  of  the  skin,  as  well  as  the  soles  of  the  feet,  by  a  pin- 
prick, by  pinching  a  fold  of  the  skin,  etc.  We  should  especially  remember  that 
in  nervous  diseases  there  is  often  a  delay  in  the  reflex,  so  that  the  reflex  contrac- 
tion appears  only  when  the  irritation  has  lasted  for  a  certain  time.  Thus  in  many 
diseases  of  the  cord,  as  we  have  often  seen,  the  reflex  follows  only  after  we  have 
kept  a  needle  sticking  into  the  skin  for  some  time  or  have  pinched  a  fold  of  skin 
continuously  for  several  (ten  or  fifteen)  seconds,  a  delay  which  has  a  connection 
with  the  fact  of  the  "  time  summation  of  reflex  irritation  "  known  from  physiol- 
ogy. The  summation  of  reflex  irritation  not  infrequently  coincides  with  the 
summation  of  irritation  from  the  sensation  of  pain  (vide  supra,  page  793),  so 
that,  after  the  irritation  has  acted  for  a  certain  length  of  time,  the  sensation 
of  pain  and  the  reflex  contraction  occur  at  the  same  time.  In  the  stroking  reflex 
(a  rapid,  vigorous  stroking  of  the  sole  of  the  foot  or  of  other  parts  of  the  skin 
with  the  handle  of  a  percussion  hammer)  we  have  a  local  summation  of  reflex 
irritation,  since  many  different  parts  of  the  skin  are  rapidly  irritated  one  after 
another.  In  the  ticlding  reflex  the  local  and  the  time  summation  of  reflex  irrita- 
tion are  united.  All  parts  of  the  skin  do  not  show  the  same  "  reflex  sensibility." 
The  reflexes  are  usually  set  free  more  readily  from  the  sole  of  the  foot  than  from 
the  skin  of  the  leg  or  thigh.  The  reflex  contraction  in  such  cases  consists  usually 
of  a  dorsal  extension  of  the  foot  and  a  coincident  flexion  of  the  knee  and  hip. 
In  the  toes,  stroking  the  sole  usually  causes  in  healthy  persons  a  flexor  reflex,  but 
in  the  paralyzed  there  is  often  a  dorsal  extension  of  the  great  toe.  After  irritat- 
ing the  skin  of  the  thigh  we  sometimes  see  reflex  contractions  in  the  extensors 
of  the  lower  leg.  The  stronger  and  more  persistent  the  irritation,  the  more  ener- 
getic and  widespread  is  the  reflex  contraction.  Where  the  reflex  irritability  is 
actively  increased,  sticking  a  needle  into  the  sole  will  often  produce  a  vigorous 
flexor  contraction  in  the  irritated  leg,  and  also  a  weaker  contraction  at  the  same 
time  in  the  other  leg. 

[The  researches  of  Babinski,  confirmed  by  many  other  obsei-vers,  have  shown 
that  dorsal  extension  of  the  great  toe,  following  stroking  of  the  sole,  is  in  adults 
a  valuable  sign  as  indicating  disturbance  of  the  central  motor  neurones,  the 
pyramidal  tract.  It  is  rarely,  if  ever,  obtained  in  health,  except  in  young  chil- 
dren, but  it  is  found  in  the  majority  of  cases  of  old  hemiplegia,  spastic  paralysis, 
etc.,  where  there  is  degeneration  of  the  pyramidal  tract,  and  it  may  occur  before 
there  is  any  notable  increase  in  the  tendon  reflexes.  The  first  response  on  irri- 
tating the  sole  of  the  foot  in  health  is  usually  a  plantar  flexion  of  the  great  or 
small  toes;  in  some  instances  there  is  only  a  contraction  of  the  tensor  vaginse 
femoris  muscle,  which  may  readily  escape  observation.  In  other  cases,  still, 
the  irritation  at  once  causes  a  sudden  withdrawal  of  the  leg.  We  rarely,  if 
ever,  fail  to  elicit  some  form  of  response,  which  is  equal  on  the  two  sides,  in 
health.— K.] 

We  must  also  mention  two  special  forms  of  cutaneous  reflex  which  are  often 
examined :  the  abdominal  reflex  and  the  cremaster  reflex.  The  abdominal  reflex 
is  best  excited  by  stroking  the  abdominal  wall  rapidly  and  with  some  force  with 
the  handle  of  a  percussion  hammer.  If  we  stroke  from  without  inward  on  the 
linea  alba,  we  can  distinguish,  according  to  the  level  of  the  irritation,  an  upper, 


840  DISEASES    OE   THE   XEEVOUS    SYSTEM 

middle,  and  lower  abdominal  reflex.  On  stroking  from  above  downward,  these 
contractions  unite.  In  bealth  tbe  abdominal  reflex  is  only  very  rarely  absent, 
chiefly  in  persons  with  a  very  lax  abdominal  wall  and  in  the  corpulent.  In  cere- 
bral hemiplegia  the  absence  of  the  reflex  on  the  paralyzed  side  is  an  important 
sign.  In  spinal  diseases  the  reflex  may  be  absent  on  one  or  both  sides,  which 
should  lead  us  to  bear  in  mind  that  the  centripetal  portion  of  the  reflex  arc  of  the 
lower  and  middle  abdominal  reflex  enters  the  spinal  cord  through  the  posterior 
roots  of  the  tenth  to  twelfth  intercostal  nerves,  and  of  the  upper  abdominal 
[epigastric]  reflex  through  the  posterior  roots  of  the  ninth  intercostal  nerve 
(Dinkier).  The  cremaster  reflex  is  a  reflex  ascent  of  the  testicle  when  the  inner 
side  of  the  thigh  is  forcibly  stroked  or  when  sudden  deep  pressure  is  exerted  by 
the  hand  a  hand's  breadth  above  the  internal  condyle.  This  reflex  is  almost 
always  present  in  healthy  boys  and  men,  although  in  varying  strength.  We 
must  take  care  not  to  confuse  the  cremaster  reflex  with  the  contraction  of  the 
dartos.  The  clinical  significance  of  the  cremaster  reflex  is  similar  to  that  of  the 
abdominal  reflex.  The  reflex  arc  of  the  cremaster  reflex  is  at  the  level  of  the 
first  and  second  lumbar  nerves.  Other  cutaneous  reflexes — the  gluteal,  the  mam.- 
millary,  etc. — have  at  present  no  special  practical  significance. 

Tendon  Reflexes. — Of  almost  greater  practical  importance  than  the  investiga- 
tion of  the  cutaneous  reflexes  is  the  test  of  the  phenomena  classed  under  the 
name  of  the  "  tendon  reflexes,"  and  first  carefully  investigated  and  described  by 
Erb  and  Westphal  in  the  year  1875.  "We  understand  by  these  those  muscular  con- 
tractions which  arise  from  the  brief  mechanical  irritation  of  the  tendons  and 
analogous  parts,  such  as  the  periosteum  and  fasciae.  Westphal  originally  held 
that  these  contractions  were  the  result  of  direct  mechanical  irritation,  but  later 
accurate  clinical  and  experimental  work  has  shown  that  the  "  tendon  reflexes,"  as 
Erb  had  maintained  from  the  beginning,  are  true  reflex  phenomena,  starting 
from  the  mechanical  irritation  of  the  sensory  nerves  in  the  tendons,  periosteum, 
etc.  The  tendon  reflex  of  most  practical  importance  is  the  patellar  reflex,  "  knee 
phenomenon"  (Westphal)  [or  "knee-jerk"  (Mitchell)] — that  is,  a  contraction 
occurring  in  the  quadriceps  after  mechanical  irritation  of  the  ligamentum  patellae 
by  a  quick  blow  with  a  percussion  hammer.  In  order  to  evoke  this  reflex  it  is 
especially  necessary  for  the  person  examined  to  avoid  all  active  muscular  tension 
in  the  leg,  especially  in  the  extensor.  If  we  examine  patients  who  are  not  in  bed, 
we  can  test  the  patellar  reflex  by  making  the  patient  while  sitting  cross  the  leg 
to  be  tested  over  the  other,  and  by  striking  the  patellar  tendon  as  the  leg  hangs 
loose ;  but  it  seems  to  us  more  convenient  to  direct  the  patient  to  extend  the  leg 
until  it  forms  an  obtuse  angle  with  the  thigh  with  the  opening  of  the  angle  below. 
If  the  sole  be  set  fully  on  the  floor  the  extensor  cruris  is  made  tense  in  this  posi- 
tion, and  we  can  very  easily  and  plainly  excite  the  contraction  of  the  quadriceps 
by  striking  the  patellar  tendon.  When  the  patient  is  in  bed  it  is  best  to  raise  the 
leg  to  be  tested  into  a  semi-flexed  position  by  putting  the  left  hand  under  the 
hollow  of  the  knee;  the  foot  remains  lying  on  the  bed,  and  the  patient  should 
avoid  any  active  muscular  tension.  If  the  patellar  reflex  be  weak  and  hard  to 
detect,  we  should  try  the  proceeding  advised  by  Jendrassik,  which  consists  in 
testing  the  reflex  while  the  patient  grips  the  two  hands  together,  and  tries  with 
all  his  strength  to  pull  them  apart.  By  this  or  any  other  vigorous  tension  of  the 
muscles  of  the  upper  extremities  the  muscles  of  the  legs  are  probably  greatly  re- 
laxed, while  any  voluntary  innervation  is  avoided,  and  thus  is  explained  the  in- 
crease of  the  reflex,  which  is  often  pronounced.  If  by  the  help  of  this  "  Jendras- 
sik's  test "  no  reflex  is  to  be  elicited,  we  may  regard  it  as  absent,  a  condition 
which  is  almost  always  of  pathological  significance,  since  complete  absence  of  the 
patellar  reflex  practically  never  occurs  in  health.  The  reflex  arc  in  the  cord  for 
the  patellar  reflex  is  found  in  the  second  lumbar  segment. 


EEMAEKS   UPON   THE   DISTUEBA:NtCES    OF   MOTILITY      811 

The  second  important  tendon  reflex  to  be  provoked  in  the  lower  extremity  is 
the  Achilles  tendon  reflex.  If  we  give  to  the  foot  of  the  person  examined  (who 
should  lie  on  his  side  in  bed)  a  passive  position  of  slight  dorsal  extension,  so  that 
the  tendo  Achillis  is  a  little  tense,  and  then  strike  the  tendon  a  quick  blow,  a 
marked  contraction  of  the  gastrocnemius  follows.  Precisely  the  same  reflex  is 
usually  to  be  elicited  by  striking  the  plantar  fascia.  The  Achilles  tendon  reflex  is 
not  quite  so  constant  in  healthy  persons  as  the  patellar  reflex,  but  it  is  usually 
present  and  well  marked.  Its  reflex  arc  in  the  cord  lies  at  the  level  of  the  third 
to  the  fifth  sacral  segments.  Where  the  tendon  reflexes  are  abnormally  increased, 
however,  the  Achilles  tendon  reflex  is  very  vigorous,  and  then  we  can  very  often 
produce  it  in  the  following  especially  characteristic  manner.  If  we  make  a  sud- 
den, short,  vigorous,  passive,  dorsal  extension  of  the  foot,  the  tendo  Achillis  is 
suddenly  made  tense,  and  thus  is  irritated  mechanically.  As  a  result  of  this, 
there  is  a  reflex  plantar  flexion  of  the  foot.  If  now,  by  persistent  passive  dorsal 
extension  of  the  foot,  the  tendo  Achillis  is  again  made  tense,  there  follow  by 
turns  new  plantar  and  dorsal  movements  of  the  foot,  so  that  the  foot  is  thus 
put  into  a  vigorous  tremor.  This  symptom,  which  can  only  exceptionally  be  pro- 
voked in  healthy  persons,  is  termed  ankle  clonus  (foot  clonus),  or  "  foot  phenom- 
enon "  (Westphal).  Where  there  is  a  very  great  increase  of  the  tendon  reflexes 
the  tremor  is  sometimes  not  confined  to  the  foot,  but  the  whole  leg  falls  into  a 
vigorous  clonus,  a  symptom  which  was  once  given  the  unsuitable  name  of  spinal 
epilepsy,  since  it  apparently  came  on  spontaneously  as  a  result  of  some  tension  of 
the  tendons.  We  can  also  obtain  the  patellar  reflex  in  the  form  of  a  clonus  if  we 
pull  the  patella  firmly  down  with  the  finger  and  force  it  downward  by  a  sudden 
blow  on  the  finger. 

The  two  symptoms  described — the  patellar  reflex,  and  the  Achilles  tendon  re- 
flex or  foot  phenomenon — are  practically  the  most  important,  and  are  the  most 
often  tested,  but  they  are  by  no  means  the  only  reflexes  in  the  lower  extremity. 
Besides  the  reflexes  from  the  special  tendons,  we  also  frequently  obtain  muscular 
contractions  by  striking  the  periosteum  and  the  fascise,  which  have  been  termed 
the  periosteal  and  fascia  reflexes.  Thus  a  contraction  in  the  quadriceps  often 
follows  a  blow  on  the  anterior  surface  of  the  tibia  when  the  reflex  excitability  is 
increased.  We  also  see  contractions  frequently  in  the  adductors  of  the  thigh  on 
striking  the  internal  condyle  of  the  femur,  contractions  in  the  muscles  of  the 
posterior  aspect  of  the  thigh  in  striking  the  calves,  etc. 

Under  normal  conditions  the  tendon  reflexes  in  the  upper  extremities  are 
sometimes  quite  weak  or  entirely  absent,  but  where  the  irritability  is  abnormally 
increased  we  see  even  here  the  most  various  and  vigorous  reflexes.  The  most 
important  and  most  constant  are  the  periosteal  reflexes,  from  striking  on  the 
lower  end  of  the  radius  and  ulna.  As  a  rule,  in  our  observations,  we  have  usually 
obtained  a  contraction  in  the  supinator  longus  and  biceps  from  a  blow  on  the 
head  of  the  radius,  and  a  weaker  contraction  in  the  same  muscles  from  the  head 
of  the  ulna,  and  also,  very  frequently,  pronation  of  the  forearm  and  flexion  of  the 
wrist  and  fingers.  The  deltoid  also  contracts  not  infrequently  from  a  blow  on  the 
lower  end  of  the  ulna.  Direct  tendon  reflexes  in  the  biceps  and  triceps  on  strik- 
ing their  own  tendons  are  also  almost  always  to  be  obtained.  [The  triceps  reflex 
seems  the  most  constant  of  all  the  reflexes  of  the  upper  extremity. — ^K.]  We  may 
also  not  infrequently  obtain  a  contraction  in  the  biceps  by  a  blow  on  the  clavicle. 
A  persistent  clonus  in  the  hand  upon  passive  volar  flexion  sometimes  occurs,  but  it 
is  rare. 

A  more  detailed  account  of  the  behavior  of  the  cutaneous  and  tendon  reflexes 
in  the  individual  diseases  of  the  nervous  system  will  be  given  later  in  the  special 
chapters,  where  we  shall  also  learn  the  present  theories  as  to  the  course  of  the 
reflex  tracts  and  the  influence  of  other  nerve  tracts  upon  them. 


842  DISEASES    OF   THE   NEEVOUS    SYSTEM 

Mechanical  Muscular  Irritability  and  Paradoxical  Contraction. — "Direct 
mechanical  irritability  of  the  muscles  "  is  shown  by  the  occurrence  of  energetic 
brief  contractions  of  single  muscular  bundles  or  of  the  whole  muscle  from  a  direct 
blow  on  the  belly  of  the  muscle  with  a  percussion  hammer.  In  such  cases,  how- 
ever, we  are  dealing,  in  my  opinion,  not  with  a  direct  muscular  irritation,  but  with 
a  mechanical  irritation  of  the  nerves  which  enter  the  muscle,  since  the  muscular 
contractions  are  always  strongest  when  we  strike  the  corresponding  point  of 
entrance  of  the  nerves,  precisely  the  same  as  faradic  irritation  of  the  muscle. 
The  ensuing  muscular  contraction,  however,  may  sometimes  be  a  reflex,  evoked 
by  mechanical  irritation  of  the  fascia  stretched  over  the  muscle.  These  contrac- 
tions just  described  are  to  be  distinguished  from  the  so-called  idiomuscular  con- 
tractions. We  see  these  most  plainly  if  we  give  a  vigorous  blow  with  the  ulnar 
side  of  the  hand  or  with  a  percussion  hammer  to  the  belly  of  a  muscle,  such  as  the 
biceps.  A  small  transverse,  circumscribed  muscular  swelling  forms  at  the  point 
struck,  and  gradually  disappears  again.  The  test  for  mechanical  muscular  irrita- 
bility has  not  yet  attained  any  special  practical  importance, 

"  Paradoxical  contraction  "  is  the  name  which  Westphal  has  given  to  a  sjTnp- 
tom  seen  especially  in  the  tibialis  anticus,  and  rarely  also  in  the  flexors  of  the  leg 
and  forearm.  It  is  when  the  foot,  after  being  put  in  passive  dorsal  extension,  re- 
mains in  this  position  even  after  the  expiration  of  a  considerable  time  (several 
minutes),  and  a  marked  prominence  of  the  tendon  of  the  tibialis  anticus  is  usu- 
ally visible.  We  can  not  at  the  present  time  give  a  definite  explanation  of  this 
phenomenon,  which  so  far  has  been  observed  in  various  spinal  and  cerebral  dis- 
eases, multiple  sclerosis,  paralysis  agitans,  etc. 

5.  General  Remarks  upon  the  Changes  of  Electrical  Excitability  in 
THE  Motor  Nerves  and  Muscles* 

Electricity,  since  the  investigations  of  Duchenne,  Eemak,  Benedikt,  Moritz 
Meyer,  von  Ziemssen,  Brenner,  Erb,  and  others,  has  become  not  only  one  of  the 
most  prominent  therapeutic  aids  in  the  treatment  of  nervous  diseases,  but  it  also 
plays  an  extremely  important  part  in  the  examination  of  nervous  patients,  since 
the  test  of  the  electrical  excitability  of  diseased  nerves  and  muscles  gives  us  a 
large  amount  of  valuable  information  in  regard  to  diagnosis  and  prognosis. 

Every  complete  electrical  examination  must  be  made  with  both  currents — the 
faradic  or  induction  current  (usually  the  secondary  current),  and  the  galvanic  or 
constant  current.  One  "  indifferent "  pole  is  usually  put  on  the  sternum  or  the 
back  of  the  neck,  and  the  other  "  testing "  pole  on  the  nerve  or  muscle  to  be 
tested.  For  the  indifferent  pole  we  use  a  large  electrode  (about  twelve  centi- 
metres long),  and  as  a  testing  pole  a  smaller  electrode,  the  best  being  Erb's 
"  normal  electrode,"  with  a  surface  of  ten  sqxiare  centimetres.  The  excitement 
of  the  muscle  from  the  nerve  is  called  indirect;  the  excitement  from  placing 
the  electrode  on  the  muscle  itself  (where,  of  course,  the  excitement  of  the  intra- 
muscular nerves  can  not  be  excluded)  is  called  direct.  Those  points  on  the  human 
body  where  the  different  nerves  and  muscles  are  most  easily  accessible  to  the  elec- 
trical excitement  are  to  be  found  in  Figs.  99  to  104,  taken  from  Erb's  handbook. 

In  faradic  examination  the  nonnal  condition  is  that  we  can  provoke  marked 
muscular  contractions  both  from  the  nerves  and  from  direct  excitement  of  the 
muscles  at  the  points  generally  accessible  to  excitement.  As  von  Ziemssen  has 
found,  the  points  at  which  the  muscle  can  most  easily  be  made  to  contract  by 

*  In  regard  to  all  the  details  of  electrical  diagnosis  and  electro-therapeutics  we  would  refer  to  Erb's 
"  Handbuch  der  Elektrotherapie."  Leipsic,  Vogel,  1886.  [Translated  by  De  Watteville.  New  York  : 
Wni.  Wood  &  Co.,  1887.]  E.  Remak's  "  Grundriss  der  Elektrodiagnostik  und  Elektrotherapie." 
Vienna,  1895,  etc. 


KEMAEKS   UPON   THE   DISTUEBANCES    OF   MOTILITY      843 

"  direct "  excitement  correspond  exactly  to  the  points  where  the  motor  nerves 
enter  the  muscle.  The  direct  faradic  muscular  excitation  is  therefore  always  a 
nerve  excitation.  In  order  to  determine  the  excitability  quantitatively  we  meas- 
ure the  distance  between  the  two  coils  of  the  induction  apparatus  (coil  distance. 


IiYontalis 

Facial 
{upper  branch) 

Corrugator  supercilii 


Orbicul.  palpebrarum 
Nasal  muscles.  < 

Zygomatic! 
Orbicularis  oris. 
Facial  {middle  br^ch), 
Masseter, 

Levator  menti. 

Quadratus  menti. 

Triangularis  menti. 

Hypoglossux. 

Facial  (lower  branch). 

Platysma  myoides, 
Hyoid  muscles. 


Omo-hyoid 


Anterior  thoracic 
(Pectoralis  major). 


Region  of  the  central 
convolutions. 


Region  of   the    third 
frontal  convolution 
and  the  insula 
(speech  center;. 

TemporaUs. 

Facial  (upper)  in 
front  of  ear. 

Facial  (trunk). 
Posterior  auricular. 
Facial  (middle  br^ch). 
i'acial  (loioer  branch). 
Splenius. 

Sterno-cleido-mastoid . 

Spinal  accessory. 
Levator  anguli 
scapulae.    ■ 

Trapezius. 
Dorsalis  scapulae. 

Axillary  (circumflex). 

Long  thoracic  (serra- 
tus  magnus;. 


Phrenic.        Supraclavicular  p)oint. 
(Erb's  point.     Deltoid, 
biceps,  bracbialis  anticus, 
and  supinator  longus.) 

Fig.  99. 


Brachial  plexus. 


Rollendbstand)  at  which  the  first  minimal  contraction  of  the  muscle  occurs.  On 
increasing  the  current,  the  minimal  contraction  gradually  passes  into  a  vigorous 
tetanic  contraction  of  the  muscles. 

Galvanic  examination  is  performed  by  the  aid  of  a  "current  reverser,"  by 
which  the  current  at  any  desired  strength  can  be  rapidly  opened  and  closed  and 
the  testing  pole  can  be  made  either  the  negative  pole  (the  cathode  or  zinc  pole) 
or  the  positive  pole  (the  anode  or  copper  or  carbon  pole). 

The  nerves  and  muscles  are  excited  not  by  the  continuous  flow  of  the  elec- 
trical current,  but  only  by  its  variations  and  the  sudden  opening  and  closing  of 
the  current. 

By  the  help  of  this  "  polar  method  of  investigation  "  (Brenner)  we  can  easily 
determine  the  law  of  contraction,  which  holds  equally  for  the  normal  motor  nerves 
and  for  the  muscles. 

With  a  very  weak  current  no  noticeable  excitement  takes  place.  If  we  grad- 
ually increase  the  strength  of  the  current,  the  first  weak  contraction  of  the  muscle 
occurs  at  the  closure  of  the  cathode — that  is,  when  the  current  is  closed  so  that 
the  cathode  is  made  the  testing  pole.  On  opening  the  cathode,  or  on  closing  or 
opening  the  anode,  nothing  follows.  If  we  increase  the  strength  of  the  current 
still  more,  the  cathodic  closure  contractions  become  stronger,  and  the  anodic 


8M 


DISEASES    OF   THE   NEEVOUS    SYSTEM 


closure  and  anodic  opening  contractions  appear,  now  the  one  being  earlier  and 
stronger,  and  now  the  other.  Opening  of  the  cathode  has  still  no  effect.  Only 
with  a  very  strong  current,  in  which  the  cathodic  closure  contractions  have 
already  become  tetanic — that  is,  they  still  persist  after  the  closure  of  the  current 
— can  we  provoke  weak  cathodic  opening  contractions.    Expressed  in  the  abbrevia- 


Triceps  (long  head). 

Triceps  (internal  head). 
Ulnar. 


Flexor  carpi  ulnaris. 
Flexor  profundus  digitorum. 


Flexor  sublimis  digitorum 
(II  and  III). 


Flexor  sublimis  digitorum 
a  and  IV). 

Ulnar. 

Palmaris  brevis. 

Abductor  minimi  digiti. 

Flexor  brevis  minimi  digiti. 

Opponens  minimi  digiti. 

Lumbricales. 


Deltoid  (anterior 
hair). 


Musculo-cutaneous 
Biceps. 
Brachialis  anticus. 


Supinator  longus. 
Pronator  radii  teres. 
Flexor  carpi  radialis. 


Flexor  sublimis  digitorum. 

Flexor  longus  poUicis. 
Median. 

Abductor  pollicis. 
Opponens  pollicis. 

Flexor  brevis  pollicis. 
Adductor  pollicis. 


Fig.  100. 

tions  now  in  general  use  in  electrical  diagnosis,  the  law  of  contraction  for  normal 
muscles  and  nerves  in  man  is  as  follows  :  " 

*  Ka  signifies  cathode,  An  =  anode,  S  =  closure,  0  =  opening,  z  (Zuckung)  =  weak  contraction, 
Z  =  stronger  contraction,  Te  =  tetanus.  Sometimes  the  increasing  strength  of  the  contractions  is 
abbreviated  by  the  signs  Z,  Z'  and  Z".    [Many  English  and  American  writers  on  electricity  use  letters 


REMAEKS   UPON   THE   DISTURBANCES    OF   MOTILITY      845 

1.  Lowest  degree  with  weak  currents  :  KaSz,  KaO — ,  AnS — ,  AnO — . 

2.  Middle  degree  with  .stronger  currents:  KaSZ,  KaO — ,  AnSz,  AnOz. 

3.  Highest  degree  with  very  strong  currents :  KaSTe,  KaOz,  AnSZ,  AnOZ. 

The  variations  from  the  normal  state  seen  under  pathological  conditions  con- 
sist of  quantitative  and  also  of  qualitative  changes  in  the  law  of  contraction.  We 
term  the  simple  increase  or  diminution  of  the  electrical  excitability  in  nerves  or 
muscles,  without  simultaneous  ehaiiges  in  the  quality  and  order  of  the  occurrence 
of  muscular  contractions,  quantitative  changes.  The  discovery  of  increased  or 
diminished  excitability  of  nerve  and  muscle  can  be  made  most  easily  in  unilateral 
diseases,  where  we  can  compare  the  strengths  of  current  required  to  obtain  the 
minimal  contraction  on  the  diseased  and  healthy  sides  with  each  other.  This  is 
now  determined  without  any  special  difficulty,  since  the  general  introduction  of 


Deltoid  (posterior  half). 


Radial  imusculo-spiral). 
Brachialis  anticvis. 

Supinator  longus. 
Extensor  carpi  radialis  longior. 
Extensor  carpi  radialis  brevior. . 


Extensor  communis  digitorum. 
Extensor  indicis. 

Extensor  ossis  metacarpi  pollicis. 
Extensor  primi  internodii  pollicis. 


Dorsal  interossei,  I  and  II. 


Triceps  (long  head). 


Triceps  (external  head). 


Extensor  carpi  ulnaris. 
Supinator  brevis. 

Exteiisor  minimi  digiti. 
-Extensor  indicis. 


Extensor  secundi  internodii 
pollicis. 


-Abductor  minimi  digiti. 

*  Dorsal  interossei, 
C      III  and  IV. 


Fig.  101. 


the  absolute  galvanometer.    With  the  galvanometer  thrown  out  of  circuit  we  find 
with  how  many  cells  or  at  what  position  of  the  rheostat  the  first  distinct  cathodic 


derived  from  the  English  names.  Thus  C  stands  for  catliode,  closure,  and  contraction.  A  and  0  have 
the  same  meaning.  It  seems  to  us  clearer  and  conducive  to  greater  harmony  to  retain  the  German 
abbreviations,  which  are  simple  and  definite. — Trans.] 


846 


DISEASES    OF   THE   KEEYOTIS    SYSTEM 


closure  contraction  (KaSZ)  occurs.    Then  the  galvanometer  is  put  into  the  cir- 
cuit and  the  strength  of  the  current  in  milliamperes  is  read  off  directly.     By 


Crural. 


Pectineus. 

Adductor  magnus. 

Adductor  longus. 


V  Tensor  vaginae  femoris. 

Sartorius. 
Ift Am — Quadriceps  femoris  (common  point). 

Rectus  femoris. 
Vastus  externus. 


Vastus  internus. 


Fig.  102. 

extensive  investigations  on  healthy  persons  Stintzing  has  found  certain  limits 
within  which  the  normal  excitability  of  the  different  nerves  varies.  Deviations 
from  these  figures  above  or  below  normal  accordingly  permit  us  to  recognize  an 
increase  or  a  diminution  of  the  galvanic  excitability.  It  is  to  be  borne  in  mind 
that  Stintzing  uses  a  small  "  normal  electrode  "  with  a  surface  of  three  square 
centimetres.  Some  of  the  most  important  averages  found  by  Stintzing  are  shown 
in  the  following  table : 

Facial  nerve 1.0-2.5  milliamperes. 

Accessory  nerve 0.1-0.4  " 

Ulnar  nerve 0.2-0.9  " 

Median  nerve 0.3-1.5  " 

Eadial  nerve 0.9-2.7  " 

Crural  nerve 0.4-1.7  " 

Peroneal  nerve 0.2-2.0  " 

Tibial   nerve 0.4-2.0  " 

An  accurate  measurement  of  the  absolute  strength  of  the  faradic  current  is 
possible,  but  it  has  as  yet  been  but  little  introduced  into  practice.  We  usually 
content  ourselves,  as  we  have  said,  with  the  statement  of  the  coil  distance  at 
which  the  first  perceptible  contraction  occurs.  Stintzing  found  as  an  average 
position  for  the  frontal  nerve,  128.5  millimetres  ;  for  the  accessory  nerve,  137  milli- 
metres ;  for  the  radial  nerve,  105  millimetres ;  for  the  median  nerve,  122.5  milli- 


EEMAEKS   UPON   THE   DISTUHBANCES    OF   MOTILITY      847 

metres;  for  the  ulnar  nerve,  130  millimetres;  for  the  crural  nerve,  111.5  milli- 
metres; for  the  peroneal  nerve,  115  millimetres;  and  for  the  tibial  nerve,  107.5 
millimetres.    We  must  refer  to  the  special  works  for  further  details. 

Changes  in  the  quantitative  electrical  excitability  are  not  txncommon  in  patho- 
logical conditions,  but  they  have  no  very  great  practical  diagnostic  significance. 
A  pathological  increase  of  electrical  excitability  is  seen  especially  in  tetany,  a 
diminution  in  many  cases  of  neuritis,  and  sometimes  also  in  myelitis,  pressure 
paralyses,  etc.  The  apparent  diminution  of  excitability  is  often  due  only  to 
increased  resistance  (dry,  thick  skin,  thick  layer  of  fat,  etc.). 

Much  more  important,  however,  than  the  simple  quantitative  changes  of  elec- 
trical excitability  are  those  not  merely  quantitative  but  also  qualitative  devia- 


Sciatic. 

Biceps  femoris  (long  head). 
Biceps  femoris  (short  head). 


Peroneal. 


Gastrocnemius  (external  head) 


Soleus. 


Flexor  longua  hallucis 


Y  Gluteus  maximus. 


Adductor  magnus. 

Semitendinosus. 

Semimembranosus. 


1 Posterior  tibial. 


Gastrocnemius  (internal  head). 


Soleus. 


Flexor  longus  digitorum. 


Tibial. 


Fig.  103. 


tions  from  the  nonnal  law  of  contraction,  which  were  first  discovered  in  certain 
forms  of  paralysis  by  Baierlacher  in  1859,  and  were  soon  generally  confirmed. 
Erb  has  given  these  the  name  of  the  "  reaction  of  degeneration,"  because  they  are 
closely  connected  with  the  progress  of  certain  anatomical  changes  in  the  para- 
lyzed muscles  and  nerves. 

In  order  to  make  the  relations  of  the  reaction  of  degeneration  clear,  let  us 
select  as  an  example  any  fresh  peripheral  paralysis  and  follow  the  changes  in 
excitability  to  the  two  currents  in  the  nerves  and  muscles.    In  a  short  time  (two 


848 


DISEASES    OE   THE   ^sTeeYOUS    SYSTEM 


or  three  days)  after  tlie  onset  of  the  paralysis  a  gradually  increasing  decline  in 
the  faradic  and  galvanic  excitability  in  the  nerve  begins.  After  one  or  two 
weeks  the  excitability  is  completely  lost,  so  that  from  the  nerve  we  can  no  longer 
provoke  any  trace  of  muscular  contraction  with  the  strongest  faradic  or  con- 
stant current.  During  this  time  the  excitability  of  the  paralyzed  muscles  to 
the  faradic  current  has  also  rapidly  diminished,  and  finally  has  wholly  disap- 
peared. The  case  is  quite  different  with  galvanic  excitement  of  the  muscles. 
Here  we  find  at  first  a  slight  diminution,  which  in  the  second  week  passes  to  a 
decided  increase  of  the  galvanic  muscular  excitability.  We  now  obtain  marked 
muscular  contractions  with  relatively  very  weak  currents.  Besides  that,  two 
other  very  important  peculiarities  are  to  be  noted :  1.  The  muscular  contractions 
are  first  of  all  not  short  and  lightning-like,  as  under  normal  conditions,  but  they 


Tibialis  anticus. 
Extensor  longus  digitorum. 


Peroneus  brevis. 


Extensor  proprius  pollicis. 


Peroneal. 


^    e-\ —  Gastrocnemius  (external). 
\ —  Peroneus  longus. 


Dorsal  interossei. 


Soleus. 


«_  -i- — Flexor  longus  hallucis. 


Extensor  brevis  digitorum. 
Abductor  minimi  digiti. 


Fig.  104. 

seem  quite  sluggish,  protracted,  "  worm-like,"  and  often  persist  during  the  whole 
duration  of  the  closure  of  the  current.  2.  The  muscular  contractions  occur  not 
only  chiefly  at  cathodic  closure  (KaS),  as  under  normal  conditions,  but  the  anodic 
closure  contractions  (AnSZ)  are  as  strong  as  the  cathodic  closure  contractions 
(KaSZ),  or  even  plainly  exceed  them.  With  stronger  currents  anodic  closure 
tetanus  (AnSTe)  is  readily  obtained.  The  cathodic  opening  contraction  (KaOZ) 
is  also  frequently  stronger.  3.  It  may  finally  be  mentioned  here  that  the  mechan- 
ical irritability  of  the  muscles  in  such  cases  is  usually  increased,  and  the  muscles 
when  struck  also  show  a  slow,  worm-like  contraction. 

This  second  degree  of  the  reaction  of  degeneration  lasts  from  four  to  eight 
weeks.  If  the  paralysis  be  severe  and  long  continued,  or  incurable,  at  the  end  of 
this  period  comes  a  decline  of  the  galvanic  muscular  excitability.     The  contrac- 


EEMARKS   UPON   THE   DISTURBANCES    OF   MOTILITY      849 

tions  become  weaker,  the  strength  of  current  necessary  to  produce  them  greater, 
and,  finally,  in  incurable  cases,  even  with  the  strongest  currents,  we  can  obtain 
only  a  little  slow  anodic  closure  contraction  (AnSZ),  or  none  at  all.  It  is  difier- 
ent,  however,  in  the  milder,  curable  cases.  In  these  the  passage  to  the  normal  con- 
dition gradually  follows  either  the  increase  of  the  galvanic  muscular  excitability, 
or,  in  more  protracted  cases,  its  secondary  decline.  The  contractions  become  more 
vigorous  and  shorter,  the  cathodic  closure  contraction  (KaSZ)  again  pre- 
dominates, the  faradic  muscular  excitability  and  the  faradic  and  galvanic  excita- 
bility of  the  nerves  finally  return,  and  with  them  the  old  normal  conditions  are 
restored.  A  fact  to  be  observed  in  these  cases  is  of  great  interest,  namely,  that 
the  voluntary  motion  in  such  cases  often  returns  decidedly  earlier  than  the  elec- 
trical excitability  of  the  peripheral  nerves.  We  see,  then,  that  a  diseased  nerve 
may  be  capable  of  conducting  excitations  coming  from  the  brain,  while  the  taking 
up  of  excitation,  its  direct  excitability,  is  still  completely  lost.  In  such  cases  we 
can  obtain  a  muscular  contraction  by  electrical  excitation  of  the  nerve  above  the 
point  of  lesion. 

Besides  the  complete  reaction  of  degeneration  just  described,  there  is  also  a  so- 
called  partial  reaction  of  degeneration,  which  is  not  infrequent  in  milder  cases. 
This  may  show  itself  in  several  forms,  but  it  is  chiefly  when  the  diminution 
of  the  faradic  and  galvanic  excitability  in  the  nerves  and  the  diminution  of 
faradic  excitability  in  the  muscles  is  only  of  a  slight  degree,  while  the  character- 
istic changes  in  the  direct  galvanic  excitement  of  the  muscles — ready  appearance 
of  anodic  closure  contractions  (AnSZ),  and  especially  the  noticeably  slow  charac- 
ter of  the  ensuing  muscular  contractions — are  fully  developed.  In  general  the 
slow  muscular  contraction  on  direct  galvanic  irritation  of  the  muscles  is  practi- 
cally the  most  important  symptom  of  reaction  of  degeneration.  We  sometimes 
see  the  occurrence  of  slow  contractions  on  faradic  excitement  of  nerves  and  mus- 
cles— "  faradic  reaction  of  degeneration,"  and  in  some  cases  we  even  see  slow 
muscular  contractions  on  indirect  galvanic  irritation  of  the  nerve  (partial  reac- 
tion of  degeneration  with  indirect  slowness  of  contraction).  In  the  course  of 
atrophic  paralyses  we  often  see  that  the  different  varieties  of  reaction  of  degen- 
eration pass  into  one  another  as  the  process  advances  or  improves  (Stintzing). 

Anatomical  Changes  of  the  Nerves  and  Muscles  in  the  Reaction  of  Degen- 
eration; its  Significance  in  Diagnosis  and  Prognosis. — As  we  have  previously 
seen,  all  paralyses  may  be  divided  into  two  great  groups — into  atrophic  paralyses, 
and  paralyses  without  marked  atrophy  of  the  affected  muscles.  We  have  learned 
to  recognize  the  necessary  hypothesis  of  the  "  trophic  "  influence  of  the  ganglion- 
cells  in  the  anterior  comua  of  the  spinal  cord  as  the  foundation  of  this  distinction, 
an  influence  which  is  easily  to  be  understood  when  we  consider  that  ganglion-cell 
and  peripheral  motor  nerve-fiber  form  an  anatomical  unit  with  which  the  muscu- 
lar fiber  is  directly  connected  as  a  terminal  organ.  In  all  cases  where  the  disease 
affects  these  ganglion-cells,  or  is  situated  in  the  peripheral  nerves,  so  that  the 
trophic  influence  of  the  ganglion-cells  on  the  muscles  can  no  longer  be  of  influ- 
ence, we  have  a  degenerative  atrophy  of  the  peripheral  portion  of  the  nerve,  and 
also  a  relatively  rapid  atrophy  of  the  muscle  belonging  to  it.  This  secondary  de- 
generation of  the  peripheral  nerves  and  the  consequent  atrophy  of  the  muscles 
are  the  anatomical  causes  of  the  phenomena  of  electrical  reaction  of  degeneration. 

If  we  have  to  do  with  a  peripheral  paralysis,  such  as  a  traumatic  lesion  of  a 
nerve-trunk,  the  portion  of  the  nerve  peripheral  to  the  point  of  lesion  is  separated 
from  its  cell  of  origin  in  the  cord,  and  begins  to  undergo  secondary  degeneratioji. 
The  first  anatomical  sign  of  the  degeneration  is  a  breaking  dovni  of  the  medullary 
sheath  at  first  into  large  and  gradually  into  smaller  flakes  and  drops.  The  axis 
cylinder  is  also  soon  destroyed,  so  that  the  sheath  of  Schwann  finally  incloses  only 
approximately  homogeneous  fluid  contents,  which  are  in  great  part  rapidly  ab- 
54 


850  DISEASES    OF   THE   NERVOUS    SYSTEM 

sorbed.  At  the  same  time  there  is  an  increase  of  the  nuclei  in  the  sheath  of 
Schwann,  and  this  increase,  v/hen  the  process  is  long  continued,  leads  to  a  de- 
cided increase  of  the  interstitial  connective  tissue  in  the  nerve.  The  diminution 
and  final  loss  of  electrical  irritability  in  the  nerve  are  perfectly  parallel  to  these 
anatomical  changes,  for  we  can  readily  understand  that  such  a  completely  de- 
stroyed nerve  can  be  excited  neither  by  the  f  aradic  nor  by  the  galvanic  current. 

The  degeneration  of  the  nerve  involves  its  finest  terminal  branches  in  the 
muscles ;  but  the  muscle  itself,  as  we  have  said,  does  not  remain  unchanged.  The 
muscular  fibers  undergo  a  marked  atrophy.  They  become  much  smaller,  their 
transverse  striation  may  be  preserved  for  a  long  time,  but  it  often  becomes  some- 
what less  distinct.  Some  muscular  fibers  show  a  peculiar  yellow  homogeneous 
consistency  which  is  called  "  waxy  degeneration."  Fatty  or  marked  granular  de- 
generation of  the  fibers  occurs  only  in  the  later  stages.  The  motor  end-plates  of 
the  nerves  in  the  muscles  are  spared  for  a  comparatively  long  time,  and  they  dis- 
appear only  when  the  degeneration  of  the  muscles  has  reached  the  highest  degree. 
There  is  also  a  considerable  increase  in  the  muscle  nuclei  and  in  the  later  stages 
a  considerable  new  formation  of  interstitial  connective  tissue,  often  associated 
with  an  abundant  deposit  of  fat.  Muscles  thus  altered  react  only  to  the  galvanic 
current  and  in  the  slow  manner  described  above.  We  recognize  from  this  that 
the  muscle  deprived  of  its  nerve  still  retains  a  certain  trophic  independence.  The 
slow  galvanic  contraction  is  the  expression  of  the  purely  muscular  irritability 
which  is  still  retained  by  itself  in  the  muscle  deprived  of  its  nerve  and  conse- 
quently atrophied,  while  the  faradic  irritability  is  lost  because  the  f aradic  irrita- 
tion of  the  muscle  can  be  accomplished  only  by  means  of  the  terminal  branches  of 
the  nerve  in  the  muscle. 

In  the  incurable  cases  the  processes  of  degeneration  just  described  gradually 
advance,  but,  in  the  cases  that  recover,  a  number  of  processes  of  regeneration 
begin  sooner  or  later.  We  can  not  here  go  into  the  finer  details.  We  would  men- 
tion merely  that  the  "  regeneration  "  in  all  probability  takes  place  only  from  the 
central  nerve-stump;  that  it  consists,  therefore,  essentially  of  a  new  outgrowth 
from  the  maimed  neurones.  The  old  nerve-sheaths  of  the  cut-off  or  degenerated 
peripheral  portion  serve  as  conduction  tubes.  The  axis  cylinders  grow  out  first, 
and  then  new  medullary  sheaths  are  formed.  The  end-plates  of  the  nerves  are 
restored  very  early,  according  to  Gessler,  even  before  the  nerve-fibers.  The  mus- 
cular fibers  also  increase  in  volume  at  the  same  time. 

Voluntary  motion  in  the  previously  paralyzed  muscle  returns  hand  in  hand 
with  the  processes  of  regeneration.  It  appears,  as  has  been  already  mentioned, 
sooner  than  the  normal  electrical  excitability  of  the  nerves  and  muscles,  because 
it  can  take  place  as  soon  as  the  axis  cylinders  are  again  formed,  while  the  normal 
electrical  excitability  of  nerves  and  muscles  can  take  place  only  after  the  restora- 
tion of  the  medullary  sheaths.  We  usually  express  this  fact  by  saying  that  the 
reception  of  peripheral  irritations  depends  upon  the  persistence  of  the  medullary 
sheath.  The  destroyed  medullary  sheaths  perhaps  form  a  sort  of  isolating  layer 
about  the  axis  cylinders,  which  is  only  a  poor  conductor  of  the  electrical  current. 
This  is  the  reason  why  in  diseases  of  the  peripheral  nerves  we  sometimes  find  re- 
action of  degeneration  in  muscles  and  nerves  which  have  lost  none  of  their  vol- 
untary motility.  In  such  cases  there  is  probably  disease  of  the  medullary  sheaths 
without  much  degeneration  of  the  axis  cylinders. 

The  same  anatomical  changes,  which  we  have  just  described  as  a  secondary 
degeneration  in  lesions  of  the  peripheral  motor  nerves,  also  develop,  if  the  pri- 
mary disease  has  its  seat  in  the  anterior  cornua  of  the  gray  matter  of  the  spinal 
cord — that  is,  in  the  trophic  centers  themselves.  In  these  cases,  of  course,  the 
form  of  the  disease  has  nothing  to  do  with  it.  Both  in  the  different  forms  of 
inflammation  and  of  primary  atrophy,  and  also  in  new  growths,  which  affect  the 


EEMAKKS   UPON   THE   DISTUEBANCES    OF   MOTILITY      851 

anterior  gray  matter  of  the  cord,  a  secondary  degeneration,  with  pronounced  reac- 
tion of  degeneration,  develops  from  the  anterior  roots  of  that  portion  of  the  cord 
affected  to  the  ends  of  the  peripheral  nerves,  and  even  to  the  corresponding  mus- 
cles. We  shall  also  learn  to  recognize  a  number  of  primary  degenerations  of  the 
peripheral  nerves,  such  as  primary  neuritis,  diphtheritic  and  toxic  paralyses,  etc. 
In  such  cases  we  find  almost  precisely  the  same  anatomical  changes  as  in  sec- 
ondary degenerations,  and,  in  consequence  of  these  changes,  there  is  also  elec- 
trical reaction  of  degeneration  in  the  paralyzed  nerves  and  muscles.  In  all  cere- 
bral paralyses,  however,  and  in  those  spinal  paralyses  where  the  cause  of  the 
paralysis  is  situated  above  the  part  of  the  anterior  gray  cornua  concerned,  the 
degeneration  of  the  peripheral  nerves,  and  also  the  reaction  of  degeneration,  are 
entirely  wanting. 

We  thus  see  that  the  reaction  of  degeneration,  in  regard  to  diagnosis,  at  once 
permits  us  to  decide  that  the  disease  is  situated  in  the  anterior  gray  cornua,  in 
the  anterior  roots,  or  in  the  peripheral  nerves.  It  does  not  permit  any  further 
distinction.  In  regard  to  prognosis,  it  teaches  us  that  anatomical  changes  have 
taken  place  in  the  nerves  and  muscles,  from  which,  under  some  circumstances 
(that  is,  if  the  ganglion-cell  bodies  are  still  preserved),  a  restoration  is  still  very 
possible,  but  at  all  events  it  can  take  place  only  after  the  lapse  of  a  considerable 
time,  at  least  two  or  three  months.  We  shall  soon  learn  to  recognize  a  number  of 
mild  peripheral  paralyses  in  which  there  is  generally  no  reaction  of  degeneration. 
Erom  the  absence  of  reaction  of  degeneration  we  can  then  draw  the  conclusion, 
with  certainty,  that  no  coarse  anatomical  changes  are  present  in  the  nerve,  and 
that  we  may  expect  a  much  more  rapid  recovery  from  the  trouble,  perhaps  in 
three  or  four  weeks.  The  partial  reaction  of  degeneration,  above  mentioned,  is 
also  an  important  symptom  in  regard  to  prognosis.  It  shows  probably  that  slight 
changes  have  occurred  only  in  the  terminal  branches  of  the  muscle  nerves,  while 
the  larger  nerve-trunks  have  remained  approximately  normal.  The  latter  have 
therefore  retained  their  electrical  excitability  while  the  terminal  branches  of  the 
nerves  have  lost  it.  The  partial  reaction  of  degeneration  therefore  always  permits 
a  more  favorable  prognosis  in  regard  to  time  than  the  complete  reaction  of  degen- 
eration.   

6.  Table  of  the  Different  Forms  of  Voluntary  Motion  and  the  Muscles 
AND  Nerves  concerned  Therein 

In  order  to  obtain  an  accurate  knowledge  of  the  extent  of  the  paralysis  in 
complicated  paralytic  conditions  (hemiplegia,  paraplegia,  muscular  atrophy,  etc.), 
it  is  imperatively  necessary  to  test  all  the  muscle  groups  in  order.  The  perform- 
ance of  these  tests  and  their  diagnostic  value  and  significance  will  be  materially 
aided  by  the  use  of  the  following  table,  arranged  according  to  movements. 

I.  MUSCLES  OP  THE  HEAD  AND  TRUNK 

1.  Facial  Muscles  and  Muscles  of  Mastication 

1.  Wrinkling  the  forehead  transversely  (Mm.  frontalis  et  occipitalis,  N. 
facialis). 

2.  Wrinkling  the  forehead  longitudinally  (M.  corrugator  supercilii,  N. 
facialis). 

3.  Closing  the  eyes  (M.  orbicularis  palpebrarum,  N.  facialis). 

4.  Dilating  the  nostrils  (M.  compressor  nasi  et  M.  levator  alse  nasi,  N. 
facialis). 

5.  Drawing  the  mouth  outward  and  upward  (Mm.  levator  labii  superioris, 
zygomatici,  risorius,  IST.  facialis). 


852  DISEASES    OF   THE   NEEVOUS    SYSTEM 

6.  Drawing  the  mouth  downward  (M.  depressor  anguli  oris  et  labii  superioris, 
]Sr.  facialis). 

7.  Raising  the  lower  lip  (M.  levator  menti,  IST.  facialis). 

8.  Protruding  the  lips  and  whistling  (M.  orbicularis  oris,  'N.  facialis). 

9.  Chewing  (Mm.  masseter  et  temporalis,  motor  branch  of  IST.  trigeminus). 

10.  Lateral  and  forward  movements  of  the  lower  jaw  (Mm.  pterygoidei  extern! 
et  interni,  'N.  trigeminus). 

2.  Ocular  Muscles 

1.  Raising  the  upper  lid  (M.  levator  palpebrse  superioris,  IST.  oculomotorius). 

2.  Looking  upward  and  inward  (M.  rectus  superior)  and  upward  and  outward 
(M.  obliquus  inferior,  IST.  oculomotorius). 

3.  Looking  inward  (M.  rectus  internus,  M.  oculomotorius). 

4.  Looking  outward  (M.  rectus  externus,  IST.  abducens). 

5.  Looking  downward  and  inward  (M.  rectus  inferior,  !N".  oculomotorius). 

6.  Looking  downward  and  outward  (M.  obliquus  superior,  N.  trochlearis). 

7.  Contraction  of  the  pupil  (sphincter  iridis,  'N.  oculomotorius). 

8.  Accommodation  (M.  ciliaris,  IST.  oculomotorius). 

3.  Tongue.     Soft  Palate.     Pharynx.     Larynx 

1.  Tongue  movements  (IST.  hypoglossus). 

2.  Soft  palate  (IST.  vago-accessorius). 

3.  Swallowing  (IST.  vago-accessorius). 

4.  Epiglottis  (Mm.  thyreo-epiglotticus  et  ary-epiglotticus,  IN",  laryngeus  supe- 
rior). 

5.  Vocal  cords  (IST.  recurrens). 

4.  Head  and  Trunk 

1.  Flexion  of  the  head  and  cervical  vertebrae  forward  (Mm.  recti  capitis  antici, 
longus  colli  rectus,  IST.  cervicales  1-3),  M.  sterno-cleido-mastoideus  (IST.  acces- 
sorius). 

2.  Movement  of  the  head  and  cervical  vertebrse  backward  (Mm.  splenius  capi- 
tis et  colli,  biventer  complexus,  recti  capitis  postici,  spinalis  et  semispinalis  cervi- 
cis,  IN",  cervicales  1-4). 

3.  Turning  the  head  (M.  sterno-cleido-mastoideus,  IST.  accessorius,  M.  obliquus 
capitis  inferior  et  obliquus  colli). 

4.  Lateral  flexion  of  the  head  (Mm.  recti  capitis  laterales,  M.  spinalis  cer- 
vicis). 

5.  Extension  of  the  vertebral  column  (Mm.  sacro-lumbalis  et  longissimus 
dorsi,  M.  spinalis  dorsi). 

6.  Flexion  of  the  vertebral  column  forward  (abdominal  muscles). 

7.  Torsion  of  the  vertebral  column  (M.  semispinalis  dorsi). 

8.  Lateral  flexion  of  the  vertebral  column  (M.  quadratus  lumborum,  inner- 
vated from  the  crural  plexus),  Mm.  intertransversarii. 

9.  Diaphragm  (IST.  phrenieus  from  IST.  cervicales  4  and  5). 

11.  SHOULDER-BLADE  AND  UPPER  EXTREMITY 

1.  Movements  of  the  Shoulder-hlade 
1.  Raising  the  shoulder-blade  (M.  trapezius,  IN",  accessorius,  M.  levator  anguli 
scapulae,  3  and  4  C.  IST.*). 

*  C.  N.  =  cervical  nerve,  L.  N.  =  lumbar  nerve,  S.  N.  =  sacral  nerve,  that  is,  the  several  anterior 
roots  arising  from  the  corresponding  segment  of  the  spinal  cord. 


EEMAEKS   UPON   THE   DISTURBANCES    OF   MOTILITY      853 

2.  Drawing  the  shoulder-blade  toward  the  median  line  (Mm.  rhomboidei.  Mm. 
thoracici  posteriores  from  4  and  5  C.  N.). 

3.  Eixation  and  rotation  of  the  shoulder-blade  in  raising  the  upper  arm  to  a 
vertical  position  (M.  serratus  anticus  major,  N.  thoracicus  major  from  5  C.  N.). 

2.  Movements  at  the  Shoulder 

1.  Raising  the  arm  forward  and  outward  (M.  deltoideus,  IST.  axillaris  *  [cir- 
cumflex] from  4  and  5  C.  IST.). 

2.  Adduction  and  drawing  downward  (Mm.  pectorales  major  et  minor,  N. 
thoracici  anteriores  from  6  C.  'N.,  M.  latissimus  dorsi,  N.  subscapularis  longus 
from  5  and  6  C.  N.). 

3.  Outward  rotation  (Mm.  supraspinalis,  infraspinalis,  teres  minor,  IST.  supra- 
scapularis  from  4  C.  JST.). 

4.  Inward  rotation  (Mm.  subscapularis  et  teres  major,  'N.  subscapularis  from 
6  C.N.). 

3.  Movements  at  the  Elbow 

1.  Flexion  (Mm.  biceps  et  brachialis  anticus,  N.  musculo-cutaneus ;  5  and 
6  C.  N.,  M.  supinator  longus,  IsT.  radialis  [musculo-spiralis]  ;  6  and  7  C.  N.). 

2.  Extension  (M.  triceps,  IST.  radialis,  6  and  7  C.  IST.). 

3.  Pronation  (Mm.  pronator  teres  et  pronator  quadratus,  N.  medianus; 
6  C.  K). 

4.  Supination  (M.  biceps,  jST.  musculo-cutaneous,  M.  supinator  brevis,  N. 
radialis;  5   C.  N.). 

4.  Movements  at  the  Wrist 

1.  Dorsal  extension  (Mm.  extensor  carpi  radialis  longus  et  brevis,  extensor 
carpi  ulnaris,  JST.  radialis;  6  and  7  C.  IST.). 

2.  Volar  flexion  (Flexor  carpi  radialis,  IST.  medianus.  Flexor  carpi  ulnaris, 
K  ulnaris;  7  and  8  C.  K). 

3.  Radial  flexion  (M.  extensor  carpi  radialis  longus). 

4.  Ulnar  flexion  (Mm.  flexor  et  extensor  carpi  ulnaris). 

5.  Movements  of  the  Fingers 

1.  Extension  of  the  proximal  phalanges  (Mm.  extensor  digitorum  communis, 
extensor  indicis,  extensor  minimi  digiti,  'N.  radialis;  6  and  7  C.  N.). 

2.  Extension  of  the  distal  phalanges  [phalangines  and  phalangettes]  (M.  in- 
terossei,  N.  ulnaris). 

3.  Flexion  of  the  proximal  phalanges  (Mm.  interossei  et  lumbricales,  N"n. 
ulnaris  et  medianus;  7  and  8  C.  N.). 

4.  Flexion  of  the  distal  phalanges  (Mm.  flexor  digitorum  sublimis  et  pro- 
fundus, the  latter  for  the  third  phalanx  [phalangettes],  N".  medianus;  7  and 
8  C.K). 

5.  Spreading  the  fingers,  abduction  (Mm.  interossei  externi  [dorsales],  N". 
ulnaris;  8  C.N.). 

6.  Adduction  of  the  fingers  (Mm.  interossei  interni  [palmares],  IST.  ulnaris). 

7.  Flexion  of  the  proximal  phalanx  and  abduction  of  the  little  finger  (Mm. 
flexor  brevis  et  abductor  digiti  minimi  in  the  hypothenar  eminence,  N.  ulnaris). 

6.  Movements  of  the  Thumh 

1.  Extension  of  the  metacarpal  and  both  phalanges  (Mm.  extensor  pollicis 
brevis  et  longus,  the  latter  for  the  second  phalanx,  N".  radialis;  8  C.  IST.). 

2.  Abduction  of  the  metacarpus  (M.  abductor  pollicis  longus,  N.  radialis). 

*  We  have  followed  Henle's  nomenclature  for  the  peripheral  nerves. — K. 


854  DISEASES    OF   THE   NEEVOUS    SYSTEM 

3.  Adduction  of  the  metacarpus  (M.  adductor  et  caput  profundum  flexoris 
brevis,  JST.  ulnaris). 

4.  Elexion  and  opposition  of  the  metacarpus,  flexion  of  the  first  phalanx  with 
simultaneous  extension  of  the  distal  phalanx  (Thenar  muscles:  Mm.  opponens, 
abductor  brevis  et  caput  superficiale  flexoris  brevis,  N.  medianus;  8  C.  IsT.). 

5.  Elexion  of  the  second  phalanx  (M.  flexor  pollicis  longus,  IST.  medianus). 

III.   LOWER   EXTREMITY 

1.  Movements  at  the  Hip 

1.  Elexion  (Mm.  ilio-psoas,  sartorius,  N.  cruralis,  M.  tensor  vagina  femoris, 
]Sr.  glutseus  superior;  2  and  3  L.  IsT.). 

2.  Extension  (M.  glutseus  maximus,  IST.  gluteus  inferior  from  the  sciatic 
plexus;  1  S.  K). 

3.  Abduction  (M.  glutseus  medius  et  minimus,  IST.  glutseus  superior;  1  S.  N.). 

4.  Adduction  (Mm.  adductor  brevis,  adductor  longus,  adductor  magnus, 
pectineus,  gracilis,  IST.  obturatorius  from  lumbar  plexus;  3  L.  IST.). 

5.  Outward  rotation  (Mm.  pyriformis,  obturatur  intemus,  gemelli,  quadratus 
femoris,  IST.  ischiadicus,  M.  obturator  extemus,  IST.  obturatorius  from  lumbar 
plexus;  6  L.  IST.). 

6.  Inward  rotation  (Mm.  glutseus  medius  et  minimus,  N.  glutseus  superior; 
1  S.  K). 

2.  Movements  at  the  Knee 

1.  Extension  (M.  extensor  cruris  quadriceps,  N".  cruralis;  3  and  4  L.^N".). 

2.  Flexion  (Mm.  biceps,  semimembranosus  et  semitendinosus,  IST.  ischiadi- 
cus; 4  and  5  L.  IST.). 

3.  Movements  at  the  AnJcle  and  of  the  Toes 

1.  Dorsal  extension  of  the  inner  edge  of  the  foot  (M.  tibialis  anticus,  IST. 
peroneus;  2  S.  IST.). 

2.  Dorsal  extension  of  the  outer  edge  of  the  foot  (Mm.  peroneus  longus  et 
brevis,  ]Sr.  peroneus;  2  S.  N.). 

3.  Plantar  flexion  of  the  foot  (Mm.  gastrocnemius  et  soleus,  IST.  tibialis; 
1  S.  K). 

4.  Adduction  of  the  inner  edge  of  the  foot  (M.  tibialis  posticus,  IST.  tibialis). 

5.  Abduction  of  the  foot  (M.  peroneus  brevis,  "N.  peroneus). 

6.  Dorsal  extension  of  the  toes  (Mm.  extensor  digitorum  communis  et  ex- 
tensor hallucis  longus,  IST.  peroneus;  1  and  2  S.N".). 

7.  Plantar  flexion  of  the  toes  (Mm.  flexores  digitorum  et  hallucis  longi  et 
flexor  digitorum  brevis,  IST.  tibialis;  1  and  2  S.IST.). 


CHAPTEE   II 
THE    DIFFEEENT    FORMS    OF    PERIPHERAL    PARALYSIS 

1.  Paralysis  op  the  Ocular  Muscles 

etiology. — The  largest  part  of  all  the  ocular  paralyses  arise  from  affections 
which  involve  either  the  peripheral  oculo-motor  nerves  or  their  nuclei  in  the 
brain-stem.    We  accordingly  make  a  distinction  between  peripheral  and  nuclear 


THE   DIFFEKENT   FOKMS    OF   PERIPHEEAL   PAEALYSIS    855 

paralyses  of  the  ocular  muscles.  As  we  shall  take  up  the  latter  more  fully  in  the 
■description  of  chronic  bulbar  paralysis,  we  have  here  to  mention  only  the  most 
important  and  most  frequent  causes  of  the  peripheral  ocular  paralyses.  These 
are  as  follows : 

1.  Injuries  which  directly  affect  the  nerve-trunks  or  their  branches :  blows  on 
the  eye,  knife-stabs,  fractures  of  the  skull  involving  the  orbit  or  the  base  of  the 
skull,  and  the  like. 

2.  Compression  of  the  nerves  from  morbid  i^rocesses  in  their  neighborhood. 
Tumors  of  the  base  of  the  skull,  especially,  very  often  lead  to  ocular  paralyses. 
Periostitis  at  the  base  of  the  skull  or  in  the  orbit  may  also  cause  similar  symp- 
toms, and  so  may  syphilitic  diseases  of  the  nerves  and  their  surroundings,  the 
meninges  or  periosteum,  aneurisms  of  the  basilar  artery,  acute  or  chronic  menin- 
g'itis  in  its  different  forms,  etc.  In  all  these  cases  we  usually  have  to  do  with  a 
pure  mechanical  compression  of  the  affected  nerves  by  the  morbid  new  growths  in 
their  immediate  vicinity.  More  rarely  the  pathological  process  directly  invades 
the  nerves  themselves. 

3.  The  so-called  rheumatic  ocular  paralyses  are  quite  common.  These  arise 
after  some  decided  exposure  to  cold,  such  as  a  draught  from  an  open  window,  and 
are  in  all  probability  very  largely  of  a  peripheral  nature.  They  depend,  as  is 
supposed,  upon  an  acute  neuritis  of  the  affected  nerve,  and  hence  correspond 
completely  to  the  other  rheumatic  paralyses,  such  as  rheumatic  facial  paralysis. 
Among  the  "  rheumatic  paralyses  "  we  usually  class  the  paralyses  which  appar- 
ently come  on  spontaneously  and  completely  recover,  for  which  no  other  special 
cause  can  be  made  out. 

4.  The  ocular  paralyses  that  sometimes  arise  after  certain  acute  diseases  are 
also  of  a  peripheral  nature,  and  are  due  to  degenerative  neuritis  of  the  affected 
nerves.  They  are  most  frequent  as  a  result  of  diphtheria,  and  are  very  much 
more  rare  in  typhoid  fever,  acute  rheumatism,  etc.  Of  chronic  diseases,  diabetes 
mellitus  may  sometimes  give  rise  to  ocular  paralyses,  especially  to  paralysis  of 
accommodation.  The  ocular  paralyses  occurring  as  a  symptom  of  alcoholic  poly- 
neuritis or  polioencephalitis  may  be  referred  to  a  toxic  influence  that  is  recog- 
nized. 

5.  Finally  we  often  see  ociilar  paralyses  as  a  symptom  of  more  extensive  nerv- 
ous disease,  especially  in  tabes,  multiple  sclerosis,  etc.  The  details  of  these  con- 
ditions will  be  found  in  the  description  of  the  several  diseases. 

Symptoms. — Since  we  must  refer  to  the  text-books  of  ophthalmology  in  regard 
to  the  more  precise  symptomatology,  and  the  more  special  methods  of  ophthalmic 
investigation,  we  will  here  give  only  a  brief  review  of  the  chief  symptoms  of  ocu- 
lar paralyses  which  are  important  in  nervous  pathology. 

The  disturbance  in  the  mobility  of  one  eye  is  usually  first  noticed  by  the 
patient  himself  from  the  appearance  of  double  images — double  vision,  or  diplopia. 
These  arise  because,  on  looking  to  one  side,  the  eye  on  the  paralyzed  side  can  not 
be  brought  into  the  corresponding  position  (strabismus),  and  consequently  the 
retinal  images  no  longer  fall  upon  the  same  spots,  the  two  images  are  no  longer 
projected  outward  in  a  corresponding  fashion,  so  that  two  different  images  are 
therefore  produced  of  the  same  external  object.  In  pathological  convergence  of 
the  visual  axes  homologous  double  images  arise,  in  pathological  divergence 
crossed  images^that  is,  in  the  first  case,  on  closing  one  eye,  the  image  disap- 
pears on  the  same  side,  in  the  second  case  it  disappears  on  the  opposite  side. 
By  alternately  fixing  the  gaze  on  one  or  the  other  of  two  fingers  held  in  line  with 
each  other,  and  by  regarding  the  disappearance,  on  closing  one  eye,  of  the  double 
image  of  the  finger  not  fixed,  we  can  easily  demonstrate  this  on  ourselves.  If, 
then,  crossed  double  images  arise,  for  example,  on  looking  to  the  right,  we  must 
have  a  divergent  strabismus — that  is,  an  imperfect  function  of  the  left  internus ; 


856  DISEASES    OF   THE   NEEVOIJS    SYSTEM 

but  if  there  are  homonymous  double  images,  there  must  be  a  convergent  strabis- 
mus, and  consequently  a  weakness  of  the  right  abducens.  It  makes  it  much  easier 
to  test  the  double  images  if  we  put  a  colored  glass  before  one  of  the  patient's  eyes. 
False  projections  of  the  visual  field  arise,  in  connection  with  the  double  images 
and  with  the  abnormal  strength  of  innervation  which  the  patient  has  to  use  for 
his  ocular  muscles,  so  that  the  patient's  judgment  of  the  position  of  external  ob- 
jects is  uncertain.  In  the  more  extensive  ocular  paralyses  this  often  leads  to  a 
pronounced  feeling  of  dizziness.  In  order  to  avoid  this  unpleasantness  many  pa- 
tients confine  themselves  to  monocular  vision,  close  the  affected  eye,  or  put  their 
heads  in  a  position  to  avoid  the  double  images. 

Finally,  we  must  mention  a  symptom  to  be  observed  in  almost  every  ocular 
paralysis — the  so-called  secondary  deviation  of  the  healthy  eye.  If,  after  the 
sound  eye  has  been  covered,  we  have  the  paretic  eye  fix  itself  upon  a  point  which 
it  can  not  reach  at  all,  or  which  it  can  reach  only  after  the  utmost  exertion,  we 
see,  when  the  covering  hand  is  taken  away  from  the  sound  eye,  that  the  latter 
has  been  moved  much  too  far  in  the  corresponding  direction.  The  abnormal 
exertions  of  innervation  with  the  affected  eye,  somewhat  after  the  analogy  of 
certain  associated  movements,  pass  over  to  the  associated  muscle  of  the  healthy 
side  and  cause  in  it  too  extensive  a  contraction. 

Physical  examination  gives  the  following  results,  according  to  the  extent  of 
the  paralysis : 

In  complete  paralysis  of  one  oculo-motor  nerve  (the  levator  palpebrse  supe- 
rioris,  the  superior,  inferior,  and  internal  recti,  the  inferior  oblique,  the  sphincter 
of  the  iris,  and  the  ciliary  muscle)  the  first  thing  that  is  noticed,  besides  the  dis- 
turbance in  the  movements  of  the  eye,  is  the  more  or  less  complete  drooping  of 
the  upper  lid — ptosis.  If  the  patient  wishes  to  lift  the  upper  lid  he  can  not  do  so 
at  all  or  only  to  a  slight  degree.  If  he  tries  very  hard  there  is  usually  an  evi- 
dent contraction  of  the  corresponding  frontalis  muscle.  If  we  ask  the  patient  to 
follow  with  his  eyes  the  motion  of  any  object,  such  as  the  finger,  held  before  him, 
while  he  keeps  his  head  still,  we  notice  at  once  that  the  affected  eye  does  not  move 
upward,  downward,  or  inward.  The  pupil  is  dilated  (mydriasis)  and  no  longer 
contracts  to  light.  Accommodation  is  lost,  and  distinct  vision  for  near  objects 
is  impossible.  As  a  rule,  the  whole  eye  seems  rather  prominent  (paralytic  ex'oph- 
thaknus),  because  the  backward  traction  of  the  recti  is  very  largely  absent.  In 
old  oculo-motor  paralysis  there  is  often  a  secondary  contracture  in  the  unpara- 
lyzed  external  rectus  (and  superior  oblique),  by  which  the  eye  is  persistently 
drawn  outward.  Partial  oculo-motor  paralyses  are  not  infrequent,  especially 
isolated  ptosis,  also  paralysis  limited  to  the  levator  palpebrse  and  superior  rectus, 
paralysis  of  the  internal,  inferior,  or  superior  rectus,  or  finally  isolated  paralysis 
of  accommodation,  and  they  may  usually  be  easily  recognized  from  what  has 
been  said. 

Paralysis  of  the  abducens  is  characterized  by  the  inability  to  move  the  exter- 
nal rectus.  The  eye  can  no  longer  be  moved,  or  it  can  be  moved  only  imperfectly, 
outward  beyond  the  median  line.  In  old  paralysis  the  eye  is  drawn  inward  from 
a  secondary  contracture  of  the  internal  rectus,  and  convergent  strabismus  arises. 
Paralysis  of  the  abducens  may  often  be  isolated,  but  it  is  sometimes  bilateral,  or 
combined  with  other  ocular  paralyses. 

Paralysis  of  the  trochlear  nerve,  the  superior  oblique  muscle,  is  not  perfectly 
easy  to  recognize ;  but  it  is  rarely  of  special  practical  importance.  The  action 
of  the  superior  oblique  coincides  mainly  with  that  of  the  inferior  rectus.  If  the 
trochlear  be  paralyzed  the  eye  turns  somewhat  inward  on  looking  downward,  be- 
cause the  superior  oblique  acts  also  to  abduct  the  eyeball,  and  therefore  acts 
chiefly  on  looking  downward  and  outward.  The  paralysis  of  the  trochlear  nerve  is 
sometimes  made  manifest  by  the  failure  of  the  eye  to  revolve,  which  rotation 


THE   DIFFEEENT   EOEMS    OF   PEEIPHEEAL   PAEALYSIS    857 

normally  takes  place  on  looking-  downward,  and  is  due  to  the  superior  oblique 
muscle.  This  latter  movement  takes  place  in  each  eye  about  a  sagittal  axis,  in 
such  a  way  that  the  left  eye  is  turned  from  the  left  and  up  to  the  left  and  down- 
ward, and  the  right  eye  from  the  right  and  up  to  the  right  and  downward.  In 
regard  to  diagnosis,  it  is  also  characteristic  that  the  double  images  in  trochlear 
paralysis  appear  only  in  the  lower  half  of  the  field  of  vision,  and  especially  on 
looking  downward.  Hence  it  happens  that  the  disturbance  of  vision  is  especially 
manifest  in  going  up  or  down  stairs,  because  in  such  cases  the  double  images  of 
the  steps  are  disturbing. 

The  following  must  be  added  in  regard  to  the  separate  clinical  forms  of  ocular 
paralysis :  Eheumatic  ocular  paralysis  affects  the  abdueens  most  frequently,  and 
not  infrequently  the  oculo-motor  or  one  of  its  branches,  as  in  isolated  ptosis.  We 
have  seen  a  rare  case  in  which  exposure  to  severe  cold  had  been  followed  by  a 
complete  paralysis  of  all  the  external  muscles  of  the  right  eye,  with  complete 
ptosis,  and  almost  absolute  immobility  of  the  eye  in  all  directions.  The  rheu- 
matic ocular  paralyses  are  almost  always  acute  in  their  onset,  and  they  are  often 
during  the  first  period  associated  with  sensations  of  pain  about  the  eye  and  in  the 
head.  Vomiting  (of  reflex  origin?)  is  also  not  rare  at  the  beginning  of  the  affec- 
tion. The  course  of  most  cases  is  favorable,  since  they  usually  completely  re- 
cover in  a  few  weeks,  though  sometimes  not  for  months.  In  some  cases  the 
paralysis  may  remain  stationary. 

The  diphtheritic  ocular  paralyses  usually  appear,  like  the  other  diphtheritic 
paralyses,  a  week  or  two  after  the  termination  of  the  disease.  They  most  fre- 
quently affect  the  muscles  of  accommodation,  so  that  the  patient  complains 
chiefly  of  indistinct  vision  for  near  objects;  but  we  sometimes  see  paralyses  of 
the  external  ocular  muscles  also,  the  abdueens  or  the  internal  rectus.  The  prog- 
nosis of  diphtheritic  paralyses  is  almost  invariably  favorable. 

Finally,  we  must  mention  here  the  so-called  "  recurrent  or  periodical  oculo- 
motor paralysis,"  to  which  Mobius  and  others  have  lately  called  attention,  and 
whose  nature  is  still  almost  wholly  inexplicable.  In  the  cases  of  this  sort  re- 
peated paralyses  of  one  oculo-motor  nerve,  often  associated  with  headache  and 
vomiting,  just  as  in  migraine,  come  on  at  longer  or  shorter  intervals  (in  women 
sometimes  at  the  menstrual  period)  in  the  same  individual,  who  has  often  had 
them  since  childhood.  All  branches  of  the  oculo-motor  are  usually  affected  alike, 
but  sometimes  the  internal  ocular  muscles  are  spared.  In  milder  cases  there  may 
be  only  ptosis.  The  individual  attack  sometimes  lasts  only  a  few  days,  but  often 
some  weeks.  The  attacks  usually  become  gradually  more  severe  later  on.  The 
nature  of  recurrent  oculo-motor  paralysis  is  still  quite  unknown,  but  it  seems 
to  be  growing  more  probable  that  in  a  part  of  the  cases  at  least  the  disease  is 
closely  related  to  migraine  (q.  v.),  and  forms  in  a  measure  only  an  unusual  devel- 
opment of  migraine — migraine  ophthalmoplegique.  The  genuine  cases  of  the 
disease,  however,  must,  of  course,  be  distinguished  from  the  recurrent  oculo- 
motor paralysis  that  sometimes  occurs  in  tabes,  cerebral  syphilis,  tumors  of 
the  base  of  the  skull,  etc.  [The  relation  to  migraine  seems  very  doubtful. 
There  is  rarely  complete  recovery  between  the  attacks,  and  there  is  a  tend- 
ency for  the  attacks  to  increase  in  frequency  and  duration  as  well  as  in 
severity.  In  three  cases  which  have  come  to  autopsy  lesions  have  been  found 
affecting  the  nerve — tumors  or  inflammatory  thickening.  Some  of  the  cases 
have  also  had  anaesthesia  in  one  or  more  branches  of  the  distribution  of  the 
trigeminus  during  the  attack.  Besides  the  recurrent  oculo-motor  paralysis  and 
recurrent  facial  paralysis  (vide  infra),  recurrent  trochlear,  and  abdueens  paraly- 
ses and  recurrent  paralysis  of  several  cranial  nerves  at  once  have  been  re- 
ported.— K.] 

Nothing  generally  applicable  can  be  said  as  to  the  course  and  prognosis  of  the 


S58  DISEASES    OF   THE   NEEVOUS    SYSTEM 

other  forms  of  ocular  paralyses,  since  in  tliem  everything  depends  upon  the  form 
of  the  underlying  disease. 

Treatment. — In  regard  to  the  fulfillment  of  any  possible  causal  indication  we 
must  remember  especially  that  ocular  paralysis  is  not  very  infrequently  of  syphi- 
litic origin.  Iodide  of  potassium  and  energetic  mercurial  inunction  may  some- 
times give  very  good  results  in  such  cases.  Hence  these  remedies  must  also  be 
tried  in  doubtful  cases. 

Of  other  remedies  galvanic  treatment  gives  the  speediest  relief.  We  pass 
-weak  currents  transversely  through  the  temples,  or,  what  is  usually  better,  we  put 
the  anode  to  the  back  of  the  neck  and  apply  the  labile  cathode  to  the  closed  eye, 
especially  to  the  region  corresponding  to  the  paralyzed  muscles.  Great  caution, 
weak  currents,  and  the  avoidance  of  any  great  variations  in  the  currents  are  of 
course  necessary.  We  may  also  try  preparations  of  strychnine  internally,  or, 
better,  subcutaneously  in  the  vicinity  of  the  eye.  We  must  refer  to  special  trea- 
tises with  regard  to  a  correction  of  the  double  images  by  covering  the  affected 
eye,  spectacles  with  one  dark  or  ground  glass,  or  prismatic  spectacles,  or  in  regard 
to  operations,  such  as  tenotomy,  that  are  sometimes  performed. 

2.  Paralysis  of  the  Motor  Branch  of  the  Trigeminus 

{Paralysis  of  the  Muscles  of  Mastication) 

Paralysis  of  the  muscles  of  mastication,  the  masseters  and  temporals,  supplied 
by  the  third  branch  of  the  trigeminus,  is  a  rare  affection.  It  is  most  frequently 
seen  in  diseases  of  the  base  of  the  skull  which  compress  the  motor  branch  of  the 
fifth.  We  shall  also  learn  later  on  to  recognize  paralysis  of  the  muscles  of  mas- 
tication as  a  rare  symptom  of  chronic  bulbar  affections. 

The  chief  symptom  of  motor  paralysis  of  the  trigeminus  is  the  difficulty  or 
impossibility  of  chewing.  In  unilateral  paralysis  the  patient  can  chew  only  on 
the  healthy  side;  in  bilateral  paralysis  he  can  no  longer  chew  at  all.  Paresis 
of  the  muscles  of  mastication  can  be  readily  determined  by  the  lack  of  strength 
in  resisting  the  attempt  to  draw  down  the  lower  jaw  or  by  the  patient's  inability 
to  make  a  deep  imprint  in  biting  a  bit  of  wood  (lead-pencil,  etc.).  In  complete 
paralysis  of  the  muscles  of  mastication  the  lower  jaw  hangs  loosely  down,  and  it 
can  also  no  longer  be  moved  sideways,  from  the  co-existing  paralysis  of  the  ptery- 
goids. We  can  not  usually  detect  clinically  disturbances  in  the  other  muscles 
supplied  by  the  trigeminus  (mylohyoid,  buccinator,  tensor  palati,  and  tensor  tym- 
pani),  but  there  are  often  sensory  disturbances  in  the  distribution  of  the  tri- 
geminus at  the  same  time. 

The  prognosis  and  treatment  depend  upon  the  primary  disease.  Local  faradi- 
zation or  galvanization  of  the  paralyzed  muscles  is  to  be  tried. 

3.  Facial  Paralysis 

(Mimetic  Facial  Paralysis.     BelVs  Palsy) 

.3]tiology. — Facial  paralysis  is  one  of  the  commonest  peripheral  paralyses,  as 
we  can  understand  from  the  superficial  position  of  the  nerve,  exposing  it  to  exter- 
nal injuries,  and  from  its  course  through  the  narrow  Fallopian  canal.  We  consider 
it  improbable  that  a  special  "  neuropathic  family  predisposition  "  plays  a  part  in 
the  occurrence  of  peripheral  facial  paralysis,  as  Charcot's  school  maintains.  The 
most  important  causes  of  facial  paralysis  are :  1.  Exposure  to  cold,  draughts, 
sleeping  by  an  open  window,  riding  in  the  cars  with  the  window  open,  etc.  The 
paralyses  arising  in  this  way  are  termed  "  rheumatic,"  and  we  also  include  in  this 
class  those  peripheral  paralyses  which  are  apparently  spontaneous — that  is,  those 
without  any  marked  exposure  to  cold  that  can  be  discovered.  In  all  these  cases 
we  probably  have  to  do  with  a  neuritis  of  the  nerve-trunk,  which  comes  on  in  a  way 


THE   DIFFERENT   FORMS    OF   PERIPHERAL   PARALYSIS    859 


as  yet  unknown  (infectious?  toxic?).  [In  a  recent  autopsy  of  a  ease  of  so-called 
^'rheumatic"  facial  paralysis,  Minkowski  found  a  simple  degenerative  parenchym- 
atous neuritis,  without  any  swelling  of  the  nerve-sheath  or  increase  of  connect- 
ive tissue. — K.]  2.  Diseases  of  the  middle  ear  and  especially  caries  of  the  petrous 
bone.  As  the  facial  passes  through  the  Fallopian  canal,  which  is  in  the  immediate 
vicinity  of  the  tynapanic  cavity,  we  can  easily  understand  how  so  often  in  caries  of 
the  petrous  bone,  and  often  perhaps  in  purulent  affections  of  the  middle  ear,  in- 
flammation may  invade  the  trunk  of  the  facial,  or  how  the  facial  may  be  com- 
pressed by  inflammatory  exudations,  etc.  3.  In  rare  cases  a  pressure  paralysis  of 
the  facial  nerve  arises  in  swelling  of  the  parotid  gland  or  tumors  in  its  vicinity.  4. 
Diseases  of  the  base  of  the  skull  or  brain,  tumors,  syphilitic  new  growths,  and 
acute  or  chronic  inflammations,  often  give  rise  to  the  development  of  a  facial 
paralysis  by  invasion  of  the  trunk  of  the  facial  or  compression  of  it.  5.  We  shall 
have  to  speak  repeatedly  in  the  following  sections  of  the  frequent  implication  of 
the  facial  nerve  in  diseases  of  the 
brain  and  medulla  and  of  the  impli- 
cation of  the  facial  muscles  in  multiple 
neuritis,  in  juvenile  muscular  dys- 
trophy, and  other  diseases. 

Symptoms  and  Course. — The  mani- 
fold character  and  different  functions 
of  the  nerves,  which  unite  in  the 
trunk  of  the  facial,  are  the  causes  of  the 
quite  large  array  of  symptoms  in  facial 
paralysis.  Most  of  these  symptoms  are 
manifest  only  in  perii^heral  facial  pa- 
ralysis, and  the  following  description, 
therefore,  refers  chiefly  to  this. 

The  paralysis  of  the  facial  muscles 
of  expression  is  the  most  striking  and 
characteristic  (see  Fig.  105).  The 
paralyzed  half  of  the  face  is  lax  and 
expressionless,  the  wrinkles  in  the 
forehead  are  obliterated,  the  eye  is 
abnormally  wide  open,  as  the  weight  of 
the  lower  eyelid  draws  it  down,  and  the 
eye  also  waters  (epiphora),  the  naso- 
labial fold  is  obliterated,  the  corner 
of  the  mouth  droops,  and  saliva  fre- 
quently flows  from  it.     The  paralysis 

becomes  still  more  marked  on  any  movement  of  the  face,  on  wrinkling  the  fore- 
hiead,  turning  up  the  nose,  laughing,  talking,  whistling,  or  inflating  the  cheeks. 
The  eye  can  be  only  partly  closed.  On  attempting  it,  the  upper  lid  sinks  down 
from  its  weight  (a  weakening  of  the  levator  palpebrse  superior  is),  the  eye  is 
turned  upward,  so  that  the  pupil  is  covered,  but  quite  a  wide  space  is  left  between 
the  eyelids  (lagophthalmus).  This  defective  closure  of  the  lids  facilitates  the 
entrance  of  dust,  etc.,  into  the  eye,  and  sometimes  giv^s  rise  to  conjunctivitis,  or 
even  to  severer  inflammation  of  the  eye.  Speech  is  rendered  difficult  and  indis- 
tinct from  defective  movements  of  the  lips,  and  mastication  becomes  impaired 
from  the  imperfect  movement  of  the  cheeks.  The  patient  can  no  longer  whistle 
because  he  can  no  longer  pucker  the  lips  sufficiently  on  the  affected  side.  If  he 
tries  to  puff  out  the  cheeks  or  keep  them  inflated  we  notice  plainly  the  flaccidity 
of  the  cheek  on  the  paralyzed  side.  On  drawing  down  the  lower  lip  the  paralysis 
of  the  platysma  myoides  is  sometimes  very  plainly  seen.     The  tongue  is  often 


Fig.  105.— Right  facial  paralysis  (after  SeeligmCi,- 
LER).  Tlie  folds  are  smoothed  out  and  in  part 
entirelj-  absent  on  the  paralyzed  side,  while  they 
are  strongly  marked  on  the  left.  The  mouth  and 
nose  are  drawn  to  the  left. 


860 


DISEASES    OF   THE   NEEVOUS    SYSTEM 


apparently  protruded  to  one  side,  but  this  is  due  merely  to  the  distorted  position 
of  the  mouth.  Very  often,  however,  we  see,  when  the  mouth  is  open  and  the 
tongue  is  at  rest,  that  the  half  of  the  tongue  corresponding  to  the  paralyzed  side 
lies  deeper  than  the  other  half,  a  condition  which  is  probably  connected  with  a 
paralysis  of  the  stylo-hyoid  and  digastric  muscles.  In  some  cases  in  which  the- 
geniculate  ganglion  or  the  facial  trunk  above  it  were  affected,  some  writers  have 

claimed  to  find  a  paresis  of  the  soft 
palate  on  the  affected  side;  the 
fibers  from  the  facial  are  said  to 
pass  through  the  superficial  petro- 
sal nerve  to  the  spheno-palatine 
ganglion,  and  thence  to  the  soft 
palate.  It  droops  more,  and  on 
phonation  the  soft  palate  is  raised 
obliquely  to  the  healthy  side.  Ac- 
cording to  more  recent  investiga- 
tions, however,  the  soft  palate  is- 
apparently  innervated  only  by 
fibers  from  the  vaso-accessory  and 
not  from  the  facial. 

Disturbances  of  taste  in  the 
anterior  two  thirds  of  the  tongue 
have  been  repeatedly  found  on  the 
paralyzed  side,  but  they  usually 
attain  only  a  slight  degree.  They 
are  explained  by  an  affection  of 
the  fibers  of  the  chorda  tympani, 
which  run  for  some  distance  in  the 
facial,  as  has  been  described  on 
page  827.  At  the  beginning  of  the 
paralysis  many  patients  complain 
of  subjective  sensations  of  taste^ 
Later  on  the  dullness  of  taste  may 
often  be  discovered  by  careful  test- 
ing. Tactile  sensibility  in  the 
tongue  is  only  exceptionally  di- 
minished (sensory  fibers  in  the 
A  diminished  secre- 
saliva  (fibers  in  the 
and     consequently     an 


Fig.  106.— Schematic  representation  of  the  trunk  of  the 
facial  from  the  base  of  the  skull  to  the  pes  anseri- 
nus.  Different  localizations  of  the  lesion  in  paralysis. 
N.f.  Facial  nerve.  JSf.p.s.  Great  superficial  petrosal. 
N.c.c.p.t.  Nerve  communicating?  with  the  tympanic 
plexus.  N.st.  Stapedius.  Ch.t.  Chorda  tympani.  Gf. 
Fibers  of  taste.  Sps.  Nerve  governing  the  secretion 
of  saliva.  N.a.  Acoustic  nei-ve.  G.g.  Geniculate  gan- 
glion. F.st.  Stylomastoid  foramen.  N.u.p.  Posterior 
auricular  nerve. 


chorda?) 

tion     of 

chorda), 

abnormal  feeling  of  dryness  in  the  patient's  mouth  on  the  paralyzed  side,  are 
sometimes  said  to  have  been  observed.  Disturbances  of  hearing  are  fre- 
quent, but  they  are  usually  due  to  some  complicating  aural  trouble  {vide- 
supra),  or  to  a  co-existing  affection  of  the  acoustic  nerve.  Paralysis  of  the  sta- 
pedius muscle,  however,  sometimes  seems  to  cause  symptoms,  including  a  marked 
sensitiveness  to  all  loud  sounds,  and  even  an  abnormal  acuteness  of  hearing,  espe- 
cially for  low  notes  (hyperacusis,  oxyokoia).  These  symptoms  are  due  to  the  fact 
that  in  paralysis  of  the  stapedius  its  antagonist,  the  tensor  tympani,  causes  a 
greater  tension  of  the  membrana  tympani.  Keflex  movements,  winking,  etc.,  are, 
of  course,  lost  in  complete  peripheral  facial  paralysis.  For  the  special  reflexes, 
which  are  often  seen  in  the  later  stages  of  facial  paralysis,  vide  infra. 

By  .testing  all  the  symptoms  described,  in  most  cases  we  can  decide  with  accu- 
racy upon  the  place  where  the  break  in  conduction  in  the  facial  must  occur.  If 
we  examine  the  accompanying  plan  of  the  facial  (Fig.  106),  devised  by  Erb,  we- 


THE   DIFFERENT   FORMS    OF   PERIPHERAL   PARALYSIS    861 

•can  easilj-  understand  the  following  chief  symptomatic  forms  of  facial  paralysis. 
Of  course  we  must  not  forget  that  many  points  (innervation  of  the  soft  palate, 
of  the  secretion  of  saliva  and  tears,  etc.)  are  still  very  much  in  need  of  further 
investigation. 

1.  Paralysis  of  the  facial  muscles ;  but  taste,  secretion  of  saliva,  hearing,  and 
soft  palate  normal;  seat  of  the  affection  in  the  portion  between  1  and  2,  usually 
the  trunk  of  the  facial  below  the  Fallopian  canal. 

2.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  and  eventually  dimin- 
ished secretion  of  saliva;  but  hearing  and  soft  palate  normal;  seat  of  the  affec- 
tion within  the  Fallopian  canal  between  2  and  3. 

3.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  diminished  secretion  of 
saliva,  abnormal  acutenessof  hearing;  but  soft  palate  normal;  seat  between  3  and  4. 

4.  Paralysis  of  the  facial  muscles,  disturbance  of  taste,  diminished  secretion 
of  saliva,  abnormal  acuteness  of  hearing,  and  paresis  of  the  soft  palate  ( ?  vide 
supra)  ;  seat  in  the  geniculate  ganglion  between  4  and  5. 

5.  Paralysis  of  the  facial  muscles,  diminished  secretion  of  saliva,  abnormal 
acuteness  of  hearing,  paresis  of  the  soft  palate  (?),  but  no  disturbance  of  taste; 
seat  above  the  geniculate  ganglion  between  5  and  6. 

The  changes  in  electrical  excitability,  and  some  other  changes,  may  be  best 
•described  in  connection  with  the  course  of  facial  paralysis.  Ordinarily  rheumatic 
paralysis  usually  begins  quite  suddenly;  less  frequently  it  is  more  gradual. 
Sometimes  there  are,  for  a  short  time,  subjective  prodromata,  such  as  abnormal 
sensations  of  taste,  slight  ringing  in  the  ears,  and  very  often  painful  sensations 
in  the  ear,  behind  the  ear,  and  in  the  face,  which  symptoms  may  be  referred  to 
the  beginning  of  acute  inflammatory  processes  in  the  nerve.  In  a  few  cases  the 
occurrence  of  herpes  vesicles  has  been  observed  in  the  distribution  of  the  affected 
facial,  a  condition  which  may  be  most  readily  explained,  in  accordance  with  what 
was  said  on  page  815,  by  reference  to  the  numerous  anastomoses  between  the 
l>ranches  of  the  facial  and  those  of  the  trigeminus.  Among  other  rare  complica- 
tions of  simple  peripheral  facial  paralysis  we  may  mention  neuralgic  pain  in  the 
different  areas  of  the  trigeminus  and  slight  optic  neuritis. 

In  regard  to  the  further  course  we  distinguish  the  three  following  forms : 

1.  The  mild  form,  of  facial  paralysis,  to  which  especially  many  rheumatic 
paralyses  belong.  The  affection  is  usually  referred  only  to  the  facial  muscles, 
disturbances  of  taste,  etc.,  being  wholly  absent.  Electrical  excitability  in  the 
facial  and  the  paralyzed  muscles  remains  entirely  normal.  Recovery  is  rapid, 
usually  in  two  or  three  weeks.  In  these  cases  we  may  certainly  suppose  that 
there  are  no  severe  and  deep-seated  anatomical  changes  in  the  nervous  or  mus- 
cular fibers. 

2.  The  middle  form  of  facial  paralysis  (Erb).  In  this  there  is  no  complete 
reaction  of  degeneration,  but  only  a  partial  one.  The  excitability  of  the  nerve  is 
•somewhat  diminished,  but  it  is  not  lost.  In  the  muscles,  however,  in  about  two 
or  three  weeks,  there  appears  a  decided  increase  of  galvanic  excitability  to  direct 
excitement.  The  anodic  closure  contraction  (AnSZ)  is  also  greater  than  the 
cathodic  closure  contraction  (KaSZ),  and  the  contractions  are  slow.  In  regard 
to  prognosis  we  may  decide  from  this  that  the  recovery  will  still  be  quite  rapid. 
It  usually  follows  in  from  four  to  six  weeks. 

3.  The  severe  form  of  facial  paralysis  is  that  in  which  there  is  a  complete 
reaction  of  degeneration  in  the  nerve  and  muscles,  the  details  of  which  we  have 
learned  in  the  previous  chapter — loss  of  faradic  and  galvanic  excitability  of  the 
nerve,  loss  of  faradic  excitability  of  the  muscles,  and  quantitative  and  qualitative 
changes  in  the  galvanic  excitability  of  the  muscles.  In  this  form  there  are  always 
coarse  processes  of  degeneration  in  the  nerve  and  atrophy  of  the  muscles,  so  that 
recovery  follows,  if  at  all,  only  after  three  to  six  months,  or  even  later,  because 


862  DISEASES    OF    THE   ElERyOUS    SYSTEM 

tlie  processes  of  regeneration  require  at  least  as  mucli  time  for  their  accomplisli- 
ment.  We  often  see  in  the  later  stages  of  these  cases  special  symptoms  of  motor 
irritation  (Hitzig) .  These  consist,  first,  of  a  slight  or  sometimes  very  pronounced 
tonic  contracture  of  the  paralyzed  muscles,  which  is  sometimes  very  striking;  if 
such  cases  are  examined  carelessly,  we  may  easily  mistake  the  (flaccid)  healthy 
side  of  the  face  for  the  paralyzed  side ;  second,  of  single  spasmodic  contractions 
of  the  muscles,  a  true  facial  tic  (vide  infra)  following  the  paralysis  of  the  facial; 
third,  of  special  associated  movements — if  the  patient  closes  his  eyes,  winks,  etc.^ 
there  always  follows  a  marked  distortion  of  the  comer  of  the  mouth,  which  can 
not  be  suppressed;  we  have  seen  this  symptom  frequently  in  students  in  whom  a 
peripheral  branch  of  the  facial  has  been  injured  in  a  duel ;  fourth,  of  an  increased 
reflex  irritability — on  pricking  the  skin,  or  blowing  on  it,  vigorous  muscular  con- 
tractions follow.  We  have  often  ourselves  seen  contractions  in  the  affected 
facial  muscles  following  a  blow  on  the  bridge  of  the  nose,  on  the  nasal  bone,  or  on 
the  forehead  on  the  healthy  side.  These  reflexes  come  from  the  skin,  or  perhaps 
in  part  from  the  periosteum  and  the  fasciae  also.  All  these  symptoms — the  con- 
tracture, the  abnormal  twitchings,  and  the  associated  movements — may  last  for  a 
very  long  time — for  years  in  incurable  or  in  imperfectly  cured  cases. 

Prognosis. — The  prognosis  of  facial  paralysis  depends,  of  course,  in  the  first 
place,  upon  the  primary  disease,  if  any  exists.  Paralysis  in  tumors  of  the  base  of 
the  brain,  caries  of  the  petrous  bone,  etc.,  is  almost  always  incurable.  The  course 
of  the  paralysis  in  affections  of  the  middle  ear  depends  upon  the  curability  of  the 
latter  disease.  Very  important  data  for  the  accurate  prognosis  of  rheumatic 
paralysis  are  given  by  the  electrical  examination,  as  has  been  carefully  described 
above.  Of  course,  we  can  never  form  a  definite  judgment  from  this  at  the  begin- 
ning of  the  paralysis,  but  only  at  the  end  of  the  first  week.  If,  at  the  end  of  the 
first  week  or  fortnight,  the  electrical  excitability  of  the  nerve  still  remains  normal, 
we  can  almost  certainly  prophesy  a  rapid  and  favorable  course.  If  reaction  of 
degeneration  appears,  we  can  not  count  upon  recovery  in  the  most  favorable  cases 
before  two  or  three  months.  Relapses  almost  never  follow  directly  upon  the 
course  of  a  paralysis,  but  it  is  by  no  means  rare  to  see  peripheral  facial  paralysis 
occur  several  times  in  the  same  patient  after  intervals  of  some  years.  We  have 
seen  a  man  of  about  thirty  who  had  a  peripheral  facial  paralysis  four  times  within 
a  few  years,  which  disappeared  each  time  after  a  few  weeks — a  condition  which 
possibly  is  to  be  regarded  as  analogous  to  the  "  periodical  oculo-motor  paraly- 
sis "  (see  page  857). 

Diagnosis. — The  symptoms  of  facial  paralysis  are  so  pronounced  that  the 
paralysis  itself  can  always  be  easily  recognized.  In  regard  to  the  precise  form  of 
the  paralysis  and  its  cause,  we  can  often  decide  only  by  considering  the  ^etiologi- 
cal  factors,  such  as  injuries,  exposure  to  cold,  or  aural  affections.  In  distinguish- 
ing between  peripheral  and  central  (bulbar  or  cerebral)  paralyses,  the  other  co- 
existing bulbar  or  cerebral  symptoms  must  first  of  all  be  considered.  We  shall 
learn  to  recognize  more  accurately  later  the  different  modes  in  which,  in  these 
cases,  facial  paralysis  may  be  combined  with  paralysis  of  the  other  cerebral  nerves, 
or  the  nerves  of  the  extremities.  In  doubtful  cases  electrical  examination  is 
often  of  decisive  value.  Reaction  of  degeneration  can  be  present  only  in  periph- 
eral paralysis,  or  in  such  bulbar  paralyses  as  affect  the  fibers  of  the  facial  below 
the  facial  nucleus  or  affect  the  nucleus  itself.  In  all  cerebral  paralyses  the  elec- 
trical excitability  is  perfectly  retained.  It  may  also  be  mentioned  here  briefly 
that  in  all  cerebral  facial  paralyses  the  frontal  muscles  and  the  orbicularis  palpe- 
brarum are  usually  unaffected,  while  in  peripheral  paralyses  they  also  are 
paralyzed. 

Treatment. — The  treatment  of  the  underlying  disease  is  of  the  greatest  impor- 
tance in  all  cases  where  any  aural  affection,  any  removable  compressing  swelling. 


THE   DIFFEEENT   FOEMS    OF   PEEIPHEEAL   PAEALYSIS    868 

as  of  the  parotid,  or  syphilis,  lies  at  the  bottom  of  the  trouble.  The  methods  of 
treatment  indicated  in  such  cases  are  self-evident.  In  fresh  rheumatic  facial 
paralysis  it  is  advisable  at  first  to' give  a  few  doses  of  salicylate  of  sodium  or 
antipyrine.  In  other  cases  electricity  is  the  only  remedy  which  can  give  sure 
results,  although  we  must  not  overestimate  its  efficiency.  In  the  earlier  stages  of 
the  paralysis  we  may  recommend  the  stabile  conduction  of  a  weak  constant 
current  through  the  auriculo-mastoid  fossae,  four  to  six  times  a  week  for  two  or 
three  minutes,  at  first  the  anode,  then  the  cathode,  to  the  affected  side.  Later  on 
the  chief  treatment  is  peripheral  galvanization,  or  eventually  faradization  of  the 
muscles.  We  place  the  anode  in  the  auricular  fossa  and  slowly  stroke  the  dif- 
ferent nerve-branches  and  the  muscles  with  the  cathode.  We  can  often  confirm 
the  fact,  immediately  after  each  sitting,  that  the  eye  closes  better  after  galvaniza- 
tion of  the  orbicularis.  Faradization  excites  a  reflex  irritation  of  the  nerves  from 
irritation  of  the  skin,  and  hence  is  perhaps  of  service.  Internal  remedies  (strych- 
nine, etc.)  are  probably  quite  useless. 

In  secondary  contractures  we  may  obtain  some  favorable  results  by  methodical 
stretching  of  the  muscles  by  wooden  wedges  inserted  under  the  cheeks  and  by 
massage. 

4.  Paralyses  ix  the  Eegion  of  the  Muscles  of  the  Shoulder 

Isolated  paralyses  of  these  muscles  are  rare,  with  the  exception  of  the  practi- 
cally important  paralysis  of  the  serratus.  Disturbances  in  their  functions  are 
more  frequent,  as  one  symptom  in  complicated  paralytic  states,  especially  in  pro- 
gressive muscular  atrophy,  and  in  diseases  in  the  neighborhood  of  the  foramen 
magnum  or  of  the  upper  cervical  vertebrae.  In  syringomyelia  paralyses  in  the 
distribution  of  the  accessory  nerve  are  not  uncommon. 

Paralysis  of  the  Sterno-cleido-mastoid  (spinal  accessory  nerve). — The  chin 
is  somewhat  raised  and  turned  toward  the  affected  side  in  consequence  of  the 
antagonistic  contracture  of  the  other  sterno-mastoid.  Motion  in  the  opposite 
direction  is  difficult.  In  bilateral  paralysis  of  this  muscle  it  is  very  difficult  to 
turn  the  head  with  the  chin  raised,  and  it  can  be  done  only  imperfectly.  The  head 
readily  falls  backward  and,  when  the  patient  is  lying  down,  it  can  be  lifted  only 
with  the  greatest  difficulty  if  at  all. 

Paralysis  of  the  Trapezius  (spinal  accessory  nerve). — The  shoulder  sinks 
downward  and  forward  so  that  the  supra-clavicular  fossa  becomes  deeper.  The 
median  border  of  the  scapula  moves  outward  and  is  not  parallel  to  the  vertebral 
column,  as  under  normal  conditions,  but  it  runs  obliquely  from  below  and  inward, 
upward  and  outward.  Voluntary  raising  of  the  shoulder,  "  shrugging  the  shoul- 
der," is  impaired,  and  it  can  be  done  only  by  the  levator  scapulas.  The  arm  sinks 
down  from  its  own  weight,  and  there  is  often  pain  in  the  shoulder  from  stretch- 
ing the  ligaments  of  the  joint.  If  the  clavicular  portion  is  paralyzed,  the  shoulder 
does  not  move  on  deep  breathing.  Eaising  the  arm  above  the  horizontal  is  also 
affected,  from  the  impaired  fixation  of  the  scapula. 

Paralysis  of  the  Pectoralis  Major  and  Minor  (anterior  thoracic  nerves). — 
Abduction  of  the  upper  arm  is  difficult,  the  hand  can  be  placed  on  the  shoulder 
of  the  healthy  side  only  by  the  help  of  the  anterior  bundle  of  the  deltoid,  and 
the  palms  can  not  be  clapped  together  hard  when  the  arms  are  stretched  forward. 
The  function  of  the  pectoral  in  forcibly  drawing  down  the  arm  when  raised  to 
the  perpendicular  (as  in  chopping  wood,  pulling  down  a  hanging  rope,  etc.)  is 
very  important. 

Paralysis  of  the  Ehomboidei  (N.  dorsaUs  scapulce)  causes  the  inner  edge  of 
the  scapula  to  be  somewhat  raised  from  the  thorax  while  its  lower  angle  moves 
outward.  It  becomes  difficult  to  approximate  the  scapula  to  the  vertebras,  and 
wholly  impossible  to  do  so  if  the  trapezius  be  also  paralyzed.     The  movements  of 


864: 


DISEASES    OF   THE   ^EEVOUS    SYSTEM 


the  extended  arm  inward  and  backward  are  also  impaired  on  account  of  the  de- 
fective fixation  of  the  scapula.  Isolated  paralysis  of  the  levator  anguli  scapulae 
causes  no  noticeable  symptoms,  but  if  the  trapezius  be  also  paralyzed  it  becomes 
wholly  impossible  to  raise  the  scapula.  Then  the  approximation  of  the  scapula 
to  the  vertebral  column  (rhomboidei)  and  the  raising  of  the  scapula  (levator  an- 
guli scapulae)  are  completely  abolished. 

Paralysis  of  the  Latissmus  Doesi  (subscapular  nerves). — There  is  no  de- 
formity when  at  rest,  but  the  arm  can  not  be  strongly  adducted  inward  and 
backward  or  held  firmly  to  the  trunk,  and  the  hand  can  not  be  placed  on  the 
sacrum.  The  latissimus,  like  the  pectoralis  major,  acts  in  drawing  down  vigor- 
ously the  raised  arm.  Finally,  when  the  latissimus  is  paralyzed,  it  affects  the 
throwing  back  of  the  shoulders,  as  in  the  position  of  the  soldier. 

Paralysis  of  the  Eotators  of  the  Humerus  Inward  asb  Outward. — Move- 
ments of  rotation  at  the  shoulder- joint  are  best  tested  when  the  forearm  is  flexed 
at  a  right  angle.    In  paralysis  of  the  inward  rotators  (especially  the  subscapular, 

innervated  by  the  sub- 
scapular    nerve),     the 
arm,  when  rotated  out- 
ward,     can      not      be 
brought  back  again  to 
its      normal     position. 
All  manipulations,  too, 
which     the     paralyzed 
arm  tries  to  make  on 
the  opposite  side  of  the 
body,   are  considerably 
impaired.    In  paralysis 
of    the    outward    rota- 
tors—the   infra-spinat- 
us,   innervated   by  the 
supra-scapular      nerve, 
and    the    teres    minor, 
innervated  by  the  axil- 
lary —  rotation  of  the 
arm    outward   is    abol- 
ished.    In  writing  and 
sewing  (using  the  nee- 
dle),      the       paralysis 
causes     very     marked 
disturbance.       Paraly- 
sis of  the  teres  major 
(subscapular        nerve) 
causes  hardly  any  no- 
ticeable      disturbance, 
since  this  muscle  acts 
merely  as  an  aid  to  the 
latissimus     dorsi     and 
pectoralis  major. 

Paralysis  of  the 
Serratus  Anticus  Ma- 
jor (paralysis  of  the  long  thoracic  nerve). — This  paralysis  is  quite  common,  and 
therefore  is  of  practical  importance.  Its  most  frequent  cause  is  mechanical  injury 
of  the  long  thoracic  nerve,  such  as  may  occur  especially  in  porters,  field-hands  who 
carry  sacks,  soldiers  in  fighting,  etc.    We  also  see  at  times  a  neuritie  paralysis  of 


Fig.  107.— Paralysis  of  the  right  serratus  (personal  observation).    Wing- 
like protrusion  of  the  right  scapula  when  the  arm  is  stretched  forward. 


THE    DIFFEEENT    FOEMS    OF    PEEIPHERAL   PAEALYSIS     865 

the  serratus,  coming  on  with  j)ain  in  the  shoulder  either  without  any  discoverable 
cause,  or  as  the  result  of  taking  cold  ("  rheumatic  serratus  paralysis  ")•  Finally, 
serratus  paralysis  may  follow  acute  infectious  diseases,  especially  typhoid  fever, 
where  it  is  probably  also  of  neuritic  origin.  We  have  seen  serratus  paralysis 
after  acute  articular  rheumatism  and  once  after  gonorrhoea.  Bilateral  paraly- 
sis of  the  serratus  is  seen  as  one  symptom  of  extensive  muscular  atrophy,  espe- 
cially in  juvenile  muscular  dystrophy.  A  congenital  absence  of  both  serrati  also 
occurs  with  the  corresponding  disturbances  of  function. 

As  the  arm  hangs  down  quietly,  the  scapula  on  the  paralyzed  side  is  some- 
what raised  and  stands  out  a  little  from  the  chest-wall,  from  the  action  of  the 
antagonists  (the  traction  of  the  levator  anguli  scapulae,  the  trapezius,  and  the  pec- 
toralis),  its  lower  angle  is  a  little  approxiraated  to  the  vertebral  column,  and 
therefore  its  median  edge  runs  obliquely  upward  and  outward  (traction  of  the 
rhomboidei).  This  faulty  position  of  the  scapula,  however,  is  in  many  cases  only 
of  slight  degree. 

If  the  patient  wishes  to  raise  his  arm,  he  can  raise  it  only  to  the  horizontal 
position,  and  we  fail  to  see  the  projection  of  the  tense  indentations  of  the  serratus 
on  the  lateral  wall  of  the  chest;  but  as  soon  as  we  seize  the  scapula  firmly 
and  push  it  forward — that  is,  supply  the  missing  action  of  the  serratus — the  pa- 
tient can  at  once  raise  the  arm.  If  the  arm  is  raised  outward  to  the  horizontal 
line,  the  scapula  approaches  the  vertebral  column.  The  somewhat  projecting 
lower  angle  then  comes  almost  behind  the  spinous  process.  The  muscular  masses 
of  the  trapezius  and  rhomboidei  are  crowded  together  and  form  a  swelling  which 
is  absent  on  the  healthy  side  when  the  arms  are  in  the  same  position.  If  the 
patient  moves  his  arm  forward,  which  has  been  raised  outward,  the  scapula  turns 
about  its  vertical  axis  and  makes  a  wing-like  projection  almost  perpendicular  to 
the  surface  of  the  back  (vide  Fig.  107).  We  can  now  take  the  scapula  between 
two  fingers  and  grasp  its  whole  inner  surface.  The  latter  forms  a  deep  hollow 
with  the  middle  part  of  the  back.  Serratus  paralysis  can  almost  always  be  recog- 
nized at  the  first  glance  from  this  extremely  characteristic  and  peculiar  position 
of  the  scapula.  In  some  cases  the  patient  can  still  raise  the  arm  almost  com- 
pletely to  the  perpendicular  in  spite  of  paralysis  of  the  serratus.  This  is  prob- 
ably done  by  the  help  of  the  middle  portion  of  the  trapezius.  Disturbances  of 
sensation  are  often  entirely  absent,  but,  on  careful  testing,  we  can  often  find  a 
slight  disturbance  in  the  region  of  the  scapula  and  shoulder  in  traumatic  and 
neuritic  paralysis. 

The  course  of  serratus  paralysis  is  usually  quite  tedious,  but,  as  a  rule,  in  ordi- 
nary peripheral  paralyses,  recovery  takes  place  after  several  months.  Many  cases 
are  incurable.  Treatment  consists  chiefly  in  the  application  of  electricity  to  the 
paralyzed  nerve  and  muscles. 

5.  Paralyses  of  the  Muscles  of  the  Back  and  Abdomen. 
The  muscles  of  the  back  and  abdomen  are  rarely  paralyzed  except  as  a  com- 
plication of  more  extensive  disease.  Paralysis  of  these  muscles  is  seen  most 
frequently  in  the  different  forms  of  juvenile  muscular  dystrophy  (q.v.).  If  the 
erector  spinse  on  both  sides  is  atrophied  and  paralyzed,  the  vertebral  column 
when  the  patient  is  sitting  forms  a  curve  with  the  convexity  backward.  The 
patient  supports  himself  by  putting  the  hands  on  the  thighs,  lest  the  trunk  fall 
forward.  When  the  trunk  is  bent  forward  it  is  difficult  or  impossible  to  regain 
the  upright  position.  On  standing,  the  trunk  sinks  backward,  so  that  a  plummet 
dropped  from  the  upper  thoracic  vertebrae  would  fall  behind  the  sacrum.  The  an- 
terior portion  of  the  pelvis  is  raised  by  the  contraction  of  the  abdominal  muscles 
necessary  to  maintain  the  equilibrium.  If  the  abdominal  muscles  are  paralyzed, 
the  patient  can  no  longer  raise  the  trunk  to  an  erect  position,  when  lying  on 
55 


866  DISEASES    OF   THE   NEKVOUS    SYSTEM 

his  back,  without  the  aid  of  the  arms.  On  standing  erect,  the  belly  is  very  promi- 
nent, the  anterior  portion  of  the  pelvis  is  sunk,  and  the  spinal  column  is  bent  in 
marked  lordosis.  A  plummet  dropped  from  the  upper  thoracic  vertebraB  would 
strike  about  in  the  middle  of  the  sacrum.  The  implication  of  the  smaller  spinal 
muscles,  not  mentioned  here,  is  difficult  to  determine  positively.  If  the  extensor 
of  the  back  as  well  as  the  abdominal  muscles  are  paralyzed,  it  is  no  longer  pos- 
sible to  keep  the  trunk  erect. 

6.  Paralyses  in  the  Region  of  the  Upper  Extremity 
Paralysis  of  the  Deltoid  Muscle  (axillary  [^circumflex]  nerve). — Deltoid 
paralysis  occurs  either  as  one  symptom  of  complicated  paralyses  involving  the 
brachial  plexus,  or  as  an  isolated  traumatic  and  rheumatic  paralysis ;  that  is,  neu- 
ritic,  beginning  with  pains  in  the  region  of  the  shoulder.  After  acute  articular 
rheumatism  {q.  v.),  when  the  shoulder  has  been  involved,  we  have  also  repeatedly 
seen  deltoid  paralysis  ("  arthritic  or  arthropathic  paralysis  ")  with  atrophy  of  the- 
muscles.  Finally  deltoid  paralysis  is  a  common  symptom  in  the  most  varied 
spinal  and  cerebral  diseases.  The  characteristic  symptom  of  deltoid  paralysis  is 
the  imj)ossibility  of  raising  the  upper  arm  when  it  is  hanging  down  vertically, 
but  we  must  remember  that  the  different  parts  of  the  deltoid  need  not  always 
be  equally  affected.  The  anterior  bundle  of  the  muscle  raises  the  arm  obliquely 
forward  and  inward,  the  middle  bundle  outward,  and  the  posterior  bundle  back- 
ward; the  latter  also  serves  chiefly  to  draw  the  arm  outward  and  backward  when 
it  has  been  raised  forward.  The  arm  is  raised  forward  and  outward  by  the 
action  of  the  deltoid  only  up  to  the  horizontal,  and  it  is  raised  backward  only  ta 
an  angle  of  about  forty-five  degrees.  To  raise  the  arm  completely  to  the  per- 
pendicular the  serratus  anticus  must  act  (vide  supra).  If  the  anterior  bundle 
of  the  deltoid  be  chiefly  paralyzed,  the  patient  can  no  longer  put  his  hand  to  his 
head,  raise  the  arm  to  the  opposite  shoulder,  etc.  If  the  posterior  bundle  be- 
paralyzed  he  can  no  longer  put  his  hand  in  his  trousers'  pocket.  In  complete 
paralysis  the  arm  usually  hangs  down  loosely.  If  the  patient,  nevertheless,  makes, 
a  vigorous  effort  to  raise  his  arm,  the  shoulder  is  usually  raised  and  the  scaptda 
turned  from  the  contraction  of  the  trapezius  and  serratus.  In  a  few  cases  only 
has  it  been  observed  that,  where  the  deltoid  is  wholly  paralyzed,  the  patient  can 
still  raise  his  arm  by  the  aid  of  the  upper  portion  of  the  pectoralis  major  or  of 
the  supra-spinatus  and  trapezius.  It  is  easy  to  avoid  mistaking  anchylosis  of  the 
shoulder-joint  for  deltoid  paralysis  by  making  a  few  passive  movements  of 
the  arm. 

Paralysis  of  the  Biceps  and  Brachialis  Anticus  {musculo-cutaneous  nerve) 
is  only  exceptionally  an  isolated  paralysis,  but  it  is  quite  often  seen  combined  with 
other  paralyses.  The  forearm,  when  in  supination,  can  not  be  flexed,  but  in  pro- 
nation the  supinator  longus  can  still  display  its  action  of  flexion.  The  action  of 
supination  by  the  biceps,  which  it  exerts  when  the  forearm  is  flexed,  is  also  absent. 
We  can  readily  recognize  this  action  on  ourselves  by  making  a  rapid  and  forcible 
movement  of  supination  when  the  forearm  is  flexed  and  then  feeling  the  contrac- 
tion of  the  biceps  with  the  flngers.  We  sometimes  see  at  the  same  time  a  disturb- 
ance of  sensibility  on  the  radial  side  of  the  forearm  from  an  affection  of  a 
cutaneous  branch  of  the  musculo-cutaneous  nerve. 

Radial  [Musculo-spiral]  Paralysis.— The  anatomical  course  of  the  radial 
nerve  causes  pressure  paralysis  of  this  nerve  to  be  among  the  commonest 
peripheral  paralyses.  It  is  seen  especially  when  the  nerve  is  pressed  against  the 
humerus  during  sleep  by  the  body  or  head  lying  on  it,  in  drunkenness,  sleeping- 
on  a  wooden  bench,  on  the  hard  ground,  etc.  The  paralysis  is  usually  noticed 
immediately  on  waking.  Other  traumatic  influences,  direct  injuries  of  the  nerve, 
compression  in  dislocation  of  the  shoulder,  in  fractures  of  the  humerus,  in  pres- 


THE    DIFFEEENT   FOEMS    OF   PEEIPHEEAL   PAEALYSIS    867 


sure  from  crutches,  in  bandaging  or  fettering  the  arm,  etc.,  are  also  frequent 
causes  of  radial  paralysis.  It  is  worthy  of  note  that  paralysis  of  the  extensor  digi- 
torum  has  been  repeatedly  seen  to  follow  subcutaneous  injections  of  ether  on  the 
extensor  side  of  the  forearm.  Exposure  to  cold  (rheumatic  radial  paralysis)  plays 
no  very  great  part  in  the  etiology  of  paralysis.  Eadial  paralysis  is  also  rare  after 
acute  infectious  diseases.  For  lead  paralysis,  which  is  localized  chiefly  in  the  dis- 
tribution of  the  radial,  vide  infra. 

The  radial  innervates  the  triceps  and  the  muscles  on  the  extensor  side  of  the 
forearm.  Paralysis  of  the  triceps  is  present  only  in  the  cases  where  the  point  of 
lesion  is  situated  quite  high  up,  as  in  crutch  paralyses,  dislocation  paralyses, 
plexus  paralyses,  etc.,  but  it  is  absent,  or  at  least  it  is  only  faintly  manifest,  in 
most  of  the  ordinary  pressure  paralyses,  in  which  the  place  where  the  radial  turns 
about  the  humerus  is  the  point  of  compression.  Triceps  paralysis  is  readily  recog- 
nized by  the  impossibility  of  extending  the  forearm,  but  we  must  always  make  the 
experiment  with  the  upper  arm  raised,  so  as  to  exclude  the  action  of  gravity  in 
extending  the  forearm. 

Paralysis  of  the  muscles  on  the  extensor  side  of  the  forearm  may  at  once  be 
recognized,  since  the  hand  hangs  down  relaxed  in  a  flexed  position  (see  Fig.  108). 
Any   dorsal   extension   by 

the  extensor  carpi  ulnaris  -  - 

and  the  extensores  carpi 
radialis  longus  et  brevis 
is  impossible,  and  the 
lateral  movements  of  the 
hand  in  abduction  and  ad- 
duction are  rendered  dif- 
ficult. The  fingers  are 
flexed,  the  first  phalanx 
can  not  be  extended  by 
the  extensor  communis 
digitorum,  extensor  indi- 
cis,  and  extensor  minimi 

digiti;  but  if  the  first  phalanges  be  extended  passively  and  supported,  the  ex- 
tension of  the  terminal  phalanges  is  perfectly  normal,  from  the  action  of  the 
interossei  which  are  supplied  by  the  ulnar  nerve.  The  thumb  is  flexed  and 
adducted,  and  can  neither  be  abducted  nor  extended  actively  (extensores 
ossis  metacarpi  et  primi  et  secundi  internodii  pollicis).  If  the  forearm 
be  extended  and  pronated  it  can  not  be  supinated  (supinator  brevis),  but  the 
flexed,  forearm  can  be  supinated  by  the  biceps.  Flexion  of  the  forearm  in  supina- 
tion, which  is  done  by  the  biceps  and  brachialis  anticus,  is  retained,  but  flexion 
when  half  pronated  ("  middle  position  ")  is  weakened,  from  the  paralysis  of  the 
supinator  longus.  If  we  have  the  patient  make  short  and  rapid  movements  of 
flexion  of  the  forearm  in  this  position  we  do  not  see  the  characteristic  normal 
prominence  of  the  tense  supinator  longus.  The  very  characteristic  prominence 
of  this  muscle  is  also  wanting  if  the  patient  tries  to  hold  his  pronated  and  semi- 
flexed forearm  firm  against  forcible  attempts  at  extension.  The  supinator  longus 
is  only  exceptionally  spared  in  radial  paralysis. 

The  functional  disturbance  of  the  hand  in  radial  paralysis  is  very  consider- 
able. The  action  of  the  flexors  is  also  weakened,  since  their  points  of  insertion 
are  approximated,  on  account  of  the  constant  drooping  of  the  hand.  "We  often 
see,  too,  sensory  disturbances,  as  well  as  motor,  in  the  distribution  of  the  radial, 
but  these  are  usually  slight.  The  chief  seat  is  on  the  radial  half  of  the  back  of  the 
hand  and  the  dorsal  surface  of  the  thumb,  and  index  and  middle  fingers  (compare 
Fig.  87,  page  801).    The  electrical  excitability  of  the  paralyzed  parts  corresponds 


Fig.  108. 


-Position  of  the  hand  in  paralysis  of  the  radial  nerve. 
(From  Seeugmuller.) 


DISEASES    OF    THE   A^EEA^OUS    SYSTEM 


to  the  laws  that  generally  obtain.  At  the  onset,  and  in  mild  cases,  it  is  normal ;  at 
a  later  period,  in  severe  cases,  there  are  pronounced  atrophy  and  reaction  of  de- 
generation. It  is  "worthy  of  note  that  in  all  forms  of  radial  paralysis,  especially  in 
lead  paralysis,  we  very  often  find  a  peculiar  chronic  thickening  and  swelling  of 
the  tendons  on  the  back  of  the  hand,  the  chief  cause  of  which  is  probably  the 
mechanical  tension  of  the  tendons. 

Ulnar  Paralysis. — Except  frora  the  frequent  implication  of  the  muscles  sup- 
plied by  the  ulnar  nerve  in  extensive  paralyses  and  atrophies,  especially  in  pro- 
gressive muscular  atrophy,  ulnar  paralysis  arises  chiefly  from  traumatic  influ- 
ences, pressure,  wounds,  fractures  of  the  humerus,  especially  fractures  of  the  in- 
ternal condyle,  dislocations  of  the  shoulder- joint,  etc.  Primary  neuritic  paralyses 
or  paralyses  following  acute  diseases,  such  as  typhoid  fever,  are  much  more  rare. 
Flexion  of  the  hand,  and  especially  its  lateral  movement  to  the  ulnar  side,  is 
disturbed  (flexor  carpi  ulnaris).  Flexion  of  the  last  three  fingers  is  imperfect 
from  partial  paresis  of  the  flexor  profundus  digitorum,  and  the  little  finger  can 
not  be  moved  at  all  (hypothenar  muscles).  Paralysis  of  the  interossei  and  the 
last  two  lumbricales  is  most  striking,  by  which  flexion  of  the  proximal  phalanges 
and  extension  of  the  terminal  phalanges  of  the  fingers  becomes  impossible.  The 
defective  extension  of  the  terminal  phalanges  is  most  plainly  seen  when  we  hold 
the  proximal  phalanges  firmly  and  ask  the  patient  to  extend  the  fingers  fully. 
The  last  two  fingers  remain  less  extended  than  the  index  and  middle  fingers, 
whose  lumbricales  are  innervated  by  the  median  nerve.  Spreading  the  fingers, 
and  still  more  bringing  them  together  again,  is  also  much  impaired  (interossei, 
lumbricales).  The  thumb  can  not  be  adducted  against  the  metacarpal  bone  of 
the  index-finger  (adductor  pollicis)  or  held  firmly  in  this  position. 

In  almost  all  old  cases  of  ulnar  paralysis  a  very  characteristic  position  of  the 
hand  is  developed,  besides  the  muscular  atrophy  which  is  especially  noticeable  in 

the  interosseal  furrows  of 
the  back  of  the  hand.  By 
the  contraction  of  the  mus- 
cles antagonistic  to  the 
paralyzed  interossei  (ex- 
tensor and  flexor  communis 
digitorum),  the  first  pha- 
langes are  put  in  marked 
dorsal  extension,  but  the 
terminal  phalanges  are 
flexed,  so  that  the  hand  as- 
sumes an  actual  clawing 
position — "  claw-like  hand," 
main  en  griffe  (see  Fig. 
109).  A  similar  position  of 
the  fingers  occurs  as  a  con- 
genital anomaly  (in  small  children),  and  is  probably  due  to  defective  develop- 
ment or  complete  absence  of  the  interossei. 

The  disturbance  of  sensibility,  if  it  be  present  at  all,  affects  the  volar  surface 
of  the  last  two  fingers,  the  dorsal  surface  of  the  last  three  fingers,  and  a  portion 
of  the  back  of  the  hand  (see  Figs.  87,  88,  and  89).  Trophic  disturbances  of  the 
skin  of  the  fingers  are  not  infrequently  seen. 

Median  Paralysis. — Isolated  peripheral  median  paralysis  is  seen  chiefly  as  a 
traumatic  paralysis,  much  more  rarely  as  neuritic  paralysis.  Disturbances  in  the 
muscles  innervated  by  the  median  are  comparatively  common  as  a  complication 
of  more  extensive  paralyses,  in  cerebral  and  spinal  diseases  (progressive  mus- 
cular atrophy). 


Fig.  109. — Paralysis  of  the  ulnar  nerve.  Atrophy  of  the  inter- 
ossei. The  terminal  phalanges  can  not  be  extended.  (From 
the  Erlangen  Medical  Clinique.) 


THE   DIFFEEENT   FOKMS    OE   PERIPHEEAL   PAEALYSIS    869 

The  disturbances  of  motion  are  very  striking.  Pronation  of  the  forearm  is 
almost  wholly  abolished  (pronator- radii  teres  and  quadratus).  The  hand  can  be 
flexed  only  toward  the  ulnar  side  by  the  flexor  carpi  ulnaris  (paralysis  of  the 
flexor  carpi  radialis).  The  terminal  phalanges  of  the  fingers  can  no  longer  be 
flexed  (flexor  sublimis  digitorum  and  a  part  of  the  profundus),  but  flexion  of  the 
primary  phalanges  is  normal  by  means  of  the  interossei.  The  patient  can  grasp 
an  object  only  by  the  last  three  fingers,  which  can  still  be  partly  flexed  by  the 
flexor  profundus  digitorum  (ulnar  nerve).  The  terminal  phalanx  of  the  thumb 
can  no  longer  be  flexed  (flexor  longus  poUicis),  and  the  first  phalanx  can  be  flexed 
only  when  the  thumb  is  also  adducted  by  the  adductor  and  the  inner  head  of  the 
flexor  brevis  (ulnar  nerve).  The  thumb  can  not  be  opposed  at  all  (touching  the 
terminal  phalanx  of  the  little  finger  with  the  thumb),  since  the  muscles  that  act 
for  opposition  (opponens,  abductor  brevis,  and  outer  head  of  the  flexor  brevis) 
are  all  innervated  by  the  median  nerve.  The  thumb  therefore  lies  with  the  meta- 
carpus turned  backward  in  extension  as  a  result  of  the  unopposed  action  of  the 
extensor  longus  ("  ape  position  "). 

If  there  is  any  disturbance  of  sensibility,  it  is  found  on  the  volar  surface  of 
the  thumb  and  the  two  adjacent  fingers,  and  also  on  the  dorsal  surface  of  the 
terminal  and  middle  phalanges  of  the  index  and  middle  fingers,  and  the  radial 
side  of  the  ring-finger  (see  Figs.  88  and  89).  In  severe  eases  trophic  disturb- 
ances, vesicles  on  the  fijigers,  a  shining  atrophic  skin,  and  changes  in  the  nails  are 
often  present. 

Combined  Paralyses  of  the  Arm  Muscles. — Combined  paralyses,  in  which  the 
affected  muscles  belong  to  the  distribution  of  several  nei'ves,  occur  in  various 
forms,  especially  as  a  result  of  injuries  which  affect  the  brachial  plexus  in  the 
neck  or  shoulder — plexus  paralyses.  There  is  either  direct  injury  of  the  nerves 
by  a  blow  or  wound,  or  indirect  injury  from  luxation  of  the  humerus,  fracture  of 
the  head  of  the  humerus  and  the  clavicle,  tumors  in  the  supra-clavicular  fossa,  etc. 
Plexus  paralyses  from  primary  neuritis  also  occur. 

Among  the  many  possible  combinations  of  plexus  paralyses,  one  form,  first 
described  by  Erb,  and  since  then  repeatedly  observed,  deserves  special  mention. 
In  this  the  deltoid,  biceps,  brachialis  anticus,  and  supinator  longus  (muscles 
whose  nerves  all  rise  from  the  roots  of  the  fifth  and  sixth  cervical  nerves)  are 
paralyzed  at  the  same  time.  The  same  combination  of  paralysis  therefore  occurs 
as  if  the  motor  roots  of  the  fifth  and  sixth  cervical  nerves  were  themselves  af- 
fected. The  arm  hangs  down  relaxed,  and  can  not  be  raised  at  all;  the  forearm 
can  not  be  flexed  at  all,  but  the  hand  and  fingers  have  their  normal  mobility. 
The  cause  of  the  paralysis  must  have  its  seat  at  the  point  where  the  nerve-fibers 
for  the  muscles  mentioned  lie  near  one  another  (see  Fig.  99).  The  supinator 
brevis  and  infra-spinatus  are  also  not  very  infrequently  paralyzed  at  the  same 
time,  so  that  the  forearm,  when  pronated  and  hanging  down,  can  not  be  supinated, 
and  the  humerus,  when  rotated  inward,  can  not  be  turned  outward.  The  supra- 
spinatus  and  subscapularis  may  also  be  involved  in  the  paralysis.  Sensory  dis- 
turbances are  usually  slight,  but  they  may  sometimes  be  found  on  the  outer  side 
of  the  upper  arm  and  forearm. 

This  same  combination  of  paralyzed  muscles  is  found  in  a  part  of  the  delivery 
paralyses  first  described  by  Duchenne.  These  are  sometimes  seen  in  infants  after 
hard  labor,  and  are  the  result  of  injuries  of  the  brachial  plexus  in  turning,  in 
bringing  down  the  raised  arm.  in  the  Prague  method,  in  extracting  the  child  by 
the  shoulders,  in  forceps  delivery,  etc.  Such  obstetrical  paralyses  may  get  entirely 
well  in  a  few  weeks  or  months,  but  not  infrequently  permanent  atrophic  paralyses 
remain. 

Another  rare  form  of  plexus  paralysis  occurs  from  injury  of  the  fibers  coming 
from  the  eighth  cervical  and  first  dorsal  nerves.     This  leads  to  paralysis  of  the 


870  DISEASES    OF    THE   XEKVOUS    SYSTEM 

smaller  muscles  of  the  hand  (thenar,  interossei)  and  the  flexor  muscles  on  the 
palmar  side  of  the  forearm.  Slight  disturbances  of  sensibilitv  are  usually 
present  at  the  same  time  in  the  ulnar  and  median  region. 

In  some  cases  of  complicated  paralyses  of  the  brachial  plexus,  which  are  usu- 
ally traumatic  (Seeligmiiller  and  others),  co-existing  symptoms  on  the  part  of  the 
sympathetic  have  been  observed,  consisting  of  contraction  of  the  pupil,  narrowing 
of  the  opening  of  the  lids,  and  a  retraction  of  the  eyeball  on  the  paralyzed  side. 
These  symptoms,  pointing  to  a  paralysis  of  sympathetic  nerves  (vide  infra,  page 
905),  are  probably  always  due  to  a  lesion  of  the  ramus  communicans  of  the  first 
dorsal  nerve,  as  follows  from  clinical  and  experimental  investigations  (Klumpke). 
Vaso-motor  symptoms  in  the  face  are  usually  absent,  but  we  sometimes  find  a 
peculiar  flattening  of  the  cheeks,  which  has  not  yet  been  correctly  explained. 

Occupation  Paralyses. — In  certain  occupations  in  which  certain  muscles  or 
groups  of  muscles  or  nerves  are  over-excited  or  exposed  to  persistent  pressure, 
paralyses  may  occur  which  merit  a  brief  mention.  Thus  we  see  not  infrequently 
atrophic  paralysis  of  the  muscles  of  the  ball  of  the  thumb  in  file-cutters,  linen- 
ironers,  basket-weavers,  locksmiths,  joiners,  etc.,  and  atrophy  of  the  interossei  in 
cigar-rollers.  Bruns  has  described  an  isolated  paralysis  of  the  flexor  poUicis 
longus  as  sometimes  occurring  in  drummers  as  a  result  of  over-exertion.  The 
prognosis  of  these  paralyses,  which  are  often  associated  with  parsesthesise  and 
slight  sensory  disturbances,  is  not  unfavorable,  provided  the  patient  can  give  up 
his  harmful  calling. 

General  Prognosis  and  Treatment  of  the  Peripheral  Paralyses  of  the  Upper 
Extremity. — In  the  prognosis  of  the  peripheral  paralyses  of  the  arm  the  same 
points  hold  good  that  have  been  spoken  of  in  the  prognosis  of  facial  paralysis. 
In  these,  too,  there  are  mild  and  severe  cases,  the  latter  having  complete  reaction 
of  degeneration,  and  a  course  that  lasts  at  least  several  months  before  recovery. 
A  number  of  traumatic  and  neuritic  paralyses  can  be  cured  only  up  to  a  certain 
point,  or  they  may  be  even  entirely  incurable. 

The  treatment  can  fulfill  a  causal  indication  only  in  comparatively  rare  cases, 
when  we  can  succeed  in  removing  by  operation  any  compressing  tumors,  cica- 
trices, splinters  of  bone,  formations  of  callus,  etc.  When  nerves  have  been  cut, 
suture  of  the  nerve  is  an  extremely  important  measure,  which  promotes  recovery 
and  which  may  be  the  only  possible  means  to  secure  recovery.  In  fresh  neuritic 
paralyses  the  well-known  anti-rheumatics  (antipyrine,  salicylate  of  soda)  are 
sometimes  used,  especially  if  there  is  also  pain. 

In  other  cases  the  electrical  treatment  of  paralyses  promises  the  best  success. 
We  use  the  galvanic  current  chiefly,  although  we  generally  employ  the  faradic 
current  at  the  same  time.  In  regard  to  the  method  of  application,  we  may  employ 
the  stabile  action  of  the  constant  current  on  the  very  point  of  the  lesion,  espe- 
cially in  fresh  cases,  but  the  chief  method  is  the  electrical  irritation  of  the  para- 
lyzed nerves  and  muscles.  We  treat  the  nerve  above  the  point  of  the  lesion  in 
order  to  act  in  some  degree  against  the  hindrance  to  conduction  from  above  and 
to  overcome  it.  The  muscles  are  irritated  by  galvanism  by  stroking  the  cathode 
over  the  individual  paralyzed  muscles.  If  there  is  reaction  of  degeneration,  with 
anodic  contractions  predominating  or  exclusively  present,  we  use  the  anode  for 
the  exciting  pole.  The  other  pole  is  placed  on  the  back  of  the  neck  or  on  the  seat 
of  the  lesion.  Faradization  of  the  muscles  may  also  be  of  service,  especially  if 
the  muscles  react  to  faradism;  but,  even  if  this  is  not  the  case,  the  sensory  far- 
adic irritation  has  perhaps  a  favorable  influence,  since  it  produces  a  reflex  irrita- 
tion of  the  motor  nerves.  The  single  sittings  should  last  five  or  ten  minutes,  and 
should  take  place  daily  or  three  or  four  times  a  week.  The  fresher  the  paralysis, 
the  more  favorable  in  general  is  the  prognosis.  Of  course  in  such  cases  it  is 
usiially  impossible  to  decide  how  much  of  the  improvement  is  to  be  referred  to 


THE    DIFFEEENT    FOEMS    OF    PERIPHERAL   PARALYSIS    871 

the  treatment  and  how  much  to  spontaneous  recovery,  but  we  can  not  deny  that 
we  sometimes  obtain  noteworthy  success  even  in  old  and  severe  cases  by  great 
patience  and  perseverance.  The  treatment  must  in  such  cases  be  kept  up  for 
months,  or  years,  with  occasional  interruptions. 

Embrocations  with  spirits  and  Avith  similar  substances  must  often  be  pre- 
scribed in  practice,  but  they  act  favorably  only  when  associated  with  methodical 
massage  of  the  paralyzed  muscles.  We  sometimes  see  a  certain  advantage,  too, 
from  local  warm  bathing,  or  from  the  use  of  the  baths  in  Teplitz,  Wiesbaden, 
Wildbad,  etc. 

7.  Paralysis  of  the  Diaphragm 

Isolated  paralysis  of  the  diaphragm  occurs  but  rarely,  from  wounds  of  the 
phrenic  nerve  in  the  neck,  also  as  primary  or  secondary  neuritic  (post-diphtheritic) 
paralysis,  and  finally  in  hysteria.  Muscular  paresis  of  the  diaphragm  seems  to  de- 
velop sometimes  as  a  result  of  inflammation  of  the  serous  layer  of  the  diaphragm. 
The  paralysis  of  the  diaphragm  which  comes  on  as  one  symptom  in  more  extensive 
paralyses,  is  more  frequent  and  practically  more  important.  In  diseases  of  the 
upper  cervical  cord,  in  ascending  myelitis,  or  in  compression  of  the  cervical  cord 
by  vertebral  caries  or  meningeal  tumors,  in  progressive  muscular  atrophy,  in  mul- 
tiple neuritis,  etc.,  the  development  of  paralysis  of  the  diaphragm  is  the  cause  of 
the  rapidly  fatal  termination  which  follows  the  appearance  of  disturbance  of 
respiration.  The  roots  of  origin  of  the  phrenic  nerve  are  the  third  and  fourth 
cervical. 

The  symptoms  of  paralysis  of  the  diaphragm  are  readily  recognized,  especially 
in  the  ordinary  bilateral  affection.  We  detect  the  modification  of  the  respiratory 
movements  at  the  first  glance.  While  we  are  struck  by  the  marked  upper  thoracic 
respiration,  which  becomes  very  labored  on  the  slightest  cause,  while  the  visible 
and  palpable  protrusion  of  the  epigastrium  on  inspiration  is  entirely  absent.  In- 
stead of  this  there  is  usually  an  inspiratory  retraction  in  the  epigastric  region. 
The  respiration  is  but  little  accelerated  in  simple  paralysis  of  the  diaphragm  as 
long  as  the  patient  is  perfectly  quiet;  but  in  other  cases  the  development  of  a 
severe  bronchitis,  from  the  defective  respiration  in  the  lower  lobes  of  the  lungs, 
causes  constant  dyspnoea.  The  explanation  of  the  bronchitis  may  be  found  in  the 
fact  that  the  action  of  abdominal  pressure  is  very  much  diminished  by  the  con- 
stant high  position  of  the  diaphragm,  which  may  be  made  out  by  percussion,  and 
consequently  the  cough  and  the  expectoration  of  secretion  are  very  imperfect. 

The  prognosis  is  favorable  only  in  hysterical  and  rheumatic  paralyses ;  other- 
wise it  is  usually  very  unfavorable.  In  regard  to  treatment,  the  only  thing  that 
can  be  tried  is  to  stimulate  the  diaphragm  from  the  phrenic  in  the  neck  by  f ara- 
dism  or  galvanism,  while  the  other  pole  is  placed  on  the  region  of  the  insertion  of 
the  diaphragm  in  the  thorax.  A  transverse  conduction  of  the  constant  current 
through  the  diaphragm,  associated  with  changes  of  the  current,  may  also  have  a 
favorable  influence. 

8.  Paralyses  in  the  Region  of  the  Lower  Extremity 
Paralysis  of  the  Crural  ISTerve. — Crural  paralysis  is  but  rarely  isolated. 
It  is  seen  after  injuries,  after  compression  of  the  nerve  by  tumors  of  the  pelvis  or 
thigh,  in  disease  of  the  vertebrae,  psoas  abscess,  etc.  There  is  also  a  primary 
neuritis  of  the  crural  nerve,  and  finally  paralysis  of  the  quadriceps  sometimes 
follows  acute  articular  rheumatism  and  other  affections  involving  the  knee-joint. 

The  most  important  muscles  innervated  by  the  crural  nerve  are  the  ilior 
psoas  and  the  extensor  cruris  quadriceps.  The  paralysis  of  these  muscles  is  read- 
ily recognized.  The  thigh  can  not  be  flexed  on  the  trunk,  and  the  trunk  can  be 
raised  from  the  recumbent  position  (ilio-psoas  muscle)  only  with  difficulty  (by 


872  DISEASES    OF    THE    JsTERVOUS    SYSTEM 

the  help  of  the  abdominal  muscles,  vide  supra).  If  the  thigh  be  flexed  passively 
in  bed  the  dependent  lower  leg  can  not  be  extended  or  raised  in  the  air  (extensor 
cruris  quadriceps).  In  peripheral  paralysis  of  the  quadriceps  the  patellar  reflex 
of  course  is  absent.  Walking  and  standing  are  very  difficult  or  almost  impossible, 
since  the  ilio-psoas  is  necessary  for  the  stride  forward  and  the  quadriceps  for 
fixation  of  the  knee-joint.  Paralysis  of  the  sartorius  and  pectineus  causes  no 
special  symptoms,  but  it  can  be  recognized  by  the  failure  of  these  muscles  to 
contract  when  their  movements  are  opposed.  If  there  is  any  disturbance  of  sen- 
sibility it  is  found  in  the  lower  half  of  the  anterior  surface  of  the  thigh  and 
on  the  inner  side  of  the  leg  down  to  the  great  toe  (saphenous  nerve,  see  Figs. 
90  and  91). 

Paralysis  of  the  Obturator  Nerve  is  very  rarely  seen  as  an  isolated  phe- 
nomenon. The  chief  symptoms  are  the  defective  adduction  of  the  thigh  (the  ad- 
ductor magnus,  longus,  and  brevis,  and  the  gracilis),  and  the  impossibility  of 
crossing  one  leg  over  the  other.  Rotation  of  the  thigh  outward  is  also  disturbed 
(obturator  externus).  Some  disturbance  of  sensibility  may  be  found  on  the  inner 
side  of  the  thigh. 

Isolated  Paralyses  in  the  Distribution  of  the  Gluteal  Nerves  are  not  common, 
but  the  muscles  supplied  by  these  nerves  are  often  very  markedly  implicated  in 
more  extensive  paralytic  conditions,  especially  in  muscular  dystrophy  and  mul- 
tiple neuritis.  Paralysis  of  the  glutasus  maximus  is  rendered  noticeable  by  the 
fact  that  this  muscle  extends  the  thigh  on  the  pelvis.  It  is  therefore  especially 
called  into  play  in  going  up-stairs,  climbing  mountains,  and  rising  from  a  sitting 
or  recumbent  position.  All  these  movements  are  rendered  nearly  impossible  when 
the  muscles  are  paralyzed.  While  walking  on  level  ground  is  only  slightly  af- 
fected, the  patient  can  not  step  up  upon  any  step,  he  can  get  up  from  a  chair  only 
with  effort,  etc.  On  rising  from  a  sitting  position  from  the  floor  the  trunk  is 
raised  by  supporting  the  arms  on  the  thighs  (see  the  illustration  in  the  chapter  on 
juvenile  muscular  atrophy).  When  the  patient  is  in  bed  we  may  test  the  func- 
tion of  the  glutseus  maximus  by  holding  the  flexed  thigh  tightly  with  the  hand 
and  making  the  patient  extend  it.  The  glutseus  medius  and  glutasus  minimus  are 
abductors  of  the  thigh,  and  also  fix  the  thigh  on  the  pelvis.  If  they  are  paralyzed 
the  patient  has  a  very  characteristic  waddling  gait.  On  account  of  the  predomi- 
nance of  the  adductors  the  feet  are  then  advanced  near  each  other  or  even  one 
over  the  other.  The  glutseus  medius  is  also  a  rotator  of  the  thigh  inward,  so 
that  when  it  is  paralyzed  the  outward  rotators  (pyriformis,  obturator  internus 
and  externus,  gemelli,  and  quadratus  femoris)  exert  a  predominant  action. 

Paralyses  in  the  Region  of  the  Sciatic  come  from  traumatic  lesions,  from 
continuous  pressure  on  the  nerve  from  working  in  a  squatting  position  (field 
work,  etc.),  from  pelvic  tumors,  and  in  hard  labors  (pressure  of  the  forceps,  or, 
with  a  narrow  pelvis,  pressure  of  the  presenting  head  on  the  nerves).  Isolated 
primary  neuritic  paralysis  in  the  sciatic  region  is  rare,  but  we  quite  frequently  see 
peroneus  paralysis  as  a  symptom  of  more  extensive  multiple  neuritis  (alco- 
holic polyneuritis,  neurotic  muscular  atrophy,  etc.).  Diabetic  neuritis  may  also  be 
localized  in  the  peroneal  nerve.  Very  marked  paralytic  symptoms  in  the  region 
of  the  sciatic  are  seen  in  diseases  of  the  conus  terminalis  and  the  cauda  equina 
(lesions  of  the  lumbar  vertebrse  and  sacrum). 

Peroneus  Paralysis. — Of  the  two  main  branches  of  the  sciatic,  the  peroneus 
and  the  tibial,  the  former  is  far  more  frequently  affected  than  the  latter.  Even 
in  injuries  of  the  sciatic  trunk,  the  peroneus  paralysis  is  usually  much  more  evi- 
dent than  the  injury  of  the  tibialis  fibers.  We  can  readily  understand  that  the 
peroneal  nerve  itself  is  quite  often  subject  to  external  injury  from  its  superficial 
position.  The  symptoms  of  peroneus  paralysis  are  very  readily  recognized.  The 
flaccid  drooping  of  the  toe  strikes  the  observer  at  once.     On  walking,  this  becomes 


THE   DIFFERENT   FORMS    OF   PERIPHERAL   PARALYSIS    873 

firy  marked,  and  the  tip  of  the  foot  often  sticks  to  the  floor.  The  patient,  there- 
fore, has  to  raise  the  thigh  higher,  and  to  put  the  foot  down  awkwardly,  toe  first 
("  high  action,"  "  steppage  ").  Dorsal  extension  of  the  foot  (tibialis  anticus)  and 
of  the  proximal  phalanges  of  the  toes  (extensor  communis  digitorum  longus  and 
brevis  and  extensor  hallucis  longus),  and  also  abduction  of  the  foot  and  raising  its 
outer  border  (the  peronei),  are  almost  impossible.  In  old  cases  a  permanent  toe- 
drop  (talipes  equinus  or  varo-equinus)  develops,  usually  as  a  result  of  secondary 
contracture  of  the  muscles  of  the  calf,  and  this  is  often  associated  with  a  perma- 
nent flexed  position  of  the  toes  from  secondary  contracture  of  the  interossei. 

Paralysis  of  the  Tibial  jSTerye  makes  jjlantar  flexion  of  the  foot  impossible 
(gastrocnemius  and  soleus).  The  patient  can  no  longer  rise  on  his  toes.  Adduc- 
tion of  the  foot  (tibialis  posticus)  and  plantar  flexion  of  the  toes  (flexor  com- 
munis digitorum  and  flexor  hallucis  longus)  are  also  abolished.  As  a  result  of 
secondary  contractures,  talipes  calcaneus  sometimes  develops,  and  also  a  claw- 
like position  of  the  toes,  with  dorsal  extension  of  the  first  and  plantar  flexion  of 
the  last  phalanges  from  paralysis  of  the  interossei.  If  the  popliteus  be  also 
paralyzed,  the  flexed  lower  leg  can  no  longer  be  rotated  inward. 

In  Paralysis  of  the  Trunk  of  the  Sciatic  there  is  sometimes  added  to  the 
symptoms  mentioned  the  inability  to  flex  the  leg  backward  on  the  thigh  (to  be 
tested  when  the  patient  is  lying  on  his  side  or  standing),  which  is  due  to  a  paraly- 
sis of  the  biceps,  semi-membranosus,  and  semi-tendinosus.  In  unilateral  paraly- 
sis of  the  sciatic,  walking  is  still  possible,  since  the  leg  is  fixed  at  the  knee  by  the 
quadriceps  extensor  and  is  rigid  like  a  wooden  leg. 

The  distribution  of  the  disturbance  of  sensibility  on  the  posterior  surface  of 
the  whole  leg  is  given  in  Fig.  91.  Vaso-motor  and  trophic  disturbances,  cyanosis, 
coldness  and  atrophy  of  the  skin,  and  changes  in  the  nails  are  often  present. 
Atrophy  and  the  electrical  reactions  of  the  paralyzed  muscles  occur  under  the 
same  conditions  as  in  all  other  peripheral  paralyses. 

Paralyses  from  diseases  of  the  cauda  equina  will  be  described  later  in  the 
chapters  on  the  pathology  of  the  spinal  cord. 

Treatment  of  all  the  paralyses  last  described  follows  the  same  rules  as  are 
given  for  the  management  of  peripheral  paralyses  in  the  upper  extremity. 

9.  Toxic  Paralyses 

Lead  Paralysis. — Of  all  the  toxic  paralyses,  that  from  lead  poisoning  is  prac- 
tically the  most  important.  It  is  a  coinmon  symptom  of  chronic  lead  poisoning, 
and  is  seen  ch  afly  in  those  persons  whose  occupation  gives  rise  to  a  long-con- 
tinued absorption  of  small  amounts  of  lead,  especially,  therefore,  in  type-setters, 
type-cutters,  and  type-founders ;  in  artists  and  house-painters,  from  lead  colors ; 
in  potters,  from  lead  glaze;  in  tinkers,  file-cutters,  etc.  Lead  paralysis  may  occur 
as  the  only  symptom  of  chronic  lead  poisoning,  or  it  may  be  associated  in  various 
ways  with  other  symptoms  (lead  colic,  lead  encephalopathy,  etc.). 

The  investigations  of  Leyden,  Zunker,  Schultze,  and  others  agree  in  their 
main  conclusions  that  the  anatomical  cause  of  lead  paralysis  is  certainly  a  degen- 
erative disease  and  ultimate  atrophy  of  the  peripheral  motor  nerve-fibers  belong- 
ing to  the  paralyzed  muscles  caused  by  the  toxic  influence  of  lead.  The  degen- 
erative atrophy  of  the  muscles  is  therefore  to  be  regarded  in  part  as  a  purely  sec- 
ondary disease,  although  it  is  possible  that  the  muscles  may  also  be  injured  by 
the  lead  at  the  same  time  with  the  nerves.  The  spinal  cord,  and  especially  the 
motor  ganglion-cells  in  the  anterior  horns  of  tBe  gray  matter,  remain,  as  a  rule, 
unaltered,  but  undoubtedly,  in  severe,  incurable  cases,  there  may  also  finally  de- 
velop a  toxic  atrophy  of  these  ganglion-cells. 

Lead  paralysis  shows  an  extremely  typical  localization  in  the  great  majority 
of  cases,  and  it  affects  by  far  the  most  frequently  a  part  of  the  radial  distribution. 


874  DISEASES    OF    THE   XEEVOUS    SYSTEM 

A  paralysis  of  the  extensor  communis  digitorum  comes  on  rapidly  or  slowly. 
Extension  of  the  proximal  phalanx  of  the  middle  and  ring,  and  later  of  the  index 
and  little  fingers,  becomes  impossible,  but  the  extension  of  the  terminal  phalanges 
by  the  interossei  remains  normal.  There  often  follows  later  a  paralysis  of  the 
extensor  and  abductor  longus  pollicis  and  the  extensors  of  the  wrist,  and  in  severe 
cases  a  paralysis  of  the  interossei  and  thenar  muscles,  while  the  supinator  longus 
and  the  triceps  almost  always  remain  free  in  a  remarkable  way.  In  much  rarer 
cases  lead  paralysis  affects  the  deltoid,  biceps,  brachialis  anticus,  and  supinators. 
Paralysis  of  the  lower  extremities  is  also  very  rare.  We  have  seen  a  very  char- 
acteristic case  in  which,  besides  extensive  paralysis  of  both  arms,  walking  was  for 
some  time  almost  impossible  on  account  of  bilateral  paralysis  of  the  ilio-psoas 
and  extensor  cruris  (crural  nerve).  The  patient  recovered  completely.  Other 
observers  have  seen  peroneus  paralysis  from  lead  poisoning  [sometimes  without 
noticeable  involvement  of  the  arm  muscles. — K.].  Paralysis  of  the  laryngeal 
muscles  has  also  been  described. 

Lead  paralysis  is  usually  bilateral.  Ordinarily  the  right  forearm  is  first 
affected  and  the  left  arm  some  days  or  weeks  later.  In  all  severe  cases  a  pro- 
nounced atrophy  and  electrical  reaction  of  degeneration  develop  in  the  paralyzed 
muscles.  It  is  an  interesting*  point  that  changes  in  the  electrical  excitability 
(slow  galvanic  contractions,  etc.)  may  sometimes  be  made  out  in  muscles  which 
can  be  perfectly  well  moved  hj  the  will  (see  page  850).  The  sensibility  is  almost 
invariably  normal,  or  at  most  only  very  slightly  altered,  so  that  the  sensory  nerves 
are  manifestly  unaffected  by  the  lead. 

Lead  paralysis  permits  a  favorable  prognosis  in  the  cases  where  the  patient 
can  be  removed  from  the  injurious  influence  of  the  poison.  Recovery  takes  place 
after  several  weeks,  or  in  severe  cases  after  some  months.  Relapses  of  paralysis 
and  complications  with  other  morbid  results  of  chronic  lead  poisoning,  however, 
are,  of  course,  frequent. 

The  treatment  is  the  same  as  in  all  other  peripheral  paralyses.  Electricity  is 
first  to  be  considered.  Local  sulphur  baths  and  the  internal  use  of  iodide  of  potas- 
sium are  also  recommended. 

[In  the  severer  forms  of  chronic  lead  poisoning  the  central  nervous  system 
may  be  affected  as  well  as  the  peripheral  nerves.  In  the  chapter  on  poisons  (q.  v.) 
brief  reference  has  been  made  to  some  of  the  other  conditions  due  to  lead  poison- 
ing. Besides  lead  colic  and  lead  arthralgia  various  forms  of  ansesthesia  and 
parsesthesia  may  occur.  In  the  forms  of  lead  encephalopathy,  besides  the  general 
symptoms  of  headache,  mental  unrest,  and  convulsions  referred  to  above,  we  some- 
times meet  with  symptoms  suggestive  of  a  localized  lesion,  monoplegia  or  hemi- 
plegia, hemianopsia,  amaurosis,  etc.  In  other  cases  the  existence  of  progressive 
dementia  with  tremors,  convulsions,  etc.,  may  lead  to  a  mistaken  diagnosis  of  gen- 
eral paralysis.  In  other  cases  the  symptoms  are  suggestive  of  combined  sclerosis 
of  the  spinal  cord — ataxic  paraplegia  (q.v.).  In  cases  of  doubtful  diagnosis  it 
may  be  of  assistance  to  examine  the  urine  for  lead,  after  iodide  of  potassium  has 
been  given  in  five-  to  ten-grain  doses  thrice  daily  for  a  week.  The  method  of  mak- 
ing such  an  examination  will  be  found  in  the  treatises  on  urinary  analysis.  If 
large  doses  of  iodide  be  given  there  is  some  danger  that  the  lead  will  be  liberated 
too  rapidly  and  that  more  acute  symptoms  may  ensue.  J.  J.  Putnam  has  shovm 
that  lead  is  sometimes  found  in  the  urine  of  healthy  persons.  The  pathology  of 
chronic  lead  poisoning  is  still  undetermined.  The  cerebral  symptoms  have  been 
attributed  to  disseminated  foci  of  encephalitis  or  to  more  chronic  degenerative 
processes.  Since  lead  poisoning  may  cause  contracted  kidney  the  possibility  of 
uraemia  is  also  to  be  considered.  Lead  has  been  found  in  the  urine  in  various 
cases  of  chronic  degeneration  of  the  spinal  cord,  and  it  may  act  as  a  cause  of  such 
affections,  especially  of  combined  scleroses.     It  is  still  uncertain  whether  such 


THE   DIFFEEENT   FORMS    OF   LOCALIZED    SPASM  875 

degeneration  is  due  directly  to  the  toxic  influence  of  the  lead,  or  to  the  severe 
anaemia  produced  by  lead  (compare- the  chapter  on  pernicious  anaemia).  In  all 
severe  cases  of  chronic  lead  poisoning  iodide  of  potassium  should  be  given  for  a 
long  time  to  insure  the  elimination  of  the  lead. — K.] 

Arsenical  Paralysis. — Arsenical  paralysis  is  rare  in  chronic  arsenical  poison- 
ing (colors  containing  arsenic,  hangings,  etc.),  but  it  is  much  commoner  after 
acute  poisoning.  After  the  first  violent  gastro-intestinal  symptoms  are  over,  a 
severe  form  of  nervous  disease  manifests  itself  either  immediately  or  two  or 
three  weeks  later.  The  chief  symptom  of  this  affection  is  an  extensive  atrophic 
paralysis  of  the  arms  and  legs.  The  legs  are  often  affected  alone,  or  at  least  the 
trouble  is  much  more  pronounced  in  them.  The  muscles  of  the  trunk  may  also 
be  involved  in  the  paralysis.  In  general  the  rule  holds  in  arsenical  paralysis  also 
that  the  extensor  muscles  are  more  affected  than  the  flexors.  Electrical  reaction 
of  degeneration  is  found  in  the  atrophied  muscles.  The  accompanying  disturb- 
ances of  sensibility  are  also  very  characteristic,  either  anaesthesia,  or  especially 
paraesthesia  and  severe  pains  in  the  sacrum,  arms,  and  legs.  The  nerve-trunks  are 
soraetimes  very  sensitive  to  direct  pressure.  Ataxic  disturbances,  similar  to  those 
in  alcoholic  neuritis,  also  occur  as  well  as  paralysis.  Trophic  disturbances  in 
the  nails,  hair,  etc.,  have  been  repeatedly  observed. 

There  are  only  a  few  investigations  in  man  as  to  the  anatomical  cause  of 
arsenical  paralysis,  but  there  can  hardly  be  a  doubt  that  the  chief  disturbance  is  a 
severe  neuritic  change.  All  the  morbid  symptoms  are  in  harmony  with  this  (see 
the  chapter  on  multiple  neuritis)  as  well  as  the  general  course  of  the  disease, 
which  in  most  cases  ends  favorably.  Of  course  we  must  not  exclude  the  fact  that 
both  in  lead  and  in  arsenical  paralysis  the  cells  in  the  anterior  horns  may  also  be 
affected  in  some  severe  cases. 

Of  the  other  less  frequent  toxic  paralyses  we  may  mention  here  phosphorus 
paralysis,  copper  and  zinc  paralysis,  and  mercurial  paralysis,  which  in  a  few  cases 
has  been  seen  after  the  therapeutic  use  of  mercury.  Polyneuritis  must  also  be 
considered  to  be  the  chief  cause  of  all  these  paralyses.  Of  organic  compounds, 
carbonic  oxide  and  bisulphide  of  carbon  may  lead  to  toxic  paralyses.  Details  as  to 
the  important  alcoholic  paralysis  will  be  found  in  the  chapter  on  multiple  neuritis. 


CHAPTER   III 
THE    DIFFERENT    FORMS    OF    LOCALIZED    SPASM 

1.  Spasm  in  the  Motor  Distribution  of  the  Trigeminus 

Tonic  spasm  of  the  muscles  of  mastication  is  called  trismus.  As  an  independ- 
ent disease  it  is  very  rare,  but  it  often  occurs  as  one  symptom  in  complicated 
forms  of  spasm  and  other  nervous  affections,  as  in  tetanus,  in  the  epileptic  attack, 
in  hysteria,  meningitis,  etc.  Both  jaws  are  pressed  firmly  together,  and  we  can 
feel  through  the  cheeks  the  hard  and  tense  masseters.  In  unilateral  spasm  of  the 
pterygoids  the  lower  jaw  is  pushed  laterally  in  the  opposite  direction. 

Clonic  spasm  of  the  muscles  of  mastication — masticatory  facial  spasm — con- 
sists of  a  paroxysmal  and  constant  movement  of  the  lower  jaw,  almost  always  in 
a  vertical,  but  rarely  in  a  horizontal  direction.  The  single  movements  follow  one 
another  usually  in  a  regular,  rapid  rhythm,  and  produce  an  audible  chattering 
of  the  teeth.  The  mucous  membrane  of  the  mouth  and  the  tongue  is  often  in- 
jured. 


876  DISEASES    OE   THE   NEEVOUS    SYSTEM 

The  cause  of  these  spasms  can  not  always  be  established.  Sometimes  they 
seem  to  be  of  reflex  origin,  as  in  affections  of  the  lower  jaw,  the  teeth,  or  even  of 
distant  parts.  We  once  saw  a  case  which  lasted  for  a  year  which  was  said 
to  have  arisen  from  a  severe  fright,  and  which  therefore  must  be  regarded  as 
"  hysterical,"  and  also  a  case  of  clonic  spasm  in  a  ten-year-old  boy  in  the  mas- 
seters  and  mylo-hyoids  of  hysterical  origin. 

The  treatment,  apart  from  the  treatment  of  the  primary  affection,  must 
aim  at  removing  the  cause  of  the  disease,  if  there  be  one,  such  as  decayed  teeth. 
In  other  respects  electricity  is  of  value  in  many  cases,  applied  either  by  passing 
the  constant  current  through  the  muscles,  by  faradizing  them,  or  by  using  the 
wire  brush.  Of  internal  remedies  we  may  try  narcotics,  bromide  of  potassium, 
atropine,  etc. 

Artificial  feeding  is  of  great  importance,  if  the  patient  can  not  take  food  vol- 
untarily from  a  persistent  trismus.  It  is  best  to  introduce  a  small  oesophageal 
tube  through  the  nose  into  the  oesophagus.  Rectal  feeding  is  insufficient  for  a 
permanent  method,  but  still  it  is  sometimes  of  service.  In  some  cases  a  suc- 
cessful attempt  has  been  made  to  overcome  the  closure  of  the  jaws  gradually  by 
pushing  v\'ooden  wedges  between  the  teeth. 

2.  Clonic  Facial  Spasm 

{Mimetic  Facial  Spasm.     Facial  Tic.     Convulsive  Tic) 

We  know  little  that  is  definite  as  to  the  aetiology  of  facial  spasm,  the  most  fre- 
quent and  practically  the  most  important  form  of  isolated  spasm.  In  some 
cases,  perhaps,  the  disease  is  to  be  referred  to  a  lesion  of  the  trunk  of  the  facial, 
from  exposure  to  cold,  aural  affections,  or  disturbances  at  the  base  of  the  skull, 
vsuch  as  aneurism  of  the  vertebral  artery  pressing  on  the  trunk  of  the  facial,  as 
was  seen  in  one  case),  or  else  to  a  refiex  irritation  of  the  nerve  as  in  trigeminal 
neuralgia,  etc.  It  may  be  that  many  cases  are  not  of  peripheral  but  of  central 
origin,  from  the  facial  center  in  the  cerebral  cortex.  The  disease  may  also  appear 
after  violent  mental  excitement.  Finally,  imitation  and  the  habit  of  grimacing 
play  a  part  in  many  cases,  especially  in  children,  that  is  not  to  be  underestimated 
(hysterical  facial  spasm).  At  any  rate  we  may  see  from  what  has  been  said  that 
we  should  not  judge  all  cases  of  mimetic  facial  spasm  in  the  same  way,  but  it  is 
the  most  characteristic  cases,  due  apparently  to  organic  causes,  which  usually 
we  are  wholly  unable  to  explain.  Repeated  observations  have  established  the 
fact  that  the  disposition  to  the  disease  is  heightened  by  a  general  hereditary 
neuropathic  taint.  The  tendency  to  twitch  the  facial  muscles  is  very  often  noticed 
in  nervous  and  irritable  persons,  but  there  is  an  essential  difference  between  this 
grimacing  and  the  true  facial  spasm  with  its  lightning-like  muscular  contractions. 

The  symptoms  of  true  convulsive  tic  consist  of  alternating,  short,  lightning- 
like contractions  in  almost  all  the  muscles  supplied  by  the  facial.  The  disease  is 
usually  unilateral,  often  extending  over  the  whole  distribution  of  the  facial,  but 
sometimes  confined  only  to  individual  parts — partial  facial  spasm.  Sometimes 
the  contractions  are  almost  constant,  though  varying  in  intensity,  so  that  the 
patient  involuntarily  makes  the  strangest  faces;  but  they  often  appear  in  sepa- 
rate attacks,  which  last  but  a  short  time,  and  are  interrupted  by  completely  free 
intervals.  The  attacks  arise  without  any  special  cause,  or  they  may  be  excited  by 
talking,  voluntary  movements,  sensory  and  mental  impressions,  etc.  In  some 
very  severe  cases  the  contractions  also  invade  the  neighboring  territory — the  mus- 
cles of  mastication,  the  tongue,  the  muscles  of  the  neck,  and  even  the  upper  arm. 
Voluntary  motion  in  the  muscles  is  perfectly  normal,  except  for  the  disturbing 
influence  of  the  spasmodic  movements.  All  sensory  disturbances  are  also  lack- 
ing; there  is  neither  anaesthesia  nor  pain. 


THE   DIFFERENT   FORMS    OF   LOCALIZED    SPASM  877 

A  common  partial  form  of  facial  spasm,  which  is  entirely  or  almost  entirely 
isolated,  deserves  special  mention^blepharospasm,  or  spasm  of  the  eyelids — that 
is,  a  tonic  or  clonic  spasm  in  the  orbicularis  palpebrarum.  The  tonic  form 
may  be  of  reflex  origin  in  affections  of  the  eye,  but  sometimes  it  is  excited  from 
other  regions  of  the  trigeminus.  It  is,  as  a  rule,  bilateral,  and  it  may  last  for 
days  or  weeks,  sometimes  with  occasional  interruptions.  Graefe  first  noticed  that 
the  spasm  could  sometimes  be  instantly  checked  by  pressure  on  the  points  of 
exit  of  the  branches  of  the  trigeminus,  and  often  by  pressure  upon  certain  parts 
of  the  vertebral  column  or  other  parts  of  the  body,  so  that  the  eyelids  "  fly  up 
as  if  by  a  spring."  The  author  has  no  doubt  that  in  such  cases  we  usually  have  to 
do  with  conditions  of  hysterical  spasm.  Clonic  spasm  of  the  lids,  nictitating 
spasm,  consists  of  a  spasmodic  winking  and  contraction  of  the  eyes,  which  is  some- 
times almost  constant.  Here,  too,  we  can  often  make  out  a  reflex  origin  for  the 
spasm,  but  frequently  we  can  not  find  any  cause. 

Facial  spasm,  in  its  severe  forms,  and  especially  blepharospasm,  is  always  a 
troublesome  disease  for  the  patient,  and  causes  very  much  disturbance.  The 
course  is  often  very  tedious.  Sometimes  there  are  long  intervals,  as  we  have 
seen  during  pregnancy,  and  then  the  spasm  begins  anew.  In  not  very  rare  cases 
the  affection  becomes  habitual  and  lasts  for  life. 

Treatment  is,  therefore,  usually  a  difficult  and  thankless  task.  The  best  results 
may  be  obtained  where  we  can  succeed  in  removing  any  reflex  cause  of  the  spasm, 
as  in  extracting  decayed  teeth,  treating  affections  of  the  eye,  or,  in  some  cases, 
resecting  the  supra-orbital  nerve.  In  applying  electricity,  our  chief  attention 
must  be  directed  to  any  pressure  points,  to  which  we  make  a  stabile  application  of 
the  anode  of  the  constant  current.  If  there  are  no  pressure  points,  we  put  the 
anode  on  the  trunk  of  the  facial  and  the  different  branches  of  the  pes  anserinus. 
In  cases  of  reflex  origin  Berger  obtained  good  results  by  applying  the  anode  to  the 
occiput,  just  under  the  protuberance,  while  the  cathode  was  held  in  the  hand — 
galvanization  of  the  medulla.  The  single  sitting  should  last  five  or  ten  minutes. 
The  f  aradic  current — a  slowly  "  swelling  current  "  * — has  also  been  recommended. 
Of  internal  remedies  we  should  first  try  bromide  of  potassium,  and  then  arsenic, 
atropine,  curare,  or  oxide  of  zinc.  The  action  of  these  drugs  is  always  very  uncer- 
tain. A  favorable  result,  however,  has  been  obtained  by  nerve-stretching,  in  a  part 
of  the  cases  operated  on,  at  least  so  far  that  the  ensuing  paralysis  troubles  the 
patient  less  than  the  constant  twitching.  When  the  paralysis  ceases  the  twitch- 
ings  usually  begin  again,  but  in  some  cases  the  benefit  has  been  permanent.  Fi- 
nally, we  must  mention  that  the  use  of  the  red-hot  iron  has  sometimes  been  fol- 
lowed by  a  decided  improvement  of  the  spasm  in  old  cases.  We  employ  cauteriza- 
tion along  the  cervical  vertebrae,  on  the  trunk  of  the  nerve,  or  on  any  existing 
pressure  points,  by  means  of  Paquelin's  thenuo-cautery. 

In  the  cases  which  are  not  to  be  regarded  as  a  form  of  organic  spasm,  but  are 
to  be  classed  as  hysterical,  due  to  bad  habits,  etc.,  a  methodical  training  of  the 
will  by  gymnastic  exercises  may  be  attended  with  the  best  results. 

3.  Spasm  in  the  Region  of  the  Hypoglossal  E'erve.  Lingual  Spasm 
Although  the  tongue  is  often  implicated  in  complicated  forms  of  spasm,  such 
as  hysterical  or  epileptic  spasms,  isolated  spasms  in  it  are  very  rarely  seen. 
They  are  relatively  most  common  in  hysteria.  They  occur,  however,  either  in  a 
clonic  or  a  tonic  form,  and  then  they  cause  a  marked  disturbance  of  speech,  or 
even  of  respiration,  if  the  spasm  draw  the  tongue  backward.  In  the  latter  case 
it  may  be  necessary  to  use  inhalations  of  ehloi-oform,  and  to  draw  the  tongue 
forward  by  force. 

[*  A  current  that  begins  weak,  and  is  gradually  made  stronger  and  then  weaker.— K.] 


878 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


4.  Spasms  in  the  Muscles  of  the  ISTeck 

Tonic  and  clonic  spasms  in  the  region  of  the  muscles  of  the  neck  are  not  very 
frequent,  but  they  appear  in  very  various  forms,  and  are  at  times  a  very  severe 
and  persistent  affection.  We  can  usually  discover  nothing  definite  as  to  the  aeti- 
ology of  this  condition.     Only  in  a  few  cases  can  we  make  out  coarse  anatomical 


Fig.  110.— Severe  case  of  spasm  of  the  accessory  nerve  (trapezius  and  sterno-mastoid  muscles). 
(From  the  Erlangen  Medical  Clinique.) 

disease  of  the  nervous  system  or  of  the  cervical  vertebrae,  rheumatic  or  other  evil 
factors,  reflex  influences,  etc.;  but  a  general  neuropathic  constitution  certainly 
plays  a  great  part  in  the  development  of  these  forms  of  spasm.  Although  the 
spasms  in  the  different  muscular  regions  are  often  combined  with  one  another, 
we  can  still  distinguish  the  chief  separate  forms. 

Spasms  in  the  Distribution  of  the  Accessory  iSTERVE. — In  clonic  spasm  of 
the  accessory  there  are  brief  or  more  persistent  twitchings  of  the  head,  which 
may  attain  great  severity.     Where  there  is  a  predominating  unilateral  spasm 


THE   DIFFEREJsTT   FORMS    OF   LOCALIZED    SPASM 


8^J 


of  the  sterno-mastoid,  the  head  is  turned  to  the  opposite  side  at  every  contrac- 
tion of  this  muscle,  and  the  chin  is  also  somewhat  raised.  In  unilateral  spasm 
of  the  trapezius,  when  only  the  upper  portion  of  the  muscle  is  usually  affected, 
the  head  is  drawn  backward  toward  the  affected  side  against  the  shoulder. 
In  bilateral  and  combined  spasm  of  these  muscles  we  see  severe  shaking  and 
nodding  movements  of  the  head — the  so-called  nodding  spasms,  "  salaam  convul- 
sions " — which  have  been  observed  chiefly  in  children.  They  may  also  be  excited 
in  like  manner  by  contractions  of  other  muscles  of  the  neck  (rectus  capitis,  longus 
colli).  In  tonic  spasm  of  the  accessory  the  head  is  constantly  fixed  in  the  ab- 
normal position  described  above,  and  it  can  not  be  brought  back  passively  to  its 
normal  position  at  all,  or  only  incompletely.  The  oblique  position  of  the  head  in 
unilateral  tonic  spasm  of  the  sterno-mastoid  is  called  spastic  torticollis  (caput 
ohstipum  spasticum).  The  affection  called  rheumatic  torticollis  hardly  belongs 
here,  since  it  is  probably  due  to  a  rheu- 
matic myositis  of  the  sterno-mastoid. 

Tonic  and  clonic  spasm  of  the  spleni- 
us  (Fig.  Ill)  is  also  isolated,  or  com- 
bined with  spasm  of  the  accessory.  In 
this  the  head  is  drawn  backward  and 
toward  the  affected  side,  and  thus  Ave 
can  feel  the  muscular  swelling  pro- 
truding to  the  outside  of  the  cervi- 
cal portion  of  the  trapezius.  Spasm  of 
the  obliquus  capitis  is  probably  the 
cause  of  the  so-called  rotatory  tic,  in 
which  there  are  genuine  spasmodic  rota- 
tory movements  of  the  head. 

The  course  of  the  forms  of  spasm 
described  is  usually  very  tedious.  There 
are  mild  cases  which  recover  in  a  short 
time,  but,  on  the  other  hand,  many  of 
these  forms  of  spasm  develop  into  a  very 
distressing,  habitual,  chronic  affection. 
In  these  cases  any  steady  occupation, 
such  as  reading  or  writing,  is  rendered 
almost  impossible  by  the  constantly  re- 
curring spasmodic  lateral  and  rotatory 

movements  of  the  head.  Any  mental  excitement,  a  feeling  that  he  is  noticed,  etc.. 
increase  the  patient's  spasms,  while  they  become  milder  when  he  is  completely  at 
ease.  In  some  cases  the  twitching  ceases  entirely  when  the  body  is  wholly  at  rest, 
but  it  returns  at  once  on  any  voluntary  movement.  Combinations  of  the  different 
forms  of  spasm  occur  in  the  most  varied  ways.  Facial  tic  may  be  associated  with 
spa;sm  of  the  muscles  of  the  neck.  In  the  severest  cases  the  spasm  may  extend 
even  to  the  muscles  of  the  upper  arm.  The  occurrence  of  mental  disturbances 
(melancholia,  confusional  insanity)  has  been  repeatedly  seen.  All  this  favors  the 
theory  of  the  central  nature  of  the  disease.  The  patient's  general  condition  may 
finally  become  very  poor.    Many  fall  into  the  morphine  habit. 

Treatment. — In  some  cases  electricity  has  brought  about  recovery,  or  at  least 
improvement.  The  method  of  treatment  consists  of  the  application  of  the  anode 
to  the  affected  nerves  and  muscles,  or  of  the  use  of  a  swelling  faradic  current,  or 
of  the  faradic  brush  to  the  skin  over  the  affected  muscles.  Very  often  we  have  to 
change  the  method,  and  we  must  try  to  find  out,  by  testing,  the  most  efiicient  way 
to  employ  electricity.  We  may  try  cautious  massage  of  the  affected  muscles.  We 
have  greater  confidence  in  methodical  gymnastic  exercises  carried  out  persistently 


Fig.  111.— Spasm  of  tlie  right  splenius  capitis. 
( From  DucHENKE.j 


880  DISEASES    OF   THE   NERVOUS    SYSTEM 

for  a  long  time.  Of  other  remedies,  narcotics,  such  as  subcutaneous  injections 
of  morphine,  are  indispensable  in  severe  cases,  but  we  must  be  very  careful  in 
their  use.  We  may  also  try  bromide  of  potassium,  antipyrine,  arsenic  [bella- 
donna], and  other  nervines.  In  severe  cases  we  resort  to  the  use  of  the  red-hot 
iron  to  the  back  of  the  neck.  Other  observers,  and  we  ourselves,  have  seen  good 
results  from  it,  but  of  course  benefit  does  not  always  follow.  We  may  also  advise 
nerve-stretching,  but  it  is  of  doubtful  advantage.  [Resection  of  the  affected 
nerves  has  also  been  performed  in  many  cases  with  some  alleged  benefit.  Brissaud 
and  other  French  observers  claim  that  many  of  the  cases  of  torticollis  are  of  psy- 
chical origin  (hysterical?),  and  that  they  are  cured  by  appropriate  mental  treat- 
ment.— Iv.]  Finally,  it  must  be  mentioned,  that  we  may  give  great  relief  to  many 
patients  by  suitably  applied  mechanical  supports. 

5.  Spasms  in  the  Muscles  of  the  Shoulder  and  Arm 
Clonic  spasms  in  the  upper  extremity  are  probably  usually  of  central  origin. 
They  are  rarely  isolated,  as  in  the  pectoralis  major,  but  are  more  frequently  com- 
bined with  other  forms  of  spasm  and  other  nervous  symptoms.  They  sometimes 
seem  to  be  of  reflex  origin,  as  in  the  clonic  spasms  associated  with  brachial  neu- 
ralgia, and  also  the  spasms  sometimes  seen  in  araputation-stumps.  For  many  of 
these  forms  of  spasm  the  cause  is  still  wholly  unknown. 

Isolated  tonic  spasms,  in  single  muscles,  or  groups  of  muscles,  in  the  upper 
extremity,  have  been  repeatedly  observed.  Tonic  spasm  of  the  rhomboidei  causes 
an  oblique  position  of  the  scapula,  so  that  its  inner  border  runs  obliquely  upward 
and  outward  from  below  and  inward.  This  makes  it  hard  to  raise  the  arm  above 
the  horizontal  line,  as  in  serratus  paralysis,  but  the  separation  of  the  scapula  from 
the  chest-wall,  which  is  so  very  characteristic  of  the  latter,  is  wanting.  Tonic 
spasm  in  the  levator  anguli  scapula  is  rare,  except  in  connection  with  spasm  of 
the  rhomboidei  or  trapezius.  In  it  the  shoulder  is  raised  and  the  head  is  bent 
a  little  to  the  affected  side.  Isolated  tonic  spasms  in  the  pectoralis  major,  latis- 
simus  dorsi,  deltoid,  etc.,  are,  on  the  whole,  easy  to  recognize,  but  they  are 
of  very  rare  occurrence.  Tonic  flexor  spasms  of  the  hand  and  fingers  are  miore 
common.  We  have  ourselves  seen  several  such  cases,  which  lasted  for  months.  In 
one  case  the  spasm  could  at  once  be  relieved  by  placing  the  anode  of  a  moderately 
strong  galvanic  current  on  the  median  neiwe.  In  another  case  the  flexor  spasm  of 
the  fingers  had  followed  a  mild  acute  inflammation  of  the  wrist-joint.  Brief 
tonic  spasms  of  the  flexors  of  the  fingers  and  of  the  thumb  muscles  are  of  quite 
common  occurrence.  They  are  seen  especially  in  persons  who  have  to  do  some 
severe  and  persistent  bodily  work,  also  in  alcoholic  subjects,  patients  with  gastric 
disease  or  chronic  nephritis,  in  hysteria,  etc.  Some  of  these  forms  of  spasm 
should  perhaps  be  classed  as  tetany,  a  special  form  of  spasm  which  will  be  fully 
described  later. 

We  can  scarcely  give  any  general  rules  for  prognosis  or  treatment.  It  is  always 
important  to  remove  any  trouble  which  may  cause  the  spasm.  We  may  also  try, 
first  of  all,  electricity  (a  stabile  galvanic  current,  applying  the  anode  to  the 
affected  muscles  and  their  nerves)  and  methodical  gymnastics,  the  latter  espe- 
cially in  all  cases  having  any  relation  to  hysteria  (q.  v.). 

6.  Spasms  in  the  Muscles  of  the  Lower  Extremity 
Clonic  spasms  in  the  muscles  of  the  lower  extremity  are  always,  with  rare 
exceptions,  a  symptom  of  spinal  or  cerebral  disease.  Of  the  tonic  spasms  the 
most  frequent  and  the  best  known  are  the  painful  spasms  in  the  calves,  or  cramps, 
which  are  apt  to  come  on  after  great  muscular  exertion,  mountain-climbing,  or 
dancing.  Many  persons  have  an  especially  marked  predisposition  to  such  cramps, 
which  readily  come  on,  especially  after  making  certain  movements  or  holding  the 


THE   DIFFEREXT    FORMS    OF   LOCALIZED    SPASM  S81 

foot  in  a  certain  position.  Similar  painful  cramps  sometimes  come  in  other 
muscles  besides  the  calves,  as  in  the  abductor  hallucis,  etc.  Constantly  recurring, 
extensive,  and  painful  spasms  in  the  leg  muscles  may,  as  we  have  seen,  form  a 
very  distressing  affection  which  is  hard  to  remove.  In  most  of  these  cases  there  ' 
are  probably  conditions  of  irritation  occurring  in  the  muscles  themselves.  Other 
tonic  spasms  in  the  muscles  of  the  lower  extremity  are  rare,  but  individual  cases 
of  isolated  tonic  spasm  in  the  abductors,  in  the  ilio-psoas,  in  the  muscles  of  the 
calves,  etc.,  have  been  observed.  More  extensive  tonic  contractures  of  the  muscles 
of  the  leg  are  not  very  rare  in  hysteria,  especially  in  the  hysteria  of  children. 

Saltatory  Reflex  Spasm,- — In  this  place  we  may  mention  a  peculiar  form  of 
spasm,  to  which  Bamberger  has  given  the  name  of  "  saltatory  reflex  spasm." 
This  shows  itself  in  the  muscles  of  the  lower  extremities,  never  when  the  patient 
is  quiet  in  bed,  but  only  when  he  tries  to  stand  or  to  walk.  As  soon  as  the  soles 
of  the  feet  touch  the  floor,  such  vigorous  contractions  are  set  up  in  the  muscles  of 
the  legs  as  to  force  the  patient  to  keep  up  a  constant  hopping,  jumping,  or  trip- 
ping. The  heels  are  also  usually  raised  spasmodically,  and  in  many  cases  the 
patient  would  certainly  fall  if  he  were  not  supported.  In  the  pure  forms  of 
saltatory  spasm,  on  physical  examination  we  can  usually  make  out  nothing  but 
an  extraordinary  increase  of  the  reflexes,  especially  of  the  tendon  reflexes,  but  in 
some  cases  there  may  also  be  other  nervous  symptoms.  According  to  our  present 
theories  there  can  scarcely  be  a  doubt  that  the  cases  described  as  "  saltatory  re- 
flex spasm  "  are  without  exception  hysterical. 

[Certain  similar  affections  exist  as  endemic  neuroses.  In  the  "  jumpers  "  of 
Maine  the  spasms  may  be  produced  by  any  excitement.  In  other  forms  the 
victims  are  compelled  to  imitate  everything  they  see  or  hear.  The  curious 
affection  observed  in  Siberia,  Java,  and  elsewhere,  known  as  latah  or  myriachit, 
is  allied  to  this  trouble.  Alcoholism,  cold,  and  privation  seem  to  be  important 
aetiological  factors,  and  these  affections  probably  have  some  relation  to  hys- 
teria.— K.] 

Arthrogryposis. — As  an  appendix  we  would  here  consider  briefly  a  remark- 
able disease,  the  so-called  arthrogryposis,  which  occurs  chiefly  in  children  in  the 
first  years  of  life,  and  consists  of  persistent  tonic  spasms  and  contractures  of  one 
or  often  of  all  four  extremities.  The  disease  usually  develops  quite  acutely,  and 
may  run  its  course  with  fever  and  rather  severe  general  symptoms.  The  legs  are 
found  either  in  a  position  of  rigid  extension,  or  they  are  drawn  up  spasmodically 
to  the  body,  and  can  not  be  extended  passively  even  with  violence.  The  arms 
are  flexed,  and  the  hands  and  fingers  are  also  fixed  in  some  position  of  contracture. 
The  milder  cases  may  recover  after  a  few  weeks,  but  we  have  seen  two  cases  which 
ended  fatally,  in  which  the  autopsy  gave  an  absolutely  negative  result.  The 
nature  of  this  quite  rare  affection  is  still  wholly  unknown  to  us.  Several  authors 
have  of  late  tried  to  identify  arthrogryposis  with  tetany  (q.  v.),  which  we  can  not 
admit,  at  least  not  in  all  cases.  In  contrast  to  tetany  we  have  in  arthrogryposis 
an  unbroken  tonic  rigidity  of  the  extremities  lasting  for  days  or  even  weeks.  In 
regard  to  treatment,  prolonged  warm  baths  are  especially  to  be  recommended. 
The  cautious  use  of  galvanism,  massage,  the  bromide  salts  internally,  etc.,  may 
also  be  tried. 

7.  Spasms  ix  the  Respiratory  Muscles 

Tonic  spasm  of  the  diaphragm  has  been  seen  in  a  few  rare  cases.  The  lower 
part  of  the  thorax  is  much  expanded,  the  epigastrium  is  protruded,  and  the 
respiration,  which  shows  intense  dyspncea,  can  be  performed  only  by  the  upper 
part  of  the  thorax.  The  depression  and  immobility  of  the  diaphragm  can  be  made 
out  on  percussion.  Many  patients  have  a  severe  pain  in  the  region  of  the  dia- 
phragm. The  condition  is  not  without  danger  and  demands  instant  interference : 
56 


882  DISEASES    OF   THE   NEEVOUS    SYSTEM 

inhalations  of  chloroform,  subcutaneous  injections  of  morphine,  a  warm  bath 
with  a  cool  shower-bath  after  it,  faradization  of  the  skin  in  the  region  of  the 
diaphragm,  galvanization  of  the  phrenics,  etc. 

Clonic  Spasm  of  the  Diaphragm. — Singultus. — The  well-known  "hiccough" 
or  "  sob,"  due  to  a  sudden  spasmodic  contraction  of  the  diaphragm,  associated 
with  a  brief  inspiratory  sound,  is  in  its  mild  forms  a  very  frequent  condition, 
which  soon  passes  off;  but  it  sometimes  increases  to  a  persistent,  obstinate,  and 
very  troublesome  affection,  which  may  last  for  weeks  or  months.  Hysterical  hic- 
cough is  the  most  frequent.  This  comes  on  especially  after  mental  excitement, 
and  it  may  sometimes  last,  with  short  interruptions,  for  weeks  or  even  months. 
Persistent  hiccough  may  also  be  excited  reflexly  in  affections  of  the  stomach,  in- 
testines, peritoneum,  etc.  In  some  cases  the  hiccough  depends  upon  a  direct 
lesion  of  the  phrenic  nerve,  as  we  have  seen  in  one  case  of  tubercular  mediastino- 
pericarditis.  We  have  also  seen  hiccough  lasting  for  hours  in  cerebral  apoplexy, 
and  in  chronic  myelitis  extending  to  the  cervical  cord. 

In  the  milder  cases  hiccough  soon  passes  off  without  special  treatment.  Hold- 
ing the  breath,  pressure  on  the  closed  glottis,  blows  on  the  back,  etc.,  are  proce- 
dures generally  known  by  the  laity,  and  they  are  often  used  to  suppress  hiccough. 
In  hysterical  hiccough  intelligent  and  at  the  same  time  energetic  mental  treat- 
ment will  often  rapidly  lead  to  the  voluntary  suppression  of  the  spasmodic  move- 
ments and  thus  to  complete  recovery.  Such  treatment  is  often  aided  by  the  in- 
fluence (in  part  merely  suggestive)  of  some  internal  remedy,  such  as  bromide  of 
potassium,  or  the  use  of  electricity.  In  severe  hiccough  due  to  organic  disease  we 
raust  sometimes  resort  to  narcotics  (large  doses  of  bromide  of  potassium,  opium, 
morphine,  inhalations  of  chloroform).  The  constant  current  to  the  phrenic 
nerve  or  faradization  of  the  region  of  the  diaphragm  sometimes  acts  beneficially. 

Complicated  respiratory  spasms,  either  in  the  form  of  spasmodically  acceler- 
ated and  forced  breathing,  or  spasms  combined  with  all  sorts  of  other  symptoms, 
with  many  gurgling  noises,  eructations,  etc.,  are  almost  exclusively  confined  to 
hysteria.  We  have  ourselves  counted  in  one  such  case  over  two  hundred  respira- 
tions a  minute !  The  best  remedy  for  most  of  these  forms  of  spasm,  and  one 
which  often  acts  instantly,  is  a  cool  bath  with  energetic  cold  shower-baths.  The 
yawning  spasm  (chasmus,  oscedo),  sneezing  spasm  (sternutatio  convulsiva, 
ptarmus),  laughing  and  weeping  spasms,  coughing  spasm,  etc.,  also  belong  to  the 
respiratory  spasms.  We  once  saw  an  instructive  example  of  the  latter  in  a  boy 
ten  years  old,  undoubtedly  due  to  hysteria.  A  peculiar,  hollow,  barking  cough 
came  on  as  a  "  reflex  "  (that  is,  due  to  association  of  ideas)  either  spontaneously 
or  on  pinching  any  part  of  the  skin.  The  affection  lasted  for  some  weeks,  and 
then  disappeared  quite  suddenly. 


CHAPTEE  IV 
WRITER'S    CRAMP    AND    ALLIED    PROFESSIONAL    NEUROSES 

Writer's  cramp  {graphospasm,  mogigraphia)  is  the  commonest  form  of  a 
whole  class  of  peculiar  disturbances  of  motion,  to  which  Benedikt  gave  the  appro- 
priate name  of  "  professional  neuroses  of  co-ordination."  Their  characteristic 
feature  is  that  the  disturbance  in  a  certain  group  of  muscles  appears  only  when 
these  muscles  come  into  harmonious  action,  in  some  definite  and  usually  some 
delicate  and  complicated  occupation.  Although  the  persons  who  suffer  from 
writer's  cramp  can  move  and  use  the  muscles  of  their  right  arm  and  hand  for 


THE   DIFFEEENT   FORMS    OF   LOCALIZED    SPASM  883 

ordinary  purposes  in  a  perfectly  normal  manner,  these  same  muscles  at  once 
refuse  their  service  wlien  the  patient  begins  to  \vrite.  In  this  case  the  disturbance 
can  not  lie  in  the  innervation  of  the  individual  muscles  themselves,  but  it  must 
be  referred  to  the  form  of  their  associated  action — that  is,  it  must  be  a  disturb- 
ance of  co-ordination.  It  therefore  becomes  very  probable  that  the  cause  of  the 
spasm  is  to  be  sought,  not  in  the  peripheral  parts,  but  in  the  centers.  We  are 
convinced  that  writer's  cramp  and  the  allied  occupation  neuroses  are  due  to  dis- 
turbances of  the  central  (cortical)  innervation.  Writer's  cramp  is  a  morbid  con- 
dition in  •writing  similar  to  stuttering  in  speaking.  Over-exertion  in  writing 
plays  the  most  important  part  as  an  setiological  factor.  Writer's  cramp  is  there- 
fore seen  chiefly,  but  of  course  not  exclusively,  in  those  persons  whose  occupation 
entails  continuous  writing,  especially  in  secretaries,  merchants,  bureau  officials, 
etc.  A  general  nervous  predisposition  seems  also  very  notably  to  increase  the 
tendency  to  writer's  cramp.  Most  cases  are  associated  with  pronounced  neuras- 
thenic symptoms.  Mental  factors  (fright,  anxiety)  sometimes  play  an  unmistak- 
able part.  Attention  has  also  been  called  to  the  fact  that  bad  pens,  such  as  hard 
steel  pens,  improper  methods  of  holding  the  pen  in  writing,  etc.,  may  favor  the 
development  of  writer's  cramp. 

Symptoms. — The  essential  symptom  of  writer's  cramp  is  the  appearance  of 
certain  disturbances  at  every  attempt  to  write,  which  render  writing  very  difficult 
or  entirely  impossible.  The  affection  usually  begins  gradually,  but  increases  quite 
rapidly.  For  the  precise  characterization  of  the  disturbance  Benedikt  has  dis- 
tinguished three  forms  of  writer's  cramp,  but  they  run  into  one  another  in  various 
ways.  The  spastic  form  is  the  most  frequent.  The  patient  scarcely  begins  to 
write  when  contractions  or  tonic  spasms  come  on  in  the  different  fingers.  The  pen 
is  either  pressed  spasmodically  deep  into  the  paper,  or,  when  it  is  moved,  it  makes 
very  faulty  irregular  movements.  We  very  often  see  a  tonic  spasm  of  the  pro- 
nators of  the  forearm  set  in  on  each  attempt  to  write.  Writing  is  under  such  cir- 
cumstances wholly  impossible,  or  it  is  done  only  with  the  greatest  exertion,  and 
the  characters  are  also  utterly  distorted,  unequal,  and  mingled  with  false  strokes 
and  blots.  Finally,  in  the  tremulous  form  of  writer's  cramp  there  is  such  a 
marked  tremor  in  the  right  hand  at  every  attempt  to  write  that  the  letters  are 
completely  illegible.  We  have  seen  several  such  cases  in  children,  which  we  have 
regarded  as  distinctly  hysterical. 

In  the  paralytic  form  the  disturbance  is  chiefly  a  tired  feeling  in  the  right 
arm  of  rapid  onset,  like  paralysis,  and  it  is  often  associated  with  pain.  This  form 
of  disturbance  in  writing  ought  not  properly  to  be  classed  with  writer's  cramp, 
since  it  is  absurd  to  speak  of  a  "  paralytic  "  form  of  "  cramp." 

As  has  already  been  said,  the  motility  of  the  right  arm  in  every  other  respect  is 
usually  perfectly  normal,  but  sometimes  analogous  symptoms  also  appear  in  the 
same  patient  in  many  other  fine  employments,  such  as  sewing,  piano-playing,  etc. 
The  sensibility  is  usually  unaffected,  except  for  the  muscular  pains  already  men- 
tioned, and  a  frequent  feeling  of  numbness  in  the  forearm  and  fijigers.  A  few 
painful  pressure-points  have  sometimes  been  found  on  the  ceiwical  and  dorsal 
vertebrae.  We  should  also  examine  the  peripheral  nerves,  since  painful  thick- 
enings are  sometimes  said  to  be  found  in  them,  which  possibly  stand  in  a  causal 
relation  to  the  disease.  If  we  are  dealing  with  people  who  are  generally  neurotic, 
as  is  almost  always  the  case,  they  often  complain  at  the  same  time  of  headaches, 
mental  uneasiness,  general  weakness,  etc.  In  such  cases  the  degree  of  the  dis- 
turbance, as  we  have  said,  is  always  very  much  influenced  by  mental  conditions 
(excitement,  anxiety),  just  as  is  the  case  in  stuttering.  We  knew  a  patient  who 
could  not  write  a  word,  in  spite  of  the  greatest  effort,  if  any  one  were  looking 
at  him,  but  othei-wise  he  wrote  a  beautiful  flowing  hand. 

The   diagnosis   of  writer's   cramp   is   almost   always   easy.     We  must  guard 


881  DISEASES    OF   THE   NEEVOUS    SYSTEM 

against  confusing  it  with  other  nervous  diseases,  such  as  chorea,  paralysis  agi- 
tans,  multiple  sclerosis,  beginning  muscular  atrophy,  or  agraphia,  which,  of 
course,  under  some  circumstances  may  lead  to  disturbances  in  writing. 

The  prognosis  is  always  to  be  given  with  reserve.  Complete  recoveries  with- 
out doubt  do  occur,  but  many  cases  are  extremely  obstinate  and  others  are 
incurable.  Relapses  are  also  very  com m  on  even  after  improvement  has  set  in. 
Many  patients  are  obliged  to  choose  another  calling  in  consequence  of  their 
trouble. 

The  treatment  begins  first  with  the  command  to  give  up  writing  entirely  for 
several  weeks.  If  this  command  can  be  obeyed,  the  mere  rest  may  be  of  service 
in  mild  incipient  cases.  Certain  contrivances  for  writing,  which  the  patient  can 
best  test  himself,  are  often  of  advantage,  such  as  sticking  the  pen-holder  through 
a  cork,  using  a  large  pen-holder,  a  change  in  the  way  of  holding  the  pen  and  in  the 
position  of  the  arm,  etc.  JSTussbaum  has  invented  a  kind  of  bracelet  to  which  the 
pen-holder  is  fastened,  and  which  is  held  firmly  by  the  outspread  fingers.  Learn- 
ing to  write  with  the  left  hand,  which  is  often  tried  by  patients,  usually  leads  to 
no  good  result,  since  the  cramp  very  soon  appears  in  the  left  hand  also. 

Of  the  special  methods  of  treating  writer's  cramp  the  application  of  galvanism 
deserves  the  first  mention.  Avoiding  all  strong  currents  and  variations  of  the 
current,  we  apply  the  stabile  anode  to  the  brachial  plexus,  and  also  to  the  different 
nerves  (especially  if  they  be  sensitive  to  pressure)  and  the  affected  muscles,  for 
five  or  ten  minutes.  The  cathode  is  placed  in  the  vicinity  of  the  cervical  vertebrae. 
If  painful  points  are  found,  they  receive  special  treatment.  We  may  also  use 
galvanism,  as  an  experiment,  through  the  head.  Of  late,  massage  and  especially 
methodical  gymnastics  have  showm  still  more  favorable  results  than  electrical 
treatment,  but  the  use  of  them  demands  special  technical  skill,  and  therefore 
they  have  so  far  obtained  excellent  results  chiefly  in  the  hands  of  certain  special- 
ists; but  such  a  methodical  re-education  in  the  movements  employed  in  writing 
should  always  be  tried.  We  can  very  rarely  promise  success  from  internal  reme- 
dies such  as  subcutaneous  injections  of  strychnine,  atropine,  etc.,  but  those  meth- 
ods of  treatment  often  act  favorably  which  aid  the  general  strength  of  the  nervous 
system,  such  as  cold-water  cures,  sea-bathing,  and  residence  at  a  mountain  resort. 
In  writer's  cramp,  just  as  in  stuttering,  we  see  very  plainly  the  influence  of 
mental  factors  (rest,  increasing  or  diminishing  self-confidence,  excitement,  etc.) 
upon  the  trouble. 

As  an  appendix  we  will  mention  here  some  other  professional  neuroses  that 
are  occasionally  seen.  They  are  the  piano-player's  cramp,  which  is  seen  espe- 
cially in  young  conservatory  pupils,  violin-  and  'cello-player's  cramp,  telegrapher's 
cramp,  tailor's  cramp,  milker's  cramp,  the  peculiar  disturbances  of  innervation  in 
the  hands  which  often  occur  in  cigar-rollers,  etc.  In  the  lower  extremities  there 
seems  to  be  an  analogous  affection  in  ballet-dancers,  and  also  in  sewing-machine 
girls,  turners,  etc.  We  have  seen  professional  cramp  in  the  tongue  in  a  clario- 
net-player. The  special  points  in  the  symptomatology  and  treatment  of  all  these 
forms  of  cramp  are  in  large  part  analogous  to  the  conditions  described  in  writer's 
cramp.  In  piano-players  the  neurosis  appears  chiefly  in  the  paretic  form — mild 
fatigue — and  is  usually  associated  with  quite  severe  pains,  that  come  on  during 
playing,  in  certain  parts  of  the  arm.  In  regard  to  treatment,  the  best  results  are 
obtained  by  energetic  massage,  but  general  treatment  (iron,  cold  baths,  a  country 
residence)  is  never  to  be  neglected.  Finally,  it  may  here  be  noted  that  in  certain 
laborious  occupations  that  are  persistently  practiced,  a  severe  group  of  nervous 
symptoms  may  also  arise.  For  example,  Hirt  has  lately  described  an  affection 
which  occurs  in  sewing-machine  girls,  and  is  characterized  by  disturbances  of  sen- 
sibility, pain,  paresthesia,  and  in  some  cases  anesthesia,  ataxia,  absence  of  the 
tendon  reflexes,  and  swaying  with  the  eyes  shut.     The  disease  thus  recalls  very 


SIMPLE   AXD   MULTIPLE   DEGENEEATIVE   NEUEITIS        885 

closely  the  picture  of  locomotor  ataxia,  but  it  is  curable  with  proper  treatment. 
Therefore  Hirt  suspected  an  affection  of  the  peripheral  nerves.  Similar  symptoms 
are  also  seen  in  other  classes  of  laborers,  as  in  farm-hands  after  laborious  toil  in 
the  fields. 


CHAPTEE   V 
SIMPLE    AND    MULTIPLE    DEGENERATIVE    NEURITIS 

1.    Simple  Neuritis 

1.  Primary  Simple  Neuritis. — In  the  previous  chapters  we  have  become  ac- 
quainted with  a  series  of  morbid  conditions  which  most  probably  are  to  be  referred 
to  primary  inflammatory  changes  of  a  particular  peripheral  nerve.  We  have  seen 
that  many  cases  of  sciatica  and  of  neuralgia  in  other  nerve  regions,  and  probably, 
too,  all  the  so-called  rheumatic  peripheral  paralyses  (rheumatic  facial  paralysis, 
deltoid  paralysis,  etc.),  are  due  to  such  a  neuritis.  We  have  very  little  infor- 
mation as  to  the  special  causes  of  such  forms  of  neuritis;  we  may  only  suspect 
that  in  such  cases  there  are  definite  infectious  or  toxic  substances  which  act  on 
the  affected  peripheral  nerves.  In  many  cases,  especially  in  most  neuralgic  affec- 
tions, it  seems  rather  to  be  slight  inflammatory  changes  in  the  nerve  sheath  and 
the  interstitial  connective  tissue  of  the  nerve,  but  in  all  forms  of  neuritis  leading 
to  motor  paralysis  it  is  chiefly  a  destruction  of  the  nerve-fiber  itself  caused  by  the 
action  of  the  injurious  substance  ("  parenchymatous  inflammation,"  or,  better, 
"degenerative  neuritis").  In  severe,  and  especially  in  acute,  cases  the  paren- 
chymatous and  the  interstitial  changes  may  develop  simultaneously.  We  will  go 
more  fully  into  the  description  of  the  anatomical  details  in  the  section  on  "  mul- 
tiple neuritis  "  below. 

We  may  merely  mention  here,  as  of  practical  importance,  those  cases  of  pri- 
mary simple  neuritis  which,  after  the  analogy  of  facial  paralysis  which  has  been 
fully  described,  lead  to  acute  peripheral  paralysis  in  other  nerve  regions.  To  this 
class  belong,  first  of  all,  neuritic  axillary  paralysis  (deltoid),  neuritic  paralysis 
in  the  ulnar,  long  thoracic  (serratus  anticus  major),  crural,  peroneus,  etc.; 
neuritic  plexus  paralyses  also  occur,  especially  in  the  brachial  plexus.  In  many, 
although  of  course  not  in  all  of  these  cases,  a  marked  exposure  to  cold  is  to  be 
looked  upon  as  the  cause  of  the  neuritis  ("rheumatic  neuritis").  The  disease 
itself  usually  begins  with  more  or  less  severe  pain  and  parsesthesia  in  the  neigh- 
borhood of  the  affected  nerve,  a  symptom  which  is  often  of  decided  significance  in 
diagnosis  and  is  usually  referred  to  the  involvement  of  the  nerve  sheath  and  in- 
terstitial tissue  (nervi  nervorum,!),  especially  when  motor  nerves  are  attacked. 
At  the  same  time  with  the  pain,  or  soon  after  it,  appear  signs  of  motor  weakness 
in  the  muscles  supplied  by  the  affected  nerve.  The  paralysis  may  vary  extreme- 
ly in  intensity.  In  mild  cases  the  symptoms  soon  disappear  and  recovery  en- 
sues. In  severer  forms  electrical  reaction  of  degeneration  and  atrophy  of  the 
paralyzed  muscles  develop;  but  even  here,  as  has  already  been  said,  we  may  usu- 
ally expect  a  favorable  issue.  The  affected  nerves  are  often  very  sensitive  to 
pressure.  Slight  disturbances  of  cutaneous  sensibility  are  often  to  be  made  out 
on  careful  examination  when  there  is  neuritis  of  a  mixed  nerve  trunk;  but,  as  a 
rule,  the  motor  disturbance  is  almost  always  much  more  apparent  than  the  sen- 
sory.   The  treatment  follows  the  methods  in  vogue  in  all  peripheral  paralyses. 

2.  Secondary  Simple  Neuritis. — There  can  scarcely  be  a  doubt  that  secondary 
neuritis  may  occur  in  consequence  of  disease  of  neighboring  organs.     Xeuritis 


886  DISEASES    OF    THE   NERVOUS    SYSTEM 

sometimes  develops  in  open  wounds  which  permit  the  direct  entrance  of  inflam- 
matory agents  to  the  nerve ;  the  inflammation  is  distributed  chiefly  in  the  sheath 
and  the  connective  tissue  of  the  nerve.  It  is,  however,  of  rare  occurrence — much 
rarer  than  we  were  formerly  disposed  to  assume.  Simple  mechanical  injuries 
and  lacerations  of  peripheral  nerves  are  much  commoner,  occurring  in  all  sorts 
of  affections  in  their  neighborhood — fractures,  luxations,  caries  of  the  bone, 
tumors,  etc.  In  such  cases  we  should  not  speak,  without  qualification,  of  "  in- 
flammation," since  we  usually  have  to  do,  as  has  been  said,  with  purely  mechan- 
ical consequences.  Apart  from  the  ordinary  secondary  descending  degeneration 
(vide  supra,  page  849),  such  mechanical  lesions  of  the  nerves  have  in  themselves 
not  the  slightest  tendency  to  extend  upward  in  the  form  of  a  "  neuritis  ascendens," 
or  "  migrans/'  as  was  formerly  believed,  and  the  assumption  of  an  "  ascending 
neuritis,"  following  diseases  of  internal  organs  (sexual  organs,  kidneys,  intes- 
tines, etc.),  and  finally  leading  not  infrequently  to  secondary  myelitis,  so- 
called  "  reflex  paralysis,"  etc.,  is  warranted  only  in  the  rarest  cases.  It  is  certain, 
however,  that  inflammatory  processes  may  sometimes  attack  neighboring  nerve 
trunks  and  that  an  acute  inflammation  may  sometimes  extend  immediately  up 
the  neurilemma  of  the  outgoing  nerve  to  the  cerebral  and  spinal  meninges.  So 
far  as  these  processes  deserve  clinical  significance  they  will  receive  special  men- 
tion in  the  appropriate  places. 

[It  has  long  been  known  that,  when  a  nerve  has  been  cut,  the  portion  below 
the  injury  rapidly  degenerates — Waller's  law  of  degeneration.  The  portions  that 
degenerate  are  the  axis-cylinder  processes  that  have  been  separated  from  the 
cell-body  of  the  neurone.  As  a  result  of  more  delicate  methods  of  research,  it  has 
been  found  that  the  rest  of  the  neurone — the  cell-body  and  the  axis-cylinder 
stump — also  undergoes  slighter  changes.  There  may  be,  therefore,  really  an 
ascending  degeneration  in  the  nerve,  but  it  is  very  slight  and  has  little  or  no 
clinical  significance. — K.] 

Those  cases  of  secondary  neuritis  which  follow  other  and  quite  different  dis- 
eases (usually  acute  infectious  diseases)  have  quite  a  different  origin.  Since  in 
such  cases  the  degeneration  often  develops  in  several  nerve  regions  at  once,  we 
will  return  more  in  detail  to  this  form  of  secondary  neuritis  in  the  next  section 
(see  the  following  pages). 

2.    Multiple  Degenerative  Neuritis 

.Sitiology. — Although  the  occurrence  of  extensive  primary  disease  in  the 
peripheral  nerves  was  practically  unknown  not  very  long  ago,  many  investiga- 
tions in  the  last  few  decades  (Dumenil,  Joffroy,  Leyden,  and  many  others)  have 
taught  us  that  no  part  of  the  entire  nervous  system  is  so  much  exposed  to  all 
possible  harmful  influences  as  the  peripheral  nerve-fiber.  We  are  at  present 
acquainted  with  a  long  list  of  types  of  nervous  disease  Avhich  are  due  exclu- 
sively, or  at  least  chiefly,  to  more  or-  less  extensive  degeneration  of  the  peripheral 
nerves.  The  more  we  investigate  the  causes  of  these  diseases,  the  more  we  be- 
come convinced  that  it  is  almost  always,  in  the  last  instance,  chemical  poisons 
which  enter  the  body  or  are  formed  in  the  body  itself  and  exert  a  destructive 
influence  on  the  peripheral  nerve-flber.  It  is  indeed  possible  that  all  such  poisons 
act  from  the  outset  upon  the  whole  peripheral  neurone — that  is,  the  ganglion-cell 
and  peripheral  nerve-fiber — but  the  visible  injury  (degeneration)  is  often  mani- 
fested exclusively  in  the  peripheral  nerve-fiber,  and  probably  first  in  the  branches 
most  remote  from  the  trophic  center,  the  nerve-cell.  Only  when  the  action  of 
the  poison  is  severe  and  long-continued  can  the  whole  neurone — that  is,  the 
motor  ganglion-cell  in  the  anterior  horn  of  the  cord — ^be  visibly  injured  or  even 
completely  degenerated.     [Changes  may  also  occur  in  the  peripheral  sensory  neu- 


SIMPLE   AND   MULTIPLE   DEGEIiTERATIVE   NEURITIS        887 

rones,  not  only  in  the  peripheral  portions  of  their  nerve-fibers,  but  also  in  their 
ganglion-cells  in  the  spinal  ganglia  and  in  their  axis-cylinder  processes  in  the 
spinal  cord. — K.]  The  toxic  origin  of  peripheral  nerve  degeneration  is  most 
clearly  seen  in  those  morbid  conditions  which  we  can  refer  with  certainty  to  a 
definite,  well-recognized  poison.  These  are  the  special  "  toxic  neuritides,"  in 
the  strict  sense  of  the  word,  with  which  we  have  already  become  acquainted 
in  the  description  of  lead  and  arsenical  paralyses.  We  have  seen  that,  by  the 
action  of  these  poisons,  extensive  destruction  of  the  peripheral  nerves  may  ensue, 
which,  of  course,  is  followed  by  serious  clinical  symptoms.  Disregarding  several 
other  rare  forms  of  poisoning  (copper,  zinc,  silver,  phosphorus,  mercury,  etc.), 
there  still  remains  one  extremely  important  and  comparatively  common  form  of 
poisoning  which  leads  to  multiple  neuritis,  and  that  is  chronic  alcoholism.  Al- 
coholic neuritis  is  by  far  the  commonest  form  of  multiple  neuritis,  and  it  will 
therefore  require  a  special  description  later. 

Besides  these  neuritides,  directly  of  toxic  origin  in  the  strict  sense  of  the 
word,  we  find  a  second  large  group  of  cases  which  come  on  secondarily  in  the 
course  of  or  as  a  sequel  to  other  diseases.  To  this  class  belong,  in  the  first  place, 
most  of  the  cases  already  mentioned  (page  832)  of  "  paralysis  after  acute  dis- 
ease." Since  it  is  usually  an  acute  infectious  disease  (diphtheria,  typhoid 
fever,  scarlet  fever,  septic  infection,  puerperal  disease  [pneumonia],  etc.),  we 
may  reasonably  assume  that  it  is  the  toxines  formed  under  the  influence  of  the 
corresponding  agents  of  infection  which  lead  to  the  death  of  the  peripheral  nerve- 
fiber;  but  similar  conditions  also  occur  in  chronic  infectious  diseases.  Tubercu- 
losis in  particular  seems  to  stand  in  close  relation  to  multiple  neuritis,  although, 
of  course,  it  is  often  hard  to  exclude  complication  with  some  septic  infection  or 
the  simultaneous  action  of  other  intoxications  (especially  alcohol,  vide  infra). 
[A  more  or  less  extensive  neuritis  is  not  uncommon  in  leprosy.  The  distribution 
of  the  neuritis  is  less  symmetrical  than  in  other  forms  of  neuritis,  and  the  morbid 
changes  in  the  peripheral  nerves,  which  involve  the  perineurium  and  interstitial 
tissue  more  than  the  nerve-fiber  itself,  are  thought  to  be  due  to  the  direct  inva- 
sion of  the  nerves  by  the  bacteria  rather  than  to  the  general  toxic  effect  of  the 
■disease.  The  chief  symptoms  are  marked  anaesthesia  and  muscular  wasting.  The 
Jansesthesia  in  the  ansesthetic  form  of  leprosy  is  due  to  these  lesions  of  the  periph- 
eral nerves. — K.]  It  is  certain  that  post-syphilitic  nervous  diseases  (tabes, 
q.  V.)  are  due,  at  least  in  part,  to  degenerations  of  the  peripheral  nerves ;  but  in 
these  cases  there  is  usually  extensive  disease  at  the  same  time  in  the  central 
nervous  system,  so  that  we  do  not  class  these  conditions  as  true  neuritis.  [Syphi- 
litic processes  may,  of  course,  involve  individual  nerves,  somewhat  in  analogy 
with  leprous  neuritis,  but  it  is  doubtful  whether  true  multiple  neuritis  is  ever 
of  syphilitic  origin.  Malaria  is  also  said  to  cause  multiple  neuritis.  Neuritis  is 
more  apt  to  follow  the  pernicious  forms  of  malaria  occurring  in  the  tropics — 
Jamaica,  India,  Madagascar,  etc.  It  may  come  on  suddenly  during  the  comatose 
period  of  a  pernicious  attack.  In  some  of  the  acute  cases  there  have  been  well- 
marked  changes  in  the  nerve-sheaths,  in  other  cases  there  have  been  ordinary 
degenerative  changes.  The  neuritis  has  been  referred  to  the  toxines  produced  by 
the  Plasmodium.  Trophic  and  vaso-motor  symptoms  (cyanosis)  seem  more 
marked  than  in  other  forms  of  neuritis.  There  is  a  possible  relation  between 
malarial  neuritis  and  beri-beri  (q.  v.). — K.]  Of  non-infectious  diseases,  diabetes 
mellitus,  first  of  all,  is  sometimes  most  closely  related  to  the  onset  of  multiple 
neuritis.  Here,  again,  we  can  scarcely  help  thinking  that  there  is  again  some  ab- 
normal chemical  substance  which  has  caused  the  neuritis,  but  the  question  of  dia- 
hetic  neuritis  is  still  in  great  need  of  further  investigation.  It  is  a  fact  that 
neuritic  affections  of  various  sorts  occur  in  severe  and  also  in  mild  forms  of  dia- 
betes, but  of  course  Ave  may  often  think,  on  the  other  hand,  that  the  glycosuria 


888  DISEASES    OE    THE   NEEYOUS    SYSTEM 

is  only  a  sequel  of  the  neuritis,  or  that  it  has  come  on  at  the  same  time  with  it 
(from  the  same  cause,  especially  previous  alcoholism).  In  a  few  cases  polyneu- 
ritis has  been  seen  in  severe  (usually  ulcerative)  carcinomata,  but  in  these  cases- 
secondary  septic  processes  may  play  the  chief  part,  as  in  tuberculosis  (vide  supra) ^ 

The  third  group,  finally,  is  composed  of  those  cases  of  multiple  neuritis  whicL 
must  be  termed  primary  multiple  degenerative  neuritis.  Of  course,  alcoholic 
or  diabetic  neuritis,  for  example,  may  come  on  apparently  as  a  primary  disease, 
but  the  true  primary  form  of  the  disease  includes  only  those  cases  where  no  other 
special  preceding  cause  can  be  discovered,  and  where  the  neuritis  apparently 
comes  on  as  an  independent  disease,  due  to  a  special  specific  cause.  The  whole- 
course  of  the  disease,  which  often  has  an  acute  febrile  character  (vide  infra), 
shows  that  we  must  in  such  cases  also  consider  toxic-infectious  influences,  but  we 
know  nothing  as  yet  as  to  the  precise  form  of  this  infection.  We  can  sometimes- 
find  no  special  cause.  There  has  often  been  previous  exposure  to  severe  cold. 
Such  cases  are  called  "  rheumatic  multiple  neuritis,"  without,  of  course,  implying 
that  they  have  any  definite  connection  with  articular  rheumatism.  It  is  worthy  of 
mention  that  primary  polyneuritis  has  sometimes  been  observed  to  occur  in  epi- 
demic form.  [The  peculiar  form  of  epidemic  neuritis  known  as  beri-beri  will  be 
spoken  of  later. — K.] 

We  must  add  in  conclusion  that  we  have  very  often  seen  cases  of  multiple- 
neuritis  where  we  could  discover  several  of  the  above-mentioned  causes  at  the 
same  time,  especially  when  alcoholism  and  tuberculosis  or  alcoholism  and  dia- 
betes mellitus  could  unite  their  noxious  effects.  We  have  also  seen  alcoholic  poly- 
neuritis come  on  directty  after  some  acute  febrile  disease  (pneumonia,  etc.)^ 
which  distinctly  reminds  us  of  the  appearance  of  delirium  tremens  in  acute 
diseases. 

Patholog'ical  Anatomy. — The  anatomical  changes  of  neuritis  consist,  as  has 
been  said,  mainly  in  a  degenerative  destruction  of  the  nerve-fibers.  We  do  not. 
know  whether  the  toxic  agents  act  directly  on  the  peripheral  nerve-fibers  or  on  the 
peripheral  motor  neurones  in  their  entirety.  The  visible  coarse  anatomical  de- 
struction is  usually  found,  at  all  events,  only  in  the  peripheral  offshoots  of  the- 
neurone — that  is,  in  the  "  peripheral  nerves,"  and  apparently  it  is  most  marked  in 
the  most  distant  terminal  arborizations  of  the  nerves.  In  the  larger  nerve-trunks 
and  plexuses  the  changes  are  xisually  much  less  pronounced  than  in  the  smaller- 
nerve-branches. 

Only  in  a  few  acute  cases  do  the  interstitial  connective  tissue  and  the  nerve- 
sheath  show  the  changes  of  true  acute  inflammation.  In  such  cases  we  find  the 
affected  nerves  swollen  and  decidedly  reddened  from  the  great  vascular  injection; 
with  the  naked  eye  we  can  sometimes  see  several  or  many  small  hasmorrhages. 
The  microscope  shows  the  nerve-sheath  and  the  interstitial  tissue  infiltrated  with 
many  round  cells,  but  as  a  rule  the  interstitial  tissue  is  little  or  not  at  all  in- 
volved in  the  disease.  The  pathological  anatomical  process  consists  exclusively 
in  a  destruction  of  the  axis  cylinder  and  medullary  sheath  (see  Fig.  112).  If 
we  stain  the  diseased  nerve-fibers  with  osmic  acid  we  see  the  sheath  of  Schwann 
filled  with  many  large  and  small  flakes  and  globules  of  the  medullary  substance 
of  the  nerve  which  are  stained  black.  The  fatty  globules  formed  by  this  degenera- 
tion are  taken  up  by  individual  leucocytes  (perhaps  also  by  the  endothelial  cells?), 
and  thus  the  so-called  "  fatty  granular  cells  "  are  formed.  If  the  process  has 
lasted  some  time  and  the  acute  symptoms  have  ceased,  either  the  regeneration  of 
the  nerve-fiber  begins,  or,  when  the  special  nerve-tissue  is  permanently  destroyed, 
there  is  a  new  formation  of  an  abundant  interstitial  connective  tissue.  If  we 
now  examine  a  transverse  section  of  a  diseased  nerve  we  find  the  individual  nerve- 
fibers  no  longer  close  together,  as  under  normal  conditions,  but  separated  from 
one  another  in  many  places,  where  some  fibers  have  wholly  disappeared,  by  a. 


SIMPLE   AND   MULTIPLE   DEGENEKATIVE   NEUEITIS        889 


large  amount  of  interstitial  connective  tissue.  If  the  new  formation  of  con- 
nective tissue  attains  a  higher  degree,  the  neiwe  then  becomes  firmer  and  denser 
than  normal,  and,  when  there  is  a  very  large  amount  of  connective  tissue  (after 
the  analogy  of  callus  formation)  it  also  becomes  thicker,  so  that  in  some  places 
we  may  sometimes  speak  of  a  neuritis  nodosa.  If,  however,  the  polyneuritis 
recovers,  it  is  due  to  regeneration — that  is,  to  a  complete  new  growth  of  the 
destroyed  nerve- 

fiber.  The  remark- 
ably great  power 
of  regeneration  of 
the  peripheral  nerves 
is  one  of  the  most 
important  facts  in 
the  pathology  of  the 
nervous  system.  It 
is  explained  in  a 
simple  naanner  by 
the  persistence  of 
the  cell  of  origin 
(the  motor  ganglion- 
cell  in  the  anterior 
horn)  from  which 
the  destroyed  termi- 
nal branches  grow 
out  again  like  the 
severed  branches  of  a 
tree.  Therefore  the 
severest  peripheral 
paralyses  and  atax- 
ias may  sometimes 
completely  recover. 

In  the  cases  of 
"  chronic  multiple 
neuritis "  the  dis- 
ease succeeds  an  acute  neuritis  or  develops  in  an  insidious  fashion  from  the  start. 
In  the  latter  case  the  first  acute  stage  of  hypersemia  and  cell  infiltration  is  wholly 
wanting  and  the  disappearance  of  nerve-fibers  and  the  secondary  new  growth  of 
connective  tissue  is  a  chronic  process  from  the  first.  Such  conditions  perhaps 
should  not  properly  be  called  "  neuritis,"  but  "  primary  chronic  degenerative 
atrophy  of  the  nerves  " ;  but  the  name  is  of  less  consequence  than  a  clear  idea  of 
the  nature  and  development  of  the  morbid  process.  There  is  also  nothing  strange 
in  finding  in  some  cases  slight  changes  in  the  motor  ganglion-cells  themselves. 
When  the  action  of  the  toxic  substance  is  severe  or  long  continued  the  whole 
motor  neurone,  including  its  cell  of  origin,  suffers.  The  paralyzed  muscles  in 
every  peripheral  neuritis  soon  become  very  much  atrophied.  Microscopic  exami- 
nation shows  all  stages  of  atrophy  of  the  fibers  up  to  complete  disappearance. 
The  transverse  striation  is  for  the  most  part  preserved,  and  the  number  of  the 
muscular  nuclei  is  much  increased.  In  individual  cases  we  also  find  degenera- 
tive destruction  of  the  muscular  fibers,  hypertrophy,  swelling,  waxy  degeneration, 
etc.  A  genuine  myositis — that  is,  the  formation  of  small  inflammatory  foci  in 
the  interstitial  tissue — is  sometimes  joined  to  the  neuritis.  In  such  cases  of 
"  neuro-myositis  "  the  poison  seems  to  act  from  the  start  simultaneously  on  the 
nerves  and  muscles. 

Besides  its  action  on  the  peripheral  motor  neurones   and  the  muscles,  the 


Fig.  118. 


-Radial  nerve  in  alcoholic  polyneuritis. 
(Personal  observation.) 


Osmic-acid  preparation. 


890  DISEASES    OF    THE   XEEYOUS    SYSTEM 

action  of  the  morbific  influence  may  extend  still  farther.  Thus  we  find  co-esist- 
ing  changes  in  the  columns  of  GoU,  and  even  in  the  brain,  which  under  some  cir- 
cumstances may  excite  sjoecial  clinical  sjinptoms. 

Symptoms  and  Course  of  the  Different  Forms  of  Multiple  Neuritis. — In 
order  to  attain  a  correct  understanding  of  the  symptomatology  of  multiple  neu- 
ritis, we  must  first  remember  that  the  disease  is  not  aatiologically  one  absolutely 
sing'le  affection,  and  that  therefore  we  must  expect  a  priori  certain  differences  in 
the  clinical  picture.  These  differences  are  due  not  only  to  the  degeneration  of 
different  nerve-trunks,  but  also,  in  part,  to  the  fact  that  the  same  specific  variety 
of  nerve-fiber  is  not  always  the  one  most  affected.  In  general,  of  course,  the 
rule  undoubtedly  holds  good  that  the  motor  nerve-fibers  afford  the  least  resistance 
to  all  the  injurious  infiuences  previously  mentioned.  Therefore  peripheral  paraly- 
ses are  the  chief  and  the  most  common  symptom  of  polyneuritis.  The  sensory 
nerves  are  usually  less  affected;  at  least  pronounced  anaesthesia  is  exceptional. 
The  involvement  of  the  sensory  nerves  is  shown  rather  by  symptoms  of  irritation 
(pain,  parsesthesia),  which  probably  are  to  be  referred  less  to  a  direct  invasion 
of  the  sensory  fibers  than  to  an  irritation  of  them  as  a  result  of  the  interstitial 
changes.  There  is,  however,  one  frequent,  important,  and  very  interesting  symp- 
tom in  multiple  neuritis,  occurring  alone  or  with  the  paralysis :  a  genuine  motor 
ataxia.  Its  origin  is  not  positively  explained,  but  we  regard  it  as  most  probable 
that  the  ataxia  is  due  to  disease  of  the  centripetal  fibers  which  also  exist  in  the 
peripheral  nerves,  whose  function  is  to  regulate  (in  a  certain  sense  reflexly)  and 
to  co-ordinate  complicated  voluntary  movements.  It  is  itseK  an  extremely  inter- 
esting fact  that  ataxia  of  movement  without  co-existing  paralysis  may  occur  in 
apparently  purely  peripheral  diseases  without  any  discoverable  changes  in  the 
spinal  cord;  but  ataxia  may  also  be  due  to  disease  of  the  spinal  processes  of  the 
spinal  ganglion-cells — that  is,  to  degeneration  in  the  columns  of  Goll.  From  a 
symptomatological  standpoint  we  must  therefore  distinguish  two  forms  of  neuritis 
— a  paralytic  form  (the  usual  form)  and  an  ataxic  form  (so-called  acute  curable 
ataxia,  and  also,  especially,  the  pseudo-tabes  of  alcoholic  subjects)  ;  but  combina- 
tions of  the  two  forms  occur,  since  paralytic  conditions  and  disturbances  of  co- 
ordination may  be  united. 

Passing  now  to  the  description  of  the  general  aspect  and  course  of  polyneu- 
ritis, it  seems  best  to  keep  separate  the  different  forms  which  may  be  distin- 
guished either  clinically  or  setiologically. 

1.  Primary  Acute  axd  Chronic  Multiple  Xeuritis 
The  disease  usually  begins  acutely,  sometimes  almost  in  an  apoplectiform 
manner,  and  without  any  definite  occasion,  precisely  like  an  acute  infectious 
disease.  Febrile  symptoms,  with  temperatures  from  102°-104°  (39°— 40°  C), 
come  on  in  persons  previously  in  good  health,  usually  in  adults  before  or  during 
middle  life,  with  severe  general  disturbance,  loss  of  appetite,  dullness,  head- 
ache, and  sometimes  even  mild  delirium.  In  these  acute  cases  albuminuria 
and  a  slight  enlargement  of  the  spleen  have  sometimes  been  observed,  which 
symptoms  also  point  toward  the  infectious  nature  of  the  disease.  In  other 
cases  the  initial  general  symptoms  are  much  less  severe,  or  they  may  be  en- 
tirely wanting.  The  pains,  which  are  hardly  ever  absent,  are  very  characteris- 
tic. They  are  described  as  pulling  and  tearing,  are  felt  chiefly  in  the  loins 
and  the  extremities,  and  sometimes  follow  approximately  the  course  of  the  large 
nerve-trunks.  Since  in  some  cases  a  number  of  the  joints  are  swollen,  the  disease 
at  first  may  be  mistaken  for  acute  articular  rheumatism.  The  first  symptoms  of 
paralysis,  usually  in  the  lower  extremities,  appear  very  soon  after  these  initial 
symptoms,  or  at  the  same  time  with  them.  The  patient  notices  that  he  can  not 
readily  move  one  leg,  and  soon  after  he  notices  the  same  of  the  other.    The  paraly- 


SIMPLE   AND   MULTIPLE   DEGENEKATIVE   NEURITIS        891 

sis  may  remain  confined  to  the  legs,  but  more  frequently  it  extends  to  one  or 
both  arms.  In  regard  to  its  distribution,  the  forearms  and  lower  legs  are  gener- 
ally more  affected  than  the  upper  arms  and  thighs,  and  the  extensors  (radial  and 
peroneal  region)  are  also  more  affected  than  the  flexors;  but  other  varieties  of 
distribution  may  occur,  for  instance,  affection  of  the  glutsei  and  thigh  muscles, 
etc.  If  we  examine  the  paralyzed  parts  more  carefully  we  find  a  perfectly  atonic 
and  more  or  less  extensive  paralysis.  The  reflexes  are  almost  always  diminished, 
the  tendon  reflexes  are  usually  entirely  absent,  and  the  cutaneous  reflexes  are 
weak,  or  they  also  have  almost  wholly  disappeared.  In  only  a  few  cases  are  the 
reflexes  increased — a  symptom  which  is  to  be  regarded  as  analogous  to  cutaneous 
hypergesthesia.  We  can  usually  make  out,  after  a  few  days,  a  decided  diminu- 
tion of  electrical  excitability  in  the  affected  nerves  and  muscles,  which  soon 
becomes  a  pronounced  reaction  of  degeneration.  If  the  paralysis  is  of  longer 
duration,  there  is  a  decided  atrophy  of  the  muscles.  In  these  cases  the  severe 
initial  symptoms  of  sensory  irritation,  as  a  rule,  rapidly  disappear,  although 
slight  pains,  parsesthesia,  and  especially  a  considerable  sensitiveness  of  the  para- 
lyzed parts  to  pressure  and  to  passive  motion,  often  last  for  a  long  time.  In 
many  acute  cases  the  hypersesthesia  of  the  skin  and  of  the  deeper  parts  reaches 
a  very  high  degree,  but  it  is  remarkable  that  the  objective  disturbances  of  sensi- 
bility are  very  slight  in  the  great  majority  of  cases;  although  on  careful  testing 
we  can  often  find  slight  diminution  of  sensibility  for  touch  or  temperature.  Other 
observers  and  we  ourselves  have  also  repeatedly  seen  the  symptom  of  so-called 
delayed  conduction— that  is,  delayed  sensation  of  pain  (vide  supra,  page  793). 
We  usually  find  no  disturbances  in  the  distribution  of  the  cerebral  and  bulbar 
nerves.  An  affection  of  the  optic  nei-ve  has  been  mentioned  in  only  a  few  cases. 
Facial  paralysis  and,  much  less  frequently,  paralysis  of  the  tongue  or  of  the  ocular 
muscles  may  also  occur.  We  have  ourselves  repeatedly  seen  total  bilateral  facial 
paralysis.  We  may  mention  as  a  rare  complication  acute  mental  disturbances 
(confusion,  anxiety,  weakness  of  memory,  vide  infra).  Details  of  this  very 
peculiar  "  polyneuritic  psychosis "  will  be  given  below  in  the  description  of 
alcoholic  polyneuritis.  The  marked  increase  in  the  frequency  of  the  pulse,  which 
is  usually  present,  is  important,  and  probably  depends  upon  a  disturbance  of 
the  vagus.  Trophic  disturbances  in  the  skin,  hair,  and  nails  are  not  very  rare. 
Profuse  sweating  sometimes  occurs.  CEdematous  swelling  of  the  affected  ex- 
tremities has  also  been  repeatedly  observed.  The  functions  of  the  bladder  and 
rectum,  however,  almost  always  remain  unaltered,  but  in  some  cases  slight  dis- 
turbances of  the  bladder  may  of  course  be  discovered. 

In  regard  to  the  course  of  the  disease,  in  the  severest  cases  it  may  soon  termi- 
nate fatally,  almost  always  because  the  paralysis  extends  to  the  muscles  of  respira- 
tion. The  inspirations  are  labored,  and  are  performed  with  the  upper  part  of  the 
thorax  only,  while  the  epigastrium  is  motionless,  or  sinks  in  on  inspiration  from 
the  paralysis  of  the  diaphragm.  There  is  also  paralysis  of  the  other  muscles  of 
respiration,  the  abdominal  muscles,  etc.,  so  that,  after  the  disease  has  lasted  a 
week  or  ten  days,  death  ensues  with  all  the  signs  of  respiratory  insufiiciency. 
Such  cases  have  been  repeatedly  described  in  the  past  under  the  title  of  acute 
ascending  paralysis  (Landry's  paralysis,  q.v.).  A  second  class  of  cases  also 
begins  quite  acutely,  but  then  takes  a  chronic  course.  The  initial  acute  febrile 
symptoms  cease  after  a  few  days,  although  the  paralysis  continues  to  develop 
to  some  extent.  Then  the  affection  seems  to  come  to  a  stand-still,  and  the  first 
signs  of  improvement  gradually  begin  to  appear.  Since  there  is  a  more  or 
less  pronounced  atrophy  of  the  muscles  in  these  cases,  it  always  takes  consid- 
erable time — usually  several  months — for  recovery;  but  it  is  often  astonishing 
to  see  how  the  most  extensive  paralysis  may  finally  get  entirely  well.  A  third 
class  of  cases  follows  a  chronic  course  from  the  outset,  although  even  in  these 


892  DISEASES    OF   THE   NEEVOUS    SYSTEM 

cases  there  may  be  more  acute  exacerbations  of  the  disease.  In  these  cases  quite 
extensive  atrophic  paralysis  gradually  develops  in  the  lower  extremities,  and 
usually  in  the  upper  extremities  also.  The  reflexes  disappear;  the  sensibility  is 
as  a  rule  somewhat,  but  very  rarely  much  diminished.  Pains  are  always  present 
at  first,  but  later  on  in  the  disease  they  often  become  subordinate.  The  blad- 
der and  rectum  usually  remain  normal  in  their  functions  or  show  only  slight 
disturbances.  If  the  disease  advance  gradually  it  may  terminate  fatally  even 
at  a  late  period,  after  a  course  of  months,  usually  from  a  final  paralysis  of  respi- 
ration; but,  on  the  other  hand,  even  after  a  protracted  course,  the  disease  may 
come  to  a  stand-still,  and  even  progress  to  a  complete  or  at  least  to  a  partial 
recovery. 

The  diagnosis  of  multiple  neuritis  is,  as  a  rule,  easy  for  one  who  is  acquainted 
with  the  disease  and  notes  the  different  symptoms  carefully.  In  regard  to  diag- 
nosis, the  chief  importance  should  be  placed  on  the  generally  acute  beginning, 
with  pronounced  symptoms  of  sensory  irritation,  with  frequently  a  very  consid- 
erable sensitiveness  of  the  nerves  and  muscles  to  pressure  and  general  cutaneous 
hyperesthesia ;  and  also  on  the  appearance  of  a  rapidly  extending  paralysis,  whose 
peripheral  nature  may  be  attested  by  the  presence  of  reaction  of  degeneration, 
muscular  atrophy,  and  the  absence  of  the  cutaneous  and  tendon  reflexes.  Such  a 
paralysis  can  be  produced  by  nothing  but  an  afi^ection  of  the  peripheral  nerves  or 
poliomyelitis  (vide  infra).  This  latter  disease  was,  in  fact,  formerly  confused 
with  multiple  neuritis,  but  a  careful  attention  to  the  initial  symptoms,  especially 
to  the  pain  and  disturbances  of  sensation,  usually  makes  the  differential  diag- 
nosis possible. 

The  prognosis  of  multiple  neuritis  is  doubtful,  as  is  shown  by  the  description 
of  the  course  of  the  disease,  but  it  is  by  no  means  very  unfavorable.  If  the  pa- 
tients gets  through  the  flrst  acute  stage  of  the  disease  without  accident,  we  may 
hope  for  recovery,  or  at  least  actual  improvement,  even  with  extensive  paralysis. 
Such  striking  results  in  the  way  of  recovery,  after  paralysis  that  has  lasted  for 
months,  are  also  important  in  regard  to  diagnosis,  since  such  extensive  processes 
of  regeneration  are  possible  in  affections  of  the  peripheral  nerves,  but  scarcely  in 
spinal  diseases;  and  hence  they  are  sometimes  an  additional  confirmation  of  the 
diagnosis  of  a  neuritis. 

Treatment. — In  the  first  stage  of  the  disease,  especially  if  severe  pains,  swell- 
ing of  the  joints,  or  high  fever  be  present,  it  is  advisable  to  try  the  exhibition  of 
salicylic  acid,  from  which  several  observers  have  seen  a  favorable  effect.  We  give 
ten  grains  (gramme  0.5)  of  the  acid  every  hour,  or  a  few  larger  doses  of  salicylate 
of  sodium,  a  drachm  to  a  drachm  and  a  half  (gramme  4-6).  Instead  of  salicylic 
acid  we  have  used  antipyrine  and  phenacetine  with  good  results.  When  the  pain 
is  very  severe  we  must  use  narcotics,  such  as  injections  of  morphine.  Embroca- 
tions of  chloroform,  and  sometimes  protracted  warm  baths,  have  also  a  palliative 
effect.  In  the  further  course  of  the  disease  proper  care,  a  suitable  position  for 
the  limbs,  and  diet — nourishing  food — are  the  main  things  for  the  patient.  The 
regenerative  processes  of  recovery  begin  spontaneously,  if  thej^  begin  at  all,  but  we 
may  hasten  recovery  and  make  it  complete  by  a  subsequent  electrical  treatment, 
especially  galvanism.  For  the  completion  of  the  recovery,  bathing  (simple  warm 
baths,  salt  baths,  etc.)  is  serviceable,  and  also  the  baths  at  Teplitz,  Wiesbaden, 
l^auheim,  and  Oeynhausen,  and  the  cautious  use  of  massage. 

2.  The  Ataxic  Form  of  Multiple  ISTeuritis 

i^'- Acute  Ourable  Ataxia^'') 

We  can  not  make  a  sharp  division  between  the  ataxic  and  the  paralytic  forms 
of  multiple  neuritis.  Both  conditions,  paralysis  and  ataxia,  may  occur  in  the 
same  patient.    It  is  important,  however,  to  know  that  almost  pure  ataxia  (without 


SIMPLE   Al^D   MULTIPLE   DEGENERATIVE   NEURITIS        893 

paralysis)  may  develop  acutely,  and  that  it  is  undoubtedly  to  be  referred  to  de- 
generation of  the  peripheral  nerves. 

Under  the  ataxic  form  of  polyneuritis  must  be  classed,  first,  the  cases  of  ataxia 
repeatedly  observed  after  various  acute  infectious  diseases,  especially  ataxia  after 
diphtheria  iq.v.),  and  also  after  typhoid  fever,  small-pox,  septic  affections,  dysen- 
tery, etc.;  but  there  is  also  a  primary  acute  ataxia  which  comes  on  without  any 
discoverable  cause  or  after  exposure  to  severe  cold  in  previously  healthy  persons. 
Severe  general  initial  symptoms  are,  as  a  rule,  not  present,  and  the  pain  is  not 
very  great.  The  ataxia  usually  develops  in  the  legs,  more  rarely  in  the  arms. 
There  may  be  slight  disturbances  of  sensibility  at  the  same  time,  but  not  neces- 
sarily. The  patellar  reflex  is  usually  but  not  always  absent.  As  a  rule,  with 
proper  care  and  nursing  the  patient  recovers  completely  in  a  few  weeks.  The 
diagnosis  of  this  primary  acute  ataxic  form  of  polyneuritis  is  usually  not  difficult. 
The  disturbance  of  the  patient's  gait  may  at  first  arouse  the  suspicion  of  tabes, 
but  the  rapid  onset,  the  perfectly  normal  pupillary  reflexes,  and  usually  also 
the  normal  micturition,  oppose  it.  We  often  find  in  some  muscular  regions  a  true 
paresis  besides  the  ataxia,  which  is  not  like  the  conditions  in  tabes.  We  once  saw, 
for  instance,  a  severe  ataxia  of  the  legs  associated  with  double  facial  paralj^sis. 
In  any  doubtful  case  a  favorable  termination  in  recovery  forms  the  final  criterion 
in  favor  of  polyneuritis. 

3.  The  Acute  and  Chronic  Neuritis  of  Alcoholic  Subjects — Alcoholic 

Paralysis 

{Pseiido-tahes  [Ataxia]  of  Alcoholic  Subjects) 

It  has  long  been  known  that  peculiar  nervous  affections  often  occur  in  alco- 
holic subjects  (M.  LIuss,  Leudet,  and  others)  ;  but  formerly  a  disease  of  the 
spinal  cord  was  assumed  to  be  the  cause  of  the  symptoms,  and  only  of  late  have 
we  obtained  the  knowledge  that  the  greatest  part  of  the  cases  of  this  class  are  to 
be  classed  as  acute  and  chronic  multiple  neuritis  (Lancereaux,  Moeli,  and  others). 
The  practical  importance  of  this  alcoholic  neuritis  is  not  slight;  first,  because  it 
may  easily  be  confused  with  other  nervous  diseases,  especially  with  myelitis  and 
tabes,  and,  second,  because  its  proper  and  timely  diagnosis  is  of  great  significance 
in  regard  to  treatment.  Alcoholic  neuritis,  furthermore,  is  by  no  means  rare, 
being  certainly  by  far  the  commonest  of  all  forms  of  polyneuritis.  The  more  we 
consider  the  significance  of  this  factor  the  more  all  other  causes  are  thrown  into 
the  background.  Not  infrequently,  of  course,  other  causes  must  be  considered  at 
the  same  time  with  alcoholism;  we  see,  for  example,  polyneuritis  very  often  in 
alcoholic  subjects  who  are  also  tuberculous,  and  sometimes  in  the  combination 
of  alcoholism  and  diabetes,  etc.;  but  in  all  such  cases  chronic  alcohol  poisoning 
probably  plays  the  chief  part.  Alcoholic  neuritis  occurs  in  drinkers  of  spirits, 
and  also,  as  we  have  often  noticed,  in  habitually  excessive  beer  drinkers.  It  is 
alleged  to  be  less  frequent  in  drinkers  of  wine. 

Alcoholic  polyneuritis,  like  the  other  varieties  of  multiple  neuritis,  occurs  in 
different  forms.  According  to  its  course  we  may  distinguish  acute  and  chronic 
cases,  and  according  to  its  symptoms  a  paralytic  and  an  ataxic  form,  but  there 
are  no  strict  boundaries  between  these  forms. 

Alcoholic  paralysis  begins  quite  suddenly  or  more  gradually.  Motor  weakness 
develops,  having  its  chief  seat  usually  in  the  legs,  and  thus  rendering  walking 
almost  wholly  impossible.  This  weakness  generally  begins  with  quite  severe  tear- 
ing and  drawing  pains  and  considerable  tenderness  on  pressure  over  the  affected 
muscles.  Most  writers  agree  that  the  muscles  on  the  anterior  side  of  the  lower 
leg  (peronei,  tibialis  anticus)  are  very  often  affected.  We  can  agree  with  this  for 
many  cases,  but  by  no  means  for  all.  We  have  often  seen  at  the  onset  the  great- 
est trouble  in  the  muscles  of  the  thigh  (crural  region),  and  especially  in  the  glu- 


894  DISEASES    OF    THE   XEEYOUS    SYSTEM 

tsei.  Such  patients  can  still  walk  witli  effort  on  level  ground,  but  they  can  not  go 
up  a  step  or  rise  from  a  chair.  With  greater  paralysis  the  patient  is  absolutely 
bedridden.  The  muscles  of  the  legs  are  flabby,  they  become  more  or  less  atrophied, 
their  electrical  excitability  diminishes,  there  is  sometimes  pronounced  reaction  of 
degeneration  (especially  the  middle  form),  and  the  patellar  reflex  and  other 
tendon  reflexes  are  usually  absent,  although  there  are  some  remarkable  exceptions 
to  this  rule.  The  bladder  and  rectum  are  entirely  normal  or  show  only  slight  dis- 
turbances. The  sensibility  of  the  legs  is  rarely  perfectly  normal  on  careful  test- 
ing, but  the  sensory  disturbances,  except  for  pain  and  parassthesia,  are  overshad- 
owed by  the  paralysis.  We  often  find  a  slight  blunting  of  sensibility  for  touch 
and  pain,  and  very  often  the  so-called  delayed  sensation  of  pain  (vide  supra, 
page  793).     The  skin  reflexes  are  diminished. 

In  many  cases  the  paralysis  extends  to  the  arms  also,  and  chiefly  in  the  radial 
distribution,  so  that  both  hands  hang  lax  in  volar  flexion,  and  they  and  the 
fingers  can  be  extended  but  little.  The  combination  of  double  radial  and  peroneal 
paralysis  has  been  often  mentioned  as  characteristic  of  alcoholic  paralysis.  Even 
in  patients  who  can  still  extend  their  hands  and  fizigers  well  we  often  find  that 
the  strength  of  the  movement  is  diminished.  In  severe  polyneuritis  the  other  arm 
muscles  may  also  be  affected.  Muscular  atrophy,  electrical  reactions,  sensibility, 
and  the  reflexes  are  the  same  as  in  the  legs. 

The  facial  muscles  are  rarely  affected,  but  they  have  been  in  a  few  cases.  In 
some  very  acute  and  severe  cases  of  polyneuritis  there  is  also  paralysis  of  the 
ocular  muscles,  so  that  the  eye  may  become  completely  immovable ;  but  in  the  few 
cases  that  have  come  to  autopsy  there  seems  usually  to  have  been  no  neuritis  of 
the  oculo-motor  nerves  themselves,  but  many  small  hgemorrhages  in  the  neighbor- 
hood of  the  third  ventricle — that  is,  in  the  region  of  the  oculo-motor  nuclei  (so- 
called  polio-encephalitis  hsemorrhagica  superior,  q.  v.). 

Mental  disturbances  ("polyneuritic  psychoses")  have  been  frequently  ob- 
served in  alcoholic  polyneuritis.  They  often  differ  little  from  delirium  tremens, 
but  in  other  cases  a  very  peculiar  type  of  disease  develops.  The  patient  is  con- 
fused, mixes  up  persons  and  places,  is  very  restless,  especially  at  night,  apparently 
has  hallucinations,  and  is  consequently  excited  and  anxious,  but  in  the  intervals 
is  happy  and  contented.  The  most  striking  disturbance  is  an  extraordinary  weak- 
ness of  memory  for  all  recent  events.  HaK  an  hour  after  eating  the  patient  no 
longer  knows  that  he  has  eaten.  If  we  show  him  an  object  or  utter  a  word  or  a 
short  sentence  to  him,  he  forgets  it  completely  in  a  few  minutes.  The  more  care- 
fully we  test  the  patient  in  regard  to  this,  the  more  frequently  shall  we  discover 
this  remarkable  disturbance  of  memory;  but  the  recollection  of  the  distant  past 
and  of  things  learned  before  the  trouble  is  not  at  all  or  very  slightly  affected. 
The  patient's  initial  confusion  is  chiefly  the  direct  result  of  this  actual  failure  of 
memory.  The  severe  mental  disturbances  sometimes  last  only  a  few  days,  but 
the  disturbances  of  memory  may  often  be  noticed  for  weeks,  when  they  gradually 
disappear. 

The  ataxic  form  of  alcoholic  polyneuritis  may  also  come  on  acutely,  so  that 
the  patient's  sudden  inability  to  walk  is  due  to  a  genuine  ataxia  of  the  legs.  The 
ataxia,  of  course,  is  generally  associated  with  manifest  paralysis,  at  least  in 
some  muscular  territories  (glutaei,  peronei,  radials).  The  ataxia  may  often  be 
masked  by  a  greater  paralysis,  so  that  we  can  discover  it  only  by  careful  exami- 
nation. The  patellar  reflex  is  usually,  but  not  invariably,  lost;  the  sensibility  is 
only  slightly  affected,  apart  from  the  pain  and  parsesthesia.  The  functions  of 
the  bladder  remain  wholly,  or  almost  wholly,  normal. 

The  chronic  form  of  alcoholic  ataxia,  the  special  pseudo-tabes  of  alcoholic 
subjects,  is  more  important  because  it  is  often  harder  to  diagnosticate.  In  this 
form  a  type  of  disease  develops  comparatively  slowly,  which  may  closely  resemble 


SIMPLE   AND   MULTIPLE   DEGENEEATIVE   NEUKITIS        895 

genuine  tabes :  ataxic  gait,  lancinating  pains,  sometimes  even  a  sort  of  girdle  sen- 
sation, absence  of  patellar  reflex,  slight  disturbance  of  the  bladder,  definite  dis- 
turbances of  sensibility,  etc.  The  disease  resembles  true  tabes  still  more  closely  if 
temporary  double  vision  occurs.  In  such  cases  we  can  avoid  mistaking  it  for  true 
tabes  only  by  careful  examination.  The  most  important  mark  of  distinction  is 
afforded  by  the  pupils,  which  almost  always  preserve  their  normal  reaction  in 
pseudo-tabes.  We  may  also  note  that  in  pseudo-tabes  the  disturbances  of  the 
bladder  are  usually  slight,  and  they  may  be  entirely  absent ;  that  the  muscles  and 
nerves  are  tender  on  direct  pressure,  and  that  from  the  first  we  can  usually  find 
besides  the  ataxia  a  slight  genuine  paresis,  which  in  some  muscles  (vide  supra) 
may  be  marked.  [We  rarely  if  ever  find  in  pseudo-tabes  the  anesthesia  or  anal- 
gesia over  the  lower  part  of  the  chest,  on  one  or  both  sides,  in  the  area  of  the 
third  to  the  seventh  dorsal  roots,  so  characteristic  of  true  tabes. — K.]  Finally,  of 
course,  the  causal  factor,  pronounced  chronic  alcoholism,  is  an  essential  considera- 
tion. It  is  worthy  of  note  that  in  alcoholic  pseudo-tabes  the  anatomical  lesion  is 
probably  not  often  limited  to  the  peripheral  nerves,  but  also  involves  the  spinal 
processes  of  the  spinal  ganglion  cells — that  is,  the  region  of  the  columns  of  Goll. 

The  course  of  this  pseudo-tabes  may  extend  over  several  years,  but  the  progno- 
sis is  far  more  favorable  than  that  of  true  tabes ;  decided  improvement  and  even, 
in  mild  cases,  complete  recovery  may  occur;  but  there  are  also  severe  incurable 
forms,  since  dangerous  complications  (tuberculosis,  etc.)  often  set  in. 

All  the  more  acute  forms  of  alcoholic  neuritis  afford  quite  a  good  prognosis, 
provided  the  abuse  of  alcohol  can  be  permanently  checked.  We  may  then  often 
see  complete  recovery  in  a  few  weeks  or  months.  On  the  other  hand,  relapses  are 
common,  and  these  usually  have  a  tedious  course. 

The  first  task  in  the  treatment  of  alcoholic  neuritis  is  to  insist  upon  the 
absolute  abandonment  of  the  use  of  alcohol.  If  this  be  done,  the  milder  cases 
usually  get  well  of  themselves.  The  favorable  course  is  aided  by  electrical  (gal- 
vanic) treatment  and  tepid  salt  baths.  Internally  we  prefer  strychnine  prepara- 
tions (pills  of  nitrate  of  strychnine  or  extract  of  nux  vomica). 

[4.  Beri-beri — Endemic  Multiple  Neuritis 
The  peculiar  disease  of  endemic  origin,  long  known  in  India  and  Japan  as 
"  beri-beri  "  or  "  Tcah-he,"  has  been  found  by  Scheube  to  be  in  its  clinical  and  ana- 
tomical relations  a  well-characterized  multiple  neuritis.  Cases  are  occasionally 
seen  in  seaport  towns  in  sailors  arriving  from.  Asiatic  ports,  and  Putnam  has  de- 
scribed cases  occurring  in  fishermen  returning  from  the  Newfoundland  banks. 
Independent  outbreaks  of  the  disease  have  also  occurred  among  the  insane  in  asy- 
lums in  Alabama,  Arkansas,  Dublin,  and  elsewhere.  Men  are  more  frequently 
affected  than  women,  and  colored  races  more  than  the  white.  The  cause  of  the 
disease  is  still  obscure.  Pekelharing  and  Winkler  attributed  it  to  a  specific  staphy- 
lococcus, but  their  observations  have  not  been  confirmed  by  later  observers. 
Insufficient  or  improper  diet  probably  increases  the  susceptibility  to  the  disease, 
but  it  is  doubtful  if  an  exclusive  diet  of  rice  or  fish,  as  was  once  believed,  can  ac- 
tually cause  beri-beri.  Bondurant  in  Alabama  found  a  close  connection  between 
the  outbreak  of  the  disease  and  the  use  of  a  pollute'^d  water-supply.  In  other  cases 
there  seems  some  association  with  malarial  poisoning.  Overcrowding  and  foul 
air  favor  its  development.  The  disease  may  begin  suddenly  or  insidiously,  and  it 
is  often  ushered  in  by  moderate  fever  and  gastro-intestinal  symptoms :  anorexia, 
vomiting,  abdominal  pain,  and  diarrhoea.  Two  forms  of  the  disease — a  "  wet  " 
and  a  "  dry  " — are  usually  recognized.  The  symptoms  in  the  "  dry  "  form  are  sim- 
ilar to  those  of  ordinary  multiple  neuritis :  pain,  parsesthesia,  tenderness,  loss  of 
power  with  degenerative  muscular  atrophy,  especially  in  the  extensors  of  the  foot, 
slight  disturbances  of  sensation,  and  diminution  or  loss  of  patellar  reflex.     The 


896  DISEASES    OF   THE   Is^EEVOUS    SYSTEM 

"  wet "  form,  which  is  commoner,  often  begins  with  dyspnoea  and  a  rapid  pulse, 
and  oedema  may  soon  follow.  The  oedema  is  most  marked  in  the  regions  supplied 
by  the  affected  nerves,  but  there  is  also  effusion  into  the  serous  cavities.  The 
heart's  action  is  weak,  and  the  heart  may  soon  become  greatly  dilated,  and  adven- 
titious murmurs  may  be  heard.  In  severer  cases  the  urine  contains  a  small 
amount  of  albumen,  the  dyspnoea  and  rapid  pulse  persist,  and  the  patient  suc- 
cumbs to  cardiac  exhaustion.  A  certain  amount  of  serous  effusion  is  usually 
present  at  the  autopsy,  together  with  the  changes  in  the  heart.  There  is  also  a 
degenerative  neuritis  of  the  peripheral  nerves,  often  including  the  vagus,  and  a 
corresponding  degeneration  of  the  muscles  supplied  by  them,  and  often  degenera- 
tion of  the  ganglion-cells  in  the  anterior  cornua.  In  some  cases  of  the  "  wet " 
form  the  disease  progresses  rapidly,  with  increasing  oedema  and  cardiac  weakness, 
leading  to  death  in  a  week  or  two.  Other  cases  may  run  a  more  chronic  course, 
with  atrophic  paralysis,  and  eventually  recover.  The  prognosis  is  grave.  Twenty 
per  cent,  of  the  cases  among  the  chronic  insane  died  in  Alabama,  and  the  mortal- 
ity has  been  even  greater  in  other  epidemics,  although  Scheube  estimates  the  aver- 
age mortality  at  five  per  cent.  In  the  way  of  prophylaxis  good  hygiene,  a  good 
soil  and  sanitary  dwellings,  pure  water  and  plenty  of  nutritious  food,  seem  essen- 
tial. Cathartics,  especially  hydragogues,  seem  of  some  benefit  in  the  early  stages. 
The  condition  of  the  heart  demands  especial  attention,  but  caution  is  necessary 
in  administering  digitalis  or  strophanthus  (the  chief  drugs  to  employ)  lest  the 
weak  heart  be  urged  to  undue  effort.  Hence  we  should  begin  with  small  doses 
(gramme  0.2-0.3,  minims  iij-v,  of  the  tincture),  increasing  gradually.  In  the 
later  stages  the  treatment  is  the  same  as  for  other  forms  of  multiple  neuritis 
(strychnine,  electricity,  massage). — K.] 


CHAPTER   VI 
NEW    GROWTHS    IN    THE    PERIPHERAL    NERVES 

The  new  growths  in  the  peripheral  nerves  are  usually  divided  into  false  and 
true  neuromata.  True  neuromata  consist  of  newly  formed,  usually  medullated, 
nerve-fibers  (neuroma  myelinicum  of  Virchow),  which  are  imbedded  in  a  con- 
nective-tissue stroma,  which  is  frequently  very  abundant.  These  neuromata  de- 
velop most  frequently  in  the  cut  ends  of  nerves  in  amputation-stumps  (amputation 
neuromata),  but  they  may  form  after  other  injuries  of  the  nerves,  and  perhaps 
many  neuralgias  and  persistent  pains  after  injuries  are  due  to  the  formation  of 
such  little  neuromata. 

The  so-called  multiple  neuromata  or  neuro-fibromata  are  of  special  pathologi- 
cal interest.  They  may  be  found  in  enormous  numbers  (many  hundreds)  on 
almost  all  the  peripheral  nerves,  on  the  sympathetic  plexuses  in  the  abdominal 
cavity,  and  on  the  cranial  nerves  (vagus,  etc.).  The  smallest  of  these  tumors 
may  be  as  large  as  a  millet^seed,  the  largest  may  grow  to  the  size  of  a  pigeon's 
egg  or  the  thumib.  The  nerves  are  changed  by  them  into  thick  cords  covered 
with  irregular  enlargements  which  can  be  felt  everywhere  under  the  skin  during 
life  (on  the  nerves  of  the  arm,  the  crural,  the  intercostal  nerves,  etc.).  This 
remarkable  condition  can  naturally  be  explained  only  by  a  congenital  abnormal 
predisposition  of  the  nervous  system  to  tumor  formation,  a  theory  which  is  sup- 
ported by  a  few  observed  cases  of  the  hereditary  occurrence  of  such  multiple 
neuromata.  The  name  "neuroma,"  however,  is  not  correctly  chosen.  It  is  rather 
a  fibroma  (a  tumor  of  connective  tissue),  through  which  the  nerve-fibers  usually 


XEW   GRO^YTHS    IX   THE   PERIPHERAL   XERVES  89T 

j)ass  in  good  condition  ("  neuro-fibroma  ").  Hence  it  happens,  as  we  have  seen 
■ourselves  in  one  case,  that,  in  spite  of  an  extensive  formation  of  neuro-fibromata, 
there  are  no  nervous  symptoms  at  all,  no  pain,  no  anaesthesia,  no  paralysis;  but 
-other  cases  have  also  been  reported  in  which  the  tumors  caused  manifest  and  even 
severe  symptoms. 

Of  other  new  growths  on  the  nerves  we  may  mention  sarcoma.  This  also  is 
■often  multiple,  and  then  it  may  lead  to  very  complicated  types  of  disease.  The 
.so-called  tubercula  dolorosa  deserve  special  mention.  By  this  term  we  mean 
little  nodules  which  may  be  felt  beneath  the  skin,  usually  readily  movable  and 
very  sensitive  to  pressure.  They  are  not  very  rare,  and  are  usually  associated 
with  drawing  pains,  which  are  rarely  decidedly  neuralgic  and  are  not  very  strictly 
localized.  They  are  situated  in  the  extremities,  especially  in  the  arms,  and  in 
the  back,  the  neck,  etc.  It  is  worthy  of  note  that  the  symptoms  are  only  at  times 
very  prominent,  and  then  they  disappear  again,  and  that  with  this  disappearance 
is  certainly  sometimes  associated  a  spontaneous  disappearance  of  the  nodule. 
The  anatomical  nature  of  the  tubercula  dolorosa  is  not  always  to  be  established 
with  certainty.  Manj'  of  them  are  true  neuromata,  but  others  belong  to  other 
iinds  of  new  growths. 

The  only  successful  treatment  of  neuromata  is  extiriDation,  which  is  to  be 
undertaken  only  when  the  symptoms  are  very  severe.  If  extirpation  be  not 
practicable,  or  if  we  have  to  do  with  multiple  neuromata,  the  patient's  trouble 
can  be  alleviated  by  symptomatic  means,  narcotics,  and  electricity.  If  we  can 
compress  the  nerve  above  the  neuroma,  we  can  often  cause  by  this  means  a  tem- 
porary cessation  of  the  pain. 
57 


898  DISEASES    OF   THE   NERVOUS    SYSTEM 


II.— VASO-MOTOR   AND   TROPHIC    NEUROSES 


CHAPTER   I 


GENERAL    PRELIMINARY    REMARKS 

{Erythromelalgia.     Acute  Angioneurotic  (Edema.     Myx(x,dema.     Acromegaly.     Hydrops  Artic2iloru7n- 
Intermittens.    Injuries  of  the  Cervical  Sympathetic) 

General  Consideration  of  Vaso-motor  Disturbances. — Physiology,  as  is  well 
known,  distinguishes  two  varieties  of  vaso-motor  nerves — the  vaso-constrictors 
and  the  vaso-dilators ;  but  since  experiments  have  detected  the  latter  variety  in 
only  a  few  places — for  example,  in  the  chorda  tympani,  the  nervi  erigentes,  and 
the  sciatic — they  have  not  acquired  a  very  great  significance  in  human  pathology. 
We  are  at  present  much  more  disposed  to  refer  every  abnormal  constriction  of 
the  vessels  to  an  excitation,  and  every  abnormal  dilatation  of  the  vessels  to 
a  paralysis  of  the  vaso-constrictor  nerves,  although  perhaps  pathological  con- 
ditions of  excitation  of  the  vaso-dilators  may  not  be  at  all  rare.  In  regard  to 
the  precise  anatomical  course  of  the  vaso-motor  nerves,  we  must  first  state 
that  vaso-motor  excitations  may  certainly  proceed  from  the  cerebrum,  as  is  shown 
by  the  well-known  symptoms  of  blushing  and  pallor  from  mental  emotions.  In 
experiments  on  dogs,  Eulenburg  and  Landois  have  succeeded  in  producing  a 
fall  of  temperature  on  the  opposite  side  by  irritating  certain  portions  of  the 
cortex  in  the  immediate  vicinity  of  the  motor  centers,  and  by  extirpation  of  the 
same  parts  they  have  produced  a  rise  in  temperature.  Furthermore,  we  know 
with  certainty  that  there  is  an  important  vaso-motor  center  in  the  medulla  oblon- 
gata (in  the  region  of  the  upper  olivary  body  in  rabbits),  the  excitation  of  which,, 
directly  or  reflexly,  is  followed  by  an  almost  universal  vascular  constriction,  and 
its  destruction  by  an  almost  universal  vascular  dilatation.  We  must  probably 
seek  the  further  course  of  the  vaso-motor  nerves  very  largely  (or  exclusively?)  in 
the  lateral  columns,  from  which  they  pass  out  chiefly  by  the  anterior  roots.  It 
is  not  known  with  certainty  whether  there  is  any  decussation  of  the  vaso-motor 
fibers,  or,  if  there  is,  where  it  occurs.  The  larger  part  of  the  vaso-motor  nerves 
collect,  at  any  rate,  in  the  principal  trunks  of  the  sympathetic,  from  which,  as  is 
well  known,  the  separate  plexuses  that  surround  the  vessels  arise.  It  is  not  im- 
probable, however,  that  there  is  also  in  part  a  direct  passage  of  vaso-motor  fibers 
from  the  cord  into  the  peripheral  nerves.  In  conclusion,  we  must  mention  that, 
according  to  Goltz's  experiments,  there  are  reflex  vaso-motor  centers  in  the  cord 
for  the  different  parts  of  the  body. 

The  clinical  vaso-motor  symptoms  are  chiefly  to  be  observed  in  the  external 
skin.    We  distinguish  them  as  follows : 

1.  Symptoms  of  Vaso-motor  Paralysis. — We  conclude  that  there  is  a  paraly- 
sis of  the  vaso-motors  if  there  is  an  abnormal  redness  of  the  skin.  Such  a  red- 
ness is  almost  always  associated  with  an  objective  and  often  a  subjective  feeling 
of  an  increase  of  temperature.  Such  conditions  are  observed  either  in  connection 
with  other  nervous  symptoms — as  in  fresh  spinal  or  cerebral  paralyses,  and  also 
very  often  in  certain  functional  neuroses,  such  as  hysteria  and  neurasthenia — or 
in  the  form  of  independent  affections — the  pure  vaso-motor  neuroses,  injuries  of 
the  cervical  sympathetic,  etc.     Of  course  in  these  eases  it  is  usually  hard  to  de- 


GENERAL   PRELIMINAEY   EEMAEKS  899 

cide  whether  there  is  really  a  vaso-motor  paralysis  or  irritation  of  the  vaso-dila- 
tors.  There  are  cases  in  ^Yhieh  thfi  only  symptoms  are  a  persistent  or  paroysmal 
diffuse  redness  of  the  skin,  especially  of  the  head,  associated  with  a  great  feeling 
of  heat,  with  palpitation  of  the  heart,  strong  pulsation  of  the  arteries,  anxiety, 
ringing  in  the  ears,  and  sweating. 

2.  Symptoms  of  Vaso-motor  Spasm,. — Spasm  of  the  small  vessels  becomes 
apparent  by  a  striking  pallor  and  coolness  of  the  skin.  There  is  often,  with  this, 
a  decided  feeling  of  formication  and  stiffness  in  the  affected  parts,  which  may 
even  increase  to  an  actual  feeling  of  pain.  Such  vaso-motor  spasms  affect  the 
hands  especially,  and  form  a  chronic  trouble  that  is  not  very  rare.  They  are 
usually  seen  in  people  who  are  generally  nervous  and  irritable,  and  sometimes 
also  in  washerwomen.  A  vascular  spasm  is  sometimes  seen  in  the  extremities  as 
one  symptom  of  complicated  paroxysms,  such  as  nervous  angina  pectoris  (q.  v.), 
especially  at  the  beginning  of  the  paroxysm.  A  persistent  spasm  of  the  small 
arteries  may  give  rise  to  considerable  subsequent  trophic  disturbance.  At  least, 
the  rare  cases  of  so-called  "  spontaneous  symmetrical  gangrene  "  (q.  v.),  and  also 
certain  forms  of  scleroderma  and  some  similar  affections,  are  referred  by  many 
observers  to  a  primary  spasm  of  the  vessels. 

General  Consideration  of  Trophic  Disturbances. — We  have  much  less  infor- 
mation concerning  the  trophic  nerves  than  we  have  concerning  the  vaso-motor. 
As  is  well  known,  the  controversy  is  still  going  on  as  to  whether  we  have  any 
right  to  assume  the  existence  of  special  trophic  nerves.  The  facts  of  clinical  neu- 
rological observation  frequently  seem  to  compel  the  hypothesis  of  special  trophic 
functions,  although,  of  course,  it  is  usually  very  hard  to  determine  this  point, 
because  we  can  seldom  wholly  exclude  the  indirect  influence  of  sensory  and  cir- 
culatory influences  (vide  supra,  anjesthesia  of  the  trigeminus). 

Among  those  symptoms  which  chiefly  support  the  theory  of  the  existence  of 
specific  trophic  nervous  influences,  we  have  already  learned  to  recognize  the  de- 
generative atrophy  of  the  muscles  and  nerves.  Various  other  sorts  of  trophic 
disturbances  in  the  skin  and  the  deeper  parts  (bones,  joints)  are  seen  in  nervous 
diseases.  Especially  after  wounds  of  the  peripheral  nerves  we  often  notice  a 
peculiar  shining,  smooth,  atrophic  condition  of  the  skin — the  "  glossy  skin " 
or  "  glossy  fingers  "  of  English  authors.  In  other  cases  anomalies  in  the  pig- 
mentation of  the  skin  seem  to  be  connected  with  the  nervous  disturbances ;  thus 
spots  deprived  of  pigment  (vitiligo)  often  develop  as  a  result  of  severe  neural- 
gias. We  must  also  bring  to  mind  here  the  appearance  of  changes  in  pigmenta- 
tion from  nervous  causes,  especially  the  astiology  of  Addison's  disease  (q.  v.) 
and  the  occurrence  of  the  so-called  nervous  nsevi.  Among  the  severe  neuro- 
trophic disturbances  of  the  skin  many  observers,  especially  Charcot,  class  the 
appearance  of  acute  bed-sores  in  many  spinal  and  cerebral  paralyses,  but  we  have 
never  been  able  to  convince  ourselves  of  the  occurrence  of  a  "  neurotrophic  decubi- 
tus," and  we  believe  that  every  bed-sore  is  due  in  the  first  instance  to  external 
injuries  (jjressure  on  the  soft  parts,  uncleanliness,  and  the  entrance  of  the  bac- 
teria of  inflammation). 

Besides  the  trophic  disturbances  in  the  skin,  we  often  see  analogous  changes 
in  the  nails  and  hair  in  nervous  patients.  The  nails  become  brittle  and  cracked, 
assume  a  darker  color,  and  often  show  abnormal  conditions  of  growth,  abnormal 
curving,  striation,  thickening  (onychogryphosis),  etc.  We  also  see  at  times  a  loss 
of  the  nails.  A  loss  of  hair  is  seen  in  frontal  neuralgia,  in  certain  forms  of  head- 
ache, and  not  infrequently  as  an  apparently  independent  nervous  disease  (alo- 
pecia). A  very  rapid  whitening  of  the  hair  after  mental  excitement  is  well  known 
to  have  occurred  in  some  cases. 

Various  disturbances  of  growth  and  nutrition  also  occur  in  the  bones  and 
joints,  and  are  to  be  regarded  as  trophic  disturbances. 


900  DISEASES    OF   THE   NERVOUS    SYSTEM 

The  implication  of  the  bones  in  atrophic  processes  is  seen  chiefly  in  pro- 
gressive unilateral  facial  atrophy  (vide  infra).  A  retarded  growth  of  bone  in  the 
affected  extremities  is  also  a  symptom  frequently  seen  in  the  spinal  and  even  in 
the  cerebral  paralyses  that  develop  in  childhood.  It  is  uncertain,  however,  how 
far  this  is  due  to  the  loss  of  direct  trophic  influences  or  to  the  indirect  influence 
of  the  loss  of  motor  functions.  In  conclusion,  we  not  infrequently  see  very  strik- 
ing and  apparently  trophic  disturbances  in  the  bones  and  joints  in  tabes  and 
syringomyelia  (q.  v.). 

Erythromelalgia. — We  should  apparently  class  here  this  peculiar  disease, 
which  is  seen  most  frequently  in  the  feet,  although  it  also  occurs  in  the  hands. 
Men  seem  to  suffer  from  it  more  frequently  than  women.  The  symptoms  are 
severe  pain,  especially  in  the  toes  and  fingers,  but  sometimes  in  the  ball  of  the 
foot,  the  heel,  etc.,  and  also  swelling,  redness,  and  marked  pulsation  of  the  ves- 
sels. In  some  cases  the  affected  parts  assume  a  very  dark-red  or  bluish-red 
color.  We  not  infrequently  see  excessive  sweating.  [In  some  cases  the  condi- 
tion seems  due  to  neuritis;  in  others  Weir  Mitchell,  who  first  described  the  dis- 
ease, has  found  arterio-sclerosis  in  the  smaller  vessels  with  no  neuritis. — K.] 

The  condition  described  either  comes  on  in  paroxysms  or  is  persistent,  al- 
though varying  in  severity.  On  standing  or  walking,  or  when  warm,  the  pain 
usually  increases.  Other  nervous  symptoms,  such  as  headache,  vertigo,  weakness, 
etc.,  are  sometimes  associated  with  erythromelalgia.  The  course  is  almost  always 
very  tedious,  and  the  prognosis  therefore  doubtful.  The  treatment  consists  in 
the  use  of  electricity,  cool  baths,  iodide  of  potassium,  antipyrine,  and  similar 
remedies.  [Mitchell  suggests  stretching  or  resection  of  the  nerves. — K.]  Com- 
pare the  section  on  acroparsesthesia  (page  822),  which  name  has  sometimes  been 
given  to  apparently  allied  conditions. 

Symmetrical  Spontaneous  Gangrene.  Raynaud's  Disease. — This  disease, 
whose  nature  is  still  quite  obscure,  begins  with  pallor  and  coldness  of  the  fingers 
("regional  ischsemia"),  associated  at  first  with  sensations  of  crawling  and 
numbness,  and  later  with  severe  pain.  After  a  short  time  the  pallor  changes 
to  a  bluish-red  color  ("  regional  cyanosis  "),  especially  in  the  terminal  phalanges, 
which  sometimes  progresses  to  the  formation  of  gangrenous  spots  and  vesicles.  In 
severe  cases  a  portion  of  the  terminal  phalanges  is  completely  destroyed  and 
thrown  off  by  dry  gangrene.  The  whole  process  may  last  for  months.  It  runs  its 
course  without  fever,  but  it  is  sometimes  associated  with  quite  severe  general 
nervous  disturbances.  In  rare  cases  spontaneous  symmetrical  gangrene  has  been 
observed  in  other  parts  of  the  body,  for  example,  in  the  thighs,  the  buttocks,  the 
ears,  the  nose,  etc.  Several  attacks  of  the  disease  may  sometimes  follow  one 
another,  so  that  the  whole  duration  of  the  trouble  may  be  for  years. 

In  regard  to  diagnosis,  we  must  first  be  convinced  that  the  disease  comes 
on  spontaneously.  Extensive  areas  of  gangrene  of  the  skin  have  repeatedly  been 
observed  in  hysteria,  produced  artificially  by  the  patient  by  means  of  caustics 
(caustic  potash,  etc.).  We  must  also  think  of  diabetic  gangrene,  severe  arterio- 
sclerosis, syringomyelia,  exophthalmic  goitre,  etc. 

The  treatment  can  be  merely  symptomatic.  Wet  applications,  baths,  cautious 
galvanization,  and  narcotics  (morphine,  chloral)  when  the  pain  is  severe,  are 
most  employed. 

Acute  Angioneurotic  (Edema  {(Edema  cutis  circumscriptum). — This  name 
has  been  given  by  Quincke,  Striibing,  and  others  to  a  disease  characterized  by 
the  sudden  onset  of  oedematous  swellings  in  various  parts  of  the  body.  These 
swellings  usually  disappear  in  a  few  hours,  but  they  are  very  often  repeated. 
Dangerous  symptoms  may  arise  if  the  OBdema  affect  the  pharynx  or  the  entrance 
to  the  larynx.  The  patient's  health  otherwise  is  sometimes  perfectly  good,  but  in 
other  cases  it  is  more  or  less  affected.    Gastric  disturbances  especially  (attacks  of 


GEl^EEAL  PKELIMINAEY   EEMAEKS  901 

vomiting  and  gastralgia)  have  been  observed  at  the  same  time  in  such  patients. 
Acute  angioneurotic  oedema  is  manifestly  closely  allied  to  urticaria  and  ery- 
thema exudativum. 

Myxcedema. — We  may  here  mention  myxoedema  (cachexie  pachydermique  of 
Charcot),  which  was  first  described  in  England  by  William  Gull  and  Ord.  The 
disease  has  taken  its  name  from  a  peculiar  thickening  and  swelling  of  the  skin, 
which  is  most  marked  in  the  face,  but  which  is  sometimes  seen  in  the  extrem- 
ities, the  trunk,  the  tongue,  and  even  in  the  internal  organs.  This  swelling  is  not 
oedema,  but  it  is  due  to  the  development  of  a  sort  of  myxomatous  new  growth, 
rich  in  mucine,  in  the  connective  tissue.  Other  trophic  disturbances  usually  coex- 
ist :  atrophy  of  the  teeth  and  nails,  [spade-like  hands,  coarseness  and]  loss  of  hair, 
failure  in  the  sweat  secretion  and  consequent  dryness  of  the  skin,  etc.  Besides 
these  there  gradually  develops  a  general  physical  and  mental  weakness,  which  may 
increase  to  great  hebetude  or  even  to  complete  dementia.  Disturbances  of  the 
sensory  functions  may  also  occur.  It  is  a  fact  of  especial  interest  that  we  find 
quite  commonly  a  diminution  and  even  a  complete  atrophy  of  the  thyroid  gland. 
It  is  not  improbable  that  all  the  symptoms  of  the  disease  may  arise  from  the  fail- 
ure of  function  of  the  thyroid  gland.  This  hypothesis  is  confirmed  by  the  re- 
peated experiments  of  Kocher  and  others,  that  after  complete  extirpation  of  the 
thyroid  in  man  almost  the  same  symptoms  ensue  as  in  myxoedema  (cachexia 
strumipriva).  From  this  we  must  suppose  that  certain  injurious  substances  accu- 
mulate in  the  body  which  are  ordinarily  rendered  innocuous  by  the  thyroid  gland. 

This  theory  has  been  materially  supported  by  recent  extremely  interesting 
experience  in  the  treatment  of  myxoedema.  The  physiologist  Schiff  made  the 
remarkable  observation  that  the  symptoms  of  cachexia  strumipriva  did  not  appear 
in  animals  if  the  thyroid  gland  of  another  animal  were  transplanted  into  the 
abdominal  cavity.  Horsley,  Bircher,  and  others  hereupon  made  the  first  experi- 
ments in  the  treatment  of  myxoedema  in  man  with  extract  of  the  thyroid  gland 
(from  sheep,  calves,  etc.).  At  first  subcutaneous  injections  of  thyroid  extract 
were  usually  employed,  but  it  was  found  that  the  internal  administration  of  the 
substance  of  the  gland  or  an  extract  thereof  had  a  far  more  favorable  influence. 
There  are  already  very  many  positive  observations  which  show  that  all  the 
symptoms  of  myxoedema  in  man  may  be  made  to  disappear  completely  in  the 
course  of  a  few  months  by  the  continued  internal  administration  of  the  thyroid 
gland.  The  most  convenient  and  certain  form  of  administration  is  in  tablets. 
Of  course  we  must  always  be  prepared  for  relapses.  [Myxoedema  is  sometimes 
associated  with  exophthalmic  goitre  and  rarely  with  acromegaly. — K.] 

[The  condition  known  as  cretinism  is  also  dependent  upon  loss  of  function  of 
the  thyroid  gland.  Endemic  cretinism  is  common  in  countries  where  endemic 
goitre  prevails,  especially  in  the  central  Alps,  and  also,  but  less  frequently,  in  the 
Carpathians,  the  Pyrenees,  the  mountain  districts  of  Central  and  South  America, 
and  the  Himalayas.  Sporadic  cretinism  may  occur  in  all  parts  of  the  world,  and 
Osier  has  collected  sixty  cases  in  America.  The  affection  comes  on  in  infancy, 
and  in  its  severer  forms  the  condition  is  unmistakable.  The  victims  are  short  and 
squat  of  figure,  with  prominent  belly,  "  blubber  lips,  retrousse  nose,  sunken  at  the 
root,  wide-open  mouth,  lolling  tongue,  small  eyes,  half-closed,  with  swollen  lids, 
stolid,  expressionless  face,  and  muddy,  dry  skin."  They  are  idiotic  and  often  una- 
ble to  talk,  walk,  or  stand  alone.  In  the  milder  cases  the  lax,  waxy  skin,  the  prom- 
inent abdomen,  and  the  failure  of  development  may  suggest  the  diagnosis.  Mar- 
velous results  have  been  attained  in  some  of  these  apparently  hopeless  cases  by  the 
early  and  persistent  use  of  the  thyroid  gland.  The  striking  cretinous  aspect  has 
disappeared  and  physical  growth  and  mental  development  have  followed. 

Closely  allied  to  these  conditions  is  the  myxoedematous  infantilism  described 
by  French  aiathors.     The  subject  preserves  the  physical  and  mental  eharacteris- 


902  DISEASES    OF   THE   NEEVOUS    SYSTEM 

tics  of  a  child  of  ten  up  to  the  age  of  thirty  or  over.  The  sexual  organs  are  unde- 
veloped, and  the  secondary  sexual  characteristics  fail  to  appear.  A  careful  exami- 
nation will  often  reveal  slight  indications  of  myxoedema — the  diminution  in  size 
or  absence  of  the  thyroid,  the  thick  lips,  thick  dry  skin,  coarse  hair,  etc. — thus 
distinguishing  it  from  the  anangioplasic  form  of  infantilism  due  to  defective 
development  of  the  arterial  system.  In  this  condition  the  administration  of 
thyroid  gland  produces  equally  striking  results. 

Adiposis  Dolorosa. — Under  this  name  Dercum  has  described  a  peculiar  con- 
dition, occurring  in  women  between  forty  and  sixty  years  of  age  with  a  neuro- 
IDathic  predisposition.  Most  of  the  victims  were  addicted  to  alcohol.  The  trouble 
begins  with  a  gradual  enlargement  of  various  portions  of  the  body,  associated 
with  pain,  parsesthesia,  and  some  tenderness.  These  enlargements  may  increase 
so  as  to  form  huge  pendulous  masses.  Muscular  weakness  is  also  present,  and 
locomotion  finally  becomes  very  difiicult  if  not  impossible.  Mental  weakness 
sometimes  supervenes.  The  masses  have  been  found  to  consist  of  fat  and  con- 
nective tissue.  Disease  of  the  thyroid  has  been  found  on  autopsy,  but  the  true 
nature  of  the  trouble  is  still  obscure.  The  coiirse  is  slow,  but  progressive.  Treat- 
ment has  thus  far  been  of  little  avail.  Every  efPort  should  be  made  to  improve 
the  nutrition,  and  thyroid  gland  should  also  be  given. 

Scleroderma. — Although  ordinarily  classed  among  the  skin  diseases,  sclero- 
denna  merits  a  brief  mention  here,  as  it  is  generally  considered  to  be  a  vaso-motor 
or  trophic  neurosis.  It  occurs  chiefly  in  neuropathic  women,  and  it  may  follow 
some  infectious  disease.  It  sometimes  occurs  with  syringomyelia,  Raynaud's 
disease,  or  other  forms  of  nervous  disease.  It  may  be  diffuse  and  symmetrical  or 
circumscribed  (morphoea) .  It  begins  gradually,  often  after  exposure  to  cold, 
with  a  feeling  of  stiffness,  most  marked  in  the  neck,  shoulders,  arms,  face,  or 
scalp.  The  skin  gradually  becomes  thickened  and  hard,  very  white  or  mottled, 
and  movements  of  the  affected  parts  become  slow  and  stiff,  and  finally  are  com- 
pletely lost  on  account  of  the  rigidity  of  the  skin.  Vaso-motor  symptoms  are 
rare,  but  pigmentation  is  occasionally  seen.  When  the  face  is  involved  a  charac- 
teristic, expressionless  "  mask  "  is  produced.  If  the  chest  be  affected,  respiration 
may  be  considerably  impaired  on  account  of  the  immobility.  Later  on  the  skin 
and  deeper  parts  may  atrophy,  although  the  hardness  and  stiffness  may  remain. 
Recovery  may  occur,  but  the  disease  is  apt  to  be  permanent,  the  patient  succumb- 
ing to  some  intercurrent  disease.  The  circumscribed  form  may  occur  in  patches, 
bands,  or  streaks,  and  may  be  confined  to  the  distribution  of  one  or  more  nerves. 
The  "white  spots  are  bordered  by  a  pinkish  zone  of  dilated  vessels.  Anatomically 
the  disease  is  characterized  by  changes  in  the  blood-vessels  and  proliferation  of 
connective  tissue  in  the  skin.  The  general  condition  should  be  strengthened  by 
nutritious  diet,  good  hygiene,  salt  baths,  arsenic,  and  cod-liver  oil.  Galvanism  is 
of  some  benefit.    Thyroid  extract  may  also  be  tried. — ^K.] 

Acromegaly. — A  "  trophic  disturbance  "  chiefly  of  the  bones,  but  also  involv- 
ing the  soft  parts,  forms  the  basis  of  that  peculiar  and  rare  disease  recently 
termed  acromegaly  (P.  Marie,  Erb,  etc.).  The  affection  develops  slowly  in 
women  and  men,  usually  in  youth  or  middle  age.  In  women  cessation  of  men- 
struation almost  invariably  precedes  the  onset  of  the  disease.  Besides  the  gen- 
eral symptoms  of  dullness,  fatigue,  and  quite  severe  neuralgic  or  drawing,  deep- 
seated  pains  in  the  head  and  the  extremities,  there  gradually  develops  a  striking 
increase  in  the  size  of  the  hands  and  feet,  and  thickness  and  plumpness  of  the 
face,  due  chiefly  to  enlargement  of  the  nose,  chin,  and  lips,  which  become  puffed 
out  to  a  considerable  size.  The  increase  in  the  lower  part  of  the  face  (especially 
the  lower  jaw)  in  contrast  to  the  nonnal  cranium  gives  a  very  characteristic 
aspect  to  acromegaly.  The  hyperplasia  of  the  lower  jaw  may  reach  so  high  a 
degree   that  the   individual  teeth   are   separated.     In   the   hands   and   feet   the 


GENERAL   PEELIMINARY   REMARKS 


903 


fingers  and  toes,  and  especially  their  terminal  phalanges,  become  thicker  and 
wider,  so  that  we  may  speak  of  actual  "  paws."  The  hyperplasia  not  only  affects 
the  bones,  but  it  makes  the  skin  thick  and  wrinkled.  A  manifest  kyphosis  of  the 
spine  usually  develops.  Other 
noteworthy  symptoms  some- 
times occur.  Thus  we  some- 
times see  marked  glycosuria, 
an  increased  secretion  of 
sweat,  and  particularly  dis- 
turbances of  vision,  either 
hemianopsia  or  amblyopia 
from  atrophy  of  the  optic 
nerves.  These  disturbances 
of  vision  are  connected  with 
the  noteworthy  fact  that  in 
most  cases  of  acromegaly  a 
tumor  of  the  hypophysis  cere- 
bri develops,  which  presses  di- 
rectly on  the  nerves  or  the 
optic  tract.  A  patient  under 
our  observation  (Fig.  113)  died 
with  symptoms  of  a  tumor  at 
the  base  of  the  brain,  and  the 
autopsy  showed  a  sarcoma- 
tous tumor  of  the  hypophysis 
which  had  grown  through  the 
adjacent  bony  parts. 

The  diagnosis  of  acromeg- 
aly is  not  difficult.  We  must 
merely  guard  against  confus- 
ing it  with  other  conditions 
also  leading  to  thickening 
of  the  bones  (partial  giant 
growth,  arthritis  and  osteitis 
deformans,  diffuse  and  local- 
ized hyperostoses,  etc.).  The 
so-called  hypertrophic  osteo- 
arthropathy is  also  to  be  dis- 
tinguished from  acromegaly. 
This  affection  is  seen  especial- 
ly in  patients  with  chronic 
bronchitis,  bronchiectasis, 

■chronic  tuberculosis,  etc., 
and  it  also  leads  to  a  paw- 
like thickening  of  the  fingers, 
hut   the  changes   in  the   lower 

jaw  so  very  characteristic  of  acromegaly  are  absent,  and  also  the  other  nervous 
symptoms,  especially  those  of  tumor  of  the  hypophysis. 

The  treatment  of  acromegaly  is,  unfortunately,  almost  wholly  unpromising. 
The  administration  of  thyroid  tablets  and  also  of  tablets  of  the  hypophysis  has 
heen  tried  without  much  benefit. 

[Gigantism.- — The  "  giants  "  who  exhibit  themselves  in  circuses  and  museums 
are  victims  of  a  disease  closely  akin  to  acromegaly  if  not  identical  with  it.  A 
study  of  giant  skeletons  has  shown  a  marked  enlargement  of  the  sella  turcica, 


Fig.  113.— Acromegaly  in  a  patient  thirty  years  old. 
(Personal  observation.) 


904  DISEASES    OF   THE   I^ERVOUS    SYSTEM 

the  site  of  the  hypophysis,  and  an  enlargement  of  the  hypophysis  has  been 
found  at  autopsies.  The  giants  themselves  often  have  enormous  hands  and  feet,, 
they  are  feeble  and  short-lived.  In  some  instances  kyphosis  has  developed  later 
in  life,  with  more  pronounced  symptoms  of  acromegaly. 

Hyperostosis  Cranii. — This  is  an  enlargement  of  the  cranium,  beginning  in 
early  life,  involving  the  anterior  part  of  the  skull  rather  more  than  the  posterior,, 
and  leading  to  enormous  thickening  of  the  bones,  from  one  to  three  or  more  centi- 
metres (one  half  to  one  and  a  half  inch).  Other  bones  are  sometimes  affected- 
The  symptoms  sometimes  resemble  those  of  cerebral  tumor,  the  cranial  nerves 
being  affected  by  the  bony  growth.  Headache  is  common  and  optic  neuritis  occa- 
sionally occurs.  Marked  exophthalmus  is  sometimes  produced  by  the  growth  of 
the  orbital  bones  which  fills  up  the  orbital  cavities.  The  trouble  is  supposed  to  be 
of  trophic  origin,  although  the  changes  in  the  bones  resemble  those  of  inflamma- 
tion. The  involvement  of  the  cranial  vault  and  the  absence  of  kyphosis  and 
changes  in  the  extremities  render  it  easily  distinguishable  from  acromegaly. 
Treatment  has  thus  far  proved  unavailing. — K.] 

Hydrops  Articulorum  Intermittens. — This  is  the  name  of  a  very  rare  disease,, 
in  which  large  swellings,  usually  of  the  knee-joint,  but  sometimes  of  the  other 
large  joints,  develop  at  perfectly  regular  intervals  of  one  to  four  weeks.  These- 
swellings  of  the  joints  run  their  course  without  fever,  and  usually  without  any 
great  pain,  and  disappear  again  in  a  few  days.  Such  attacks  may  be  repeated  at. 
intervals  of  different  lengths,  during  many  years.  Their  nervous  character  is- 
attested  especially  by  the  rapid  onset  and  disappearance  of  the  affection,  and  also- 
by  the  combination  of  it  with  other  nervous  disturbances,  such  as  angina  pec- 
toris, exophthalmic  goitre,  vaso-motor  symptoms,  hysterical  symptoms,  etc., 
which  combination  has  often  been  observed.  In  regard  to  treatment,  salicylic 
acid,  quinine,  Eowler's  solution,  and  subcutaneous  injections  of  ergotine  have 
been  tried,  but  the  trouble  is  usually  very  obstinate. 

Disturbances  of  Secretion. — In  addition  to  the  vaso-motor  and  trophic  dis- 
turbances we  must  consider  the  disturbances  of  secretion.  These  are  not  infre- 
quent. We  have  already  learned  to  recognize  anomalies  in  the  secretion  of  saliva', 
in  facial  paralysis,  and  of  the  lachrymal  secretion  in  trigeminal  neuralgia. 
Analogous  symptoms  are  occasionally  noticed  in  other  nervous  diseases.  Dis- 
turbances of  the  sweat  secretion  are  the  easiest  to  confirm.  Our  understanding  of 
them  comes  substantially  from  the  discovery  of  the  "  sweat  nerves,"  arising- 
mainly  from  the  sympathetic,  which  was  made  by  Luchsinger.  In  nervous- 
patients  we  have  seen  quite  frequently,  on  the  one  hand,  an  abnormal  increase  of 
the  sweat  secretion  (Jiyperidrosis,  ephidrosis) ,  and,  on  the  other,  a  diminution 
or  a  complete  disappearance  of  it.  The  former  is  seen  on  the  paralyzed  side  in 
many  hemiplegias  and  in  spinal  paralyses,  the  latter  in  tabes  dorsalis.  Anomalies^ 
of  the  sweat  secretion  are  quite  frequent,  and  are  usually  combined  with  vaso- 
motor disturbances  in  certain  general  neuroses,  such  as  hysteria  and  neuras- 
thenia. In  a  few  rare  cases  a  genuine  Jicematidrosis  (bloody  sweat)  has  been 
confirmed.  [Colored  sweating  (chromatidrosis)  has  been  reported  in  some  very 
rare  cases  of  hysteria. — K.]  The  condition  known  as  unilateral  hyperidrosis 
(unilateral  sweating)  is  also  especially  interesting.  In  this  there  is  an  abnormal 
secretion  of  sweat,  chiefly  in  one  half  of  the  face,  more  rarely  in  one  arm  or  over 
the  whole  of  one  side.  The  affection  has  usually  been  observed  in  connection  with 
tabes,  syringomyelia,  hemicrania,  exophthalmic  goitre,  hysteria,  etc.,  and,  in  at 
least  a  number  of  cases,  it  seems  to  be  due  to  direct  lesions  of  the  sympathetic. 
On  the  other  hand,  we  have  repeatedly  seen  persons,  who  were  otherwise  perfectly 
healthy,  in  whom  the  secretion  of  sweat,  coming  on  under  normal  conditions  from 
heat  or  physical  exertion,  remained  limited  to  one  half  of  the  body,  especially^ 
the  face. 


MIGEAINrE  905 

Injuries  and  Diseases  of  the  Cervical  Sympathetic. — In  conclusion,  we  would 
briefly  mention  here  the  symptoms  which  have  been  observed  in  direct  injuries 
of  the  cervical  sympathetic,  trauma,  pressure  of  neighboring  tumors,  etc.  If  we 
have  to  do  with  a  paralysis  of  the  sympathetic,  we  see  almost  constantly  on  the 
affected  side  a  contraction  of  the  pupil  from  paralysis  of  the  dilator  pupillse  sup- 
plied from  the  sympathetic,  in  many  cases  associated  with  a  slow  reaction  to 
light.  We  also  frequently  see  a  narrowing  of  the  opening  of  the  lids  from  paraly- 
sis of  Miiller's  muscle,  and  in  old  cases  a  retraction  of  the  bulbus  oculi,  flatten- 
ing of  the  affected  half  of  the  face,  and  occasionally  increased  redness  and 
warmth  in  the  ear  and  cheeks  from  vaso-motor  disturbance.  In  a  few  cases 
we  see  an  increased  sweat  secretion.  We  may  add  that,  according  to  Mobius,  the 
normal  reflex  dilatation  of  the  pupil,  from  a  painful  irritation  of  the  skin  of 
the  face,  is  absent  in  paralysis  of  the  sympathetic.  The  opposite  symptoms  are 
found  in  conditions  of  irritation  of  the  sympathetic.  The  occurrence  of  sympa- 
thetic symptoms  in  certain  injuries  of  the  brachial  plexus  has  already  been  men- 
tioned above  (page  870). 


CHAPTEE    II 

MIGRAINE 

{Hemicrania.     Megrim.     Sick  Headache) 

.ffitiology. — By  migraine  or  hemicrania  we  mean  a  peculiar  form  of  headache, 
coming  on  in  separate  attacks,  usually  unilateral,  and  associated  with  consider- 
able disturbance  of  the  general  condition  and  with  pronounced  nervous  gastric 
symptoms  (complete  loss  of  appetite,  nausea,  vomiting).  The  affection  occurs  in 
women  and  men,  somewhat  more  rarely  in  the  latter,  and  almost  always  begins  in 
youth,  generally  at  the  period  of  puberty,  although  typical  cases  of  migraine  have 
been  repeatedly  observed  in  school-children.  Quite  frequently,  but  not  always  by 
any  means,  the  disease  affects  persons  who  must  be  regarded  as  "  generally  nerv- 
ous," who  are  anaemic,  or  who  suffer  from  disturbances  of  menstruation.  Heredity 
often  plays  a  part,  since  hemicranija  is  both  hereditary  as  such,  and  often  appears 
in  families  which  have  suffered  from  other  nervous  diseases,  such  as  epilepsy, 
hysteria,  or  the  psychoses.  We  may  mention  as  exciting  causes,  which  may 
be  made  answerable  both  for  the  onset  of  the  disease  and  especially  for  the 
individual  attacks,  physical  and  mental  over-exertion,  great  mental  excitement, 
disturbances  of  digestion,  indulgence  in  alcohol,  etc.  [Eye-strain  {vide  supra) 
may  rarely  have  some  influence  in  causing  migraine  as  well  as  other  forms  of 
headache,  and  a  careful  search  for  any  errors  of  refraction  should  therefore  be 
made. — K.]  The  special  cause  of  the  disease,  however,  is  probably,  as  a  rule,  a 
congenital  predisposition. 

Many  writers  lay  great  stress  upon  certain  vaso-motor  symptoms  which  some- 
times accompany  migraine,  and  therefore  believe  that  the  disease  is  to  be  consid- 
ered in  the  main  an  affection  of  the  sympathetic ;  but  we  must  agree  with  Mobius 
that  this  assumption  is  very  improbable,  and  that  the  accompanying  sympathetic 
symptoms  are  probably  only  secondary  and  of  reflex  origin,  in  consequence  of  the 
pain,  or  are  merely  a  part  of  the  whole  attack  of  migraine.  We  are  still  utterly 
ignorant  of  the  special  nature  of  migraine — that  is,  of  the  kind  or  the  place  of  the 
change  which  forms  the  basis  of  the  clinical  symptoms.  The  conjecture  is  inter- 
esting, but  of  course  wholly  unconfirmed,  that  there  is  in  the  attacks  an  "  auto- 
intoxication "  of  the  body — that  is,  the  action  of  some  poison  developing  from 
time  to  time  in  the  body  itself;   but  we  do  not  know  upon  what  part  of  the 


^06  DISEASES    OF   THE   NERVOUS    SYSTEM 

nervous  system  this  poison  may  act;  we  can  merely  conjecture  that  the  place  of 
irritation,  upon  which  the  pain  and  other  migrainous  symptoms  depend,  is  in  the 
brain  itself  (in  the  cortex  or  deeper  parts).  This  conjecture  is  supported  espe- 
cially by  the  nature  of  many  of  the  symptoms  which  accompany  the  pain  of 
migraine — the  sensitiveness  of  the  sensory  organs,  the  slight  mental  change,  the 
scintillating  scotoma,  etc. 

Symptomatology. — Migraine  always  comes  on,  as  has  been  said,  in  separate 
attacks,  which  are  repeated  at  intervals  of  varying  lengths,  although  some  cases 
often  show  a  remarkably  great  regularity.  The  onset  of  the  attack  in  women 
often  has  some  relation  to  the  menses;  in  other  cases  it  is  due  to  one  of  the  ex- 
citing causes  mentioned  above. 

The  attack  of  migraine  usually  begins  with  certain  prodromal  symptoms, 
which  the  patient  soon  recognizes  as  sure  signs  of  his  approaching  suffering. 
These  prodromal  symptoms  consist  of  general  uneasiness,  discomfort,  pressure  in 
the  head,  vertigo,  at  times  tinnitus,  spots  before  the  eyes,  darkening  of  the  visual 
field,  chills,  malaise,  abnormal  yawning,  etc.  In  a  short  time  the  pain  begins.  It 
is  felt  most  either  in  the  anterior  frontal  region  or  in  the  temporal  or  parietal  re- 
gion ;  it  generally  shows  a  continuous  character,  not  intermittent  as  in  neuralgia, 
and  it  may  increase  to  a  very  great  intensity.  Usually  one  side  of  the  head  (the 
left  most  commonly)  is  the  chief  seat  of  the  pain,  particularly  the  forehead  and  the 
neighborhood  of  the  eyes ;  but  it  may  also  happen  that  the  pain  affects  the  right  and 
left  sides  alternately,  and  it  is  sometimes  not  limited  to  one  side,  but  embraces 
nearly  the  whole  head.  The  scalp  is  usually  hypersesthetic  on  the  affected  side,  and 
the  points  of  exit  of  the  nerves  may  be  sensitive  to  pressure,  but  firm  pressure  on 
the  head  (with  the  hands  or  by  tying  a  towel  tight  around  it)  sometimes  gives  relief. 

The  second  chief  symptom  in  migraine,  besides  the  headache,  is  the  com- 
plete loss  of  appetite  and  great  nausea.  Sometimes  vomiting  comes  on  only  at 
the  end  of  an  attack,  but  often  there  is  almost  uncontrollable  vomiting  through- 
out the  whole  attack.  The  patient  not  infrequently  notices  that  the  vomitus  has 
a  very  sour  taste,  and  we  have  ourselves  found  a  decided  hypersecretion  of  gastric 
juice  in  several  cases  of  migraine.  The  patients'  general  condition  is  almost 
always  very  much  disturbed.  They  feel  very  wretched  and  dull,  and  are  very 
sensitive  to  external  imj^ressions,  any  bright  light,  any  noise,  etc.  They  are  in- 
capable of  any  mental  exertion.  In  many  cases  remarkable  ocular  symptoms  oc- 
cur (ophthalmic  migraine)  :  slight  or  marked  ptosis  of  one  eyelid,  bright  flashes 
before  the  eyes,  scintillating  scotoma,  and  not  infrequently  pronounced  hemi- 
anopsia. These  symptoms  very  often  forebode  the  special  attack  of  pain.  Other 
severe  nervous  symptoms,  such  as  parsesthesia  in  the  hands  and  fingers,  tinnitus, 
disturbances  of  speech,  etc.,  have  occasionally  been  observed. 

The  vaso-motor  symptoms  accompanying  the  headache  may  occur  in  two 
different  forms.  From  them  raigraine  was  formerly  divided  into  two  sub- 
divisions— hemicrania  sympathico-tonica  or  spastica,  and  hemicrania  sympathi- 
co-paralytica  or  angio-paralytica.  In  hemicrania  spastica,  first  described  by  Du 
Bois-Reymond  from  observations  on  himself,  the  forehead  and  ear  on  the  affected 
side  are  pale,  the  skin  is  cool,  the  temporal  arteries  contracted,  the  pupil  is  often 
decidedly  dilated,  the  secretion  of  saliva  increased — in  short,  there  are  a  whole 
series  of  symptoms  present  which  all  agree  in  pointing  to  a  condition  of  irritation 
of  the  sympathetic  {vide  supra).  In  hemicrania  paralytica,  however,  which  was 
first  described  by  Mollendorff,  also  from  observations  on  himself,  the  face  is  red- 
dened on  the  affected  side,  it  feels  hot,  the  temporal  arteries  are  dilated  and 
pulsate  strongly,  there  is  sometimes  unilateral  sweating  of  the  face,  the  pupil  is 
contracted — all  symptoms,  therefore,  which  can  depend  only  on  a  paralysis  of 
the  sympathetic. 

As  has  already  been  said,  the  significance  of  all  these  symptoms  is  not  abso- 


MIGEAINE  907 

lutely  certain.  We  must  also  add  that  this  division  is  more  theoretical  than  real, 
and  that  the  cases  which  occur  in  practice  can  not  by  any  means  always  be 
inserted  into  one  or  the  other  typical  scheme  without  further  ceremony.  The 
vascular  symptoms  are  often  only  slight,  conditions  of  paralysis  and  of  irritation 
of  the  sympathetic  sometimes  seem  to  alternate  with  each  other  in  the  same 
attack,  and  we  may  even  frequently  meet  with  apparently  contradictory  symp- 
toms at  the  same  time,  such  as  pallor  joined  with  contraction  of  the  pupil.  The 
vascular  changes,  when  present,  are  almost  never  unilateral,  but  they  are  approx- 
imately alike  in  the  two  halves  of  the  face.  In  severe  attacks  the  whole  face 
usually  looks  pale  and  sunken,  but  the  initial  pallor  may  give  place  to  redness. 

The  duration  of  the  attacks  of  migraine  differs  very  much.  It  usually  lasts 
several  hours,  or  a  whole  day;  then  the  pain  gradually  disappears,  and  there  is 
often  considerable  vomiting  and  sometimes  a  profuse  discharge  of  urine  toward 
the  end  of  the  attack.  In  the  intervals  between  the  different  attacks  most  pa- 
tients are  perfectly  well  and  free  from  pain.  There  are  also  severe  forms  of  mi- 
graine where  the  individual  attacks  may  last  for  several  days  or  more  ("  etat  de 
mal ") .  Without  an  accurate  history  these  severe  conditions  of  intense  head- 
ache and  persistent  vomiting  may  readily  be  falsely  interpreted. 

The  whole  course  of  migraine  is  very  chronic,  and  it  may  last  for  years  and 
years.  It  is  usually  a  trouble  to  which  the  patient  finally  becomes  accustomed. 
We  must  generally  be  quite  guarded  in  our  prognosis,  for  many  cases  resist  very 
obstinately  all  attempts  at  cure.  We  can  give  the  patient  only  the  consolation 
that  the  trouble  generally  disappears  of  itself  in  advanced  life.  It  is  not  usually 
attended  with  any  special  danger.  In  only  a  few  cases  has  it  been  noticed  that 
attacks  of  hemicrania  of  years'  duration  have  preceded  a  severe  cerebral  disease 
that  developed  later. 

Diagnosis. — The  diagnosis  of  migraine  is  not  difficult,  if  we  hold  strictly  to 
the  definition  of  the  disease.  The  laity,  especially  women,  of  course,  delight  in 
calling  every  headache  and  all  sorts  of  other  nervous  and  hysterical  conditions 
*'  migraine."  Especially  characteristic  of  true  migraine  are  the  heredity,  the 
beginning  in  youth,  the  occurrence  in  attacks,  the  accompanying  vomiting,  and 
the  other  attendant  nervous  symptoms.  Errors  in  diagnosis  may  arise  from  the 
fact  that  attacks  of  symptomatic  migraine  may  also  occur  in  severe  organic  dis- 
eases (tabes,  brain  tumor,  etc.).  We  have  seen  a  patient  who  suffered  for 
years  with  severe  "  migraine."  He  finally  died,  and  the  autopsy  revealed  a 
■cysticercus  in  the  fourth  ventricle  with  secondary  hydrocephalus. 

Treatment. — Very  many  patients  who  suffer  from  migraine  finally  renounce 
any  special  treatment,  after  they  have  exhausted  all  possible  remedies.  They  with- 
draw to  their  rooms  when  the  attack  comes  on,  darken  the  windows,  take  noth- 
ing but  some  tea,  Seltzer-water,  or  cracked  ice,  put  a  cold  compress  about  the 
head,  perhaps  try  a  foot-bath,  and  for  the  rest  wait  quietly  until  the  attack  is 
over.  In  fact,  our  remedies  for  cutting  the  attack  short  are  quite  uncertain. 
They  sometimes  aid,  but  they  often  leave  us  in  the  lurch,  especially  if  used  re- 
peatedly. We  must  note  especially  that  narcotics,  such  as  morphine,  are  almost 
always  ill  borne  in  migraine,  and  do  no  good;  but  antipyrine,  sodic  salicylate 
(20-30  grains  [grammes  1.5-2.0],  in  strong  black  coffee),  antifebrine,  phenace- 
tine,  salipyrine,  etc.,  in  many  cases  undoubtedly  have  a  favorable  action.  Which 
remedy  acts  the  best  must  usually  be  tested  in  the  individual  case.  We  have 
ourselves  seen  excellent  results  formerly  from  sodic  salicylate,  and  lately  from 
antipyrine,  pure  or  mixed  with  the  other  remedies  mentioned;  the  attacks  of 
migraine,  when  the  remedy  was  taken  immediately  upon  the  onset  of  the  first 
symptoms,  have  become  distinctly  milder  and  have  run  their  course  more  rapidly. 
Of  course  the  action  often  ceases  with  time,  and  we  must  then  try  another  of  the 
remedies  mentioned.      Of  the   other   remedies   used  we  may  mention  guarana 


908  DISEASES    OF   THE   ITERYOUS    SYSTEM 

(PauUinia  sorhilis),  half  a  drachm  to  a  drachm  (grammes  2-4)  of  the  powder,  and 
caffeine,  or  sodio-salicylate  of  caffeine,  in  three-  to  five-grain  doses  (gramme 
0.2-0.3),  which  is  sometimes  very  serviceable.  Caffeine  is  also  the  chief  constitu- 
ent of  "  migrainine,"  which  has  lately  been  much  praised.  On  theoretical  grounds,, 
inhalations  of  nitrite  of  amyl,  three  to  five  drops  on  a  napkin,  have  been  used  in 
spastic  hemicrania,  and  subcutaneous  injections  of  ergotine  in  the  paralytic  form 
(aqueous  extract  of  ergot,  2.5;  dilute  alcohol  and  glycerine,  each  5;  or  one  part 
of  dialyzed  ergotine  in  four  parts  of  distilled  water :  injections  of  either,  three  to 
fifteen  minims).  The  practical  benefit,  however,  is  very  doubtful.  Many  other 
nervines,  such  as  bromide  of  potassium  and  Fowler's  solution,  have  been  recom- 
mended for  continued  use,  and  also  extract  of  cannabis  indica ;  and,  lately,  nitrite 
of  sodium,  two  parts  in  120  of  water,  a  teaspoonful  one  to  three  times  a  day,  and 
nitro-glycerine,  in  troches  containing  y|o  to  ^V  grain  (gramme  0.0005-0.001). 
Their  action  is  similar  to  that  of  nitrite  of  amyl.  In  ophthalmic  migraine  the 
treatment  by  large  doses  of  bromide  of  potassium  is  praised,  especially  in  France, 
as  being  very  successful. 

In  many  cases  the  general  treatment  is  very  important.  Preparations  of  iron,, 
sea-bathing,  a  mountain  residence,  and  cold-water  cures  are  often  of  decided  serv- 
ice. We  have  seen  remarkably  good  permanent  results  in  several  cases  of  severe 
migraine  from  the  moderate  use  of  Carlsbad  water,  either  at  Carlsbad  itself  or 
taken  at  home.  We  always  strongly  recommend  a  trial  of  this,  especially  when 
there  are  also  symptoms  of  hypersecretion  of  the  gastric  juice  (vide  supra). 
With  the  moderate  use  of  Carlsbad  water  we  usually  combine  methodical  hydro- 
therapy (cold  sponging,  half  baths  with  douches,  etc.)  and  an  appropriate  diet. 
The  persistent  application  of  electricity  has  also  shown  some  good  results,  but  we 
must  not  build  very  great  hopes  upon  it.  In  the  spastic  form  the  action  of  the 
anode  on  the  sympathetic  is  especially  recommended,  and  in  the  paralytic  form 
the  action  of  the  cathode,  while  the  other  electrode  is  to  be  placed  on  the  cervical 
cord,  or  as  high  as  possible  on  the  occiput  in  the  region  of  the  raedulla.  Cautious- 
galvanization  of  the  head,  and  weak  primary  faradic  currents,  may  also  be  used^ 
Specialists  in  massage  praise  their  mode  of  treatment  in  migraine ;  they  massage 
either  certain  painful  spots  in  the  head,  or  the  gastric  region.  Finally,  we  must 
mention  that  migraine  often  seems  to  be  connected  with  diseases  of  the  nose,  espe- 
cially with  hyperplasia  of  the  erectile  tissue  in  the  nose,  and  that  in  such  cases 
treatment  of  the  primary  disease  with  the  galvano-cautery  may  result  in  the 
cessation  of  the  migraine. 


CHAPTER  III 

PROGRESSIVE  FACIAL  HEMIATROPHY 

( JJnilatei-al  Progressive  Facial  Atrophy) 

Unilateral  facial  atrophy  is  an  extremely  rare  disease,  which  consists  of  a 
very  slow  and  gradual  but  usually  constantly  progressive  atrophy  of  one  half  of 
the  face,  and  affects  the  skin,  and  also  the  fatty  tissue,  the  muscles,  and  the 
bones,  either  in  a  uniform  or  a  very  diverse  manner.  The  affection  usually  be- 
gins in  youth.  The  female  sex  seems  to  be  more  disposed  to  the  disease  than  the 
male. 

The  atrophy,  which  has  its  seat  much  more  frequently  on  the  left  side  than 
on  the  right,  begins  usually  in  a  circumscribed  spot  either  on  the  cheeks  or  on  the 
chin.  The  skin,  as  a  rule,  gradually  assumes  a  whitish  or  brownish  color.  The 
affected  part,  and  finally  the  whole  half  of  the  face,  gradually  sink  in  more  and 


EXOPHTHALMIC    GOITEE 


909 


more,  so  that  the  disease  can  be  recognized  at  the  first  glance.  The  atrophy- 
shows  a  sharp  limitation  at  the  median  line.  In  many  cases  the  muscles  appar- 
ently remain  almost  wholly  intact,  hut  in  some  cases  they  show  a  marked  atrophy, 
especially  the  muscles  of  mastication.  The  corresponding  half  of  the  tongue  and 
the  soft  palate  has  sometimes  been  found  implicated.  Exceptionally,  the  atrophy 
involves   the   neighboring   region   of 


the  shoulder  and  the  upper  extremity. 
The  bones  also  atrophy,  especially  in 
the  cases  which  arise  in  early  youth. 
The  hair  on  the  affected  half  of  the 
head  often  falls  out  in  great  amount, 
and  it  becomes  thin  and  atrophic. 
The  sensibility  remains  perfectly  in- 
tact. Marked  vaso-motor  and  secre- 
tory "disturbances  have  only  rarely 
been  observed.  The  accompany- 
ing illustration  (Fig.  114)  shows  a 
patient  who  was  described  by  Rom- 
berg many  years  ago,  and  who  I 
a  long  time  frequented  the  Germ 
"cliniques  in  order  to  show  himself 

iN'othing  definite  is  known  in 
^ard  to  the  nature  of  the  affecti 
Most  observers  at  present  agree  tl 
it  is  a  trophic  neurosis,  an  affection 
■of   trophic    nerves    or    nerve-centers, 
but   where   we    are    to   look   for  the 
.special  seat  of  the  disease,  whether 
in  the  trigeminus  or  in  the  sympa- 
thetic,   we    do    not    know.      Mendel 
lately  found  in  a  case  which  came 
geminus. 

The  disease  is  not  dangerous  in  itself,  and  usually  causes  no  special  subjective 
disturbance,  but  it  seems  to  be  incurable.  In  cases  at  their  beginning  we  can 
at  most  make  an  attempt  to  bring  the  disease  to  a  standstill  by  a  long-continued 
application  of  electricity. 


Fig.  114.— Left  facial  hemiatrophy. 


to  autopsy  a  definite  neuritis  in  the  tri- 


As  an  appendix  it  may  be  briefly  mentioned  here  that  there  is  a  unilateral 
liypertrophy,  which  is  also  possibly  connected  with  neurotrophic  disturbances. 
We  saw  at  Leipsic  a  ten-year-old  boy,  otherwise  perfectly  healthy,  in  whom  a 
striking  hypertrophy  of  the  left  side  of  his  face  and  of  the  left  arm  had  gradually 
■developed. 


CHAPTER  IV 

EXOPHTHALMIC    GOITRE 

{Parry's  Disease.     Morho  di  j^lajani.     Graves's  Disease.     Dasedow''s  Disease) 

iEtiology. — The  special  group  of  symptoms  to  which  the  name  of  exophthal- 
mic goitre  has  been  given,  and  whose  three  cardinal  symptoms  are  acceleration 
of  the  pulse,  goitre,  and  exophthalmus,  was  first  carefully  described  in  Germany, 
in  the  year  1840,  by  the  Merseburg  physician  Basedow,  although  similar  but  less 


910  DISEASES    OF    THE   NEEVOUS    SYSTEM 

precise  observations  had.  been  published  in  England  by  Graves  five  years  earlier, 
[Parry,  in  England,  was  the  first  accurately  to  describe  the  disease  in  1786,  and 
it  was  also  recognized  by  Flajani  in  Italy  in  1800. — ^K.] 

In  the  aetiology  of  the  disease  all  those  factors  play  a  part  which  are  important 
in  the  aetiology  of  neuroses  in  general.  In  many  cases  a  hereditary  predisposition 
can  certainly  be  discovered.  The  disease  has  been  repeatedly  seen  in  several 
members  of  the  same  family.  We  have  ourselves  seen  severe  exophthalmic  goitre 
in  two  sisters.  Furthermore,  exophthalmic  goitre  is  also  quite  frequent  in  those 
families  in  which  there  is  a  hereditai-y  predisposition  to  neuroses  in  general — 
epilepsy,  the  psychoses,  or  hysteria.  Among  the  exciting  causes  we  must  first  men- 
tion great  mental  excitement — grief,  terror,  anger.  Sometimes  real  injuries,  as 
well  as  these  "  psychical  injuries,"  seem  to  have  an  influence  on  the  development 
of  the  disease— that  is,  great  general  bodily  concussion,  such  as  a  fall.  Many 
authors  have  laid  considerable  weight  on  diseases  of  the  female  sexual  organs,  but 
the  importance  of  this  factor  seems  to  us  to  be  exaggerated.  It  is  certain,  how- 
ever, that  the  first  symptoms  of  exophthalmic  goitre  often  develop  at  the  period 
of  pregnancy. 

The  influence  of  sex  upon  the  origin  of  the  disease  is  plain,  since  women, 
especially  somewhat  anaemic,  "  nervous "  women,  are  much  more  frequently- 
affected  than  men.  Exophthalmic  goitre  usually  appears  in  middle  life,  while  it. 
is  seen  only  exceptionally  in  children  and  old  people. 

Symptomatology. — Of  the  three  cardinal  symptoms  of  exophthalmic  goitre 
named  above,  of  which,  of  course,  one  or  another  is  often  absent  or  only  slightly 
developed,  the  acceleration  of  the  pulse  is  the  most  constant  and  usually  the  ear- 
liest. The  frequency  of  the  pulse  averages  100  to  120,  sometimes  only  80  or  90,. 
but  in  other  cases  even  140  or  160.  It  is  not  alike  at  all  times,  but  has  many 
variations — the  symptoms  lasting  for  long  periods  and  also  coming  on  in  single 
paroxysms.  In  sleep  the  frequency  of  the  pulse,  as  we  have  ourselves  confirmed^ 
is  sometimes  almost  normal,  and  sometimes  also  rapid,  but  usually  less  sa 
then  when  the  patient  is  awake.  A  very  vigorous  action  of  the  heart,  and 
as  a  rule  the  subjective  feeling  of  palpitation,  are  usually  associated  with  the 
acceleration  of  the  pulse.  There  is  a  vigorous  pulsation  of  the  carotids,  and 
sometimes  of  the  smaller  arteries.  We  do  not  discover  any  qualitative  changes 
of  the  pulse.  The  pulse  is  usually  quite  regular,  but  arhythmia  has  been  excep- 
tionally observed.  In  some  eases  the  patients  suffer  from  pronounced  angina 
pectoris. 

Physical  examination  of  the  heart  in  many  cases  shows  nothing  especial,  ex- 
cept an  accelerated  and  violent  action  of  the  heart,  but  we  sometimes  find,  as 
we  can  affirm  from  several  cases  in  our  own  experience,  a  manifest  hypertrophy 
of  the  left  ventricle,  and  also  dilatation  of  the  heart,  and  even  actual  valvular 
disease.  In  the  diagnosis  of  the  latter  some  caution  is  necessary,  because  func- 
tional heart  murmurs,  especially  at  the  base  of  the  heart,  are  often  present  in 
exophthalmic  goitre. 

The  goitre  usually  develops  somewhat  later  than  the  first  symptoms  in  the 
heart.  In  many  cases  it  is  entirely  absent,  or  present  only  in  a  slight  degree.  The 
swelling  of  the  thyroid  gland  is  generally  only  exceptionally  very  marked. 
There  are  sometimes  decided  variations  in  it  in  the  course  of  the  same  case.  The 
comparative  softness  of  the  tumor,  the  frequent  and  strong  pulsations  in  it,  and 
the  loud  vascular  murmurs,  which  are  often  but  not  always  heard,  and  which 
arise  in  the  dilated  vessels  of  the  thyroid  gland,  are  characteristic  of  the  goitre  in 
Basedow's  disease.  By  laying  the  hand  on  it  we  can  often  feel  the  thrill  and 
pulsation. 

The  exophthalmus,  the  protrusion  of  the  eyeballs  from  their  orbits,  is  always 
bilateral,  although  it  is  sometimes  more  marked  on  one  side  than  on  the  other 


EXOPHTHALMIC   GOITEE 


911 


(see  Fig.  115).  In  many  cases  it  is  entirely  absent;  in  others  it  may  attain  so  high, 
a  degree  that  an  actual  "  dislocation  of  the  eyeball "  has  been  described.  In  the 
marked  degrees  of  exophthalmus  there  is  often  a  peculiar  staring  expression  to  the 
countenance.  This  is  due  chiefly  to  the  unusual  size  of  the  palpebral  fissure  and 
to  the  less  frequent  winking  than  normal  (Stellwag's  sign).  A  peculiar  symptom, 
first  described  by  Graefe,  is  also  worthy  of  mention.  On  raising  and,  still  plainer,, 
on  lowering  the  eyes,  the  corresponding  associated  movements  of  the  upper  eye- 
lid, which  are  always  present  under  normal  conditions,  are  absent.  This  "  Graefe 
symptom  "  may  sometimes  be  one  of  the  earliest  signs  of  the  disease,  and  may 
therefore  be  of  diagnostic  value;  but  we  must  maintain,  after  much  personal 
experience,  that  it  is  on  the  whole  rare,  and  that  it  may  often  be  wholly  absent 
even  in  the  severest  cases  of  the  disease.  Disturbances  of  the  pupils  and  of  ac- 
commodation are  unknown  in  exophthalmic  goitre,  but  paralyses  of  the  external 
ocular  muscles  sometimes  oc- 
cur, and  we  have  ourselves 
repeatedly  observed  anoma- 
lies in  the  movements  of  the 
eyeball,  especially  temporary 
strabismus.  We  might  men- 
tion one  symptom,  which  Mo- 
bius  first  noticed,  and  which 
we  also  have  repeatedly  but 
not  constantly  seen,  especially 
in  patients  with  rather  marked 
exophthalmus.  It  consists  in 
the  fact  that  one  eye  very  soon 
deviates  outward  if  we  have 
the  patient  converge  the  eyes 
strongly,  as  in  fixation  of  a 
near  object—"  insufficiency  of 
convergence."  Inflammatory 
processes  in  the  eye  are  some- 
times seen,  which  are  probably 
due  to  the  fact  that  the  upper 
lid  can  not  so  well  protect  the 
protruding  eye. 

Besides  the  chief  symptoms 
of  exophthalmic  goitre  thus 
far    described,    we    must    also 


/ 


Fig.  115. — Patient  with  Basedow's  disease  (exophthalmus, 
goitre).     (Personal  observation.) 

mention  a  list  of  other  symp- 
toms which  come  under  our  observation,  both  in  the  typical  cases  and  still  more 
often  in  anomalous  cases — the  so-called  "  formes  frustes  "  of  the  French.  Among 
them  are  some  nervous  symptoms,  especially  a  peculiar  tremor  to  which  Marie  first 
called  attention.  This  tremor  affects  the  whole  body,  or  the  extremities  alone ;  it 
shows  at  times  temporary  remissions  and  exacerbations,  and  it  may  be  so  severe 
as  to  form  the  patient's  chief  complaint.  A  moderate  tremor  of  the  fingers  and 
hands  is  one  of  the  most  constant  symptoms  of  exophthalmic  goitre.  In  a  case 
under  our  observation  marked  tremor  was  one  of  the  first  symptoms  of  the  dis- 
ease. It  may  become  so  violent  at  times  that  there  are  even  spasmodic  twitchings 
in  the  extremities  and  in  the  muscles  of  the  face.  We  may  also  mention  headache, 
vertigo,  weakness  of  memory,  and  sleeplessness.  The  peculiar  nervous  anxiety 
and  the  irritable  disposition  of  the  patient  are,  however,  very  frequent,  and  in 
fact  very  characteristic,  in  many  cases  of  the  disease.  The  anxiety  and  the  haste 
in  all  movements,  in  speaking,  etc.,  often  show  themselves,  even  during  the  physi- 


912  DISEASES    OF   THE   NEKYOUS    SYSTEM 

■clan's  examination,  in  so  striking  a  way  that  they  must  be  regarded  as  not  unim- 
portant factors  in  diagnosis.  The  easily  occurring  flushing  of  the  face,  the 
marked  subjectiye  feeling  of  heat,  and  the  hot  hands,  from  which  many  patients 
suffer,  are  probably  due  to  vaso-motor  disturbances.  Objective  elevations  of  tem- 
perature up  to  100°  or  101.5°  (38°-38.8°  C.)  have  also  been  repeatedly  confirmed 
by  others  (Eulenburg)  and  by  ourselves.  A  marked  increase  of  the  sweat  pro- 
duction, which  in  rare  cases  is  only  unilateral,  is  often  associated  with  the  feel- 
ing of  heat.  On  the  other  hand,  one  of  our  patients  complained  of  a  constant 
•dryness  in  the  mouth. 

Of  symptoms  which  are  referred  to  other  organs  we  must  first  consider  some 
disturbances  on  the  part  of  the  respiration.  The  respiration  is  usually  moderately 
accelerated,  and  many  patients  complain  of  dyspnoea  and  of  a  feeling  of  oppres- 
sion in  the  chest.  In  one  case  we  saw  at  times  deep  spasmodic  inspirations;  in 
other  cases  a  peculiar  dry,  "  nervous  cough  "  appears,  such  as  we  not  infrequently 
see  in  patients  with  goitre.  There  are  also  symptoms  on  the  part  of  the  digestive 
organs.  Paroxysmal  vomiting  is  common,  and  in  severe  cases  it  may  become  so 
persistent,  distressing,  and  uncontrollable  as  to  constitute  one  of  the  chief  dan- 
gers of  the  disease.  In  one  of  our  female  patients  the  disease  began  with  an 
attack  of  almost  uncontrollable  vomiting  lasting  for  several  weeks.  We  less  fre- 
quently see  peculiar  paroxysmal  sero-mucous  or  even  bloody  diarrhoea.  We  have 
once  seen  severe  jaundice.  Finally  we  must  mention  certain  disturbances  in  the 
skin :  vitiligo  has  often  been  observed,  and  also  diffuse  brownish  pigmentation  of 
the  skin  or  chloasma-like  pigment-spots  and  urticaria.  It  is  a  noteworthy  fact, 
first  discovered  by  Yigouroux,  that  the  galvanic  resistance  of  the  skin  is  remark- 
ably small  in  patients  with  exophthalmic  goitre.  This  condition  is  probably  due  to 
the  fact  that  the  skin  is  made  wet  by  the  profuse  sweating,  and  also,  perhaps,  to 
some  form  of  atrophy  of  the  skin.  A  very  rare  but  dangerous  occurrence,  of 
which  we  ourselves  have  seen  a  striking  example,  is  an  apparently  spontaneous 
g'angrene  of  the  extremities.  In  our  case,  which  ended  fatally,  the  gangrene 
affected  the  right  leg.  ISTot  the  slightest  anomaly  could  be  made  out  in  the  ves- 
sels at  the  autopsy. 

The  general  nutrition  of  the  patient  suffers  in  most  cases ;  a  certain  degree  of 
anaemia  and  emaciation  is  often  present.  In  severe  cases,  especially  in  those  of 
rapid  development,  there  is  often  in  a  very  short  time  a  high  degree  of  emacia- 
tion associated  with  much  general  weakness.  Muscular  atrophy  frequently  de- 
velops, chiefly  in  certain  regions — the  arm  or  leg  muscles.  We  may  mention,  in 
conclusion,  that  in  many,  though  not  in  all,  female  patients  disturbances  of 
menstruation  (especially  amenorrhoea)  occur.  In  a  few  cases  peculiar  atrophic 
•conditions  have  also  been  found  in  the  genitals  and  the  breasts. 

Special  complications  are  not  very  common  in  exophthalmic  goitre.  We  may 
mention  as  most  important  that  other  neuroses  (hysteria,  epilepsy)  and  true 
psychoses  may  also  occur  with  exophthalmic  goitre.  The  complication  with  dia- 
betes, or,  as  a  rule,  more  properly,  with  alimentary  glycosuria,  is  also  of  interest. 
Tabes  has  also  been  found  associated  with  exophthalmic  goitre.  [Myxoedema 
and  acromegaly  may  also  be  present. — K.] 

Pathological  Anatomy  and  Pathogenesis. — Although  all  the  symptoms  of 
exophthalmic  goitre  point  to  an  affection  of  the  nervous  system  as  a  cause  of  the 
■disease,  as  we  see  from  the  symptomatology,  the  results  of  pathological  investiga- 
tions are  still  very  meager.  There  is  a  class  of  cases  in  which  changes  in  the  sym- 
pathetic, and  especially  in  the  lowest  cervical  ganglion,  are  said  to  have  been  pres- 
ent; but  the  pathological  significance  of  the  discovery  is  not  placed  beyond  all 
doubt;  and  in  other  cases  nothing  abnormal  at  all  could  be  found  in  the  sympa- 
thetic. The  theory  that  all  the  symptoms  of  exophthalmic  goitre  are  derived 
from  a  disturbance  of  the  sympathetic  also  meets  many  difficulties  and  contradic- 


EXOPHTHALMIC   GOITEE  913 

tions.  If  we  regard  only  the  three  cardinal  symptoms,  we  can  bring  the  accelera- 
tion of  the  pulse,  and  perhaps  the  exophthalmus,  into  harmony  with  the  theory  of 
irritation  of  the  sympathetic;  but  not  the  goitre,  which  is  due  to  a  dilatation  of 
the  vessels.  The  theory  of  a  paralysis  of  the  sympathetic  explains  the  goitre,  and 
also  the  exophthalmus — if  we  assume  as  the  cause  of  the  latter  a  dilatation  of  the 
vessels  in  the  back  of  the  orbit — but  again  the  acceleration  of  the  pulse  remains 
unexplained.  The  experiments  by  Filehhe,  in  which  symptoms  said  to  be  similar 
to  those  of  exophthalmic  goitre  were  produced  by  dividing  the  restif  orm  bodies  in 
young  rabbits,  have  had  up  to  the  present  time  no  bearing  upon  human  pathology, 
since  the  restiform  bodies  have  been  found  as  a  rule  to  be  perfectly  normal  in 
autopsies  of  patients  with  exophthalmic  goitre.  The  theory  of  the  disease  ad- 
vanced by  Mobius  is  by  far  the  most  probable  and  the  most  in  accord  with  our 
present  scientific  views.  According  to  this,  exophthalmic  goitre  is  due  to  a  pri- 
mary morbid  change  in  the  function  of  the  thyroid  gland,  either  from  the  abnor- 
mally great  formation  of  certain  irritating  substances  in  the  gland,  or  from  the 
imperfect  destruction  of  such  substances.  At  any  rate,  the  peculiar  contrast  be- 
tween the  symptoms  of  cachexia  strumipriva  (vide  supra,  myxoedema)  and  those 
of  exophthalmic  goitre  is  striking.  In  cachexia  strumipriva  there  are  absence  of 
the  thyroid,  and  then  thickening  of  the  skin,  slow  pulse,  motor  and  mental  slow- 
ness, but  in  exophthalmic  goitre  there  are  general  emaciation  and  atrophy  of  the 
skin  (diminished  electrical  resistance),  tachycardia,  mental  irritability,  tremor, 
etc.  The  results  of  thyroidectomy  in  exophthalmic  goitre  (vide  infra)  also 
favor  the  view  that  a  change  in  the  function  of  the  thyroid  gland  is  the  main 
feature  of  the  whole  symptom-complex.  [Overdoses  of  thyroid  gland  will  give 
rise  to  certain  symptoms  like  those  of  exophthalmic  goitre  (nervousness,  tachy- 
cardia, etc.),  while  even  small  doses  of  the  gland  may  aggravate  the  symptoms  if 
given  to  a  patient  with  exophthalmic  goitre. — K.] 

Course  and  Diagnosis. — The  course  of  the  disease  is  in  most  cases  very  chronic, 
and  it  may  extend  over  years  and  years,  but  there  are  also  more  acute  cases  with  a 
rapid  development  of  all  the  symptoms.  We  may  often  see  considerable  variation 
in  the  intensity  of  the  symptoms.  All  the  symptoms  of  the  disease  may  often  al- 
most wholly  disappear,  to  recur  after  the  lapse  of  years.  In  other  cases,  especially 
of  the  milder  form,  there  is  not  complete  recovery,  but  there  is  a  permanent  arrest 
of  the  disease.  In  general,  the  cases  beginning  in  youth  give  a  more  unfavorable 
prognosis  than  those  arising  in  later  years.  Complete  recoveries  have  certainly 
been  observed,  but  they  are  not  very  common,  although  marked  improvement  in 
all  the  symptoms  is  by  no  means  rare.  In  some  acute  and  apparently  very  severe 
cases  especially  we  have  seen  almost  complete  recovery;  there  was  usually  only  a 
certain  amount  of  exophthalmus  after  all  the  other  symptoms  had  disappeared. 
The  disease  sometimes  terminates  fatally  with  the  signs  of  general  weakness  and 
finally  paralysis  of  the  heart,  but  more  frequently  from  complications  in  the  heart 
or  lungs. 

In  fully  developed  cases  of  exophthalmic  goitre  a  positive  diagnosis  can  almost 
always  be  made  without  difficulty.  The  peculiar  facial  expression,  altered  by 
emaciation  and  exophthalmus  and  associated  with  goitre,  often  permits  the  recog- 
nition of  the  disease  at  the  first  glance;  but  the  diagnosis  is  often  very  uncertain 
in  the  milder,  undeveloped  cases.  In  many  patients  with  slight  or  even  marked 
goitre  we  find  some  "  Basedow  symptoms  "  without  being  able  to  call  it  actually 
"  Basedow's  disease."  If  there  be  no  evident  goitre,  we  must  be  very  slow  in  our 
judgment,  but  absence  of  exophthalmus  with  other  plainly  developed  symptoms 
is  often  seen.  On  the  other  hand,  when  there  really  is  exophthalmus  it  is  one  of 
the  most  unequivocal  symptoms.  In  all  doubtful  cases  we  should  consider  care- 
fully the  mode  of  onset  and  the  associated  symptoms,  especially  emaciation,  tre- 
mor, general  nervous  irritability,  the  feeling  of  heat,  the  tendency  to  sweating,  etc. 
58 


914  DISEASES    OF   THE   NEEVOUS    SYSTEM 

Treatment. — ^In  the  first  place  we  must  consider  the  general  treatment  of  the 
patient.  Physical  and  mental  rest,  good  food,  and  the  avoidance  of  all  stimulants 
• — such  as  alcohol  or  strong  coffee — and  the  cautious  use  of  cold-water  cures,  espe- 
cially sponging,  salt  baths,  etc.,  may  cause  a  decided  improvement  of  the  condi- 
tion. For  anaemic  patients  we  prescribe  iron,  alone  or  in  combination  with  small 
doses  of  arsenic.  A  course  at  the  springs  at  Franzensbad,  Schwalbach,  Pyrmont, 
Elster,  and  Cudowa,  is  also  sometimes  attended  with  good  results.  Residence  in 
mountainous  regions  or  by  the  sea  often  seems  to  act  still  more  favorably. 

Of  other  remedies,  electricity  is  first  to  be  mentioned,  especially  the  application 
of  galvanism  to  the  neck — the  so-called  galvanization  of  the  sympathetic  at  the 
inner  border  of  the  stemo-mastoid.  The  slowing  of  the  pulse,  which  sometimes 
comes  on  at  once  ("vagus  irritation,"  or  mental  quieting!),  is  striking.  Vigou- 
roux  praises  faradization  of  the  sympathetic  and  of  the  goitre  as  the  best  method 
of  treatment.  Among  internal  remedies  we  may  recommend  atropine  or  tinc- 
ture of  belladonna,  and  ergot  or  ergotine.  We  believe  we  have  repeatedly  seen 
good  results  from  the  latter.  Many  physicians  reject  the  use  of  preparations 
of  iodine  as  without  benefit,  but  we  have  ourselves  at  times  seen  decidedly  good 
results  from  the  long-continued  use  of  small  doses  of  iodide  of  sodium,  etc. 
The  administration  of  preparations  of  thyroid  gland,  however,  are  not  to  be 
advised,  both  for  theoretical  and  practical  reasons  \_vide  supra^.  Digitalis 
has  often  been  prescribed  for  the  palpitation,  but  usually  without  any  good  result. 
With  great  exophthalmus  the  eyes  must  be  protected  from  external  injuries.  The 
occasional  severe  sjrmptoms  on  the  part  of  the  digestive  organs  (vomiting,  diar- 
rhoea) must  be  treated  symptomatically,  by  ice,  opium,  and  champagne. 

In  view  of  the  above-mentioned  theories  as  to  the  nature  of  exophthalmic 
goitre,  partial  extirpation  of  the  goitre  has  of  late  been  frequently  tried.  Very 
favorable  results  have  been  reported  by  different  physicians,  but,  on  the  other 
hand,  there  have  of  course  been  some  sad  experiences.  In  general  we  should 
advise  the  operation  only  in  severe  cases  where  all  other  methods  of  treatment 
had  proved  of  no  avail. 


DISEASES    OF   THE    SPmAL   MENINGES  915 


III.— THE   DISEASES   OF   THE   SPINAL   CORD 


CHAPTEK   I 
DISEASES    OF    THE    SPINAL    MENINGES 

1.  Acute  Inflammations  of  the  Spinal  Meninges 

etiology  and  Pathology. — Isolated  acute  inflammation  of  the  spinal  me- 
ninges is  very  rarely  primary,  so  far  as  we  know,  but  inflammatory  processes  in 
the  neighborhood  quite  frequently  involve  the  meninges,  or  a  spinal  meningitis 
occurs  as  one  symptom  of  a  general  cerebro-spinal  meningitis.  This  latter  con- 
dition is  seen  chiefly  in  the  idiopathic,  generally  epidemic,  cerebro-spinal  menin- 
gitis— a  specific  infectious  disease,  which  has  already  been  described  in  detail 
in  a  previous  chapter.  A  tubercular  spinal  meningitis  is  also  very  often 
combined  with  tubercular  inflammation  of  the  cerebral  meninges,  but,  since  the 
symptoms  of  the  latter  are  usually  in  the  foreground  of  the  picture,  we  will  treat 
of  tubercular  cerebro-spinal  meningitis  in  the  section  on  diseases  of  the  cerebral 
meninges.  Secondary  cerebro-spinal  meningitis  is  sometimes  seen  in  the  course 
of  certain  other  infectious  diseases,  and  is  then  probably  to  be  regarded  as  a 
special  localization  of  the  specific  poison  of  the  disease.  This  is  the  explanation 
of  the  occurrence  of  acute  spinal  and  cerebral  meningitis  as  a  sequel  of  croupous 
pneumonia,  and  also  of  its  occurrence  in  pysemic  and  septic  diseases,  and,  very 
rarely,  in  typhoid  fever  and  the  acute  exanthemata.  We  must  mention,  finally,  the 
occurrence  of  a  purulent  cerebro-spinal  meningitis  as  a  sequel  of  empyema,  pul- 
monary gangrene,  etc.,  which,  although  very  rare,  we  have  repeatedly  noticed. 
In  these  cases  the  infection  of  the  meninges  also  results  from  the  primary  foci  of 
disease,  but  the  channel  of  infection  is  not  yet  exactly  known.  Perhaps  the 
intercostal  nerves  are  the  media  of  communication. 

In  all  the  cases  so  far  mentioned  we  have  chiefly  an  inflammation  of  the  pia 
mater,  a  so-called  lepto-meningitis ;  the  dura  mater  is  not  implicated  in  the  dis- 
ease at  all,  or  only  to  a  slight  degree.  The  condition  is  different  in  those  inflam- 
matory processes  which  gradually  invade  the  meninges  from  the  neighboring 
parts  outside  the  cord.  Thus  we  very  often  see  circumscribed  inflammations  on 
the  outer  surface  of  the  dura  (pachymeningitis)  in  caries  of  the  vertebrse,  and 
these  inflammations  often  invade  the  inner  surface  of  the  dura,  or  more  rarely 
reach  the  pia  mater.  Acute  purulent  peripachymeningitis  is  a  very  rare  disease ; 
it  is  a  purulent  inflammation  of  the  connective  tissue  between  the  dura  mater 
and  the  vertebral  column,  which  is  always  of  secondary  origin.  We  have  seen 
a  very  characteristic  case  of  this  sort  in  the  course  of  a  puerperal  pyaemia.  The 
inflammation  had  spread  from  a  purulent  inflammation  of  the  pelvic  cellular 
tissue,  through  the  foramina  of  the  vertebral  canal,  and  had  finally  set  up  a 
purulent  inflammation  on  the  outer  surface  of  the  dura,  extending  up  to  the 
cervical  cord.  We  meet  with  an  inflammation  of  the  pia  mater  chiefly  in  diseases 
of  the  spinal  cord,  from  an  extension  of  the  process,  as  the  pia  is  involved  to  a 
greater  or  less  extent  in  many  cases  of  myelitis. 

We  do  not  know  with  certainty  whether  other  influences,  especially  injuries 
and  exposure  to  cold,  can  lead  directly,  as  has  often  been  claimed,  to  inflammation 
of  the  spinal  meninges. 


916  DISEASES    OF   THE   NEKVOTJS    SYSTEM 

We  need  to  say  but  little  in  regard  to  the  pathological  anatomy  of  acute  spinal 
meningitis.  The  changes  in  purulent  inflammation  of  the  pia  mater  have  been 
described  in  the  chapter  on  epidemic  meningitis.  Precisely  the  same  conditions 
are  found  in  the  other  forms  of  acute  leptomeningitis.  The  changes  in  pachy- 
meningitis are  completely  analogous.  The  dura  mater  is  traversed  by  dilated  ves- 
sels, and  therefore  is  reddened;  it  is  also  thickened,  and  on  its  internal  or  ex- 
ternal surface  (pachymeningitis  interna  or  externa,  or  peripachymeningitis) 
there  is  usually  found  a  purulent  or  a  sero-purulent  exudation. 

Symptoms. — An  accurate  distinction  between  acute  inflammations  of  the  pia 
mater  and  those  of  the  dura  mater  can  not  be  made  clinically.  The  symptoms 
of  the  disease  include  the  symptoms  of  any  primary  disease  present,  the  general 
symptoms,  such  as  fever,  etc.,  and  in  addition  the  necessary  consequences  which 
the  presence  of  a  disturbance  of  the  meningeal  circulation  and  of  the  meningeal 
exudation  exerts  on  the  cord  and  nerve-roots.  These  consequences  are  due  both 
to  a  mechanical  compression  of  the  parts  named,  and  often  probably  to  an  inva- 
sion of  the  substance  of  the  cord  itself  by  the  inflammation.  To  these  is  added 
the  frequent  combination  of  spinal  symptoms  with  the  symptoms  of  a  co-existing 
cerebral  meningitis. 

The  symptoms  of  acute  spinal  meningitis  are  already  known  to  us  from  the 
description  of  epidemic  meningitis  (see  page  111),  Eecapitulating  them  briefly, 
we  may  mention  chiefly  the  very  severe  pain  in  the  back,  the  great  sensitiveness  of 
the  vertebral  column,  and  the  stiffness  of  the  back  and  neck.  To  these  may  be 
added  usually  symptoms  of  irritation  on  the  part  of  the  nerve- roots:  eccentric 
pains  in  the  trunk  and  the  extremities,  hypersesthesia  of  the  skin  and  of  the 
deeper  parts,  symptoms  of  direct  or  reflex  motor  irritation,  muscular  tension, 
contractions,  etc.  The  cutaneous  and  tendon  reflexes  are  often,  but  not  always, 
much  diminished  or  abolished  in  consequence  of  the  lesion  of  the  nerve-roots. 
There  are  at  times  disturbances  in  the  passage  of  urine  and  faeces.  If,  in  the  later 
course  of  the  disease,  there  are  actual  paralysis  and  anesthesia,  they  are  usually 
a  sign  of  a  more  marked  implication  of  the  cord  itself. 

Diagnosis. — From  the  symptoms  named,  we  can  in  many  cases  make  a  diag- 
nosis of  spinal  meningitis.  Of  course  a  meningitis  is  found  often  enough  on  the 
autopsy-table  whose  symptoms  during  life  were  completely  obscured  by  other  se- 
vere general  symptoms,  while,  on  the  other  hand,  with  severe  constitutional  symp- 
toms the  symptoms  of  meningitis  may  be  illusory,  as  in  typhoid  fever  or  pyasmia. 
Fuller  information  as  to  the  seat  and  the  extent  of  the  inflammation  is  afforded 
by  considering  the  most  painful  parts  of  the  vertebral  column,  the  predominance 
of  pain  and  cutaneous  hyperesthesia  in  the  arms  (cervical  region)  or  legs  (lum- 
bar region),  etc.  When  the  meningitis  involves  the  upper  portion  of  the  cord 
and  the  medulla  there  may  also  be  disturbances  of  respiration,  symptoms  in 
the  pupils,  and  anomalies  in  the  innervation  of  the  heart.  We  can  decide  as 
to  the  form  of  the  meningitis,  whether  purulent  or  tubercular,  only  by  a  con- 
sideration of  the  history,  the  other  morbid  symptoms,  and  the  course  of  the 
disease. 

Prognosis. — ^We  have  seen  an  undoubted  recovery,  in  severe  eases,  only  in  epi- 
demic cerebro-spinal  meningitis,  and  in  the  sporadic  cases  of  idiopathic  menin- 
gitis, which  are  probably  identical  in  aetiology.  In  all  other  eases  reported  with 
a  favorable  termination  the  diagnosis  may  be  doubted,  for  in  general  the  rule 
is  certain  that,  in  extensive  acute  purulent  leptomeningitis  and  pachymeningitis 
the  prognosis  is  almost  absolutely  unfavorable,  whether  it  be  secondary  to  another 
infectious  disease  or  arise  from  propagation  from  some  neighboring  focus  of 
inflammation.  We  may,  perhaps,  make  an  exception  of  certain  mild,  circum- 
scribed cases,  which  do  not  come  to  suppuration,  but  these  are  always  uncertain 
in  regard  to  diagnosis. 


DISEASES    OF   THE    SPIITAL  MEOTNGES  917 

Treatment. — ^In  regard  to  treatment  we  must  refer  entirely  to  wliat  has  been 
said  under  epidemic  and  tubercular-meningitis. 

2.  Chronic  Spinal  Leptomeningitis 

Although  chronic  leptomeningitis  (usually  wrongly  termed  chronic  spinal 
meningitis)  once  played  quite  a  large  part  in  the  diagnosis  and  pathology  of  dis- 
eases of  the  spinal  cord,  we  must  at  present  assert  that  its  occurrence  as  an  inde- 
pendent disease  is  exceedingly  rare.  Most  of  the  reported  cases  of  chronic  men- 
ingitis were  published  at  a  time  when  the  diagnosis  of  many  diseases  of  the  cord 
itself  was  still  perfectly  impossible,  and  when  the  thickenings  and  opacities  of 
the  meninges  were  much  more  striking  at  the  autopsy  than  far  more  essential 
changes  in  the  substance  of  the  cord  itself,  which  could  be  made  out  only  by  a  care- 
ful microscopic  examination,  and  not  by  the  naked  eye.  In  recent  years  only 
a  very  few  cases  have  been  published  which  can  be  regarded,  at  least  with  some 
reason,  as  primary  chronic  meningitis.  It  is  especially  hard  to  determine  this 
since  syphilitic  disease  of  the  spinal  meninges  (vide  infra)  shows  almost  precisely 
the  same  anatomical  appearance.  Clinical  experience  is  also  entirely  against  the 
idea  of  the  frequent  occurrence  of  chronic  spinal  meningitis.  Among  many  cases 
of  spinal  disease  we  shall  scarcely  be  induced  even  to  assume  the  probability  of 
the  existence  of  primary  chronic  meningitis. 

The  case  is  different  with  secondary  chronic  leptomeningitis.  This,  in  the 
first  place,  is,  in  rare  cases,  the  termination  of  an  acute  meningitis.  Secondary 
leptomeningitis  may  certainly  be  detected,  especially  in  epidemic  meningitis. 
We  also  find  chronic  meningitis  frequently  as  a  secondary  affection  in  primary 
diseases  of  the  cord  and  the  vertebrae.  Thus,  for  example,  in  old  cases  of  chronic 
spinal  disease,  associated  with  atrophy,  such  as  tabes  dorsalis,  progressive  muscu- 
lar atrophy,  etc.,  the  pia  is  almost  always  quite  opaque,  thickened,  and  often 
united  to  the  cord  and  the  dura  by  very  many  firm  adhesions,  while  a  cloudy 
sero-gelatinous  exudation  is  found  in  the  meshes  of  the  arachnoid.  All  these 
anomalies,  however,  are  of  a  secondary  nature,  and  have  no  clinical  significance ; 
for  the  same  changes,  though  rarely  so  marked,  are  quite  often  found  in  old 
people,  where  they  are  analogous  to  the  equally  frequent  opacities  of  the  cerebral 
meninges,  the  pleuritic  adhesions,  etc.,  and  where,  during  life,  they  have  not 
caused  the  slightest  symptoms  of  spinal  disease. 

The  symptoms  which  have  been  set  down  as  characteristic  of  leptomeningitis 
correspond  precisely  to  those  of  acute  meningitis,  except,  of  course,  that  they  are 
relatively  less  intense,  and  that  the  course  of  the  disease  is  more  protracted. 
Pain  and  stiffness  in  the  back  and  neck,  abnormal  painful  sensations  and  parses- 
thesia  in  the  extremities,  a  girdle  sensation,  and  finally  paresis,  anaesthesia,  and 
vesical  disturbances,  are  the  leading  features  of  the  type  of  disease  as  constructed, 
in  whose  fabrication  there  have  been,  at  any  rate,  many  confusions  with  myelitis, 
spinal  syphilis,  spondylitis,  beginning  tabes,  multiple  neuritis,  etc.  In  the  few 
cases  confirmed  by  autopsy  the  clinical  picture  resembled  in  some  degree,  from 
the  intention  tremor  of  the  arms  and  the  spastic  symptoms  in  the  legs,  that  of 
multiple  sclerosis.  It  is  strange  that  often  there  were  scarcely  any  shooting  pains 
during  life  in  spite  of  marked  meningeal  changes. 

It  is  clear  that  under  such  circumstances  no  special  rules  for  the  diagnosis  or 
even  the  treatment  of  chronic  spinal  meningitis  can  be  given.  Given  a  case,  we 
would  try  local  applications  to  the  vertebral  column;  painting  with  iodine;  dry, 
or,  exceptionally,  in  strong  patients,  wet  cups;  also  protracted  tepid  baths,  90° 
to  95°  (26°-28°  R.),  or  cautious  cold-water  treatment;  and  finally  the  use  of  the 
galvanic  current.  Of  internal  remedies,  iodide  of  potassium  would  be  most  indi- 
cated. We  may  refer  to  the  description  of  the  treatment  of  myelitis  in  regard  to 
all  further  details. 


DISEASES    OF   THE  l^EVOUS    SYSTEM 


3.  Pachymeningitis  Cervicalis  Hypertrophica 

Pachymeningitis  cervicalis  hypertrophica  was  first  fully  described,  as  a  spe- 
cial yet  very  rare  form  of  disease,  by  Cbarcot  in  1871,  and  later  by  his  pupil 
Joffroy.  ^tiologically,  it  is  still  utterly  obscure.  Alcoholism,  exposure  to  cold, 
and  injury  have  been  alleged  to  cause  it.  'No  small  number  of  cases  seem  to  have 
some  connection  with  syphilis. 

Anatomically,  the  disease  is  characterized  by  a  chronic  and  often  very  con- 
siderable thickening-  of  the  dura,  almost  always,  as  it  seems,  in  the  cervical  por- 
tion of  the  cord,  while  the  pia  takes  but  a  comparatively  small  part  in  the  affec- 
tion. The  dura  may  attain  a  thickness  of  six  or  seven  millimetres,  and  usually 
appears  composed  of  a  number  of  concentric  layers.  Histologically,  the  hyper- 
trophy consists  of  a  new  growth  of  dense  connective  tissue.  The  clinical  symp- 
toms of  the  disease  arise  from  the  fact  that,  first,  the  penetrating  nerve-roots, 
and  later  on  the  cord  itself,  undergo  a  considerable  mechanical  compression.  If 
this  is  of  high  degree  and  persistent,  there  are,  as  a  necessary  result,  secondary 
degenerations  of  the  motor  nerves  and  muscles,  and  a  secondary  descending  de- 
generation of  the  pyramidal  tract  in  the  cord. 

The  clinical  symptoms  are  easily  understood  from  this.  The  disease  almost 
always  begins  with  severe  pain,  which  shoots  from  the  neck  into  the  occiput  and 
the  arms.  Besides  this,  there  are  paresthesia  and  a  numb  feeling  in  the  arms  and 
hands.  Rarely  there  is  an  eruption  of  herpes.  All  these  symptoms  depend  upon 
the  irritation  of  the  posterior  roots. 

After  this  first  period  of  the  disease  (periode  douloureuse  of  Charcot)  has  lasted 
some  two  or  three  months,  the  second  period  begins — the  period  of  paralysis. 

An  atrophic  paralysis  in  the  upper 
extremities  gradually  develops, 
mainly  as  a  result  of  the  compres- 
sion of  the  anterior  motor  roots. 
This  affects,  in  a  remarkable  man- 
ner, chiefly  the  distribution  of  the 
ulnar  and  median  nerves,  while  the 
distribution  of  the  radial  on  both 
sides  usually  remains  free.  The 
hand,  therefore,  assumes  a  charac- 
teristic position  (Fig.  116),  as  a  re- 
sult of  the  contracture  of  the  an- 
tagonistic extensors.  The  paralyzed 
muscles  rapidly  become  atrophic  and 
In  this  stage  there  may  also  be  partial 


Fig.  116. — Position  of  the  hand  in  pachymeningitis 
cervicalis  hypertrophica.    (From  Charcot.) 


show  a  marked  reaction  of  degeneration 
anaesthesia  of  the  skin. 

If  the  compression  of  the  cord  advances,  the  motor  fibers  for  the  lower  ex- 
tremities, which  pass  through  the  cervical  cord,  must  necessarily  at  last  be  in- 
volved sympathetically — the  third  period  of  tbe  disease.  The  result  of  this  is  a 
spastic  paralysis  of  the  lower  extremities — that  is,  a  paresis  or  paralysis  with 
increased  tendon  reflexes,  but  of  course  without  muscular  atrophy,  because  the 
trophic  centers  for  the  muscles  of  the  legs,  in  the  anterior  cornua  of  the  lumbar 
cord,  remain  perfectly  intact.  The  compression  of  the  cervical  cord,  however, 
may  finally  lead  also  to  anassthesia  of  the  lower  extremities,  to  paralysis  of  the 
bladder,  and  bed-sores,  under  which  symptoms  death  ensues;  but,  on  the  other 
hand,  it  must  be  mentioned  that  probably  cases  of  recovery,  or  at  least  of  actual 
improvement  in  pachymeningitis  cervicalis  hypertrophica,  may  occur  even  after 
it  has  lasted  for  years. 

The  diagnosis  of  the  disease  is  based  first  upon  the  fact  that  the  affection  bo- 


DISEASES    OE    THE    SPIXAL   MEXIXGES  919 

gins  Tvith.  pains  in  the  arms,  and  upon  the  later  appearance  of  the  characteristic 
paralyses.  It  may  easily  be  confused  with  tumors  in  the  cervical  cord  and  with 
cervical  spondylitis.  Amyotrophic  lateral  sclerosis  is  distinguished,  however,  by 
the  absence  of  disturbances  of  sensibility,  by  the  bulbar  symptoms,  and  by  the 
fact  that  the  functions  of  the  bladder  remain  intact. 

Treatment  can  do  little  directly,  and  it  must  be  chiefly  symptomatic.  Baths, 
iodide  of  potassium,  and  electricity  are  most  used.  Joffroy  recommends  the  appli- 
cation of  the  actual  cautery  to  the  neck. 

4.   HEMORRHAGE    IXTO    THE    SpIXAL    MENINGES 
{Ho&matorrliacMs.    Meningeal  Apoplexy.    Fachymeninyitis  spinalis  Ticemon-Jiagica  interna) 

Large  hsemorrhages  into  and  between  the  spinal  meninges  are  of  rare  occur- 
rence. They  arise  chiefly  from  traumatic  influences,  from  concussion  or  fracture 
of  the  vertebral  column,  or  from  direct  injuries  of  the  meninges,  such  as  stabs  or 
gun-shot  wounds.  In  a  few  cases  great  physical  exertion  may  also  lead  to  a  me- 
ningeal apoplexy.  Diseases  of  the  vertebrae,  caries,  and  carcinoma,  may  also  lead 
to  a  hsemorrhage  from  the  erosion  of  a  vessel.  The  frequent  little  meningeal  hsem- 
orrhages  which  appear  as  a  complication  of  meningitis,  in  hemorrhagic  diseases, 
in  the  course  of  severe  general  infectious  diseases,  septic  infection,  typhoid  fever, 
and  small-pox,  and  as  a  result  of  severe  general  convulsions,  very  rarely  have  any 
clinical  significance.  Finally,  it  may  be  mentioned  that  aneurism  of  the  aorta  or 
its  branches  may  rupture  into  the  vertebral  canal. 

The  clinical  symptoms  of  meningeal  hgemorrhage  are  almost  always  sudden 
and  "  apoplectiform,"  but  are  unattended  by  any  disturbance  of  consciousness. 
Their  intensity  depends  entirely  upon  the  degree  of  compression  which  the  nerve- 
roots  and  the  cord  undergo  from  the  effused  blood.  The  symptoms  of  irritation 
usually  predominate — severe  pain  in  the  back,  parsesthesia,  and  neuralgic  pains  in 
the  extremities;  and  also  symptoms  in  the  motor  distribution,  tension,  tremors, 
and  contractures  of  the  muscles.  With  large  haemorrhages,  symptoms  of  paraly- 
sis, partial  anaesthesia,  disturbances  of  the  bladder,  symptoms  of  unilateral 
lesion,  etc.,  may  ensue,  but  the  different  types  of  the  disease  of  course  vary  with 
the  seat  of  the  haemorrhage.  On  the  whole,  the  diagnosis  of  meningeal  haemor- 
rhage can  but  rarely  be  made  with  any  certainty,  unless  suggestive  setiological 
factors  precede  and  the  symptoms  and  manner  of  beginning  are  especially  char- 
acteristic. 

The  course  is  quite  favorable  in  many  eases  if  the  blood  be  rapidly  reabsorbed, 
but  sometimes  a  permanent  disturbance  of  function  is  left. 

In  regard  to  treatment,  complete  rest  and  the  energetic  local  use  of  ice  are 
chiefly  to  be  recommended,  and  also  local  blood-letting — dry  cups,  or  leeches, 
where  there  are  severe  initial  symptoms  of  irritation.  Under  some  circumstances 
we  may  try  to  remove  a  part  of  the  blood  by  lumbar  puncture,  and  thus  relieve  the 
pressure  on  the  cord.  [When  the  diagnosis  of  haemorrhage  into  the  meninges  is 
reasonably  certain,  an  attempt  should  be  made  to  relieve  the  condition  by  opening 
the  spinal  canal  and  removing  the  clot. — K.]  If  permanent  disturbances  be  left, 
they  should  be  treated  by  the  ordinary  methods — iodide  of  potassium,  baths,  and 
electricity. 

We  must  here  speak  of  pachymeningitis  interna  hsemorrhagica  as  a  special 
form  of  disease,  which  usually  occurs  at  the  same  time  with  hsematoma  of  the 
cerebral  dura  mater  {vide  infra),  and  is  precisely  analogous  to  it  in  its  aetiology 
and  pathological  anatomy.  Encapsulated  collections  of  blood  are  found  on  the 
inner  surface  of  the  dura;  these  often  have  a  considerable  circumference,  and 
contain  blood  already  disintegrated,  detritus,  hsematoidine  crystals,  etc.,  since 
they  are  usually  of  old  standing.    Besides  this,  there  are  also  the  signs  of  a  fibri- 


920  DISEASES    OE   THE  E"EEVOUS    SYSTEM 

nous  inflammation — as  in  tlie  cerebral  dura — ^wliich,  according  to  the  opinion  of 
most  observers,  is  the  primary  process,  so  that  the  haemorrhages  into  the  newly 
formed  false  membrane  are  secondary.  The  symptoms  of  the  affection — which 
has  been  observed  chiefly  in  the  chronic  insane  (general  paralytics)  and  drunk- 
ards— are  rarely  pronounced,  and  consist  chiefly  of  pain  in  the  back,  stiffness  of 
the  vertebrae,  and  some  signs  of  compression  on  the  part  of  the  nerve-roots  and 
the  cord;  but  we  can  very  rarely  make  a  definite  diagnosis. 


CHAPTEK   II 


PRELIMINARY  REMARKS  ON  THE  LOCALIZATION  AND  TOPICAL 
DIAGNOSIS  (SEGMENTAL  DIAGNOSIS)  OF  DISEASES  OF  THE 
SPINAL   CORD 

The  pathological  processes  that  take  place  in  the  spinal  cord  may  be  divided 
into  two  groups,  according  to  their  localization.  In  the  first  group  the  anatomical 
changes  are  limited  with  remarkable  regularity  to  definite  neurone  territories 
which  are  associated  both  anatomically  and  physiologically.  These  diseases  are 
called  system  diseases,  since  the  entire  group  of  functionally  associated  neurones 
is  called  a  "  system."  We  may,  in  all  probability,  conceive  that  these  affections 
arise  in  one  of  two  ways :  either  certain  neurone  systems  in  some  individuals 
have  from  the  outset  a  congenital  (inherited)  weak  and  morbid  predisposition, 
and,  in  consequence  thereof,  they  are  not  able  to  perform  their  functions,  but 
atrophy  prematurely;  or,  that  certain  external,  usually  toxic,  influences  exert 
their  morbid  action;  not  on  the  whole  nervous  system  or  fortuitous  circumscribed 
parts  thereof,  but  only  on  certain  definite  neurones  (cells  or  fibers) — "  elective 
injuries."  The  latter  hypothesis  finds  a  fitting  and  instructive  example  in  the 
behavior  of  many  well-known  poisons  (curare,  strychnine,  morphine,  lead,  etc.), 
which  injure  only  certain  very  definite  neurones  and  parts  of  nerves,  while  they 
leave  all  other  neurones  completely  intact.  According  as  the  disease  involves  one 
or  more  neurone  systems  we  speak  of  simple  or  combined  system  diseases.  Spinal 
muscular  atrophy,  amyotrophic  lateral  sclerosis,  etc.,  are  due  to  disease  of  the 
motor  neurones  in  the  cortico-muscular  tract;  they  are  simple  system  diseases. 
Hereditary  ataxia,  on  the  other  hand,  is  an  example  of  a  combined  system  dis- 
ease, since  in  this  usually  not  only  certain  peripheral  sensory  neurones  but  also 
motor  neurones  undergo  simultaneous  degeneration.  Since  the  processes  of  many 
neurones  extend,  on  the  one  hand,  from  the  spinal  cord  or  spinal  ganglia  into 
the  peripheral  nerves,  and,  on  the  other,  from  the  cord  to  the  brain,  and  vice 
versa,  we  can  not,  strictly  speakng,  class  the  systematic  neurone  diseases  with 
diseases  of  the  spinal  cord  in  their  limited  sense.  Only  for  practical  and,  in 
part,  purely  conventional  reasons  do  we  consider  the  system  diseases  in  this 
section. 

In  distinction  from  the  system  diseases  there  is  a  second  group  of  diseases  of 
the  spinal  cord  where  either  there  is  no  such  limitation  of  the  anatomical  process 
to  definite  neurone  territories,  or  the  limitation  is  only  very  slight.  In  these  cases 
the  disease  extends  a  greater  or  less  distance  transversely  and  longitudinally  in 
the  cord,  forming  either  one  large  focus  of  disease  of  irregular  outline,  or  many 
smaller,  irregularly  disseminated  foci.  To  this  group,  the  ^insystemic,  diffuse 
diseases  of  the  spinal  cord,  belong  all  the  traumatic  destructions,  also  the  htem- 
orrhages,  new  growths,  and  inflammations  of  the  spinal  cord  (myelitides),  mul- 
tiple sclerosis,  etc.  ,, 


SPIXAL   LOCALIZATIONS^ 


921 


The  diagnosis  of  diseases  of  the  spinal  cord  is  usually,  first  of  all,  a  topical 
diagnosis.  From  the  symptoms  present  in  the  individual  case  we  try  to  deter- 
mine first  that  place  in  the  spinal  cord  where  an  affection  must  be  situated  to 
explain  the  given  symptoms.  By  appraising  all  the  existing  symptoms  of  dis- 
ease, and  also  all  the  functions  that  are  still  in  normal  activity,  we  can  deter- 
mine whether  the  disease  is  limited  to  one  definite  neurone  system  or  whether  it 
must  spread  diffusely  over  a  larger  portion  of  the  spinal  cord.  Only  after  the 
topical  diagnosis  of  the  disease  is  thus  established  do  we  try  to  form  a  judgment 
as  to  the  nature  of  the  disease  by  connecting  it  with  well-known  typical  forms 
of  disease  or  by  considering  the  whole  course  of  the  disease  and  any  accompany- 
ing symptoms. 

The  topical  diagnosis  naturally  presupposes  an  accurate  knowledge  of  the 
functions  of  all  the  different  parts  of  the  spinal  cord — a  knowledge  which  at 
present  we  by  no  means  possess,  but  we  know  at  least  the  distribution  of  the 
motor  and  sensory  functions  in  the  different  portions  of  the  cord  in  their  main 
outlines,  and  upon  this  basis  we  can  often  determine,  at  least  with  approximate 
certainty,  the  localization  of  the  disease,  the  so-called  segmental  diagnosis,  in  the 
transverse  lesions  of  the  spinal  cord. 

1.  In  regard  to  the  localization  of  motor  functions  we  know  definitely  that  the 
motor  fibers  of  the  anterior  roots  all  arise  from  the  ganglion-cells  of  the  anterior 
cornua.  To  each  individual  muscle  belongs  a  group  of  cells  in  the  anterior 
cornu  of  the  cord,  from  which  the  corresponding  motor  nerves,  which  innervate 
the  muscle,  arise.  These  different  muscle  nuclei,  however,  apparently  do  not  lie 
simply  beside  and  above  one  another,  but  they  encroach  upon  one  another,  so  that 
naturally  their  accurate  definition  becomes  difficult.  Furthermore,  the  fibers  of 
one  muscle  nucleus  do  not  always  pass  out  from  a  single  anterior  root,  but  often 
from  two  or  more  roots.  The  following  summary  of  the  arrangement  of  the 
spinal  muscle  nuclei  in  the  different  segments  of  the  spinal  cord  has  been  com- 
piled by  the  aid  of  the  well-known  tables  of  Allen  Starr,  Kocher,  and  others,  but 
it  can  be  regarded  as  only  an  approximate  expression  of  the  actual  conditions. 
Many  details  will  be  changed  and  many  gaps  filled  by  later  investigations.  The 
muscles  printed  in  italics  derive  the  main  part  of  their  nerves  from  the  corre- 
sponding' spinal  segment. 


Segments  or  Anterior  Roots 
1st  Cervical  Segm.ent. 


2d  Cervical  Segment. 


3d  Cervical  Segment. 


IMUSCLES 

Small  muscles  of  the  neclt. 

(Obliqmis  capitis  su[)erior  et  inferior,  rectus  capitis  posti- 
cus major  et  minor.) 
Sterno-hyoidens.      ) 

Sterno-thyroideus.  >  Ramus  descendens  hypoglossi. 
Omo-hyoideus.  ) 

Thyro-hyoideus. 
Trapezius. 
Sterno-cleido-raastoideus. 

Rectus  capitis  anticus  major. 

Longus  colli. 

Complexus  major  et  minor  (trachelo-mastoideus). 

Cervicalis  ascendens. 

Splenius  capitis  et  colli. 

Sterno-cleido-mastoideus. 

Trapezius. 

Rectus  anticus  major. 
Longus  colli. 
Complexus. 
Cervicalis  ascendens. 
Splenius. 
Trapezius. 


922 


DISEASES    OF   THE   NERVOUS    SYSTEM 


Segments  or  Anterior  Roots 
4th.  Cervical  Segment. 


5th  Cervical  Segment. 


6th  Cervical  Segment. 


7th  Cervical  Segment. 


8th  Cervical  Segment. 


1st  Dorsal  Segment. 


2d  to  13th  Dorsal  Segment. 
2d  to  11th  Dorsal  Segment. 
7th  to  12th  Dorsal  Segment. 
1st  Lumbar  Segment. 


Muscles 

Splenius,  trachelo-mastoideus,  longus  colli. 

Scaleni. 

Diaphragma  (N.  phrenicus). 

Levator  scapulsB. 

Supra-spinatus. 

Infra-spinatus. 

Deltoideus. 

Biceps,  supinator  longus. 

Rhomboidei. 

Rhomhoidei  (S.  dorsalis  scapulae). 

Supra-  et  infra-spinatus  (N.  supra-scapularis). 

Deltoideus  (N.  axillaris). 

Biceps.  1 

Coraco-irachialis.     >■  N.  musculo-cutaneus. 

BracJiialis  internus.  ) 

Supinator  longus  et  brevis, 

Diaphragma. 

Pars  clavicularis  pectoralis  majoris. 

Serratus  anticus  major. 

Teres  minor. 

Latissimus  dorsi. 

Serratus  anticus  major  (N.  thoracicus  longus). 

Pectoralis  major  et  minor. 

Latissimus  dorsi. 

Subscapularis. 

Teres  major. 

Triceps. 

Pronator  teres  et  pronator  quadratus. 

Biceps,  brachialis  internus. 

Pai's  clavicularis  pectoralis  majoris. 

Extensors  of  the  hand  and  fingers. 

Scaleni. 

Extensors  of  the  hand. 

(Radiales    externi,  s.   extensor   carpi   radialis   longus   et 

brevis,  ulnaris  externus,  s.  extensor  carpi  ulnaris.) 
Flexors  of  the  hand. 
(Radialis  internus,  s.  flexor  carpi  radialis,  ulnaris  internus, 

s.  flexor  carpi  ulnaris.) 
Extensors  of  the  fingers. 
Pronators  of  the  forearm. 
Portio  sterno-costalis  pectoralis  majoris. 
Latissimus  dorsi. 
Subscapularis,  teres  major. 

Long  extensors  of  the  fingers. 

(Extensor  communis  digitorum,  extensor  pollicis  longus  et 

brevis,  extensor  indicis.) 
Long  flexors  of  the  fingers. 
(Flexor  digitorum  sublimis  et  profundus,  flexor  pollicis 

longus.) 
Small  muscles  of  the  hand. 

Small  muscles    of    the    hand    and  fingers.     (Literossei, 

thenar,  hypothenar.) 
Long  extensors  of  the  thumb. 
Dilatator  pupillcB  (to  N.  sympatheticus,  vide  p.  905). 

Back  muscles. 

Intercostal  muscles. 

Abdominal  muscles. 

Lowest  abdominal  muscles. 
Quadratus  lumborum. 
llio-psoas. 
Sartorius. 


SPINAL   LOCALIZATION 


923 


Segments  or  Anterior  Roots 
2d  Lumbar  Segment. 

3d  Iium.bar  Segment. 


4th  Lumbar  Segment. 


5th.  Lumbar  Segment. 


1st  Sacral  Segment. 


2d  Sacral  Segment. 


3d  Sacral  Segment. 

4th  Sacral  Segraent. 

5th  Sacral  Segment  and  Coc- 
cygeal Segment. 


Muscles 

Cremaster. 
Ilio-psoas. 

Ilio-2}Soas  (psoas,  iliacus  internus). 

Sartorins. 

Adductors  of  the  thigh. 

Pectineios. 

Extensor  cruris  quadriceps. 
Obturator  exteriius  !' 
Gracilis,  adductores. 

Ghdceus  medius  et  minimus. 

Semimemhranosus,  semitendinosus, 

Bice2JS  femoris. 

Tensor  fasciae  latae. 

Dorsal  extensors  of  the  foot  and  toes. 

Pyriformis.  ] 

Obturator  internus.   \   r,  <.„-,„i +„+ „  „*  ti,^  fi  ;^i 

p       jj-  -  Outward  rotators  ot  the  tliigh. 

Qiiadratus  femoris.  J 

Dorsal  extensors  of  the  foot  and  toes. 

(Tibialis  anticus,  peronei,  extensor  digitorum  communis.) 

Flexors  of  the  foot  (gastr-oeneraius,  soleus). 

Flexor  digitorum  communis,  flexor  hallucis  longus. 

Tibialis  posticus. 

Small  muscles  of  the  foot. 

Erection. 

Perineal  muscles. 

Ejaculation  (ischio-cavernosus,  bulbo-cavernosus). 


SpMncter  et  detrusor  vesicce. 
Sphincter  ani,  levator  ani. 


Considering  tlie  muscles  with  regard  to  their  function,  we  obtain  the  follow- 
ing table  of  the  motor  functions  of  the  spinal  segments : 


Cervical  Cord 

1st  Cervical  Segmejit :  Turning  the  head. 
Bending  the  head  backward. 

8d  and  '3d  Cervical  Segments:  Bending  the 
head  forward.     Raising  the  shoulders. 

4th  Cervical  Segment :  Inspiration.  Drawing 
the  shoulders  backward. 

5th  Cervical  Segment :  Raising  and  outward 
rotation  of  the  upper  arm.  Flexion  and 
supination  of  the  forearm. 

6th  Cervical  Segment :  Adduction  and  in- 
ward rotation  of  the  upper  arm.  Exten- 
sion and  pronation  of  the  forearm. 

7th  Cervical  Segment :  Flexion  and  extension 
of  the  hand. 

Sth  Cervical  Seg-  )  Flexion  and  extension 
ment :  I    of  the  fingers.   Move- 

is^  Dorsal  Segment :  )    ment  of  the  thumb. 


Lumbar  Cord 

£d  and  3d  Lumbar  Segment:  Flexion   and 

adduction  of  the  thigh. 
4th  Lumbar  Segment:  Extension  of  the  lower 

leg. 
Sth  Lumbar  Segment :  Abduction  and  inward 

rotation  of  the  thigh.     Flexion  of  the  lower 

leg. 
1st  Sacral  Segment :  Extension  and  outward 

rotation  of  the  thigh.     Dorsal  extension  of 

the  foot. 
Sd  Sacral  Segment :    Plantar  flexion  of  the 

foot.     Toe  muscles. — Erection. 
3d  Sacral  Segment :  Ejaculation. 
4th  Sacral  Segme7it :  Bladder. 
5th  Sacral  Segment :  Rectum. 


If  there  is  disease  of  the  anterior  horns  of  the  gray  matter  (poliomyelitis, 
syringomyelia,  ha3matomyelia)  or  compression  of  the  anterior  motor  roots,  the 
muscles  paralyzed  will  correspond  directly  to  the  affected  segments;  but  with 
more   extensive  transverse   disease    (myelitis,  tumors,   compression)    of   course 


92i 


DISEASES    OF   THE   NEEVOUS    SYSTEM 


those  muscles  will  also  be  paralyzed  whose  nuclei  lie  below  the  seat  of  the  lesion, 
since  the  fibers  of  the  pyramidal"  tract  leading  to  them  will  be  interrupted. 
Erom  what  has  already  been  said  (page  851),  we  may  readily  distinguish  the 
nuclear  or  root  paralyses  from  the  pyramidal  (lateral)  tract  paralyses  by  the 
greater  atrophy,  and  especially  by  the  electrical  reaction  of  degeneration. 

2.  The  distribution  of  the  sensory  conducting  path  to  the  different  segments 
of  the  spinal  cord  corresponds  in  general  to  the  territories  of  distribution  of  the 
sensory  fibers  arising  from  each  spinal  ganglion  {vide  page  796  et  seq.)  ;  but  since 


' — L3. 


L¥. 


Fig.  117.— Distribution  of  the  sensory  root-areas  from  tiie  lumbo-sacral  plexus  (from  Thorburn).  "• 

the  outgoing  posterior  root-fibers  are  mixed  with  one  another  in  the  plexuses, 
•each  region  of  the  skin  is  supplied  by  sensory  fibers  from  at  least  two  and  prob- 
ably three  spinal  segments,  or  from  two  or  three  posterior  spinal  roots.  The 
accompanying  diagram,  devised  by  Kocher  (Table  1),  gives,  as  far  as  our  present 
}inowledge  admits,  a  good  representation  of  the  extent  of  the  different  root  terri- 
tories. We  must  be  prepared  for  individual  variations.  We  see  that  in  the  arms 
the  radial  region  is  innervated  from  the  upper  (fourth  and  fifth)  roots  of  the  bra- 
chial plexus  and  the  ulnar  region  from  the  lowest  roots  (first,  and  probably  second 


rig.  2. 


Fig.  I 


DlSTRIBUTIOX   OF   THE    ArEAS    OF    THE   Se.VSORY    RoOTS    UPOX    THE    SURFACE    OF    THE    BODY 

(FROM    KOCHER). 

Red :  Area  of  the  cervical  roots  (C.  2  to  C.  7). 
Yellow :  Area  of  the  dorsal  roots  (T).  1  to  D.  12). 
Green  :  Area  of  the  lumbar  roots  (L.  1  to  L.  4). 
Blue:  Area  of  the  sacral  roots  (S.  1  to  S.  4). 


SPIXAL   LOCALIZATION 


925 


dorsal  roots).  If  we  conceive  of  the  arm  raised  horizontally  with  the  thumb 
directed  upward,  we  can  in  a  way  imagine  a  horizontal  segmental  division  of  the 
arm  according  to  the  different  sensory-root  areas.  On  the  trunk  the  segmental 
arrangement  of  the  different  sensory  root-areas  is  very  plain;  although  the  seg- 


FiQ.  118. 
Lesion  at  the  level  of  the  second  lumbar  segment. 


Fig.  119. 
Lesion  at  the  level  of  the  third  lumbar  segment. 


ments  do  not  run  parallel  to  the  ribs  and  intercostal  nerves,  but  they  are  strictly 
horizontal.  In  the  legs  Kocher's  diagram  fails  to  give  the  area  of  distribution  of 
the  fifth  sensory  lumbar  root.  We  therefore  add  for  comparison  the  diagram 
given  by  Thorburn  for  the  distribution  of  the  sensory  root-areas  from  the  lumbo- 


FiG.  120. 
Lesion  at  the  level  of  the  fifth  lumbar  segment. 


Fin.  121. 
Lesion  of  the  first  sacral  segment. 


sacral  plexus  (Fig.  117).  The  two  diagrams  differ  considerably  from  each  other, 
so  that  further  investigations  are  very  desirable.  Figs.  118  to  124  (from  work 
conducted  in  the  author's  clinique  by  L.  R,  Miiller)  show  summarily  the  distribu- 


926 


DISEASES    OF   THE   NERVOUS    SYSTEM 


tion  of  tiie  ansestlietic  (shaded)  areas  of  the  skin  in  transverse  lesions  of  the 
spinal  cord  at  different  levels  of  the  lumbo-sacral  cord. 

In  subsequent  chapters  we  will  return  to  many  details  in  regard  to  the  sig- 
nificance of  disturbances  of  sensation  in  accurate  segmental  diagnosis.  "We 
can  here  speak  of  only  two  important  points.  Symptoms  of  sensory  irritation  are 
regarded  in  spinal  diseases  almost  exclusively  as  root  symptoms,  due  to  an  irrita- 


FiG.  122. 
Lesion  of  the  second  sacral  segment. 


Fig.  123. 
Lesion  of  the  third  sacral  segment. 


tion  of  the  affected  posterior  roots  by  pressure,  laceration,  etc.  Such  symptoms 
of  irritation,  therefore,  are  seen  chiefly  in  diseases  which  arise  in  the  coverings 
of  the  spinal  cord  (the  vertebrae  and  the  spinal  meninges).  Then  we  must  also 
refer  once  more  to  the  circumstance  mentioned  on  page  799,  that  the  tracts  for 

the  conduction  of  sensations  of  pain  and 
temperature  after  their  entrance  into 
the  cord  probably  go  at  once  to  the  gray 
matter  of  the  posterior  horns,  while  the 
simple  sensations  of  touch  are  conducted 
to  the  brain  through  the  white  posterior 
columns.  If  we  find,  therefore,  in  spinal 
diseases  the  so-called  dissociated  anaes- 
thesia, especially  anaesthesia  for  pain  and 
temperature  with  retained  sensibility  for 
touch,  we  may  be  quite  certain  that  there 
is  a  central  lesion  in  the  posterior  gray 
cornua,  such  as  is  found  especially  in 
syringomyelia,  injury  of  the  cord,  and 
central  glioma. 

[Brissaud    and    other    recent    French 
writers  lay  much  stress  upon  the  differ- 
ence between  the  sensory  areas  supplied  by 
the  spinal  roots   (radicular  metamerism) 
and  the  sensory  areas  supplied  by  the  dif- 
ferent spinal  segments  (spinal  metamerism).    The  former  have  already  been  de- 
picted.   It  is  claimed  that  the  latter  areas  surround  the  limb,  their  boundaries  be- 
ing perpendicular  to  its  long  axis.    They  correspond,  therefore,  to  areas  covered  by 


Fig,  124.— Lesion  of  the  fourth  sacral  segment. 


SPINAL  LOCALIZATION 


927 


a  glove,  a  sleeve,  a  stocking,  etc.  (geometrical  anaasthesia).  The  determination  of 
the  areas  of  ansesthesia  may  therefore  be  of  importance  in  deciding  whether  dis- 
ease affects  merely  the  spinal  roots  or  the  substance  of  the  cord.  Dejerine,  how- 
ever, denies  any  spinal  metamerism,  and  various  German  observers  claim  that 
in  syringomyelia,  where  the  central  gray  matter  is  affected,  the  areas  of  anaes- 
thesia correspond  to  the  root  distribution  as  given  above,  and  are  not  arranged 
in  bands  about  the  limb;  that  there  is  no  difference  between  radicular  and 
spinal  metamerism,  and  that  lesions  of  any  spinal  segment  cause  practically  the 
same  distribution  of  ansesthesia  whether  the  roots  or  the  central  gray  mat- 
ter be  involved.  The  question  is  still  unsettled,  and  further  study  is  neces- 
sary.— ^K.] 

3.  The  presence  or  absence  of  certain  reflexes  may  also  aid  the  segmental 
diagnosis.  Of  course  the  conditions  here  are  often  very  ambiguous,  since  the 
reflex  may  be  absent  either  from  an  interruption  of  its  particular  centripetal  or 
centrifugal  roots  or  from  an  interruption  in  any  part  of  the  reflex  arc  itself.  The 
centripetal  and  centrifugal  portions  of  the  reflex  arc  are  not  always  necessarily 
at  the  same  level.  Our  knowledge  is  by  no  means  absolutely  definite  as  to  the  po- 
sition of  the  reflex  arc  itself.  The  statements  as  to  the  relation  of  definite  segments 
of  the  cord  to  certain  reflexes  therefore  refer  in  general  only  to  afferent  (centripe- 
tal) posterior  nerve-roots  involved  in  such  reflexes.  The  assumption  that  the 
transmission  of  the  irritation  to  the  appropriate  motor  ganglion-cells  takes  place 
in  the  same  corresponding  segment  of  the  spinal  cord,  is  warranted  at  most  for 
certain  simple  mono-muscular  reflexes  (patellar  reflex,  abdominal  reflex,  etc.).  For 
more  extensive  reflexes  (general  flexion  reflex  in  the  leg,  etc.)  we  must  assume  from 
the  outset  that  the  reflex  process  spreads  over  many  segments  of  the  spinal  cord. 

We  have  set  forth  the  relations  of  the  spinal  segments  (or  posterior  roots)  to 
the  different  reflexes  in  the  following  table,  which  represents  our  present  knowl- 
edge of  the  subject,  although  it  is  still  very  uncertain : 


Biceps  tendon  reflex. 

Triceps  tendon  reflex. 

Tendon  reflexes  in  the  forearm. 

Upper  abdominal  reflex. 

Middle  and  lower  abdominal  reflex. 

Cremasier  reflex. 

Patellar  reflex. 

Glutseal  reflex. 

Plantar  flexor  reflex. 

Achilles  tendon  reflex. 


5th  cervical  segment? 
6th  cervical  segment? 
7th  and  8th  cervical  segments' 
8th  and  9th  dorsal  segments. 
10th  to  12th  dorsal  segments. 
1st  to  3d  lumbar  segments. 
2d  to  4th  lumbar  segments. 
4th  and  5th  lumbar  segments. 
1st  and  2d  sacral  segments. 
2d  sacral  sesrment  ? 


Many  details  as  to  the  behavior  of  the  reflexes  in  different  spinal  diseases  will 
be  mentioned  in  later  chapters.  We  may  here  state  briefly  that  in  general,  the 
absence  of  a  reflex  points  to  a  lesion  of  the  corresponding  segment  of  the  spinal 
cord.  Transverse  diseases  above  any  given  reflex  arc  are  usually  (but  not  always, 
vide  infra)  associated  with  a  pronounced  increase  of  the  reflex.  In  diseases  of 
the  lumbar  cord  the  tendon  reflexes  in  the  lower  extremities  are  therefore  lost  as 
a  rule,  while  in  diseases  of  the  dorsal  and  cervical  cord  they  are  usually  much 
increased. 

4.  At  this  point  we  must  mention  some  important  anatomical  relations  be- 
tween the  position  of  the  different  portions  of  the  spinal  cord  and  the  surround- 
ing vertebrse.  It  is  well  known  tTiat  the  lower  end  of  the  spinal  cord  extends  only 
to  the  level  of  the  second  lumbar  vertebra.  The  vertebral  canal  below  this  point 
is  filled  partly  by  the  filum  terminale,  but  chiefly  by  the  bundles  of  roots  of  the 
Cauda  equina.  The  greatest  breadth  of  the  cervical  enlargement  is  at  the  level  of 
the  fifth  and  sixth  cervical  vertebrse.    The  dorsal  cord  begins  at  the  level  of  the 


928 


DISEASES    OE   THE  NEEVOIJS   SYSTEM 


; 


second  dorsal  vertebra,  the  lurabar  cord  at  the  level  of  the  tenth  dorsal  vertebra. 
The  lumbar  enlargement  attains  its  greatest  circumference  at  the  eleventh  dorsal 

vertebra.    The  position  of  the  coniis  terminalis  cor- 
responds to  the  upper  half  of  the  second  lumbar 
//v'#     .,^' J  vertebra. 

The    topical    relations    between    the    different 
spinal  segments   and  spinal  roots  and  the  bodies 
C- 1   ^^\34Vii-  —  -  3  of  the  vertebrae  are  also  of  great  practical  impor- 

tance.    Since  the  spinal  segments  are  shorter  in 
the  vertical  direction  than  the  bodies  of  the  verte- 
brae, the  spinal  roots,  from  above  downward,  must 
[7|F^  travel  farther  and  farther  downward  to  reach  their 

U.X^^         '  corresponding    intervertebral    foramina.      The    ac- 

companying   diagram    from    Gowers     (Fig.    125) 

I5-'fC-0§^  ^J2.i) 1  D      makes  this  relation  plain.     A  lesion  of  the  eighth 

dorsal  segment,  for  example,  lies  opposite  the  body 

-  -  2  of  the  seventh,  and  not  of  the  eighth  dorsal  verte- 

-  -  3  bra ;  but  since  the  spinous  process  also  has  a  de- 
. .  4          scending  direction,  the  lesion  must  be  sought  at  the 

level  where  we  can  feel  the  seventh  or  even  the 
■  ■  ^  sixth  spinous  process.     These  relations  have  great 

-  0  practical  significance  for  any  operative  procedure, 

but  we  must  also  remember  that  there  may  be  indi- 
vidual variations  from  the  rule. 

10  j 


'4 


10 

11 

12 


11 


CHAPTER   III 


12 


1  S 


Co. 


Fig.  125. — Diagram  to  explain  the 
relation  between  the  points 
where  the  different  i^pinal  roots 
are  given  off  from  the  cord  and 
the  different  vertebral  bodies 
and  spinous  processes. 


DISTURBANCES    OF    CmCULATION,    H^MOR- 
RHAGES,       TRAUMATIC       LESIONS,       AND 
1  L  FUNCTIONAL      DISTURBANCES      OP      THE 

SPINAL    CORD 


1.  Disturbances  of  Circulation. — Our  knowl- 
edge as  to  the  occurrence  and  as  to  the  clinical  sig- 
nificance of  pure  disturbances  of  circulation  in  the 
spinal  cord  is  very  slight.  Most  that  is  stated  in 
regard  to  them  in  the  older  descriptions  of  the 
pathology  of  the  spinal  cord  corresponds  much  more 
to  theoretical  hypotheses  than  to  the  actiial  ob- 
jective facts. 

It  goes  without  saying  that  a  complete  anaemia 
of  the  spinal  cord  must  destroy  its  function;  this 
fact  is  best  illustrated  by  the  well-known  experi- 
ment of  Stenson:  if  we  compress  the  abdominal 
aorta  of  an  animal,  and  thus  cut  off  the  blood-sup- 
ply to  the  lumbar  cord  almost  completely,  a  paraly- 
sis of  the  posterior  portion  of  the  body  very  rapidly 
ensues.  Embolic  (or  thrombotic)  obstruction  of 
the  aorta  also  leads  to  flaccid  paralysis  of  the  legs  in 
man,  but  this  paraplegia  is  to  be  referred  to  anae- 
mia of  the  peripheral  nerves  and  muscles,  and  not 
to  any  change  in  the  spinal  cord,  as  we  must  main- 


DISTUEBAXCES  OF  CIKCULATION,  HiEMOREHAGES,  ETC.   929 

lain  after  a  personal  observation  upon  this  point.  The  spinal  cord  is  abundantly- 
supplied  with  blood  by  the  spinal^  arteries  coming  from  the  vertebral  artery. 
•Some  precisely  analogous  observations  have  been  made  in  man  in  the  rare  cases 
of  obstruction  of  the  aorta  by  emboli  or  thrombi.  Pronounced  spinal  symptoms 
in  general  anaemia,  which  may  be  referred  to  a  co-existing  anaemia  of  the  cord, 
are  rare,  and  at  any  rate  are  of  much  less  clinical  prominence  than  the  important 
results  of  a  co-existing  cerebral  ansemia  (vide  infra).  In  only  a  few  cases  has  para- 
plegia been  seen  after  a  great  general  loss  of  blood,  as  after  metrorrhagia  or  intes- 
tinal hsemorrhage.  The  severe  spinal  symptoms  sometimes  occurring  in  pernicious 
anaemia  are  due  to  combined  columnar  degeneration  in  the  cord  (vide  infra). 

All  statements  as  to  the  occurrence  and  clinical  significance  of  hypergemia  of 
the  spinal  cord  are  still  more  dubious.  We  do  not  know  whether  there  is  active 
hypersemia  of  the  cord.  The  hypersemia  from  stasis,  in  general  disturbances  of 
the  circulation,  in  which  certainly  the  spinal  cord  often  takes  part,  causes  no 
especially  marked  symptoms. 

2.  Haemorrhage  into  the  Substance  of  the  Spinal  Cord — Spinal  Apoplexy — 
Haematomyelia. — Primary  haemorrhage  into  the  spinal  cord  is  as  rare  as  haemor- 
rhage into  the  brain  is  common.  It  is  due  most  frequently  to  traumatic  influ- 
ences (fall  on  the  buttocks,  blow  on  the  back,  etc.).  We  will  return  to  this 
traumatic  haematomyelia  later.  The  sudden  onset  of  spinal  paralysis  has  also 
been  seen  after  great  physical  exertion,  and  this  is  probably  due  to  a  spinal 
apoplexy.  It  is  possible,  but  it  is  not  yet  absolutely  certain,  that  primary  vas- 
cular disease  (small  aneurisms)  may  favor  the  occurrence  of  haemorrhage  in  such 
cases.  Small  capillary  spinal  haemorrhages  are  not  infrequently  seen  as  a  second- 
ary complication  in  tumors  of  the  cord,  and  in  inflammatory  affections  such  as 
myelitis,  epidemic  meningitis,  etc.,  and  in  the  general  haemorrhagic  diathesis,  as 
in  scurvy  or  severe  general  infectious  diseases,  and  after  great  congestion,  convul- 
sions, etc.  F.  Schultze  has  also  found  haemorrhages  into  the  gray  matter  of  the 
posterior  horns  in  new-born  infants  who  have  come  into  the  world  asphyxiated 
after  difficult  labor,  and  these  haemorrhages  may  perhaps  be  of  some  significance 
in  later  life. 

Anatomical  experience  in  regard  to  primary  spinal  apoplexy  is  still  quite 
slight.  The  commonest  situation  for  spinal  haemorrhage  is  the  gray  matter,  either 
in  the  cervdcal  or  the  lumbar  enlargement.  If  the  haemorrhage  be  abundant,  we 
find  the  substance  of  the  cord  destroyed  to  a  great  extent.  The  apoplectic  center 
usually  extends  principally  in  the  long  axis  of  the  cord.  The  blood  is  still  fluid 
in  fresh  cases.  Later  on  it  undergoes  all  those  changes  which  are  fully  described 
in  the  chapter  on  cerebral  apoplexy.  It  is  not  improbable  that  some  cases  of 
syringomyelia  may  be  referred  to  a  primary  haemorrhage  into  the  spinal  cord. 

The  s;sTnptoms  of  spinal  apoplexy  must  in  the  first  place  depend  entirely  upon 
the  seat  and  extent  of  the  haemorrhage.  The  sudden,  apoplectiform  onset  of  the 
symptoms  is  always  characteristic.  It  usually  begins  with  severe  pain  in  the 
back,  followed  very  speedily  by  more  or  less  widespread  paralysis,  anaesthesia, 
vesical  disturbances,  etc.  Since  the  liEemorrhage  is  usually  situated  in  the  gray 
matter,  the  localization  of  the  muscular  paralyses  and  the  form  of  sensory  dis- 
turbance (dissociated  anaesthesia !)  often  show  the  peculiarities  attendant  upon 
such  a  lesion.  Haemorrhage  into  one  half  of  the  cord  sometimes  shows  very 
definite  symptoms  of  unilateral  lesion  (vide  infra).  Thus  in  some  cases  of 
haemorrhage  into  the  cervical  cord,  in  particular.  Minor  has  observed  the  fol- 
lowing symptom-complex:  partial  atrophic  paralysis  of  one  arm,  spastic  paralysis 
of  the  leg  on  the  same  side,  partial  anaesthesia  (just  as  in  syringomyelia)  in  the 
extremities  of  the  opposite  side. 

The  course  of  haemorrhage  of  the  cord  may  in  many  cases  be  comparatively 
favorable.  If  the  blood  be  absorbed,  and  essential  paths  of  conduction  be  not  per- 
59 


930  DISEASES    OF    THE   XEEYOUS    SYSTEM 

manently  destroyed,  the  symptoms  of  paralysis  gradually  pass  away,  and  recovery 
or  at  least  improvement  and  an  arrest  of  tlie  symptoms  follow.  In  many  cases^ 
of  course,  the  severe  type  of  spinal  paralysis  develops,  with  bed-sores,  cystitis,  etc.^ 
and  this,  after  a  longer  or  shorter  time,  leads  to  death. 

We  must  always  be  very  guarded  in  making  a  diagnosis  of  spinal  hsemorrhage. 
We  can  do  so  with  some  probability  only  when  the  symptoms  begin  in  a  pro- 
nounced apoplectiform  manner,  and  when  definite  setiological  factors  (trauma) 
are  to  be  made  out;  but,  as  we  shall  see  later,  central  softening  without  actual 
haemorrhage  may  follow  trauma  and  cause  precisely  the  same  symptoms  as- 
hsematomyelia.  We  should  also  not  forget  that  many  forms  of  acute  myelitis,  and 
even  chronic  spinal  affections  (especially  spinal  syphilis),  may  also  show  a  re- 
markably sudden  onset  or  at  least  may  suddenly  become  worse.  The  distinction 
between  genuine  spinal  apoplexy  and  meningeal  hsemorrhage  is  often  difficult. 
Initial  symptoms  of  marked  sensory  irritation  favor  meningeal  hsemorrhage,  while 
the  occurrence  of  symptoms  pointing  to  an  affection  of  the  gray  matter,  especially 
the  combination  of  atrophic  muscular  paralysis  with  partial  anaesthesia  (thermo- 
ansesthesia,  analgesia),  warrants  the  suspicion  of  central  hsematomyelia. 

Treatment. — If  we  have  the  rare  opportunity  to  be  able  to  interfere  at  the 
beginning  of  the  symptoms,  we  should  prescribe  a  perfectly  quiet  position  in  bed, 
local  use  of  ice,  and  eventually  ergotine.  Later  on  the  treatment  should  be 
directed  according  to  the  methods  generally  in  use  in  spinal  paralysis. 

3.  Traumatic  Lesions  of  the  Spinal  Cord. — In  spite  of  the  protected  position 
of  the  spinal  cord,  it  is  often  the  seat  of  severe  acute  traumatic  lesions.  Frac- 
tures and  dislocations  of  the  vertebrae  are  the  most  frequent,  and  these  may  give 
rise  to  considerable  injury  of  the  spinal  cord  by  the  dislocation  of  the  vertebrae,  or 
by  the  projection  of  a  fragment  of  bone.  Dislocations  occur  most  frequently  in 
the  cervical  region  (between  the  atlas  and  axis  or  very  often  between  the  fifth  and 
the  sixth  cervical  vertebrae).  The  upper  vertebra  in  such  cases  is  usually  dis- 
located forward.  The  spinous  process  of  the  lower  vertebra  therefore  projects 
backward,  while  the  spinous  process  of  the  dislocated  vertebra  is  pushed  forward. 
The  head  is  bent  forward.  Every  movement  of  the  head  is  painful,  and  is  there- 
fore anxiously  avoided.  Fractures  are  very  often  situated  in  the  middle  cervical 
vertebrae  or  at  the  twelfth  dorsal  and  first  lumbar  vertebrae. 

Besides  the  indirect  lesions  of  the  cord  by  displaced  vertebrae,  the  action  of 
the  injury  (fall  on  the  back,  etc.)  may  also  extend  immediately  to  the  spinal  cord. 
In  many  cases  there  may  be  at  the  moment  of  the  injury  a  temporary  distortion 
of  the  vertebral  column  associated  with  local  laceration  of  the  cord;  but  some- 
times severe  traumatic  lesions  of  the  cord  occur  without  any  vertebral  injury. 
These  consist  of  haemorrhages,  which  are  usually  central  (haematomyelia  {vide 
supra),  or  traumatic  softening,  which  is  also  usually  central.  Haemorrhage  and 
softening  may  also  be  associated.  Some  writers  hold  that  an  effusion  of  cerebro- 
spinal fluid  may  sometimes  cause  laceration  and  injury  of  the  tissues.  The  dif- 
ferent actions  of  the  traumatic  force  are,  of  course,  very  often  associated;  thus 
we  not  infrequently  see,  in  particular,  above  and  below  the  destruction  of  the 
cord  caused  by  a  vertebral  lesion,  central  haemorrhages,  or  softening  in  the  an- 
terior and  posterior  horns. 

Gun-shot  wounds  of  the  cord  are  quite  frequent,  in  which  the  bullet  either 
penetrates  the  cord  itself  or  produces  injuiy  of  the  vertebrae  and  haemorrhage, 
which  involve  the  cord  indirectly.  Stabs  and  incised  wounds  of  the  cord  have 
been  repeatedly  seen.  The  point  of  a  knife  or  sword  may  penetrate  the  spinal 
canal  from  behind  through  the  soft  parts  and  cause  a  pai'tial  section  or  at  least 
a  contusion  of  the  cord.  In  such  cases  a  secondary  "  traxunatic  inflammation  " 
may  be  added  to  the  direct  injury. 

The  symptomatology  of  injuries  of  the  spinal  cord  follows  the  general  rules 


DISTUEBANCES  OF  CIECULATION,  H.EMOEEHAGES,  ETC.    931 

for  the  localization  of  disease  of  the  cord  laid  down  in  the  previous  chapter. 
There  is  usually  at  first  a  pronounced  and  often  complete  motor  paralysis  of  the 
lower  extremities.  There  is  also  anaesthesia,  and  very  often  vesical  and  rectal 
paralysis.  In  many  severe  cases  the  secretion  of  urine  seems  at  first  much 
diminished  or  wholly  wanting.  If  the  spinal  roots  be  affected  there  are  severe 
shooting  pains  and  parsesthesia.  Above  the  limit  of  total  cutaneous  anaesthesia 
we  sometimes  find  a  zone  with  dissociated  anaesthesia  (analgesia  and  thermo- 
antesthesia).  This  symptom  points  to  a  hsematomyelia  or  a  central  softening 
ill  the  corresponding  posterior  cornu  of  the  gray  matter  above  the  seat  of 
the  special  lesion  (vide  supra).  The  reflexes  are  usually  diminished  at  first,  but, 
later,  if  the  injury  be  above  the  reflex  arc,  they  are  increased;  but  if  the  arc 
itself  be  broken,  they  are  permanently  absent.  This  rule,  however,  undergoes  an 
interesting  exception,  since  we  often  find  after  severe  injury  of  the  cervical  cord, 
and  especially  after  a  complete  transverse  lesion  thereof,  a  flaccid  paralysis  of  the 
lower  extremities  and  complete  absence  of  the  tendon,  and  more  rarely  of  the 
cutaneous,  reflexes  (Bastian,  Thorburn,  Bruns,  and  others).  To  explain  this 
striking  fact  we  must  suppose  that  the  reflex  path  in  the  lumbar  cord  has  also  un- 
dergone some  disturbance,  either  from  the  initial  general  concussion  or  from  its 
separation  from  all  the  higher  parts  in  the  brain.  With  the  loss  of  reflex  is  often 
associated  paralysis  of  the  bladder  and  rectum.  We  often  see  in  men,  especially 
after  injury  of  the  cervical  cord,  a  more  or  less  complete  and  persistent  erection 
of  the  penis,  which  is  probably  due  to  a  direct  or  reflex  irritation  of  the  nerves 
of  erection.  In  injuries  of  the  cervical  cord  particularly,  we  often  see  a  great  and 
general  increase  of  temperature,  up  to  110°  or  112°  (43°-44°  C),  especially  in 
severe  and  rapidly  fatal  cases;  this  is  of  physiological  interest,  and  agrees  with 
the  results  of  experiments.  On  the  other  hand,  there  are  also,  especially  in 
injuries  of  the  dorsal  cord,  as  it  seems,  great  falls  of  temperature,  down  to  90°  or 
86°  (32°-30°  C). 

The  further  course  of  the  affection  differs  very  much.  In  the  worst  cases  death 
ensues  in  a  few  hours  or  days.  In  other  cases  the  patients  recover  from  the  first 
"  shock,"  but  permanent  paralysis  remains,  which  may  sooner  or  later  lead  to 
death  from  the  ensuing  sequelae,  cystitis  and  bed-sores ;  but  we  often  see  partial 
improvement  and  a  cessation  of  all  the  symptoms.  Although  certain  functional 
disturbances  remain  permanently,  life  is  not  further  endangered.  Finally,  in 
comparatively  mild  cases,  there  may  be  a  complete  recovery. 

The  very  characteristic  injuries  of  the  conus  terminalis  and  the  cauda  equina 
yet  demand  special  mention.  The  conus  terminalis  is  sometimes  crushed  in 
fracture  of  the  first  lumbar  vertebra.  The  symptoms  consist  of  paralysis  of  the 
bladder,  rectum,  and  sexual  functions,  with  anaesthesia  of  the  skin  over  the  sa- 
crum and  about  the  anus,  perineum,  and  genitals  (cutaneous  branches  of  the  last 
sacral  nerves,  compare  Fig.  117,  page  924).  If  the  injury  extends  higher  there 
are  also  sensory  disturbances  on  the  posterior  aspect  of  the  lower  extremities,  and 
paralysis  in  the  region  of  the  sciatic  (see  Figs.  118-124,  pages  925,  926).  A  pre- 
cisely similar  type  of  disease,  however,  also  develops  from  injury  of  the  cauda 
equina  (for  example,  from  fracture  of  the  lowest  end  of  the  vertebral  column  or 
fracture  of  the  sacrum),  since  injury  of  the  root-fibers  of  the  sacral  and  coccygeal 
plexuses  must  of  course  cause  the  same  symptoms  as  injury  of  the  corresponding- 
spinal  segments  themselves.  In  such  cases  we  also  see  the  peculiar  distribution  of 
the  sensory  disturbances  and  the  paralyses  localized  in  the  sciatic  region,  especial- 
ly the  double  peroneal  paralysis  that  is  so  verji-  characteristic.  The  differential 
diagnosis  between  an  affection  of  the  cauda  and  a  lesion  of  the  lowest  portion  of 
the  cord  is  not  always  easy,  but  it  is  of  practical  importance,  especially  in  regard 
to  the  question  of  any  surgical  interference.  Besides  the  consideration  of  the 
chief  point  of  action  of  the  injury,  we  must  consider  especially  that  symptoms 


932  DISEASES    OF   THE   JSteEYOUS    SYSTEM 

of  severe  sensoiy  irritation  (shooting  pains,  parsesthesia)  favor  in  general  an 
affection  of  the  cauda,  while  the  existence  of  dissociated  disturbance  of  sensa- 
tion is  of  value  in  assuming  a  (central)  disease  of  the  spinal  cord. 

The  treatment  of  the  primary  affections  belongs  to  the  domain  of  surgery; 
especially  any  attempt  to  lay  open  the  vertebral  canal,  in  order,  if  possible,  to  re- 
lieve the  existing  pressure  on  the  cord  by  reducing  the  dislocation  of  the  verte- 
brae or  the  splinters  of  bone.  In  most  cases,  particularly  in  all  cases  where  the  in- 
jury is  confined  to  the  cord,  we  have  to  confine  ourselves  to  putting  the  patient  in 
a  proper  position  on  a  water-bed,  and  guarding  as  carefully  as  possible  against 
bed-sores  and  cystitis.  Locally,  the  constant  application  of  ice  is  most  to  be 
recommended.  We  can  expect  but  little  from  local  blood-letting,  inunctions  with 
mercurial  ointraent,  etc.  If  the  first  acute  stage  pass  off  favorably,  the  treatment 
of  any  paralytic  symptoms  remaining  follows  the  ordinary  rules  (baths  and 
electricity). 

4.  Diseases  of  the  Spinal  Cord  after  a  Sudden  Reduction  of  the  Atmospheric 
Pressure  [Caisson  Disease]. — In  bridge-builders  and  others,  who  have  worked  for 
hours  under  water  in  the  so-called  "  caissons,"  under  an  external  pressure  of  two 
or  three  atmospheres,  we  sometimes  observe  peculiar  nervous  symptoms  after 
they  leave  the  caisson — that  is,  on  the  sudden  reduction  of  the  atmospheric  pres- 
sure. These  symptoms  do  not  come  on  immediately  after  the  change  to  the  ordi- 
nary atmospheric  pressure,  but  usually  some  minutes  or  even  half  an  hour  later. 
They  progress  very  rapidly,  so  that  in  a  few  hours  at  the  latest  the  disease  is 
fully  developed.  Besides  the  frequent  mild  and  transitory  symptoms  of  pain  in 
the  ears  and  haemorrhage  from  the  ears,  articular  and  muscular  pains  in  the  back 
and  the  extremities,  slowing  of  the  pulse  and  vomiting,  vertigo,  tinnitus,  dis- 
turbances of  vision  and  speech,  clouding  of  consciousness,  or  even  complete  men- 
tal confusion,  there  are  also  more  persistent  and  severe  disturbances  of  motil- 
ity and  sensibility,  which  point  unequivocally  to  an  affection  of  the  spinal  cord. 
Usually  the  spinal  symptoms  affect  the  lower  extremities  chiefly ;  more  rarely  they 
also  involve  the  arms.  Paralysis  of  the  diaphragm  has  also  been  observed.  The 
type  of  disease  differs  much  in  its  details;  as  a  rule  the  symptoms  of  spastic 
paraplegia  predominate,  but  in  other  cases  there  are  marked  disturbances  of  sen- 
sation or  co-ordination.  The  bladder  is  often  involved;  there  is  usually  retention 
of  urine.  The  patient  sometimes  recovers  in  a  few  weeks,  but  in  other  cases  the 
condition  terminates  fatally  in  a  comparatively  short  time — in  a  few  weeks  or 
months.  Anatomical  investigations  (Leyden,  F.  Schultze,  von  Schrotter,  and 
others)  show  in  such  cases  a  disseminated  but  extensive  affection  in  the  dorsal 
cord,  chiefly  in  the  posterior  columns  and  the  posterior  portions  of  the  lateral 
columns.  The  nervous  tissue  in  the  diseased  parts  is  completely  destroyed,  and 
instead  of  it  is  found  detritus  and  a  collection  of  large,  round,  fatty  granular 
cells.  Haemorrhages  into  the  cord,  which  might  perhaps  be  expected,  have  not 
been  seen.  The  cause  of  these  small  multiple  foci  of  softening  is  to  be  found  in 
the  occurrence  of  many  gas  emboli.  During  the  workman's  stay  in  the  compressed 
air  the  blood  absorbs  an  abnormal  amount  of  gas,  especially  nitrogen  (Hoppe- 
Seyler,  P.  Bert,  and  others).  With  too  sudden  a  return  to  the  ordinary  con- 
ditions of  atmospheric  pressure,  bubbles  of  gas  form  in  the  blood,  and,  in  case  they 
can  not  be  thrown  off  fast  enough  by  the  lungs,  they  lead  to  numerous  emboli  in 
the  smaller  vessels  with  their  consequences.  The  anatomical  arrangement  of  the 
vessels  seems  to  be  the  reason  why  the  embolic  foci  are  situated  chiefly  in  the 
dorsal  cord. 

The  treatment  is  the  same  as  in  acute  myelitis.  The  prophylactic  measures  to 
be  employed  in  a  given  case  are  of  course  very  important.  The  onset  of  morbid 
symptoms  can  be  certainly  avoided  by  the  cautious  and  slow  reduction  of  the 
atmospheric  pressure.     [Ko  person  suffering  from  any  disease,  especially  of  the 


DISTUKBANCES  OF  CIRCULATION,  HiEMORRHAGES,  ETC.    933 

heart  or  kidneys,  no  one  addicted  to  alcohol,  and  no  old  or  very  stout  person, 
should  enter  a  caisson.  It  is  probably  safer  not  to  enter  a  caisson  fasting.  Be- 
ginners should  remain  in  the  caisson  a  comparatively  short  time — not  over  an 
hour.  Eor  more  experienced  workmen  a  day's  work  should  not  exceed  four 
hours,  divided  into  two  shifts  with  four  hours'  interval.  Great  precautions 
must  also  be  taken  against  cold.  The  process  of  "  unlocking "  must  be  slow, 
at  least  five  minutes  for  each  atmosphere  of  pressure.  It  is  said  that  when  the 
symptoms  first  come  on  they  may  be  averted  by  restoring  the  victim  to  the 
caisson  or  to  a  cabinet  capable  of  affording  increased  atmospheric  pressure.  Fluid 
extract  of  ergot  (a  drachm  [gramme  4.0]  every  hour  for  a  few  doses)  is  said  to 
give  great  relief  at  the  outset. — K.] 

5.  Functional  Disturbances  (Spinal  Irritation — Spinal  Neurasthenia). — In 
practice  we  very  often  see  cases  where  the  patient  complains  of  a  set  of  symptoms 
which  are  in  all  probability  of  spinal  origin;  but  since  all  the  objective  signs  of  a 
severe  spinal  affection  are  entirely  absent,  and  since  the  whole  development  and 
further  course  of  these  cases  oppose  the  theory  of  a  coarse  anatomical  disturbance 
in  the  cord,  we  have  a  right  to  regard  them  as  mere  "  functional  disturbances," 
and  thus  to  express  their  relation  to  certain  injurious  setiological  influences,  and 
their  comparative  freedom  from  danger.  It  is  often  very  hard  to  judge  as  to  the 
special  origin  of  the  symptoms.  The  hypothesis  of  "  fine  molecular  changes  "  and 
also  the  hypothesis  of  "  abnormal  vaso-motor  influences  and  disturbances  of  the 
circulation  "  are  forms  of  speech  without  any  actual  basis.  In  Yerj  many  cases — 
though  of  course  not  in  all — the  influence  of  a  morbid  imagination  and  of  men- 
tal anxiety  is  very  evident.  The  spinal  symptoms  are  also  very  often  associated 
with  certain  cerebral  symptoms,  so  that  the  former  are  only  a  part  of  a  general 
neurasthenia.     We  raust  therefore  refer  to  the  description  of  the  latter. 

If  we  look  for  the  cause  for  the  development  of  the  disease,  we  find,  as  a  rule, 
one  or  more  of  those  injurious  factors,  which  have  an  undoubted  influence  in 
the  development  of  ahnost  all  the  neuroses :  severe  and  persistent  emotional  ex- 
citement, mental  and  physical  over-exertion,  improper  methods  of  living,  poisons, 
such  as  alcohol  and  nicotine,  and  sexual  excesses,  such  as  masturbation,  etc. 
Besides  these  there  is  very  often  a  hereditary  predisposition,  a  congenitally  weak 
resistance  of  the  nervous  system,  which  is  often  further  enfeebled  by  a  poor 
state  of  the  general  nutrition.  Finally,  a  hypochondriacal  disposition  is  of  great 
significance,  as  it  causes  not  only  an  abnormally  increased  attention  to  the  symp- 
toms, but  also  an  abnormal  hypersesthesia  to  all  subjective  sensations,  and  even 
the  development  of  new  subjective  sensations.  The  constant  anxiety  about  the 
dreaded  results  of  any  excesses  committed  (especially  with  many  patients  the 
fear  of  the  supposed  effects  of  previous  masturbation)  is  often  much  more  injuri- 
ous than  the  excesses  themselves.  Hypochondriacal  dread,  too,  usually  plays  the 
largest  part  in  the  spinal  neurasthenic  conditions  frequent  among  physicians 
(tabophobia). 

The  symptoms  of  the  morbid  conditions  in  question  usually  begin  gradually. 
The  patient  begins  to  complain  of  weakness  and  fatigue  in  walking,  and  also  very 
often  of  pains  in  the  back  and  loins,  and  not  infrequently  in  the  extremities  also. 
In  spite  of  the  vivid  description  which  the  patients  give  of  their  pain,  they  usually 
have  to  admit,  if  questioned  abo^^t  it  closely,  that  the  intensity  of  the  pain  is 
really  not  very  great.  Besides  the  pain  there  are  usually  many  forms  of  parass- 
thesia — numbness,  formication,  cold  feelings,  etc.  The  more  the  patient  knows, 
or  at  least  believes  he  knows,  of  the  symptomatology  of  spinal  diseases  from 
reading  and  from  associating  with  other  patients,  the  more  detailed  are  his  com- 
plaints. Disturbances  of  the  bladder  are  usually  present  only  in  a  slight  degree, 
but  still  they  do  occur.  They  often  depend  merely  upon  the  disturbance  of 
the  involuntary  reflex  mechanism,  due  tf)  the  added  factor  of  increased  voluntary 


934  DISEASES    OF   THE   NERVOUS    SYSTEM 

attention.  There  are  very  often  sexual  disturbances  (pollutions,  sexual  weakness, 
etc.),  whicli  are  usually  to  be  referred  to  former  excesses,  especially  to  masturba- 
tion or  to  the  hypochondriacal  condition  of  the  patient. 

If  we  make  a  physical  examination  of  the  patient  we  can  not  discover  definite 
signs  of  a  spinal  affection.  In  some  of  the  cases  we  find  an  increased  sensitive- 
ness of  the  vertebrae  on  pressure,  which  may  be  limited  to  a  few  definite  spots, 
a  symptom  to  which  the  name  of  "  spinal  irritation  "  is  often  given';  but  we  often 
fail  to  find  this  tenderness  of  the  vertebrae.  Nothing  abnormal  is  to  be  discovered 
in  the  pupils  or  the  reflexes.  The  tendon  reflexes  are  sometimes  quite  lively  and 
sometimes  weak.  The  sensibility  is  objectively  perfectly  normal;  neither  can  we 
discover  actual  paresis  or  atrophy  of  the  muscles.  Vaso-motor  disturbances, 
however,  are  often  seen :  abnormal  coldness,  pallor  or  redness  of  the  hands,  tend- 
ency to  sweating,  etc.  The  manifold  cerebral  symptoms,  that  are  usually  present 
at  the  same  time,  will  be  mentioned  in  the  description  of  neurasthenia.  The 
condition  of  the  general  nutrition  in  many  patients  remains  unchanged,  but,  of 
course,  some  become  pale,  thin,  and  weak. 

The  diagnosis  of  functional  disturbances  of  the  spinal  cord  is  usually  not 
difficult,  as  we  have  said,  and  it  may  often  be  made  from  the  history,  from  the 
patient's  whole  outward  behavior,  and  from  the  manner  of  his  complaints ;  but  we 
can  not  lay  too  much  stress  upon  the  injunction  that  a  careful  physical  examina- 
tion should  always  be  made,  in  order  to  avoid  confusion  with  an  incipient  serious 
disease.  We  shall  repeatedly  call  attention  in  what  follows  to  the  symptoms  which 
must  chiefly  be  observed  for  this  purpose. 

In  regard  to  prognosis  and  treatment  we  will  refer  to  what  is  said  in  the  chap- 
ter on  neurasthenia. 


,      CHAPTER  IV 

THE    PRESSURE    PARALYSES    OF    THE    SPINAL    CORD 

{Slow  Compression  of  the  Spinal  Oord,  especially  in  Caries  and  Carcinoma  of  the  Vertehroi) 

.3itiology.— Many  pathological  processes  in  the  vicinity  of  the  spinal  cord 
exert  a  gradually  increasing  pressure  upon  it,  and  thus  inhibit  the  conduction  of 
nervous  irritation,  and  even  cause  coarse  organic  changes  in  the  substance  of  the 
cord.  The  seat  of  such  affections  is  in  the  first  place  in  the  membranes  of  the 
spinal  cord.  In  the  chapter  on  meningitis  we  have  already  mentioned  the  com- 
pressing action  of  the  masses  of  inflammatory  exudation  on  the  nerve-roots  and 
the  cord,  and  we  have  learned  to  recognize,  especially  in  pachymeningitis  cervi- 
calis  hypertrophica,  a  characteristic  example  of  a  gradually  increasing  compres- 
sion of  the  cervical  cord.  Precisely  similar  conditions  are  found  in  the  not  very 
rare  meningeal  tumors,  whose  special  pathology  will  be  described  in  connection 
with  the  tumors  of  the  cord  itself. 

By  far  the  most  frequent  pressure  paralyses  of  the  spinal  cord,  and  hence  the 
most  important  practically,  are  caused  by  certain  diseases  of  the  vertebrae,  and 
first  of  all  by  chronic  caries  of  the  vertebrae  (spondylitis,  Pott's  disease,  spondyl- 
arthrocace).*  There  is  no  longer  any  doubt  that  in  almost  all  cases  vertebral 
caries  is  of  tubercular  origin — a  local  tuberculosis  of  the  vertebrae.     Although 

*  In  the  kyphoscolioses  of  the  vertebral  column,  not  due  to  spondylitis,  but  caused  by  abnormal 
mechanical  conditions  or  conditions  of  growth,  there  are  practically  never  any  symptoms  of  compres- 
sion in  the  cord,  even  in  very  pronounced  cases.  In  these  cases  the  cord  manifestly  shows  quite  a 
great  adaptability. 


THE   PRESSURE   PARALYSES    OF   THE    SPINAL   CORD      935 


these  facts  were  formerly  rendered  very  probable  by  the  histological  conditions  of 
the  process,  and  by  its  frequent  relation  to  other  unquestionable  tubercular  dis- 
eases, such  as  phthisis,  miliary  tuberculosis,  and  tubercular  meningitis,  they 
have  of  late  been  confirmed  beyond,  a  doubt  by  the  almost  invariable  discovery 
of  tubercle  bacilli  in  the  cheesy  nodules  of  the  vertebral  caries.  Tubercular 
spondylitis  occurs  at  almost  any  age;  it  is  rare  only  in  old  people.  It  often  de- 
velops in  children,  but  it  is  ahnost  as  frequent  in  adults.  The  ^etiological  signifi- 
cance of  injuries,  such  as  a  fall  or  a  blow,  which  are  often  mentioned  by  the 
patients  themselves  or  their  parents,  is  in  most  cases  doubtful,  but  not  wholly  to 
be  ignored.  As  a  rule  vertebral  caries  apparently  develops  quite  independently  as 
a  primary  disease.  Of  course  we  can  very  often  succeed  in  finding  setiological 
factors  rendering  tubercular  disease  likely — the  tubercular  habit,  hereditary 
tendency,  or  previous  tubercular  disease  elsewhere,  such  as  phthisis,  pleurisy, 
other  affections  of  the  bones,  etc. 

Cancer  of  the  vertebrae,  as  well  as  caries,  leads  to  pressure  paralysis  of  the 
spinal  cord;  but  it  is  relatively  much  rarer  than  caries,  it  develops  chiefly  in 
older  persons,  and  it  occurs  only  as  a  secondary  new  growth  in  cancer  of  other 
organs — the  breast,  the  stomach,  the  oesophagus,  etc.  Sarcoma  is  the  chief  pri- 
mary tumor  of  the  vertebrae ;  but  it  may  also  involve  the  vertebrae  secondarily  by 
extension  from  growths  in  the  vicinity. 

We  must  mention  here  briefly,  as  very  rare  causes  of  compression  of  the  spinal 
cord,  aneurism  of  the  aorta,  which  gradually  erodes  the  vertebras,  echinococci  in 
the  vertebral  canal,  exostoses  of  the  vertebrae,  [myeloma,]  and  syphilitic  new 
growths. 

Pathological  Anatomy. — Vertebral  caries  is  by  far  most  frequent  in  the  dorsal 
portion  of  the  vertebral  column  (dorsal  spondylitis),  less  frequent  in  the  cervical 
portion  (cervical  spondylitis),  and  rarest  in  the  lumbar  por- 
tion (lumbar  spondylitis)  and  in  the  sacrum  (sacral  spon- 
dylitis). It  usually  extends  over  several  adjacent  vertebrae, 
or  more  rarely  two  separate  foci  of  disease  are  seen.  The 
process  itself,  the  details  of  which  can  not  be  discussed  here, 
probably  always  begins  in  the  spongy  substances  of  the  bod- 
ies of  the  vertebrae.  We  see  here,  on  section,  in  incipient 
cases,  roundish,  pale  reddish,  or  yellowish  nodules,  which 
consist  of  newly  formed  fungous  tissue — that  is,  tubercular 
granulation-tissue.  The  bony  substances  become  more  and 
more  destroyed  by  the  invasion  of  the  new  growth,  which  it- 
self shows  the  characteristic  tendency  of  all  tubercular  new 
growth  to  cheesy  degeneration.  Thus  there  is  often  an  ex- 
tensive destruction  of  the  bodies  of  the  vertebrae,  which  later 
on  involves  the  vertebral  processes  also,  the  intervertebral 
disks,  and  the  other  articular  connections  between  the  differ- 
ent vertebrae. 

There  are  essentially  two  factors  to  be  considered  in  re- 
gard to  the  question  which  chiefly  interests  us  here — that  is,  in  regard  to  the  occur- 
rence of  compression  of  the  spinal  cord.  In  the  first  place,  it  is  clear  that  the  com- 
plete or  partial  destruction  of  the  bodies  of  one  or  even  more  vertebrae,  and  of  their 
articular  connections,  can  not  remain  without  influence  upon  the  i)osition  of  the 
other  adjacent  vertebrae.  In  fact,  we  very  often  see  dislocations  of  the  vertebrae 
as  a  result  of  it,  usually  by  the  pushing  backward  of  the  partly  destroyed  verte- 
bra by  the  movements  of  the  vertebra?  above  and  below  the  diseased  portion  on  one 
another  (see  Fig.  126).  There  arises,  on  the  one  hand,  a  contraction  of  the  ver- 
tebral canal,  and  with  it  often  a  very  considerable  limitation  of  the  space  for  the 
•cord;  and,  on  the  other  hand,  that  characteristic  projection  of  the  spinous  pro- 


FiG.  126.  —  Schematic 
representation  of  ver- 
tebral displacement  in 
spondylitis.  The  point 
of  compression  of  the 
cord,  at  the  level  of 
the  second  dorsal  ver- 
tebra, is  at  C. 


936  DISEASES    OF   THE   KEEVOUS    SYSTEM 

cesses  in  the  region  of  the  diseased  portion  of  the  vertebral  column  which  forms 
the  so-called  Pott's  boss — the  angular  kyphosis  (Eig.  127,  page  938).  In  very- 
slight  degrees  of  the  disease  there  is  only  a  trifling  projection  of  one  or  more 
spinous  processes,  but  in  other  cases  it  gradually  becomes  an  extensive  deformity 
of  the  vertebral  column,  which  strikes  us  at  the  first  glance ;  but  it  must  be  espe- 
cially borne  in  mind  that  in  very  many  cases  of  vertebral  caries,  where  the  body 
of  no  vertebra  is  wholly  or  mainly  destroyed,  there  is  no  knuckle  formed  at  all. 
The  line  of  the  spinous  processes  in  such  cases  preserves  completely  its  normal 
external  form. 

The  second  factor,  which  is  very  often  to  be  considered  in  the  mechanism  of 
compression  of  the  cord,  is  the  formation  of  tubercular  granulation  tissue  or  of 
foci  of  cheesy  pus  on  the  posterior  surface  of  the  bodies  of  the  vertebrse.  Since- 
the  inflammatory  tubercular  new  growth  involves  the  periosteum,  there  .are  often 
formed  here  large  collections  of  cheesy  pus,  which  are  situated  beneath  the  peri- 
osteum, raise  it,  and  push  it  out  far  into  the  vertebral  canal.  Still  more  com- 
monly, the  tubercular  new  growth  directly  involves  the  outer  surface  of  the  dura,, 
and  forms  here  extensive  cheesy  masses  which  of  course  may  also  cause  a  com- 
pression of  the  cord.  The  inner  surface  of  the  dura  at  the  corresponding  parts 
is  usually  a  little  injected,  but  otherwise  perfectly  normal.  A  direct  invasion  of 
the  inner  surface  of  the  dura  or  of  the  pia  by  the  tubercular  process  through  the 
dura  is  rare. 

If  now  a  greater  or  less  contraction  of  the  vertebral  canal  has  arisen  from.' 
dislocation  of  the  vertebrae,  or  from  the  projection  inward  of  the  cheesy  purulent 
masses  into  the  canal,  the  consequences  of  pressure  on  the  spinal  cord  itself  are- 
not  long  wanting.  In  cases  where  there  has  been  much  displacement  of  the  verte- 
brae or  an  abundant  formation  of  cheesy  purulent  masses  on  the  outer  surface  of 
the  dura  with  considerable  narrowing  of  the  vertebral  canal,  the  direct  and  purely 
mechanical  injury  of  the  nervous  elements  certainly  plays  a  part;  but  we  not 
infrequently  see  during  life  marked  paraplegia  in  vertebral  caries,  where  the- 
autopsy  shows  only  a  comparatively  slight  narrowing  of  the  vertebral  canal,  usu- 
ally from  granulations  on  the  outer  surface  of  the  dura  mater.  In  such  cases 
there  are  a  number  of  other  factors,  for  the  most  part  also  of  a  mechanical  nature, 
which  lead  to  destruction  of  the  substance  of  the  cord.  In  the  first  place  the  com- 
pression of  the  epispinal  lymph-space  causes  a  stasis  of  lymph  (Schmaus)  in  the 
periadventitial  and  also  in  the  periganglionic  lymph-spaces  and  in  the  lymph- 
spaces  between  the  axis  cylinders  and  the  medullary  sheaths.  The  retained 
lymph  has  a  mechanical  and  probably  a  toxic  action  on  the  nerve  elements.  We 
also  see  not  infrequently  thrombosis  of  the  small  afferent  arteries,  causing 
anaemic  necrosis  of  their  respective  vascular  territories.  It  is  hard  to  decide 
how  much  effect  may  be  ascribed  to  direct  compression  of  the  vessels ;  and  equally 
hard  to  say  whether  toxines  from  the  tubercular  nodules  may  perhaps  reach  the 
substance  of  the  cord,  and  there  exert  an  injurious  action.  In  no  case,  however,, 
have  we  a  right,  in  our  opinion,  based  upon  a  comparatively  large  number  of  cases 
seen  in  hospital  and  private  practice,  to  speak  of  a  "  compression  myelitis."" 
Myelitis — that  is,  inflammation — always  implies  agents  of  inflammation  at  the 
place  of  inflammation,  and  of  that  there  is  no  suggestion  in  compression  of  the- 
cord.  The  histological  changes  at  the  point  of  compression  (vide  infra)  are  not 
of  an  inflammatory  nature,  but  they  may  all  be  explained  by  the  above-mentioned 
mechanical  factors. 

If  we  find  a  gTcater  narrowing  of  the  vertebral  canal,  the  spinal  cord  is  also 
smaller  at  the  point  of  compression.  If  the  narrow  part  correspond  to  a  bend  in 
the  vertebral  column,  we  can  very  often  see  a  marked  angle  of  bending  on  the-^ 
anterior  surface  of  the  cord.  The  whole  configuration  of  the  cord  and  the  ar- 
rangement of  the  nervous  elements  may  be  considerably  disturbed  and  distorted 


THE  PEESSUEE  PAEALYSES  OE  THE  SPINAL  COED   937 

mechanically.  The  consistency  of  the  cord  at  the  part  affected,  the  extent  of 
which  seldom  exceeds  a  few  centimetres,  is  usually  diminished;  the  cord  is  soft 
and  may  be  easily  bent.  In  old  cases  only  do  we  find  the  cord  itself  harder  than 
normal  and  sclerosed  (vide  infra).  It  is  very  remarkable,  however,  that  often, 
as  we  have  repeatedly  seen,  marked  symptoms  of  paralysis  may  be  present  during- 
life  without  finding  any  coarse  mechanical  lesion  of  the  cord  in  the  cadaver,  so 
that  the  cord  may  have  an  almost  perfectly  normal  appearance.  As  in  the  periph- 
eral nerves,  so  in  the  spinal  cord,  a  moderate  pressure  is  manifestly  enough  to 
excite  a  partial  break  in  the  conduction,  without  being  at  the  same  time  neces- 
sarily associated  with  an  actual  mechanical  destruction  of  nervous  elements.  On 
careful  microscopic  examination  of  the  cord,  we  find  in  such  cases,  in  spite  of  the 
existence  of  a  complete  paraplegia  during  life,  that  most  of  the  nerve-fibers  are 
still  completely  preserved,  and  that  there  are  only  here  and  there  a  few  lacunse, 
corresponding  to  circumscribed  lymph-spaces  (vide  supra),  and  to  single  fibers 
which  have  been  destroyed.  This  discovery  is  especially  interesting  because  it 
makes  us  understand  the  possibility  of  recovery,  even  in  apparently  severe  cases 
(vide  infra). 

If  we  take  a  portion  from  the  soft  place  of  compression  for  examination  in  the 
fresh  state,  we  find  usually  many,  sometimes  (in  old  cases)  only  a  few,  granular 
cells,  according  to  the  amount  of  disintegrated  nerve-medulla,  the  remains  of 
which  are  taken  up  by  the  white  blood-corpuscles  (the  wandering  cells),  and  prob- 
ably also  by  the  glia  cells.  If  we  make  stained  cross-sections  of  the  hardened  cord, 
we  see  under  the  microscope  no  signs  of  hyper^emia,  or  accumulation  of  cells  about 
the  vessels,  and  only  exceptionally  a  little  hssmorrhage;  but  we  do  find,  besides 
many  still  preserved  nerve-fibers,  other  fibers,  which  are  involved  in  the  disinte- 
gration or  are  already  destroyed.  Very  commonly  the  changes  are  distributed  in 
the  form  of  nodules.  We  find  groups  of  greatly  swollen  axis-cylinders,  or  of  axis- 
cylinders  torn  off  and  rolled  up  in  a  spiral.  The  medullary  sheaths  are  every- 
where involved  in  the  disintegration,  until  they  blend  with  the  disintegrated  axis- 
cylinders.  The  products  of  disintegration  developing  everywhere  serve,  as  was 
said  above,  to  form  the  granular  cells.  The  ganglion-cells  and  the  glia  also  show 
signs  of  disintegration.  We  not  infrequently  find  the  so-called  corpora  amylacea, 
whose  origin  is  still  somewhat  obscure.  If  the  destruction  of  the  nervous  tissue 
have  advanced  to  a  certain  degree,  there  is  in  the  later  stages,  as  in  all  analogous 
processes,  a  secondary  implication  of  the  neuroglia.  ISTow  follows  an  increase 
of  the  interstitial  connective  tissue.  Its  proliferations,  which  take  the  place  of 
the  destroyed  nervous  tissue,  seem  broad  and  thick — at  first  loose,  but  later  firm 
and  fibrillary.  Thus  it  happens  that  in  old  cases  we  find  nothing  at  the  point  of 
compression  but  a  loss  of  nerve-fibers  in  the  cord,  and  instead  a  firm  fibrous  tissue. 
We  can  sometimes  notice  processes  of  regeneration  in  the  nei*ve-fibers  (vide 
infra).  In  general  the  changes  are  much  more  marked  in  the  white  matter  of  the 
cord  than  in  the  gray. 

Finally,  after  every  protracted  compression  of  the  cord  we  find  an  ascending 
and  descending  secondary  degeneration  of  certain  systems  of  fibers  in  the  cord 
(vide  infra). 

We  need  not  go  more  fully  into  the  details  of  compression  of  the  cord  from 
other  causes,  since  the  results,  as  far  as  they  are  of  a  purely  mechanical  natiire, 
are  precisely  the  same.  In  cancer  of  the  vertebrae  there  may  also  be  dislocations 
of  the  vertebral  column  after  the  destruction  of  some  of  the  vertebrae,  but  usually 
the  compression  depends  upon  the  direct  growth  of  the  newly  formed  tissue  into 
the  dura.  In  these  cases  the  compression  of  the  nerve-roots  in  the  intervertebral 
foramina  is  also  of  importance. 

Clinical  History. — 1.  The  Pressure  Paralyses  in  Vertebral  Caries. — Many 
cases  of  spondylitis  run  their  course  without  involving  the  cord,  or  at  least  they 


938 


DISEASES    OF   THE   NERVOUS    SYSTEM 


involve  it  only  in  quite  a  subordinate  fashion.  In  other  cases  the  symptoms  of 
disease  of  the  vertebrse  exist  for  a  long  time  alone,  until  at  last,  slowly  or  sud- 
denly, the  signs  of  compression  of  the  cord  are  added  to  them.  Finally,  in  a 
third  groiip  of  cases,  the  vertebral  disease  is  so  latent  that  only  the  cord  symp- 
toms are  prominent  in  the  type 
of  the  disease,  and  the  disease  of 
the  vertebra  is  easily  entirely 
overlooked. 

Usually  the  symptoms  of  the 
developing  primary  disease,  the 
affection  of  the  vertebrae,  precede 
the  appearance  of  the  first  cord 
symptoms  by  some  time.  The 
patient  feels  a  dull  pain  at  a 
definite  part  of  the  spine,  which 
is  increased  by  movements  of 
the  trunk,  by  bending  or  straight- 
ening up.  Many  patients  notice 
the  stijBfness  of  the  vertebral  col- 
umn of  themselves,  and  some- 
times even  a  beginning  deform- 
ity. In  characteristic  cases  we 
notice  at  once,  on  examining  the 
vertebral  column,  an  angular 
kyphosis  (gibbus,  Fig.  127)  of 
considerable  extent  or  limited 
to  a  few  vertebrae;  but  some- 
times there  is  only  a  slight  prom- 
inence of  a  single  vertebra,  and 
not  infrequently  there  is  exter- 
nally no  change  in  the  formation 
of  the  vertebral  column.  The 
tenderness  on  pressure  on  the 
spinous  processes  is  also  not  a 
constant  symptom;  it  may  be 
very  pronounced,  but  it  is  not 
infrequently  absent  even  in 
marked  kyphosis.  The  first  cord 
symptoms  usually  consist  of  pain- 
ful sensations,  which  are  not  con- 
fined to  the  place  of  the  disease, 
but  spread  out  along  the  course 
of  the  nerve-paths.  These  pains 
are  due  to  the  compression  and 
the  consequent  irritation  of  the  nerve-roots,  and  therefore  extend,  according  to 
the  seat  of  the  affection,  into  the  shoulders  and  arms,  into  the  lateral  portions  of 
the  trunk,  or  into  the  lower  extremities.  The  initial  pains  are  most  frequently 
felt  in  the  region  of  the  lower  ribs  or  of  the  epigastrium,  corresponding  to  the 
most  frequent  situation  of  vertebral  caries  in  the  lower  dorsal  vertebrae.  They  are 
sometimes  very  severe,  and  then  they  usually  have  a  pronounced  neuralgiform 
character,  or  they  may  be  more  dull,  pressing,  dragging,  etc.  Besides  the  special 
pains,  there  are  also  many  forms  of  paraesthesia,  such  as  formication,  cold  feel- 
ings, and  burning  feelings. 

The  disturbances  of  motility  begin  to  appear  at  the  same  time  with  these 


Fig.  127. — Angular  kyphosis  in  vertebral  caries. 
(Personal  observation.) 


THE  PRESSUEE  PARALYSES  OF  THE  SPINAL  CORD   939 

symptoms  or  soon  after  them.  A  stiffness  and  weakness  arise  which  impede  the 
^ait  more  and  more,  usually  not  in-both  legs  at  once,  but  first  in  one  and  then  in 
the  other,  although,  as  a  rule,  both  legs  are  soon  involved.  This  paresis  increases 
rapidly  or  slowly,  and  it  may  finally  go  on  to  a  complete  motor  paralysis.  If  the 
seat  of  the  aflection  be  in  the  dorsal  vertebrae,  as  it  usually  is,  or  if  it  be  in  the 
lumbar  vertebrae,  the  paralysis  affects  the  lower  extremities  only,  and  the  arms, 
of  course,  remain  intact;  but  in  cervical  spondylitis  the  arms  are  usually  first 
and  chiefly  affected.  Only  on  great  compression  of  the  cervical  cord  is  the  con- 
duction of  the  fibers  passing  through  it  for  the  lower  extremities  impaired,  and 
then  there  are  also  disturbances  of  function  in  these.  Ataxia  of  the  legs  is  not 
very  common,  but  it  certainly  does  occur  in  compression  of  the  cord.  The  ataxia 
of  course  is  usually  concealed  by  the  co-existing  paresis  of  the  muscles  or  the  ex- 
isting spastic  conditions.  We  see  ataxia  most  frequently  in  the  stages  of  devel- 
opment or  recovery  of  compression  paralyses. 

Disturbances  of  sensibility  are  quite  often  found,  independently  of  the  pains 
and  paraesthesise  above  mentioned,  but  in  many  cases  of  pressure  paralysis  they 
are  present  in  only  a  comparatively  slight  degree.  It  seems  that  the  sensory 
nerves  resist  pressure  more  than  the  motor  nerves,  just  as  in  the  pressure  paraly- 
ses of  peripheral  nerves;  but  possibly  their  position  in  the  gray  matter  of  the 
posterior  cornua  protects  them  better  from  the  above-mentioned  mechanical  in- 
juries than  is  the  case,  for  example,  with  the  motor  fibers  in  the  pyramidal  tract. 
The  fact  is  that  often,  even  in  complete  motor  paraplegia,  there  is  little  if  any 
diminution  of  sensibility,  and  that  marked  anaesthesia  is  rare,  and  is  seen  only  in 
the  last  stages  of  the  disease.  We  find  most  frequently  a  slight  blunting  of  sen- 
sibility equally  to  all  forms  of  sensation,  especially  to  the  sense  of  pain,  in  other 
cases  partial  disturbances  of  the  sense  of  temperature  with  the  sensibility  to 
touch  and  pain  well  preserved,  sometimes  partial  anaesthesia  of  the  sense  of 
pressure,  etc.  The  different  parts  of  the  skin  not  infrequently  act  differently,  so 
that  we  find  portions  with  quite  normal  sensibility,  as  well  as  very  anaesthetic 
portions.  There  may  also  be  hyperaesthetic  areas  of  the  skin  (especially  at  the 
Tipper  boundary  of  the  disturbance  of  sensation),  particularly  with  marked  hyper- 
sesthesia  to  pain  (pin-pricks). 

The  condition  of  the  reflexes  is  interesting.  If  the  seat  of  the  compression  be 
above  the  reflex  arc,  which  we  must  assume  to  be  in  the  lumbar  cord  for  the  re- 
flexes of  the  lower  extremities,  we  should  expect  that  the  reflexes  would  persist, 
and  in  many  cases  even  be  increased,  corresponding  to  the  decline  in  the  inhibi- 
tory influences  coming  from  above.  The  latter  takes  place  in  most  cases  with  the 
tendon  reflexes.  The  increase  of  the  tendon  reflexes,  and  the  coincident  increase 
of  muscle  tonus,  may  reach  so  great  a  degree  in  many  cases  of  compression  of  the 
dorsal  and  cervical  cord  as  to  show  in  the  lower  extremities  the  pronounced  type  of 
spastic  rigidity  and  spastic  paralysis.  The  legs  are  then  found  in  a  rigid  tonic  ex- 
tension, with  the  knees  pressed  firmly  together,  or  there  is  spastic  contracture  of 
the  flexors  and  adductors.  All  passive  movements  of  the  legs  can  be  performed  only 
with  the  greatest  difficulty,  and  the  attempt  often  causes  a  general  tremor  of  the 
leg.  All  the  tendon  reflexes  (patellar  reflex,  adductor  reflex,  ankle  clonus,  etc.)  are 
much  increased,  but  we  must  remember  that  even  in  apparently  flaccid  paraplegia 
the  reflexes  are  sometimes  quite  lively.  In  cervical  spondylitis  the  tendon  and 
periosteal  reflexes  in  the  arms  are  also  increased  sometimes,  but  in  other  cases,  if 
the  reflex  arc  be  injured,  they  are  absent.  Where  the  seat  of  the  compression  is 
above  the  lumbar  cord,  the  cutaneous  reflexes  sometimes  show  considerable  vigor, 
hut  their  increase  is  much  less  frequently  decided  than  is  the  increase  of  the 
tendon  reflexes.  In  severe  pressure  paralyses  in  the  dorsal  cord  the  cutaneous 
reflexes  are  sometimes  diminished.  They  are  rarely  entirely  absent,  but  one  must 
xmderstand  testing  them,  and  must  employ  long-continued  cutaneous  irritation. 


940  DISEASES    OF    THE   NEEVOUS    SYSTEM 

such  as  pinching  and  pricking-,  in  different  parts  of  the  skin  in  order  to  provoke 
them  (vide  supra,  page  839).  [In  spastic  conditions  the  Babinski  reflex  is  usu- 
ally found. — K.]  In  many  cases  of  total  compression  of  the  cervical  cord  we 
find  a  flaccid  paraplegia  with  absence  of  the  tendon  reflexes  in  the  legs,  just  as 
in  traumatic  total  transverse  lesion  of  the  cervical  cord.  In  these  cases  we  shall 
usually  be  able  to  find  secondary  changes  in  the  lumbar  cord  on  careful  examina- 
tion (vide  page  931). 

Disturbances  of  the  rectum  and  bladder  occur  in  almost  all  severe  cases  of 
pressure  paralysis.  The  difficulty  of  micturition  is  often  an  early  symptom  of  the 
disease;  later  on  there  is  complete  retention  of  urine,  and,  in  the  more  advanced 
stages  of  the  disease,  there  is  usually  incontinence.  With  this  the  danger  of  the 
development  of  cystitis  becomes  very  great.  The  bowels  are  usually  constipated, 
but  sometimes  there  is  also  incontinence  of  faeces. 

Trophic  disturbances  are  often  found  in  the  paralyzed  parts.  If  there  be 
severe  symptoms  of  sensory  irritation  there  may  sometimes  be  eruptions  of  her- 
pes, corresponding  to  the  course  of  the  nerves.  More  frequently  there  are  chronic 
disturbances  in  the  nutrition  of  the  skin  in  severe  and  long-continued  cases.  It 
becomes  dry,  the  epidermis  scales  off,  and  the  nails  become  brittle.  Bed-sores 
form  very  easily  in  severe  cases  on  the  sacrum,  on  the  buttocks,  on  the  inner  side 
of  the  knees,  and  on  the  heels,  especially  when  the  patient  has  insufficient  care. 
The  muscles  retain  their  normal  volume  and  their  normal  electrical  excitability 
in  many  cases  as  long  as  their  trophic  center  remains  uninjured;  but  sometimes, 
even  when  the  point  of  compression  is  above  the  lumbar  cord,  there  is  a  gTeat 
flaccidity  (vide  supra)  and  atrophy  of  the  muscles  of  the  legs,  although  the  elec- 
trical reaction  of  the  nerves  is  normal,  or  at  most  a  little  reduced  in  quantity. 
In  cervical  spondylitis  with  lesion  of  the  cervical  cord  or  of  the  anterior  cervical 
roots  there  may  be  atrophic  paralysis  in  the  arms.  If  there  be  compression  of 
the  lumbar  cord  there  is  atrophic  paralysis  of  the  leg  muscles.  We  have  already 
learned  to  recognize  the  peculiar  type  of  nervous  symptoms  in  disease  of  the 
lowest  portion  of  the  cord  or  of  the  cauda  equina  (page  931).  We  sometimes  see 
the  same  type  in  caries  of  the  upper  lumbar  vertebrae  with  compression  of  the 
conus,  or  in  caries  of  the  sacrum  with  compression  of  the  cauda  equina.  The 
points  to  be  noticed  in  distinguishing  between  affections  of  the  conus  and  affec- 
tions of  the  cauda  have  already  been  mentioned  on  page  931. 

Thus  we  see,  under  some  circumstances,  in  compression  of  the  cord,  the  whole 
group  of  symptoms  arising  which  are  the  necessary  consequence  of  the  break 
in  conduction  in  the  spinal  cord,  and  which  we  shall  likewise  meet  again  in  vari- 
ous other  spinal  affections,  especially  in  myelitis  and  in  tumors.  The  intensity 
and  number  of  the  symptoms  must,  of  course,  vary  very  much  in  the  different 
cases.  If  the  compression  be  quite  slight,  there  are  only  mild  symptoms  of  sen- 
sory irritation  and  slight  paresis.  One  of  the  earliest  and  most  constant  signs 
of  a  compression  of  the  cord,  in  the  dorsal  or  cervical  region,  is  a  decided  increase 
of  the  patellar  reflex.  We  sometimes  flnd  it  at  a  time  when  there  is  scarcely  a 
single  other  cord  symptom  present.  If  the  compression  increases,  the  paresis 
becomes  more  marked,  the  disturbance  of  sensibility  is  greater,  and  vesical  dis- 
turbances arise,  until  finally  the  complete  type  of  an  entire  transverse  interrup- 
tion of  conduction  in  the  cord  is  developed.  The  precise  limitation  of  the  symp- 
toms, especially  the  distribution  of  the  sensory  disturbance,  follows  the  rules 
already  given  (page  920).  There  is  only  rarely,  however,  a  complete  transverse- 
destruction  of  the  spinal  cord  in  vertebral  caries.  The  conduction  of  sensory 
impressions,  at  least,  is  usually  not  wholly  abolished.  The  time  required  for  the 
development  of  the  symptoms  of  spinal  compression  differs  very  much.  They 
sometimes  attain  a  considerable  height  in  a  short  time,  and  sometimes  they  de- 
velop only  after  a  course  of  months.    Variations  in  the  intensity  of  the  symptoms. 


THE  PEESSUEE  PAEALYSES  OF  THE  SPINAL  COED   941 

are  frequent,  and  they  point  perhaps  to  a  corresponding  variation  in  the  severity 
of  the  compression. 

In  regard  to  the  result  of  pressure  paralyses  in  vertebral  caries,  spondylitic 
processes  without  doubt  can  recover,  which  is  by  no  means  in  contradiction  to 
their  character  as  a  local  tubercular  process.  In  this  connection  the  fact  is  of 
g-reat  practical  importance  that  even  the  pressure  paralyses  may  be  completely 
restored,  as  far  as  the  cause  of  the  compression  can  be  removed  by  the  absorption 
of  inflammatory  and  tubercular  new  growths,  so  that  a  complete  and  permanent 
recovery  may  take  place  even  after  the  paralysis  has  lasted  for  some  months,  or 
a  year,  or  even  a  year  and  a  half.  Such  recoveries  have  been  seen  in  a  consider- 
able number  of  cases  by  others  and  also  by  ourselves.  They  are  explained  in  part 
by  the  restoration  of  function  in  fibers  which  were  rendered  merely  incapable  of 
conduction  by  pressure,  but  not  completely  destroyed  (page  937),  and  in  part  per- 
haps in  old  eases  by  the  occurrence  of  regeneration.  Fickler  has  made  the  inter- 
esting observation  in  the  author's  clinique  that  the  ends  of  the  pyramidal  fibers  in 
the  lateral  tract  may  grow  out  above  an  old  compression,  pass  around  the  scar  of 
the  compression  through  the  anterior  fissure,  and  enter  the  cord  below  it  to  their 
anterior  horns. 

Although,  according  to  this,  the  prognosis  in  a  part  of  the  cases  of  pressure 
paralysis  from  spondylitis  is  comparatively  good,  still  many  other  cases  terminate 
unfavorably.  The  cause  lies  either  in  the  occurrence  of  dangerous  sequelae  of 
the  paralysis,  such  as  bed-sores,  cystitis,  or  pyelo-nephritis,  with  fever  and  in- 
creasing- general  weakness ;  or  in  the  development  of  other  tubercular  diseases, 
especially  phthisis,  or  more  rarely  miliary  tuberculosis  or  tubercular  meningitis, 
which  prove  fatal.  In  some  cases  there  is  a  stationary  paralytic  condition,  since 
the  vertebral  disease  recovers  and  sclerosis  ensues  in  the  cord,  which  is  capable 
of  no  further  change. 

2.  The  Pressure  Paralyses  in  Cancer  of  the  Vertebrae. — In  pressure  paralysis 
from  cancer  of  the  vertebrse,  which  is  not  very  rare,  the  spinal  affection  may 
seem  to  be  primary,  especially  when  the  primary  growth  (breast,  etc.)  has  not  up 
to  that  time  caused  any  very  striking  clinical  symptoms.  The  first  symptom  is 
usually  pain,  both  in  the  region  of  the  new  growth  and  radiating  in  neuralgic 
form.  The  pain  becomes  distressing  if  the  tumor  grows  about  and  compresses  the 
posterior  roots  ("paraplegia  dolorosa").  The  other  spinal  symptoms  are  pre- 
cisely analogous  to  those  in  compression  of  the  cord  by  vertebral  caries,  and 
therefore  they  need  not  be  described  again  in  detail.  Changes  in  the  shape  of 
the  vertebral  column  sometimes  occur,  but  we  only  rarely  find  a  characteristic 
angular  gibbus,  as  in  vertebral  tuberculosis.  The  general  cancerous  cachexia  is 
usually  soon  apparent.  The  course  is  in  general  more  rapid  than  in  caries.  The 
disease  rarely  lasts  more  than  nine  to  eighteen  months  before  its  invariably 
fatal  end. 

Diagnosis. — The  frequency  of  the  pressure  paralyses  of  the  spinal  cord  admon- 
ishes us  to  examine  the  vertebral  column  carefully  in  every  case  of  spinal  disease, 
especially  if  the  case  in  question  can  not  be  referred  to  one  of  the  special  types  of 
systemic  diseases  (vide  infra).  We  should  look  especially  for  the  stiffness  of  spe- 
cial parts  of  the  vertebral  column  on  movements  of  the  head  or  triink,  and  also  for 
the  pronounced  tenderness  of  single  vertebra?  to  pressure,  and,  finally,  as  a  most 
important  and  most  certain  sign,  for  the  deformity  of  the  vertebral  column,  the 
marked  projection  of  a  single  spinous  process,  or  the  formation  of  an  evident 
angular  kyphosis.  If  we  find  such  a  Pott's  boss  the  diagnosis  is  easy,  and  we  can 
then  at  any  rate  refer  the  existing  cord  symptoms  to  a  compression  of  the  cord 
caused  by  a  disease  of  the  vertebrse. 

The  diagnosis  is  more  difficult  if  the  signs  of  an  affection  of  the  vertebras  be 
not  evident.    It  must  once  for  all  be  stated  that  vertebral  caries  does  not  inva- 


942  DISEASES    OF   THE   NEEVOUS    SYSTEM 

riably  and  necessarily  result  in  a  manifest  knuckle,  and  that  even  the  tender- 
ness of  the  vertebrse  to  pressure  is  sometimes  very  slight  in  spondylitis.  In  such 
cases  the  examination  of  the  vertebral  column  must  be  repeated  frequently, 
since  even  slight  anomalies  obtain  a  diagnostic  value  if  constantly  present;  and 
the  whole  course  of  the  disease  is  also  to  be  considered.  The  most  characteristie 
features  of  a  compression  of  the  cord  are  its  beginning  with  symptoms  of  sensory 
irritation,  the  persistent  and  more  or  less  severe  pain  in  the  back,  the  preponder- 
ance of  symptoms  of  motor  paralysis  with  comparatively  little  disturbance  of  sen- 
sibility, and  finally  the  frequent  asymmetry  of  the  symptoms  on  the  two  sides, 
which  may  even  recall  the  type  of  the  so-called  "  unilateral  lesion  "  of  the  spinal 
cord  (vide  infra).  Sometimes  the  cause  of  the  spinal  symptoms  is  at  first  obscure, 
and  later  on  in  the  disease  a  marked  anomaly  of  the  vertebral  column  develops. 

If  the  diagnosis  of  an  ailection  of  the  vertebrae  be  certain,  the  next  question  i& 
as  to  the  nature  of  it,  especially  whether  we  have  to  do  with  a  spondylitis,  or  with 
a  cancer  of  the  vertebrse.  Since  spondylitis  is  by  far  the  more  frequent  disease, 
we  must  always  think  of  that  first,  especially  in  young  people  predisposed  to 
tuberculosis,  and  where  we  have  the  formation  of  a  pronounced  angular  kyphosis^ 
In  cancer  of  the  vertebrae  the  coarser  changes  in  the  form  of  the  vertebral  column 
are  generally  less  marked.  This  develops  usually  in  older  people,  after  the  age- 
of  forty,  and  is  manifested,  as  we  have  said,  by  the  great  intensity  of  the  initial 
symptoms  of  sensory  irritation.  The  discovery  of  a  primary  nodule  of  cancer  (in 
women  the  breasts  require  particular  examination)  and,  as  we  ourselves  have- 
seen,  the  appearance  of  a  cancerous  swelling  of  the  inguinal  lymph-glands,  may 
serve  to  support  the  diagnosis.  Finally,  a  certain  stress  is  to  be  laid  on  the  well- 
known  general  habit  of  patients  with  cancer,  on  the  peculiar  cancerous  cachexia, 
and  on  the  whole  course  of  the  disease. 

In  regard  to  the  distinction  between  caries  of  the  vertebrae  and  sarcoma  of  the- 
dura  mater,  see  the  chapter  on  tumors  of  the  spinal  cord. 

The  place  of  compression  is,  in  the  majority  of  cases,  to  be  recognized  by  the 
evident  localization  of  the  disease  of  the  vertebras.  In  other  respects  the  same 
rules  hold  for  localization  which  we  have  given  in  detail  in  the  second  chapter  of 
this  section  (page  920  et  seq.). 

Treatment. — In  regard  to  the  special  treatment  of  spondylitis,  especially  the 
orthopedic  treatment,  we  must  refer  to  the  text-books  of  surgery.  The  most 
benefit  is  to  be  expected  from  the  various  contrivances  for  extension  of  the  spinal 
column.  It  can  not  be  denied,  and  we  have  ourselves  several  times  seen,  that 
such  extension  sometimes  produces  a  decided  diminution  of  the  pressure  on  the- 
cord,  which  is  followed  by  a  remarkably  rapid  improvement  of  certain  symptoms 
of  paralysis.  Such  observations  are  strongly  in  favor  of  our  theory  that  the  ac- 
tion of  vertebral  caries  is  usually  purely  mechanical.  Very  often,  however,  we- 
have  had  to  admit  that  the  extension  apparatus  was  of  no  benefit  or  only  of  tempo- 
rary benefit,  or  that  it  even  materially  aggravated  the  patient's  distress.  In 
vertebral  caries  with  co-existing  spinal  symptoms  we  must  therefore  use  extension 
of  the  vertebrae,  plaster  jackets,  etc.,  with  caution.  Surgical  interference  to  re- 
move dislocated  vertebrae,  compressing  masses  of  pus,  etc.,  has  been  repeatedly 
tried  in  vertebral  caries,  sometimes  with  benefit,  but  often  without  success.  In 
most  cases  we  shall  be  limited  to  a  general  symptomatic  and  dietetic  treatment.. 
Persistent  rest  in  bed,  on  the  back,  is  of  the  greatest  importance,  and  it  must 
always  be  strongly  advised.  Several  eases  of  complete  recovery  from  severe  pres- 
sure paraplegia,  which  we  have  had  under  our  own  observation,  were  due  to  this 
alone.  The  most  careful  treatment  of  the  general  condition  (fresh  air,  good  food, 
cod-liver  oil,  arsenic,  iron,  etc.)  of  course  also  demands  attention.  We  have  seen 
very  unfavorable  action  from  Koch's  tuberculine.  Local  applications  to  the  verte- 
bral column  are  much  used — dry  cups,  painting  with  iodine,  and  especially  the  hot 


ACUTE   AND   CHEONIC   MYELITIS  94a 

iron.  The  use  of  the  Litter  in  spondylitis  has  even  to-day  warm  advocates,  and, 
in  fact,  deserves  to  be  tried,  the  procedure  with  Paquelin's  themio-cautery  being 
especially  easy;  we  make  some  three  or  four  eschars  on  each  side  of  the  diseased 
vertebrae. 

Among  other  remedies  we  may  mention  stabile  galvanization  at  the  point  of 
pressure,  and  the  electrical  treatment  of  the  paralyzed  extremities;  also  the  use 
of  baths,  especially  salt-baths.  In  regard  to  the  symptomatic  treatment,  we  will 
refer  to  the  following  chapter. 


CHAPTEE   Y 


ACUTE    AND    CHRONIC    MYELITIS 

( Transverse  Myelitis.     Diffuse  Myelitis) 

Definition  and  .etiology  of  Myelitis. — "  Myelitis  "  is  the  name  we  give  to 
those  inflammatory  degenerative  diseases  of  the  spinal  cord  which  develop  pri- 
marily in  the  substance  of  the  cord  itself  and  lead  to  a  more  or  less  extensive 
destruction  of  the  nervous  elements.  We  know  very  little  of  the  causes  of  these 
diseases,  and  of  the  precise  nature  and  manner  in  which  these  causes  exert  their 
morbid  influences.  The  name  of  myelitis  has  probably  been  used  up  to  the  pres- 
ent time  for  several  quite  distinct  morbid  processes,  since  it  is  often  by  no  means 
easy  to  recognize  the  precise  origin  of  the  anatomical  changes.  At  any  rate,  we 
must  recognize  this  uncertainty  in  the  definition  of  myelitis,  and  at  least  try  as 
much  as  possible  to  keep  separate  the  forms  which  surely  do  not  belong  in  the 
same  group.  Thus  we  have  said  expressly  in  the  previous  chapter  that  the  purely 
mechanical  traumatic  changes  in  the  spinal  cord  are  to  be  differentiated  from 
true  myelitis  and  that  the  inflammatory  processes  in  these  cases  are  at  most  sec- 
ondary. We  must  also  emphasize  the  fact  that  anaemic  necrosis  of  the  cord  from 
vascular  obstruction  (from  primary  endarteritis,  thrombosis,  or  embolism  of  the 
vessels)  does  not  seem  to  have  the  significance  in  the  cord  that  it  does  in  the 
brain,  but  that  we  must  always  bear  in  mind  the  possibility  of  its  occurrence,  and 
hold  firmly  to  the  fundamental  distinction  between  such  anfemic  softening  or 
infarction  and  primary  degenerative  inflammation.  It  is  very  difficult  to  deter- 
mine the  position  which  syphilis  holds  in  relation  to  the  deflnition  of  myelitis. 
The  distinction  is,  of  course,  easy  in  the  rare  cases  where  there  is  an  actual 
gumma  in  the  cord,  but  there  are  also  a  good  many  cases  of  apparently  genuine 
degenerative  myelitis  in  persons  who  have  previously  had  syphilis.  In  these  cases 
the  anatomical  findings  often  leave  us  in  the  lurch,  if  the  question  of  the  syphi- 
litic origin  of  the  disease  is  to  be  answered  with  certainty.  Even  in  cases  where 
this  origin  is  recognized,  the  way  in  which  the  syphilitic  agent  acts  is  still  utterly 
obscure.  Most  stress  is  generally  laid,  of  course,  upon  the  "  specific  syphilitic  " 
changes  in  the  blood-vessels ;  but  these  criteria  are  not  wholly  unequivocal  in 
their  nature,  and  the  question  of  the  mutual  relations  between  the  disease  of  the 
vessels  and  the  true  parenchymatous  changes  still  needs  further  discussion.  It 
is,  however,  of  great  practical  importance  to  know  that  syphilis  apparently  plays 
a  considerable  part  in  the  aetiology  of  the  spinal  disease  hitherto  classed  as  mye- 
litis. The  myelitis  of  the  upper  dorsal  cord,  which  runs  its  course  chiefly  under 
the  form  of  spastic  spinal  paralysis  (g.  v.),  seems  frequently  to  be  due  to  previous 
syphilis. 

We  can  call  only  those  processes  genuine  myelitis  in  Avhich  some  excitants  of 
inflammation  act  locally  upon  the  substance  of  the  spinal  cord  and  cause  diffiise 
inflammatory  degenerative  changes  therein.     Such  genuine  myelitides  are  decid- 


514  DISEASES    OF   THE   I^EEVOUS    SYSTEM 

edly  rare,  and  little  definite  is  yet  known  as  to  their  causes.  We  sometimes 
see  the  disease  develop  in  previously  healthy  persons,  who  are  ignorant  of  any 
special  harmful  influence  to  which  to  attribute  their  illness.  In  other  cases 
the  blame  is  laid  upon  exposure  to  cold,  repeated  wettings,  physical  over-exer- 
tion (such  as  military  maneuvers),  etc.  In  women,  the  first  symptoms  of  the 
disease  sometimes  follow  childbed.  These  alleged  causes,  however,  play  at 
most  the  part  of  an  exciting  cause.  It  is  wholly  out  of  the  question  that 
sexual  excesses,  as  was  formerly  believed,  can  of  themselves  lead  to  anatom- 
ical disease  of  the  spinal  cord;  the  same  is  true  of  severe  emotional  disturb- 
ances. 

We  may  assume  that  the  special  cause  of  true  acute  myelitis  is  in  all  proba- 
bility some  infectious  germ.  This  has  been  maintained  for  some  time  in  regard 
to  acute  poliomyelitis  (q.  v.)  ;  but  the  evidence  is  increasing  in  favor  of  the  infec- 
tious nature  of  acute  transverse  myelitis  also.  Thus  we  have  seen  a  case  follow, 
a  felon,  and  staphylococci  were  found  in  the  cerebro-spinal  fluid,  which  was  with- 
drawn by  lumbar  puncture.  Flirstner  found  pneumococci  in  the  foci  of  inflam- 
mation in  a  case  of  acute  disseminated  myelitis.  In  short,  it  is  probable  that  we 
shall  obtain  still  clearer  ideas  of  the  etiology  of  acute  myelitis  by  continued  in- 
vestigations. There  is  no  doubt  that  infectious  causes  are  to  be  considered  in  the 
rare  cases  of  purulent  inflammation  of  the  cord  (abscess  of  the  cord)  ;  the  same 
is  true  of  the  myelitides  following  acute  infectious  diseases  (typhoid  fever, 
small-pox,  erysipelas,  influenza,  malaria,  gonorrhoea,  etc.).  As  to  the  causes  of 
chronic  myelitis — that  is,  of  the  "  myelitic  "  transverse  diseases  of  the  cord 
which  are  chronic  from  the  outset — our  knowledge  is  the  more  uncertain  since 
it  is  very  hard  strictly  to  define  this  morbid  process.  We  will  return  to  this 
point  later. 

That  secondary  myelitis  may  arise  by  direct  extension  of  the  inflammatory 
process  from  the  vicinity  has  been  definitely  determined  only  in  acute  purulent 
meningitis  (especially  the  epidemic  cerebro-spinal  form)  and  tubercular  menin- 
gitis. In  the  other  cases  formerly  classed  under  this  heading,  we  have  to  do,  as 
has  repeatedly  been  said,  mainly  with  purely  mechanical  consequences.  The 
hypothesis  that  neuritic  processes  may  extend  to  the  cord  (ascending  neuritis) 
we  have  already  (page  886)  characterized  as  doubtful  and  practically  unim- 
portant. 

Pathological  Anatomy. — Macroscopic  examination  of  the  cord  in  its  fresh 
condition  shows  no  marked  pathological  changes  except  in  a  small  number  of 
cases.  At  the  first  glance,  the  spinal  cord  often  seems  almost  completely  nor- 
mal, even  if  there  have  been  severe  spinal  symptoms  during  life,  and  sometimes 
the  opacities  and  adhesions  of  the  pia,  which  often  strike  us  at  first,  have  no  prac- 
tical importance.  If  we  test  the  consistency  of  the  cord  carefully  by  toiiching  it, 
of  course  a  change  in  it  often  strikes  the  practiced  examiner,  since  the  cord  over  a 
definite  extent  is  either  softer  and  more  flexible,  or,  on  the  other  hand,  harder  and 
firmer,  than  normal.  If  we  now  make  a  number  of  cross-sections  through  the  cord, 
we  notice  that  the  substance  of  the  cord  rises  up  more  on  section,  that  the  outline 
of  the  gray  matter  is  less  distinct,  and  especially  that  the  white  matter  is  of  a 
reddish-gray  color,  and  that  sometimes  there  is  also  a  reddish,  hyperasmic  coloring 
of  the  gray  matter.  In  some  cases  we  can  recognize  small  capillary  haemorrhages 
with  the  naked  eye.  The  more  acute  the  disease  the  softer,  as  a  rule,  is  the  cord 
in  the  part  diseased  ("  acute  inflammatory  softening").  If  the  disease  is  chronic 
or  if  some  time  has  elapsed  since  the  expiration  of  the  acute  initial  stage,  the  cord 
in  the  diseased  spot  is  denser,  firmer,  and  sclerosed,  and  grayer  in  color  on  section, 
but  it  is  not  possible  to  determine  precisely  in  the  fresh  cord  the  extent  and  degree 
of  the  disease. 

The  changes  are  much  more  plainly  visible  if  we  harden  the  cord  in  chromic 


ACUTE   AND   CHRONIC   MYELITIS  945 

acid,  or  Miiller's  fluid,"  for  at  least  eight  or  teij  weeks.  All  the  normal  parts  of 
the  white  matter  of  the  cord  assume  -a  dark-green  color,  which  is  really  due  to  the 
staining  of  the  medullary  sheaths  by  the  chromic  acid.  The  diseased  portions,  in 
which  the  medullary  sheaths  are  mainly  if  not  entirely  absent,  are  thus  often 
very  sharply  distinguished  from  the  healthy,  dark-green  portions.  Since  similar, 
although  less  sharply  defined,  differences  in  color  between  healthy  and  diseased 
tissue  are  also  noticed  in  the  gray  matter,  the  cross-section  of  the  cord,  well 
hardened  in  chromic  acid,  usually  gives  quite  a  correct  idea  of  the  extent  of  the 
disease. 

We  obtain  more  precise  disclosures,  however,  as  to  the  form  of  the  anatomical 
changes  by  microscopical  examination.  When  made  on  the  fresh,  unhardened 
■cord,  it  affords  little  information.  The  presence  of  numerous  granular  cells  (vide 
infra)  in  fresh  teased-out  preparations  is  the  only  thing  that  is  important,  since 
they  show  with  certainty  the  existence  of  a  pathological  change.  If,  however,  we 
make  thin  cross-sections  of  the  hardened  cord,  and  stain  them  with  carmine  or 
some  similar  staining  fluid,  even  the  naked  eye  notices  at  once  a  marked  difference 
between  the  diseased  and  the  healthy  tissue,  since  the  former,  which  is  almost 
always  richer  in  connective  tissue,  has  a  much  darker  staining,  and  thus  is  dis- 
tinguished from  the  brighter  normal  tissue.  The  microscopic  examination  now 
shows  that  in  the  diseased  parts  the  normal  nerve-tissue  has  been  almost  wholly 
or  at  least  partly  destroyed.  Only  occasionally  do  we  see  nerve-fibers  of  normal 
appearance  remaining  here  and  there.  In  other  places  the  fibers  that  are  still 
visible  are  smaller  and  atrophied,  and  the  axis-cylinders  have  in  part  lost  their 
medullary  sheaths,  or  are  swollen.  The  changes  in  the  ganglion-cells  are  harder 
to  follow,  but  in  more  advanced  cases  they  also  show  marked  signs  of  destruction; 
they  are  contracted,  rounder,  and  have  lost  their  processes.  The  increase  of  the 
neuroglia  tissue  corresponds  to  the  destruction  of  the  nerve-substance.  The 
meshes  of  the  neuroglia  extend  and  swell,  so  that  the  space  formed  by  the  destruc- 
tion of  the  nerve-tissue  is  in  great  measure  taken  up  by  connective  tissue.  The 
older  the  process,  the  firmer  and  more  fibrous  is  the  connective  tissue.  The 
nuclei  of  the  neuroglia  increase  in  number,  and  we  often  find  a  very  great  increase 
in  those  peculiar,  flat  cells  with  many  processes,  first  described  by  Deiters,  and 
named  after  him — the  so-called  "  Deiters'  spider-cells."  The  fatty  granular  cells 
are  also  easily  recognized  in  hardened  preparations,  provided  they  are  not  treated 
with  alcohol.  They  lie  in  the  interstices  between  the  meshes  of  the  neuroglia, 
and  are  especially  numerous  about  the  vessels.  They  are  to  be  regarded  either  as 
white  blood-corpuscles,  or  perhaps  as  endothelial  cells  from  the  sheaths  of  the 
vessels,  which  have  taken  up  the  fat  from  the  disintegrated  nerve-substance.  If, 
therefore,  the  process  be  still  fresh,  or  if  it  be  still  advancing,  the  fatty  granular 
globules  are  to  be  met  with  in  great  numbers,  while  in  old,  sclerosed  nodules,  only 
a  few  of  them,  or  scarcely  any,  are  to  be  found.  The  changes  in  the  vessels  are 
usually  very  striking.  They  are  often  dilated  and  congested.  Here  and  there 
there  may  be  haemorrhages.  The  vascular  walls  are  thickened,  especially  in  old 
cases,  and  sometimes  have  become  peculiarly  homogeneous — "  hyaline  degenera- 
tion " ;  and  a  large  accumulation  of  nuclei,  lines  of  fatty  granular  cells  or  peculiar 
epithelioid  cells,  may  be  found  about  the  vessels.  The  so-called  corpora  amylacea 
are  sometimes  present  in  chronic  cases  in  great  numbers,  and  sometimes  they 
are  only  scanty.     Their  significance  and  their  genesis  are  still  unknown. 

The  extent  of  the  whole  process  varies  very  much  in  different  cases.  We  usu- 
ally find  one  main  focus  of  myelitis,  which  extends  in  a  diffuse  manner  over  the 
greatest  part  of  the  transverse  section  of  the  sjiinal  cord,  and  which  may  reach  up- 


[*  The  formula  for  Miiller's  fluid  is  as  follows  :  Two  and  a  half  parts  of  potassic  biohromate,  one 
part  of  sodic  sulphate,  and  oiiu  hundred  parts  of  water. — K.| 
60 


946  DISEASES    OF   THE   NERVOUS    SYSTEM 

ward  and  downward  for  a  space  of  five  to  ten  centimetres  or  more.  The  dorsal  por- 
tion of  the  cord  is  most  frequently  affected  (dorsal  myelitis),  the  upper  half  being- 
usually  most  involved,  but  in  some  cases  the  lower  half  is  chiefly  affected.. 
Nearly  the  whole  of  the  dorsal  cord  is  often  the  seat  of  a  diffuse  inflammatory 
affection,  which,  of  course,  differs  in  extent  at  different  levels.  In  other  much 
rarer  cases  the  chief  focus  of  disease  is  in  the  cervical  cord  (cervical  myelitis),, 
somewhat  more  frequently  in  the  lumbar  cord  (lumbar  myelitis).  We  often  find 
small,  distinct  foci  in  the  vicinity  of  the  main  focus.  In  all  severe  and  long-con- 
tinued cases  there  develops  later  a  systemic  ascending  and  descending  second- 
ary degeneration  (vide  infra). 

Acute  disseminated  myelitis  has  a  special  form  of  anatomical  distribution 
It  occurs  in  many  small  foci  which  may  extend  almost  throughout  the  whole  length, 
of  the  cord.  Individual  columns  of  the  cord,  especially  the  posterior  columns, 
are  often  chiefly  affected.  In  rare  cases,  as  has  already  been  said,  true  purulent' 
inflammation — that  is,  circumscribed  abscess  with  purulent  breaking  down  of 
tissue— has  also  been  observed. 

The  Individual  .Symptoms  of  Myelitis. — The  course  of  transverse  myelitis 
differs  so  much  in  different  cases  that  it  is  impossible  to  give  a  picture  of  the- 
disease  which  will  be  generally  applicable.  According  as  one  or  another  part  of 
the  cord  is  involved,  the  clinical  symptoms  will  relate  chiefly  to  the  sensibility  or 
the  motility,  the  trophic  functions  or  the  reflexes,  and  will  be  present  in  the  upper 
or  the  lower  extremities,  or  in  both  at  once.  The  following  description  will,  there- 
fore, be  devoted  first  to  the  single  symptoms,  and  will  give  the  inferences  which, 
according  to  the  present  state  of  our  knowledge,  may  be  drawn  from  their  pres- 
ence as  to  the  seat  and  the  extent  of  the  anatomical  process ;  not  until  then  will 
wo  endeavor  to  distinguish  the  different  clinical  forms  of  myelitis. 

1.  Symptoms  of  Motor  Paealysis  are  not  only  the  chief  symptoms,  as  a  rule,, 
in  well-developed  myelitis,  but  are  often  the  first  sign  of  the  beginning  of  the  dis- 
ease. The  patient  feels  at  first  only  a  slight  weakness  in  one  or  both  legs ;  he  gets- 
tired  more  easily  in  walking,  and  begins  to  "  drag  "  his  legs  after  him.  Sooner  or 
later  the  motor  weakness  gradually  becomes  greater  and  increases  to  complete 
paralysis.  The  patient  is  then  bed-ridden,  and,  finally,  can  not  make  the  least 
active  movement  with  his  legs.  The  symptoms  of  paralysis  in  the  arms  are- 
analogous. 

Since  the  chief  paths  for  the  conduction  of  voluntary  motion  are  situated,  as- 
we  have  seen,  in  the  lateral  columns  of  the  spinal  cord,  and  especially  in  the- 
lateral  pyramidal  tract,  we  conclude,  in  every  spinal  disease  where  symptoms  of 
paralysis  are  present,  that  there  is  an  interruption  of  this  tract — that  is,  an 
implication  of  the  posterior  portions  of  the  lateral  columns.  Since  in  transverse- 
myelitis  the  whole  cross-section  of  the  cord  is  more  or  less  involved,  the  paralysis 
also  extends  to  the  two  halves  of  the  body :  motor  paraplegia  is  the  characteristic 
form  of  paralysis  for  transverse  myelitis.  Paraplegia  of  the  lower  extremities 
may  of  course  arise  wherever  the  myelitis  is  situated,  whether  in  the  lumbar, 
dorsal,  or  cervical  region ;  but  the  upper  extremities  necessarily  remain  entirely 
free  in  every  dorsal  or  lumbar  myelitis.  The  occurrence  of  paretic  symptoms 
here,  and  the  final  development  of  a  brachial  paraplegia,  point  with  certainty  to 
an  implication  of  the  cervical  region,  to  a  cervical  myelitis.  If  the  symptoms  of 
paralysis  are  not  alike  in  the  two  corresponding  extremities,  but  are  more  marked 
on  one  side  than  on  the  other,  the  anatomical  affection  must  also  be  more  intense 
on  that  side  of  the  cord  than  on  the  opposite  side. 

2.  Symptoms  of  Motor  Irritation  of  various  sorts  are  often  seen,  both  at  the- 
beginning  and  during  the  whole  course  of  myelitis.  Single  twitchings  come  on 
spontaneously  in  the  limbs,  which  are  at  the  same  time  paralyzed,  or  at  least 
paretic,  and  these  twitchings  are  short  and  rapid  or  slow  and  persistent.     The- 


ACUTE   AND   CHRONIC   MYELITIS  947 

thighs  are  drawn  up  ou  the  abdomen,  or  there  are  severe  spasms  of  the  extensors. 
The  interpretation  of  these  symptoms  is  not  always  easy.  It  is  often  particularly 
hard  to  decide  whether  they  are  the  result  of  a  direct  irritation  of  motor  fibers 
in  the  cord,  or  whether  they  represent  reflexes  {vide  infra).  The  value  of  the 
symptoms  of  motor  irritation  for  the  localization  of*  the  disease  is  accordingly 
slight,  but,  of  course,  in  these  cases  we  must  consider  chiefly  the  motor  tracts  in 
the  lateral  columns. 

3.  Ataxia. — There  can  be  no  doubt  that  actual  ataxia  also  occurs  in  transverse 
myelitis,  but  it  is  rarely  pronounced  because  the  co-existing  spastic  or  paralytic 
symptoms,  which  are  almost  always  present,  of  course  conceal  the  ataxia.  We 
therefore  see  evident  ataxic  disturbances  rather  in  slow  cases  which  do  not 
speedily  become  paraplegic,  or  sometimes  not  until  the  disease  improves.  In  re- 
gard to  the  localization  of  the  disease,  we  may  usually  conclude,  when  there  is 
ataxia,  that  the  posterior  columns  are  involved.  Very  marked  ataxia  of  the 
arms  and  legs  occurs  in  the  acute  disseminated  myelitis  of  the  posterior 
columns. 

4.  Disturbances  of  Sensibility. — The  disturbances  of  sensibility  usually  ap- 
pear to  a  marked  degree  only  in  the  later  stages  of  the  disease.  At  the  outset  we 
generally  notice  merely  mild  symptoms  of  sensory  irritation  in  the  legs,  such  as 
formication,  prickling,  numbness,  a  woolly  feeling,  etc.,  while  severe  pain  is  hardly 
ever  present  in  transverse  myelitis,  and  hence  it  always  points  rather  to  some 
affection  of  the  vertebrae  or  the  meninges.  In  very  acute  myelitis  there  may  be 
at  first  a  severe  local  pain  in  the  back.  Slight  diminution  of  sensibility  is  often 
to  be  made  out  early  on  careful  examination,  but,  in  many  cases,  the  sensibility 
remains  for  a  long  time  wholly,  or  almost  wholly,  intact,  either  because  the  locali- 
zation of  the  disease  spares  the  sensory  portions  of  the  cord,  or  because  the  sen- 
sory paths  of  conduction  are  more  resistant,  or  they  can  act  vicariously  for  one  an- 
other to  a  higher  degree.  The  more  carefully  we  examine,  the  earlier  shall  we  be 
able  as  a  rule  to  find  at  least  partial  disturbances  of  sensibility.  The  examination 
of  the  sensibility  to  temperature,  especially,  should  never  be  neglected.  Partial 
anaesthesia  of  the  pressure  sense,  analgesia,  etc.,  also  occur.  We  must  also  pay 
attention  to  the  not  uncommon  delayed  sensibility  to  pain  (page  793).  In  the 
further  course  of  the  disease,  however,  there  are  almost  always  more  marked  dis- 
turbances of  sensibility,  and  finally  frequently  a  complete  angesthesia.  On  the 
other  hand,  we  see  in  many  cases  a  striking  hyperaesthesia  to  painful  stimuli,  such 
as  a  pin-prick. 

From  the  presence  of  marked  disturbances  of  sensibility  we  can  conclude  with 

certainty  that  there  is  an  affection  of  the  posterior  cokunns,  and  especially  of  the 

posterior  cornua  of  the  gray  matter.     With  marked  analgesia  and  thermo-anaes- 

thesia  the  latter  are  always  involved.     Disease  of  the  lateral  columns  also  may 

'probably  cause  disturbances  of  sensibility  (page  799). 

The  disturbance  of  sensibility  gives  important  service  in  estimating  the  height 
at  which  the  affection  in  the  cord  is  situated.  If  we  search  on  the  trunk  for  the 
line  where  the  cutaneous  sensibility  becomes  normal,  we  may  from  this  determine 
the  upper  boundary  of  the  myelitis  in  accordance  with  the  data  furnished  on 
page  924;  but  since  each  cutaneous  region,  as  has  been  said,  is  supplied  with 
sensory  fibers  from  at  least  two  or  three  spinal  segments,  we  must  look  for  the 
upper  boundary  of  the  disease  not  simply  in  the  segment  corresponding  to  the 
upper  boundary  of  the  anaesthetic  area,  but  one  or  two  segments  higher.  In 
myelitis  in  the  lumbar  region  the  disturbance  of  sensibility  reaches  to  the 
umbilicus,  or  even  a  little  higher ;  in  myelitis  in  the  lower  dorsal  region  it  reaches 
about  to  the  lower  end  of  the  sternum;  in  myelitis  in  the  upper  dorsal  region  to 
the  level  of  the  axillae;  and  in  cervical  myelitis  the  sensibility  of  the  upper  ex- 
tremities is  also  impaired,  but  complete  anaesthesia  is  very  rare. 


948  DISEASES    OF    THE   NEEYOUS    SYSTEM 

5.  Cutaneous  Eeflexes.— As  is  generally  assumed,  the  reflex  arcs  in  the  cord 
are  found  at  about  the  same  level  as  the  centripetal  sensory  and  the  centrifugal 
motor  fibers.  They  are  also  connected  with  fibers  which  come  from  above  and 
have  properties  of  reflex  inhibition.  If  these  fibers  above  the  reflex  arc  are  put 
into  a  state  of  irritation,  the  reflex  is  thereby  impaired;  but  if  the  conduction 
be  broken  in  these  fibers,  the  reflex  activity  appears  increased,  the  reflex  comes  on 
with  a  weaker  irritation,  and  the  contraction  is  more  vigorous.  If  the  reflex  arc 
itself  be  broken  at  any  point,  the  reflex  must  disappear. 

The  data  from  the  examination  of  the  patient  may  generally  be  harmonized 
with  this  scheme,  although,  of  course,  the  reality  probably  shows  more  compli- 
cated conditions.  In  extensive  lumbar  myelitis,  by  which  the  reflex  path  in  the 
lumbar  cord  is  broken,  the  cutaneous  reflexes  in  the  lower  extremities  must  be 
diminished  or  absent.  In  these  cases  the  loss  of  sensibility  runs  about  parallel 
to  the  diminution  of  the  reflexes.  In  dorsal  and  cervical  myelitis,  however,  the 
reflex  arc  in  the  lumbar  cord  remains  unimpaired,  but  the  conduction  of  sensory 
impressions  to  the  brain  may  very  well  be  interrupted.  In  these  cases  the  cutane- 
ous reflexes  are  retained,  even  when  there  is  ansesthesia ;  or,  if  the  reflex  inhibitory 
influences  be  removed,  they  are  decidedly  increased.  [There  is  often  dorsal  ex- 
tension of  the  great  toe  on  irritating  the  sole  of  the  foot — ^the  Babinski  reflex. 
— K.]  The  cutaneous  reflexes  in  the  legs,  however,  may  also  be  diminished  or 
delayed  in  myelitis  of  the  lower  dorsal  cord,  in  which  case  we  must  imagine  as 
a  rule  a  secondary  loss  of  excitability  of  the  fibers  and  cells  presiding  over  the 
refiex,  or  perhaps  an  irritation  of  inhibitory  fibers.  It  is  often  important  in 
determining  the  seat  of  myelitis  to  examine  the  cremaster  reflex,  the  abdominal 
reflex,  etc.  If  the  reflex  paths  described  above  (page  927)  be  interrupted,  the 
reflexes  of  course  must  be  absent. 

6.  Tendon  Reflexes. — The  same  rules  generally  hold  in  judging  of  the  ten- 
don reflexes  as  are  to  be  considered  in  judging  of  the  condition  of  the  cutaneous 
reflexes.  We  know  that  the  reflex  arc  of  the  patellar  reflex  is  at  the  level  of  the 
second  to  the  fourth  lumbar  segments  (page  927).  If  the  entrance  zones  of  the 
posterior  sensory  roots  or  the  ganglion-cells  in  the  anterior  horns  be  diseased  at 
this  level,  the  patellar  reflex  must  disappear.  The  Achilles  tendon  reflex  and  the 
ankle  clonus  have  their  reflex  arcs  in  the  sacral  segments  of  the  cord.  The  Achilles 
tendon  reflex  is  always  absent  in  extensive  disease  of  the  posterior  columns  and 
of  the  gray  matter  in  the  corresponding  portion  of  the  lumbar  cord.  The  absence 
of  the  tendon  reflexes  in  the  lower  extremities  is  therefore  one  of  the  most  impor- 
tant points  besides  the  other  symptoms  for  the  diagnosis  of  a  myelitis  of  the  lum- 
bar cord.  In  almost  all  inflammations  above  the  lumbar  cord — that  is,  in  dorsal 
and  cervical  myelitis — there  is,  however,  a  very  decided  increase  of  the  tendon 
reflexes,  the  result,  as  we  must  suppose,  of  the  loss  of  the  reflex  inhibitory  influ- 
ences. We  have  much  reason  to  assume  that  the  fibers  which  influence  the  condi- 
tion of  the  tendon  reflexes  run  chiefly  in  the  lateral  columns  (pyramidal  tract)  of 
the  spinal  cord,  but  that  they  are  not  identical  with  the  fibers  of  the  lateral  pyram- 
idal tracts  which  serve  for  voluntary  motion  (see  the  chapter  on  spastic  spinal 
paralysis).  We  may  therefore  assert  that,  with  a  considerable  increase  of  the  ten- 
don reflexes  in  the  lower  extremities,  the  seat  of  the  myelitis  must  be  above  the 
lumbar  cord — that  is,  in  the  cervical  or  dorsal  cord — and  that  in  these  cases  we 
have  to  suppose  that  the  lateral  columns  are  chiefly  implicated.  In  cervical 
myelitis  the  tendon  reflexes  in  the  upper  extremities  are  often  considerably  in- 
creased. 

We' have  already  said,  on  page  840  et  seq.,  what  is  necessary  in  regard  to  the 
different  signs  of  the  increased  tendon  reflexes,  the  exaggerated  patellar  reflex, 
ankle  clonus,  the  periosteal  reflexes,  etc.  The  peculiar  character  which  the 
paralysis  of  the  legs  assumes  from  a  considerable  simultaneous  increase  of  the 


ACUTE   AND   CHEONIC   MYELITIS  949 

tendon  reflexes  (spastic  paraplegia)  will  be  described  more  fully  in  the  chapter 
on  "  spastic  spinal  paralysis  "  {vide  infra). 

7.  Disturbances  in  the  Bladder  and  Rectum. — Disturbances  in  micturition 
are  one  of  the  commonest  symptoms  of  myelitis.  The  first  manifestation  is  usu- 
ally a  difficulty  in  micturition ;  the  patient  has  to  strain  and  to  wait  longer  before 
urinating.  There  may  finally  be  a  complete  retention  of  urine  from  paralysis  of 
the  detrusor  urinas.  In  the  later  stages  of  the  disease,  however,  there  is  usually  a 
paralysis  of  the  sphincter  vesicae,  and  consequently  more  frequent  desire  to 
micturate,  and  finally  incontinence  of  urine.  The  disturbances  of  the  bladder 
give  no  points  for  the  localization  of  myelitis,  since  they  may  occur  with  disease 
at  any  level  of  the  spinal  cord ;  but  we  believe  we  are  right  in  assuming  that  they 
always  permit  us  to  decide  that  the  posterior  columns  of  the  cord  are  involved. 

The  clinical  significance  of  disturbances  of  the  bladder  in  myelitis,  and  in 
many  other  diseases  of  the  cord,  apart  from  the  great  distress  and  discomfort  for 
the  patient,  lies  in  the  fact  that  they  very  often — almost  always  in  severe  cases — 
give  rise  to  the  development  of  cystitis.  In  retention  of  urine  the  use  of  the 
catheter,  by  which  infiammatory  irritants  are  often  brought  into  the  bladder,  in 
spite  of  all  attempts  at  disinfection,  leads  to  decomposition  of  the  urine  and  to 
cystitis ;  but  where  there  is  also  incontinence,  the  imperfect  closure  of  the  sphinc- 
ter and  the  constant  presence  of  stagnating  and  decomposing  urine  in  the  urethra 
are  the  causes  of  the  entrance  of  these  irritants  into  the  bladder.  If  cystitis  have 
developed,  it  may  be  followed  under  some  circumstances  by  pyelitis  and  purulent 
pyelo-nephritis  (q.  v.),  which  conditions  are  often  the  immediate  cause  of  death 
from  the  sequelae  connected  with  them,  such  as  fever — sometimes  associated 
with  chills — general  weakness,  and  emaciation. 

Defecation  is  also  disturbed  in  many  cases  of  myelitis.  There  is  usually  con- 
stipation at  first,  which  may  depend  either  upon  weakness  of  the  intestinal  peri- 
stalsis, or  upon  paresis  of  the  abdominal  muscles.  Sometimes  the  constipation 
reaches  such  a  degree  that  the  bowels  move  only  at  intervals  of  one  or  two  weeks. 
In  many  severe  cases  there  is  finally  incontinence  of  faeces,  as  a  result  of  paralysis 
of  the  sphincter  ani.  We  can  give  no  details  as  to  the  localization  of  the  nerve- 
tracts  in  the  cord  which  take  part  in  defecation. 

We  have  yet  to  note  that  micturition  and  defecation  are  often  aroused  reflexly 
in  an  abnormal  fashion  where  there  is  increased  reflex  irritability.  On  irritation 
of  the  skin  over  the  thighs,  the  perineum,  the  gluteal  region,  etc.,  there  is  often  an 
involuntary  contraction  of  the  bladder,  associated  with  loss  of  urine. 

In  conclusion,  we  may  mention,  as  an  addendum,  that  the  sexual  functions  are 
often  considerably  disturbed  in  many  cases  of  myelitis,  and  finally  they  may  be 
wholly  lost. 

8.  Trophic  Disturbances.- — The  trophic  condition  of  the  paralyzed  muscles 
affords  extremely  important  points  for  diagnosis.  In  cervical  and  dorsal  myelitis 
the  trophic  centers  in  the  lumbar  cord  for  the  muscles  of  the  legs  remain  intact; 
the  paralyzed  muscles,  therefore,  retain  essentially  their  normal  volume,  and  espe- 
cially their  normal  electrical  excitability.  Even  in  such  cases  the  muscles  are 
sometimes  flabbier  and  of  less  girth  than  under  normal  conditions,  but  this 
depends  partly  on  the  decline  in  the  general  nutrition,  and  partly  perhaps  on  the 
lack  of  movement,  the  "  atrophy  of  inactivity."  Only  occasionally  do  we  find 
more  marked  muscular  atrophy,  but  without  reaction  of  degeneration ;  but  if 
we  find  in  myelitis  a  marked  atrophy,  with  reaction  of  degeneration  in  the  muscles 
of  the  lower  extremities,  we  can  from  this  draw  a  definite  conclusion  that  the 
anterior  gray  cornua  or  the  fibers  of  the  anterior  roots  in  the  lumbar  cord  are 
affected  (see  page  851).  In  an  analogous  fashion  degenerative  atrophy  with 
reaction  of  degeneration  in  the  muscles  of  the  upper  extremities  points  to  an 
affection  of  the  anterior  gray  matter  in  the  cervical  cord. 


950  DISEASES    OF   THE   NEEVOUS    SYSTEM 

Trophic  disturbances  in  the  6kin  are  also  frequent.  We  often  find  the  skin 
dry,  hard,  with  a  scaly  epidermis,  and  the  nails  thickened  and  brittle.  Excep- 
tionally there  are  eruptions  of  herpes,  urticaria,  etc.  Vaso-motor  disturbances 
also  occur.  Sometimes  the  paralyzed  extremities  show  a  mottled,  cyanotic  redden- 
ing, and  feel  cold.  Slight  cedema  is  quite  frequently  present  in  the  paralyzed 
parts.  Disturbances  of  the  sweat  secretion  are  not  infrequent.  We  find  either 
that  it  is  absent  or  that  there  is  a  great  increase  in  it,  so  that  the  paralyzed  parts 
are  constantly  moist.  All  these  symptoms  have  no  value  at  present  for  the  special 
topical  diagnosis. 

The  frequent  occurrence  of  bed-sores  in  the  sacral  region,  over  the  glutsei,  or 
more  rarely  over  the  trochanters  on  the  feet  or  the  inner  side  of  the  knees,  is  of 
great  practical  importance.  Although  trophic  and  vaso-motor  influences  may  play 
a  part  in  their  origin,  still  their  ultimate  cause  is  always  to  be  found  in  external 
conditions,  pressure,  uncleanliness,  etc.  The  more  faulty  the  care  of  the  patient 
is,  the  easier  bed-sores  arise.  With  completely  paralyzed  and  anaesthetic  patients, 
with  incontinence  of  urine  and  fseces,  of  course  they  sometimes  can  not  be  wholly 
and  permanently  avoided,  even  with  the  most  careful  management.  The  extent 
which  a  bed-sore  may  reach  is  sometimes  absolutely  frightful.  A  large  part  of 
the  sacrum  may  be  laid  bare,  after  the  overlying  soft  parts  and  the  periosteum 
have  become  gangrenous  and  been  thrown  off. 

9.  Disturbances  in  the  Region  of  the  Cerebral  Nerves  are  entirely  absent 
in  most  cases  of  transverse  myelitis.  In  rare  cases  of  cervical  myelitis  the  pro- 
cess may  gradually  extend  upward  and  give  rise  to  bulbar  symptoms.  We  some- 
times see  changes  in  the  pupils  in  cervical  myelitis,  such  as  inequality  and  spinal 
myosis;  and  finally  myelitis  has  been  repeatedly  combined  with  an  optic  neuritis. 
In  general,  however,  any  co-existing  cerebral  symptoms  always  require  a  special 
explanation.  They  are  either  co-existent  from  the  same  cause  (for  example, 
syphilis),  or,  instead  of  an  ordinary  transverse  myelitis,  there  is  multiple  scle- 
rosis, or  some  other  disease. 

Different  Forms  of  Myelitis.  Acute  and  Chronic  Myelitis. — The  whole  pic- 
ture of  transverse  myelitis  in  its  different  forms  may  be  constructed  from  the 
symptoms  described  in  detail  in  the  preceding  paragraphs.  We  can  usually 
determine  without  difficulty,  at  least  approximately,  the  seat  and  extent 
of  the  disease.  If  we  group  the  chief  symptoms  of  the  different  forms  of  mye- 
litis together,  according  to  the  location  of  the  disease  in  the  cord,  they  are 
as  follows : 

Cervical  Myelitis. — Paraplegia  of  the  legs,  combined  with  more  or  less  ex- 
tensive disturbances  in  the  upper  extremities,  and  eventually  distiirbances  of 
sensibility  over  a  like  extent.  At  times  atrophy  of  single  muscular  regions  in  the 
arms.  No  marked  atrophy  in  the  legs.  Increased  tendon  reflexes  and  spastic 
symptoms  in  the  legs  and  often  in  the  arms.  Cutaneous  reflexes  in  the  legs  re- 
tained, and  sometimes  even  increased.  Disturbances  of  the  bladder  and  rectum. 
Sometimes  changes  in  the  pupils. 

Dorsal  Myelitis. — Upper  extremities  free.  Motor,  and  eventually  sensory, 
paraplegia  of  the  legs,  without  degenerative  atrophy.  Increased  tendon  reflexes 
and  pronounced  spastic  symptoms  in  the  legs  (especially  in  myelitis  in  the  upper 
dorsal  cord) ;  cutaneous  reflexes  retained,  sometimes  increased.  Disturbances 
of  the  bladder  and  rectum. 

Lumhar  Myelitis. — Upper  extremities  free.  Motor,  and  eventually  sensory, 
paraplegia  of  the  legs.  Cutaneous  and  tendon  reflexes  in  the  legs  diminished  or 
absent.  Under  some  circumstances  degenerative  muscular  atrophy  in  the  legs 
with  reaction  of  degeneration.  Disturbances  of  the  bladder  and  rectum.  In 
myelitis  of  the  lower  sacral  cord  the  paralysis  is  confined  chiefly  to  the  distribu- 
tion of  the  sciatics  and  the  bladder  and  rectum.    The  disturbance  of  sensation  is 


ACUTE   A^D   CHRONIC   MYELITIS  951 

found  on  the  posterior  aspect  of  the  thighs,  the  buttocks,  and  the  genitals  (page 
925). 

The  above  division  of  the  different  forms  of  myelitis  refers  only  to  the 
different  locations  of  the  disease  and  the  difference  in  symptoms  thereby  pro- 
duced, so  that  we  must  further  discuss  the  division  of  myelitis  into  an  acute 
and  a  chronic  form.  This  division  is  made  solely  by  observing  the  course  of  the 
disease,  or  from  the  statements  in  the  history  of  the  ease  as  to  duration;  but 
we  must  bear  in  mind  that  this  refers  only  to  the  iirst  stage  of  the  disease,  to 
the  rapidity  with  which  the  myelitic  symptoms  develop  at  the  start.  In  most  cases 
of  genuine  primary  myelitis  the  myelitic  symptoms  come  on  very  suddenly,  lead  in 
a  very  short  time  (sometimes  in  a  few  days  or  a  few  weeks)  to  the  most  complete 
paralysis  (paraplegia,  vesical  paralysis,  anaesthesia,  bed-sores,  etc.),  and  advance 
irresistibly,  causing  death  in  a  short  time  (from  four  to  twelve  weeks).  Such 
cases  are,  of  course,  called  acute  transverse  myelitis.  We  sometimes  see,  how- 
ever, the  disease  beginning  acutely,  and  rapidly  developing  a  more  or  less  com- 
plete paraplegia,  which  after  some  time  remains  entirely  stationary,  or  at  least 
shows  only  extremely  slight  further  changes.  Such  cases  must  also  be  classed 
definitely  as  acute  myelitis,  although  they  present  later  a  chronic  type  of  spinal 
disease,  which  sometimes  lasts  for  many  years ;  but  they  are  also  undoubtedly  cases 
of  acute  myelitis,  ending  in  relative  recovery — that  is,  in  recovery  with  a  scar  or 
defect  in  the  cord.  We  can  call  only  those  cases  actual  chronic  myelitis  which 
are  chronic  from  the  first — that  is,  which  begin  slowly  and  progress  gradually — 
but  such  forms  of  actual  chronic  myelitis  are  very  rare,  for  the  not  very  rare 
-cases  which  seem  to  belong  under  this  heading  during  life  usu:dly  prove  at  the 
autopsy,  at  least  as  far  as  our  experience  goes,  to  be  something  different — multiple 
sclerosis,  tumor,  combined  columnar  or  systemic  disease,  etc.  We  might  rather 
speak  of  chronic  myelitis  in  those  cases  which  have  an  acute  initial  stage,  and 
then  take  later  a  chronic  progressive  course.  At  any  rate,  in  our  definition  of 
■chronic  myelitis  we  must  pay  especial  attention  to  the  clinical  course  and  an 
accurate  history,  for  the  pathological  lesions  alone  can  not  be  conclusive.  The 
pathologist  can  not  determine  whether  a  given  transverse  sclerosis  of  the  cord 
is  the  result  of  a  process  chronic  from  the  first  or  of  a  long-past  acute  process. 

We  can  not  give  at  present  a  definite  picture  of  acute  disseminated  myelitis. 
We  would  be  most  ready  to  suspect  this  form  of  myelitis  if  an  acute  type  of 
spinal  disease  developed  apparently  primarily  or  especially  as  a  sequel  of  some 
previous  acute  infectious  disease,  and  if  it  indicated  an  isolated  or  combined 
columnar  affection  rather  than  a  transverse  affection.  Acute  ataxia  with  loss  of 
tendon  reflexes  and  evident  vesical  disturbances,  or  a  combination  of  ataxia  with 
paresis  and  spastic  symptoms,  have  been  most  frequently  observed. 

Recovery  from  acute  myelitis  is  perhaps  not  impossible,  but  it  is  certainly 
very  rare.  We  know  of  no  case  that  recovered  completely  where  the  diagnosis 
could  be  made  with  certainty.  The  cases  reported  where  a  recovery  is  claimed 
are  usually  cases  of  pressure  paralysis,  multiple  neuritis,  poliomyelitis,  etc. 
We  may  speak  somewhat  more  frequently  of  relative  recovery  if  the  severe  initial 
symptoms  subside  in  part  and  change  to  a  mild,  stationary,  morbid  state.  The 
fatal  termination  of  acute  or  chronic  myelitis  is  the  result  of  the  general  weak- 
ness which  finally  sets  in ;  or  it  comes  from  cystitis  or  pyelo-nephritis,  both  of 
which  arc  often  combined  with  pya^mic  conditions;  or  from  extensive  bed-sores; 
or  finally  from  some  complication,  such  as  tuberculosis  or  acute  diseases. 

Diagnosis. — The  diagnosis  of  diffuse  transverse  myelitis  is  always  made  by 
considering  the  whole  group  of  symptoms  prominent  in  the  individual  case.  The 
possibility  of  a  compression  of  the  cord  must  be  exchided  by  a  careful  examina- 
tion of  the  vertebral  column,  and  by  consideration  of  the  course  of  the  disease. 
We  must  also  be  sure  that  the  existing  symptoms  do  not  correspond  to  a  definite 


952  DISEASES    OF   THE   NEEVOUS    gYSTEM 

typical  disease,  or  a  systemic  disease,  but  that  they  can  agree  only  with  the 
assumption  of  a  diffuse  transverse  disease  at  a  certain  point  in  the  cord,  to  be 
made  out  accurately  according  to  the  symptoms.  The  further  decision,  as  to- 
whether  this  diffuse  transverse  disease  is  a  myelitis,  may  be  made  quite  positively 
in  acute  cases  or  cases  beginning  acutely,  but  in  cases  chronic  from  the  outset 
it  can  hardly  ever  be  made  definitely,  for  precisely  the  same  type  of  disease  may 
sometimes  be  produced  by  multiple  sclerosis  (q.  v.),  by  new  growths  in  the  cord 
(glioma),  and  finally  by  combined  systemic  disease.  In  the  description  of  all 
these  diseases  we  will  once  more  return  to  the  likeness  sometimes  observed  be- 
tween them  and  transverse  chronic  myelitis. 

Treatment. — Although  our  therapeutic  endeavors  are  rarely  crowned  with  per- 
manent and  complete  success,  still  in  many  cases  we  can  relieve  the  suffering  and 
delay  the  end. 

We  can  try  to  meet  the  causal  indication  in  cases  where  the  history  or  the 
examination  shows  evidence  of  the  existence  of  previous  syphilis  (page  943). 
Even  if  the  connection  between  previous  syphilis  and  myelitis  can  not  be  as- 
sumed with  absolute  certainty — and  usually  it  can  not — still  we  must  always  try 
inunction  thoroughly,  using  half  a  drachm  to  a  drachm  (grammes  3-5)  of  mer- 
curial ointment  a  day.  We  give  twenty  to  thirty  grains  (grammes  1.5-2.0)  of 
iodide  of  potassium  daily  at  the  same  time.  We  sometimes  see  decided  improve- 
ment from  this ;  but  in  some  eases,  of  course,  the  result  is  uncertain,  or  the  treat- 
ment seems  to  exert  even  an  unfavorable  influence  upon  the  disease.  In  the 
latter  case  we  must  stop  it  at  once. 

Of  the  other  methods  of  treatment  the  chief  are  electricity,  baths,  and  cold- 
water  cures.  We  alternate  these.  ISTew  attempts  at  cure  raise  the  patient's  cour- 
age and  hope  afresh. 

Electricity  may  give  symptomatic  improvement  in  many  cases,  but  of  course 
it  causes  recovery  only  exceptionally,  at  most.  In  severe  and  hopeless  cases,  how- 
ever, it  is  at  least  the  best  means  of  consoling  the  patient.  The  constant  current 
has  the  greatest  therapeutic  value.  We  use  large  electrodes  placed  on  the  verte- 
bral column,  and  pass  not  too  strong  a  stabile  or  slowly  labile  current  through  the 
cord  for  about  four  or  five  minutes,  chiefly  through  the  region  where  we  suppose 
the  seat  of  the  disease  to  be.  We  usually  take  the  ascending  current,  and  alter- 
nate with  the  two  poles  on  the  diseased  part.  We  should  avoid  reversals  and  great 
variations  in  the  strength  of  the  current.  We  associate  with  this  peripheral  gal- 
vanization, and  often  faradization  of  the  muscles  and  nerves  of  the  paralyzed  ex- 
tremities. Single  symptoms  sometimes  deserve  special  attention — faradization  of 
the  skin  in  anaesthesia,  galvanization  of  the  bladder  in  vesical  weakness,  etc.  The 
sittings  should  take  place  daily  or  every  other  day.  If  we  would  be  successful,  the 
treatment  must  be  kept  up  persistently  for  months. 

The  treatment  of  myelitis  by  baths,  if  prudently  used,  may  also  be  of  evident 
service.  Even  simple  tub-baths,  such  as  can  be  had  in  almost  every  household, 
do  good  service  under  some  circumstances.  The  chief  rules  are  never  to  make  the 
baths  too  warm — about  88°  or  95°  at  most  (25°-28°  R.) — to  limit  them  at  first  to 
ten  or  fifteen  minutes,  and  to  give  them  at  first  not  oftener  than  three  or  four 
times  a  week.  Sometimes  hot  baths  (95°-100°  F.  [28°-30°  R.]  or  more)  seem 
to  act  well,  but  in  other  cases  they  certainly  are  injurious.  If  the  baths  are  well 
borne,  they  may  be  employed  daily.  We  should  be  most  cautious  in  incipient  and 
still  advancing  cases.  The  best  action  of  the  simple  warm  bath  is  seen  in  chronic 
myelitis  with  predominant  spastic  symptoms.  In  these  cases  the  duration  of  the 
baths  may  be  increased  to  an  hour  or  more.  Sometimes  the  bnths  work  still 
better  when  certain  substances  are  added,  especially  if  we  use  salt-baths,  which 
are  made  by  the  addition  of  five  or  ten  pounds  of  common  salt  (Stassfurt  salt), 
or  four  to  six  pounds  of  brine  salt,  or  one  to  three  quarts  of  brine  to  the  water. 


ACUTE   AND    CHKONIC   MYELITIS  953 

By  introducing  carbonic  acid  into  the  water  through  a  perforated  tube  in  the  floor 
of  the  tub  we  can  easily  make  artificial  carbonic-acid  salt  baths. 

If  we  can  send  patients  in  easy  circumstances  to  a  health-resort,  the  carbonic- 
acid  thermal  salt  springs  at  Oeynhausen  and  Nauheim  are  most  suitable  for  this 
purpose,  also  the  baths  at  Kissingen,  Wiesbaden,  and  Baden-Baden,  the  thermal 
baths  of  Ragatz,  Teplitz,  Wildbad,  and  Gastein,  the  mnd-baths  in  Elster,  Marien- 
bad,  etc. 

A  methodical  cold-water  treatment  sometimes  gives  quite  good  results;  but  in 
these  cases  we  should  wholly  avoid  all  the  more  heroic  treatments,  such  as  douches, 
violent  rubbing,  and  very  cold  baths,  and  employ  only  short,  cool,  full  or  half 
baths  or  packs  or  mild  cold  sponging.  Hydro  therapeutics  are  usually  combined 
with  electricity. 

We  can  expect  but  little  success  from  internal  treatment,  but  it  can  not  be 
dispensed  with  in  practice.  A  trial  of  strychnine  (subcutaneously  or  by  the 
mouth)  is  most  to  be  recommended,  and  also  ergotine,  nitrate  of  silver,  and  espe- 
cially iodide  of  potassium.    Salicylate  of  sodium  may  be  tried  in  fresh  acute  cases. 

The  general  hygienic  and  symptomatic  treatment  is  very  important.  If  the 
first  symptoms  of  a  beginning  spinal  disease  show  themselves,  we  should  urgently 
advise  the  patient  to  take  the  best  possible  care  of  himself  (avoiding  all  physical 
Gver-exertion),  and  to  enjoy  mental  rest.  The  diet  should  be  strengthening  but 
easily  digestible.  Large  amounts  of  spirits,  much  smoking,  much  tea  and  coffee, 
etc.,  are  to  be  avoided.  If  the  patient  becomes  bedridden,  we  must  employ  the 
utmost  care  to  get  a  good  bed  in  order  to  guard  against  bed-sores.  In  severe 
cases,  especially  where  there  are  disturbances  of  sensibility,  a  water-cushion  is 
most  desirable.  The  patient's  position  must  also  be  frequently  changed,  and  the 
sacral  region  must  often  be  washed  and  rubbed.  Every  incipient  bed-sore  must 
be  very  carefully  treated  by  Peruvian  balsam  ointment  (1  to  30),  iodoform, 
salicylate  plaster,  or  mercurial  plaster,  which  acts  very  well,  in  order  to 
prevent  its  spreading.  When  the  bed-sore  is  very  extensive  the  continuous  bath 
is  the  best  remedy. 

If  there  is  retention  of  urine  and  the  patient  has  to  be  catheterized,  the  most 
extreme  care  must  be  employed  in  cleaning  and  disinfecting  the  catheter,  or  else 
cystitis  will  develop  in  a  few  days.  If  it  does,  it  is  best  in  severe  cases  to  wash 
out  the  bladder  regularly  with  boracic-acid  solution,  permanganate  of  potassium, 
and  like  remedies.  In  milder  cases  we  may  try  chlorate  of  potassium  internally, 
fifty  to  seventy-five  grains  a  day  (grammes  3-5),  salol,  urotropine,  or  balsams. 
If  there  is  complete  incontinence  it  is  advisable  to  introduce  a  permanent  cath- 
eter (sonde  a  demeure)  into  the  bladder — that  is,  a  ISTelaton's  catheter,  which  lies 
in  the  bladder  and  is  fastened  to  the  thighs  by  strips  of  plaster.  The  urine  runs 
away  through  a  rubber  tube,  and  we  avoid  the  constant  wetting  of  the  skin  and 
linen.  In  men,  good  urinals  are  often  perfectly  satisfactory,  but  in  women,  their 
application  usually  causes  great  difficulties. 

Constipation  must  be  met  according  to  the  general  rules.  We  should  be  as 
sparing  as  possible  with  cathartics  at  first,  and  try  to  make  an  appropriate  diet 
and  enemata  suffice.  If  there  is  severe  pain,  subcutaneous  injections  of  morphine 
are  unavoidable,  but  we  always  delay  this  as  long  as  possible,  although  finally  we 
let  the  dose  of  morphine  be  unlimited  in  hopeless  cases. 


954 


DISEASES    OF   THE   NEEVOTJS    SYSTEM 


CHAPTEE   VI 

MULTIPLE    SCLEROSIS    OF    THE    BRAIN    AND    SPINAL    CORD 

(Disseminated  Nodular  Sclerosis.     Sclerose  en  plaques) 

etiology  and  Pathology. — Multiple  sclerosis  of  the  central  nervous  system 
is  a  special  chronic  form  of  disease,  whose  anatomical  basis  consists  in  the  devel- 
opment of  numerous  disseminated  "  sclerotic  nodules  "  (^vide  infra)  in  the  brain 
and  cord.  We  know  practically  nothing-  as  to  its  aetiology,  for  the  significance  of 
exposure  to  cold,  over-exertion,  and  mental  emotions,  sometimes  given  as  causes  of 
the  disease,  is  wholly  doubtful.  It  is  also  very  improbable  that  syphilis  plays  any 
part  in  the  aetiology  of  multiple  sclerosis.  P.  Marie  claims  to  have  seen  the  dis- 
ease come  on  very  frequently  as  a  consequence  of  some  acute  infectious  disease 

(typhoid  fever,  scarlet  fever,  etc.), 
and  therefore  he  suspects  that  the  dif- 
ferent foci  of  disease  have  an  infec- 
tious inflammatory  origin;  but  our 
own  experience  does  not  permit  us  to 
confirm  this,  nor  does  our  experience 
pronounce  in  favor  of  a  relation  be- 
tween multiple  sclerosis  and  chronic 
intoxication,  as  Oppenheim  supposes; 
on  the  contrary,  in  the  majority  of 
our  own  observations  we  could  find  ab- 
solutely no  material  external  cause,  in 
spite  of  careful  inquiry.  We  are 
therefore  disposed  to  regard  the  dis- 
ease as  of  endogenous  nature,  as  a 
multiple  gliosis  due  to  congenital  ab- 
normal predisposition.  The  anatom- 
ical data  also  harmonize  very  well 
with  this  view.  Any  injury  preceding 
the  development  of  the  disease,  acute 
diseases,  intoxications,  emotional  dis- 
turbances, etc.,  would  therefore  act  at  most  as  exciting  causes.  If,  however,  a 
"  disseminated  myelitis  "  should  actually  at  any  time  follow  an  acute  disease  and 
lead  to  the  formation  of  multiple,  sclerotic  nodules  in  the  nervous  system  with 
corresponding  symptoms,  this  would  be  an  affection  similar  to  multiple  sclerosis, 
but  yet  essentially  difl^erent. 

A  hereditary  predisposition  seems  to  be  present  in  only  a  few  cases.  The 
affection  occurs  chiefly  in  youth,  somewhere  between  the  ages  of  eighteen  and 
thirty-five,  but  we  have  ourselves  seen  one  case,  which  came  to  an  autopsy,  in  a 
man  of  sixty.  The  disease  also  occurs  in  children.  'No  material  distinction  has 
been  made  out  as  to  sex. 

In  regard  to  the  development  of  the  different  sclerotic  nodules,  nothing  defi- 
nite has  been  established  at  present  as  to  their  genesis.  The  suspicion  has  re- 
peatedly been  uttered  that  the  disease  is  due  to  primary  changes  in  the  vessels, 
but  no  proof  of  this  can  be  given.  The  nodules  are  in  part  easy  to  recognize  with 
the  naked  eye,  from  their  gray  color,  and  we  can  also  feel  an  increased  resistance. 
They  are  scattered  over  the  whole  central  nervous  system.  Their  favorite  seats 
in  the  brain  are  the  centrum  ovale,  the  walls  of  the  lateral  ventricles,  and  the 
corpus  callosum;  but  on  careful  examination  we  usually  find  many  nodules  in  the 
gray  matter  of  the  central  ganglia  and  the  cortex;  the  nodules  are  also  quite 


Fig.   128.  —  Distribution  of  the  sclerosed  nodules  on 
the  surface  of  the  pons. 

(From  Leube.) 


MULTIPLE  SCLEEOSIS  OF  THE  BRAIN  AND  SPINAL  CORD    955 


^^  I 


abundant,  as  a  rule,  in  the  pons,  less  frequent  in  the  medulla,  and  very  abundant 
and  variously  distributed  in  the  cord  (see  Figs.  128  and  129),  chiefly  in  its 
white  substance.  Examined  microscopicallj^  the  nodules  consist  of  an  abundant, 
reticulated,  fibrillary  neuroglia  tissue,  in  which  the  nerve-fibers  are  lessened  in 
number,  but,  as  a  rule,  not  wholly  destroyed;  on  the  contrary,  we  usually  find 
many  axis-cylinders  preserved  in  the  nodules,  as  Charcot  first 
found  and  as  has  often  been  confirmed  since  by  other  observers. 
This  fact  is  important  clinically,  because  it  explains  why  multi- 
ple sclerosis  only  rarely  or  only  in  its  advanced  stages  leads  to 
complete  paralysis.  It  also  indicates,  as  it  seems  to  us,  that  the 
process  does  not  start  from  the  nervous  tissue,  but  from  the 
interstitial  neuroglia  tissue.  It  also  explains  the  remarkable 
fact  that  the  ordinary  secondary  degenerations  are  almost  al- 
ways absent,  in  spite  of  the  presence  of  many  nodules  in  the 
spinal  cord.  In  the  vessels  we  usually  notice  thickening  of  the 
walls,  which  may  be  surrounded  by  neuroglia  cells.  The  author 
regards  these  changes  as  of  secondary  nature.  Fatty  granular 
■  cells  are  often  to  be  found  in  fresh  cases. 

Clinical  History. — From  the  variations  which  the  number 
and  the  localization  of  the  nodules  show,  it  may  be  understood 
from  the  outset  that  a  picture  of  the  disease  which  repre- 
sents all  cases  can  not  be  drawn;  but  many  cases  show  so 
characteristic  a  group  of  symptoms  that  the  diagnosis  can 
often  be  made  with  considerable  certainty.  We  will  first 
describe  this  typical  form  of  disease,  for  the  knowledge  of 
which  we  must  thank  Charcot  chiefly,  and  then  we  will  add 
some  remarks  upon  the  cases  which  differ  from  this  type 
("  formes  frustes  "),  which  are  by  no  means  very  rare. 

The  symptom  of  the  typical  cases  of  multiple  sclerosis 
which  we  must  first  mention  is  an  extremely  striking  dis- 
turbance of  motion  which  manifests  itself  either  as  actual 
ataxia  or  as  the  so-called  "  intention  tremor."  This  "  tremor  " 
was  apparently  the  reason  why  multiple  sclerosis  was  repeat- 
edly confounded  in  former  years  with  paralysis  agitans,  al- 
though the  two  diseases  have  not  the  slightest  resemblance  one 
to  the  other.  The  one  fact  that  the  motor  disturbance  of  mul- 
tiple sclerosis  comes  on  only  exceptionally  when  at  rest,  but 
almost  always  on  voluntary  movement,  affords  an  effectual 
distinction.  Moreover,  the  motor  disturbance  of  multiple  scle- 
rosis can  be  called  an  actual  tremor  only  in  part  of  the  cases. 
Such  a  true  oscillatory  tremor  is  often  seen,  for  example, 
in  the  arms  when  the  patient  tries  to  hold  them  out  unsup- 
ported, but  the  tremor,  in  distinction  from  that  of  paralysis 
agitans,  seems  to  occur  less  in  the  fingers  than  in  the  larger 
joints.  We  have  scarcely  ever  seen  oscillatory  tremor  in  the 
legs  in  multiple  sclerosis.  In  purposive  movements  there  is 
rarely  a  true  oscillatory  tremor  in  the  arms,  but  rather  an 
ataxic  motor  disturbance — that  is,  an  uncertainty  and  an  ex- 
cursive movement,  which  is  especially  plain  when  the  patient 
tries  to  touch  a  given  point  with  his  forefinger,  to  put  the  tips  of  the  forefingers 
together,  to  bring  a  glass  of  water  to  the  mouth,  to  pour  water  from  one  test-tube 
into  another,  etc.  In  the  legs  the  ataxia  usually  occurs  precisely  as  in  tabes 
dorsalis  (as  in  putting  the  heel  on  the  other  knee).  We  sometimes  see  consider- 
able wavering  and  shaking  of  the  head  when  unsupported.     The  ataxia  of  the 


E:lMli,.- 


FiG.  129.  — Example 
of  disease  of  the 
cord  in  multiple 
sclerosis.  The  dark 
portions  are  the 
parts  diseased. 


956  DISEASES    OF   THE   ^^eeYOUS    SYSTEM 

trunk  is  usually  very  evident.  If  we  make  the  patient  stand  witli  the  feet  to- 
gether, it  usually  causes  a  marked  swaying  of  the  whole  body.  This  swaying  is 
often  much  greater  when  the  patient  shuts  his  eyes.  We  therefore  find  "  Rom- 
berg's system"  in  multiple  sclerosis  precisely  as  in  tabes  dorsalis  (g.  v.).  If  the 
patient  with  multiple  sclerosis  is  excited,  his  uncertainty  and  unrest  usually  be- 
come greater. 

In  two  other  muscular  regions  the  motor  disturbance  often  makes  itself  mani- 
fest in  a  very  characteristic  way — in  the  muscles  of  articulation  (tongue)  and  the 
muscles  of  the  eye.  Even  on  protruding  the  tongue  we  sometimes  see  an  uncer- 
tainty of  movement,  but  the  disturbance  is  still  more  evident  when  the  patient 
speaks.  Many  patients  with  multiple  sclerosis,  though  of  course  not  all,  show 
a  very  characteristic  disturbance  of  speech.  The  speech  is  slow,  monotonous, 
scanning,  indistinct,  and  sometimes  finally  almost  unintelligible.  The  patient 
sometimes  pronounces  almost  every  syllable,  or  even  every  sound,  separately,  thus : 
"  S-w-al-low."  We  sometimes  notice  that  the  voice  often  breaks  into  a  falsetto. 
There  can  hardly  be  a  doubt  that  this  disturbance  of  speech  indicates  the  presence 
of  sclerotic  nodules  in  the  pons  and  medulla,  and  that  the  anomaly  of  motion 
at  the  bottom  of  it  is  analogous  to  the  ataxia  of  the  arms  and  legs  described 
above.  The  nystagmus  sometimes  seen  in  multiple  sclerosis,  especially  when 
looking  to  one  side,  is  also  nothing  but  ataxia  of  the  ocular  muscles ;  but  we  must 
confess  that  we  have  seen  manifest  nystagmus  in  multiple  sclerosis  much  less  fre- 
quently than  might  be  expected  from  the  statements  of  some  writers. 

Besides  ataxia  and  intention  tremor,  actual  paresis  or  even  paralysis  of  the 
muscles  may  be  wholly  absent  or  may  be  only  a  late  symptom.  At  any  rate,  in 
spite  of  marked  ataxia  the  gross  strength  of  the  arms  and  legs  may  be  very  well 
preserved  for  a  long  time.  The  thing,  however,  which,  in  addition  to  the  ataxia, 
gives  the  motor  disturbance  of  multiple  sclerosis  its  special  stamp  is  the  almost 
constant  increase  in  the  reflexes,  and  the  associated  spastic  symptoms.  In  the 
upper  extremities  the  spastic  symptoms  are  less  prominent,  but  even  here  we 
almost  always  find  very  vigorous  tendon  and  periosteal  reflexes  on  striking  the 
lower  ends  of  the  bones  of  the  forearm  or  the  tendon  of  the  biceps  or  triceps.  In 
the  lower  extremities  we  see  not  only  a  marked  patellar  reflex  and  a  very  in- 
tense and  persistent  ankle  clonus,  but  often  an  evident  hypertonicity  of  the  mus- 
cles, or  even  a  pronounced  tonic  rigidity  of  both  legs. 

It  is  the  spastic  symptoms  which  materially  affect  the  patient's  gait.  If  they 
are  comparatively  slight  the  gait  is  simply  uncertain,  wavering,  stumbling,  and 
ataxic,  although  even  here  the  stiffness  and  jerkiness  of  the  spastic  gait  is  usually 
plainly  to  be  seen  ("  spastic-ataxic  gait").  The  ataxia  of  the  gait  is  due  (un- 
like the  ordinary  tabetic  gait)  not  to  the  uncertainty  of  the  legs,  but  to  the 
swaying  of  the  whole  body,  as  in  cerebellar  ataxia.  If  the  spastic  symptoms  are 
more  prominent,  the  gait  also  becomes  more  spastic,  but  the  individual  steps  are 
always  quick  and  long  on  account  of  the  absence  of  paresis.  In  many  cases  with 
slight  ataxia  and  marked  hypertonicity  of  the  muscles  the  gait  is  almost  purely 
spastic.  Only  when  paresis  of  the  legs  ensues  does  the  gait  become  more  dragging 
and  labored,  with  slow,  stiff  steps  ("  spastic-paretic  gait").  The  ataxia  is  then 
of  course  no  longer  very  noticeable. 

It  is  not  easy  to  explain  the  occasion  of  all  these  motor  s^nnptoms  of  multiple 
sclerosis  thus  far  described,  but  we  may  certainly  say  this :  that  the  persistence 
of  the  axis-cylinders  in  the  sclerotic  nodules  mentioned  above  explains  the  fact 
that  there  is  so  often  in  multiple  sclerosis  not  a  real  paralysis,  but  only  ataxia 
(intention  tremor)  and  spastic  symptoms  (increased  tendon  reflexes).  The  gen- 
eral tendency  is  to  refer  the  ataxia  to  nodules  in  the  posterior  columns  or  in  the 
superior  leminiscus,  and  the  spastic  symptoms  to  nodules  in  the  lateral  tracts. 
The  occasion  of  the  oscillatory  tremor  is  still  wholly  unknown. 


MULTIPLE  SCLEROSIS  OE  THE  BRAIN  AND  SPINAL  CORD   957 

Other  symptoms  besides  the  motor  symptoms  jiist  mentioned  are  much  less 
common  in  multiple  sclerosis.  It  is  .especially  noteworthy  in  respect  to  diagnosis 
that  disturbances  of  sensation  and  of  the  bladder  are  usually  quite  subordinate. 
On  careful  testing  we  of  course  find  not  infrequently  in  some  places  slight  or  tem- 
porary diminution  of  the  cutaneous  sensibility  or  insignificant  disturbances  of 
micturition,  but  such  symptoms  are  not  part  of  the  characteristic  picture  of  mul- 
tiple sclerosis.  The  cutaneous  reflexes  usually  show  no  special  disturbances,  but 
we  have  so  frequently  found  certain  reflexes  absent,  especially  the  abdominal  re- 
flex, that  we  must  ascribe  to  this  symptom  a  certain  significance  in  diagnosis. 

A  number  of  cerebral  symptoms  are  far  more  important,  although  they  are 
present  only  in  a  part  of  the  cases.  Eirst  to  be  mentioned  are  the  not  uncommon 
ocular  disturbances.  The  disturbances  of  vision  are  the  most  important;  these 
may  be  either  a  simple  diminution  of  the  acuteness  of  vision  or  a  contraction  of 
the  visual  field  and  disturbance  of  the  color  sense.  These  symptoms  are  due 
to  an  atrophy  of  the  optic  nerve,  which  as  a  rule  appears  first  in  the  temporal  half 
of  the  papilla.  The  disturbance  of  vision  only  rarely  goes  on  to  complete  blind- 
ness. The  atrophy  of  the  optic  nerves  may  sometimes  develop  from  an  optic 
neuritis.  Motor  disturbances  of  the  eyes  are  also  not  uncommon,  and  sometimes 
they  may  even  be  the  first  noticeable  symptom  of  the  disease.  The  paralysis 
almost  always  affects  the  external  ocular  muscles  only,  and  usually  causes  diplopia. 
It  may  affect  one  or  both  eyes,  and  sometimes  there  is  associated  paralysis.  Re- 
fiex  immobility  of  the  pupils  is  hardly  ever  seen. 

Of  other  cerebral  symptoms  we  may  mention  headache  and  especially  ver- 
tigo. The  latter  is  often  a  very  early  symptom  of  the  disease.  It  may  be  parox- 
ysnaal  or  persistent.  In  the  course  of  the  disease  there  often  appears  a  certain 
mental  weakness,  an  imbecility,  which  sometimes  increases  to  marked  dementia. 
Conditions  of  melancholy  or  exaltation  are  much  rarer.  We  must  also  mention 
the  occurrence  of  apoplectiform  attacks  as  a  symptom  which  is  often  important 
in  diagnosis.  After  slight  prodromal  symptoms,  such  as  headache  and  vertigo, 
loss  of  consciousness  and  hemiplegia  come  on  quite  suddenly.  With  this  the  face 
is  usually  red,  the  pulse  is  frequent,  and  the  temperature  may  rise  to  104°  or  106° 
(40°-41°  C).  After  a  day  or  two  the  consciousness  gradually  returns,  and  the 
hemiplegia  soon  disappears.  Epileptiform  attacks  are  much  rarer.  We  saw  these 
repeatedly  in  a  typical  case;  they  were  mainly  unilateral,  and  were  followed  by 
a  hemiplegia  which  soon  passed  away.  The  precise  cause  of  these  attacks  is  still 
wholly  unknown.  We  know  only  that  they  are  not  due  to  complicating  gross 
changes  in  the  brain,  but  that  they  arise  merely  from  functional  conditions  of 
paralysis  or  irritation.  Finally,  we  must  mention  an  interesting  symptom  not 
infrequently  observed  in  multiple  sclerosis,  which  may  also  be  of  value  in  diag- 
nosis— namely,  the  so-called  impulsive  laughing  and  crying.  In  many  patients 
these  emotional  manifestations  occur  very  frequently  and  in  an  uncontrollable 
fashion,  either  almost  spontaneously  or  especially  upon  the  slightest  occasion. 
Not  infrequently  the  two  manifestations  pass  almost  directly  into  each  other. 

In  regard  to  the  general  course  of  typical  cases,  the  disease  develops  very  slowly 
and  gradually.  Motor  symptoms,  tremor,  uncertainty  of  movements,  and  disturb- 
ances in  gait,  usually  appear  in  the  extremities  first.  The  patient  often  com- 
plains at  the  same  time  of  occasional  headache  and  vertigo.  The  speech  gradually 
becomes  more  indistinct,  the  intelligence  weaker,  and  the  other  symptoms  of  the 
disease  described  above  develop.  The  affection  almost  always  lasts  for  years  and 
years.  Variations  in  the  course,  temporary  improvement,  and  new  relapses  are 
common.  It  would  even  seem  in  mild  cases  as  if  there  were  sometimes  a  recovery 
or  at  least  an  arrest  of  the  symptoms,  but  in  general  we  must  always  regard 
the  prognosis  as  very  unfavorable.  We  often  see  the  condition  rapidly  grow 
worse,  especially  after  the  above-mentioned  apoplectiform  attacks.    The  last  stage 


958  DISEASES    OF   THE   NEEVOUS    SYSTEM 

is  characterized  by  the  gradually  increasing  disturbance  of  the  general  nutrition, 
and,  finally,  by  paralysis  and  bed-sores.  Death  ensues  from  intercurrent  diseases, 
from  the  increasing  weakness,  or  sometimes  in  an  apoplectiform  attack. 

Unusual  Forms. — Besides  the  typical  form  of  multiple  sclerosis  described, 
there  are  often,  as  we  have  said,  cases  that  vary  from  the  type  ("  formes  frustes  ")- 
We  will  mention  briefly  the  following  possibilities : 

1.  The  disease  may  be  very  latent.  We  saw  one  case  in  which,  for  a  long 
time,  the  only  symptom  was  a  complaint  of  slight  headache  and  vertigo.  Finally, 
there  was  a  transitory  apoplectiform  attack,  several  months  later  an  epileptiform 
attack,  and  a  few  days  after  that  death  took  place.  The  autopsy  showed  a  com- 
pletely developed  multiple  sclerosis. 

2.  Sometimes  the  disease  appears  under  the  exact  type  of  a  chronic  myelitis. 
The  cerebral  nodules  cause  no  symptoms,  they  are  present,  perhaps,  only  in  small 
numbers,  and  the  spinal  nodules  cause  a  gradually  increasing  paraplegia  of  the 
legs,  with  vesical  disturbance,  loss  of  sensibility,  etc.  We  have  notes  of  several 
autopsies  of  multiple  sclerosis  in  which,  during  life,  the  diagnosis  of  a  simple 
transverse  myelitis  had  been  made  (vide  supra,  page  951). 

3.  Cases  have  been  repeatedly  known  where  multiple  sclerosis  has  appeared 
under  almost  the  exact  type  of  a  spastic  spinal  paralysis  (vide  infra).  In  these 
cases  many  nodules  were  situated  in  the  lateral  columns  of  the  cord.  If  the  spas- 
tic symptoms  be  combined  with  muscular  atrophy  (nodules  in  the  anterior  gray 
cornua),  the  disease  may  even  simulate  the  type  of  an  amyotrophic  lateral  scle- 
rosis, with  at  times  co-existing  bulbar  symptoms  (vide  infra.)  If  multiple  scle- 
rosis be  localized  to  an  unusual  extent  in  the  pons  and  medulla,  the  s;sanptoms  of 
a  chronic  bulbar  paralysis  may  be  prominent. 

4.  Much  less  frequently  the  type  of  the  disease  may  resemble  tabes  (immobile 
pupils,  ataxia,  pain).  We  do  not  know  whether  absence  of  the  patellar  reflex  has 
been  seen  in  undoubted  multiple  sclerosis.  There  are,  however,  combinations  of 
multiple  sclerosis  and  gray  degeneration  of  the  posterior  columns  (syphilis?). 

5.  It  sometimes  happens  that  multiple  sclerosis  is  the  reason  for  a  slowly  de- 
veloping hemiplegia,  which  may  then  be  falsely  regarded  as  cerebral,  while  the 
autopsy  shows  several  nodules  in  the  corresponding  side  of  the  cord  and  pons. 

6.  In  some  cases  the  mental  disturbances  (dementia)  are  so  prominent  that 
there  is  the  pronounced  picture  of  paralytic  dementia  with  disturbances  of 
speech,  etc. 

Diagnosis. — In  all  such  atypical  cases  the  diagnosis  of  multiple  sclerosis  is 
sometimes  quite  impossible,  or  at  best  it  can  be  made  with  a  fair  amount  of  proba- 
bility only  when  some,  at  least,  of  the  characteristic  symptoms  of  the  disease  are 
present  besides  the  anomalous  sjTnptoms.  The  circumstance,  indeed,  that  the 
anomalous  cases  will  not  properly  fit  the  moulds  of  any  other  form  of  disease, 
should  make  us  thinlv  of  the  possibility  of  a  multiple  sclerosis;  for  in  these 
anomalous  cases,  of  course,  there  may  be  all  possible  combinations  of  symptoms. 

In  typical  cases,  however,  the  diagnosis  is  easy,  and  often  it  can  be  made  with 
absolute  certainty.  The  slow  development  of  the  disease,  usually  without  any 
discoverable  cause,  the  comparative  youth  of  the  patient,  the  ataxia  of  the  legs 
and  the  ataxia  or  tremor  of  the  arms,  the  swaying  of  the  body  when  standing 
with  the  feet  together,  the  uncertain  spastic-ataxic  gait,  the  occasional  absence 
of  the  abdominal  reflex,  the  increased  tendon  reflexes  in  the  arms  and  legs,  the 
absence  of  any  marked  disturbances  of  sensation  or  of  the  bladder,  in  some  cases 
also  the  disturbance  of  speech,  the  nystagmus,  the  impulsive  laughing  and  crying, 
the  slight  mental  weakness  which  often  comes  on  later,  and  flnally  the  occasional 
apoplectiform  or  epileptiform  attacks — all  these  symptoms  give  a  veiy  character- 
istic picture,  which  is  usually  quickly  recognized  and  correctly  interpreted.  It  is 
hardly  possible  to  confiise  it  with  paralysis  agitans  (q.  v.)  if  we  remember  the 


THE    SO-CALLED    PSEUDO-SCLEROSIS  959 

characteristic  attitude  of  the  latter  affection,  the  osciUatory  tremor  of  the  fingers 
when  at  rest,  the  rigidity  of  the  face,  etc.  It  is  very  seldom  difficult  to  distin- 
guish it  from  true  tabes  dorsalis.  It  is  easier  to  confuse  multiple  sclerosis  with 
Friedreich's  hereditary  ataxia  (q.  v.) ;  but  the  condition  of  the  tendon  reflexes  is 
usually  decisive;  these  are  wholly  absent  in  tabes  and  Friedreich's  disease,  but 
they  are  almost  invariably  increased  in  multiple  sclerosis.  It  sometimes  happens 
that  hysteria  assumes  a  form  very  similar  to  multiple  sclerosis  (tremor,  ataxia,  in- 
creased tendon  reflexes,  etc.),  but  in  such  cases  we  can  usually  arrive  at  a  correct 
diagnosis  by  careful  observation  if  we  pay  attention  to  the  whole  condition  of 
the  patient,  the  course  of  the  disease,  and  the  characteristic  hysterical  "  stigmata." 
There  is,  however,  a  combination  of  multiple  sclerosis  and  hysteria  (especially 
hysterical  hemiansesthesia),  as  has  been  maintained  especially  by  Charcot's  pupils. 
The  distinction  between  multiple  sclerosis  and  the  so-called  pseudo-sclerosis  will 
be  stated  below. 

Prognosis. — The  most  important  features  in  prognosis  have  already  been  men- 
tioned. We  have  seen  that  an  improvement  in  the  symptoms  is  not  uncommon, 
but  that  the  final  outcome  of  the  disease,  with  perhaps  a  few  exceptions,  is  un- 
favorable.   The  disease  may  last  for  many  years. 

Treatment. — In  the  treatment  we  may  make  a  trial  of  the  same  remedies  that 
have  been  mentioned  in  the  description  of  chronic  myelitis.  Absolute  rest  and 
good  care,  which  many  patients  can  obtain  only  in  a  good  sanitarium,  are  often 
beneficial.  We  may  also  use  galvanism,  baths,  and  sponging,  and  internally 
iodide  of  potassium,  ergotine,  and  nitrate  of  silver.  The  uncertainty  of  move- 
ment can  sometimes  be  distinctly  improved  by  methodical  gymnastic  exercises 
(see  the  following  chapter). 

APPENDIX 

THE    SO-CALLED    PSEUDO-SCLEROSIS 

Cases  of  disease  have  been  observed,  first  by  C.  Westphal  and  later  by  the 
author  and  others,  the  symptoms  of  which  seemed  to  warrant  the  diagnosis  of 
multiple  sclerosis,  but  the  autopsy  proved  wholly  negative.  The  victims  are 
usually  young  and  often  have  a  predisposition  to  nervous  disease.  The  symptoms 
of  the  disease  consist  of  a  marked  rapid  or  slow  oscillatory  tremor  with  wide  ex- 
cursions, which  sometimes  occurs  during  rest,  but  which  becomes  unusually  vio- 
lent on  motion.  The  tremor  affects  the  arms  particularly,  but  also  the  trunk  and 
legs.  There  seems  to  be  no  real  ataxia  as  in  multiple  sclerosis.  The  tendon  reflexes 
are  increased  and  a  distinct  spastic  rigidity  may  develop  in  the  legs.  The  speech 
is  sometimes  quite  as  decidedly  scanning  as  in  multiple  sclerosis.  iJ^ystagmus  is 
usually  absent.  We  have  seen  apoplectiform  attacks  in  a  pronounced  form,  and 
also  impulsive  laughing  and  crying.  The  face  often  has  a  peculiar  rigid  ex- 
pression. Certain  mental  disturbances  are  very  characteristic,  especially  a 
marked  tendency  to  outbursts  of  wrath  and  actual  maniacal  attacks.  Signs  of 
confusion  and  hallucinations  are  less  common.  The  course  may  extend  over  many 
years.  The  disease  seems  to  be  incurable.  Death  ensues  through  increasing 
general  weakness  or  in  an  apoplectiform  attack.  Anatomical  investigation,  as  has 
been  said,  is  essentially  entirely  negative,  even  with  a  careful  microscopical  ex- 
amination of  the  nervous  system. 

The  resemblance  between  the  type  of  this  "  pseudo-sclerosis  "  and  true  mul- 
tiple sclerosis  is  evident;  nevertheless,  now  that  we  know  the  disease,  we  can  often 
make  the  distinction.  The  chief  points  to  bear  in  mind  are  the  very  marked  true 
oscillatory  tremor,  the  absence  of  real  ataxia,  and  the  mental  disturbances  just 
mentioned. 

The  treatment  of  pseudo-sclerosis  is  the  same  as  that  of  multiple  sclei'osis. 


960  DISEASES    OF   THE   NEEVOUS    SYSTEM 


CHAPTER   VII 

TABES    DORSALIS 

{Locomotor  Ataxia.     Gray  Degeneration  of  the  Posterior  Columns.     Posterior  Spinal  Sclerosis) 

We  give  at  present  the  old  name  of  tabes  dorsalis,  "  consumption  of  the  spinal 
cord,"  to  a  perfectly  definite  chronic  disease  of  the  central  nervous  system,  whose 
chief,  but  by  no  means  sole,  anatomical  basis  is  regarded  as  a  primary  systemic 
degeneration  of  the  peripheral  sensory  neurones,  and  especially  of  their  processes 
in  the  posterior  columns  of  the  spinal  cord.  The  first  description  of  tabes,  which, 
of  course,  is  defective  in  many  respects,  is  found  in  a  work  of  W.  Horn  in  1827. 
We  must  thank  especially  the  investigations  of  Romberg  in  Germany,  in  1851, 
and  of  Duchenne  in  France,  in  1858,  for  a  more  comprehensive  knowledge  of  the 
disease,  and  for  a  precise  distinction  between  it  and  the  other  chronic  diseases 
of  the  spinal  cord. 

.ffitiology.— But  little  that  is  definite  was  known  until  lately  as  to  the  cause  of 
tabes  dorsalis.  Hereditary  conditions  play  a  very  slight  part  in  genuine  cases, 
and  even  a  general  "  neuropathic  taint "  can  only  rarely  be  made  out  in  ataxic 
patients.  Much  weight  in  regard  to  aetiology  was  formerly  laid  upon  previous 
exposure  to  cold.  It  can  not  be  denied  that  sometimes  the  first  symptoms  of  the 
disease  follow  some  pronounced  exposure  to  wet  or  cold,  but  much  more  fre- 
quently nothing  of  the  sort  can  be  made  out.  The  case  is  similar  with  regard  to 
physical  and  mental  over-exertion,  which  were  formerly  made  answerable  for  the 
origin  of  tabes.  It  is  an  utterly  ungrounded  assertion  that  sexual  excesses  may 
be  the  cause  of  tabes.  Tabes  may  rarely  develop  as  a  result  of  acute  diseases 
or  somewhat  more  frequently  as  a  result  of  injury  (general  concussion  of  the 
body  from  a  fall,  fractures,  etc.) ;  but  we  may  ascribe  to  these  factors  merely 
the  significance  of  an  exciting  cause.  In  these  rare  cases,  too,  it  is  hard  to 
confirm  the  connection.  The  earlier  teaching  that  tabes  develops  after  "  sup- 
pression of  the  foot-sweat "  is  manifestly  due  to  a  confusion  of  cause  and 
effect.  The  absence  of  foot-sweat  is  not  the  cause,  but  a  symptom  of  incipient 
tabes. 

The  only  setiological  fact  which  in  our  opinion  is  beyond  any  doubt  is  the 
relation  of  tabes  to  a  previous  syphilitic  infection.  This  relation  of  the  two  dis- 
eases to  each  other  was  first  confirmed  in  France  by  Fournier  and  in  Germany  by 
Erb,  and  in  spite  of  the  vigorous  contradiction  which  the  views  of  these  observers 
at  first  met  with  on  many  sides,  this  theory  of  tabes  is  constantly  acquiring  more 
and  more  general  recognition. 

The  connection  between  tabes  and  syphilis  can  be  confirmed,  first  of  all,  by 
statistics.  Erb  was  able  to  find  a  history  of  syphilis,  with  secondary  symptoms, 
in  about  62  per  cent,  of  his  patients ;  and  Fournier,  in  103  cases,  found  syphilitic 
antecedents  as  many  as  94  times.  Our  own  observations  agree  exactly  with  Erb's 
data,  since  61  per  cent,  of  our  patients  stated  definitely  that  they  had  formerly 
suffered  from  syphilis.  If  we  also  reckon  the  cases  where  the  patients  admit  a 
former  sore  but  no  secondary  symptoms,  the  percentage  becomes  much  greatei' — 
90  per  cent.  In  general  it  is  worthy  of  note  that,  as  a  rule,  in  most  cases  of  tabes 
the  previous  syphilis  has  not  had  a  great  intensity.  Only  quite  infrequently  do 
we  find  tertiary  syphilitic  symptoms  as  well  as  tabes;  we  have  seen,  for  example, 
severe  ulcers  of  the  skin,  gummatous  periostitis,  etc.  The  time  between  the  in- 
fection and  the  beginning  of  the  first  symptoms  of  tabes  varies  very  much;  it 
may  be  from  two  to  twenty  years. 

The  connection  between  tabes  and  previous  syphilis  also  explains  naturally  a 
number  of  peculiarities  in  the  occurrence  of  tabes,  especially  the  fact  that  tabes 


TABES    DORSALIS  961 

is  much  commoner  in  men  than  in  women,  that  it  is  particnhirly  very  rare  in 
women  of  the  better  class,  while  it  is  found  much  more  frequently  in  women  of 
the  lower  classes,  that  it  comes  on  particularly  in  middle  life,  that  it  is  much 
more  common  in  the  higher  classes  and  in  urban  populations  than  in  the  country, 
that  certain  classes  (merchants,  artists,  officers)  show  a  much  larger  percentage 
of  cases  of  the  disease  than  others  (clergymen,  teachers,  etc.)-  If  we  see,  however, 
any  cases  of  tabes  which  show  striking  differences  in  these  respects,  we  can  al- 
most always  find  evidence,  even  in  such  cases,  of  a  previous  syphilitic  infection. 
Such  individual  cases  therefore  afford  material  for  the  most  convincing  proof  of 
the  connection  between  the  two  diseases.  Thus  we  sometimes  see  tabes  in  per- 
fectly irreproachable  women;  here  we  can  almost  always  detect  previous  syphilis 
in  the  husband  which  has  been  transmitted  to  the  wife.  We  ourselves  and  other 
observers  have  seen  tabes  arise  in  this  way  in  both  husband  and  wife.  We  may 
also  find  tabes  in  very  young  or  very  old  persons,  and  then  we  can  discover  that 
syphilis  was  acquired  at  a  very  early  or  a  very  advanced  age.  A  few  cases  of 
tabes  occur  in  children,  and  are  in  all  probability  to  be  referred  to  hereditary 
syphilis. 

Although  the  connection  between  tabes  and  previous  syphilis  may  be  regarded 
as  definitely  established,  the  nature  of  this  connection,  on  the  other  hand,  is  not 
yet  fully  explained.  This  much,  of  course,  is  certain,  that  tabes  is  not  an  ordinary 
tertiary  syphilitic  disease.  Both  its  anatomical  changes  (vide  infra)  and  the 
extremely  slight  effect  of  antisyphilitic  treatment  remove  every  doubt  as  to  this. 
The  connection  between  the  two  diseases  must  be  of  some  other  nature,  and 
therefore  we  long  ago  expressed  the  opinion  that  tabes  was  due  only  to  certain 
<3hemical  poisons  (toxines),  which  develop  in  the  body  from  the  action  of  the 
syphilitic  infection.  Such  toxines  may  very  well  cause  definite  systems  of  fibers 
(vide  infra)  to  degenerate,  and  their  presence  is  also  a  good  explanation  of  cer- 
tain clinical  peculiarities  of  tabes,  especially  the  paroxysmal  occurrence  of  cer- 
tain symptoms  (the  so-called  crises).  Many  of  these  crises,  especially  the  gastric 
and  intestinal  crises,  are  very  similar  to  toxic  symptoms  (vomiting,  pain,  pro- 
nounced general  debility  and  weakness,  etc.).  Tabes  and  the  closely  allied  gen- 
eral paralysis  therefore  stand  in  the  same  relation  to  syphilis  as  "  post-syphi- 
litic nervous  diseases,"  that  the  common  "  nervous  sequelfe  "  do  to  the  acute  infec- 
tious diseases- — for  exaraple,  as  post-diphtheritic  paralysis  and  ataxia  do  to  previ- 
ous pharyngeal  diphtheria.  Of  course  this  hypothesis  does  not  afford  a  complete- 
ly clear  insight  into  the  nature  of  the  tabetic  process.  Thus  the  constant  advance 
of  most  (but  of  course  not  all)  cases  of  tabes  requires  a  further  special  explana- 
tion. We  may  perhaps  imagine  the  process  thus:  that  the  toxines  absorbed  at 
first  merely  injure  the  affected  nervous  system  (vide  infra),  but  that  the  complete 
atrophy  and  cessation  of  function  comes  on  gradually  through  the  wear  and  tear 
associated  with  the  normal  functioning  of  the  nervous  elements.  In  this  sense 
other  external  influences  (fatigue  and  physical  over-exertion,  exposure  to  cold, 
injury)  may  be  regarded  as  aiding  the  process. 

It  can  not  at  present  be  maintained  that  every  tabes  is  of  syphilitic  origin, 
although  we  have  never  yet  seen  a  typical  genuine  tabes  in  which  syphilis  could 
•certainly  be  excluded;  but  it  would  not  be  impossible  that  other  noxious  influ- 
ences might  cause  the  same  s^^stems  of  fibers  to  degenerate  as  in  tabes,  and  thus 
produce  a  form  of  disease  similiar  to  that  of  genuine  tabes.  Thus  we  know  at 
present,  from  the  investigations  of  Tuczek,  that  symptoms  may  develop  in  chronic 
ergot  poisoning  (ergotism)  which  are  perfectly  analogous  to  those  of  t:ibes  and 
depend  iipon  a  corresponding  disease  of  the  posterior  columns  of  the  cord  which 
can  be  demonstrated  anatomically.  These  cases  of  "  tabes,"  however,  which  are 
traced  to  some  other  cause,  must  later  be  distinguished  from  the  post-syphilitic 
cases  which  constitute  by  far  the  great  majority. 
61 


962 


DISEASES    OE    THE    NERVOUS    SYSTEM 


Pathological  Anatomy. — As  we  have  seen  on  page  796,  the  cell  bodies  of  the 
peripheral  sensorj-  neurones  lie  in  the  spinal  ganglia.  The  processes  of  the  spinal 
ganglion-cells  divide  into  two  branches.  One  goes  to  the  periphery  of  the  body, 
the  cutaneous  surface;  it  forms  the  so-called  peripheral  sensory  nerve.  The 
other  process   serves  for  the   centripetal  conduction   of   sensory  irritations;  it 

enters  the  cord  through  the 
a  posterior  roots  and  goes,  as 

we  have  said  above,  either 
upward  in  the  posterior  col- 
umns or  into  the  posterior 
gray  cornua,  there  to  connect 
with  spinal  sensory  neurones 
of  the  second  order.  Upon 
this  peripheral  (first)  sen- 
sory neurone  system  (spinal 
ganglion  system), whose  ana- 
tomical arrang'ement  we 
have  just  briefly  described, 
the  (toxic)  cause  of  tabes 
acts  especially  and  causes  it 
slowly,  fiber  by  fiber  or  neu- 
rone by  neurone,  to  degen- 
erate. In  tabes,  as  in  most 
other  primary  systemic  dis- 
eases, we  find  that  the  evi- 
dent visible  anatomical  de- 
generation of  the  different 
neurones  always  begins  in 
the  prolongations,  and  the 
destruction  of  the  cell  body 
itself  follows  later,  if  at  all, 
and  is  the  last  process. 
Since  the  prolongations  of 
the  spinal  ganglion-cells  are, 
first,  the  peripheral  sensory 
nerves,  and,  second,  the 
fibers  in  the  posterior  col- 
umns, and,  in  part,  in  the 
posterior  horns  of  the  spinal 
cord,  we  understand,  with- 
out further  explanation,  that 
the  anatomical  process  in 
tabes  must  manifest  itself  as 
a  degeneration  both  in  the 
peripheral  nerves  and  in  the 
posterior  columns  and  pos- 
terior horns  of  the  spinal 
cord.  So  far  as  we  can  at 
present  appreciate  the  con- 
ditions, the  spinal  process  of 
the  neurone  cells  in  the  spinal  ganglia  seem  to  be  affected  earlier,  more  regu- 
larly, and  more  extensively  than  the  peripheral  process ;  but  it  seems  to  us  prob- 
able that  there  are  individual  differences  in  this  respect,  and  that  many  differences 
in  the  course  of  the  disease  in  different  cases  of  tabes  may  be  explained  by 


Fig.  130.— Degeneration  of  the  posterior  columns  in  advanced 
tabes,  a.  Cervical  cord.  b.  Dorsal  cord.  c.  Lumbar  cord. 
(Personal  observation.) 


TABES    DOESALIS  963 

such  variations  in  the  particular  anatomical  localization  of  the  tabetic  de- 
generation. 

If  we  examine  the  spinal  cord  of  a  patient  who  has  died  in  the  advanced  stage 
of  tabes,  the  smallness  and  thinness  of  the  cord  usually  strike  us  at  once.  The 
pia  mater  is  thickened  and  opaque,  especially  on  the  posterior  surface.  We  often 
see  the  posterior  columns  appearing  through  the  pia  as  a  gray  band  extending  the 
whole  length  of  the  spinal  cord.  On  cross-section  we  notice  that  the  smallness 
of  the  cord  is  due  chiefly  to  the  atrophy  of  the  posterior  columns,  which  is  often 
very  considerable.  These  no  longer  protrude  at  all  backward,  as  they  normally 
do,  but  seem  flat  and  sunken.  From  their  pronounced  gray  color  they  are  very 
plainly  distinguished  on  cross-section  from  the  rest  of  the  white  matter  of  the 
cord.  The  posterior  cornua  of  the  gray  matter,  and  the  posterior  nerve-roots, 
show  exceptionally  a  considerable  atrophy,  and  appear  very  small  and  thin  and 
also  of  a  gray  color. 

Microscopic  examination  gives  more  exact  information  as  to  the  extent  and 
form  of  the  degeneration.  This  shows  (Fig.  130,  a,  h,  c)  that  all  portions  of  the 
posterior  columns  are  not  affected  in  like  manner,  but  only  those  portions  which 
contain  the  processes  and  collaterals  of  the  posterior  root-fibers,  which  therefore 
belong  to  the  system  of  spinal  ganglion  neurones.  The  other  tracts  (short  tracts, 
commissural  fibers)  are  spared.  The  degeneration  is  almost  always  most  intense 
in  the  lumbar  cord ;  here  it  affects  chiefly  the  middle  and  posterior  portions  of  the 
posterior  columns,  while  the  most  anterior  portion  and  the  so-called  dorso-median 
sacral  bundle  (Fig.  130,  c)  remain  normal  in  almost  all  cases.  These  are  indeed 
fibers  which  have  another  origin  and  do  not  belong  to  the  spinal  ganglion  system. 
In  the  dorsal  cord  (Fig.  130,  &)  the  posterior  columns  are  almost  completely  de- 
generated. There  are  usually  small  normal  areas  still  preserved  in  the  posterior 
external  and  the  most 
anterior  portions.  In 
the  cervical  cord  (see 
Fig.  130,  a)  the  so- 
called  columns  of  Goll 
are  chiefly  affected, 
together  with  the  pro- 
longation of  the  fibers 
from  the  root-zones  of 

the    lumbar    cord     and  Fig.  l.Sl.— Dorsal  region.  Fig.  132.— Lumbar  region. 

1        ,-,       u  1    ,         i'         .         Transverse  section  through  the  posterior  columns  of  the  cord  in  beginning 

also  the     lateral  root-  tabes  dorsaiis. 

areas  " — that  is,  those 

portions  in  the  columns  of  Burdach  where  fibers  enter  directly  from  the 
posterior  nerve-roots,  and  from  which  fibers  may  be  traced  farther  into 
the  gray  matter  of  the  posterior  cornua;  but  the  so-called  posterior  external 
areas,  and  also  two  little  antero-lateral  areas,  remain  entirely,  or  at  least 
for  a  long  time,  free  from  the  disease,  because  these  are  also  bundles  of  fibers 
which  do  not  belong  to  the  system  of  the  spinal  ganglia  or  posterior  roots.  If 
we  examine  cases  of  tabes  in  the  earlier  stages  which  happen  to  come  to  autopsy, 
we  find  in  the  posterior  columns  only  a  few  root  territories  affected — that  is, 
the  fibers  arising  from  individual  spinal  ganglia  or  posterior  roots  and  lying  near 
one  another,  while  other  root  territories  remain  free  from  degeneration  (Figs. 
131  and  132).  A  system  of  very  fine  fibers,  entering  through  the  posterior  roots, 
is  affected  very  early,  as  a  rule.  It  branches  outward  immediately  after  the 
entrance  of  the  roots,  and  occupies  a  small  but  very  sharply  defined  territory  at 
the  point  of  the  posterior  cornua,  between  the  posterior  and  lateral  columns  (the 
so-called  zone  of  Lissauer).  In  all  the  affected  root  territories  the  degeneration 
slowly  involves  fiber  after  fiber.     The  order  in  wbich  the  different  root  territories 


964  DISEASES    OF   THE   NEEVOUS    SYSTEM 

degenerate,  after  one  another  and  in  part  at  the  same  time  with  one  another,  is 
certainly  not  always  the  same  in  individual  cases,  as  is  evident  from  the  varia- 
tions in  the  clinical  course  of  the  disease.  As  a  rule,  the  neurones  of  the  lumbar 
and  lower  dorsal  spinal  ganglia  certainly  degenerate  first,  and  the  neurone  sys- 
tems of  the  cervical  ganglia  later. 

We  must  state,  with  reference  to  the  participation  of  the  gray  matter  in  the 
disease,  that  the  posterior  comua,  as  we  have  already  said,  are  also  found  con- 
siderably affected,  which  is  explained  mainly  by  the  atrophy  of  the  posterior  root- 
fibers  which  enter  them  directly.  It  also  can  not  appear  strange  that  the  medul- 
lated  fibers  found  in  Clarke's  columns  seem  very  much  reduced  in  number,  since, 
they  also  are  direct  processes  of  the  posterior  root-fibers.  The  cells  of  the  col- 
umns of  Clarke  remain  normal.  The  ganglion-cells  of  the  posterior  horns,  which 
belong  to  the  second  sensory  neurones,  also  remain  normal,  and  no  changes  are 
found  in  the  processes  of  these  cells  in  the  lateral  columns.  The  lateral  and  ante- 
rior columns  of  the  cord  usually  remain  unaltered  {vide  infra). 

On  the  other  hand,  the  peripheral  sensory  nerves — that  is,  peripheral  pro- 
cesses of  the  spinal  ganglion-cells — are  by  no  means  spared.  In  all  cases  of  tabes 
which  have  been  carefully  examined  thus  far,  we  find  in  the  peripheral  nerve- 
trunks  (sciatic,  crural,  etc.),  and  usually  still  more  in  the  finer  branches  of  the 
sensory  nerves,  a  considerable  number  of  degenerated  centripetal  fibers  (Dejerine, 
Oppenheim  and  Siemerling,  and  others).  We  regard  this  degeneration  as  precise- 
ly analogous  to  the  disease  of  the  posterior  columns  and  by  no  means  a  secondary 
degeneration.  Like  the  degeneration  of  the  posterior  columns,  it  also  is  an  ex- 
pression of  the  primary  disease  of  the  peripheral  sensory  neurone  system.  In 
regard  to  the  cell-bodies  in  the  spinal  ganglia,  those  certainly  are  well  preserved 
for  a  long  time,  at  least  in  regard  to  their  external  aspect,  but  finally  we  may  find 
more  or  less  definite  changes  in  them,  although  hardly  ever  complete  atrophy. 

The  anatomical  process  of  tabes  is  by  no  means  limited  exclusively  to'  a 
chronic  degeneration  of  the  first  sensory  neurone  system.  Other  neurones  and 
neurone  systems  may  also  be  involved  in  the  disease.  The  occasional  affection  of 
the  trigeminal  neurones  is  of  course  wholly  analogous  to  the  degeneration  of  the 
sensory  spinal  neurones;  but  other  regions  sometimes  become  degenerated,  espe- 
cially the  optic  nerve,  more  rarely  the  vagus  and  acoustic,  and  also  certain  motor 
regions,  especially  the  ocular  nerves,  other  peripheral  motor  nerves,  the  pyramidal 
lateral  tract,  etc.  We  will  return  more  fully  to  these  "  complications,"  or,  to 
speak  more  correctly,  to  these  rarer  localizations  of  the  tabetic  process,  in  the 
clinical  portion  of  this  chapter.  If  we  consider,  however,  that  the  whole  neurone 
territory  of  the  spinal  ganglia  evidently  contains  neurones  of  very  different 
physiological  importance  (fibers  for  the  conduction  of  the  different  qualities  of 
sensation,  for  the  co-ordination  of  movement,  for  the  innervation  of  the  bladder 
and  rectum,  for  reflex  processes,  etc.),  and  that  also  other  most  diverse  neurone 
territories  may  be  involved  in  tabes,  we  can  understand  that  tabes  can  be  termed, 
not  a  simple,  but  far  more  properly  a  "  combined  systemic  disease." 

The  form  of  the  tabetic  affection  consists  of  a  primary  degenerative  atrophy  of 
the  nerve-fibers,  and  a  corresponding  secondary  increase  of  the  connective  tissue. 
The  gray  color  of  the  posterior  columns  is  due  to  the  loss  of  the  medullary 
sheaths.  Since  the  destruction  of  the  nerve-fibers  advances  but  very  slowly,  we 
find  only  a  few  fatty  granular  cells.  In  old  cases  we  find  numerous  corpora 
amylacea,  whose  origin  and  significance  are  still  unknown.  The  thickening  of. 
the  pia  mater  is  a  purely  secondary  phenomenon,  which  is  always  most  marked 
on  the  posterior  surface  of  the  periphery  of  the  cord,  corresponding  to  the  atrophy 
of  the  posterior  columns. 

Clinical  History. — A  disease  which  has  as  its  basis  so  definite  and  strictly  lim- 
ited an  anatomical  change  as  is  the  case  with  tabes  dorsalis  would  also  be  ex- 


TABES   DOKSALIS  965 

pected.  to  give  a  very  characteristic  clinical  ijicture.  This  supposition  is  entirely 
correct,  and  there  are  few  diseases  which  can  be  diagnosticated,  even  in  their 
earliest  stages,  with  as  much  certainty  as  tabes.  This  fact  is  explained  only  by 
regarding  tabes  as  a  systemic  disease,  in  which  certain  systems  of  fibers  are  always 
affected,  while  others  are  as  constantly  spared  by  the  disease.  The  difference 
between  individual  cases  of  tabes  lies,  therefore,  less  in  the  symptoms  themselves 
than  in  their  intensity,  their  duration,  and  the  order  of  their  occurrence.  In  this 
regard,  however,  the  differences  in  the  clinical  pictures  are  extremely  varied,  so 
that,  even  with  a  comi^aratively  great  personal  experience,  we  often  see  new  com- 
binations of  symptoms  and  also  peculiarities  in  their  course. 

For  the  majority  of  cases  we  may  sketch  the  following  general  description  of 
the  disease,  in  which  it  is  better  to  divide  the  whole  course  into  several  stages; 
but,  of  course,  this  division  can  have  only  a  schematic  value. 

Tabes  dorsalis  begins,  as  a  rule,  with  a  stage  of  initial  symptoms,  which  de- 
velop very  gradually  and  insidiously,  and  which  may  be  of  very  varying  dura- 
tion. The  most  characteristic  symptoms  of  this  stage  are  those  of  sensory  ii-rita- 
tion,  most  frequently  in  the  form  of  the  so-called  lightning-like,  "  lancinating  " 
pains  in  the  lower  extremities.  They  are  sometimes  very  severe,  but  at  other 
times  only  of  slight  intensity,  and  are  comparatively  little  noticed  by  the  patient, 
who  regards  them  as  "  rheumatism."  Many  patients  have  a  feeling  of  numbness 
and  tingling  in  the  tips  of  the  fingers,  especially  of  the  ring  and  little  fingers,  and 
there  is  often  a  pronounced  girdle  sensation  in  the  trunk.  In  some  cases,  too, 
neuralgic  and  migraine-like  pains  in  the  head  may  appear  in  the  early  stages. 

Besides  these  symptoms  of  sensory  irritation,  which  may  often  be  for  years 
the  only  symptoms  of  which  the  patient  complains,  two  objective  symptoms  ap- 
pear very  early,  which  are  of  the  greatest  importance  in  the  diagnosis  of  incipient 
tabes :  the  disappearance  of  the  patellar  reflex  and  the  reflex  immobility  of  the 
pupils.  The  absence  of  the  patellar  reflex  is  the  most  constant  of  all  the  known 
symptoms  of  tabes.  It  is,  as  a  rule,  to  be  found  so  early  that  we  can  hardly  ever 
decide  with  exactness  upon  the  time  of  its  occurrence.  The  reflex  immobility  of 
the  pupil — that  is,  the  failure  of  the  pupil  to  contract  to  light,  while  the  changes 
on  accommodation  may  be  perfectly  retained — is,  indeed,  not  so  constant  as  the 
failure  of  the  patellar  reflex,  but  it  is  present  in  almost  all  cases.  If  all  three 
symptoms- — lancinating  pains,  absence  of  patellar  reflex,  and  immobility  of  the 
pupils — are  present  at  the  same  time,  the  diagnosis  of  tabes  is  absolutely  certain, 
even  if  all  other  symptoms  are  wanting,  because  this  peculiar  combination  of 
three  such  apparently  heterogeneous  symptoms  is  seen  in  this  disease  alone.  If 
only  two  of  these  symptoms  are  present,  but  if  the  reflex  immobility  of  the  pupils 
be  one,  the  diagnosis  is  also  practically  certain ;  but  if  this  symptom  be  absent  we 
should  be  very  cautious  in  admitting  that  the  affection  is  genuine  tabes. 

Among  the  rarer  initial  symptoms  we  shall  also  learn  to  recognize  diplopia, 
caused  by  paralysis  of  certain  ocular  muscles,  and  loss  of  vision,  from  optic  atro- 
phy. In  many  other  cases  certain  disturbances  of  cutaneous  sensibility  (a  girdle 
feeling,  parsesthesia,  a  furry  feeling)  announce  the  approach  of  the  disease. 
Sometimes  disturbances  in  micturition  appear  quite  early,  while  in  other  cases 
gastric  crises  (vide  infra)  or  some  joint  affection  are  the  first  symptoms  which 
the  patient  notices. 

After  this  first  stage  of  the  disease  has  lasted  for  a  very  varying  period,  from 
a  few  months  to  two  or  five  or  even  twenty  years,  the  second  stage  begins ;  this 
we  usually  term  the  ataxic  stage  of  tabes. 

The  beginning  of  this  stage  is  recognized  by  the  appearance  of  disturbances  of 
gait.  The  gait  becomes  more  difficult  and  more  uncertain,  and  there  are  certain 
peculiarities  which  we  will  describe  more  fully  later.  Careful  examination  shows 
that  the  disturbance  in  gait  is  due  not  to  a  paresis  of  the  muscles  but  to  a  disturb- 


966  DISEASES    OE   THE   NERVOUS    SYSTEM 

ance  of  co-ordination,  ataxia  of  the  lower  extremities.  This  symptom  usually 
increases  very  slowly,  until  it  reaches  a  degree  where  the  patient  can  walk  only 
with  assistance,  and  finally  can  not  walk  at  all.  There  is  often  later,  but  almost 
always  not  for  years,  ataxia  of  the  upper  extremities. 

Besides  the  persisting  symptoms  of  the  first  stage,  there  are  often  now  more 
marked  disturbances  of  sensibility,  as  well  as  ataxia.  The  patient  has  a  feeling  as 
if  he  were  walking  on  wool,  felt,  or  similar  substances.  If  he  closes  his  eyes  there 
is  great  swaying  of  the  whole  body — "  Romberg's  symptom."  Physical  examina- 
tion of  the  sensibility  almost  always  shows  considerable  disturbance  of  the  cuta- 
neous sensibility,  especially  of  sensibility  to  pain,  or  even  of  other  forms  of  sen- 
sibility. A  loss  of  muscular  sense  is  very  common.  The  disturbances  of  micturi- 
tion, such  as  incontinence,  gradually  become  more  marked,  and  very  often  cystitis 
gradually  develops.  This  stage  also  may  last  for  years.  Sometimes  the  disease 
seems  to  stand  still,  frequently  even  manifest  improvement  is  seen,  but  then  the 
condition  becomes  worse  again. 

The  third  stage,  the  terminal  stage  of  the  disease,  develops  if  the  patient  has 
not  previously  succumbed  to  an  intercurrent  disease.  The  symptoms  are  the 
same  as  in  most  of  the  other  chronic  diseases  of  the  spinal  cord.  The  patient 
gradually  becomes  more  and  more  wretched  and  helpless,  and  finally  is  confined 
almost  wholly  to  his  bed.  The  ataxia  reaches  an  extreme  degree,  and  finally  there 
is  sometimes  an  actual  motor  weakness  or  complete  paralysis  of  the  legs.  In 
these  cases,  which  are  by  no  means  frequent,  we  are  correct  in  calling  the  third 
stage  of  tabes  the  "  paralytic  stage."  A  severe  pyelo-cystitis  usually  develops, 
bed-sores  appear,  and  death  finally  frees  the  patient  from  his  lamentable  con- 
dition. 

We  must  now  complete  this  briefly  sketched  picture  of  the  disease  by  a  more 
careful  description  of  the  single  symptoms. 

1.  Disturbances  of  Motility  in  the  Extremities. — The  typical  motor  symp- 
tom of  developed  tabes  dorsalis  is  the  disturbance  of  co-ordination,  the  ataxia 
(see  page  837).  This  is  almost  always  seen  in  the  lower  extremities  first.  To 
test  the  ataxia  it  is  most  convenient  to  ask  the  patient  to  touch  the  knee-pan  of 
one  leg  with  the  heel  of  the  other  foot  ("  knee-heel  test  ").  We  see  then  that  the 
leg  moved  is  often  carried  beyond  the  point  designated  several  times  before 
it  reaches  it.  The  ataxia  is  often  noticeable,  even  in  crossing  one  leg  over 
the  other,  as  the  leg  raised  makes  much  too  great  and  too  "  throwing "  a 
movement. 

The  alteration  of  the  gait  is  very  characteristic — the  ataxic  gait,  from  which 
we  can  often  perceive  the  patient's  disease  at  the  first  glance.  If  the  patient  sits 
down  and  tries  to  get  up  again  to  walk,  there  is  difiiculty  in  rising.  He  separates 
his  legs  to  find  a  firra  point  of  support,  he  takes  a  stick  to  help  himself  if  he 
can,  and  he  often  gets  the  proper  balance  to  keep  himself  erect  only  after  several 
attempts.  The  gait  itself  is  straddling,  and  the  legs  are  raised  abnormally  high 
and  set  down  with  a  stamp.  The  direction  of  the  gait,  however,  is  as  a  rule 
well  preserved,  and  the  trunk  (vide  infra)  is  often  but  little  involved  in  the 
swaying.  This  is  the  distinction  between  the  ataxic  gait  of  tabes  (due  to  ataxia 
of  the  legs)  and  the  staggering,  wavering  gait  in  cerebellar  disease  ("  cerebellar 
ataxia  "  with  ataxia  of  the  legs  and  trunk),  in  multiple  sclerosis,  etc.  If  we  have 
the  patient  turn  rapidly  or  make  a  proper  military  "  about  face,"  the  uncertainty 
of  movement  is  still  more  marked,  as  it  also  is  if  the  patient  rises  suddenly  and 
begins  to  walk  or  makes  a  sudden  halt  when  walking.  These  methods  of  testing 
are  therefore  especially  suitable  for  ascertaining  the  first  beginnings  of  ataxia. 
Very  often  the  first  uncertainty  in  the  gait  is  noticed  in  going  down-stairs,  be- 
cause the  patient  can  not  put  his  foot  securely  on  the  next  step  below.  Going 
up-stairs  is  at  first  far  less  affected  because  the  perpendicular  rise  of  the  stairs 


TABES   DOESALIS  967 

prevents  any  excessive  movement.  If  the  ataxia  reaches  a  higher  degree,  most 
tabid  patients  always  walk  with  a  &tick  and  control  the  movements  of  their  legs 
by  keeping  their  eyes  fixed  on  the  floor  as  they  walk.  This  control  is  particularly 
necessary  when  the  sensibility  of  the  legs,  especially  the  muscular  sensibility,  is 
diminished  at  the  same  time. 

In  more  advanced  cases  the  ataxia  becomes  apparent  even  on  standing  with 
the  feet  close  together  (static  ataxia).  We  see  continually  in  the  muscles  and 
tendons  of  the  legs  slight  contractions  which  are  necessary  to  maintain  the  con- 
stantly shifting  equilibrium.  These  contractions  become  much  more  marked  as 
soon  as  the  patient  stands  with  his  eyes  shut.  There  is  then  usually  an  evident 
swaying  of  the  body,  which  is  sometimes  so  great  that  the  patient  is  in  danger  of 
falling.  This  phenomenon  (Romberg's  symptom)  is  due  chiefly  to  the  defective 
control  of  the  muscular  movements,  which  are  necessary  to  preserve  the  equilibri- 
um, as  a  result  of  the  impaired  sensibility  of  the  skin  of  the  soles  of  the  feet  and 
that  of  the  joints  and  the  muscles  themselves.  If  this  control  be  supplied  by  the 
eyes,  the  swaying  is  insignificant,  but  it  at  once  becomes  more  marked  if  the  con- 
trol by  the  eyes  is  lost.  From  a  like  reason  it  is  much  harder  for  most  ataxic 
patients  to  walk  in  the  dark  than  by  daylight. 

In  many  cases  of  tabes,  especially  when  the  disease  is  far  advanced,  the  co- 
ordination of  the  maintenance  of  the  position  of  the  trunk  is  evidently  dis- 
turbed. Such  patients  finally  can  not  sit  up,  since  the  trunk  sways  so  ranch.  The 
gait  of  tabid  patients  with  great  ataxia  of  the  trunk  is  still  more  uncertain  and 
also  plainly  staggering. 

If  ataxia  of  the  upper  extremities  occur  in  the  course  of  the  disease,  it  is 
easily  recognized  if  the  patient  tries  to  take  hold  of  some  definite  object,  such 
as  his  ear,  or  if  he  brings  the  tips  of  his  two  forefingers  together  from  a  certain 
distance,  or  if  he  tries  to  touch  exactly  with  the  tip  of  his  finger  the  finger  of  the 
physician  when  held  before  him.  The  ataxia  is  of  course  also  apparent  in  all  fine 
complicated  movements  (eating,  sewing,  writing,  tying  a  knot,  drawing  straight 
lines,  etc.).  The  movements  are  irregular  and  uncertain,  and  the  excursions  are 
marked.  If  there  be  at  the  same  time  any  sensory  disturbance  in  the  arms,  the 
anomaly  in  their  movements  is  still  greater  with  the  eyes  shut. 

There  has  been  much  written  and  much  argued  as  to  the  cause  of  the  ataxia  in 
tabes  dorsalis.  The  main  reason  why  it  is  at  present  impossible  to  give  an  in- 
controvertible explanation  of  the  occurrence  of  ataxia  lies  in  the  fact  that  we 
are  not  yet  in  a  condition  to  know  and  to  analyze  with  sufficient  accuracy  the 
process  of  normal  co-ordination  of  motion  (page  837) ;  for  manifestly  every  theory 
as  to  the  causes  of  ataxia  must  begin  with  the  processes  involved  in  the  co-ordina- 
tion of  normal  movements.  If  we  try  to  get  a  clear  idea  of  this,  the  most 
essential  point  to  bear  in  mind  is  that  co-ordination  of  motion  is  not  a  con- 
genital function,  but  a  power  of  our  organs  of  motion  acquired  by  practice.  The 
movements  of  little  children  who  are  learning  to  walk  are  ataxic,  and  even  in 
later  life  it  often  happens  that  we  have  to  learn  how  to  perform  certain  compli- 
cated and  difiicult  movements  (so-called  manual  dexterity,  exercises  of  skill).  We 
can  get  no  other  idea  of  this  "  learning  how  to  co-ordinate  "  than  that  it  takes 
place  by  the  aid  of  the  constant  action  of  controlling  and  correcting  impressions 
coming  from  the  periphery — that  is,  centripetal — but  we  must  bear  in  mind  that 
these  actions  are  mainly  unconscious.  The  surer  we  become  in  the  execution  of 
the  movements,  the  more  the  regulatory  influence  of  the  centripetal  irritations 
falls  into  the  background,  without  ever  wholly  disappearing.  In  these  cases  we 
must  not  consider,  by  any  means,  merely  the  irritations  which  are  brought  to  the 
central  organs  from  the  skin  of  the  parts  moved ;  but  we  should  consider,  just  as 
much  or  even  more,  those  irritations  which  are  due  to  the  varying  tension  and 
position  of  the  deeper  parts,  the  muscles,  the  fasciae,  the  ligaments,  and  the  articu- 


968  DISEASES    OF   THE   NERVOUS    SYSTEM 

lar  surfaces.    Even  the  special  organs  of  sense,  particularly  the  eye,  under  some 
circumstances,  assist  materially  in  regulating  motion. 

A  disturbance  of  co-ordination  must  accordingly  take  place  when  this  con- 
stant regulation  of  our  movements  by  centripetal  irritations  ceases.  Since  the 
anatomical  lesion  in  tabes,  as  we  have  seen,  consists  almost  exclusively  of  a  degen- 
eration of  centripetal  systems  of  fibers  passing  through  the  posterior  roots,  there 
can  scarcely  be  a  doubt  in  our  opinion  that  tabetic  ataxia  is  due  to  the  degenera- 
tion of  centripetal  fibers  regulating  movements;  but  we  must  emphasize  the  fact 
that  these  centripetal  co-ordinating  fibers  must  not  be  identified  without  further 
proof  with  the  centripetal  fibers  serving  for  conscious  sensibility,  for  we  can  by 
no  means  establish  a  parallelism  between  the  degree  of  ataxia  and  the  severity  of 
the  sensory  disturbances  (in  the  skin  and  in  the  muscles),  although  of  course 
disturbances  of  co-ordination  and  disturbances  of  sensibility  very  often  co-exist 
in  this  disease.  There  are,  however,  undoubtedly  cases  of  tabes  with  marked 
ataxia  of  the  legs  in  which  we  can  find  on  examination  only  slight  disturbances 
of  the  cutaneous  and  muscular  sensibility.  This  is  still  more  frequently  the  case 
in  other  diseases  attended  with  ataxia. 

We  may  therefore  very  well  imagine  that  ataxia  is  the  consequence  of  a 
degeneration  of  those  collaterals  which  go  from  the  centripetal  neurones  to  the 
motor  ganglion-cells,  and  there  provide  for  the  regulation  of  the  strength  of 
motor  innervation,  although  there  are  still  enough  conducting  paths  to  conduct 
sensory  impressions  to  the  centers  of  consciousness.  We  do  not  as  yet  know, 
however,  in  what  part  of  the  motor  tract  the  regulatory  influence  of  centripetal 
irritations  takes  place;  whether  in  the  cells  of  the  anterior  horns  of  the  cord,, 
which  is  the  simplest  explanation  of  the  theory  of  tabetic  ataxia,  or  higher  up  fn 
the  motor  cortex  or  in  part  in  the  cerebellum,  etc.  This  can  be  made  perfectly 
clear  only  by  further  investigation. 

Ataxia  is  the  chief  motor  disturbance  in  tabes.  The  crude  strength  of  the 
muscles  may  be  perfectly  normal,  and  it  is  chiefly  a  service  of  Duchenne's  to  have 
made  clear  for  the  first  time  the  principal  distinction  between  ataxia  and  paraly- 
sis. He  showed  that  ataxics,  who  can  no  longer  walk  a  step  alone,  can  never- 
theless exert  the  greatest  strength  with  their  legs.  We  have  ourselves  treated  a 
teacher  of  gymnastics  who,  in  spite  of  the  most  marked  ataxia  of  the  arms,  had. 
still  so  much  strength  in  them  that  he  could  support  himself  in  bed  on  his- 
arms  and  keep  his  whole  body,  with  his  legs  extended,  in  the  air.  It  sometimes 
happens,  however,  that  the  crude  strength  also  disappears  in  tabes,  and  that 
the  muscles  become  paretic.  There  may  be  a  simulation  of  a  certain  "  pseudo- 
paresis,"  since  the  patient  with  severe  ataxia  loses  the  ability  to  concentrate  his 
muscular  strength  in  the  necessary  direction.  There  is  also  in  tabes  occasionally, 
as  we  have  said,  an  actual  paralysis  of  the  legs  ultimately.  We  have  stated 
above  that  even  a  complete  paraplegia  may  finally  develop  in  the  course  of  the 
disease.  In  these  cases  we  find,  on  anatomical  examination,  that  the  process  is  ne 
longer  confined  to  the  posterior  columns,  but  that  there  is  also  a  systemic  de- 
generation of  the  lateral  pyramidal  motor  tracts  in  the  lumbar  cord.  In  some 
cases  paraplegia  has  been  observed  to  come  on  quite  suddenly  even  in  the  early 
stages  of  the  disease,  and  usually  to  disappear  again  in  the  course  of  a  few 
weeks.  Its  origin  has  not  yet  been  explained.  The  rare  paralyses  of  certain  motor 
nerves  have  another  significance.  They  have  usually  been  noted  at  the  begin- 
ning of  the  disease,  and  affect  the  radial,  peroneal,  accessory,  etc.  They  are 
probably  due  to  changes  in  the  affected  peripheral  nerves,  but  as  a  rvde  they  are 
transitory,  and,  in  our  opinion,  so  far  as  they  are  not  accidental  complications 
(such  as  pressure  paralyses),  they  are  to  be  put  in  the  same  category  with  tabetic 
oculo-motor  paralyses  (vide  infra). 

We  may  add,  finally,  that  slight  symptoms  of  motor  irritation,  slight  twitch- 


TABES   DOESALIS  969 

ings  in  the  muscles,  especially  in  the  fingers,  are  not  uncopamon,  but  they  are 
noticed  only  when  the  attention  is  especially  directed  to  them.  It  is  not  certainly 
known  how  they  arise ;  perhaps  they  are  of  reflex  origin,  or  perhaps  they  are  con- 
nected with  the  ataxia  and  loss  of  muscle  sense. 

The  condition  of  the  muscles  on  passive  motion  is  very  characteristic.  We 
notice  in  most  cases  a  very  striking  flaccidity  of  the  limbs,  so  that  there  is  hardly 
any  muscular  resistance  to  be  felt.  In  bedridden  tabid  patients  we  can  often,  for 
example,  flex  the  leg  with  ease  at  the  hip  far  enough  to  touch  the  head.  There 
is  evidently  a  diminution  of  muscular  tonus,  a  so-called  hypotonia  of  the  muscles. 
Since  there  are  many  reasons  for  believing  that  the  normal  muscular  tonus  is  of 
reflex  origin,  we  are  led  to  think  of  a  connection  between  the  absence  of  muscular 
tonus  and  the  loss  of  centripetal  irritations.  The  diminution  of  the  muscular 
tonus  in  tabes  is  evidently  in  close  relation  to  the  absence  of  the  tendon  reflexes. 

The  electrical  excitability  of  the  nerves  and  muscles  remains  perfectly  normal 
in  uncomplicated  tabes. 

2.  Disturbances  of  the  Cutaneous  and  Muscular  Sensibility. — As  we  have 
already  said,  tabes  begins,  in  the  great  majority  of  cases,  with  symptoms  of  sen- 
sory irritation,  which  usually  persist  in  the  later  course  of  the  disease.  Be- 
sides the  simple  paresthesia — the  feeling  of  tingling  and  numbness  in  the  legs, 
and  sometimes,  too,  a  similar  feeling  which  appears  quite  early  in  the  upper  ex- 
tremities (especially  often,  as  we  have  said,  in  the  ulnar  region) — the  tabetic 
pains  are  remarkably  characteristic  of  the  disease. 

The  intensity  of  the  pains  differs  very  much  in  different  cases ;  but  we  very 
rarely  see  a  complete  absence  of  them.  The  patient's  attention  is  often 
first  called  to  his  slight  and  infrequent  pains  by  direct  questioning;  but  in 
some  cases  the  severe  pains  are  a  constant  distress  to  him.  The  pains  most 
characteristic  of  tabes  are  the  lightning-like,  "  lancinating  "  pains,  which  shoot 
like  neuralgic  pains  for  some  distance  along  the  course  of  the  nerves.  They  often 
come  on  in  very  severe  paroxysms  ("  pain  crises,"  sometimes  associated  with  con- 
siderable disturbance  of  the  general  condition,  loss  of  appetite,  etc.),  last  one  or 
more  days,  and  then  disappear  for  a  shorter  or  longer  time.  There  are  also  boring, 
stabbing  pains,  which  are  fixed  at  one  point  and  have  their  seat  especially  in  the 
vicinity  of  the  joints;  and  finally  "constricting  pains,"  which  are  felt  most  fre- 
quently in  the  back  and  loins.  The  well-known  "  girdle  feeling  "  of  tabid  patients 
— that  is,  the  sensation  of  a  band  tightly  encircling  the  trunk,  or  a  tight,  "  drawn- 
together  "  pressure  on  the  lateral  portions  of  the  trunk — is  a  similar  symptom  of 
sensory  irritation.  The  girdle  feeling  is  manifestly  due  to  irritative  processes 
in  the  region  of  the  lower  dorsal  or  upper  lumbar  nerves.  Since  it  is  compara- 
tively frequent,  and  often  appears  quite  early,  it  also  has  a  certain  diagnostic 
significance. 

The  tabetic  pains  almost  always  show  themselves  first  in  the  legs,  but  parses- 
thesia  also  occurs,  and  often  very  early,  in  the  intercostal  region  (girdle  sen- 
sation). In  the  ulnar  region  quite  analogous  pains  sometimes  appear,  and  in 
very  advanced  cases  we  have  also  observed  pains  in  the  region  of  the  occipital 
nerves  and  of  the  trigeminus.  On  the  other  hand,  neuralgic  pains  in  the  face, 
especially  in  the  region  of  the  frontal  nerve,  or  in  the  occiput,  or  even  migraine- 
like attacks,  also  occur,  even  in  the  initial  stage  of  tabes,  as  we  have  ourselves 
observed.  In  some  cases  the  lancinating  pains  in  tabes  may  be  accompanied  by 
the  appearance  of  herpes  zoster. 

Usually  much  later  than  the  pains  appears  also  a  diminution  of  sensibility 
which  can  be  made  out  objectively.  As  a  rule,  it  may  be  stated  that  in  most,  but 
not  in  all,  cases  of  tabes  the  sensibility  does  not  remain  normal;  although  well- 
marked  ansesthesia  never  appears  until  the  more  advanced  stages  of  the  disease. 

The  form  of  the  disturbances  of  sensibility  varies  extremely,  and  no  disease 


970  DISEASES    OF    THE    NERVOUS    SYSTEM 

furnishes  so  many  opportunities  for  the  study  of  interesting  details  in  the  region 
of  anomalies  of  sensation  as  tabes  dorsalis.  Our  knowledge  of  the  occurrence  of 
partial  paralyses  of  sensation  especially  is  very  largely  based  on  the  examination 
of  tabid  patients.  In  order  to  form  a  correct  opinion  upon  the  condition  of  the 
cutaneous  sensibility  it  is  therefore  absolutely  necessary  to  test  carefully  all  the 
different  qualities  of  sensation.  Beginning  with  the  examination  of  simple 
sensibility  to  contact  (tactile  sense),  we  often  find  this  very  well  preserved  even 
in  advanced  cases.  There  is  often,  of  course,  a  certain  blunting  of  sensibility. 
A  slight  touch  with  a  camel's-hair  brush  is  often,  even  in  the  early  stages,  no 
longer  felt,  or  felt  only  very  indistinctly,  on  the  lower  legs  and  feet,  or  on  certain 
zones  on  the  trunk  (vide  infra).  The  disturbance  of  the  sensibility  to  pain  is 
more  marked.  A  blunting  of  the  sensibility  to  pain  on  the  legs  is  one  of  the 
most  constant  and  early  symptoms  of  tabes,  but,  in  order  to  determine  it,  it  is 
absolutely  necessary  to  test  at  first  only  by  brief  pricks.  We  then  find,  as  a  rule, 
that  such  pricks  can  not  be  positively  distinguished  from  a  touch  with  the 
head  of  the  pin  or  with  the  finger,  because  the  specific  sensation  of  pain  from  the 
pin-prick  is  lost.  The  case  is  quite  different  if  we  keep  up  a  continuous  pin-prick. 
In  that  case  the  patient  at  first  usually  feels  only  a  painless  touch,  but  after  a 
short  time  (sometimes  only  some  seconds  later)  there  ensues  often  considerable 
pain  accompanied  by  a  reflex  twitch  in  the  leg  pricked.  This  symptom  was  for- 
merly explained  by  Naunyn,  E.  Remak,  and  others  as  "  double  sensation,"  due  to 
"  delayed  conduction  of  the  sensibility  to  pain,"  but,  in  our  opinion,  it  is  depend- 
ent merely  upon  the  slow  summation  of  pain  irritation  which  requires  a  longer 
time  (vide  page  793),  but  there  is  also  perhaps  a  delay  in  conduction.*  Only 
in  far-advanced*  cases  can  the  analgesia,  especially  in  certain  parts  of  the  skin, 
reach  so  great  a  degree  that  even  continuous  painful  irritants  can  no  longer  excite 
a  sensation  of  pain.  The  patient  may  be  nearly  or  wholly  insensible  to  deep 
pin-pricks  or  strong  faradic  currents. 

The  after-sensations  of  tabid  patients  are  another  peculiar  symptom.  It  may 
happen  that  a  patient  after  a  single  prick  may  have  five,  six,  or  more  painful 
after-sensations  at  varying  intervals. 

Disturbances  of  the  sense  of  pressure,  and  still  more  that  of  temperature,  are 
also  quite  frequently  found,  especially  as  partial  paralyses  of  sensation,  when  the 
sensibility  is  otherwise  well  preserved.  We  should  note  particularly  the  occur- 
rence of  partial  anaesthesia  of  the  sensibility  to  heat  or  cold.  On  the  other  hand, 
the  sensibility  to  temperature  may  sometimes  be  very  keen,  while  in  other  re- 
spects there  is  quite  a  high  degree  of  anaesthesia.  Fischer  has  termed  a  peculiar 
disturbance  of  sensibility  occurring  in  tabes,  polysesthesia ;  the  patient  asserts, 
when  examined  with  an  sesthesiometer,  that  he  feels  several  (four  or  five)  points, 
although  he  was  touched  with  but  one. 

The  considerable  anomalies  of  the  rauscular  sense,  which  are  often  to  be  made 
out  in  more  advanced  cases,  have  a  special  interest  (see  page  794).  If  the  patient 
shuts  his  eyes,  he  is  often  entirely  unaware  of  the  situation  and  position  of  his 
limbs.  He  makes  an  indefinite  or  wholly  false  report  as  to  the  direction  and 
extent  of  passive  motions.f  If  the  muscular  sense  in  the  arms  be  disturbed,  and 
we  put  the  arms  into  any  unusual  position,  the  patient  has  considerable  trouble 
in  bringing  the  hands  together  with  his  eyes  shut.  He  gropes  about  in  the  air 
with  his  arms  until  he  accidentally  touches  one  arm  with  the  other  hand,  and 

*  If,  while  the  patient's  eyes  are  shut,  we  prick  the  leg  and  the  arm  or  neek  as  nearly  as  possible 
at  the  same  time,  the  prick  on  the  leg  would  necessarily  be  felt  much  later  than  that  on  the  arm,  if 
there  is  a  delayed  conduction  of  sensory  impressions  from  the  leg ;  but  we  have  never  as  yet  been 
able  to  make  out  this  condition  with  certainty. 

t  We  can  describe  different  letters  and  figures  in  the  air  with  the  patient's  extremities,  and  try 
whether  they  can  be  correctly  recognized  with  the  eyes  shut. 


TABES   DOESALIS  971 

then  he  feels  down  this  to  the  hand.  The  action  of  ataxia  and  muscular  anaes- 
thesia are  accordingly  combined  in_  these  cases.  Pitres  has  lately  described  pe- 
culiar attacks  of  muscular  rigidity,  and  attacks  of  a  decided  feeling  of  fatigue  in 
the  muscles,  apparently  coming  on  spontaneously  in  incipient  tabes  ("  crises  de 
courhature  mitsculaire  "). 

The  limitation  of  the  anaesthetic  or  hypoaesthesic  cutaneous  territories  is  of 
much  interest,  if  we  consider  them  with  regard  to  the  territories  of  distribution 
of  the  different  spinal  ganglia  (page  924  et  seq.).  We  would  mention  in  par- 
ticular that  in  the  very  early  stages  of  the  disease  we  can  often  find  one  or  more 
girdling  zones  of  hyperaesthesia  [or  hypoalgesia]  on  the  trunk,  especially  in  the 
region  of  the  upper  and  middle  dorsal  nerves  (Hitzig  and  Lahr  and  others).  In 
the  legs  very  anaesthetic  and  more  sensitive  regions  sometimes  alternate. 

Only  in  rare  and  far-advanced  cases  is  there  finally  a  complete  anaesthesia  of 
the  lower,  and  exceptionally  of  the  upper  extremities.  We  then  see  also  at  times 
disturbances  of  sensibility  in  the  region  of  the  trigeminus,  in  the  skin  of  the  face. 
We  must  also  mention  the  fact  that  the  peripheral  nerve-trunks,  especially  the 
ulnar  nerve  at  the  elbow,  are  often  insensitive  to  direct  pressure  (ulnar  phe- 
nomenon [Biernacki's  symi^tom]). 

That  the  cause  of  all  these  disturbances  of  sensation  is  to  be  looked  for  in 
the  disease  of  the  peripheral  sensory  neurones  needs  no  further  argument.  It  is  a 
question  only  what  share  the  peripheral  nerves  and  what  share  the  spinal  fibers 
and  cells  have  in  the  causation,  and  how  far  in  general  such  a  localization  of  the 
symptom  is  justified.  In  general  we  regard  it  as  most  probable  that  the  tabetic 
pains  and  par^esthesiae  are  due  to  irritation  in  the  processes  of  the  spinal  ganglia 
leading  to  the  periphery — that  is,  in  the  sensory  peripheral  nerves.  Anaesthesia 
must  of  course  arise  from  any  degenerative  destruction  of  sensory  fibers.  If  there 
is  marked  anaesthesia,  and  especially  analgesia  and  thermoanaesthesia,  we  may 
always  assume  an  atrophy  of  the  root-fibers  entering  the  posterior  horns.  With 
sensory  disturbances  in  the  region  of  the  trigeminus,  we  may  look  for  anatomical 
disturbances  in  the  neurones  of  this  nerve. 

3.  Disturbances  of  the  Reflexes. — The  cutaneous  reflexes  show  no  constant 
changes  in  tabes.  They  are  usually  approximately  normal,  but  sometimes  they 
are  diminished,  especially  if  there  be  at  the  same  time  a  marked  disturbance  of 
sensibility.  In  many  respects  their  condition  corresponds  to  the  condition  of  the 
sensibility  to  pain.  The  abdominal  and  cremaster  reflexes  are  often  preserved  for 
a  very  long  time. 

The  absence  of  the  tendon  reflexes,  especially  of  the  patellar  and  Achilles 
tendon  reflexes,  is,  however,  an  almost  constant  sign  of  tabes,  and  is  a  sign  of  the 
highest  diagnostic  value.  As  we  have  already  said,  the  disappearance  of  the 
patellar  reflex  is  one  of  the  earliest  symptoms  of  the  disease,  and  is  therefore  of 
the  greatest  significance  in  the  diagnosis  of  initial  tabes.  Since  this  symptom 
was  first  discovered  by  Westphal  it  is  not  infrequently  called  "  Westphal's  sign." 
There  are  certainly  cases  of  tabes  in  which  the  patellar  reflex  may  persist  for  a 
long  time,  in  spite  of  the  development  of  many  other  morbid  symptoms.  These, 
however,  are  only  very  rare  exceptions,  which  do  not  disprove  the  rule,  and  do 
not  at  all  contradict  our  general  views  as  to  tabes.  In  individual  cases  those 
fibers  which  serve  to  set  free  the  reflex  may  be  spared  for  a  long  time,  just  as 
any  other  characteristic  sjmptom  of  the  disease  may  under  some  circumstances 
occasionally  be  absent.  Concerning  the  precise  anatomical  cause  of  the  dis- 
appearance of  the  patellar  reflex,  it  can  be  due  only  to  a  degeneration  in  the 
centripetal  portion  of  the  affected  reflex  arc — that  is,  only  in  the  fibers  which 
belong  to  the  territory  of  the  posterior  roots.  It  is  in  accordance  with  this  that 
disease  of  the  middle  portion  of  the  posterior  columns  in  the  lumbar  cord  (that  is, 
the  root-zones,  see  Fig.  132)  always  seems  to  be  accompanied  by  a  failure  of  the 


972 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


patellar  reflex.    The  direct  mechanical  irritability  of  the  muscles,  especially  of  the 
quadriceps,  is  almost  always  retained  in  tabes. 

4.  Disturbances  in  the  Eye  and  the  Other  Organs  of  Special  Sense. — The 
justification  for  regarding  tabes  as  a  combined  systemic  disease  lies  in  the  fre- 
quency with  which  certain  cerebral  symptoms,  as  well  as  the  spinal,  are  found 
in  it. 

The  symptoms  in  the  eyes  deserve  the  first  attention.  We  find,  of  course  not 
in  all  cases,  but  still  in  the  great  majority  of  them,  that  the  pupils  show  no 

trace  of  contraction  to  light, 
although  the  well  -  known 
changes  in  the  pupils  are,  as 
a  rule,  yet  not  invariably, 
very  manifest  upon  any  varia- 
tion of  the  accommodation — 
dilatation  of  the  pupils  on 
looking  at  distant  objects  with 
approximately  parallel  axes  of 
vision  and  contraction  of  the 
pupils  on  fixing  a  near  object 
with  the  greatest  possible  con- 
vergence of  the  eyeballs.  We 
give  this  phenomenon,  first 
described  by  Argyll  Robert- 
son, but  the  precise  anatom- 
ical cause  of  which  is  not  yet 
known,  the  name  of  reflex  im- 
mobility of  the  pupils  with  re- 
tained mobility  on  accommo- 
dation [reflex  iridoplegia] . 
It  is  a  very  characteristic 
feature  that  the  immobile  pu- 
pils are  often  not  perfectly 
round,  but  on  careful  inspec- 
tion seem  rather  irregular  or 
polygonal.  As  we  have  al- 
ready said,  the  immobility  of 
the  pupils  is  often  a  very  early 
symptom,  so  that  it  also  has  a  very  great  diagnostic  importance,  the  more  so 
that  it  is  rarely  found  except  in  genuine  tabes  and  the  allied  general  paralysis. 
In  regard  to  the  average  size  of  the  pupils,  they  are  often  about  normal,  but  we 
very  often  find  both  pupils  unusually  contracted  (spinal  myosis)  or  more  rarely 
dilated.  Quite  frequently  we  find  in  tabes  inequality  of  the  pupils  and,  as  a 
rare  symptom,  a .  striking  change  in  the  size  of  the  pupils,  so  that  first  one  and 
then  the  other  pupil  is  the  larger  ("springing  pupil")-  We  may  also  add 
that  the  dilatation  of  the  pupil  which  is  normally  produced  by  painful  irritation 
of  the  skin  of  the  cheek  is  often  absent  in  tabes  (Erb). 

The  paralyses  of  the  ocular  muscles  in  tabes  are  also  very  interesting  (see  Fig. 
133).  They  are  usually  unilateral,  but  sometimes  bilateral,  and  often  appear 
even  at  the  beginning  of  the  disease,  so  that  diplopia  may  be  the  fii'st  subjective 
symptom  of  which  the  patient  complains.  In  every  sudden  oculo-motor  or  abdu- 
cens  paralysis,  coming  on  without  any  other  cause,  we  must  think  of  the  possibil- 
ity of  an  incipient  tabes.  It  is  remarkable  that  these  paralyses  in  many  cases 
disappear  permanently  and  entirely  after  some  time,  but  it  is  always  possible  that 
they  may  recur  later.     We  once  saw  a  case  of  tabes  with  pronounced  periodical 


Fio.  133. — Paralysis  of  the  left  oculo-motor  nerve  in  tabes. 
(Eriangen  Medical  Clinique.) 


TABES   DORSALIS  973 

oculo-motor  paralysis  (vide  page  857).  The  oculo-motor  paralysis,  however,  when 
it  has  once  appeared,  may  be  permanent,  as  we  have  repeatedly  seen,  especially 
in  a  case  with  bilateral  abducens  and  unilateral  oculo-motor  paralysis,  and  also  in 
a  case  with  almost  complete  bilateral  oculo-motor  paralysis.  In  the  autopsies  on 
such  cases  we  find  the  trunks  of  the  affected  nerves  and  their  nuclei  markedly 
atrophic,  but  it  is  very  probable  that  the  temporary  ocular  paralyses  in  tabetic 
patients  depend  upon  changes  in  the  peripheral  nerves  of  the  ocular  muscles. 

The  third  complication  in  the  eyes  in  tabes  is  optic  atrophy.  It  occurs  in 
about  ten  or  fifteen  per  cent,  of  all  cases,  and  is  usually  an  initial  symptom,  at 
a  time  when  the  absence  of  the  tendon  reflexes,  which  may  usually  also  be  no- 
ticed, is  the  only  thing,  except  this,  to  render  the  diagnosis  of  the  disease  pos- 
sible. The  patient  complains  of  diminution  of  vision;  and  the  power  to  distin- 
guish colors,  especially  green,  disappears  quite  early.  On  objective  examination, 
we  find,  besides  this  anomaly  in  the  color  sense,  usually  a  limitation  of  the  field  of 
vision,  and  the  beginning  gray  degeneration  of  the  optic  nerve  can  easily  be  made 
out  on  ophthalmoscopic  examination.  The  affection  sometimes  makes  little  halts 
and  slight  apparent  improvements,  but  it  usually  ends  with  complete  blindness. 
The  optic  atrophy  more  rarely  may  not  appear  until  the  later  stages  of  the  dis- 
ease, when  all  the  other  symptoms  are  already  fully  developed. 

Auditory  disturbances  are  much  rarer  than  those  of  sight,  but  they  also  occur. 
The  cause,  in  at  least  a  part  of  the  cases,  is  an  atrophy  of  the  acoustic  nerve. 
We  had  a  patient  with  tabes  under  treatment  for  a  long  time  who  was  finally 
entirely  blind  in  both  eyes,  entirely  deaf  in  both  ears,  and  almost  entirely  anges- 
thetic  up  to  the  forehead.  The  only  possible  way  of  communication  was  by  writ- 
ing the  different  letters  of  each  word  on  his  forehead  with  the  finger!  Symp- 
toms are  also  frequently  seen  which  resemble  those  of  Meniere's  disease — tin- 
nitus, vertigo,  and  deafness. 

Changes  in  the  senses  of  taste  and  smell  have  been  observed  only  in  a  few 
cases. 

5.  DlSTURB.^JSX'ES  IN  THE  BLADDER,  THE  EeCTUM,  AND  THE  SeXUAL  OrGANS. Diffi- 
culty in  emptying  the  bladder  is  an  almost  constant  symptom  in  the  later  stages 
of  tabes.  It  sometimes,  indeed,  appears  very  early.  The  patient  feels  the  desire 
to  urinate  more  frequently  than  normal,  there  is  often  a  slight  involuntary  mic- 
turition or  dribbling  of  urine,  and  at  other  times  there  is  retention  of  urine, 
sometimes  coming  on  quite  suddenly;  in  advanced  stages  there  is  frequently 
complete  incontinence.  A  cystitis  very  often  develops  as  a  result  of  all  these 
disturbances,  which  may  be  the  starting-point  of  severe  pyelo-cystitis  and  pyelo- 
nephritis, and  thus  be  the  cause  of  death. 

Persistent  constipation  is  also  a  very  frequent  symptom  of  tabes,  the  reason 
for  which  is  perhaps  to  be  sought  in  the  defective  refiex  excitation  of  intestinal 
peristalsis.  The  constipation  may  in  many  cases  give  rise  to  very  painful  sensa- 
tions in  the  loins  and  abdomen.  The  coccygodynia,  which  sometimes  occurs  in 
tabes,  has  already  been  mentioned  (see  page  820).  Incontinence  of  fseces  occurs 
quite  rarely  in  the  last  stages  of  the  disease. 

A  diminution  in  sexual  power  is  found  almost  constantly  in  advanced  cases ; 
and  it  is  also  often  one  of  the  initial  symptoms. 

6.  Symptoms  in  the  Internal  Organs. — We  see,  not  very  infrequently,  in  tabes 
certain  nervous  symptoms  in  the  internal  organs  which  are  in  part  very  charac- 
teristic. The  most  important  and  the  most  frequent  are  the  so-called  "  gastric 
crises."  These  almost  always  come  on  suddenly  and  paroxysmally,  and  consist 
of  an  extremely  severe  cardialgic  pain,  which  is  accompanied  by  violent  vomiting. 
The  vomitus  usually  consists  of  fluid  slimy  masses  stained  with  bile,  and  usually 
contains  so  much  hydrochloric  acid  that  we  can  call  it  an  actual  hypersecretion 
(vide  page  459).     In  these  attacks  the  patient  feels  very  wretched,  and  there  is 


974 


DISEASES    OE   THE   NERVOUS    SYSTEM 


often  at  the  same  time  palpitation,  acceleration  of  the  pulse,  vertigo,  etc.  The 
attacks  last  about  two  or  three  days.  In  many  patients  they  are  repeated  every 
few  months.  As  we  have  said,  the  gastric  crises  may  appear  very  early.  We 
ourselves  know  cases  where,  in  consequence  of  severe  gastric  crises,  a  serious  gas- 
tric affection  has  been  falsely  diagnosticated,  in  the  beginning  of  the  disease. 
Attacks  of  diarrhoea,  "  intestinal  crises,"  usually  not  associated  with  pain,  have 
also  been  repeatedly  observed. 

We  term  attacks  of  severe  dyspnoea  "  laryngeal  crises."  These  depend  per- 
haps upon  a  (reflex?)  spasm  of  the  glottis,  and  may  attain  a  very  alarming  degree. 
They  are  also  associated  with  a  severe  spasmodic  nervous  cough  like  an  attack 
of  whooping-cough.  These  laryngeal  crises  may  come  on  so  suddenly  that  the 
patient  may  sink  to  the  floor  with  symptoms  of  the  most  extreme  suffocation. 
Paralysis  of  the  laryngeal  muscles  (posterior  crico-arytsenoids)  has  also  been 
observed,  and  it  is  analogous  to  the  other  tabetic  paralyses  (ocular  muscles,  etc.). 
We  may  assume  changes  in  the  vagus-accessory  nucleus,  or  in  the  vagus  or  recur- 
rent itself  (Oppenheim),  as  the  anatomical  cause  of  all  these  symptoms. 

In  a  few  cases  "  renal  crises  "  ("  crises  nephritiques  ")  have  also  been  de- 
scribed. They  consist  of  severe  attacks  of  pain,  like  renal  colic.  French  authors 
also  describe  "  urethral  crises  "  and  "  crises  clitoridiennes,^^  the  paroxysmal  ap- 
pearance of  voluptuous  feelings  with  a  vaginal  secretion  in  women,  in  the  begin- 
ning of  the  disease. 

We  may  mention,  finally,  that  we  sometimes  see  in  tabetic  patients  a  constant 
and  very  great  frequency  of  the  pulse,  100  to  120  a  minute.     We  also  frequently 

see  the  combination  of  tabes  with  aortic  in- 
sufficiency which  has  been  mentioned  by 
some  authors.  The  essential  connection  be- 
tween the  two  affections  lies  probably  in  the 
previous  syphilis. 

7.  Trophic  Disturbances.  —  Although 
trophic  disturbances  are  wholly  absent  in 
many  cases  of  tabes,  they  may,  on  the  other 
hand,  occur  so  frequently  and  in  such  mani- 
fold forms  as  actually  to  be  classed  among 
the  most  interesting  although  least  under- 
stood symptoms  of  tabes.  We  must  first 
mention  that  the  general  nutrition  of  many 
patients  with  tabes,  although  of  course  not 
of  all,  gradually  suffers  in  a  marked  fash- 
ion. The  patients  grow  thin  and  have  a 
peculiar  suffering,  faded  look.  We  can  not 
wholly  deny  a  possible  connection  between 
this  symptom  and  the  primary  disease.  The 
trophic  disturbances  in  the  different  tissues 
are  still  more  striking.  We  have  already 
spoken  of  the  occasional  appearance  of 
herpes  zoster.  In  some  cases  a  marked  ex- 
foliation of  the  epidermis  has  been  seen, 
and  also  a  falling  out  of  the  hair,  nails,  and  teeth.  Peculiar  paraesthesiae 
and  hypoassthesia  of  the  mucous  membrane  of  the  jaws  and  gums  often  pre- 
cede the  loosening  and  falling  out  of  the  teeth.  Sometimes  there  are  small 
haemorrhages,  apparently  spontaneous,  into  the  skin  or  into  the  visible  mu- 
cous membranes,  especially  into  the  conjunctiva,  as  we  have  seen  in  several 
cases.  The  so-called  mal  perforant  du  pied  is  the  worst  trophic  disturbance  of 
the  skin;  this  is  a  round,  deep  ulceration,  situated  on  the  ball  of  the  foot  or  on 


Fig.  134.— Tabetic  arthropathy  of  the  rig'ht 
knee  and  left  ankle.     (Personal  observation.) 


TABES   DOESALIS 


975 


P 


\ 


\ 


the  heel,  which  is  very  hard  and  slow  to  cure  in  spite  of  the  most  careful  treat- 
ment. 

The  most  interesting  trophic  disturbances  in  tabes,  however,  are  sometimes 
found  in  the  bones  and  joints.  These  are  the  tabetic  osteopathies  and  arthropa- 
thies, first  accurately  described  by  Charcot  (Fig.  134).  In  the  bones  there 
sometimes  develops  a  peculiar  brittleness,  which  may  lead  to  a  sudden  fracture, 
which  apparently  occurs  quite  spontaneously  or  on  the  slightest  occasion,  even 
in  bed.  The  painlessness  of  these  fractures,  which  is  due  to  the  tabetic  analgesia, 
is  very  striking;  the  bones  get  out  of  place  without  the  patient's  noticing  it,  and 
thus  the  fracture  often  heals  with 
displacement  and  an  unusual  callus 
formation.  The  tabetic  joint  affec- 
tions are  found  most  frequently  in 
the  knee  and  hip,  more  rarely  in  the 
foot,  shoulder,  or  even  in  one  thumb. 
They  often  seem  to  begin  very  acute- 
ly, a  very  great  serous  eifusion  some- 
times taking  place  into  the  cavity  of 
the  joint.  Besides  this  effusion  there 
gradually  develop  the  manifold  pro- 
cesses of  a  chronic  arthritis  defor- 
mans: on  the  one  hand,  atrophy  of 
the  articular  ends  of  the  bones;  on 
the  other,  thickening  of  the  cap- 
sule, the  formation  of  osteophytes, 
etc.  In  connection  with  the  artlirop- 
athy  there  is  often  permanent  dislo- 
cation of  the  joint.  Thus  we  often 
see,  following  a  tabetic  affection  of 
the  knee,  a  genu  recurvatum  (Fig. 
135).  Arthropathic  muscular  atro- 
phy is  often  seen,  and  is  worthy  of 
note  (atrophy  of  the  quadriceps  in 
disease  of  the  knee-joint,  etc.).  Ta- 
betic arthropathy  may  thus  finally 
lead  to  monstrous  changes  in  the 
joints  such  as  can  scarcely  be  found 
under  other  circumstances.  Corre- 
sponding changes  are  also  seen  in  the 
vertebral  column.  They  may  give 
rise  to  fracture  of  the  vertebra3, 
spinal  curvature,  etc.  The  develop- 
ment of  the  so-called  "  pied  tabe- 
iique "  (Charcot)  is  also  an  osteo- 
pathic process;  this  consists  chiefly 
of  a  considerable  thickening  and  pro- 
trusion of  the  dorsum  of  the  foot 
with  a  marked  flattening  of  the  sole. 

We  are  not  yet  able  to  explain  fully  the  occurrence  of  all  these  changes.  It  is 
hard  to  avoid  entirely  the  assumption  of  trophic  nervous  disturbances.  It  has 
been  claimed  that  degenerative  changes  have  been  found  in  cases  of  tabetic  os- 
teopathy and  arthropathy  in  the  nerves  leading  to  the  bones  and  joints;  but  it  is 
also  possible,  on  the  other  hand,  that  many  of  the  so-called  tabetic  arthropathies 
may  be  of  syphilitic  origin.    It  is  an  important  fact  that  conditions  may  exist  in 


\ 


'■■X ' 


\ 


\ 


Fig.  135. — Genu  recurvatum  in  tabes  dorsalis. 
( Personal  observation. ) 


976  DISEASES    OF    THE   Is^EEVOUS    SYSTEM 

tabes,  which  must  have  a  very  unfavorable  influence  upon  any  existing  bone  or 
joint  affection.  The  most  important  of  these  is  analgesia.  That  is  the  reason  why 
patients,  in  spite  of  a  beginning  arthropathy,  do  not  spare  the  affected  joint  but 
continue  to  irritate  it  still  more.  We  saw  a  patient,  for  example,  where  an  affec- 
tion of  the  knee-joint  developed  in  a  comparatively  very  early  stage  of  tabes, 
which  up  to  that  time  had  not  been  diagnosticated  at  all.  As  the  patient  felt  no 
pain  whatever  in  his  knee,  he  hunted  most  vigorously  through  a  whole  autumn, 
until  finally  an  extremely  severe  swelling  of  the  knee-joint  and  an  actual  subluxa- 
tion of  the  leg  ensued.  It  is  also  possible  that  pronounced  ataxic  movements  may 
frequently  aid  in  irritating  the  articular  surfaces. 

The  muscles  preserve  in  general  their  normal  state  of  nutrition,  except  as  they 
take  part  in  some  joint  affection  or  in  a  general  emaciation.  Charcot  described 
a  case  of  a  combination  of  tabes  with  genuine  progressive  muscular  atrophy,  in 
which  the  autopsy  showed  a  degeneration  of  the  anterior  gray  cornua  in  the  spinal 
cord  besides  the  atrophy  of  the  posterior  columns.  The  first  report  upon  a  unilat- 
eral atrophy  of  the  tongue,  which  sometimes  develops  quite  early  in  tabes,  is  due 
to  the  same  observer.  These  and  similar  atrophies  sometimes  seen  in  other  mus- 
cular territories  are  due  to  degeneration  of  the  corresponding  motor  nuclei  (hypo- 
glossal nucleus,  etc.)  ;  but  peripheral  neuritis  may  also  lead  to  muscular  atrophy 
in  tabes.  Joffroy  described  a  special  form  of  tabetic  club-foot  ("  pied  hot  ta- 
hetique  "),  which  seems  to  be  due  to  an  atrophy  of  the  calf  muscles. 

Some  observations  of  apparently  spontaneous  rupture  of  the  tendons  (Achilles 
tendon,  ligamentum  patellae)  show  that  peculiar  trophic  disturbances  may  also 
develop  in  them. 

8.  Cerebral  Symptoms. — ^Besides  the  frequent  important  disturbances  on  the 
part  of  certain  cerebral  nerves,  such  as  the  optic  and  oculo-motor,  which  have 
already  been  discussed,  we  must  mention  here  the  relation  between  tabes  and 
progressive  general  paralysis  (g.  v.).  On  the  one  hand,  the  symptoms  of  tabes 
are  often  present  in  the  course  of  general  paralysis,  so  that  the  autopsy  shows  a 
typical  degeneration  of  the  posterior  columns  (Westphal)  ;  and,  on  the  other 
hand,  it  also  happens  that  the  whole  process  begins  with  tabes,  which  may  exist 
alone  for  years  without  any  mental  symptoms,  and  then  only  at  the  close  do  the 
symptoms  of  paralytic  dementia  (mental  weakness,  disturbances  of  speech,  para- 
lytic attacks,  delusions  of  grandeur,  etc.)  appear.  This  combination  of  the  two 
diseases  is  nothing  strange,  since  general  paralysis  is  also  a  post-syphilitic  neiw- 
ous  disease,  and  is  to  be  regarded  as  almost  wholly  analogous  to  tabes.  Paralytic 
dementia  has  been  called,  not  without  reason,  "  tabes  of  the  brain." 

The  complication  of  tabes  with  hemiplegia  repeatedly  occurs.  The  latter  de- 
pends upon  a  cerebral  haemorrhage  or  an  embolic  or  thrombotic  softening,  so  that 
the  two  diseases  are  probably  connected  only  so  far  as  they  are  both  perhaps  re- 
lated to  previous  syphilis.  It  seems  to  us  worthy  of  note  that  in  two  such  cases 
we  saw  scarcely  any  contracture  develop  in  the  paralyzed  limbs. 

Course  and  Prognosis. — Although  most  of  the  characteristic  symptoms  of 
tabes  develop  in  almost  all  cases,  still  the  order  and  the  intensity  of  their  onset 
vary  greatly.  We  have  already  briefly  described  the  general  type  of  the  disease 
which  most  frequently  comes  under  observation,  and  many  other  peculiarities  in 
its  course  have  been  mentioned  from  time  to  time. 

We  have  stated  that  the  initial  period  is  usually  characterized — apart  from 
the  symptoms  that  can  be  made  out  only  objectively,  such  as  absence  of  the  patel- 
lar reflex  and  reflex  immobility  of  the  pupils — by  the  lancinating  pains;  that  these 
may  differ  very  much  in  intensity;  and  that  the  duration  of  this  flrst  stage  may 
vary  between  a  few  months  and  ten  or  twenty  years.  The  optic  atrophy,  the 
ocular  paralyses,  gastric  crises,  vesical  disturbances,  etc.,  were  mentioned  as 
rarer  initial  symptoms.    The  passage  from  the  first  stage  to  the  second — the  stage 


TABES   DOESALIS  977 

of  ataxia — is  sometimes  very  gradual,  but  in  other  cases  very  rapid  and  sudden. 
We  have  repeatedly  seen  such  transitions.  Frequently  they  come  on  clearly 
after  some  special  exciting  cause,  as  after  some  injury,  some  physical  over-exer- 
tion, etc.  If  the  previous  symptoms  were  slight,  the  patient  dates  his  disease 
from  this  point,  and  says  that  he  was  quite  suddenly  broken  down  by  some  cause, 
and  that  since  then  he  has  not  been  able  to  walk  at  all,  or  else  only  with  diffi- 
culty. Even  in  such  cases  there  is  often  slow  improvement  following  the  sud- 
den change  for  the  worse,  but  the  gain,  of  course,  is  not  permanent.  In  other 
cases,  however,  the  ataxia  develops  only  very  slowly  and  never  reaches  a  very 
marked  degree.  Experience  teaches,  in  particular,  that  tabid  patients  with  early 
atrophy  of  the  optic  nerves  or  with  unusually  severe  attacks  of  pain  are  often 
without  more  than  a  trace  of  ataxia  for  a  very  long  time — many  years ! 

No  rules  of  general  value  can  be  given  as  to  the  further  advance  of  the  disease, 
the  invasion  of  the  arms  by  the  ataxia,  or  the  occurrence  of  the  rarer  symptoms, 
such  as  the  joint  aifections,  etc.  Almost  every  individual  case  affords  its  idiosyn- 
crasies, since  one  group  of  symptoms  is  often  especially  prominent,  while  another 
is  entirely  absent  or  developed  only  to  a  slight  degree.  On  the  whole,  however,  we 
can  almost  always  make  out  a  gradual,  even  if  a  very  slow,  advance  in  the  disease. 
ITew  symptoms  appear,  the  old  ones  increase,  the  general  condition  becomes  worse, 
until  finally  the  last  stage  of  the  disease  comes  on. 

Recovery  from  tabes  in  the  sense  that  all  the  existing  symptoms  (immobile 
pupils,  absence  of  patellar  reflex,  etc.)  wholly  disappear,  have  never  yet  been 
observed  with  certainty,  and  a  Tpriori  such  a  thing  is  hardly  conceivable;  but  it 
is  not  so  very  rare  for  the  tabetic  process  to  be  arrested  for  at  least  a  year.  We 
liave  become  acquainted  with  such  cases  only  since  we  have  been  able  to  recognize 
with  certainty  the  initial  stages  of  the  disease.  We  have  ourselves  known  for 
many  years  a  number  of  mild  cases  of  tabes  in  whom  it  is  scarcely  possible  to 
■detect  any  recognizable  progress  in  the  disease  and  who  regard  themselves  as 
almost  perfectly  well.  They  go  to  their  business  and  have  little  or  no  trouble 
from  their  disease.  Of  course  we  must  be  prepared  for  an  ultimate  change  for  the 
"worse  even  in  such  cases.  In  more  advanced  tabes,  treatment  may  at  most  cause 
some  improvement,  delay  the  course  of  the  disease,  and  alleviate  certain  symp- 
toms ;  many  patients,  especially  under  favorable  external  conditions,  may  even  in 
this  stage  lead  a  tolerable  existence  for  years. 

Diagnosis. — There  is  scarcely  any  other  disease  of  the  spinal  cord  whose  diag- 
nosis can  in  most  cases  be  made  with  so  great  certainty  and  such  comparative 
ease.  Since  tabes  is  a  combined  systemic  disease,  it  affords  a  definite  combina- 
tion of  symptoms  such  as  can  occur  under  no  other  conditions.  The  diagnosis, 
therefore,  is  never  to  be  made  from  any  one  single  symptom,  but  only  from  the 
combination  of  all  and  from  the  whole  course  of  the  disease. 

The  diagnosis  of  initial  tabes  is  especially  important.  In  every  case  of  obsti- 
nate "  rheumatic  "  pains,  or  similar  pains  in  the  lower  extremities,  we  should 
think  of  the  possibility  of  tabes,  and  examine  the  tendon  reflexes  and  the  pupils. 
The  combination  of  characteristic  pains,  absence  of  the  patellar  reflex  on  the  two 
•sides,  and  reflex  immobility  of  the  pupils,  usually  makes  the  diagnosis  almost 
absolutely  certain,  as  was  said  above;  two  of  these  symptoms,  especially  if  the 
reflex  immobility  of  the  pupils  be  one,  make  it  at  least  very  probable.  Ocular 
paralyses,  temporary  ptosis,  or  temporary  diplopia,  may  be  very  important  for  the 
-diagnosis.  We  should  also  remember  that  the  disease  may  begin  with  optic  atro- 
phy, and  that  early  gastric  crises  may  simulate  a  gastric  affection,  early  disturb- 
ance in  micturition  a  vesical  trouble,  or  swelling  of  the  joints,  a  joint  disease, 
until  careful  examination  of  the  other  symptoms  explains  the  true  nature  of  the 
disease.  The  essential  point  is  to  think  at  once  in  every  such  case  of  the  possi- 
bility of  tabes,  and  look  for  the  distinctive  objective  symptoms.  Among  the  latter 
62 


978  DISEASES    OF   THE   NEEVOUS    SYSTEM 

we  would  call  especial  attention  here,  besides  the  symptoms  generally  recognized 
(absence  of  tendon  reflexes,  immobile  pupils,  slight  vesical  weakness),  to  the 
limited  girdle-like  disturbance  of  sensation  on  the  trunk,  since  in  doubtful  cases 
this  is  often  of  decided  significance  in  diagnosis. 

In  the  fully  developed  ataxic  stage  of  tabes  the  diagnosis  is  almost  always 
easy,  and  it  often  can  be  made  at  the  first  glance.  The  history,  the  characteristic 
ataxic  gait,  the  swaying  with  the  eyes  shut,  the  absence  of  the  reflexes,  etc.,  ex- 
clude every  doubt.  The  diagnosis  may  be  more  difiicult  if  we  happen  to  see  the 
patient  for  the  first  time  in  the  final  stage,  when  actual  paralysis  has  set  in,  when 
a  complicating  hemiplegia  has  arisen,  etc.  In  such  cases  we  must  lay  stress  on 
the  development  of  the  disease  and  find  out  what  characteristic  tabetic  symptoms 
— pupillary  symptoms,  absence  of  patellar  reflex,  vestiges  of  ataxia,  or  pains — can- 
now  be  discovered.  With  proper  attention  and  knowledge  of  the  case,  the  diag- 
nosis can  even  then  almost  always  be  made  correctly. 

Vertebral  affections  are  to  be  mentioned  first  of  the  diseases  which  may  be 
confused  with  tabes.  These  also  cause,  under  some  circumstances,  lancinating- 
pains  and  an  absence  of  the  patellar  reflex,  as  a  result  of  compression  of  the  spinal 
Toots;  but  in  these  cases  the  later  course  of  the  disease  is  entirely  different, 
apart  from  the  changes  in  the  vertebral  column  and  the  absence  of  other  charac- 
teristic symptoms  of  tabes,  especially  the  immobile  pupils.  The  same  holds  true- 
of  certain  deep-seated  tumors  in  the  vicinity  of  the  spinal  cord.  We  have  already 
said  that  in  rare  cases  a  multiple  sclerosis  may  offer  symptoms  similar  to 
those  of  tabes.  In  these  cases  the  chief  stress  in  regard  to  diagnosis  is  to  be- 
laid on  the  condition  of  the  tendon  reflexes,  the  pupils,  the  disturbances  of  sen- 
sation, and  the  bladder.  It  is  of  greater  practical  importance  that  certain  toxie 
nervous  diseases  may  have  a  great  similarity  to  tabes.  Chronic  alcoholic  neuritis 
has  already  been  spoken  of  in  this  connection — the  so-called  pseudo-tabes  of  alco- 
holic subjects.  In  these  cases,  however,  the  reflex  immobility  of  the  pupils  and  the 
disturbances  of  the  bladder  are  usually  absent,  while  atrophic  paralysis  may 
develop  at  the  same  time,  which  hardly  ever  happens  in  tabes.  The  setiological 
factors  (alcoholism)  are  also,  of  course,  to  be  taken  into  account.  In  adults  post- 
diphtheritic ataxia  may  be  mistaken  for  tabes.  In  such  cases  a  consideration 
of  the  aetiology,  and  especially  the  condition  of  the  pupils  and  of  the  vesical  dis- 
turbances, will  usually  make  the  correct  diagnosis  easy.  "  Diabetic  tabes  "  (page 
758)  can  scarcely,  with  proper  attention,  be  mistaken  for  true  tabes.  The  dif- 
ferential diagnosis  between  tabes  and  Friedreich's  hereditary  ataxia  will  be  de- 
scribed in  the  next  chapter. 

Finally,  it  may  be  mentioned  here  that  we  have  twice  seen  a  group  of  nerv- 
ous symptoms  in  men  who  have  worked  many  years  in  tobacco  factories,  which 
resembled  tabes  in  so  many  points  that  we  might  term  it  "  nicotine  tabes."  The 
morbid  symptoms,  which  resemble  tabes,  consist  of  painful  sensations,  absence  of 
the  patellar  reflex,  contracted  pupils  with  reflex  immobility,  and  uncertainty  of 
gait ;  but  the  whole  type  of  the  disease  is  distinguished  from  tabes  by  a  peculiar 
tremor,  by  a  marked  increase  of  the  cutaneous  reflexes,  especially  in  the  lower 
extremities,  etc. 

Treatment. — The  tedious  course  of  tabes  demands  that  the  physician  have  at 
hand  a  number  of  remedies  and  methods  of  treatment  which  he  can  vary  according- 
to  the  predominating  circumstances,  either  to  obtain  a  certain  amount  of  improve- 
ment by  a  new  way  of  attacking  the  disease,  or  at  least  constantly  to  kindle  the 
patient's  hope  and  courage  anew. 

The  first  question  which  is  usually  raised  at  present  in  regard  to  the  treat- 
ment of  tabes  is  in  regard  to  the  efficacy  of  a  specific  antisyphilitic  treatment. 
In  our  opinion,  the  ability  to  answer  this  question  correctly  depends  not  merely- 
on  recognizing  the  fact  of  the  connection  between  tabes  and  syphilis,  but  also  on 


TABES   DOESALIS  979 

forming  a  clear  conception  of  the  nature  of  this  connection.  There  can  then  be 
no  doubt  that  in  tabes  there  is  not  even  a  remote  question  of  such  efficacy  of  mer- 
cury or  iodide  as  we  see  almost  as  a  rule  in  true  tertiary,  gummatous  syphilitic 
diseases.  We  very  often  see  in  tabes  no  benefit  at  all  from  an  inunction  cure 
or  from  the  internal  use  of  iodide  of  potassium,  and  in  some  cases  the  con- 
dition seems  even  to  grow  worse  under  such  treatment.  Such  observations  were 
for  a  long  time  cited  as  the  chief  evidence  against  the  connection  between  the 
two  diseases.  If,  however,  we  adopt  the  position  which  we  have  advanced  that 
tabes  is  a  post-syphilitic  degenerative  nervous  disease,  just  as  ataxia  may  some- 
times be  a  post-diphtheritic  disease,  we  can  easily  understand  the  inefficacy 
of  a  specific  remedy,  which  acts  only  on  syphilitic  new  formation  of  tissue. 
Nevertheless  we  may  not  wholly  exclude  antisyphilitic  methods  of  treatment  from 
the  therapy  of  tabes;  for,  in  the  first  place,  it  is  always  possible  (and  it  seems  to 
us  to  be  confirmed  by  many  trials)  that  an  antisyphilitic  treatment  (inunction, 
iodide  of  potassium)  may  infiuence  in  a  way  beneficial  to  the  patient  the  con- 
ditions which  cause  tabes  to  advance.  It  has,  furthermore,  been  fully  attested  by 
repeated  observations  that,  besides  the  tabetic  changes  in  the  cord,  there  may  also 
be  at  the  same  time  actual  syphilitic  gummatous  processes,  which  of  course  may 
contribute  their  part  to  the  symptoms  of  the  disease.  That  these  morbid  processes 
require  thorough  specific  treatment  is  certain,  and  therefore 'we  regard  it  as  justi- 
fiable and  even  desirable  to  make  a  trial  of  inunction  in  beginning  tabes,  and 
under  some  circumstances  even  in  advanced  tabes,  especially  if  any  anomalies  in 
the  type  of  the  disease  suggest  the  possibility  of  co-existing  gummatous  changes. 
Very  experienced  observers,  especially  Erb,  have  gained  the  impression  that  a 
careful  inunction  treatment  sometimes  visibly  benefits  the  patient.  We  can  not, 
of  course,  report  much  that  is  favorable  from  our  own  experience,  but  we  often 
employ  specific  treatment,  especially  iodine  preparations,  in  cases  that  seem 
suitable.  Every  inunction  treatment  prescribed  in  tabes  must  be  carefully 
watched,  that  no  injury  be  done  to  the  patient  by  this  potent  remedy.  In  many 
advanced  cases  of  tabes,  especially  where  the  patient's  general  condition  is  feeble, 
we  must  abstain  wholly  from  mercurial  treatment. 

If  the  antisyphilitic  treatment  be  not  indicated,  or  if  it  has  been  unsuccessful, 
electricity  and  balneo-therapeutics  or  hydro-therapeutics  deserve  relatively  the 
most  confidence,  although  of  course  we  must  beware  of  exciting  too  sanguine 
hopes. 

The  electrical  treatment  consists  chiefly  of  the  passage  of  the  ascending  con- 
stant current  through  the  spinal  cord.  The  current  must  not  be  too  strong,  and 
the  sittings  should  take  place  daily,  or  every  other  day.  Erb  recommends  placing 
the  medium-sized  cathode  in  the  vicinity  of  the  sympathetic,  and  the  large  anode 
close  to  the  spinous  processes  on  the  other  side  of  the  vertebral  column,  moving  it 
at  intervals  from  above  downward.  This  procedure  lasts  about  four  or  five  min- 
utes for  each  side.  We  also  obtain  good  results  symptomatically  when  there  are 
severe  pains,  vesical  weakness,  etc.,  by  peripheral  galvanization.  If  we  find  pain- 
ful points  on  the  vertebral  column,  as  is  rarely  the  case,  they  should  be  especially 
treated  with  the  stabile  anode.  The  treatment  recommended  by  Rumpf  with  the 
faradic  brush  has  also  been  used  at  times  with  good  results.  This  consists  in 
brushing  the  skin  of  the  back  and  the  extremities  with  a  strong  current  for  five 
or  ten  minutes.  Every  form  of  electrical  treatment,  in  order  to  obtain  results, 
must  be  kept  up  for  months. 

Hydro-therapeutics,  used  rationally,  have  often  resulted  in  considerable  im- 
provement in  tabes,  although  they  may  cause  much  mischief.  Hot  baths,  espe- 
cially vapor-baths,  are  often  followed  by  a  rapid  change  for  the  worse — a  fact 
which,  unfortunately,  we  can  often  observe  where  vapor-baths  have  been  pre- 
scribed for  patients  at  the  beginning  of  their  disease  "  for  rheumatism."     Con- 


980  DISEASES    OF   THE   NERVOUS    SYSTEM 

tinuous  wet  packs  and  severe  rubbings  are  also  often  accompanied  by  unfavorable 
results.  Tepid  half  or  full  baths,  however,  of  75°  to  86°  at  most  (20°-24°  R.), 
associated  with  gentle  rubbing  of  the  skin,  or  brief  cold  sponging,  etc.,  often  do 
good  service.  Wet  compresses,  applied  around  the  abdomen  or  the  legs  at  night, 
often  have  a  favorable  iniluence  on  the  pains.  In  general,  it  is  a  good  plan  to 
send  well-to-do  patients  in  summer  to  a  water-cure  establishment  which  is  con- 
ducted by  an  experienced  director  and  well  equipped,  but  the  necessary  procedures 
may  also  be  undertaken  at  home. 

Of  the  baths  whose  use  is  recommended  in  tabes,  Oeynhausen  has  the  greatest 
reputation.  The  baths  in  ISTauheim  have  a  composition  and  action  very  similar  to 
those  at  Oeynhausen.  We  have  also  seen  very  good  results  from  the  baths  at 
Kissingen.  Many  physicians  praise  mud-baths  and  iron-baths  (Pyrmont,  Dri- 
burg,  Cudowa,  Elster,  Franzensbad,  etc.),  while  the  indifferent  thermal  baths 
(Teplitz,  Wildbad,  Eagatz,  etc.),  formerly  much  in  favor,  are  at  present  rarely 
used  in  tabes.  For  the  preparation  of  artificial  carbonic-acid  salt  baths  see 
pages  952,  953. 

Besides  the  methods  of  treatment  thus  far  mentioned,  there  are  still  a  number 
of  internal  remedies,  the  use  of  which  seems  sometimes  to  be  of  advantage.  The 
chief  ones  to  be  mentioned  are  nitrate  of  silver,  first  recommended  by  Wunderlich, 
one-sixth-of-a-grain  pills  (gramme  0.01),  at  first  three,  gradually  increasing  to 
six  a  day,  before  meals;  and  ergotine,*  one-grain  pills  (gramme  0.05),  three  to 
six  a  day;  we  may  also  try  iodide  of  potassium,  phosphorus,  arsenic,  etc.  All 
these  remedies,  especially  the  two  first  named,  may  be  used  for  a  long  time,  and, 
with  interruptions,  even  for  years. 

In  consequence  of  a  somewhat  too  sanguine  indorsement  by  Langenbuch, 
nerve-stretching  (usually  the  operative  stretching  of  both  sciatics)  was  for  some 
time  practiced  on  many  tabid  patients,  but  since  experience  has  taught  us  that 
nerve-stretching,  in  spite  of  some  apparent  successes,  scarcely  ever  exerts  a  perma- 
nent favorable  action,  and  is  also  not  wholly  without  danger,  the  operation  has 
been  almost  entirely  given  up  in  tabes.  It  may  still  be  tried  in  those  cases  where 
we  have  unusually  severe  attacks  of  pain  in  the  region  of  definite  neiwes.  In 
such  cases  we  should  first  try  bloodless  stretching  (page  820).  The  "suspension 
treatment "  of  tabes  has  also  had  only  a  brief  vogue.  This  consisted  in  hang- 
ing up  the  patient  for  a  short  time  by '  an  apparatus  fastened  under  the  chin 
[and  arms],  thus  stretching  the  spinal  cord  and  the  nerve-roots  by  the  weight  of 
the  body.  The  successes  at  first  reported  are  of  very  doubtful  significance,  while 
there  were  certainly  some  very  unfortunate  consequences.  We  ourselves  can 
not  advise  the  use  of  this  method.  The  treatment  of  tabes  by  firmly  fitting 
corsets  is  also  much  praised  and  recommended.  If  we  listen  to  the  patients  who 
have  just  left  the  sanitarium  of  some  eminent  orthopaedic  surgeon,  they  know 
no  end  to  their  praise.  If  we  see  them  again  in  a  year  and  a  day,  we  find  them 
ataxic  as  before,  and  the  corsets — in  some  corner !  Temporary  symptomatic  bene- 
fit should  not  be  denied,  but  of  course  the  corset  treatment  can  not  affect  the 
tabetic  process  itself. 

Symptomatically,  the  same  remedies  are  to  be  considered  as  were  mentioned 
in  the  treatment  of  chronic  myelitis.  We  try  to  alleviate  the  pains  by  narcotic 
embrocations  and  bandaging  the  legs.  Of  internal  remedies,  sodic  salicylate  and 
antipyrine,  and  also  antifebrine,  phenacetine,  or  a  mixture  of  these  remedies, 
sometimes  undoubtedly  alleviate  and  shorten  the  pains.     [Chloride  of  aluminium, 

*  There  is  only  an  apparent  contradiction  in  the  fact  that,  in  spite  of  the  occurrence  of  an  "  er^o- 
tine  tabes"  (vide  supra),  ergotine  is  also  used  as  a  remedy  against  tabes.  It  may  very  well  be  that 
the  same  remedy,  which  in  large  doses  causes  certain  systems  of  fibers  to  atrophy,  may  in  smaller 
doses  have  some  favorable  (stimulating)  action  on  the  same  system  of  fibers  ;  but  we  must  always  be 
cautious  in  the  use  of  ergotine. 


HEEEDITAEY    (JUVENILE)    ATAXIA     '  981 

in  doses  of  two  to  four  grains  (gramme  0.1-0.25)  three  times  a  day,  occasionally 
relieves  the  pain. — K.]  Some  observers  praise  the  action  of  the  so-called  points  de 
feu  (circumscribed  burning  of  the  skin  with  the  thermo-cautery)  along  the  spine 
at  the  points  of  exit  of  the  affected  nerve-roots.  In  bad  cases  morphine  is  indis- 
pensable. We  try  to  remove  the  constipation  by  prescriptions  as  to  diet,  or  by  mild 
cathartics,  such  as  the  bitter  waters,  tamarinds,  and  rhubarb,  by  enemata,  or  by 
electrical  treatment  and  massage  of  the  abdomen.  Galvanic  treatment  often 
acts  very  favorably  on  the  bladder  symptoms.  For  these  symptoms  Charcot 
praises  the  action  of  ergot,  and  other  physicians  recommend  strychnine.  Mor- 
phine is  the  best  remedy  in  the  gastric  crises.  We  may  also  try  warm  poultices, 
washing  out  the  stomach,  belladonna,  chloral,  cocaine,  etc.  Severe  laryngeal 
crises  also  require  morphine  injections  as  a  rule.  Optic  atrophy  unfortunately 
defies  any  treatment.  We  usually  try  strychnine  injections  to  encourage  the 
patient. 

One  method  for  the  symptomatic  treatment  of  tabes  deserves  special  mention, 
and  that  is  the  treatment  of  ataxia  by  methodical  exercises  (G.  Frenkel).  If 
ataxic  patients  are  systematically  admonished  to  execute  all  the  movements  of 
the  several  joints  slowly  and  as  regularly  as  possible  several  times  each  day  for  a 
definite  time,  and  also  to  perform  certain  other  movements  (touching  a  definite 
point  with  the  fingers  or  toes,  walking  a  chalk  mark,  walking  between  the  rungs 
of  a  ladder,  seizing  swinging  balls,  putting  stoppers  into  definite  holes,  etc.), 
we  may  often  recognize  that  the  practice  actually  has  an  influence  upon  the 
certainty  of  the  movements  and  leads  to  an  improvement  in  the  ataxia.  Certain 
sanitaria  carry  out  this  method  of  treatment  by  the  use  of  complicated  apparatus. 
The  benefit,  however,  should  not  be  overvalued. 

It  is  also  of  the  greatest  importance  that  the  physician  should  regulate  and 
supervise  the  patient's  mode  of  life  in  its  general  hygienic  and  dietetic  aspect. 
We  must  warn  him  especially  against  any  physical  or  mental  over-exertion, 
prescribe  a  prudent  but  strengthening  diet,  withdrawing  all  large  amounts  of 
alcoholic  drinks,  and  enjoin  good  air,  a  country  residence  in  summer,  or  a  medium 
mountain  climate,  and  in  winter  at  times  southern  resorts.  How  effective  this 
general  dietetic  treatment  of  tabes  is,  may  be  seen  in  hospitals,  where  tabid  pa- 
tients of  the  lower  classes  are  sometimes  much  benefited  by  simple  rest  and  good 
care.  The  earlier  we  get  the  patient  under  treatment,  the  more  persevering  and 
careful  should  we  be  in  our  treatment,  because  then  we  can  still  hope  for  a  cer- 
tain success.  In  old  and  far-advanced  cases  we  must  confine  ourselves  to  a  purely 
symptomatic  treatment. 


CHAPTEE  VIII 
HEREDITARY    (JUVENILE)    ATAXIA    (FRIEDREICH'S    DISEASE) 

.Sltiology  and  Pathological  Anatomy. — In  1861  Friedreich  first  described  a 
peculiar  disease  observed  by  him  in  several  members  of  the  same  family.  He  at 
first  regarded  the  disease  as  a  special  form  of  tabes  on  account  of  the  marked 
ataxia  attending  it,  but  later  investigations  have  shown  that  this  "  Friedreich's 
disease  "  has  nothing  in  common  with  true  tabes  except  a  certain  similarity  of 
symptoms  (especially  ataxia),  which  is  due  to  the  fact  that  the  anatomical 
changes  in  the  cord  agree  in  part  in  the  two  affections.  While  tabes  represents 
an  acquired  degeneration  of  different  neurone  systems,  Friedreich's  disease  is 
undoubtedly  due  to  a  congenital  morbid  predisposition  of  certain  neurone  sys- 
tems, as  a  consequence  of  which  these  neurone  systems  have  not  developed  their 


982  DISEASES    OF   THE   NERVOUS    SYSTEM 

full  and  permanent  functions  and  therefore  atrophy  slowly  and  prematurely. 
This  congenital  origin  of  the  disease  is  most  evident  from  the  fact  that  the  disease 
is  not  infrequently  seen  in  several  (two  to  five)  brothers  and  sisters,  and  in  some 
cases  in  members  of  two  or  more  generations  of  the  same  family.  Of  course 
sporadic  cases  of  Friedreich's  disease  are  seen  with  comparative  frequency,  but 
in  such  cases  the  youthful  age  at  which  the  first  symptoms  of  the  disease  are  no- 
ticed indicates  the  congenital  abnormal  tendency.  The  first  symptoms  sometimes 
appear  at  the  age  of  seven  to  ten  years,  but  frequently  not  until  puberty,  and  in 
some  cases  even  somewhat  later  (eighteen  to  twenty  years).  It  is  usually  hard  to 
determine  accurately  the  period  of  onset,  because  the  disease  begins  very  gradual- 
ly, and  therefore  its  onset  may  certainly  remain  unnoticed  for  a  long  time.  The 
disease  is  about  equally  common  in  the  two  sexes,  perhaps  a  little  commoner  in 
the  male.  The  first  symptoms  sometimes  seem  to  follow  some  acute  disease 
(scarlet  fever,  measles,  influenza),  injury,  etc.,  but  these  are  exciting  causes 
which  make  the  existing  morbid  tendency  manifest. 

Clinical  History.- — The  first  symptom  invariably  to  be  noticed,  which  is  by  far 
the  most  important  later,  is  ataxia.  It  shows  itself  at  first  as  a  slowly  increasing 
uncertainty  of  gait;  almost  at  the  same  time  or  only  a  little  later  the  ataxia 
is  noticed  in  the  upper  extremities.  When  the  disease  is  fully  developed  the  gait 
is  unusually  characteristic.  In  regard  to  the  ataxic  movements  of  the  legs  the 
gait  resembles  that  of  tabes,  but  it  usually  differs  from  it  in  the  much  greater 
swaying  of  the  trunk.  In  this  respect  the  gait  is  more  like  that  of  the  so-called 
cerebellar  ataxia.  The  fact  that  in  Friedreich's  disease  the  muscles  of  the  trunk 
and  pelvis  are  also  affected  by  the  ataxic  disturbance,  and  even  to  a  greater  de- 
gree, is  the  reason  why  the  patient  usually  manifests  more  of  the  so-called  static 
ataxia  than  is  the  case  in  tabes — that  is,  that  he  continually  sways  very  much 
when  standing  quietly  (vide  Fig.  136).  The  patient  therefore  always  stands  and 
walks  with  the  legs  wide  apart  to  give  the  body  a  better  support.  If  we  make 
him  stand  still  with  the  legs  as  close  together  as  possible,  we  notice  the  constant 
muscular  contractions  necessary  to  maintain  the  equilibrium.  With  the  removal 
of  the  visual  control  by  closing  the  eyes,  the  uncertainty  and  swaying  of  the 
body  increases.  The  ataxia  is  also  very  well  marked  in  the  legs,  as  is  most  readily 
shown  by  the  well-known  "knee-heel  test,"  and  also  in  the  arms,  as  tested  by 
bringing  the  finger-tips  together,  by  reaching  for  an  object  held  before  one, 
writing,  etc.  The  disturbance  of  speech,  which  is  often  noticed  in  the  later 
stages,  is  due  to  an  ataxia  of  the  muscles  requisite  for  speech,  and  consists  of 
an  indistinct  articulation  and  a  slow,  scanning,  badly  modulated  manner  of 
speaking.  ISTystagmus  of  the  eyes,  especially  on  looking  far  to  one  side,  some- 
times occurs  as  a  further  ataxic  symptom,  just  as  in  multiple  sclerosis,  but  it  is 
by  no  means  invariable,  or  at  least  it  may  not  appear  rmtil  late  in  the  disease. 

Besides  the  ataxia,  which  finally  becomes  very  pronounced,  for  a  long  period 
we  can  usually  detect  only  one  other  important  sjinptom,  which  is  probably 
always  of  very  early  occurrence — the  complete  absence  of  the  patellar  reflex.  All 
other  nervous  functions  may  remain  wholly  unaffected  for  a  long  time.  The 
motor  strength  of  the  muscles  is  very  well  retained.  We  know  a  patient  who,  in 
spite  of  the  most  marked  ataxia,  has  traveled  several  miles  a  day  by  the  aid 
of  a  cane.  The  muscles  are  usually  not  remarkably  well  developed,  but  they  show 
no  striking  atrophy,  apart  from  rare  complications.  Many  patients  show  a 
peculiar  choreic  muscular  unrest.  The  sensibility  of  the  skin  and  deeper  parts 
(joints,  muscular  sense)  may  for  a  long  time  remain  perfectly  normal,  a  condi- 
tion which  has  been  justly  brought  forward,  especially  by  Friedreich,  as  an  argu- 
ment against  the  dependence  of  ataxia  upon  sensory  disturbances.  Of  course  this 
preservation  of  sensibility  must  not  be  too  much  emphasized,  since  many  other 
observers   and  we  ourselves  have  repeatedly  found  slight   disturbances   of  sen- 


HEREDITAEY    (JUVENILE)    ATAXIA 


98.- 


sibility  (especially  on  the  feet,  toes,  and  lower  legs)  on  careful  testing:  for  ex- 
ample, a  slight  diminution  of  the  tactile  sense,  the  pressure  sense,  sometimes  the 
muscular  sense,  etc.  The  sensibility  to  pain  seems  almost  always  to  remain  un- 
affected. Parsesthesiae  and  spontaneous  pains  are  also  entirely  absent.  The 
cutaneous  reflexes  show  no  material  disturbance  and  the  pupil  reflexes  are  always 
preserved.  Disturbances  of  the  bladder  are  also  absent.  In  some  cases,  however, 
there  may  be  atrophy  of  the  optic  nerves,  just  as  in  tabes.  We  may  also  note  that 
the  toes,  especially  the  great  toes, 
have  a  very  striking  tendency  to 
assume  a  position  of  extreme  dor- 
sal extension,  and  we  sometimes 
see  a  tendency  for  the  foot  to  as- 
sume the  equinus  position.  The 
vertebral  column  often  shows  an 
evident  scoliosis. 

The  course  of  the  disease  is 
very  chronic  and  it  may  last  for 
years  and  years.  The  ataxia 
finally  becomes  so  great  that  the 
patient  is  bedridden.  In  such 
cases  there  is  finally  actual  paraly- 
sis, greater  disturbance  of  sensa- 
tion, disturbances  of  intelligence, 
etc.  Death  often  ensues  from 
some  intercurrent  disease. 

Pathological  Anatomy. — He- 
reditary ataxia  was  the  first  form 
of  disease  in  which  a  combined 
systemic  lesion  of  the  spinal  cord 
was  discovered  by  careful  anatom- 
ical investigation  by  Kahler  and 
Pick.  Later  observers  (F. 
Schultze,  Eiitimeyer,  and  others) 
have  confirmed  these  discoveries. 
We  find  the  posterior  roots  and 
the  posterior  columns  most  dis- 
eased, and  chiefly  the  zone  of  the 
entering  root-fibres.  Lissauer's 
areas  are  usually  exempt,  in  con- 
trast to  the  degeneration  of  tabes. 
The  cerebellar  lateral  tract  (in- 
cluding probably  the  cells  of 
Clarke's  columns)  is  also  regular- 
ly affected,  and  also  Gowers'  tract 
(see  the  chapter  on  secondary  de- 
generations in  the  cord)  and  the 
neighborhood  of  the  pyramidal  lat- 
eral tract,  although  in  lesser  degree.  The  histological  process,  as  in  all  systemic 
diseases,  consists  of  a  degenerative  atrophy  of  the  nervous  elements  and  a  con- 
siderable secondary  increase  of  the  neuroglia. 

It  would  be  very  interesting  to  make  a  careful  comparison  between  the  ana- 
tomical lesions  and  the  symptoms  in  Friedreich's  disease,  on  the  one  hand,  and 
in  tabes  on  the  other;  but  we  are  still  greatly  in  want  of  a  sufficient  number  of 
careful  observations.     The  absence  of  marked  sensory  disturbances  and  of  lan- 


FiG.  136.- 


-Attitude  of  a  patient  with  hereditaiy  ataxia. 
(Personal  observation.) 


984  ■  DISEASES    OF   THE   NEEVOUS    SYSTEM 

cinating  pains  in  hereditary  ataxia  is  striking.  The  absence  of  pain  is  explained 
perhaps  by  the  integrity  of  the  peripheral  nerves,  or  perhaps  by  the  different 
nature  of  the  disease :  in  tabes  we  have  the  action  of  irritating  toxines,  in  hered- 
itary ataxia  simple  endogenous  atrophy. 

Diagnosis. — The  diagnosis  of  Friedreich's  disease  is  easy,  if  we  are  acquainted 
with  the  disease,  and  it  is  usually  perfectly  definite.  The  marked  ataxia,  espe- 
cially the  tottering,  uncertain  gait,  besides  the  youth  of  the  patient,  and  at  times 
the  hereditary  conditions,  as  a  rule  soon  render  a  correct  decision  possible.  The 
absence  of  immobility  of  the  pupils,  of  marked  sensory  disturbances,  of  symptoms 
of  sensory  irritation,  of  vesical  disturbances,  etc.,  distinguish  the  disease  from  or- 
dinary tabes.  It  is  easier  to  mistake  it  for  multiple  sclerosis,  since  this  also  comes 
on  in  youth;  but  Friedreich's  disease  often  begins  in  childhood,  which  is  only 
exceptionally  the  case  with  multiple  sclerosis.  The  examination  of  the  patellar 
reflex  is  most  distinctive ;  this  is  entirely  absent  in  hereditary  ataxia  and  increased 
in  multiple  sclerosis.  The  condition  of  the  patellar  reflex  also  distinguishes 
Friedreich's  disease  from  hereditary  cerebellar  ataxia,  soon  to  be  described  {vide 
infra).  The  distinction  from  post-diphtheritic  and  similar  forms  of  ataxia  should 
also  give  rise  to  no  difficulty. 

Treatment. — Although  there  are  some  variations  in  the  course  of  the  disease, 
it  seems  in  general  always  to  advance  and  to  be  incurable.  We  can  therefore 
merely  try  to  obtain  temporary  improvement  and  an  arrest  of  the  disease  by  in- 
telligent care  of  the  patient  and  by  all  the  methods  employed  in  chronic  nervous 
diseases  (see  the  previous  chapter). 


APPENDIX 

HEREDITARY  CEREBELLAR  ATAXIA 

{Heredo-ataxie  Cerebelleuse) 

As  an  appendix  to  Friedreich's  ataxia  we  must  here  mention  still  another 
remarkable  hereditary  and  family  disease,  the  chief  symptom  of  which  is  also 
ataxia,  while  the  most  essential  anatomical  change  consists  of  an  atrophy  of  the 
cerebellum  (ISTonne,  P.  Marie,  Londe,  and  others). 

The  disease  occurs  in  brothers  and  sisters  and  members  of  different  generations 
of  the  same  family,  but  there  are  probably  sporadic  cases  besides.  The  two  sexes 
are  about  equally  affected;  the  male  sex  seems  to  predominate  somewhat.  The 
first  symptoms  of  the  disease  usually  appear  between  the  twentieth  and  the  thir- 
tieth year,  sometimes  earlier,  rarely  later.  They  consist  of  the  slow  onset  of 
ataxia  of  the  extremities  and  particularly  of  a  staggering,  reeling  gait.  Stand- 
ing is  also  insecure,  but  on  the  whole  it  is  only  slightly  altered  by  closing  the 
eyes.  In  the  arms  the  ataxia  may  become  so  great  as  to  render  all  the  finer 
occupations  (writing,  etc.)  almost  impossible.  The  ataxia  of  the  facial  muscles 
causes  mimetic  movements  of  expression  which  are  often  extremely  peculiar  and 
bizarre;  the  speech  is  usually  considerably  disturbed.  The  muscular  strength  is 
not  diminished,  although  the  patient  often  complains  of  feeling  fatigued.  The 
sensibility  is  perfectly  retained  and,  in  particular,  we  find  the  muscular  sense 
wholly  unaffected.  The  cutaneous  reflexes  are  normal  or  somewhat  diminished, 
but  the  tendon  reflexes  are  almost  invariably  increased,  although  marked  spastic 
symptoms  are  absent.  The  innervation  of  the  bladder  undergoes  no  change.  The 
pupils  usually  retain  their  normal  reaction,  but  atrophy  of  the  optic  nerves  with 
the  corresponding  disturbance  of  vision  has  been  repeatedly  observed.  Pro- 
nounced mental  disturbances,  such  as  weakness  of  memory,  abnormal  irritability, 
etc.,  may  also  develop. 


PEIMAEY  DEGENERATIONS  OE  THE  MOTOE  TEACT   985 

The  disease  has  a  very  tedious  course  and  usually  lasts  many  years.  The 
prognosis  is  absolutely  unfavorable.  Death  ensues  from  some  intercurrent  dis- 
ease or  as  a  result  of  the  ultimate  general  weakness.  Anatomical  examination,  as 
has  been  said,  shows  as  the  most  striking  change  an  atrophy  of  the  cerebellum,, 
which  is  diminished  about  one  half  in  size.  The  spinal  cord  is  sometimes  poorly 
developed  on  the  whole,  but  it  shows  no  columnar  degeneration. 

The  disease  is  distinguished  very  essentially  from  Friedreich's  hereditary 
ataxia,  which  otherwise  is  very  similar  to  it,  by  this  anatomical  condition,  which 
is,  however,  still  in  urgent  need  of  thorough  study.  Clinically  the  two  diseases 
are  to  be  distinguished  particularly  by  the  condition  of  the  tendon  reflexes  and 
the  fact  that  cerebellar  ataxia  usually  comes  on  somewhat  later  in  life.  The 
differential  diagnosis  between  cerebellar  ataxia  and  multiple  sclerosis  is  often 
very  difficult.    The  generic  (family)  occurrence  is  the  chief  distinction. 

The  treatment  can  be  merely  symptomatic,  and  it  has  little  prospect  of  success. 


CHAPTEE   IX 

THE  PRIMARY  DEGENERATIONS   OF  THE   MOTOR  TRACT,   INCLUDING 

THE   MUSCLES 

1.  Preliminary  Eemarks 

In  the  two  preceding  chapters  we  have  become  acquainted  with  two  diseases 
whose  anatomical  basis  is  a  primary  degeneration  of  a  number  of  systems  of 
fibers  whose  conduction  was  chiefly  centripetal.  In  tabes  we  found  the  cause  of 
the  degeneration  to  be  exogenous,  acquired  noxious  influences,  coming  from  with- 
out and  probably  of  chemical  nature;  in  hereditary  ataxia,  on  the  contrary,  the 
cause  was  endogenous  anomalies — that  is,  anomalies  in  the  embryonic  predisposi- 
tion, and  therefore  congenital,  which  caused  a  premature  atrophy  of  nerve-fibers 
which  had  from  birth  an  abnormally  weak  power  of  resistance.  In  this  chapter 
we  shall  become  acquainted  with  a  number  of  diseases,  which  are  due  chiefly  to 
primary  degeneration  of  the  great  centrifugal  motor  conducting  tract,  especially 
the  pyramidal  tract.  We  will  see  that,  just  as  with  hereditary  ataxia,  the  basis 
of  the  disease  is  chiefly  an  endogenous,  congenital  weakness  of  this  portion  of  the 
nervous  system,  so  that  it  is  therefore  very  often  a  family,  generic  disease; 
although  in  some  cases  exogenous  noxious  influences  are  probably  also  to  be  con- 
sidered. 

In  order  to  obtain  a  preliminary  review  of  the  whole  group  of  diseases  here 
under  consideration,  we  may  picture  to  ourselves,  as  in  the  accompanying  dia- 
gram ((Fig.  13Y),  the  course  of  the  long  conducting  tract  leading  from  the 
central  convolutions  to  the  muscles,  as  has  been  fully  described  on  page  829. 
In  the  first  place  we  will  consider  a  form  of  disease  in  which  ultimately  the 
whole  cortico-muscular  conducting  tract,  from  the  cortical  cell,  C,  up  to  and 
including  the  muscle,  M,  is  found  degenerated.  This  is  amyotrophic  lateral 
sclerosis.  We  will  next  describe  a  form  of  disease  in  which  only  the  second 
portion  (the  so-called  second  neurone)  of  the  whole  tract — namely,  the  portion 
from  the  ganglion-cell  in  the  anterior  horn  of  the  cord  (V)  up  to  and  including 
the  muscle — is  affected.  This  is  spinal  muscular  atrophy,  and  the  completely 
analogous  progressive  bulbar  paralysis.  In  the  third  place  we  shall  see  that  the 
first  main  portion  of  the  tract,  PyS,  may  be  alone  affected  up  to  the  cell  of  the 
anterior  horn,  but  without  involving  it.    We  then  have  the  true  primary  pyramidal 


986 


DISEASES    OF    THE    NEKYOUS    SYSTEM 


lateral  sclerosis,  with  the  clinical  picture  of  pure  spastic  spinal  paralysis.  In  the 
fourth  place  the  disease  may  involve  only  the  peripheral  motor  nerve,  m,  with 
its  corresponding  muscles  {neurotic  muscular  atrophy),  and  finally  we  may  also 
place  here  by  far  the  commonest  form  of  disease,  the  progressive  muscular  dys- 
trophy— that  is,  that  disease  in  which  only  the  terminal  apparatus  of  the  whole 
tract,  the  muscle  itself,  undergoes  a  progressive  atrophy. 

The  forms  of  disease  just  mentioned  are  probably,  so  far  as  they  are  endoge- 
nous diseases,  all  closely  allied,  but  it  is  still  necessary  for  a  time  to  keep  them 

separate,  at  least  so  far  as  they  show 
very  definite  marks  of  distinction, 
both  clinically  and  anatomically. 
Only  with  a  more  advanced  knowl- 
edge of  the  special  nature  of  all  these 
morbid  conditions  can  we  make  a 
strict  Eetiological  division  of  them. 
At  present  we  must  remember  that 
we  can  not  consider  the  different  clin- 
ical and  anatomical  forms  as  different 
diseases,  strictly  separate  from  one 
another.  The  more  our  knowledge 
increases,  the  more  prominent  seem 
to  be  transitions  and  connecting  links 
between  the  different  forms. 


2.  Amyotrophic  Lateral  Sclerosis 

.^Etiology  and  Pathological  Anat- 
omy.— For  the  first  accurate  knowl- 
edge of  amyotrophic  lateral  sclerosis 
we  must  thank  Charcot,  who  pub- 
lished in  1869,  in  company  with 
Joffroy,  his  first  observations  upon 
such  cases,  and  who  in  1874  was  able 
to  give  quite  a  complete  description 
of  the  disease;  but  an  exact  knowl- 
edge of  amyotrophic  lateral  sclerosis 
was  first  made  possible  by  Flechsig's 
investigations  upon  the  course  of  the 
conducting  tracts  in  the  spinal  cord. 
From  these  we  can  now  say  that  the 
disease  is  manifested  anatomically 
essentially  as  a  primary  systemic  de- 
generation of  the  whole  cortico-mus- 
cular  conducting  tract,  and  not  only  of  the  spinal  portion  thereof  belonging 
to  the  extremities,  but  also  of  the  bulbar  portion  belonging  to  the  muscles  of  the 
face,  tongue,  soft  palate,  etc.  These  two  parallel  portions  must  be  regarded  as 
completely  equivalent  parts  of  one  great  motor  system — a  point  to  which  we  shall 
frequently  return  later.  The  motor-nerve  nuclei  in  the  medulla  and  pons  (for  the 
hypoglossus,  facial,  motor,  trigeminus,  etc.),  and  also  the  nuclei  for  the  oculo- 
motor nerves,  are  to  be  regarded  as  precisely  analogous  to  the  ganglion-cell  groups 
in  the  anterior  horns  of  the  cord  for  the  muscles  of  the  extremities. 

In  amyotrophic  lateral  sclerosis  a  large  part  of  this  motor  conducting  tract 
undergoes  degeneration,  and  sometimes,  as  it  seems,  throughout  almost  its  whole 
extent.  If  we  examine  the  nervous  system  in  such  a  case  we  find  in  the  spinal 
cord  that  the  large  ganglion-cells  of  the  anterior  horns  in  the  cervical  and  lumbar 


Fig.  137. — Diagram  of  the  motor  tract.  C  Motor  gan- 
glion-cell in  the  cortex.  PyS.  Pyramidal  lateral 
tract.  V.  Ganglion-cell  of  the  anterior  horn.  in. 
Motor  nerve.    M.  Muscular  fiber. 


PEIMAEY   DEGE:N'ERATI0N"S  OF   THE   MOTOE   TEACT       987 

cord,  or  in  the  cervical  cord  only,  are  atrophied  and  in  part  wholly  absorbed 
(Fig.  138).     We  find  the  pyramidal  tracts  greatly  degenerated  in  both  lateral 
columns,  and,  of  course,  in  one  or  both  anterior  columns  when  there  is  an  anterior 
pyramidal  tract.     In  the  anterior  horns  also  the  number  of  medullated  fibers, 
part    of    which    are    cer- 
tainly  processes    of    the 
pyramidal    lateral     tract 
(PyS)  *  fibers,  is  dimin- 
ished.    Farther  upward, 
as  was  first  discovered  by 
Charcot   and   Marie,   we 
can  follow  the  degenera- 
tion    of     the     pyramidal  "  '^{'  "  ; 
tract,  not  in  all,  but  cer- 
tainly    in     many     cases,         X-^^                                                   •. 
through  the  pyramids  of 
the    medulla,    the    pons,                 "*    ...             ■      •  .>                          -si        """ 

tne  crura,   and  the  inter-  -^^^  138.— Section  of  the  cervical  cord  iu  amyotrophic  lateral  sclerosis, 

nal  capsule  to  the  central  Degeneration  of  the  pyramidal  tracts,  in  part  of  the  other  antero- 

T    , .                .             ,  lateral  ti-acts.  pronounced  atrophy  of  the  anterior  horns.    (Person- 

COnvolutlOns,      m      whose  al  observation.) 

ganglion-cells  we  can  also 

find  atrophy.  The  bulbar  motor  nuclei,  especially  the  hypoglossus  nucleus  and  the 
vagus-accessory  nucleus,  more  rarely  the  facial  nucleus,  etc.,  are  also  atrophied 
as  a  rule,  just  like  the  anterior  horns  of  the  cord.  From  all  these  bulbar  and 
spinal  ganglion-cells  a  further  (secondary?)  degeneration  also  extends  toward  the 
periphery  into  the  corresponding  nerve-roots  (hypoglossus,  etc.,  spinal  anterior 
roots)  and  nerve-trunks.  It  is  difficult  to  make  out  atrophied  fibers  in  the  periph- 
eral nerves,  and  up  to  t£e  present  time  they  have  not  always  been  looked  for  with 
sufficient  care,  but  it  can  scarcely  be  doubted  that  the  affected  motor  fibers,  which 
are  processes  of  the  atrophied  ganglion-cells,  are  likewise  to  be  found  in  a  condi- 
tion of  degeneration.  Finally,  the  muscles  show  a  considerable  atrophy,  as  is 
plainly  manifest  even  during  the  life-time  of  the  patient.  Their  volume  is  much 
diminished ;  many  muscles  (for  details  vide  infra)  finally  almost  whollj"  disap- 
pear, so  that  in  their  place  there  is  little  left  but  connective  tissue  and  fat.  In 
the  other  muscles  we  find,  besides  a  number  of  normal  fibers  still  preserved,  many 
very  small  fibers,  showing  various  degrees  of  atrophy,  with  their  transverse  stria- 
tion  usually  preserved,  but  more  rarely  indistinct.  The  nuclei  of  the  sarcolemma 
are  much  increased,  and  the  interstitial  fat  tissue  is  often,  but  not  always,  abun- 
dantly developed. 

Although  we  may  undoubtedly  designate  amyotrophic  lateral  sclerosis  as,  in 
the  main,  a  primary  degeneration  of  the  pyramidal  tract,  yet  in  many  cases  the 
disease  is  not  limited  absolutely  to  this  one  system.  It  has  long  been  noticed 
that  the  diseased  area  in  the  lateral  columns  extended  farther  foi'ward  and  inward 
than  the  actual  pyramidal  lateral  tract,  PyS,  and  that,  accordingly,  bundles  of 
fibers  in  the  anterior  portion  of  the  lateral  columns  and  in  the  so-called  lateral 
limiting  layer  were  involved  in  the  disease.  Indeed,  it  often  seems  as  if  the 
whole  region  of  the  anterior  and  lateral  columns  were  poorer  in  fibers  than  the 
area  of  the  posterior  columns.  Only  toward  the  lateral  cerebellar  tract,  KIS,  is 
the  degeneration  almost  always  verj^  sharply  limited — that  is,  the  lateral  cere- 
bellar tract  remains  as  a  rule  perfectly  normal,  but  disease  has  repeatedly  been 


*  Abbreviations  in'' frequent  use  iu  what  follows  :  PyS  =  pyraniidul  lateral  tract  (Pyramiden-Seit- 
enstrangbahn) ;  Py  V  =  anterior  pyramidal  tract  (Pyramiden-Vorderstrangbaliu)  ;  KIS  =  lateral  cere- 
bral tract  ("Kleinhirn-Seitenstran^bahn."! 


DISEASES    OF   THE   IsTeeVOUS    SYSTEM 

found  in  Goll's  columns.  All  these  degenerations,  last  mentioned,  have  no  known 
clinical  significance.  They  show  only  how  other  bundles  of  fibers  may  sometimes 
suffer  under  the  same  noxious  influence  as  well  as  the  pyramidal  tract. 

Our  knowledge  in  regard  to  the  questions  as  to  where  the  degeneration  begins,. 
in  what  way  it  progresses,  and  what  is  primary  and  what  secondary  atrophy,  is 
most  uncertain.  The  anatomical  examination  gives  only  the  result  of  the  destruc- 
tion, but  it  shows  very  few  details  of  its  course.  Much  may  be  inferred  from 
clinical  observation,  but  much  work  is  still  needed  to  attain  perfectly  clear  knowl- 
edge. Perhaps  different  possibilities  should  be  considered,  which  would  explain 
many  variations  in  the  clinical  course.  At  any  rate,  the  different  portions  of  the 
system  may  be  affected  in  varying  sequence,  and  the  disease  may  also  extend  with, 
varying  rapidity,  but  the  destruction  of  the  nerve-fibers  is  always  the  primary 
process;  the  increase  of  the  interstitial  connective  tissue  and  the  slight  changes 
in  the  vessels  are  a  secondary,  accidental  process. 

We  know  as  yet  hardly  anything  definite  as  to  the  causes  of  amyotrophic 
lateral  sclerosis.  For  one  class  of  cases  we  believe  we  may  assume  a  congenital 
weakness  of  the  motor  system.  The  disease  usually  begins  at  the  period  between 
thirty-five  and  fifty,  but  not  infrequently  later.  ISTo  special  external  causes  of  the 
disease  have  thus  far  been  found.  The  male  sex  seems  to  be  affected  somewhat 
more  frequently  than  the  female. 

Clinical  History. — In  all  typical  cases  the  clinical  symptoms  give  a  perfectly 
characteristic  type  of  disease,  limited  strictly  to  the  motor  sphere,  corresponding- 
to  the  perfectly  systemic  anatomical  lesions  just  described. 

The  first  signs  of  the  disease  almost  always  begin  in  the  arm.  The  patient 
notices  a  difficulty  in  working,  and  becomes  easily  tired.  The  weakness  of  the 
arm  gradually  increases,  and  finally,  usually  some  months  later,  involves  the 
other  arm.  A  wasting  of  certain  muscles,  which  gradually  increases  and  becomes 
more  extensive,  is  now  often  noticed  by  the  patient.  About  six  months  or  a 
year  later,  symptoms  appear  in  the  lower  extremities.  The  gait  becomes  stiff 
and  uncertain,  the  patient  gets  tired  more  easily,  and  quite  a  marked  tremor  of 
the  legs  often  comes  on,  apparently  spontaneously. 

If  we  now  examine  the  patient  carefully,  the  type  of  the  disease  is  usually 
perfectly  plain.  We  notice,  first  in  the  upper  extremities,  a  very  pronounced 
and  more  or  less  extensive  muscular  atrophy.  This  is  usually  most  marked 
where  it  begins — namely,  in  the  thenar  and  hypothenar  eminences.  The  inter- 
ossei  are  also  plainly  atrophied,  and  the  muscles  on  the  extensor  side  of  the 
forearms,  but  the  flexors  of  the  hand  and  of  the  terminal  phalanges  of  the  fingers 
remain  intact  longer.  In  the  upper  arm  the  triceps  and  the  deltoid  are  usually 
the  most  atrophied,  and  later,  and  to  a  less  degree,  the  biceps  and  the  muscles  of 
the  shoulder.  We  find  a  functional  disturbance  of  the  muscles — a  paresis — corre- 
sponding to  the  degree  of  atrophy.  The  functional  capacity  depends  upon  how 
much  muscle  is  left,  and  only  with  a  complete  disappearance  of  the  muscle  is 
there  a  complete  loss  of  the  corresponding  motion,  but  a  marked  paresis  can 
sometimes  be  noticed  in  muscles  which  are  not  yet  much  atrophied.  Fibrillary 
m.uscular  contractions  are  almost  filways  to  be  detected  in  the  affected  muscles 
on  careful  observation.  The  electrical  excitability  of  the  muscular  fibers  still 
preserved  is  normal.  The  strength  of  contraction  of  the  muscle  irritated  by  the 
faradic  current  is  therefore  proportional  to  the  amount  of  muscular  substance 
still  present.  In  the  much  atrophied  muscles  the  effects  of  irritation  are  finally 
very  slight,  and  then  we  can  always  detect  a  distinct  reaction  of  degeneration  in 
the  muscular  fibers  that  are  still  left,  especially  in  the  ball  of  the  thumb.  We 
can  scarcely  ever  make  out  with  certainty  a  loss  of  excitability  in  the  nerve-trunk, 
probably  because  here  a  greater  number  of  normal  fibers  are  always  present. 

The  examination  of  the  tendon  reflexes  is  very  important.  They  are  invariably 


PEIMAEY   DEGENERATIOis^S  OF    THE   MOTOR   TRACT       989 

much  increased,  eveu  from  the  early  stages  of  the  disease.  We  obtain  vigorous 
reflex  contractions  from  a  gentle  blow  on  the  tendons  of  the  biceps  and  the  triceps, 
and  on  the  lower  ends  of  the  bones  of  the  forearm.  This  increase  of  the  tendon 
reflexes  is  extremely  important  in  diagnosis,  because  it  never  occurs  in  this  way 
in  ordinary  "  progressive  muscular  atrophy  " — that  is,  in  that  disease  in  which  the 
degeneration  extends  merely  from  the  muscles  to  the  motor  ganglion-cells  in  the 
anterior  cornua,  while  the  lateral  motor  tracts  remain  free  (vide  infra).  In  the 
later  stages  of  the  disease  marked  contractures  in  the  arms  and  hands  sometimes, 
but  not  always,  develop.  The  sensibility  of  the  skin  and  deeper  parts,  however, 
remains  absolutely  normal. 

The  first  morbid  symi^toms  usually  develop  in  the  lower  extremities  some 
months  later  than  in  the  arms.  The  pure  spastic  sjTiiptoms  are  here  remarkably 
prominent,  while  the  muscular  atrophy  is  late  in  its  development,  and  is  but  slight. 
The  legs  become  stiff,  and  oppose  considerable  muscular  resistance  to  attempts 
at  passive  motion,  but  the  crude  strength  of  the  muscles  is  decidedly  below  the 
normal.  There  is  an  obvious  paresis,  although  there  is,  as  it  seems,  hardly  ever 
a  complete  paralysis  of  the  legs;  and  the  disturbance  of  motion,  at  any  rate,  is 
considerably  increased  by  the  spastic  symptoms  (vide  infra,  spastic  spinal  paraly- 
sis). The  spastic  sjTxiptoms  are  connected  with  the  hypertonicity  of  the  muscles 
(the  increased  muscle  tonus)  and  the  increased  tendon  reflexes.  These  symptoms 
•depend  mainly  upon  the  great  increase  of  the  tendon  reflexes.  The  patellar  reflex 
is  very  vigorous,  and  we  often  find  a  marked  and  persistent  ankle  clonus.  The 
patient  can  still  walk  quite  a  distance,  but  the  gait  is,  of  course,  difficult  and 
laborious.  The  patient  walks  with  short,  slow,  dragging  steps — the  spastic-paretic 
gait.  Only  in  a  few  cases  does  a  marked  atrophy  of  the  muscles  appear  in  the 
early  stages  in  the  legs  as  well  as  in  the  arms.  The  sensibility  of  the  skin  and 
deeper  parts  is  also  perfectly  preserved  in  the  legs  in  amyotrophic  lateral  sclero- 
sis. The  cutaneous  reflexes  from  the  soles  of  the  feet  show  no  striking  changes. 
[There  may  be  dorsal  extension  of  the  great  toe  on  testing  the  plantar  reflex — 
Rabinski's  reflex. — K.]  Disturbances  in  micturition  are  also  entirely  absent. 
The  bowels  may  be  somewhat  costive,  but  they  are  otherwise  normal. 

After  the  condition  has  lasted  for  some  time  (a  year  or  two)  in  this  form — 
muscular  atrophy  and  increased  tendon  reflexes  in  the  upper  extremities  and 
spastic  paresis  in  the  lower — and  has  slowly  grown  worse,  bulbar  symptoms  come 
on  in  the  third  and  last  stage  of  the  disease.  The  speech  gradually  becomes  more 
indistinct,  and  there  is  difliculty  in  swallowing.  If  we  examine  closely  we  find 
the  lips  atrophied,  so  that  puckering  the  mouth,  whistling,  etc.,  are  difiicult.  We 
also  notice  a  decided  atrophy  of  the  tongue.  Its  surface  is  uneven,  and  we  notice 
more  or  less  marked  fibrillary  twitchings  of  single  muscular  bundles.  The  sensi- 
bility is  also  normal  here.  We  sometimes  find  a  vigorous  masseter  reflex  (jaw- 
jerk)  on  striking  the  lower  jaw,  analogous  to  the  increased  tendon  reflexes  in  the 
extremities.  The  other  muscles  of  the  face,  the  muscles  of  mastication  and  the 
ocular  muscles,  usually  remain  unaffected.  The  patient's  intelligence  is  un- 
changed. The  ready  onset  of  marked  mimetic  emotional  movements  is  sometimes 
striking.  Many  patients  with  amyotrophic  lateral  sclerosis  break  out  into  spas- 
modic laughter  or  weeping  and  wailing  upon  the  slightest  provocation  ("  impul- 
sive laughing  and  crying").  This  remarkable  symptom,  which  also  occurs  in 
multiple  sclerosis  (page  957),  is  probably  due  to  the  disappearance  of  certain 
fibers  which  inhibit  affective  movements.  The  face  is  sometimes  peculiarly  dis- 
torted and  broadened  by  a  persistent  tonic  contraction  of  the  facial  muscles  (see 
Eig.  156,  page  1010).  In  one  ease  under  our  observation  there  were  frequent 
attacks  of  severe  spasm  of  the  glottis  with  danger  of  suffocation. 

If  the  patient  have  trouble  in  taking  food,  from  difficulty  in  swallowing,  the 
state  of  the  general  nutrition  soon  becomes  worse.     Respiratory  disturbances  are 


990  DISEASES    OF   THE   NEEVOUS    SYSTEM 

usually  the  final  immediate  cause  of  death,  if  an  intercurrent  disease,  such  as  in- 
halation pneumonia,  etc.,  does  not  previously  put  an  end  to  the  patient's  melan- 
choly condition. 

Variations  from  this  typical  picture  of  the  disease  sometimes  occur,  but  only 
as  the  sequence  may  vary  in  which  the  different  symptoms  come  on  or  the  differ- 
ent muscular  regions  are  affected.  If  the  anatomical  lesion  begins  exclusively  in 
the  central  motor  neurones,  there  are  at  first  purely  spastic  symptoms,  either 
spastic  rigidity  of  the  lower  extremities  only  or  rigidity  of  the  trunk  and  arms  as 
well,  and  a  distorted  facial  expression;  and  only  later,  when  the  second  motor 
neurones  are  affected,  is  added  atrophy  of  the  muscles,  at  first  usually  either  in 
the  forearms  and  hands  or  in  the  bulbar  region  (tongue,  lips,  etc.).  In  other  cases 
however,  the  type  of  progressive  muscular  atrophy  is  from  the  first  more 
prominent,  and  the  spastic  symptoms,  if  marked  anywhere,  appear  only  in  the 
legs.  In  these  cases  the  disease  of  the  peripheral  motor  neurones  is  at  first  evi- 
dently greater  than  that  of  the  central  motor  neurones ;  but  even  here  the  in- 
creased tendon  reflexes  point  from  the  outset  to  an  implication  of  the  central 
motor  neurones.  Increased  tendon  reflexes,  however,  can  of  course  occur  only  in 
those  muscles  whose  ganglion-cells  in  the  anterior  horns  are  not  yet  completely 
destroyed.  The  bulbar  symptoms  are  wholly  analogous  to  the  other  muscular 
atrophies;  they  are  due  to  the  degeneration  of  the  nerve-nuclei  in  the  medulla. 
We  shall  become  more  fully  acquainted  with  them  later  (vide  infra,  progressive 
bulbar  paralysis). 

The  diagnosis  of  the  disease  is  rarely  difficult.  Its  usually  typical  course,  the 
muscular  atrophy  co-existing  with  increased  tendon  reflexes,  the  rigidity  in  other 
muscles,  especially  in  the  legs,  the  complete  absence  of  sensory  or  vesical  disturb- 
ances, and  the  final  appearance  of  bulbar  symptoras,  are  chiefly  to  be  considered 
in  diagnosis.  Mistakes  may  arise  from  the  fact  that  tumors  or  myelitis  may  for 
a  long  time  have  a  similar  localization,  as  in  the  gray  matter  of  the  cervical  cord, 
and  therefore  provoke  analogous  symptoms.  It  is  probable  that  in  the  past  there 
was  often  confusion  with  syringomyelia  (q.  v.),  but  such  mistakes  may  easily  be 
avoided  if  we  remember  the  sensory  disturbances  in  the  arms  which  are  so  very 
characteristic  of  this  disease.  The  distinction  between  amyotrophic  lateral  scle- 
rosis and  the  other  primary  diseases  of  the  motor  system  will  be  self-evident  from 
the  description  of  these  diseases  which  follows. 

The  prognosis  of  amyotrophic  lateral  sclerosis  must  be  regarded  as  absolutely 
unfavorable.  The  disease  advances  slowly  but  unceasingly,  and  usually  leads  to 
death  in  a  few  years.  Only  in  a  few  cases,  occurring  in  early  youth  (Seelig- 
mltller),  does  the  disease  seem  to  come  to  a  standstill. 

We  can  therefore  expect  but  slight  results  from  treatment.  At  most  we  can 
perhaps  check  the  advance  of  the  disease  by  an  electrical  or  gymnastic  treatment, 
kept  up  with  very  great  patience  and  perseverance. 

3.  Spinal  Progressive  Muscular  Atrophy 
Preliminary  Remarks  and  Pathological  Anatomy. — Few  diseases  of  the 
spinal  cord  have  been  the  subject  of  such  different  conceptions  and  inter- 
pretations as  progressive  muscular  atrophy.  The  reason  for  this  lies  chiefly  in 
the  fact  that  its  main  symptom,  the  progressive  atrophy  of  the  voluntary  muscles, 
may  be  found  in  many  totally  distinct  diseases,  and  hence  this  has  given  rise  to 
constant  confusion  and  mistakes.  If,  at  the  present  time,  we  read  the  older  and 
even  a  part  of  the  newer  literature  on  this  subject,  we  find  everywhere  a  mixture 
of  different  cases,  not  at  all  of  the  same  disease,  and  only  the  latest  accurate  clin- 
ical and  anatomical  methods  of  investigation  have  enabled  us  to  bring  at  least 
some  order  out  of  this  chaos. 

Except  for  a  few  earlier  observations,  Duchenne  and  Aran,  in  1849  and  1850, 


PEIMAEY   DEGENEEATIONS  OF   THE   MOTOR   TRACT       991 

gave  the  first  good  description  of  progressive  muscular  atrophy.  The  French 
observers,  therefore,  at  present  speak  of  the  disease,  in  distinction  from  other 
similar  affections,  as  "  atrophie  musculaire  progressive,  type  Duchenne-AranJ' 
A  short  time  after,  in  1855,  Cruveilhier,  on  the  ground  of  a  positive  lesion  on 
autopsy,  first  pronounced  the  opinion  that  a  disease  of  the  gray  matter  in  the 
spinal  cord  was  to  be  regarded  as  the  special  anatomical  cause  of  the  disease. 
Since  then  a  tedious  dispute  has  been  carried  on,  and  even  in  part  kept  up  to  the 
present  time,  as  to  whether,  in  fact,  the  disease  has  its  seat  in  the  spinal  cord,  or 
in  the  muscles  themselves — a  dispute  which  was  necessarily  without  results  for 
a  long  time ;  the  more  because  the  actual  pathological  data  were  very  scanty,  and 
because  the  results  of  examinations  often  contradicted  one  another,  owing  to  the 
confusion  between  different  morbid  processes  which  did  not  belong  together  at  all. 

At  present  we  know  that  the  great  majority  of  progressive  muscular  atrophies 
certainly  have  their  starting-point  in  the  muscles  themselves  (vide  infra,  pro- 
gressive muscular  dystrophy),  but  that  there  is  also  a  rare  but  definitely  estab- 
lished spinal  form  of  progressive  muscular  atrophy.  This  is  closely  allied  to  amy- 
otrophic lateral  sclerosis,  which  we  have  just  described,  but  although  in  amyo- 
trophic lateral  sclerosis  the  whole  pyramidal  motor  tract  may  be  degenerated,  and 
the  lateral  pyramidal  tracts  in  the  cord  are  in  particular  always  affected,  in 
"  spinal  progressive  muscular  atrophy  "  the  degeneration,  as  we  have  said,  is  con- 
fined to  the  peripheral  motor  neurone — that  is,  to  that  portion  of  the  motor  con- 
ducting tract  which  extends  from  the  ganglion-cells  of  the  anterior  cornua  to  the 
muscular  fibers  themselves.  The  second  central  motor  neurone — that  is,  the  lat- 
eral pyramidal  tract — remains  perfectly  normal.  It  is  very  improbable  that  this 
difference  in  the  extent  of  the  anatomical  localization  causes  a  fundamental  dis- 
tinction between  the  two  diseases  mentioned.  The  clinical  distinctions  due  to 
the  different  anatomical  localization  are,  however,  of  sufficiently  marked  promi- 
nence to  justify,  at  least  provisionally,  a  special  limitation  of  amyotrophic  lateral 
sclerosis  on  the  one  side  and  spinal  progressive  muscular  atrophy  on  the  other, 
as  two  different  clinical  forms  of  the  same  morbid  process. 

The  precise  anatomical  lesion  in  progressive  (spinal)  muscular  atrophy  is  as 
follows : 

In  the  spinal  cord,  particularly  in  the  cervical  cord,  we  find  the  ante- 
rior gray  cornua  very  small ;  the  ganglion-cells  have  wholly  or  largely  disap- 
peared, and  those  remaining  are  atrophied;  and  the  neuroglia  is  changed  to  a  fine 
fibrous  tissue,  sometimes  studded  with  spider-cells ;  but  the  lateral  columns,  espe- 
cially the  pyramidal  tracts — that  is,  the  portion  of  the  motor  conducting  tract 
central  to  the  ganglion-cells  of  the  anterior  cornua — are  perfectly  normal ;  the  an- 
terior roots  and  the  affected  motor  fibers  in  the  peripheral  nerves,  however,  are 
atrophied,  although  in  the  nerve-trunks  the  discovery  of  degenerated  fibers  mixed 
with  many  other  normal  fibers  is  not  perfectly  easy.  In  the  muscles  the  atrophy 
is,  of  course,  still  more  noticeable  on  a  post-mortem  examination  than  on  exami- 
nation during  life.  The  muscles  most  affected  are  reduced  to  small,  pale,  and 
flabby  bundles,  in  which  fat  and  connective  tissue  outweigh  the  proper  muscular 
tissue.  On  histological  examination,  we  find)  besides  some  muscular  fibers  which 
are  still  of  normal  diameter  or  even  hypertrophied,  all  degrees  of  diminution  and 
atrophy  in  the  other  fibers,  so  that  finally  all  that  seems  to  be  left  of  many  fibers 
is  merely  the  empty  sheaths  of  sarcolemma;  but  most  of  the  diminished  fibers 
retain  their  transverse  striation  to  the  last,  and  only  occasionally  do  we  see  signs 
of  granular  (fatty?)  and  waxy  degeneration  of  the  muscular  fibers,  a  splitting 
longitudinally  and  transversely,  etc.  The  interstitial  connective  tissue  is  always 
hyperplastic,  the  muscular  nuclei  are  considerably  increased  in  number,  and  we 
often  find  an  abundant  deposit  of  fat  between  the  fibers  which  are  still  preserved. 

So  far  the  actual  lesion.     In   comprehending  it,  the   only  difficulties   arise 


992 


DISEASES    OE    THE   NIERVOUS    SYSTEM 


from  the  questions  as  to  the  mode  of  development,   and   as  to  the   reciprocal 
dependence  of  the  different  disturbances.     Is  the  atrophy  of  the  anterior  cor- 

nua  to  be  regarded  as  primary, 
and  the  atrophy  of  the  nerves  and 
muscles  as  a  secondary  descend- 
ing degeneration;  or  does  the 
process  begin  in  the  muscles  or 
nerve-endings,  and  extend  up- 
ward from  them  to  the  spinal 
cord;  or,  finally,  do  we  have  to  do 
with  an  approximately  simultane- 
ous degeneration  of  the  whole 
motor  portion  affected?  These 
are  questions  to  which  at  present 
no  definite  answer  can  be  given. 
Many  reasons  seem  to  us  to  favor 
the  belief  that  the  degenerative 
process  begins  in  the  last  ter- 
minal branches  of  the  motor 
nerves,  and  from  these  ascends 
gradually  to  the  spinal  cord. 
This,  however,  is  not  yet  proved, 
and  possibly  the  starting-point  of 
the  disease  and  its  further  prog- 
ress may  differ  in  different  cases. 
.ffitiology  and  Clinical  His- 
tory.— Progressive  muscular  atro- 
phy is  an  extremely  slow  and 
chronic  disease  from  the  begin- 
ning. The  special  causes  are  as 
little  known  as  those  of  amyotro- 
phic lateral  sclerosis.  Here,  too, 
we  shall  probably  have  ultimately 
to  fall  back  iipon  the  hypothesis  of 
conditions  of  congenital  weakness 
in  the  affected  systems  of  fibers. 
Hereditary  and  generic  influences 
are  often  not  to  be  detected,  but 
they  are  sometimes  undoubtedly 
present.  "We  ourselves  and  other 
obserA^ers  have  repeatedly  seen 
spinal  muscular  atrophy  occur  in 
several  members  of  the  same  fam- 
ily. The  disease  sometimes  be- 
gins in  childhood  and  sometimes 
in  youth,  but  often  in  more  ad- 
vanced age  (from  forty  to  fifty). 
Although,  as  we  have  said,  a  con- 
genital weakness  of  the  motor 
system  is  probably  always  to  be 
regarded  as  the  special  cause  of 
the  disease,  in  some  cases  certain 
especially  persistent  over-exertion  of  the  muscles  in  hard 


Fig.  141. 
Figs.  139-141.— Atrophy  of  the  small  muscles  of  the  hand, 
especially  of  the  thenar  and  hypothenar  muscles,  in  spi- 
nal progressive  muscular  atrophy,    a.  Hand  of  a  healthy 
man.    b.  Atrophied  hand.    (Erlangen  Jledical  Clinique') 


external  conditions 

work,  seem  to  favor  its  outbreak 


PEIMAEY  DEGENERATIONS  OE  THE  MOTOR  TRACT   993 


The  disease  begins,  by  far  the  most  frequently,  in  the  upper  extremities,  and 
■especially,  as  it  seems,  in  the  right  arm,  but  sometimes  in  the  left,  or  in  both  arms 
at  once.  As  a  rule,  it  begins  with  an  atrophy  of  the  short  muscles  of  the  thumb 
and  of  the  hypothenar  eminence,  which  is  accompanied  by  a  corresponding  dis- 
turbance of  functions  (see  the  accompanying  figures,  139  to  141).  Other 
symptoms — disturbances  of  sensibility,  parsesthesia,  or  pain — are  usually  en- 
tirely absent.  The  atrophy  usually  affects  the 
abductor  pollicis  brevis  and  the  opponens  first, 
and  then  the  flexor  brevis  and  the  adductor. 
We  notice  very  early  the  characteristic  sinking 
in  and  flattening  of  the  ball  of  the  thumb,  and 
the  abnormal  position  of  the  thumb,  which  is 
persistently  approximated  to  the  second  meta- 
carpal bone — the  "  ape  hand."  It  becomes  con- 
stantly harder  and  finally  impossible  to  oppose 
the  thumb  to  the  other  fingers  (performed  by 
the  fiexor  brevis  for  the  index  and  middle  fingers 
and  by  the  abductor  brevis  and  opponens  for 
the  ring  and  little  fingers).  At  the  same  time, 
•or  a  little  earlier  or  later,  the  interossei  begin 
to  atrophy,  as  is  recognized  by  the  sinking  in 
of  the  interosseous  spaces  and  the  increasing 
incomplete  extension  of  the  terminal  phalanges 
■of  the  fingers.  The  atrophy  of  the  lumbricales 
■causes  a  visible  flattening  of  the  hollow  of  the 
hand.  If  the  disturbance  in  the  function  of 
the  interossei  has  reached  a  certain  degree,  the 
same  claw-like  position  of  the  fingers  appears, 
as  we  have  already  learned  to  recognize  in 
ulnar  paralysis  (see  Fig.  142),  due  to  the  con- 
tracture of  the  antagonist  of  the  interossei,  the 
extensor  communis  digitorum. 

In  the  further  progress  of  the  disease  the 
atrophy  either  extends  to  the  muscles  of  the 
forearm,  or,  what  is  not  at  all  rare,  it  jumps 
■over  these  and  attacks  the  muscles  of  the  shoul- 
der, usually  the  deltoid  first.  In  the  forearm 
it  is  usually  the  muscles  on  the  extensor  side 
which  are  first  attacked,  the  abductor  and  ex- 
tensor longus  pollicis,  the  extensors  of  the 
wrist  and  fingers,  and  only  later  the  supinators, 
flexors,  etc.  In  the  upper  arm  the  deltoid  al- 
most always  atrophies  first,  and  then  the  biceps, 
while  the  triceps  may  remain  intact  somewhat 
longer.  There  are  also  cases  in  which  the  atro- 
phy begins  in  the  deltoid  and  the  muscles  of  the 

upper  arm,  while  the  small  muscles  of  the  hands  and  fingers  are  not  affected  until 
later.  The  muscles  of  the  trunk  are  usually  added  to  the  list  quite  late :  the  mus- 
cles that  extend  the  head  and  keep  it  erect,  so  that  the  head  sinks  forward,  the 
trapezii,  the  infra-spinati  and  supra-spinati,  the  rhomboidei,  the  latissimi  dorsi, 
the  pectorals,  etc.  (see  Figs.  143  and  144).  The  disturbance  of  function  caused 
by  the  atrophy  of  all  these  muscles  is  readily  apparent  from  what  was  said  in 
the  chapter  on  the  different  form  of  paralysis.  In  advanced  cases  the  arms  hang 
down  laxly  by  the  sides  of  the  trunk.  Only  with  the  greatest  difficulty,  if  at 
63 


Fig.  142.— Atrophy  of  the  small  muscles 
of  the  hand  and  the  muscles  on  the 
extensor  side  of  the  forearm  in  spinal 
progressive  muscular  atrophy.  The 
last  three  fingers  can  no  longer  be  ex- 
tended.   (Personal  t)bservation.) 


994 


DISEASES    OF    THE    IsTervOUS    SYSTEM 


all,  can  the  patient  do  anything  with  them — as  to  dress  or  undress  himself;  but  he 
sometimes  learns  to  help  himself,  at  least  in  some  degree,  by  "  throwing  "  move- 
ments, by  motions  of  the  trunk,  by  using  his  mouth  in  taking  hold  of  things, 
etc.  Quite  rarely  the  atrophy  finally  attacks  the  muscles  of  the  neck.  The 
severest  respiratory  disturbances,  and  finally  a  fatal  termination,  may  be  brought 
about  by  an  implication  of  the  diaphragm  and  the  other  muscles  of  respiration. 

The  time  which  elapses  before  the  gradual  appearance  of  the  more  marked 
disturbances  of  function  is  almost  always  very  long.     Years  may  elapse  before 

the  atrophy  extends  from 
the  little  muscles  of  the 
hand  to  the  other  mus- 
cles of  the  arm.  In  the 
muscles  of  the  legs  the 
first  signs  of  atrophy  al- 
most always  develop  very 
late  if  at  all.  The  arms- 
are  often  perfectly  use- 
less when  the  patient 
can  still  walk  for  hours. 
Of  course  there  are  some 
exceptions  to  this  rule, 
and  then  the  muscles  of 
the  lower  leg  (peronei) 
especially  seem  to  be  first 
affected. 

Besides  the  atrophy, 
and  the  loss  of  function 
that  runs  parallel  to  it,  we 
must  mention  some  other 
changes  in  the  muscles. 
The  fibrillary  muscular 
twitchings  are  often  very 
striking.  A  constant 
tremor  and  wave  of  the 
muscle  may  be  provoked 
by  them.  In  some  cases 
they  are  weak  and  they 
can  be  detected  only  by 
special  attention.  They 
usually  become  vigorous 
if  one  irritates  the  mus- 
cle mechanically  by  a  blow.  The  electrical  excitability  of  the  diseased  muscles 
varies,  inasmuch  as  it  depends  entirely  upon  the  number  of  normal  fibers  still  pre- 
served in  the  muscle.  Since  the  atrophy  affects  only  one  fiber  after  another,  the 
faradic  and  galvanic  excitability  decrease  gradually,  and  are  lost  completely  only 
when  the  greatest  part  of  the  muscle  is  destroyed.  On  careful  testing,  we  can 
then,  however,  almost  always  make  out  a  decided  galvanic  reaction  of  degeneration 
in  single  muscles  that  are  much  diseased,  especially  in  the  form  of  the  so-called 
partial  reaction  of  degeneration :  the  excitability  of  the  nerves  is  retained,  but  the 
contractions  in  the  muscles  themselves  seem  very  slow,  and  the  anodic  closure 
contractions  (AnSZ)  predominate  (seepage  851). 

In  many  eases  there  is  an  increase  of  the  fatty  tissue  (which  is  always  of  mod- 
erate degree)  at  the  same  time  with  the  atrophy  of  the  muscular  substance,  and 
this  often  makes  it  very  hard  to  judge  of  the  atrophy;  but  the  loss  of  function  in 


Fig.  143.  Fig.  144. 

Figs.  143  and  144. — Spinal  progrressive  muscular  atrophy. 
(Personal  observation.) 


PRIMARY  DEGENERATIONS  OF  THE  MOTOR  TRACT   995 

the  muscles,  the  diminished  electrical  excitability,  and  the  peculiar  soft  feeling 
which  atrophied  muscles  have  when  covered  with  fat,  reveal  the  true  condition  of 
things.  There  are  no  trophic  disturbances  in  the  skin.  Almost  all  the  former 
statements  in  regard  to  this  refer  probably  to  the  confusion  between  progressive 
muscular  atrophy  and  similar  forms  of  disease,  especially  syringomj-elia.  The 
coldness  and  cyanosis  sometimes  seen  in  the  hands  is  due  to  the  fact  that  the 
arms  constantly  hang  down  and  to  the  lack  of  any  muscular  movement. 

The  examination  of  the  tendon  reflexes  is  of  great  diagnostic  importance. 
While  they  are  invariably  decidedly  increased  in  the  upper  extremities  in  amyo- 
trophic lateral  sclerosis,  they  are  only  feebly  manifest  or  entirely  absent  in  genu- 
ine progressive  muscular  atrophy,  a  condition  which  is  easily  explained  by  the 
atrophy  of  the  motor  ganglion-cells  belonging  to  the  reflex  arc,  or  by  the  atrophy 
of  the  centrifugal  motor  fibers.  Since  no  degeneration  of  the  lateral  pyramidal 
tract  precedes  this  atrophy,  it  goes  without  saying  that  the  muscular  rigidity, 
associated  with  paresis  and  increase  of  the  tendon  reflexes,  so  characteristic  of 
amyotrophic  lateral  sclerosis,  is  also  absent.  Muscular  weakness  and  muscular 
atrophy  are  completely  parallel  in  spinal  progressive  muscular  atrophy.  In  the 
lower  extremities  the  patellar  reflex  is  retained  as  long  as  the  disease  spares  the 
legs,  but  it  is  not  increased.  If  the  atrophy  involve  the  legs,  the  patellar  reflex 
is  usually  lost. 

In  distinction  from  all  these  manifest  disturbances  in  the  motor  region,  the 
sensibility  of  the  skin  and  deeper  parts  remains  perfectly  preserved.  A  careful 
test  of  the  sensibility  is  therefore  indispensable  to  avoid  mistaking  it  for  similar 
morbid  conditions,  such  as  syringomyelia.  There  are  also  never  any  morbid  symp- 
toms on  the  part  of  the  bladder  or  rectum. 

In  many  cases  the  affection  finally  invades  the  muscular  region  innervated 
from  the  medulla;  the  symptoms  of  "progressive  bulbar  paralysis"  (vide  infra)  are 
added  to  those  of  progressive  muscular  atrophy.  This  combination  of  spinal  and 
bulbar  disease,  as  we  have  previously  shown,  is  a  usual  occurrence  in  amyotrophic 
lateral  sclerosis,  even  when  the  disease  has  lasted  a  comparatively  short  time. 
In  genuine  progressive  muscular  atrophy,  however,  the  bulbar  symptoms  usually 
develop,  if  at  all,  only  after  the  disease  has  gone  on  for  years.  Then  the  speech 
begins  to  become  indistinct  from  the  atrophy  of  the  tongue,  swallowing  is  diffi- 
cult, and  the  patient  finally  succumbs  to  increasing  inanition  or  to  respiratory 
disturbances.  In  their  principal  characteristics  the  muscular  atrophy  of  the  ex- 
tremities and  the  bulbar  symptoms,  as  we  have  said,  are  precisely  analogous  phe- 
nomena, inasmuch  as  the  nerve  nuclei  in  the  medulla  have  precisely  the  same  sig- 
nificance for  the  muscles  of  the  tongue,  the  pharynx,  and  the  face,  as  the  anterior 
gray  cornua  of  the  cord  have  for  the  muscles  of  the  trunk  and  the  extremities.  In 
many  cases,  however,  bulbar  symptoms  do  not  develop  at  all,  since  the  patients  die 
early  of  some  intercurrent  disease,  or  the  fibers  of  the  bulbar  region  are 
not  involved  in  the  morbid  process;  but  the  whole  process  may  begin,  as  we  shall 
see  later,  in  the  region  of  the  bulbar  nerves  as  "bulbar  paralysis,"  while  the 
spinal  muscular  atrophy  does  not  come  on  in  the  arms  until  afterward. 

Diagnosis. — The  diagnosis  of  spinal  progressive  muscular  atrophy  can  easily 
be  made  if  we  confine  ourselves  strictly  to  the  definition  of  the  disease,  and  do  not 
confuse  it  with  other  affections  in  which  the  muscular  atrophy  is  only  one  symp- 
tom which  may  have  an  entirely  different  origin — muscular  atrophies  in  extensive 
diffuse  myelitis,  in  tumors,  in  the  formation  of  cavities  in  the  cord,  in  multi- 
ple neuritis,  as  a  result  of  articular  affections  and  injury,  etc.  We  should  con- 
sider especially  the  typical  course  of  the  affection  in  most  cases  of  genuine 
progressive  muscular  atrophy,  its  beginning  in  the  upper  extremities,  the  small 
muscles  of  the  hand,  or  more  rarely  the  muscles  of  the  shoulder  and  upper 
arm,    its    slow    advance,  the  peculiar    "  individualization "    of    the     atrophy — 


996  DISEASES    OE   THE   NeeVOUS    SYSTEM 

that  is,  the  affection  of  some  muscles  while  other  neighboring  muscles  remain 
completely  normal ;  the  special  form  of  atrophy  recognizable  by  fibrillary  contrac- 
tions and  electrical  reaction  of  degeneration ;  and,  finally,  the  absence  of  all  dis- 
turbances of  sensibility  or  of  the  sphincters.  Progressive  muscular  atrophy  is 
doubtless  nearly  allied  to  amyotrophic  lateral  sclerosis,  but  the  latter  is  distin- 
guished by  its  more  rapid  course,  and  especially  by  the  increase  of  the  tendon 
reflexes  due  to  the  affection  of  the  lateral  columns,  and  the  corresponding  appear- 
ance of  spastic  symptoms.  The  differential  diagnosis  between  the  spinal  and  the 
myopathic  (juvenile)  muscular  atrophy  (muscular  dystrophy),  which  is  also  per- 
fectly certain  at  present  in  most  cases,  will  be  described  later. 

The  prognosis  of  progressive  muscular  atrophy  is  to  be  regarded  as  absolutely 
unfavorable.  The  disease  appears  comparatively  benign  only  from  the  fact  that 
it  is  apt  to  advance  very  slowly,  since  it  may  last  for  ten  or  fifteen  years,  or  even 
longer.  As  we  have  already  said,  the  fatal  termination  at  last  appears  from  some 
intercurrent  disease,  or  as  a  result  of  the  final  appearance  of  dangerous  bulbar 
symptoms,  paralysis  of  deglutition  and  respiration. 

The  results  of  treatment  are  accordingly  very  slight.  An  electrical  treatment, 
continued  for  months  and  years  with  very  great  persistence,  can  alone  produce 
a  little  improvement  or  check  the  advance  of  the  atrophy  somewhat.  Temporary 
improvement  may  also  sometimes  be  attained  by  methodical  massage  of  the 
muscles  and  a  rationally  conducted  gymnastic  treatment.  In  other  respects,  the 
treatment  must  be  symptomatic.  [Gowers  claims  that  daily  subcutaneous  injec- 
tions of  strychnine,  grains  y-g-Q  to  jV  (granune  0.0005-0.002),  often  arrest  the 
disease. — K.] 

4.  Neurotic  Muscular  Atrophy 

(  Type  Charcot- Marie.     Peroneal- Forearm  Type  of  Progressive  Muscular  Atrophy) 

This  name  is  given  to  a  form  of  progressive  muscular  atrophy  which  has  be- 
come known  through  many  recent  observations  (Charcot  and  Marie,  Tooth,  J. 
Hoffmann,  and  others),  and  which  is  manifested  by  several  very  characteristic 
clinical  features.  The  disease  is  often  a  pronounced  hereditary  and  family  affec- 
tion, which  can  sometimes  be  traced  through  four  or  five  generations,  but,  on  the 
other  hand,  it  also  occurs  in  members  of  the  same  generation  without  being  pres- 
ent in  the  antecedents,  and  individual  cases  have  also  repeatedly  been  observed  in 
which  there  was  apparently  no  hereditary  predisposition.  The  first  symptoms 
of  the  disease  usually  appear  in  childhood,  but  some  cases  have  also  been  ob- 
served in  later  life.    There  is  no  essential  difference  between  the  two  sexes. 

IText  to  the  conditions  mentioned  (beginning  in  childhood,  generic  occur- 
rence), the  most  noticeable  feature  is  the  very  regular  localization  of  the  muscu- 
lar atrophy  (see  Fig.  145).  The  atrophy  almost  always  begins  symmetrically  in 
the  portions  of  the  extremities  most  distant  from  the  trunk — that  is,  in  the  hands 
and  forearms  and  the  feet  and  lower  legs.  The  lower  extremities  are  often  af- 
fected for  a  longer  or  shorter  time  (even  for  years)  before  the  upper,  but  the  con- 
trary sequence  may  also  occur.  Since  the  atrophy  of  the  small  muscles  of  the 
feet  causes  symptoms  that  attract  little  attention  (a  claw-like  position  of  the 
toes),  the  disease  may  often  remain  unnoticed  until  the  peronei,  the  tibiales  an- 
tici,  and  the  long  extensors  of  the  great  toe  are  involved.  The  gait  then  becomes 
impaired  from  the  dropping  of  the  toes  and  shows  all  the  characteristic  peculiar- 
ities of  bilateral  peroneal  paralysis  {q.  v.).  In  older  cases  there  often  develops' 
on  both  sides  a  complete  talipes  equinus  or  varo-equinus.  As  the  atrophy 
progresses,  the  muscles  of  the  calves  gradually  become  affected,  and  finally  the 
muscles  of  the  thigh  as  well.  Atrophy  and  paresis  of  the  muscles  go  always  hand 
in  hand.  The  same  is  seen  in  the  upper  extremities.  Here  the  small  muscles  of 
the  hand,  the  interossei  and  thenar  and  hypothenar  muscles,  atrophy  first,  just 


PKIMAEY  DEGENEKATIONS   OF  THE   MOTOE   TKACT      997 


as  in  spinal  muscular  atrophy  and  amyotrophic  lateral  sclerosis.  The  fingers 
therefore  assume  the  claw  position;  the  movements  of  the  thumb  become  more 
and  more  impaired,  so  that  it  lies  addueted  against  the  hand.  The  atrophy  then 
extends  to  the  forearms,  where  the  extensors  are  earlier  and  more  markedly 
affected  than  the  flexors.  Later  in  the  course  of  the  disease,  when  the  forearms 
and  hands  are  already  greatly  emaciated,  we  can  usually  discover  the  beginning 
of  atrophy  in  the  muscles  of 
the  shoulder  and  upper  arm. 
The  muscles  belonging  to 
the  trunk  resist  the  morbid 
process  the  longest.  The 
facial  muscles  also  are  usu- 
ally spared,  although  mani- 
fest changes  may  finally  oc- 
cur even  in  them,  but  no 
disturbances  have  thus  far 
been  observed  in  the  domain 
of  the  bulbar  nerves.  Final- 
ly we  may  mention  the  ob- 
servations reported  by  Hanel 
where  the  disease  was  traced 
in  many  members  of  one 
family  through  four  genera- 
tions and  was  always  con- 
fined to  the  upper  extrem- 
ities. 

It  is  of  the  greatest  im- 
portance for  our  compre- 
hension of  the  whole  disease 
that  the  atrophying  muscles 
show  fibrillary  contractions, 
usually  slight  but  sometimes 
lively,  and  that  we  can 
invariably  find  the  most 
marked  changes  in  the  elec- 
trical excitability  of  the 
muscles  and  their  corre- 
sponding nerves.  The  nerves 
soon  show  a  marked  diminu- 
tion or  even  a  total  loss  of 
galvanic  and  faradic  excita- 
bility. In  the  muscles  we 
find  either  the  same  condi- 
tions or  a  pronounced  galvanic  reaction  of  degeneration.  It  is  a  very  interesting 
fact  that,  on  electrical  examination,  we  can  often  detect  manifest  changes  in 
excitability,  just  as  in  lead  paralysis,  in  muscles  which  apparently  show  no 
atrophy  or  paralysis  at  all. 

The  mechanical  excitability  of  the  muscles  is  also  diminished.  The  tendon 
reflexes  of  the  affected  muscles  are  wholly  absent  or  much  diminished.  They  are 
never  increased.  The  sensibility  is  never  much  affected,  but  it  is  often  not  per- 
fectly normal.  Parsesthesise  and  painful  sensations  in  particular  are  often  pres- 
ent, and  there  is  sometimes  a  manifest  but  slight  blunting  of  the  cutaneous  sensi- 
bility.   The  functions  of  the  bladder  and  rectum  remain  normal. 

From  the  clinical  facts  just  described  the  conclusion  may  be  drawn  that  the 


Fig.   145. — Neurotic  muscular  atrojjhy.     The  disease  cauie  ou  in 
almost  the  same  fashion  in  three  members  of  one  family. 
(Personal  observation). 


998 


DISEASES    OE    THE    l^EEVOUS    SYSTEM 


form  of  muscular  atrophy  under  discussion  must  liave  a  neurotic  or  a  spinal  ori- 
gin. The  assumption  of  a  neurotic  origin  is  favored  not  only  by  the  results  of  the 
electrical  examination  and  the  occurrence  of  pain  and  slight  sensory  disturbances, 
but  also  by  the  results  of  the  anatomical  investigations  thus  far  reported,  al- 
though they  are  of  course  still  few 
■  I  in  number.  According  to  these, 
'  the  disease  seems  to  be  confined 
X  mainly  to  the  muscles  and  the 
peripheral  motor  nerves,  while  the 
anterior  roo'ts  and  the  ganglion- 
cells  in  the  anterior  horns  show 
no  perceptible  alteration,  but  a 
moderate  loss  of  fibers  is  some- 
times found  in  the  region  of  the 
columns  of  Goll. 

Further  observations  and  in- 
vestigations must  teach  us  whether, 
as  is  probable,  we  shall  find  closer 
relations  and  transition  forms  be- 
tween neurotic  and  spinal  atrophy ; 
but  meanwhile  the  disease  just  de- 
scribed is  a  form  of  progressive 
muscular  atrophy  so  well  charac- 
terized and  so  readily  recognizable 
in  its  clinical  aspect  that  a  sepa- 
rate description  of  it  is  undoubt- 
edly warranted. 


{The 


5.  Progressive  Muscular 
Dystrophy 

Myopathic   Juvenile   Forms   of  Pro- 
gressive Muscular  Atrophy) 


Fig.  146. 


-Peroueal  muscular  atrophy.    Legs  of  the  bi-other 
of  the  patient  shown  in  Fig.  145. 


The  so-called  purely  myopathic 
muscular  atrophies  are  much  com- 
moner than  the  forms  of  muscular 
atrophy  thus  far  described,  in  which,  besides  th6  wasting  of  the  muscular 
fiber,  there  is  a  more  or  less  extensive  atrophy  of  the  motor  nervous  sys- 
tem. Myopathic  muscular  atrophy  is  the  name  given  to  all  those  forms  in 
which  anatomical  investigation  has  thus  far  found  atrophic  processes,  not  in 
the  cord  or  in  the  peripheral  nerves,  but  exclusively  in  the  muscles  themselves. 
The  old,  long  contest  whether  the  "  seat "  of  progressive  muscular  atrophy  was 
to  be  looked  for  in  the  spinal  cord  or  in  the  muscles  themselves,  has  thus  at  last 
been  decided :  that  each  of  these  hypotheses  was  correct  for  certain  cases.  Thanks 
to  persistent  clinical  and  anatomical  investigations,  we  are  now  in  a  position  to 
distinguish,  easily  and  positively  for  the  most  part,  the  spinal  (and  neurotic) 
from  the  myopathic  cases  even  during  the  patient's  life.  Of  course  many  facts 
even  now  seem  to  indicate  that  there  is  no  very  strict  division,  and  that  even 
here  transition  forms  may  occur  which  can  be  fully  understood  only  by  a  still 
more  accurate  insight  into  the  nature  of  the  morbid  process  in  question. 

In  spite  of  many  common  peculiarities,  the  individual  cases  of  myopathic 
muscular  atrophy  differ  in  many  respects  from  one  another.  These  differences 
relate  either  to  the  localization  of  the  muscles  chiefly  or  at  least  first  affected,  or 
to  the  special  variety  of  change   in   the  muscles    (simple   atrophy   or   atrophy 


PEIMAEY  DEGENEEATIONS  OF  THE  MOTOR  TRACT   999 

with  a  large  interstitial  development  of  fat).  These  differences  were  the  reason 
why  it  was  formerly  believed  that  several  forms  of  disease  could  be  recognized, 
whereas  in  reality  we  are  dealing  only  with  different  types  of  the  same  disease. 
These  varieties,  of  course,  have  so  much  individuality  and  so  constantly  recur 
in  the  .same  way  that  we  are  perfectly  justified  in  differentiating  them, 
from  a  clinical  standpoint;  but,  on  the  other  hand,  there  are  so  many  transitions 
between  the  different  types  that  their  intimate  relationship  is  undoubted.  Erb 
has  therefore  been  perfectly  correct  in  proposing  to  group  together  all  these  differ- 
ent types  under  one  common  name — progressive  muscular  dystrophy — in  order  to 
attest  their  kinship.  We  can  then  distinguish  the  different  sub-t;v"pes  by  spe- 
cial terms. 

Before  we  proceed  in  what  follows  to  describe  these  different  sub-types  in 
greater  detail,  we  would  first  mention  the  most  important  points  which  are 
common  to  all  forms  of  myopathic  mxiscular  atrophy — that  is,  of  so-called  mus- 
cular dystrophy.  They  are  as  follows :  1.  All  forms  of  dystrophy  occur  gener- 
ically  or  hereditarily.  We  therefore  see  the  disease  most  frequently  in  brothers 
and  sisters,  or  more  rarely  in  members  of  the  same  family  in  different  genera- 
tions. On  the  other  hand,  sporadic  cases  are  of  course  not  uncommon.  If  the 
•disease  occurs  in  members  of  the  same  family  it  usually  assumes  the  same  form  in 
each  of  them;  but  different  forms  may  exceptionally  occur  in  one  family — a  cir- 
cumstance strongly  suggesting  an  intimate  relation  between  the  different  types. 
2.  The  first  symptoms  of  the  disease  almost  always  appear  in  youth,  sometimes  in 
childhood,  sometimes  not  until  puberty.  Only  in  rare  cases  does  the  disease 
begin  between  thirty  and  forty  or  even  later.  It  is  worthy  of  note  that  certain 
forms  usually  begin  in  childhood  ("  infantile "  form  with  implication  of  the 
facial  muscles,  pseudo-hypertrophy),  and  other  forms  only  at  puberty  ("  juvenile  " 
form  with  implication  of  the  shoulder  and  upper-arm  muscles).  3.  The  localiza- 
tion of  the  muscular  atrophy  is  extremely  irregular.  The  different  forms  or  types 
are  of  course  distinguished  by  their  special  localization;  but  as  the  disease  ad- 
vances, or  in  the  frequent  transition  cases,  it  often  happens  that  other  muscular 
regions  besides  those  chiefly  affected  are  also  involved  to  a  lesser  degree.  It  thus 
appears  that  in  all  forms  it  is  finally  the  same  muscular  regions  which  are  chiefly 
affected  with  atrophy,  while,  on  the  other  hand,  in  all  forms  certain  muscular  re- 
gions with  scarcely  an  exception  remain  intact.  The  groups  of  muscles  most 
exposed  to  the  disease  are :  (a)  Facial  muscles,  as  far  as  they  are  innervated  by 
the  facial  nerve,  especially  the  orbicularis  palpebrarum  and  orbicularis  oris. 
(h)  Muscles  of  the  shoulder-girdle:  pectoralis,  latissimus  dorsi,  serratus  anticus 
major,  rhomboidei,  trapezius,  (c)  Muscles  of  the  upper  arm:  biceps,  brachialis 
anticus,  supinator  longus,  triceps,  (d)  Long  extensors  of  the  back  (erectores 
-spinse).  (e)  Pelvic  muscles  (glutsei)  and  muscles  of  the  thigh.  Other  muscles, 
however,  are  almost  always  spared  in  muscular  dystrophy:  (a)  Deltoids,  supra- 
spinati,  and  infra-spinati.  (&)  Forearm  muscles,  and  especially  the  small  mus- 
cles of  the  hand  and  fingers,  (c)  Lower  leg  muscles,  especially  the  gastrocnemius 
and  the  small  muscles  of  the  foot,  (d)  Tongue  and  muscles  of  deglutition.  All 
these  statements  are  not  absolutely  without  exception,  but  they  show  the  usual 
rule,  which  must  depend  upon  the  essential  nature  of  the  disease.  4.  The  ana- 
tomical changes  in  the  muscles  are  essentially  the  same  in  all  the  different  forms 
of  dystrophy.  They  consist  first  of  the  most  varied  changes  in  volume  of  the  indi- 
vidual muscular  fibers.  Many  fibers  show  an  atrophy  which  progresses  finally  to 
complete  disappearance,  while,  on  the  other  hand,  so-called  hypertrophic  (hypervo- 
luminous)  fibers  are  also  almost  always  to  be  found.  Erb  suspects  that  the  hyper- 
trophy is  the  first  stage  of  the  disease  of  the  fiber,  and  that  the  atrophy  follows 
this  later.  Besides  these  changes  in  volume,  we  see  regularly  an  evident  increase 
in  the  muscle  nuclei  and  a  considerable  increase  in  the  interstitial  connective 


1000 


DISEASES    OE   THE   NERVOUS    SYSTEM 


tissue.  If  there  is  pronounced  pseudo-hypertrophy  the  interstitial  tissue  is  per- 
meated with  an  abundant  accumulation  of  fat-cells.  In  the  muscular  fibers  them- 
selves the  transverse  striation  is  almost  always  preserved  to  the  last,  and  we 
never  find  granular  or  fatty,  so-called  degenerative  destruction  in  any  great 
degree.  The  peripheral  motor  nerves  and  the  motor  ganglion-cells  in  the  anterior 
horns — that  is,  the  peripheral  motor  neurones — remain  perfectly  normal.  Two 
clinical  facts,  which  are  very  important  in  diagnosis,  are  associated  with  this  cir- 
cumstance :  (a)  In  all  forms  of  dystrophy  the  fibrillary  contractions  in  the  dis- 
eased muscles,  which  are  so  common  in  spinal  atrophies,  are  almost  invariably 
absent,  (h)  Distinct  electrical  reaction  of  degeneration  is  almost  never  found  in 
dystrophy  (in  contrast  to  the  spinal  atrophies).  Since  the  disease  is  also  a 
motor  system  disease,  like  all  the  other  forms  of  progressive  muscular  atrophy,. 


3  4 

Fig.  147.— Positions  of  a  child  with  hereditary  (pseudo-hypertrophic)  muscular  atrophy,  on  rising  to  an 

erect  attitude.    (From  Gowers.) 

it  is  self-evident  that  in  dystrophy  the  sensibility,  the  functions  of  the  bladder, 
etc.,  remain  perfectly  normal. 

Since  we  have  mentioned  the  most  important  features  common  to  all  forms  of 
dystrophy,  we  will  pass  to  the  description  of  the  chief  individual  clinical  types. 
We  would  emphasize  the  fact  once  more  that  transition  forms  between  these 
types  are  by  no  means  rare. 

1.  Pseudo-hypertrophy  of  the  Muscles  (Lipomatosis  luxurians  muscularis 
progressiva  of  Heller;  Atrophia  musculorum  lipomatosa  of  Seidel). — Pseudo- 
hypertrophy is  the  rarest  form  of  muscular  dystrophy,  but  it  was  the  first  to  be- 
come accurately  known,  on  account  of  its  striking  aspect.  It  was  quite  fully  de- 
scribed in  Germany  by  Griesinger  (1864),  while  in  France  Duchenne  gave 
in  1868  a  very  complete  clinical  description  of  it.  In  1866  M.  Eulenburg  and 
Cohnheim  had  already  shown,  by  the  careful  anatomical  examination  of  a  case, 
that  the  nervous  system  remained  perfectly  normal,  a  statement  which  was  con- 
firmed by  all  subsequent  investigations  (Charcot,  F.  Schultze,  and  others). 

Pseudo-hypertrophy  develops  almost  invariably  in  childhood,  somewhere  be- 
tween the  ages  of  five  and  eight  years.  It  is  a  pronounced  family  or  even  hered- 
itary disease.  The  male  sex  is  decidedly  more  disposed  to  the  disease  than  the 
female    [but  the  disease   seems  to  be   transmitted  through  the   female   in   the 


PEIMARY  DEGENERATIONS    OF   THE   MOTOR   TRACT     1001 


hereditary  cases. — K.]  Sometimes,  but  not  always,  we  also  find  in  the  affected 
families  some  disposition  to  a  nei-vons  taint,  such  as  hysteria,  epilepsy,  feeble- 
mindedness, anomalies  of  the  skull,  etc. 

The  disease  begins  gradually  and  almost  always  without  a  special  exciting 
cause.  The  parents  notice  that  the  child,  who  had  been  previously  perfectly 
well  and  strong,  becomes  insecure  on  his  legs,  so  that  he  can  no  longer  jump  or 
go  up-stairs  as  well  as  he  used  to  do.  This  points  to  the  first  characteristic  pecul- 
iarity wherein  pseudo-hypertrophy  differs  from  spinal  progressive  muscular 
a\rophy.  It  begins,  with  rare  exceptions,  in  the  muscles  of  the  trunk,  especially 
in  the  muscles  of  the  back  and  pelvic  muscles  (glutsei),  and  in  the  muscles  of  the 
lower  extremities,  especially  in  those  of  the  thigh.  While 
the  arms  and  hands  are  still  perfectly  normal,  walking 
constantly  grows  more  and  more  difficult,  and  the  gait 
very  soon  assumes  so  characteristic  a  type  that  from  this 
alone  the  diagnosis  can  often  be  made  at  the  first  glance. 
The  gait  becomes  waddling  (chiefly  on  account  of  the 
weakness  of  the  glutsei  medii),  the  belly  appears  very 
prominent,  the  vertebral  column  is  arched  forward  in 
the  lumbar  region  in  marked  lordosis,  and  the  whole 
upper  part  of  the  body  is  balanced  on  the  legs.  The  legs 
are  raised  slowly  and  with  difficulty,  and  the  toes  usually 
droop  from  paresis  of  the  dorsal  extensors.  The  child's 
movements,  when  he  tries  to  raise  himself  from  the  floor 
or  pick  up  any  object,  are  very  characteristic,  and  are  alike 
in  almost  all  cases,  as  a  result  of  paresis  of  the  extensors 
of  the  thigh  and  leg  (glutsei  and  extensores  cruris).  Since 
it  is  impossible  to  raise  the  trunk,  the  child  usually  first 
gets  on  all  fours,  and  then  gradually  straightens  himself 
"up  ["  climbs  up  his  thighs  "]  by  leaning  his  arms  on  his 
knees  (see  Fig.  147).  Later  on  disturbances  of  motion 
appear  in  the  upper  extremities  also,  and  in  general  they 
are  very  similar  to  those  to  be  described  more  fully  in  the 
next  type. 

If  we  inspect  the  patient  more  closely  we  shall  usually 
find  at  the  first  glance  an  extraordinary  increase  in  the 
volume  of  single  muscles  (see  Fig.  148).  The  calves  are 
disproportionately  thick,  and  sometimes  the  thighs  also ; 
the  arms  are  affected  later,  especially  the  deltoids,  the 
triceps,  etc.  This  increase  of  volume  is  caused  by  an  ab- 
normal interstitial  development  of  fat,  "  pseudo-hyper- 
trophy." Hence  the  muscles  do  not  feel  firm,  but  soft 
and  spongy.  It  is  by  no  means  rare,  however,  that,  be- 
sides the  pseudo-hypertrophy  in  some  muscles,  a  genuine  atrophy  develops  in 
others,  with  a  pronounced  loss  of  substance  and  without  any  co-existing  de- 
velopment of  fat.  This  is  seen  especially  in  the  upper  extremities  in  the 
groups  of  muscles  previously  mentioned.  Finally,  there  seems  to  be  in  addi- 
tion even  a  genuine  muscular  hypertrophy.  In  several  cases  we  have  seen  a 
marked  increase  in  volume  in  the  muscles  of  the  calves,  which  were  capable 
of  quite  an  extraordinary  display  of  strength.  In  such  cases,  however,  there  is, 
probably,  in  our  opinion,  a  sort  of  compensatory  hypertrophy,  since  the  muscles 
that  are  still  able  to  work  are  exerted  excessively. 

Fibrillary  twitchings  of  the  muscles  are  scarcely  ever  seen.  Electrical  exami- 
nation shows  a  diminution  of  excitability  corresponding  to  the  atrophy  and  to 
the  increased  deposit  of  fat,  but  never  reaction  of  degeneration.     The  sensibility 


Fig.  148.  —  Pseudo-hyper- 
trophy of  the  muscles. 
(From  DucHENNE.) 


1002 


DISEASES    OE   THE   JS^EEVOUS    SYSTEM 


V 


/ 


\ 


remains  perfectly  normal,  and  also  micturition  and  defecation.  The  patellar  reflex 
is  sometimes  absent,  because  the  quadriceps  is  involved.  It  is  noticeable  that 
the  skin,  especially  in  the  legs,  very  often  shows  a  peculiar  bluish  marbled  color- 
ing. Bulbar  symptoms  ap- 
parently never  occur.  The 
intelligence  in  most  cases 
is  perfectly  normal,  but 
exceptionally  children  with 
hereditary  muscular  atro- 
phy also  show  manifest 
signs  of  mental  or  even  of 
moral  weakness. 

The    disease    advances 

very    slowly    but    without 

Vj|=,  remissions.       Finally    the 

r    *•-:'*-.■'  '  patient    can    not    walk    at 

~^~-.-,_^  all;  he  is  confined  to  the 

^^  \.^  bed,  and  becomes  more  and 

■--,  more  helpless.    Death  usu- 

ally ensues  from  some  in- 
/  tercurrent      disease,      but 

/'  1  sometimes     from     insuffi- 

ciency   of    the    respiratory 
muscles. 

2.  The  Infantile  Atro- 
phic FoRii  OF  Muscular 
Dystrophy  usually  with 
Implication  of  the  Facial 
Muscles. — Simple  atrophic 
forms  of  progressive  raus- 
cular  wasting  develop  far 
more  frequently  in  early 
childhood  than  pseudo-hy- 
pertrophy. They  may  be 
combined  with  pseudo-hy- 
pertrophy, as  we  have  said  above,  especially  in  the  form  where  there  is  lipoma- 
tosis in  the  lower  extremities  and  simple  atrophy  in  the  shoulders  and  arms ; 
but  what  gives  the  simple  atrophic  infantile  form  a  special  stamp  is  the  com- 
paratively frequent  implication  of  the  facial  muscles.  These  muscles  may  not 
be  involved,  and,  on  the  other  hand,  they  may  be  affected  in  rare  instances  in 
the  juvenile  form  as  well,  but  marked  atrophy  of  the  facial  muscles  is  a  peculiarity 
chiefly  of  the  infantile  atrophic  form. 

Duchenne  had  already  observed  that  in  children  there  is  a  form  of  muscular 
atrophy  which  begins  in  the  muscles  of  the  face ;  but  his  statements  were  almost 
forgotten  until,  a  few  years  ago,  Landouzy  and  Dejerine  called  attention  anew 
to  this  subject,  and  demonstrated,  contrary  to  previous  belief,  that  implication  of 
the  facial  muscles  is  by  no  means  an  unusual  symptom.  If  the  atrophy  is  already 
plainly  pronounced,  characteristic  sjTuptoms  ensue :  the  eyes  can  no  longer  be 
completely  closed,  and  the  movements  of  the  mouth  in  whistling,  laughing,  and 
talking  become  impaired.  From  the  sinking  in  of  the  cheeks,  the  drooping  of  the 
under  lip,  etc.,  there  develops  a  very  characteristic  type  of  countenance  ("  fades 
myopathique"),  by  which  the  practiced  eye  can  recognize  the  affection  almost 
at  once  (Fig.  149).  There  may  finally  ensue  complete  rigidity  and  immobility  of 
the  face.    At  the  same  time  or  somewhat  later,  as  a  rule,  other  muscular  regions 


Fig.  149. — Juvenile  mj-opachie  muscular  atrophy  iu  a  teu-j-ear-old 
child,  with  marked  impUcaUon  of  the  facial  muscles.  Inabili- 
ty to  close  the  eyes  or  move  the  lips,  .itrophy  of  the  pecto- 
rals, etc.    (From  the  Erlangen  3Iedical  Clinique.) 


PEIMAEY  DEGENERATIONS    OF  THE   MOTOR   TRACT     1003 

may  be  affected,  and  again,  as  in  other  forms,  chiefly  the  shoulder  muscles,  the 
muscles  of  the  upper  arms,  the  extensors  of  the  spine,  and  the  muscles  of  the 
pelvis  and  thigh.  The  child's  gait  becomes  as  waddling  as  that  of  children  with 
pseudo-hypertophy,  which  we  have  just  described.  The  spine  has  a  lordotic  curva- 
ture, the  child  rises  from  the  floor  by  the  aid  of  the  arms  (Fig.  147),  etc.  The 
sequence  in  which  the  different  muscles  are  attacked  by  the  atrophy  is  not  always 
the  same.  The  facial  muscles,  for  example,  may  often  be  attacked  later  than  the 
muscles  of  the  shoulder,  upper  arm,  and  trunk.  In  order  to  detect  the  slighter 
degrees  of  implication  of  the  face,  it  is  advisable  to  have  the  patient  close  his 
eyes  when  the  head  is  bent  backward;  we  can  then  readily  detect  the  fissure 


Fig.  150.— Two  brothers  with  juvenile  muscular  atrophy.      (Personal  observation  from  the  Eriangen 

Medical  Clinique.) 


left  between  the  eyelids  (insufficiency  of  the  orbicularis  palpebrarum).  We 
can  also  notice  in  the  early  stages  that  the  patient  can  not  protrude  the  lips 
to  whistle. 

The  muscles  of  mastication,  the  internal  ocular  muscles,  and  the  muscles  of 
the  forearm  and  hand  almost  always  remain  normal.  A  slight  persistent  con- 
tracture of  the  biceps  is  sometimes  present  and  is  characteristic.  Fibrillary  con- 
tractions and  reaction  of  degeneration  are  almost  always  absent. 

3.  The  Juvenile  Form  of  Dystrophy. — The  peculiarities  of  this  form  were 
fi.rst  carefully  studied  by  Erb.  It  usually  does  not  begin  until  after  actual  child- 
hood, in  the  years  of  puberty  or  sometimes  later  (between  twenty  and  forty). 
It  occurs  sporadically  occasionally,  but  it  is  also  frequently  hereditary  or  generic 
(that  is,  occurring  in  families),  and  the  girls  of  the  family  are  often  attacked 


1004 


DISEASES    OE    THE    NEEVOUS    SYSTEM 


by  this  form,  wliile  the  infantile  form  is  seen  especially  in  boys.  The  disease 
is  also,  like  pseudo-hypertrophy,  sometimes  seen  to  begin  in  the  pelvic  muscles 
and  the  legs,  but  more  often  the  shoulders  and  upper  extremities  are  first  at- 
tacked. There  is  also  a  remarkable  regularity  in  the  choice  of  the  muscles 
attacked,  as  has  been  mentioned  above.  According  to  Erb,  the  following  muscles 
are  almost  constantly  diseased  in  the  trunk  and  the  upper  extremities :  the 
pectoralis  major  and  minor,  the  trapezius,  the  latissimus  dorsi,  the  serratus 
anticus  major,  the  rhomboidei,  the  sacro-lumbalis  and  longissimus  dorsi,  and 
later  the  triceps.  The  following,  however,  almost  always  remain  normal;  the 
sterno-mastoid,  the  levator  anguli  scapulse,  the  coraco-brachialis,  the  teres  major 
and  minor,  the  deltoid,  the  supra-spinatus  and  infra-spinatus,  and,  as  must 
be  mentioned  especially  in  distinction  from  spinal  muscular  atrophy,  the  small 

muscles  of  the  hand.  The 
muscles  of  the  forearm, 
too,  except  the  supinator 
longus,  remain  intact  for 
a  long  time,  if  not.  per- 
manently; but  exceptions 
also  occur:  for  example, 
the  accompanying  illus- 
tration (Fig.  150)  shows 
two  brothers  with  juvenile 
muscular  atrophy  which 
in  other  respects  is  char- 
acteristic, but  the  muscles 
on  the  extensor  side  of 
the  forearm  are  also  eom- 
pletelj^  atrophied.  In  the 
lower  extre^lities  the 
atrophy  attacks  chiefly 
the  glutsei  and  the  quadri- 
ceps, more  rarely  the  per- 
onei  and  the  tibialis  an- 
ticus, while  the  sartorius 
and  the  muscles  of  the 
calf  are  usually  wholly 
exempt.  Fibrillary 
twitchings  in  the  affected 
muscles  are  generally  ab- 
sent, and  there  is  hardly 
ever  any  reaction  of  de- 
generation. 

The  disturbances  of 
function  due  to  this  condition  are  self-eviden1>,  so  that  a  full  description  of  them 
may  be  omitted.  The  arms  usually  suffer  first,  as  we  have  said.  The  marked 
projection  of  the  scapulae,  from  the  paralysis  of  the  serratus,  is  especially  char- 
acteristic (Fig.  152).  If  we  try  to  take  the  patient  inider  the  shoulders  and  lift 
him,  the  shoulders  are  perfectly  limp.  They  are  therefore  immediately  raised  so 
high  that  the  head  comes  between  the  shoulders  ("loose  shoulders  ").  The  most 
striking  features  in  the  anterior  wall  of  the  chest  are  the  flattening  in  the  region 
of  the  pectoralis  and  the  peculiar  folds  of  skin  on  the  anterior  edges  of  the  axillae. 
If  the  patient  walks  we  can  often  recognize  the  disease  at  a  distance  at  the 
first  glance  by  the  peculiar  gait.  The  upper  part  of  the  body  is  carried  back- 
ward (lordosis  of  the  lumbar  vertebrae),  and  the  gait  is  waddling,  since  the  pelvis 


Fig.  151.— Juvenile  muscular  dj' strophy.^  Prominence  of  the  scapulae 
when  the  arms  are  raised  in  consequence  of  atrophy  of  the  ser- 
ratus and  rhomboidei.  (Personal  observation  from  the  Erlangen 
Medical  Clinique.) 


PEIMAEY  DEGENERATIONS    OE   THE   MOTOR   TRACT     1005 


Fig.  152. — Muscular  d3'Strophy.  Prominence 
of  the  scapulte  when  the  arms  are  hanging 
down.    (Erlangen  Medical  Clinique.) 


been  seen  to  begin  at  a  more  ad- 
vanced age — from  forty  to  fifty — 
but  in  other  respects  these  cases  do 
not  differ  from  the  general  type,  al- 
though  we   have    noticed    that,    in 
such  cases  as  begin  relatively  late 
in  life,  the  muscles   of  the   pelvis 
and  thighs  were  chiefly  affected,  so 
that    the    patient    could    not 
stand  or  walk  while  the  arms 
still  performed  their  functions 
tolerably  well  (Fig.  154). 

Diag-nosis  of  Myopathic 
Muscular  Atrophy  (Muscular 
Dystrophy). — Now  that  the 
type  of  myopathic  muscular 
dystrophy  has  been  established 


can  no  longer  be  held  properly  by  the  weak 
glutsei.  On  stooping  and  rising,  the  same 
symptoms  are  seen  as  have  previously  been 
described  (Fig.  147).  As  a  rule,  in  the 
juvenile  form  the  face  is  not  involved,  but 
we  can  sometimes  detect  slight  disturb- 
ances of  the  facial  muscles,  especially  defec- 
tive closure  of  the  lids  and  inability  to 
whistle  (Fig.  153).  We  once  made  the 
interesting  observation  that  the  adult 
brother  of  a  young  girl  suffering  from 
juvenile  dystrophy  showed  these  (congeni- 
tal?) anomalies  in  the  face  from  earliest 
childhood,  without  showing  any  further  in- 
dications of  dystrophy.  Bulbar  symptoms 
are  as  rare  as  in  the  other  forms.  It  is  of 
significance  that  the  intercostal  muscles 
and  the  diaphragm  may  finally  atrophy,  and 
the  consequent  respiratory  disturbance  may 
be  the  cause  of  death. 

The  course  of  juvenile  dystrophy  is  very 
chronic,  like  that  of  all  the  other  forms. 
The  disease  progresses  very  slowly  and 
often  seems  almost  to  stand  still  for  a  long 
time.  Many  cases  have  been  under  ob- 
servation for  twenty  or  thirty  years. 

We  may  mention  in  conclusion  that  in 
some   cases   of   dystrophy  the  trouble   has 


Fig.  ]58. — Juvenile  muscular  ilystri^iiliy 
the  eyes.    Myopathic  fades.     iPert 


Insufiicient  closure  of 
iiial  observation.) 


1006 


DISEASES    OF    THE    NEKVOUS    SYSTEM 


in  all  its  details  by  numerous  observations,  the  diagnosis  is  usually  no  longer 
difficult.  The  generic  occurrence  of  the  disease,  its  development  usually  in  child- 
hood or  youth,  the  remarkable  regularity  in  the  selection  of  muscles  affected,  the 
absence  of  fibrillary  contractions  and  also  of  electrical  reaction  of  degeneration  in 
the  affected  muscles,  are  the  chief  points  upon  which  the  diagnosis  is  to  be  based 
in  the  individual  case.  If  we  bear  in  mind  these  peculiarities,  the  distinction  from 
the  spinal  and  neurotic  amyotrophies  or  from  other  similar  types  of  disease  (syr- 
ingomyelia) is  usu- 
ally easy.  Only  a  few 
cases,  which  clinic- 
ally seem  to  present 
transition  forms,  re- 
main for  a  time  un- 
certain in  their  ana- 
tomical determina- 
tion. We  must,  how- 
ever, indicate  one 
condition  which  may 
sometimes  give  rise  to 
mistakes  in  diagnosis 
— namely,  congenital 
muscular  defects.  In 
some  persons  we  find 
that  certain  muscles 
or  parts  of  muscles 
are  absent  from  birth, 
and  it  is  remarkable 
that  it  is  most  fre- 
quently the  same 
muscles  which  are 
most  often  affected 
in  muscular  dystro- 
phy, especially  the 
pectoralis  major,  or 
at  least  its  sternal 
portion,  the  serrati, 
the  rhomboidei,  the 
trapezii,    etc.      Such 

patient  in  sitting;  he  can  neither  stand  nor  walk.    (Personal  observa-    ^""S'-'"^""^ 

tion.)  defects  naturally  pre- 

sent at  the  first  glance 
a  very  similar  picture  to  that  of  a  patient  with  dystrophy;  but  we  can  usu- 
ally decide  correctly  as  to  the  condition  by  careful  inquiry,  since  in  case  of 
congenital  muscular  defects  the  abnormalities  have  always  been  present,  and 
they  also  show  no  noticeable  increase  in  the  course  of  years. 

Treatment. — The  treatment  of  myopathic  muscular  dystrophy  is  seldom  suc- 
cessful. We  may  sometimes  obtain  a  certain  improvement  by  persistent  treat- 
ment by  electricity  or  massage;  but  at  present  any  considerable  alteration  in 
the  coure  of  the  disease  is  beyond  the  domain  of  possibility.  [Persistent  and 
systematic  gymnastic  exercises  sometimes  have  a  decidedly  beneficial  effect. — K.] 


Fig.  1.54. — Progressive  myopathio  muscular  atrophy  of  the  pectorals,  upper 

arms,  and  muscles  of  the  pelvis  and  thigh.    Ordinary  position  of  the    conffCnital 

'"a^\r     (Personal  observa-  ° 


PEIMAEY   DEGENEEATIONS    OF   THE   MOTOE   TEACT     lOOY 


6.  Primary  Degeneration  op  the  Pyramidal  Tracts 

{Primary  Lateral  Sclerosis.     Spastic  Spinal  Farali/.sls.     Motor  Tabes.     Spusmodlc  Talts  DorsaUs) 

While  in  all  the  forms  of  primary  disease  of  the  motor  system  thus  far  de- 
scribed the  muscles  are  involved  primarily  or  secondarily,  and  muscular  atrophy 
therefore  plays  a  leading-  part  in  the  clinical  picture  of  all  the  diseases  described 
above,  in  rare  cases  the  degeneration  may  be  limited  to  the  central  neurone 
{PyS  of  Fig.  137,  page  986)  of  the  motor  tract.  In  such  cases  a  type  of  disease 
develops,  in  which  indeed  the  disturbances  are  exclusively  motor,  but  in  which 
muscular  atrophy  is  completely  absent — a  type  of  disease  to  which  has  been  given 
the  name  of  ^^  spastic  spinal  paralysis  ^^  (Erb,  Charcot).  There  is  no  doubt  that 
such  primary,  isolated  degeneration  of  the  pyramidal  tract  may  occur,  without 
involving  the  peripheral  motor  neurone  (cell  of  the  anterior  horn  with  its  process, 
the  peripheral  motor  nerve) ;  but  we  must  add  that  primary  degeneration  of  the 
pyramidal  tract  is  especially  apt  to  be  associated  with  degeneration  of  other  sys- 
tems of  neurones  (lateral  cerebellar  tract,  fibers  of  the  posterior  columns),  so  that 
the  anatomical  picture  of  the  disease  is  not  a  simple  one,  but  corresponds  to  a 
"  combined  system  diseased 

Type  of  Spastic  Spinal  Paralysis. — Three  symptoms  predominate  in  the  pic- 
ture of  spastic  spinal  paralysis :  motor  paresis,  hypertonicity  of  the  muscles  (mus- 
cular rigidity),  and  the  increase  of  the  tendon  reflexes — the  patellar  reflex,  and 
ankle  clonus.  The  loss  of  motor  power — we  are  speaking  at  present  only  of  the 
spastic  paralysis  of  the  legs,  which  is  by  far  the  most  frequent  and  the  most 
clearly  marked — is  found  in  various  degrees,  from  a  simple  weakness  of  move- 
ment to  a  complete  and  more  or  less  extensive  paralysis.  The  other  two  symp- 
toms, however — the  hypertonicity  (rigidity)  of  the  muscles,  and  the  increase  of 
the  tendon  reflexes— give  the  disturbance  of  motion  its  characteristic  "  spastic  " 
feature.  Both  symptoms,  indeed,  are  to  be  regarded  as  in  part  identical,  for  the 
rigidity  of  the  muscles  is  also  of  reflex  origin.  If  the  tendon  reflexes  be  much  in- 
creased, the  reflex  tension  of  the  muscles  comes  on  even  upon  the  stretching  and 
pulling  of  the  tendons,  which  are  excited  by  the  weight  of  the  limbs,  or  by  any 
active  or  passive  movements.  The  reflex  muscular  tension  opposes  any  attempt 
at  motion.  The  muscles  feel  rigid  and  firm,  and  the  legs  are  often  found  in 
almost  permanent  contracture  and  extended,  with  the  feet  in  plantar  flexion.  If 
we  try  to  flex  the  leg  passively  at  the  knee,  or  if  we  try  to  extend  the  foot  dorsally, 
we  find  it  almost  impossible  to  do  so.  The  more  rapidly  and  suddenly  we  try  to 
produce  the  motion,  the  more  marked  is  the  muscular  resistance,  which  can 
scarcely  be  overcome.  If,  however,  we  go  to  work  very  slowly  and  cautiously,  and 
avoid  any  sudden  tension  of  the  tendons,  we  can  almost  always  flex  the  leg  with- 
out special  trouble.  If  we  put  the  patient  on  the  edge  of  the  bed,  the  legs  do  not 
hang  down  laxly,  but  they  usually  fall  at  once  into  a  vigorous  extensor  tetanus, 
since  the  weight  of  the  leg  puts  the  quadriceps  into  contraction  by  the  tension  on 
the  ligamentum  patellse.  A  convulsive,  reflex  tremor  of  the  whole  leg  often  comes 
on  at  once,  similar  to  ankle  clonus.  If  we  examine  the  patient  while  in  the  bath 
we  find  the  spasms  decidedly  less,  because  in  the  water  the  influence  of  the  weight 
of  the  limb  is  diminished.  It  must  still  remain  undecided  whether  the  existence 
of  muscular  rigidity  in  spastic  paralysis  is  to  be  explained  exclusively  by  the 
increase  in  the  tendon  reflexes.  In  some  muscles  there  is  sometimes  so  persistent 
a  condition  of  tonic  irritation  that  we  are  led  to  think  of  processes  of  direct, 
abnormal  motor  irritation.  Thus  the  adductors  of  the  thigh,  in  particular, 
and  often  the  dorsal  extensors  of  the  great  and  other  toes,  etc.,  show  a  constant 
rigidity  and  tension,  the  reflex  origin  of  which  can  not  be  established,  at  least 
with  any  certainty. 


1008  DISEASES    OF    THE    NEEVOFS    SYSTEM 

Active  motion,  as  is  easily  explained,  must  also  be  impaired  from  the  inhibi- 
tory action  of  the  tonic  and  reflex  spasms.  The  degree  of  disturbance  of  motion 
is  thus  increased,  and  the  paresis  often  seems  greater  than  is  really  the  case.  The 
influence  of  the  muscular  tension  is  especially  manifest  in  the  gait  of  the  patient. 
As  long  as  walking  is  still  possible,  we  notice  very  plainly  that  it  is  rendered  diffi- 
cult, not  only  by  the  muscular  paresis,  but  also  by  the  stiffness  of  the  legs.  The 
patient  walks  with  short  and  difficult  steps,  the  legs  are  scarcely  flexed  at  the 
knee,  and  the  feet  are  scarcely  raised  at  all.  The  feet  "  stick  to  the  floor  "  and 
are  slowly  slid  forward,  and  there  is  a  marked  tendency  to  walk  on  the  toes,  from 
the  contraction  in  the  muscles  of  the  calves.  The  weight  of  the  body  alone  presses 
the  feet  downward.  We  term  this  very  characteristic  form  of  gait  the  spastic- 
paretic  gait.  It  is  also  characteristic  of  spastic  paralysis  of  the  legs  that  the 
patient  is  unable  to  execute  certain  isolated  movements.  Thus  the  patient,  like 
a  hemiplegic  (vide  infra),  often  can  not  dorsally  extend  the  foot  by  itself;  but  if 
he  flexes  the  whole  leg  and  draws  it  up  to  the  trunk,  there  always  follows  a  marked 
dorsal  extension  of  the  foot  with  great  tension  of  the  tendon  of  the  tibialis  anti- 
cus  muscle. 

The  increase  in  the  tendon  reflexes  may  also  exist  without  the  presence  of  any 
special  motor  paresis  of  the  muscles  at  the  same  time;  but  since  the  motion 
is  not  a  little  influenced  in  such  a  case  by  the  constant  spasms,  a  disturbance  of 
motility  may  be  produced,  which  we  have  called  "  spastic  pseudo-paralysis,"  or, 
more  properly,  pseudo-paresis.  In  these  cases  the  muscular  strength  is  almost 
normal,  and  the  patient  can  walk  for  quite  a  long  time.  ISTevertheless,  all  his 
movements  are  stiff  and  difficult,  and  the  gait  shows  all  the  peculiarities  of  the 
pure  spastic  gait.  The  steps  are  not  very  short  and  they  follow  one  another  quite 
rapidly,  but  the  legs  remain  perfectly  stiff  and  are  scarcely  raised  from  the 
ground,  and  the  patient  walks  almost  entirely  on  his  toes.  In  the  house  the 
patient  walks  with  a  noisy  shuffle,  and  in  soft  sand  we  can  see  the  furrows  drawn 
by  the  feet  as  they  slide  along  the  ground.  Since  the  Achilles  tendon  is  made 
tense  at  each  step,  and  since  a  reflex  contraction  of  the  muscles  of  the  calf  re- 
sponds to  this  tension,  each  step  is  often  followed  by  a  short  lifting  of  the  whole 
hody  ("teetering"  spastic  gait). 

Although  the  symptoms  mentioned  are  the  characteristic  positive  features  of 
■"  spastic  spinal  paralysis,"  yet,  in  the  original  sense  of  the  word,  the  affection  is 
also  characterized  by  the  fact  that  certain  other  spinal  symptoms,  especially  dis- 
turbances of  sensibility,  disturbances  in  micturition  and  defecation,  muscular 
atrophy,  and  other  trophic  symptoms,  are  entirely  absent.  Only  when  such  was 
the  case  have  Erb  and  Charcot  claimed  that  a  special  anatomical  cause  must  lie 
at  the  bottom  of  the  peculiar  group  of  symptoms,  which  they  suspected  to  be  a 
primary  disease  of  the  lateral  columns — that  is,  of  the  pyramidal  tracts  particu- 
larly. This  suspicion  was  entirely  warranted,  since  the  picture  of  pure  spastic 
spinal  paralysis  could  be  explained  by  no  other  anatomical  theory.  A  degenera- 
tion in  the  lateral  columns  explains  the  motor  paresis,  explains  the  increase  of 
the  tendon  reflexes  by  the  loss  of  reflex  inhibitory  influences,  and  finally  it  also 
explains  any  direct  tonic  contraction  of  the  muscles  by  the  hypothesis  of  processes 
of  motor  irritation.  Actual  evidence  of  the  occui-rence  of  primary  systemic  de- 
generation in  the  lateral  columns  could  of  course  be  furnished  only  by  anatom- 
ical observation.  This  has  now  actually  taken  place,  so  that  at  present  there  can 
no  longer  be  any  doubt  of  the  occurrence  of  a  "  spastic  spinal  paralysis  "  in  the 
original  sense  of  Charcot  and  Erb.  If  we  observe  the  same  morbid  picture  not 
only  in  primary  degeneration  of  the  pyramidal  tract,  but  also  in  other  cases,  it  is 
due  to  the  fact  that,  under  certain  circiunstances,  other  diseases  may,  at  least  for 
a  time,  involve  the  lateral  columns  almost  exclusively,  and  especially  the  pyrami- 
dal tracts. 


PEIMAEY   DEGENERATIONS    OF    THE   MOTOR   TRACT     1009 


So  far  as  our  present  knowledge  extends,  the  affection  domes  on  in  two  some- 
what distinct  clinical  forms.  The  first  may  be  brought  into  the  closest  relation 
with  amyotrophic  lateral  sclerosis.  As  we  have  seen  above  (page  989),  we  often 
find  in  typical  amyotrophic  lateral  sclerosis  a  pure  spastic  paresis  in  the  legs 
without  any  trace  of  muscular  atrophy, 
while  in  the  arms  and  the  bulbar  region 
there  is  a  more  or  less  marked  muscu- 
lar atrophy  besides  the  spastic  symptoms. 
There  are  also  cases  of  disease — ^they  oc- 
cur usually  in  somewhat  advanced  life 
and  sporadically,  that  is,  not  generically 
as  a  family  disease — where  spastic  rigid- 
ity and  paresis  develop  not  only  in  the 
legs,  but  also  in  the  trunlc,  the  arms, 
and  the  face,  without  a  trace  of  muscu- 
lar atrophy.  In  the  course  of  a  few  years 
the  patient  finally  becomes  almost  com- 
pletely stiff  (Fig.  155),  without  being 
entirely  paralyzed.  The  stiffness  is  due 
solely  to  the  muscular  rigidity.  The 
arms  also  show  pronounced  hyper  tonicity 
on  passive  movement.  Impulsive  laugh- 
ing and  crying  also  occur,  just  as  in 
amyotrophic  lateral  sclerosis  (Fig.  156). 
If  we  have  the  rare  opportunity  to  make 
an  autopsy  on  such  a  case,  we  find  a 
marked  systemic  degeneration  in  both 
lateral  columns,  chiefly  in  the  region  of 
the  pyramidal  tract,  PyS,  but  usually  in- 
volving other  bundles  of  fibers  in  the  lat- 
eral columns  as  well.  The  degeneration  of 
the  pyramidal  tract,  Py8,  may  be  traced 
upward  through  the  pyramids,  the  pons, 
and  the  crus  to  the  internal  capsule.  The 
ganglion-cells  in  the  anterior  horns  of  the 
spinal  cord  are  entirely  normal  or  they 
show  only  insignificant  chang'es.  The  close 
relationship  between  this  form  of  "  pure 
lateral  sclerosis  "  and  amyotrophic  lateral 
sclerosis  is  shown  by  the  fact  that  the  one 
disease  may  develop  into  the  other.  After 
the  typical  affection  of  lateral  sclerosis  has 
continued  in  its  pure  form  for  some  years, 
atrophy  may  sometimes  finally  develop  in 
the  small  muscles  of  the  hand,  the  tongue, 
etc. — in  short,  there  is  clinical  evidence 
that  the  peripheral  motor  neurone  has  be- 
gun to  degenerate ;  but  the  atrophy,  as  a 
although  different  degrees  of  transition  forms  probably  occur. 

A  second  well-characterized  form  of  primary  degeneration  of  the  pyramidal 
tract  is  the  hereditary  or  family  spastic  spinal  paralysis  which  has  been  described 
by  us.  This  shows  itself  in  several  members  of  the  same  family,  especially  in 
brothers  and  sisters ;  in  this  form  there  very  gradually  develops,  in  the  course  of 
years  and  years,  a  constantly  increasing  rigidity  of  the  legs  with  increased  tendon 
64 


<<^£^ 


Fig.  155.— Spastic  spinal  paralysis.  Enormous 
muscular  rigidity  of  the  trunk,  arms,  and 
legs.  When  supported  from  behind,  the  pa- 
tient can  stand  as  stiff  as  a  post.  (Erlangen 
Bledical  Clinique.) 


rule,  remains   comparatively  slight, 


1010 


DISEASES    OE   THE   NERVOUS    SYSTEM 


reflexes  and  all  the  motor  disturbances  dependent  thereon.  The  gait  is  pro- 
nouncedly spastic,  the  feet  cling  to  the  floor,  the  legs  are  pressed  firmly  together 
from  the  contracture  of  the  adductors,  and  on  walking,  one  foot  can  pass  the  other 
only  with  difficulty.  The  patient  treads  only  on  the  anterior  part  of  the  foot ;  the 
whole  body  is  projected  stiffly  forward,  so  that  the  patient  has  to  hold  a  cane  in 
front  of  himself  to  keep  from  falling  forward  (Fig.  157).  Eor  a  long  time  the 
purely  spastic  symptoms  outweigh  the  paretic  (spastic  pseudo-paralysis),  and 
only  very  gradually  does  the  spastic  gait  become  spastic-paretic,  and  an  actual 
loss  of  muscular  strength  ensue.     The  general  condition,   the  sensibility,  the 

bladder  and  the  mus- 
cular nutrition  may  re- 
main unaffected  for  a 
long  time  or  until  the 
end.  The  disease  usu- 
ally begins  somewhere 
between  twenty  and 
thirty,  but  some  cases 
apparently  occur  in 
children  also.  There 
can  hardly  be  any  doubt 
that  the  disease  is  due- 
to  a  congenital  morbid 
predisposition  of  the- 
pyramidal  tract,  and 
that  thus  it  is  closely- 
connected,  setiological- 
ly,  with  the  other  forms 
of  hereditary  systemic- 
disease,  especially  with 
hereditary  muscular- 
atrophy;  but  the  ana- 
tomical examination  of" 
the  spinal  cord,  which 
has  been  possible  thus 
far  in  only  a  few  cases,, 
has  shown  disease  in  the 
lateral  cerebellar  tract 
(KIS)  and  the  columns 
of  Goll,  besides  degen- 
eration in  the  pyramidal  lateral  tract  (PyS) — that  is,  in  the  territory  of  the 
neurones  of  the  lumbar  spinal  ganglia.  Anatomically,  therefore,  hereditary 
spastic  spinal  paralysis  must  also  be  termed  a  combined  systemic  disease. 

Besides  the  two  forms  of  primary  degeneration  of  the  pyramidal  lateral  tracts- 
(PyS)  already  mentioned,  which  in  our  opinion  are  perfectly  well  established" 
clinically  and  anatomically,  there  are  in  reality  several  other  forms  of  disease 
whose  clinical  symptoms  are  in  the  main  those  of  spastic  spinal  paralysis,  while 
the  anatomical  changes  consist  of  a  primary,  more  or  less  strictly  systemic  dis- 
ease of  the  lateral  columns  alone,  or  of  the  lateral  and  posterior  columns.  In  the 
latter  case  ataxia,  bladder  disturb.mces,  slight  disturbances  of  sensation,  etc., 
may  at  times  be  added  to  the  spastic  symptoms ;  but  since  we  have  very  little 
definite  knowledge  of  these  rare  forms  of  disease,  we  can  not  at  present  give  any 
suitable  description  of  them.  Many  of  these  diseases  seem  to  be  exogenous  in 
origin  and  to  be  especially  connected  with  previous  syphilis.  Other  cases  are- 
related  setiologically  to  severe  general  constitutional  diseases,  especially  perni- 


FiG.  156. — Spastic  spinal  paralysis.  Impulsive  laughing.  The  same  pa- 
tient as  Fig.  155.  Symptoms  of  amyotrophic  lateral  sclerosis  came 
on  later.    (Erlangen  Medical  Clinique.) 


PKIMAKY   DEGENEEATIONS    OF    THE    MOTOR  TRACT    1011 


cious  anaemia  (page  723).  We  may  also  mention  that  a  pure  type  of  spastic 
spinal  paralysis  may  be  produced  by  chronic  poisoning  with  lathyrus  seeds 
(lathyrus  sativus  and  lathyrus  cicera,  the  so-called  vetches,  which  are  used  to 
make  bread  in  southern  countries).  Systemic  degenerations  of  the  spinal  cord 
also  occur  in  pellagra,  which  is  common  in  northern  Italy  from  the  continued  use 
of  diseased  or  fermented  maize.  This  sometimes  causes  especially  marked  spastic 
symptoms,  besides,  of  course,  many  other  spinal  and  mental  symptoms  (Tuczek). 
[Gowers  has  given  the  name  of  ataxic  paraplegia  to  a  class  of  cases  of  com- 
bined degeneration  of 
the  lateral  and  posterior 
columns,  which  are  by 
no  means  rare.  The 
disease  comes  on  grad- 
ually in  middle  life, 
usually  without  any 
definite  cause.  Men 
are  much  more  fre- 
quently affected  than 
women.  The  early  symp- 
toms resemble  those  of 
spastic  paraplegia,  with 
the  addition  of  atax- 
ic unsteadiness,  which 
may  be  at  first  the 
most  prominent  symp- 
tom. There  are  very 
rarely  any  lightning- 
pains,  but  there  is  at 
times  a  dull  pain  in  the 
legs  or  the  sacrum. 
There  is  rarely  any  im- 
pairment of  sensation. 
The  tendon  reflexes  are 
usually  much  exagger- 
ated. Sexual  power 
may  be  lost  early,  and 
the  bladder  and  rectum 
are  often  affected.  Re- 
flex immobility  of  the 
pupils  and  optic  atro- 
phy are  rare,  but  nys- 
tagmus is  occasionally*' 
noticed.  The  arms  are 
usually  involved  later. 
Mental  symptoms  are  rare.  The  disease  is  slowly  progressive,  but  it  rarely 
proves  fatal,  death  being  usually  due  to  some  intercurrent  disease.  The  extent 
of  the  degeneration  in  the  cord  varies,  but  it  is  never  so  well  marked  in  the  pos- 
terior columns  as  it  is  in  true  tabes.  Putnam  has  also  described  a  type  of  degen- 
eration occurring  also  in  adult  life,  but  much  more  frequent  in  women.  In  his 
cases  the  trouble  seemed  to  be  not  infrequently  associated  with  profound  angemia 
or  other  forms  of  malnutrition.  Paraisthesia  is  a  very  prominent  symptom  of 
the  earlier  stages  of  the  disease,  and  it  may  come  on  suddenly  or  rapidly 
increase.  Its  appearance  in  an  anaemic  person  of  middle  age  is  therefore 
suggestive  of  the  onset  of  this  form  of  disease.     Disturbances  of  micturition 


Fig.  157.— Family 'silastic  siiiiial  paralysis 
(Erlangeii  Medical  Cliniqne. ) 


1012  DISEASES    OF    THE    NERVOUS    SYSTEM 

are  also  very  common  in  the  early  stages.  Inco-ordination  and  muscular  weak- 
ness develop  later,  and  the  weakness  may  increase  to  complete  paraplegia.  The 
reflexes  are  usually  exaggerated,  but  they  may  be  absent.  The  disease  is  apt 
to  terminate  fatally  within  four  or  five  years.  The  pathological  changes  are 
of  a  degenerative  nature,  and  are  most  marked  in  the  posterior  and  lateral 
columns,  but  they  are  quite  diffuse,  so  that  this  type  of  disease  is  more  closely 
allied  to  diffuse  chronic  myelitis  than  to  a  systemic  degeneration.  In  some 
cases  systematic  gymnastic  exercises,  by  Erankel's  method,  prove  of  de- 
cided benefit.  The  treatment  otherwise  is  the  same  as  that  of  chronic  mye- 
litis.—K] 

Diagnosis. — Since  the  symptom-complex  of  spastic  spinal  paralysis  must  al- 
ways arise  if  the  pyramidal  tracts  are  affected  by  any  disease  in  any  part  of 
the  two  lateral  columns  of  the  spinal  cord  or  even  higher  up,  it  is  easily  seen 
that  it  may  often  be  very  difficult  or  even  quite  impossible  to  decide  in  a  given 
case  whether  we  have  to  do  with  a  primary  systemic  degeneration  or  with  some 
other  circumscribed  disease  of  the  pyramidal  tracts.  The  chief  weight  in 
diagnosis  should  always  be  laid  on  the  general  development  of  the  morbid  condi- 
tion, the  setiological  conditions  (several  in  a  family  affected),  and  the  strict 
limitation  of  the  symptomatic  picture  (absence  of  any  sensory  or  bladder  disturb- 
ances,  etc.). 

The  morbid  conditions  chiefly  to  be  considered  in  differential  diagnosis  are 
the  following:  1.  Multiple  sclerosis.  As  previously  stated  (page  956),  this  may 
for  some  time  resemble  very  closely  the  type  of  pure  spastic  spinal  paralysis. 
2.  Syphilitic  disease  of  the  upper  dorsal  cord,  the  so-called  syphilitic  spastic  spinal 
paralysis.  We  will  consider  this  important  disease  more  fully  in  a  subsequent 
chapter  on  syphilis  of  the  spinal  cord.  3.  Chronic  hydrocephalus  (vide  infra, 
the  section  on  diseases  of  the  brain).  4.  Subacute  and  chronic  myelitis  following 
other  acute  diseases  (typhoid  fever,  influenza,  etc.).  This  can,  as  a  rule,  be 
easily  distinguished  from  genuine  spastic  spinal  paralysis  by  the  mode  of  ori- 
gin, and  also  by  the  clinical  symptoms.  5.  Slight  compression  of  the  spinal 
cord,  from  vertebral  caries,  tumors,  traumatic  affections  of  the  vertebrae,  etc., 
may  for  some  time  give  rise  to  typical  symptoms  of  spastic  spinal  paralysis, 
but  with  careful  attention  and  longer  observation  there  will  only  rarely  be  any 
mistake. 

Prognosis  and  Treatment. — The  prognosis  of  genuine  spastic  spinal  paralysis 
is  naturally  as  unfavorable  as  that  of  any  other  systemic  disease.  The  treat- 
ment can  therefore  be  merely  symptomatic.  The  spastic  symptoms,  which  are 
often  very  troublesome,  are  most  readily  alleviated  by  the  use  of  long-continued 
warm  baths.  In  other  respects  the  treatment  follows  the  rules  that  obtain  in  all 
chronic  affections  of  the  spinal  cord. 


APPENDIX 

CONGENITAL    SPASTIC    PARAPLEGIA   IN    CHILDREN 

(Spastic  Cerebral  Paralysis.     Infantile  Spastic  Diplegia.     Little^s  Disease) 

In  this  place  we  would  also  speak  briefly  of  a  morbid  condition,  first  described 
by  J.  Heine  and  the  English  physician  Little,  which  is  not  very  rarely  observed 
in  children.  The  symptoms  in  these  cases  are  probably  usually  congenital,  or  at 
least  they  arise  during  birth  {vide  infra'),  but  from  reasons  that  are  easy  to 
understand  they  are  not  noticed  until  later.  When  the  children  come  under 
medical  observation  they  are  usually  from  three  to  six  years  old,  or  even  older. 


CONGENITAL    SPASTIC    PAKAPLEGIA    IN    CHILDKEN     1013 


The  most  striking-  symptom  is  that  the  child  can  not  walk  at  all,  or  he  walks  only 
with  difficulty  and  with  assistance.  If  we  examine  the  legs  carefully  we  usu- 
ally find  that  they  are  quite  stiff.  The  thighs  are  usually  somewhat  flexed  and 
firmly  adducted,  and  also  rotated  inward.  The  knees  are  also  slightly  bent,  while 
the  feet  are  often  in  a  position  of  equinus  or  equino-varus  (Fig.  158).  From  the 
contracture  of  the  thighs  in  adduction  it  readily  happens  that  the  legs  cross  each 
other  when  the  child  lies  down,  or  especially  when  he  tries  to  walk.  Passive  move- 
ments of  the  legs  can  be  performed  only  by  overcoming-  more  or  less  muscular 
resistance.  The  tendon  reflexes,  especially  the 
patellar  reflex,  are  much  increased,  and  there  is 
often  a  persistent  ankle  clonus.  The  sensibility 
and  micturition  are  normal.  The  arms,  as  a  rule, 
are  readily  moved,  but  slighter  spastic  symptoms 
may  also  occur  in  them.  Many  of  these  children 
are  mentally  perfectly  normal,  learn  to  talk  and 
write  well,  etc. ;  but  in  other  cases  cerebral  disturb- 
ances are  also  plainly  manifested,  feeble  intelli- 
gence, defective  speech,  epileptic  attacks,  strabis- 
mus, etc.  As  the  child's  physical  development  pro- 
ceeds the  symptoms  often  improve,  but  in  general 
the  condition  is  stationary  and  not  progressive. 

Our  knowledge  is  still  very  defective  as  to  the 
causes  of  these  congenital  spastic  paraplegias  and 
the  anatomical  changes  which  underlie  them.  First 
of  all  we  must  make  a  fundamental  division  of 
the  cases  into  two  groups.  In  the  one  we  have  to 
do  with  children  who  are  born  with  great  difficulty 
and  with  artificial  aid  (forceps,  etc.).  In  this 
group  we  can  probably  assume  injuries  of  the  brain 
in  parturition  from  haemorrhage,  etc.,  which  result 
in  permanent  disturbances  of  function.  In  the 
other  group,  where  the  history  affords  no  such  evi- 
dence (except  that  often  the  children  are  born 
prematurely),  we  usually  have  to  assume  some  con- 
genital defect  (so-called  porencephaly  in  the  cere- 
brum, congenital  aplasia  of  the  motor  centers  or  of  the  whole  pyramidal  tract). 
This  congenital  form  of  spastic  paraplegia  may  also  occur  generically,  but  it  is 
to  be  distinguished  from  the  hereditary  spastic  paralysis  above  described,  which 
develops  slowly  and  only  in  later  life  and  is  progressive. 

In  the  way  of  tfeatment,  we  may  expect  most  from  regular  gymnastic  exer- 
cises. Surgical  interference  (tenotomy,  transplantation  of  tendons)  and  ortho- 
paedic appliances  may  sometimes  considerably  improve  the  child's  ability  to 
walk. 


Fig.  158.— Position  of  the  legs  in 
congenital  spastic  cerebral  pa- 
ralysis. (Sketch  from  personal 
observation.) 


1014 


DISEASES    OE    THE    ^teeVOUS    SYSTEM 


CHAPTEE   X 
ACUTE    AND    CHRONIC    POLIOMYELITIS 

1.  Spinal  Paralysis  of  Children 

(Acute  Poliomj/elitis  in  Children) 

etiology  and  Pathological  Anatomy. — In  children  there  occurs  quite  fre- 
quently a  definite  and  well-characterized  form  of  paralysis,  for  the  first  accurate 
knowledge  of  which  we  must  thank  Jacob  von  Heine  in  1840.  Although  Heine 
subsequently,  in  1860,  expressed  the  opinion  that  a  disease  of  the  spinal  cord 
formed  the  basis  of  the  paralysis,  the  first  actual  confirmation  of  this  opinion  was 
furnished  by  Prevost  and  Vulpian,  Charcot  and  JoSroy,  and  others,  so  that  at 
present  we  are  justified  in  exchanging  the  old  term  "  essential  paralysis  of  chil- 
dren "  for  the  name  of  "  spinal  paralysis  of  children." 

As  the  name  indicates,  the  affection  occurs  chiefly,  if  not  exclusively  {vide 
infra),  in  children,  and  is  most  frequent  in  the  earlier  years,  somewhere  between 
one  and  four.    An  exciting  cause,  such  as  taking  cold,  has  hardly  ever  been  made 

out.  The  children  are  almost 
always  perfectly  healthy*  pre- 
viously, and  come  of  healthy 
families  without  any  neuro- 
pathic predisposition.  The 
whole  course  of  the  disease 
makes  the  hypothesis  very 
probable  that  we  have  to  do 
with  an  acute  infectious  dis- 
ease— ^with  an  infectious  pro- 
cess, which  often  causes  first 
a  mild  or  severe  general  in- 
fection of  the  body,  and  then 
is  localized  chiefly  in  a  cir- 
cumscribed portion  of  the 
spinal  cord.  It  also,  perhaps, 
bears  some  relation  to  this 
hypothesis  that  most  of  the 
cases  occur  in  warm  weather. 
The  fact  should  also  be  mentioned  that  small  and  even  extensive  epidemics  of 
spinal  paralysis  of  children  have  been  repeatedly  observed.  We  have  ourselves 
seen  three  children  fall  ill  in  a  little  village  in  a  few  days  with  acute  poliomyelitis. 
With  reference  to  its  anatomy,  the  disease  may  be  defined  as  an  acute  inflam- 
mation, which  affects  chiefly  a  definite  portion  of  the  anterior  gray  matter  of  the 
spinal  cord,  usually  attacking  only  the  anterior  gray  horn  of  one  side;  yet  it  does 
not  always  limit  itself  strictly  to  this,  but  it  may  involve  the  white  matter  in  the 
vicinity  somewhat,  although,  of  coiirse,  to  a  lesser  extent  than  the  gray  matter. 
Although  fresh  cases  have  so  far  been  examined  in  very  scanty  numbers,  still  we 
can  sometimes  make  out  clearly  the  signs  of  inflammation  in  the  older  centers 
of  disease.  The  lesion  which  is  most  frequently  found  in  old  cases  consists 
of  a  considerable  atrophy  of  one  anterior  horn,  which  is  cicatrized  and  shriv- 


FiG.  159.— Section  through  the  cervical  enlargement  in  anterior 
poliomyelitis ;  the  left  anterior  column  is  very  much  con- 
tracted and  is  without  ganglion-cells.    (From  Charcot  and 

JOFFROY.) 


*  The  paralyses  arising  after  acute  diseases — such  as  measles,  scarlet  fever,  small-pox,  etc. — are 
perhaps  partly  of  spinal  origiu,  but  they  can  not  be  identified  with  tlie  idiopathic  spinal  paralysis  of 
children. 


ACUTE   AND   CHEONIC  POLIOMYELITIS  1015 

eled  and  changed  to  a  dense  sclerosed  tissue,  often  pierced  by  dilated  and  thick- 
ened vessels,  and  containing  scarcely  a  single  normal  ganglion-cell.  If  the 
j)aralysis  affects  one  arm,  the  corresponding  anterior  horn  in  the  cervical  enlarge- 
ment is  atrophied  (see  Fig.  159)  ;  if  the  leg  be  paralyzed,  the  process  is  seated 
in  the  lumbar  enlargement.  In  bilateral  paralysis  we  must  think  of  an  affec- 
tion of  both  anterior  horns  at  the  corresponding  level  of  the  cord. 

This  inflammation  of  the  anterior  horn,  the  poliomyelitis,  is  to  be  regarded  as 
the  primary  focus  of  disease,  dependent  upon  the  local  action  of  the  excitants  of 
inflammation.  Erom  this  point,  as  in  every  severe  lesion  of  the  motor  ganglion- 
cells  there  situated,  there  develops  a  secondary  degeneration,  which,  extending 
to  the  periphery,  affects  the  corresponding  anterior  roots,  and  later  their  appro- 
priate motor  nerves  and  the  muscles  supplied  by  them.  In  the  paralyzed  muscles 
and  nerves  we  accordingly  find  a  high  degree  of  degeneration  and  atrophy,  such 
as  we  have  learned  to  recognize  in  severe  peripheral  paralyses. 

Although  at  present  the  spinal  origin  of  the  atrophic  paralysis  of  children  is 
regarded  as  sufficiently  certain,  we  must  mention  that  it  is  not  improbable,  at 
least  in  many  cases,  that  the  peripheral  nerves  are  also  primarily  involved;  the 
poliomyelitis  may  be  combined  with  a  multiple  neuritis,  produced  by  the  same 
causes  and  thus  co-ordinate.  Under  this  heading  should  be  classed  those  cases 
where  there  is  at  first  great  pain  in  the  extremities,  especially  on  pressure  and 
passive  movement.  The  rapid  disappearance  of  many  of  the  initial  paralytic 
symptoms  may  perhaps  be  referred  in  part  to  the  presence  of  co-existing  neuritie 
processes.  We  shall  also  see  later  that  there  are  perhaps  etiological  relations  be- 
tween spinal  and  cerebral  infantile  paralysis. 

Clinical  History. — The  disease  almost  always  begins  suddenly.  A  child  who 
was  previously  perfectly  well  and  lively  is  all  at  once  attacked  with  severe  fever, 
often  reaching  105°  or  106°  (40°-41°  C),  and  quite  severe  general  symptoms  are 
also  associated  with  the  fever  even  from  the  beginning.  The  child  complains  of 
headache,  and  sometimes  of  pain  in  the  loins  and  in  the  limbs  (vide  supra},  and  is 
decidedly  stupid  and  somnolent.  Very  often  still  more  marked  cerebral  symptoms 
develop :  complete  loss  of  consciousness,  single  twitchings  in  the  face  or  the  ex- 
tremities, or  general  convulsions.  The  eclamptic  attacks,  turning  of  the  eyes,  and 
clonic  contractions  in  the  face  and  extremities,  sometimes  appear  even  at  the 
beginning  of  the  disease.  On  the  part  of  other  organs  we  see  most  frequently 
gastro-intestinal  symptoms,  especially  vomiting,  more  rarely  diarrhoea.  All  the 
initial  symptoms,  whose  intensity  varies  very  much  in  the  different  cases,  some- 
times last  only  a  very  short  time — a  day  or  two — although  they  often  continue 
for  a  week  or  two.  Indeed,  we  even  know  cases  in  which,  as  the  mothers  have 
assured  us,  the  children  are  said  to  have  "  lain  in  spasms,"  almost  uninterrupt- 
edly, even  for  four  or  five  weeks  before  the  beginning  of  the  paralysis — that  is, 
before  it  became  noticeable.  On  the  other  hand,  however,  it  may  happen  that  the 
initial  symptoms,  especially  the  severe  cerebral  symptoms,  are  entirely  absent  or 
greatly  modified. 

After  the  initial  period  of  the  disease  just  described  has  passed  away,  the 
parents  usually  notice  that  the  child  is  attacked  by  a  more  or  less  extensive 
paralysis.  If  its  development  can  be  followed  closely,  we  always  find  that  it 
spreads  rapidly,  often  in  single  spurts  which  quickly  follow  one  another,  so  that 
it  usually  reaches  a  considerable  extent  in  a  short  time.  Either  both  legs,  or  the 
legs  and  one  arm,  or  all  the  extremities,  and  even  the  muscles  of  the  trunk,  are 
affected.  In  some  cases  one  oculo-motor  or  facial  nerve  has  been  observed  to 
be  affected  at  the  beginning,  a  symptom  which  we  would  most  readily  refer  to 
a  neuritie  process.  The  paralysis  scarcely  ever  remains  permanently  as  exten- 
sively distributed  as  at  first ;  it  diminishes  rapidly,  and  soon  is  limited  to 
a   definite   muscular   region,   which  remains   permanently   paralyzed.      In   some 


1016 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


cases  the  paralysis  may  entirely  disappear,  but  as  a  rule  a  complete  paralysis 
is  left  in  one  extremity,  or  at  least  in  a  portion  of  it;  most  frequently 
in  one  leg,  especially  in  the  peroneal  muscles ;  somewhat  more  rarely  in  the  arm, 
chiefly  in  the  deltoid ;  sometimes  in  both  legs ;  or,  very  rarely  in  spinal  paralysis, 
in  one  arm  and  leg  on  the  same  side  or  on  opposite  sides.  Meantime  the  child's 
general  health  has  been  completely  restored.  He  is  well  and  vigorous,  has  an  ex- 
cellent appetite,  never  shows  any  permanent  cerebral  disturbance — only  the  pain- 
less, flaccid  paralysis,  the  inability  to  use  the  affected  extremity,  is  left  behind. 
In  the  following  weeks  and  months  a  further,  slower  improvement  in  the  power 

of  motion  often  becomes  noticeable,  but, 
as  a  rule,  a  permanent  and  more  or  less 
complete  paralysis  of  certain  muscles  re- 
mains. 

In  regard  to  the  more  intimate  pecul- 
iarities of  this  remaining  paralysis,  it 
may  invariably  be  characterized  as  a  flac- 
cid atrophic  paralysis.  A  marked  atrophy 
of  the  paralyzed  muscles  shows  itself  a 
few  weeks  after  the  beginning  of  the  pa- 
ralysis. This  atrophy  gradually  spreads, 
and  it  may  finally  attain  the  highest  de- 
gree. The  atrophy  is  often,  but  not  al- 
ways, partly  concealed  by  a  more  abun- 
dant development  of  fat  tissue.  The 
changes  in  the  electrical  excitability  of 
the  paralyzed  nerves  and  muscles  come 
on  still  more  rapidly  than  the  visible  atro- 
phy. Since  we  have  to  do  with  a  com- 
plete degeneration  of  the  nerves,  as  fol- 
lows from  the  anatomical  basis  of  the  dis- 
ease, a  pronounced  electrical  reaction  of 
degeneration  must  necessarily  develop  in 
the  affected  parts.  Duchenne  found  that 
usually  the  faradic  excitability  of  the 
nerves  and  muscles  is  completely  lost  after 
a  week  or  two.  On  galvanic  examina- 
tion, we  can  at  first  detect  an  increase  of 
excitability  in  the  muscles  with  a  pre- 
dominance of  slow  anodic  closure  contrac- 
tions (AnSZ),  while  later,  after  two  or 
three  months,  the  galvanic  excitability 
also  sinks  very  considerably ;  but  the  mus- 
cular contractions  preserve  their  qualita- 
tive peculiarities  characteristic  of  reac- 
Very  often  the  whole  affected  extremity 
remains  backward  in  its  growth,  so  that  later  the  bones  may  show  a  shortening 
of  several  centimetres  (Fig.  160).  The  parallelism  between  the  muscular  atrophy 
and  the  stunted  growth  is  not,  however,  present  in  all  cases,  as  Volkmann,  in 
particular,  has  stated. 

Passive  motion  of  the  paralyzed  extremity  is  at  first,  on  account  of  the 
absence  or  diminution  of  the  muscular  tonus,  perfectly  free,  and  so  remains 
except  for  the  contractures  that  finally  set  in  (vide  infra).  Many  joints  are 
so  flaccid  that  we  can  actually  make  flapping  movements  with  the  paralyzed  limbs 
and  give  them  the  most  extraordinary  positions.    The  tendon  reflexes  are  invaria- 


FiG.  160.— Old  spinal  infantile  paralysis,  acquired 
at  the  age  of  six.    (Personal  observation.) 


tion  of  degeneration  (see  page  847). 


ACUTE  AND   CHRONIC  POLIOMYELITIS  1017 

bly  completely  absent  in  the  paralyzed  extremities,  and  so  almost  always  are  the 
cutaneous  reflexes — a  condition  which  is  to  be  referred  to  the  interruption  of  the 
reflex  arc  in  the  anterior  horns,  which  may  sometimes  be  of  diagnostic  signifi- 
cance. The  skin  often  shows  certain  trophic  disturbances  (atrophy,  anomalies  in 
the  growth  of  the  hair  and  in  the  secretion  of  sweat)  ;  it  almost  always  feels 
cool  and  has  a  cyanotic  appearance.  Its  sensibility,  however,  is  completely  re- 
tained in  all  cases.  Micturition  is  sometimes  a  little  disturbed  at  the  beginning 
of  the  disease,  but  in  most  cases  this  disturbance  completely  disappears  later. 

After  the  paralysis  has  existed  for  a  time,  certain  secondary  contractures 
almost  always  develop  in  the  paralyzed  parts,  some  of  which  are  of  a  very 
characteristic  type.  In  the  legs  especially  the  "paralytic  club-foot"  (talipes 
varo-equinus)  is  a  condition  long  known.  It  is  due  to  the  fact  that,  from  the 
paralysis  of  the  peronei  muscles  and  of  the  tibialis  anticus,  the  point  of  the  foot 
constantly  droops,  and  that  a  contracture  is  g-radually  developed  in  the  antago- 
nistic unparalyzed  muscles  of  the  calf,  whose  points  of  insertion  are  permanently 
approximated.  In  paralysis  of  the  muscles  of  the  calf  there  arises,  on  the  other 
hand,  a  moderate  deg'ree  of  calcaneus  from  the  contracture  of  the  antagonists. 
In  the  arms  and  in  the  vertebral  column,  in  paralyses  of  the  spinal  muscles,  the 
most  manifold  and  sometimes  very  considerable  contractures  and  deformities 
may  also  arise,  which  are  in  the  main  always  to  be  referred  to  the  contracture  of 
unparalyzed  antagonists  and  to  external  mechanical  conditions,  such  as  weight 
and  pressure. 

In  conclusion,  if  we  simply  compare  the  type  of  disease  sketched  with  its  ana- 
tomical cause,  the  general  agreement  of  the  two  may  at  once  be  seen.  The  affec- 
tion of  the  anterior  gray  cornua  must  have  as  a  result  a  paralysis  with  a  subse- 
quent atrophy  and  reaction  of  degeneration,  in  which  the  reflexes  must  be  lost  by 
the  destruction  of  the  reflex  arc,  but  the  sensibility  must  remain  perfectly  normal 
from  the  persistence  of  the  sensory  conduction  (the  posterior  columns  and  the 
posterior  gray  cornua),  and  the  vesical  functions  must  also  remain  normal.  The 
subsequent  paralysis  is  the  result  of  the  permanent  destruction  which  the  morbid 
process,  in  itself  completely  ended,  has  caused  in  the  spinal  cord. 

We  must  also  mention  the  peculiar  fact  which  has  been  observed  in  some  cases, 
that  progressive  muscular  atrophy  may  come  on  in  later  life  in  persons  who  long 
before  have  had  spinal  infantile  paralysis.  The  cells  of  the  anterior  horns  once 
injured  by  the  acute  disease  seem  never  to  have  become  equal  to  the  functional 
demands  made  upon  them,  and  therefore  they  succumb  to  a  premature  atrophy. 

Diagnosis. — The  diagnosis  of  the  spinal  paralysis  of  children  is  almost  always 
easy  to  make  correctly,  if  we  hold  strictly  to  the  deflnition  and  peculiarities  of 
the  disease,  and  do  not  reckon  as  spinal  paralysis  every  paralysis  appearing  in  a 
child.  We  should  consider  chiefly  the  acute  beginning,  the  subsequent  flaccid 
paralysis  with  atrophy  and  reaction  of  degeneration,  with  the  loss  of  the  reflexes, 
but  with  retained  sensibility.  If  we  observe  these  features,  we  are  sufliciently 
protected  against  confusion  with  cerebral  diseases  and  other  diseases  such  as 
spondylitis,  hereditary  muscular  atrophy,  or  spastic  cerebral  and  spinal  paralysis. 
We  have  already  mentioned  above  that  transitional  forms  between  acute  polio- 
myelitis and  acute  polyneuritis  probably  occur;  but  we  would  constantly  empha- 
size one  principal  distinction  between  polyneuritis  and  genuine,  circumscribed 
acute  poliomyelitis — polyneuritis  has  a  general,  hfematogenous,  toxic  or  toxic-in- 
fectious origin,  while  acute  poliomyelitis  seems  to  be  a  true  local  inflammiition, 
dependent  upon  the  local  presence  of  the  (organized?)  excitants  of  inflammation. 
In  the  clinical  differential  diagnosis  we  should  consider  chiefly  the  existence  of 
any  initial  pains  and  any  initial  sensitiveness  of  the  peripheral  nerves  and  mus- 
cles. The  further  course  of  the  disease  may  also  be  decisive,  since  the  neuritic 
paralyses  afford  a  much  better  prognosis  than  the  paralyses  of  poliomyelitis. 


1018  DISEASES    OF   THE    NEEVOUS    SYSTEM 

Prognosis. — It  is  not  impossible,  but  it  is  not  yet  proved,  that  many  of  the 
cases  where  children  die  speedily  with  convulsions  are  to  be  regarded  as  the  initial 
stage  of  acute  poliomyelitis.  If,  however,  the  first  stage  of  the  disease  be  past, 
the  prognosis  as  regards  life  is  entirely  favorable,  since  the  rest  of  the  child's 
physical  development  is  no  further  affected  in  any  way.  The  prognosis  as  regards 
the  complete  restoration  of  the  disturbance  of  function  is,  however,  much  more 
unfavorable.  Although  we  should  not  forget  that  the  paralysis  is  at  first  much 
more  extensive  than  it  is  later,  nevertheless  this  lessening  of  the  paralytic  symp- 
toms occurs  only  in  the  first  weeks  or  months.  A  limb  which  has  not  recovered 
in  six  to  nine  months  usually  remains  paralyzed  for  life.  Nevertheless,  this 
should  not  restrain  us  from  persevering  in  treatment,  at  least  in  the  first  years, 
since  sometimes  a  very  noticeable  improvement  in  the  functions  of  the  paral- 
yzed parts  is  thus  procured. 

Treatment. — If  we  have  an  opportunity,  even  during  the  initial  stage  of  the 
disease  (when,  of  course,  the  diagnosis  can  not  usually  be  made  with  certainty), 
to  attack  the  disease  by  our  treatment,  we  may  prescribe  cold  compresses  or  an 
ice-bag  to  the  head,  and  eventually,  when  there  is  high  fever  or  great  stupor,  a 
tepid  bath  with  cool  affusions.  We  are  but  rarely  led  to  try  blood-letting  by 
leeches  behind  the  ears  or  on  the  temples,  when  there  are  signs  of  marked  cere- 
bral hypersemia.  Internally  we  usually  prescribe  a  mild  "  intestinal  derivative," 
such  as  half  a  grain  or  a  grain  (gramme  0.03-0.05)  of  powdered  calomel  every  two 
or  three  hours,  infusion  of  senna,  etc. 

After  paralysis  appears,  we  may  expect  the  most  success  from  electrical  treat- 
ment, kept  up  consecutively  for  months,  and,  with  interruptions,  for  years.  We 
put  a  large,  broad  electrode  on  the  vertebral  column  at  the  spot  which  corresponds 
to  the  place  of  the  lesion  in  the  spinal  cord — on  the  cervical  vertebrae  in  paralysis 
of  the  arm,  and  the  lower  dorsal  in  paralysis  of  the  leg — ^while  the  other  electrode 
serves  for  peripheral  application  to  the  paralyzed  nerves  and  muscles.  In  this 
way  we  apply  a  moderately  strong  constant  current,  reversing  it  occasionally,  for 
two  or  three  minutes,  partly  stabile  and  partly  labile,  passing  the  cathode,  or  even- 
tually the  anode,  slowly  over  the  paralyzed  muscles  and  nerves.  We  may  also 
employ  occasional  interruptions  and  reversals  of  the  current.  Duchenne  has  also 
found  persistent  treatment  by  the  faradic  current  of  advantage.  The  sittings 
should  take  place  three  or  four  times  a  week,  and  later  even  of tener,  if  possible. 

Besides  electrical  treatment,  methodical  gymnastic  exercises  of  the  muscles, 
that  can  still  be  moved  to  some  degree  actively,  may  also  be  of  distinct  advantage. 
Regular  and  persistent  massage  of  the  muscles  is  also  to  be  recommended  in  the 
later  stages.  In  practice  we  can  not  avoid  prescribing  certain  embrocations,  such 
as  spirit  of  camphor,  spirit  of  mustard,  or  spirit  of  formic  acid.  Passive  mo- 
tion is  very  important  to  guard  against  contractures,  and  to  improve  the  already 
existing  deformities. 

The  use  of  baths,  of  brine  or  ferruginous  waters,  is  to  be  recommended, 
although,  of  course,  they  must  not  be  overvalued.  They  may  be  given  at  home. 
If  circumstances  permit  sefiding  the  child  to  a  bath  during  the  summer  months, 
we  should  chiefly  consider  the  brine  baths  at  Reichenhall,  Kreuznach,  Kosen,  and 
Colberg;  the  acid  salines  at  Rehme,  ISTaiiheim,  and  Soden;  and  eventually,  with 
weak  and  ansemic  children,  the  use  of  the  iron  baths  at  Dribvirg,  Pyrmont,  or 
Schwalbach.  Good  results  are  sometimes  obtained  at  the  indifferent  thermal 
baths  at  Teplitz,  Wildbad,  Ragatz,  or  Gastein,  but  these  must  be  used  only  with 
caution.  We  also  obtain  good  results,  especially  with  older  children,  at  the  cold- 
water  cures. 

Very  little  is  to  be  expected  from  the  use  of  internal  remedies.  Iodide  of  po- 
tassium and  strychnine  are  recommended,  the  latter  in  the  form  of  subcutaneous 
injections,  -^o  to  ,W  grain  (gramme  0.001-0.003)  daily. 


ACUTE   A^'D   CHROl^IC  POLIOMYELITIS  1019 

When  the  acute  process  is  wholly  past  and  we  can  no  longer  count  on  any  fur- 
ther regenerative  process,  the  mechanical  surgical  treatment  of  the  patient  may 
often  be  of  material  service.  In  the  first  place  the  power  of  movement  may  be 
improved  by  orthopaedic  appliances,  and  troublesome  contractures  may  also  be 
relieved  by  tenotomy.  The  therapeutic  attempts  to  join  the  tendons  of  muscles 
which  can  still  contract  to  the  tendons  of  the  paralyzed  muscles,  in  order  to  ren- 
der it  once  more  possible  to  obtain  the  effect  of  movement  of  these  muscles 
(Nicolodoni,  Vulpius,  and  others),  are  of  especial  interest.  The  symptomatic 
benefit  thus  obtained  is  very  considerable.  Details  as  to  all  the  orthopaedic  and 
surgical  methods  of  treatment  are  to  be  found  in  the  special  treatises.  When  we 
can  no  longer  hope  for  any  further  improvement  in  the  paralysis  worth  mention- 
ing, the  treatment  is  limited  to  improving  the  patient's  general  condition  and 
strengthening  him  as  much  as  possible  by  proper  food  and  good  air. 

2.  Acute  Poliomyelitis  of  Adults 

{Acute  Atrophic  Spinal  Paralysis  of  Adults) 

Although  it  had  been  believed  for  a  long  time  that  the  form  of  acute  atrophic 
spinal  paralysis,  just  described,  occurred  only  in  children,  later  observations  by 
Moritz  Meyer,  Duchenne,  Erb,  F.  Schultze,  F.  Miiller,  and  others,  have  established 
the  fact  that  precisely  analogous  cases  of  disease  may  also  develop,  although 
far  less  frequently,  in  adults,  especially  in  young  persons  under  thirty.  There  is 
no  longer  any  doubt  of  this  fact,  especially  if  we  consider  an  authentic  ana- 
tomical lesion  found  by  F.  Schultze.  We  have,  however,  once  before  had  to  say 
that  for  a  long  time  we  have  regarded  the  diagnosis  of  acute,  and,  as  we  shall  soon 
see,  of  chronic  poliomyelitis  also,  as  too  lightly  made,  and  that  certainly  very 
many  of  the  cases  diagnosticated  and  published  as  poliomyelitis  are  to  be  classed 
as  primary  neuritis  (see  page  885).  Since  we  know  that  primary  degenerative 
processes  may  develop  acutely  and  subacutely  in  the  motor  nerves,  and  may  also 
lead  to  an  atrophic  paralysis,  a  greater  part  of  the  teaching  on  poliomyelitis  needs 
new  and  careful  revision  in  order  to  exclude  what  does  not  belong  to  it. 

The  type  of  acute  poliomyelitis  of  adults,  so  far  as  it  has  been  established  by 
definite  observations,  which  at  present  are  not  numerous,  is  not  materially  differ- 
ent from  the  type  of  the  spinal  paralysis  of  children. 

We  often  can  not  make  out  any  ^etiological  conditions ;  sometimes  exposure 
to  cold,  over-exertion,  etc.,  seem  to  favor  the  development  of  the  disease.  Cases 
are  seen  more  frequently  in  men  than  in  women. 

The  disease  likewise  begins  with  quite  severe  initial  symptoms,  fever,  head- 
ache, somnolence,  delirium,  and  vomiting,  which  may  last  from  a  few  days  to  a 
week  or  two.  The  violent  spontaneous  pains  which  are  very  often  reported  in  the 
extremities  usually  belong  probably  to  those  cases  in  which  a  primary  neuritis, 
but  not  a  poliomyelitis,  is  the  chief  anatomical  lesion;  but  severe  pain  in  the 
back  may  also  occur  in  genuine  poliomyelitis  in  the  first  acute  stage  of  the  dis- 
ease. After  the  end  of  this  first  stage  the  paralysis  appears.  This  develops  with 
varying  distribution,  usually  in  single  spurts,  but  always  rather  rapidly.  The 
paralyzed  muscles  are  perfectly  flaccid,  the  cutaneous  and  tendon  reflexes  are 
wholly  absent,  and  very  soon  a  pronounced  atrophy  and  reaction  of  degeneration 
appear,  while  the  sensibility  and  the  vesical  and  sexual  functions  remain  normal. 

The  distribution  of  the  paralysis  shows  certain  peculiarities,  which  must  be 
briefly  described  here,  since  they  can  be  studied  much  better  in  adults  than  in 
children.  The  paralysis  may  be  very  extensive,  it  may  aft'eet  all  four  extremities, 
or  it  may  occur  in  the  form  of  paraplegia,  or  even  of  monoplegia.  In  the  ex- 
tremities we  very  often  find  certain  groups  of  muscles  paralyzed,  to  which  E. 
Remak  first  called  attention.     Since  the  muscles  that  are  paralyzed  at  the  same 


1020  DISEASES    OF   THE    I^EEVOUS    SYSTEM 

time  are  not  supplied  by  the  same  peripheral  nerves,  but  usually  are  connected 
in  their  functions,  we  may  suppose  that  the  corresponding  ganglion-cells  in  the 
anterior  comua  of  the  spinal  cord  also  lie  together,  without  regard  to  the  dis- 
tribution of  their  peripheral  processes  in  the  different  motor  nerves.  Thus,  for 
example,  it  is  worthy  of  note  that,  in  paralysis  of  the  crural  region,  the  sartorius 
often  remains  entirely  free;  that  in  the  leg  the  tibialis  anticus,  on  the  one  hand, 
and  the  peronei  and  the  extensor  dig'itorum  on  the  other,  may  be  separately  dis- 
eased; that  in  the  forearm  the  supinator  longus,  supplied  by  the  radial  nerve, 
remains  free,  while  all  the  other  muscles  on  the  extensor  side  of  the  forearm  are 
paralyzed  ("  forearm  type  "  of  E.  Remak)  ;  and  that,  on  the  other  hand,  the  supi- 
nator may  be  paralyzed  alone  or  together  with  the  biceps,  brachialis  anticus,  and 
deltoid  ("upper-arm  type"  of  E.  Eemak).  From  the  group  of  muscles  para- 
lyzed we  can  determine  with  some  degree  of  accuracy  the  location  of  the  disease 
in  the  cord  according  to  the  statements  previously  made  in  regard  to  the  position 
of  the  spinal  motor  centers  (page  921). 

In  regard  to  diagnosis,  especial  attention  must  be  paid  to  the  distinction  be- 
tween poliomyelitis  and  neuritis.  The  greatest  stress  is  to  be  laid  on  the  initial 
pains  and  any  other  slight  disturbances  of  sensibility.  In  other  respects,  the 
course  of  the  two  diseases  is  so  similar  that  we  can  indeed  imagine  that  they  are 
closely  allied  in  their  setiological  relations,  and  exhibit  merely  different  forms  of 
localization  of  the  same  (probably  infectious)  morbid  agency.  It  always  seems 
to  us,  however,  as  we  have  said  above,  that  the  principal  distinction  is  that  in 
genuine  circumscribed  poliomyelitis  there  is  an  actual  local  focus  of  inflamma- 
tion, but  in  polyneuritis  there  is  a  toxic  (hematogenous)  degeneration  of  the 
peripheral  motor  neurones.  In  the  latter  case,  of  course,  the  motor  ganglion-cell 
itself  may  also  be  destroyed  if  the  disease  be  severe,  but  this  would  always  be  a 
different  process  from  the  local  poliomyelitic  inflammation. 

The  prognosis  is  not  wholly  unfavorable,  as  sometimes  a  complete  recovery 
has  been  observed,  although  only  after  months.  Of  course,  it  is  very  possible  that 
such  cases  are  multiple  neuritis.  On  the  other  hand,  however,  the  same  perma- 
nent paralyses  as  in  spinal  paralysis  of  children  may  be  left,  with  atrophy  and 
contractures. 

The  treatment  follows  precisely  the  same  rules  that  we  have  mentioned  in  the 
spinal  paralysis  of  children.  The  internal  or  subcutaneous  use  of  ergotine  may 
be  added  on  the  recommendation  of  some  physicians.  F.  Miiller  recommends  a 
solution  of  two  and  a  half  drachms  of  ergotine  (grammes  10)  with  a  third  of  a 
grain  of  sulphate  of  atropine  (gramme  0.02)  in  five  drachms  of  water  (grammes 
20),  of  which  he  injects  seven  to  fifteen  minims  twice  a  day. 

3.  Subacute  and  Chronic  Poliomyelitis 

{Subacute  and  Chronic  Atrophic  Spinal  Paralysis.     Paralysie  generale  spinale  anterieure 

suhaigue  [Duchenne]) 

While  the  anatomical  basis  of  acute  poliomyelitis  in  adults  still  leaves  much 
to  be  desired,  our  anatomical  knowledge  of  the  occurrence  of  a  subacute  and 
chronic  poliomyelitis,  in  the  sense  of  the  authors  who  have  described  it.  is  still 
more  defective.  Confusions  with  multiple  neuritis  are  also  undoubtedly  very 
common  here,  and  the  diagnosis  is  not  incontestable  in  all  the  cases  published 
under  the  name  of  "  subacute  poliomyelitis  " ;  but  there  can  be  no  doubt,  from 
some  recent  and  perfectly  accurate  observations  (Oppenheim,  ISTonne,  and 
others),  that  extensive  subacute  and  chronic  diseases  may  occur  in  the  anterior 
horns  of  the  cord  and  lead  to  the  development  of  extensive  paralysis.  The 
setiological  and  general  pathological  conception  of  these  cases  is  of  course  still 
wholly  unsettled. 


SO-CALLED   ACUTE   ASCENDING   SPINAL   PARALYSIS     1021 

In  the  cases  classed  under  this  heading  a  paralysis,  first  of  both  legs  and 
somewhat  later  usually  of  both  arms,  develops  in  a  comparatively  short  time — 
in  the  course  of  some  days,  or  weeks  at  most.  It  usually  has  no  special  cause 
or  any  severe  initial  symiatoms.  The  patient  complains  at  first  of  weakness 
in  the  legs ;  he  can  no  longer  walk,  and  he  is  confined  to  the  bed.  A  short  time 
later  the  same  disturbances  appear  in  the  arms,  and  lead  to  a  more  or  less  com- 
plete paralysis.  More  rarely  the  opposite  condition  obtains,  that  the  arms  are 
affected  first  and  the  legs  later,  but  the  sensibility  always  remains  wholly  unaffect- 
ed, except  at  most  for  slight  paraesthesia,  and  there  is  also  no  pain,  either  spon- 
taneous or  occurring  on  i^ressure.  Soon  after  the  paralysis  an  equally  exten- 
sive atrophy  develops,  and  a  distinct  loss  of  electrical  excitability,  running 
parallel  to  it ;  which  passes  over  into  a  partial  or,  in  all  severe  cases,  a  com- 
plete reaction  of  degeneration.  The  cutaneous  and  tendon  reflexes  are  very 
much  diminished  and  often  entirely  lost.  The  bladder  and  rectum,  however, 
remain  intact,  and  bed-sores  never  develop  if  the  patient  has  proper  care.  We 
sometimes  notice  a  striking  diminution  of  the  sweat  secretion.  In  rare  cases 
the  muscles  of  the  neck,  the  lips,  the  tongue,  and  the  pharynx  are  attacked  by 
the  disease. 

After  the  paralysis  has  reached  its  greatest  extent  there  is  usually  a  pause. 
The  condition  remains  stationary  for  months  sometimes,  and  then  a  gradual 
improvement  begins,  which  perhaps  may  go  on  to  complete  recovery ;  but  often,  of 
course,  the  recovery  remains  incomplete,  so  that  the  patient  has  a  more  or  less 
marked  disturbance  of  function  for  life.  The  "  middle  form  of  chronic  polio- 
myelitis "  described  by  Erb,  in  which  there  is  only  a  partial  reaction  of  degenera- 
tion in  the  paralyzed  muscles,  almost  always  gives  a  good  prognosis.  The  disease 
takes  an  unfavorable  course,  if  the  respiration  be  impaired  through  involvement 
of  the  respiratory  muscles,  or,  if  the  patient  can  not  swallow,  through  involvement 
of  the  muscles  of  deglutition,  or  if  inhalation  pneumonia  set  in.  The  autopsy 
then  shows  extensive  degenerative  inflammatory  changes  in  the  anterior  gray 
columns  of  the  cord  with  a  great  destruction  of  ganglion-cells,  while  we  can 
usually  discover  only  very  slight  changes  (secondary  degeneration)  in  the 
peripheral  nerves. 

As  a  consequence  of  what  has  been  said,  we  shall  be  compelled  to  make  a  diag- 
nosis of  chronic  poliomyelitis  when  extensive  paralysis  comes  on  with  subsequent 
atrophy  and  electrical  reaction  of  degeneration  and  without  any  neuritic  symp- 
toms (pain!),  and  without  disturbances  of  sensation  or  of  the  bladder.  It  is  dis- 
tinguished from  "  spinal  muscular  atrophy  "  proper,  by  the  fact  that  in  this  there 
is  a  slow  atrophy,  attacking  fiber  after  fiber,  so  to  speak,  and  that  the  atrophy  and 
muscular  weakness  go  absolutely  parallel,  while  in  chronic  poliomyelitis  the  pa- 
ralysis precedes  the  atrophy,  and  whole  muscles  or  muscular  regions  are  affected 
from  the  start. 

The  treatment  is  not  absolutely  hopeless,  as  is  shown  by  the  above  description. 
A  persistent  electi'ical  treatment  is  always  most  advisable. 


CHAPTER   XI 

THE     SO-CALLED    ACUTE     ASCENDING     SPINAL    PARALYSIS 

( Parol i/sis  A><ei!nili;iis  Aoifo.     Lmolri/'s   /'uraJi/s/'s) 

In  the  year  1859  Landry  described  a  disease  under  the  name  of  "  paralysie 
ascendante  aigue,"  which  is  chiefly  characterized  clinically  by  the  fact  that  first 


1022  DISEASES    OE    THE    jSTERVOUS    SYSTEM 

the  lower  and  soon  after  the  upper  extremities,  and  finally  a  number  of  the 
muscular  regions  supplied  by  the  medulla,  are  attacked  by  a  rapidly  advancing 
paralysis,  while  the  sensibility  and  the  functions  of  the  bladder  and  rectum 
remain  normal.  In  many  cases  the  disease  terminates  fatally.  Examination  of 
the  nervous  system  has  so  far,  however,  shown  no  lesion  which  can  be  regarded 
with  certainty  as  the  anatomical  cause  of  the  disease.  Considering  the  continued 
and  quite  numerous  observations  of  the  disease,  it  seems  questionable,  at  any 
rate,  whether  we  can  establish  a  uniform  anatomical  basis  for  it  (vide  infra)  ;  but 
the  clinical  picture  of  Landry's  paralysis  is  so  striking  that  a  comprehensive  de- 
scription of  it  seems  demanded. 

General  Symptomatology. — Acute  ascending  paralysis  attacks  chiefly  persons 
previously  strong  and  healthy,  in  youth  or  middle  life,  somewhere  between  twenty 
and  thirty-five  years  of  age.  Some  cases  also  have  been  seen  in  children  and  older 
people.    The  disease  seems  to  be  m.ore  frequent  in  men  than  in  women. 

The  affection  almost  always  begins  with  certain  prodromata.  These  consist  of 
general  malaise,  moderate  febrile  symptoms,  headache,  loss  of  appetite,  and  quite 
frequently  of  dragging  and  tearing  pains  in  the  back  and  the  extremities.  After 
these  symptoms  have  lasted  some  days,  or  more  rarely  some  weeks,  during  which 
they  are  either  comparatively  slight,  or  so  severe  that  many  patients  are  already 
confined  to  the  bed,  there  usually  comes  on  quite  suddenly,  or  sometimes  more 
gradually,  a  paresis,  first  of  one  leg,  but  very  soon  of  both  legs,  which  rapidly  in- 
creases, and  usually  in  a  few  days  leads  to  an  almost  complete  motor  paraplegia. 

The  paralysis  is  flaccid  in  almost  all  cases.  The  legs  may  be  moved  passively 
without  any  muscular  resistance,  and  the  muscles  show  neither  active  nor  reflex 
tension.  Their  electrical  excitability  remains  perfectly  normal  in  many  cases, 
but  there  is  sometimes  a  rapid  loss  of  faradic  rauscular  excitability.  It  is  not  yet 
proved  whether  complete  reaction  of  degeneration  occurs.  The  reflexes,  both 
cutaneous  and  tendon  reflexes,  seem  to  be  diminished  or  wholly  lost  in  the  major- 
ity of  cases,  but  some  exceptions  to  this  rule  have  been  known. 

Sensibility  is  sometimes  perfectly  intact,  but  slight  alterations  do  occur,  and 
quite  rarely  there  may  be  even  marked  anesthesia.  At  times  a  noticeable  delay 
of  sensation  is  observed.  We  find  no  changes  in  the  nerves  of  special  sense. 
There  is  occasionally  a  slight  oedema  in  the  legs,  which  is  perhaps  to  be  regarded 
as  a  vaso-motor  disturbance.  The  marked  sweating,  from  which  many  patients 
suffer,  is  also  worthy  of  mention.  The  bladder  and  rectum  in  most  cases  are  not 
at  all  affected,  or  they  present  merely  slight  and  temporary  disturbances. 

A  short  time  after  the  legs  are  attacked  the  aiTQS  also  begin  to  be  paretic. 
A  marked  motor  weakness  appears  first  in  one,  then  in  the  other  arm,  and  this 
may  also  increase  to  almost  complete  paralysis.  The  sensibility,  the  reflexes,  and 
the  electrical  excitability  show  conditions  like  those  in  the  lower  extremities. 
The  muscles  of  the  trunk  are  also  affected  at  the  same  time  as,  or  still  earlier 
than,  the  arms.  The  patient  can  no  longer  sit  up  in  bed,  turn  on  his  side,  or  make 
similar  movements.  In  some  cases  a  paralysis  of  the  muscles  of  the  neck  has  also 
been  observed. 

The  third  and  last  stage  of  the  disease  is  characterized  by  the  appearance  of 
respiratory  disturbances  and  bulbar  symptoms.  Manifest  signs  of  a  beginning 
respiratory  paralysis  appear;  the  respiration  is  labored  and  difiicult,  the  move- 
ments of  the  diaphragm  are  impaired,  and  the  paroxysms  of  coughing  grow 
weaker.  Disturbances  in  swallowing,  difficulty  in  articulation,  and  paresis  of 
the  soft  palate  and  the  lips  may  set  in.  In  a  few  cases  a  facial  paralysis  and 
disturbances  of  the  ocular  muscles  have  been  observed.  The  condition  grows 
worse  acutely,  and,  as  we  have  said,  in  many  cases  death  ensues. 

Besides  the  symptoms  thus  far  mentioned,  referable  to  the  nervous  system,  we 
find  certain  other  symptoms  in  almost  every  case,  which  are  less  striking,  but  yet 


SO-CALLED   ACUTE   ASCENDING   SPINAL   PAEALYSIS     1023 

of  greater  significance  in  judging  of  the  disease.  The  first  of  these  is  fever.  The 
temperature  is  usually  elevated  from  the  beginning;  it  may  temporarily  show 
a  considerable  increase,  up  to  104°  (40°  C),  and  later  it  varies  between  100°  and 
102°  (38°-39°  C),  but  between  times  it  may  even  sink  to  normal.  Of  the  inter- 
nal organs  the  spleen  shows  the  most  frequent  changes.  It  is  usually  swollen 
moderately,  but  appreciably.     There  is  also  sometimes  a  slight  albuminuria. 

In  the  cases  with  a  fatal  termination  the  whole  duration  of  the  disease  is  some- 
times only  a  few  days,  and  as  a  rule  a  week  or  two,  or  rarely  more.  Fortunately, 
however,  all  cases  do  not  terminate  fatally.  The  disease  may  come  to  a  stand- 
still at  any  time,  even  if  the  most  threatening  symptoms  be  present.  Then  the 
paralysis  shows  no  further  advance,  the  disturbances  present  disappear,  and  recov- 
ery ensues  after  a  course  of  several  weeks.  It  is,  of  course,  usually  quite  a  long 
time  before  the  patient  again  feels  himself  in  possession  of  his  full  powers. 

Pathological  Anatomy  and  Pathogenesis. — If  we  consider  the  whole  picture 
of  acute  ascending  paralysis,  the  idea  is  necessarily  forced  upon  us  that  we  have 
to  do  here  with  an  acute  infection  or  auto-intoxication  of  the  body,  with  a  pre- 
dominating localization  in  the  motor  nervous  system.  The  beginning  of  the  dis- 
ease with  general  malaise  corresponds  perfectly  to  the  prodromal  stage  of  many 
other  acute  infectious  diseases.  The  fever,  the  acute  splenic  tumor,  and  the  occa- 
sional albuminuria  also  can  scarcely  be  explained  in  any  other  way,  according  to 
our  present  views,  except  by  the  above  hypothesis.  There  are,  of  course,  no 
definite  and  positive  data  as  yet  in  support  of  this  hypothesis.  A  notable  case, 
published  by  Baumgarten,  in  which  many  bacilli,  like  those  of  splenic  fever, 
were  found  in  the  spinal  cord,  is  at  present  wholly  unique.  Further  investiga- 
tions as  to  the  anatomical  changes  in  "  acute  ascending  spinal  paralysis  "  are 
still  very  desirable.  In  the  earlier  observations  there  is  usually  the  statement  of 
an  "  absolutely  negative  anatomical  examination  " ;  but  these  statements  usually 
refer  only  to  the  spinal  cord.  The  peripheral  nerves  were  formerly  not  examined 
at  all;  and  yet,  as  we  have  long  proclaimed  and  as  is  now  quite  generally  ac- 
cepted, it  is  extremely  probable  from  the  clinical  symptoms  (pain,  loss  of  electri- 
cal excitability,  condition  of  the  reflexes)  that  most  cases  of  so-called  Landry's 
paralysis  are  multiple  neuritis  {q.v.),  and  are  nothing  more  than  the  most  acute 
form  thereof.  Some  recent  anatomical  investigations  have  already  confinned 
this  hypothesis. 

It  would,  however,  be  distinctly  false  at  present  to  identify  acute  ascending 
paralysis  completely  with  multiple  neuritis,  for  in  some  observations  (R.  Schulz 
and  F.  Schultze,  von  den  Velden)  extensive  acute  myelitic  changes  have  also 
been  found  in  the  motor  portions  of  the  spinal  cord  (lateral  columns,  anterior 
gray  columns).  We  must  therefore  wait  for  many  more  observations  and  not 
decide  prematurely  upon  the  nosological  position  of  the  disease.  [Recent  in- 
vestigations show  that  Landry's  paralysis  is  an  affection  of  the  whole  peripheral 
motor  neurone,  but  that  the  ganglion-cells  in  the  anterior  horns  show,  as  a  rule, 
greater  changes  than  the  peripheral  nerve-fibers. — K.] 

Diagnosis  and  Prognosis. — In  every  paralysis  of  the  lower  extremities  begin- 
ning acutely  and  accompanied  by  general  symptoms  and  fever  we  must  consider 
the  possibility  of  an  acute  ascending  paralysis,  but  only  the  further  coiarse  of  the 
disease  can  decide  the  question.  Inasmuch  as  merely  a  well-characterized  clinical 
group  of  symptoms  is  meant  by  the  above  term,  the  diagnosis  is  always  easy  to 
make,  with  attention  to  the  peculiarities  given  above.  It  is  more  difficult,  how- 
ever, to  decide  accurately  whether  the  case  corresponds  rnther  to  the  type  of  an 
acute  multiple  neuritis  or  to  the  type  of  an  acute  ascending  spinal  paralysis.  We 
can  judge  as  to  this  point  only  by  carefvil  attention  to  the  single  symptoms,  espe- 
cially the  condition  of  the  sensibility  (pains,  anaesthesia),  of  the  reflexes,  and  of 
the  electrical  excitability. 


1024  DISEASES    OF   THE    NERVOUS    SYSTEM 

The  prognosis  must  at  first  be  made  with  great  reserve,  and  we  must  especially 
bear  in  mind  the  possibility  of  a  rapidly  fatal  teraiination.  If  the  first  acute 
stage  pass  ofF  fortunately  and  there  be  a  decided  cessation  in  the  extension  of  the 
symptoms  of  paralysis,  the  prognosis  is  quite  favorable,  for  we  may  then  expect 
that  the  patient  will  be  completely  restored. 

Treatment. — We  can  not  be  certain  whether  an  energetic  "  derivative  treat- 
ment "  is  of  advantage  in  the  beginning  of  the  disease.  Dry  cups  along  the  verte- 
bral column  are  recommended,  and  even  the  use  of  the  hot  iron  to  the  back.  We 
would  hardly  advise  the  latter.  It  may  be  advisable,  however,  to  prescribe 
inunctions  with  mercurial  ointment,  thirty  to  forty-five  grains  a  day,  as  in  anti- 
syphilitic  treatment.  Of  internal  medicines,  we  should  try  at  the  beginning  sal- 
icylic acid  or  salicylate  of  sodium  in  large  doses  (30  grains,  grammes  2,  of 
salicylate  of  sodium  three  times  a  day),  and  also  antipyrine.  We  may  also  try 
extract  of  ergot  (ergotine)  and  perhaps  iodide  of  potassium.  It  also  seems  to  be 
a  good  plan  to  begin  galvanic  treatment  early,  applied  to  the  spine  and  periph- 
erally. If  alarming  attacks  of  respiratory  insufficiency  occur,  electrical  ex- 
citation of  the  phrenic  nerve  and  of  the  respiratory  muscles  sometimes  affords 
relief  to  the  patient. 

If  the  symptoms  be  arrested,  electrical  treatment  and  the  use  of  baths  may 
do  most  to  hasten  convalescence. 


CHAPTER    XII 
NEW    GROWTHS    OF    THE    SPINAL    CORD    AND    OF    ITS    MEMBRANES 

Pathological  Anatomy. — Tumors  of  the  spinal  cord  in  the  strict  sense  of  the 
word  are  rare.  The  commonest  primary  new  growth  is  the  glioma,  which  arises 
from  the  neuroglia,  and  forms  a  cellular  and  vascular  tumor.  This  is  situated 
most  frequently  in  the  cervical  or  upper  dorsal  cord.  It  often  develops  at  the 
beginning  in  the  posterior  half  of  the  cord,  but  later  it  may  attain  a  consid- 
erable length  and  a  transverse  diameter  of  several  centimetres,  so  that  the 
spinal  cord  in  the  part  affected  may  have  a  considerable  tumor-like  thickening, 
or  it  may  even  be  changed  throughout  almost  its  whole  length  into  a  thick,  shape- 
less mass.  Inside  the  glioma  we  sometimes  find  secondary  haemorrhages  and 
(myxomatous)  softenings.  Central  gliosis  is  distinct  from  real  glioma.  The 
former  never  leads  to  any  special  enlargement  of  the  cord  (tumor  formation),  but 
to  a  gliomatous  degeneration,  and  especially  to  an  abnormal  cavity  formation  in 
the  cord,  particularly  in  a  longitudinal  direction.  We  will  speak  of  this  impor- 
tant and  by  no  means  very  rare  disease  more  fully  in  a  subsequent  chapter. 

Of  other  rare  new  growths  in  the  spinal  cord  we  may  mention  solitary  tuber- 
cles, syphilomata,  and  sarcomata.  Solitary  tubercle  usually  begins  in  the  central 
gray  matter.    Cysticerci  have  also  been  repeatedly  observed  in  the  spinal  cord. 

In  the  spinal  meninges  have  been  found  sarcomata,  fibromata,  lipomata,  myxo- 
mata,  and  syphilomata.  Sarcoma  of  the  dura  mater  is  the  commonest  and  prac- 
tically the  most  important  of  these  growths.  It  almost  always  seems  to  start 
from  the  endothelium  on  the  inner  surface  of  the  dura,  and  it  is  then  sometimes 
called  endothelioma.  Sarcoma  of  the  dura  has  a  great  tendency  to  spread  as  a  flat 
growth,  so  that  it  may  finally  surround  a  considerable  portion  of  the  cord  with 
its  mass  of  growth.  Sarcoma  is  often  multiple;  thus  it  may  co-exist  on  the  spinal 
dura  mater  and  at  the  base  of  the  brain,  etc.  As  a  rule,  it  does  not  invade  the 
pia  mater  or  the  substance  of  the  cord  itself.    Lipoma  develops  on  the  outer  sur- 


NEW    GEOWTHS    OF    THE    SPINAL    CORD  1025 

face  of  the  dura,  starting  from  the  fatty  tissue  between  the  vertebral  canal  and 
the  dural  sac.  A  carcinoma  arising'  from  the  vertebrae  may  also  reach  the  spinal 
meninges  by  direct  invasion. 

We  know  practically  nothing  of  the  aetiology  of  most  new  growths  in  the  spinal 
cord.  In  all  probability  there  is  an  abnormal  congenital  predisposition  of  the 
tissues,  which  furnishes  the  germ  for  the  subsequent  development  of  the  new 
growth.  It  is  worthy  of  note  that  the  Onset  of  the  first  symptoms  is  very  often 
preceded  by  an  injury  (fall  on  the  back,  etc.),  which  thus  seems  sometimes  to  give 
the  first  impetus  to  the  formation  of  a  tumor. 

Symptoms  and  Course. — New  growths  in  the  spinal  meninges,  especially  sar- 
coma of  the  dura  mater,  are  apt  to  cause  at  the  beginning  pronounced  root  symp- 
toms, and  usually  at  first  symptoms  of  irritation  of  the  posterior  roots.  The  first 
symptoms  of  the  disease  are  therefore  radiating  pains,  either  persistent  and  burn- 
ing or  paroxysmal  and  neuralgic,  and  parsesthesise  in  certain  root  territories. 
There  may  also  be  local  pain,  a  feeling  of  stiffness  and  pressure  in  the  back,  etc. 
There  is  rarely  any  characteristic  tenderness  over  the  spine.  Anaesthesia  and 
paralysis  may  also  arise  as  pure  root-symptoms,  but  only  when  the  disease  is 
extensive,  since,  as  was  mentioned  above  (page  921),  the  complete  division  of  one 
sensory  or  motor  root  does  not  cause  complete  anaesthesia  or  paralysis  in  any 
region.  Extensive  paraplegic  symptoms  therefore  point  usually  to  an  implication 
of  the  cord.  The  cord  itself  also  suffers,  as  we  have  described  more  fully  in  the 
account  of  pressure  paralysis  from  tuberculosis  of  the  vertebrae  (page  935).  Only 
exceptionally  does  the  growth  itself  invade  the  cord.  The  symptoms  of  spinal 
compression  are  exactly  the  same  as  in  the  other  transverse  diseases  of  the  cord. 
The  differential  diagnosis  between  meningeal  tumors  and  compression  of  the  cord 
due  to  vertebral  caries  is  therefore  often  very  difficult,  if  we  can  detect  no  changes 
in  the  spine  itself  (Pott's  boss).  We  must  then  pay  chief  attention  to  the  general 
symptoms  of  tuberculosis  (heredity,  habitus,  fever,  other  tubercular  affections). 
If  a  meningeal  sarcoma  occurs  as  a  metastasis  or  as  one  manifestation  of  multiple 
sarcomatosis,  the  discovery  of  a  sarcoma  in  some  other  place  (such  as  the  skin) 
may  put  us  on  the  right  track  in  our  diagnosis. 

In  glioma  of  the  cord  itself  the  initial  symptoms  of  sensory  irritation  may  be 
almost  wholly  absent,  or  at  least  they  may  be  only  slight.  A  complicated  type  of 
spinal  disease  gradually  develops,  in  which  all  the  spinal  symptoms  may  occur  in 
the  most  varied  combinations.  The  disease  sometimes  exhibits  from  the  begin- 
ning the  ordinary  type  of  a  transverse  spinal  paralysis.  In  such  cases  it  is  hardly 
possible  to  distinguish  between  a  tumor  and  chronic  myelitis.  In  other  eases, 
however,  certain  peculiarities  in  the  type  lead  us  to  suspect  the  possibility  of  a 
tumor.  Among  them  especially  is  the  early  asymmetry  of  the  symptoms  on  the 
two  sides.  Since  a  tumor  may  at  first  be  confined  to  one  half  of  the  spinal  cord 
(which  scarcely  ever  happens  in  myelitis),  the  signs  of  a  unilateral  lesion  of  the 
spinal  cord  (vide  infra,  Chapter  XVII)  are  often  observed  in  tumors  in  a  more  or 
less  pronounced  fashion.  Only  later  in  the  course  of  the  disease  does  the  clinical 
type  of  unilateral  lesion  gradually  change  to  the  ordinary  transverse  paralysis.  A 
certain  alternation  in  the  symptoms,  improvements,  and  new  and  quite  sudden 
changes  for  the  worse,  are  also  noticed  at  times  with  tumors,  a  condition  which 
Is  probably  to  be  referred. to  changes  in  the  fullness  of  the  vessels,  or  to  haemor- 
rhages in  the  substance  of  the  tumor.  The  manner  in  which  the  disease  pro- 
gresses is  also  to  a  certain  degree  characteristic.  If  we  find  on  repeated  exami- 
nations evident  indications  that  the  spinal  affection  is  slowly  extending  upward, 
especially  if  the  cutaneous  anaesthesia  is  moving  upward  and  the  paralysis  is 
invading  higher  muscular  territories,  this  condition  is  decidedly  in  favor  of  the 
diagnosis  of  tumor,  since  it  is  far  less  frequently  observed  in  other  fqfms  of  dis- 
ease. We  may  also  consider  in  diagnosis  the  fact  that  glioma  often  develops  in 
65 


1026  DISEASES    OF   THE    NEEVOUS    SYSTEM 

the  cervical  cord,  or  at  least  gradually  invades  the  cervical  cord;  consequently 
sensory  disturbances  and  paralysis  occur  in  the  upper  extremities  in  addition  to 
the  paraplegia  of  the  legs.  This  is  of  rare  occurrence  in  chronic  myelitis,  which 
is  usually  situated  in  the  dorsal  cord.  The  diagnosis  of  a  tumor  of  the  spinal 
cord,  however,  can  at  best  be  merely  probable. 

The  accurate  determination  of  the  seat  of  the  tumor,  the  "  segmental  diagno- 
sis," is  of  great  practical  significance,  if  there  is  any  question  of  operative  treat- 
ment. It  is  evident  that  only  new  growths  of  the  spinal  meninges  can  be  the 
subject  of  surgical  interference.  Such  new  growths  have  in  a  number  of  cases  of 
late  been  operated  upon  successfully,  but  of  course  the  number  of  cases  in  which 
a  correct  diagnosis  can  be  made  and  an  operation  can  be  successfully  performed  is 
limited.  We  need  not  repeat  here  the  details  of  a  segmental  diagnosis;  they 
follow  the  general  rules  which  hold  for  all  lesions  of  the  spinal  cord  (page  920)  ; 
but  we  must  once  again  remind  the  reader  that  total  antesthesia  of  a  given 
cutaneous  territory  means  not  only  an  involvement  of  the  corresponding  posterior 
root  as  given  in  the  diagram,  but  also  an  affection  of  the  neighboring  roots,  espe- 
cially the  two  roots  above.  After  determining  the  upper  boundary  of  the  anaes- 
thesia we  should  therefore  always  suspect  that  the  upper  boundary  of  the  lesion  in 
the  cord  is  one  or  two  segments  higher  than  would  correspond  to  the  diagram, 
because  the  individual  cutaneous  territories  are  always  in  relation  with  several 
spinal  roots.  The  same  rule  also  holds  when  the  segmental  diagnosis  is  based 
upon  the  motor  symptoms.  The  disregard  of  this  relation,  which  was  first  clearly 
established  by  Sherrington,  is  the  reason  why  formerly  the  location  was  usually 
put  too  low,  even  when  the  tumor  itself  had  been  correctly  diagnosticated.  In 
determining  the  upper  boundary  of  the  tumor,  furthermore,  we  should  consider 
not  only  the  ansesthesi-a,  but  also  the  symptoms  of  sensory  irritation.  These 
very  often  manifest  themselves  above  the  angesthetic  zone  and  then  point  with 
considerable  certainty  to  an  irritation  of  the  corresponding  posterior  roots  by 
the  upward  growth  of  the  tumor.  The  accurate  determination  of  the  position  of 
the  different  spinal  segments  and  roots  in  relation  to  the  bodies  and  spinous  pro- 
cesses of  the  vertebrae  is  also  of  great  practical  importance.  In  regard  to  this,  we 
will  refer  to  Eig.  125,  page  928. 

A  tumor  of  the  spinal  cord  may  last  for  many  years.  In  new  growths  of  the 
meninges  the  symptoms  of  sensory  irritation  alone  may  continue  for  several  years 
before  there  are  any  well-developed  transverse  symptoms.  Other  cases,  of  course, 
run  a  much  more  rapid  course.  The  prognosis  of  tumors  of  the  cord  is  wholly 
unfavorable  unless  there  is  a  possibility  of  operative  treatment;  but,  as  we  have 
said  above,  this  presents  itself  in  but  few  cases.  Otherwise  the  treatment 
is  merely  symptomatic.  If  there  is  a  suspicion  of  previous  syphilis  we  should 
necessarily  try  inunction  and  the  exhibition  of  iodide  of  potassium.  In  sarcoma 
arsenic  in  large  doses  is  perhaps  of  some  service. 


CHAPTER   Xin 
THE    SYPHILITIC    ArFECTIONS    OF    THE    SPINAL    CORD 

.31tiology  and  Pathology. — The  affections  of  the  spinal  cord  provoked  by 
syphilis  must  be  divided  into  two  principal  groups.  The  first  group  is  formed  by 
diseases  in  which  a  slow  degeneration  of  certain  systems  of  neurones  develops  in 
a  somewhat  obscure  fashion  under  the  influence  of  previous  syphilitic  infection 
(probably  from  the  action  of  some  toxine).    These  diseases  are  called  most  prop- 


SYPHILITIC   AFFECTIONS    OF   THE    SPINAL   COED        1027 

erly  "  metasyphilitic  "  (so-called  metasyphilis).  Chief  among  them,  as  we  have 
already  seen,  is  tabes  dorsalis  (the  metasyphilitic  degeneration  of  the  posterior 
root  neurones),  and  also,  probably,  certain  rare  cases  of  degeneration  of  the 
lateral  columns,  and  of  combined  systemic  disease  in  the  lateral  and  pos- 
terior columns  (PyS,  KIS,  and  the  columns  of  Goll).  The  second  group  of  syphi- 
litic diseases  is  to  be  classed  as  genuine  tertiary  syphilis  in  distinction  from 
metasyphilis.  These  affections  are  characterized  by  the  development  of  a  specific 
gummatous  new  growth  in  the  cord,  especially  in  the  membranes  (meningitis 
gummosa)  and  in  the  blood-vessels  (endarteritis  syphilitica).  This  is  usually 
quite  extensive  and  not  infrequently  associated  with  corresponding  syphilitic  dis- 
ease in  the  brain.  Since  metasyphilis  of  the  cord  has  already  been  discussed 
in  another  part  of  this  work,  there  remains  to  be  considered  here  only  the  specific 
syphilitic  (gummatous)  affections  of  the  cord. 

Indications  of  syphilis  of  the  cord  may  appear  in  six  months  to  a  year  after 
the  infection;  but  they  develop  more  frequently  in  from  two  to  five  years  after 
the  infection,  or  even  later.  In  only  a  few  cases  does  a  circumscribed  gumma 
form,  which  then  causes  the  symptoms  of  an  intramedullary  tumor.  Diffuse  gum- 
matous meningitis  is  far  more  common ;  this  almost  always  arises  from  the  spinal 
pia  mater,  and  only  exceptionally  from  the  dura  mater  (page  917) .  In  such  cases 
the  spinal  cord  seems  surrounded,  in  an  irregular  fashion,  but  to  a  considerable 
extent,  by  a  newly- formed,  vascular  granulation  tissue  several  millimetres  thick. 
The  meningeal  blood-vessels  are  also  almost  always  much  diseased,  their  walls 
are  thickened  by  endarteritic  new  formations,  and  their  lumen  obliterated  or 
filled  with  thrombi.  The  posterior  border  of  the  cord  is  usually  most  affected. 
The  disease  usually  has  a  considerable  longitudinal  extent.  The  region  of 
the  dorsal  cord  is  often  most  affected,  but  in  other  cases  it  may  be  the 
cervical  or  lumbar  cord,  or  sometimes  the  region  of  the  conus  medullaris  and 
the  Cauda  equina.  The  spinal  roots  especially  are  often  surrounded  by  a  thick 
sheath  of  newly-formed  gummatous  tissue.  Rootlets  of  newly-formed  tissue 
may  extend  from  the  pia  mater  into  the  substance  of  the  cord,  or  the  syphilitic 
new  growth  may  extend  to  the  vessels  of  the  cord  itself;  in  such  cases  secondary 
tissue-changes  (destruction  of  nerve-tissue,  proliferation  of  neuroglia)  develop 
as  a  result  of  the  defective  blood-supply  of  the  tissue.  In  many  cases  certain 
secondary  sequelae  also  develop  in  the  tissues  of  the  cord,  similar  to  those  we  have 
become  acquainted  with  in  compression  of  the  cord  from  tubercular  new  forma- 
tions on  the  dura  mater  (vide  page  936).  It  is  also  worthy  of  mention  that  in 
a  few  cases  genuine  gummatous  disease  may  apparently  be  associated  with  meta- 
syphilitic degeneration. 

Symptoms  and  Course. — It  is  evident  that  syphilis  of  the  spinal  cord  can  not 
afford  any  single  definite  type  of  disease  on  account  of  the  multiple  localization 
of  the  anatomical  changes.  We  may  say  rather  that  syphilis  of  the  spinal  cord 
is  characterized  by  the  irregularity  and  the  often  unusual  combination  of  its 
symptoms,  and  its  changeable  and  varying  course.  From  the  different  combina- 
tions of  symptoms  that  occur  we  may  best  distinguish,  relatively  speaking,  the 
following  two  forms  of  the  affection: 

1.  Chronic  Gummatous  Spinal  Meningitis  and  Meningo-myelitis. — The  dis- 
ease at  first  shows  definite  root  symptoms,  especially  symptoms  of  irritation  of 
the  posterior  roots:  parsesthesia,  hyperesthesia,  shooting  pains,  neuralgia.  Asso- 
ciated with  these  we  sometimes  find  well-defined  local  pain  in  the  back  or  in  the 
sacral  region,  pain  on  pressure  and  on  movement  of  the  vertebral  column.  Motor 
symptoms  appear  somewhat  later  as  a  rule,  sometimes  motor-root  symptoms 
(atrophic  paralyses  in  definite  muscular  territories,  for  example,  in  the  muscles 
of  the  forearm  and  hand  on  one  side  or  in  the  sacral  distribution,  etc.)  ;  or  more 
frequently  motor  symptoms  from  implication  of  the  cord  itself;  spastic  paretic 


1028  DISEASES    OF    THE    NERVOUS    SYSTEM 

symptoms  in  one  or  both  legs,  sometimes,  in  disease  of  the  cervical  cord,  in  both 
legs  and  one  arm.  Associated  therewith  are  various,  but  usually  slight,  disturb- 
ances of  sensibility,  vesical  disturbances,  etc.  If  the  region  of  the  posterior  col- 
umns and  posterior  roots  be  chiefly  affected,  affections  resembling  tabes  may 
develop  (syphilitic  pseudo-tabes  of  Oppenheim).  Not  very  rarely  unilateral  dis- 
ease may  also  present  the  more  or  less  clearly-developed  picture  of  Brown- 
Sequard's  unilateral  lesion.  It  is  of  course  impossible  to  describe  exhaustively 
all  the  combinations  of  symptoms  that  may  be  observed. 

The  whole  course  of  the  disease  is  usually  chronic  and,  as  has  been  said,  very 
variable.  In  mild  cases  we  may  sometimes  see  almost  complete  recovery  under 
appropriate  treatment,  but  this  is  unfortunately  a  rare  event,  since  the  secondary 
tissue  necroses,  the  results  of  compression,  obliteration  of  vessels,  etc.,  are  in- 
capable of  complete  restoration.  We  see  improvement  quite  frequently,  espe- 
cially with  timely  treatment,  which  finally  passes  into  a  stationary  condition. 
We  must  be  prepared  for  relapses,  fresh  exacerbations,  and  the  onset  of  new  symp- 
toms, which  may  also  be  cerebral.  The  disease  may  last  for  many — even  twenty — 
years.  The  affection  becomes  directly  fatal  through  the  occurrence  of  dangerous 
complications  (pyelo-cystitis)  or  severe  attendant  symptoms  (apoplexy),  etc. 

2.  Syphilitic  Myelitis  and  Syphilitic  Spastic  Spinal  Paralysis. — In  many 
cases  syphilis  of  the  spinal  cord  exhibits  from  the  outset  the  symptoms  of  a 
myelitic  affection.  This  form  probably  always  arises  from  the  vessels  of  the  cord. 
The  syphilitic  endarteritis  of  the  smaller  vessels  leads  to  a  rapid  or  slow  necro- 
sis of  tissue  and  the  symptoms  of  spinal  disease  which  necessarily  result  there- 
from. The  disease  often  develops  as  rapidly  as  an  acute  myelitis.  A  more  or  less 
complete  paraplegia  comes  on  within  a  few  days.  Only  on  careful  inquiry  do  we 
sometimes  learn  that  it  has  been  preceded  for  some  time  by  mild  precursory  symp- 
toms (weakness,  parsesthesias,  etc.).  In  other  cases  the  paraplegia  develops  more 
slowly,  but  yet  within  a  few  weeks  or  months.  Since  the  anatomical  lesion  is 
very  often  in  the  dorsal  cord,  the  paraplegia  far  most  frequently  shows  the  signs 
of  spastic  paralysis.  Erb  has  therefore  grouped  certain  cases  under  the  name 
of  syphilitic  spastic  spinal  paralysis.  This  form  of  spinal  syphilis,  which  in 
our  experience  is  in  fact  very  characteristic,  is  found  especially  in  young 
persons  of  the  male  sex.  Weakness,  stiffness,  and  often  a  lively  tremor  (ankle 
clonus !)  occur  first  in  one  leg  and  soon  after  in  the  other.  The  gait  constantly 
grows  more  laborious,  slower,  and  decidedly  spastic-paretic.  The  sensory  dis- 
turbances are  at  first  very  slight ;  and  there  is  no  pain.  Later,  on  careful 
examination  slight  changes  in  sensibility  are,  of  course,  often  to  be  found.  Dis- 
turbances of  the  bladder  are  also  rarely  very  prominent,  but  they  are  often  plainly 
existent  in  a  slight  degree  from  the  beginning.  The  condition  may  improve,  espe- 
cially with  timely  treatment,  but,  for  reasons  already  mentioned,  a  morbid  con- 
dition may  often  remain  stationary  for  years,  or  new  symptoms  even  may  ensue. 

Diagnosis. — So  far  as  any  diagnosis  of  syphilis  of  the  spinal  cord  is  possible, 
it  is  evident  from  what  has  been  said.  The  chief  rule  is  to  consider  the  possibility 
of  syphilitic  disease  in  all  spinal  affections  that  are  atypical  from  the  beginning. 
If  a  previous  infection  is  certain,  or  if,  at  least,  it  is  rendered  probable  by  the 
special  antecedents,  the  diagnosis  is  the  more  warranted.  Of  course  a  previous 
infection  often  enough  can  not  be  established,  even  when  there  is  certainly  syph- 
ilis of  the  cord,  and,  on  the  other  hand,  other  forms  of  spinal  disease  may,  of 
course,  occur  in  those  who  have  been  previously  infected.  The  most  characteristic 
features  of  syphilis  of  the  cord  have  been  mentioned  above.  Similar  types  of  dis- 
ease may  be  produced  by  multiple  sclerosis,  by  sarcomatosis  of  the  spinal  me- 
ninges, by  tuberculosis  of  the  vertebrte,  etc.  We  must  therefore  consider  these 
affections  chiefly  in  the  differential  diagnosis.  Sometimes  the  success  or  failure 
of  specific  treatment  may  be  of  significance  in  diagnosis. 


SYEINGOMYELIA  AND   HYDROMYELUS  1029 

Treatment. — In  every  case,  even  where  there  is  merely  a  suspicion  or  a  possi- 
bility of  syphilitic  disease  of  the  spinal  cord,  we  should  institute  at  once  a  thor- 
ough antisyphilitic  treatment.  We  think  the  best  treatment  is  inunction  with 
mercurial  ointment  (grains  xlv-lxxv,  grammes  3-5,  daily).  Other  physicians  rec- 
ommend subcutaneous  injections  of  corrosive  sublimate,  salicylate  of  mercury, 
etc.  The  inunction  is  almost  always  combined  with  the  internal  exhibition  of 
iodine  preparations,  especially  iodide  of  potassium  (at  first  grains  xx-xxx, 
grammes  1.5-2,  and  later  still  larger  doses  daily),  iodide  of  sodium,  or  one 
of  the  newer  iodine  preparations,  of  which  iodalbacid  seems  to  us  the  best.  [It 
is  often  necessary  to  give  iodide  of  potassium  in  much  larger  doses.  If  the  diag- 
nosis of  syphilis  be  probable,  it  is  advisable  to  begin  with  doses  of  half  a  drachm 
(grammes  2)  or  more  three  times  a  day,  which  should  be  increased  rapidly 
until  the  patient  is  taking  five  or  six  drachms  daily  (grammes  20-25),  and 
sometimes,  as  in  cerebral  syphilis,  it  may  be  necessary  to  push  the  dose  to  one 
or  two  ounces  a  day  (grammes  30-60). — K.]  If  circumstances  permit,  it  is 
well  to  combine  inunction  with  a  course  at  some  bath  (sulphur  baths  in  Aix, 
Nenndorf,  also  Tolz,  Hall  in  Austria,  Wiesbaden,  etc.).  Every  antisyphilitic 
treatment  must  be  kept  up  a  sufficient  length  of  time  and  repeated  after  certain 
intervals,  as  is  the  general  custom  in  the  treatment  of  syphilis.  Besides  the 
specific  treatment,  the  other  therapeutic  methods  which  are  efficacious  in  chronic 
spinal  affections  also  have  their  appropriate  use  (warm  baths,  mineral  baths,  gal- 
vanization). Individual  symptoms  (neuralgic  pains,  vesical  troubles)  require 
special  attention. 

The  properly  conducted  treatment  of  spinal  syphilis  may  give  results  which 
are  sometimes  excellent  and  often  at  least  satisfactory.  We  can  understand  from 
what  has  been  said  why  our  hopes  are  naturally  only  too  often  disappointed. 


CHAPTEE   XIV 
SYRINGOMYELIA    AND    HYDROMYELUS 

Pathological  Anatomy  and  Pathogenesis. — The  formation  of  abnormal  cav- 
ities in  the  spinal  cord  is  due  either  to  a  dilatation  of  the  central  canal  (hydro- 
myelus)  or  to  a  peculiar  process,  which  is  called  central  gliosis,  with  the  secondary 
formation  of  cavities  (syringomyelia  proper).  The  cases  of  genuine  hydro- 
myeius  are  recognized  by  the  fact  that  the  cavity  is  found  in  the  middle  of  the 
cord,  corresponding  to  the  position  of  the  central  canal,  and  that  its  walls  are  cov- 
ered by  cylindrical  epithelium.  Slight  degrees  of  hydromyelus,  in  which  the 
dilated  central  canal  has  a  diameter  of  a  millimetre  or  a  millimetre  and  a  half, 
are  not  infrequently  found.  The  dilatation  usually  extends  over  only  one  seg- 
ment of  the  cord.  Greater  degrees  of  hydromyelus,  where  the  central  canal  is 
dilated  to  a  diameter  of  half  a  centimetre  or  a  centimetre  and  the  longitudinal 
extent  is  greater,  are  much  rarer. 

In  regard  to  the  origin  of  hydromyelus,  we  may  assume,  according  to  the 
teaching  of  Leyden,  that  the  cause  is  quite  generally  some  anomaly  of  develop- 
ment in  the  formation  of  the  central  canal.  The  hypothesis  of  Langhans,  that 
processes  of  stasis  in  the  central  canal,  such  as  compression  of  the  upper  end 
by  a  tumor  in  the  posterior  cranial  fossa,  may  lead  to  hydromyelus,  is  certainly 
not  applicable  to  the  great  majority  of  eases. 

The  conditions  are  different  in  syringomyelin,  which  is  of  much  greater  prac- 
tical importance.     In  this  affection,  according  to  many  investigators  (Westphal, 


1030  DISEASES    OE   THE   NEEVOUS    SYSTEM 

SirQon,  E.  Sehultze,  J.  Hoiiniami,  and  others),  the  whole  process  apparently 
begins  with  a  gliomatous  new  formation  or  transformation  of  tissue  in  the  cen- 
tral portions  of  the  spinal  cord.  This  peculiar  process,  which  probably  starts  in 
the  ependymal  cells  about  the  central  canal,  is  called  central  gliosis.  It  consists 
of  a  replacement  of  nerve-tissue  by  fibrous  glia-tissue.  The  central  gliosis,  which 
extends  toward  either  the  posterior  or  the  anterior  horns,  has  a  decided  tendency 
to  break  down  and  thus  to  form  secondary  cavities,  which  unite  with  the  central 
canal  or  remain  independent,  and  these  cavities  may  extend  longitudinally  in  the 
central  portions  of  the  cord  with  numerous  ramifications  and  projections.  To  this 
secondary  formation  of  cavities  we  give  the  name  of  syringomyelia.  In  this  con- 
dition the  central  canal  itself  hardly  ever  remains  normal;  it  is  usually  dilated 
and  shows  many  projections,  reduplications,  and  the  like,  circumstances  which 
clearly  indicate  that  we  must  consider  disturbances  of  development  as  factors  in 
the  origin  of  syringomyelia  and  central  gliosis.  We  do  not  find  any  special  en- 
largement of  the  cord  in  the  nature  of  a  tumor.  Gliosis  is  thus  distinct  from 
true  glioma  formation  (gliomatosis),  but  in  some  cases  the  distinction  between 
gliosis  and  the  formation  of  cellular  glioma  is  ill-defined.  In  ordinary  gliosis  with 
syringomyelia,  however,  the  cord  appears  normal  externally,  or,  when  the  syr- 
ingomyelia is  extensive,  it  may  appear  flabbier,  saccular,  and  flattened  in  the 
parts  affected.  Only  on  section  do  we  recognize,  even  with  the  naked  eye,  the 
cavity  formation  in  the  center  or  to  one  side  in  the  gray  matter  and  extending 
into  the  horns  of  the  cord.  Under  the  microscope  we  find  about  the  cavity  the 
newly-formed  tissue,  still  proliferating  peripherally  and  disintegrating  toward 
the  edge  of  the  cavity.  This  tissue  contains  many  newly-formed  ependymal  cells 
in  Its  central  portion;  toward  the  periphery  the  cells  are  fewer,  and  the  tissue 
consists  chiefly  of  a  mesh-work  of  fine  glia-fibers.  "We  can  not  say  definitely  to 
what  circumstances  we  may  refer  the  destruction  of  tissue  and  the  cavity  forma- 
tion. Changes  in  the  vessels,  which  are  often  found  dilated,  may  perhaps  play 
some  part  (hgemorrhage,  thrombosis,  etc.).  In  most  cases  central  gliosis  and 
syringomyelia  begin  in  the  cervical  cord  and  there  attain  their  greatest  extent ; 
but  they  may  extend  do'wriward  in  a  lesser  degree  into  the  lumbar  cord  and 
upward  into  the  medulla  oblongata. 

We  must  probably  always  look  for  the  final  cause  of  gliosis  and  syringomyelia 
in  a  defective  congenital  constitution  of  the  spinal  cord.  According  to  F. 
Schultze,  injuries  at  birth  in  eases  of  dilficult  labor  may  perhaps  lead  to  hsemato- 
myelia  and  afford  a  basis  for  the  later  anomaly.  Injury  in  later  life  is  also  fre- 
quently accused  of  producing  the  trouble. 

Clinical  Symptoms. — Slight  degrees  of  hydromyelus  or  of  syringomyelia  may 
be  met  with  at  autopsies  as  accidental  findings  which  have  given  rise  to  no  clin- 
ical symptoms  whatever.  Other  cases  of  extensive  cavity  formation  give  rise  to 
various  complex  forms  of  spinal  disease,  which  usually  escape  correct  interpre- 
tation during  life.  Thus  we  recall,  for  example,  Spath-Schiippel's  well-known 
case  of  general  anaesthesia,  a  case  under  our  own  observation  which  presented  the 
apparently  pure  type  of  spastic  spinal  paralysis,  etc. 

Opposed  to  such  isolated  cases,  however,  the  great  majority  of  cases  of  cen- 
tral gliosis  and  syringomyelia  of  the  cervical  cord  present  an  unusually  character- 
istic picture,  so  that  we  can  often  make  a  diagnosis  with  absolute  certainty. 
Since  the  investigations  of  E.  Schultze  and  Kahler  we  know  that  this  type  is  by 
no  means  rare.  It  is  therefore  certain  that  it  was  often  seen  in  the  past,  but 
it  was  usually  falsely  interpreted.  The  fact  that  the  gliosis  begins  as  a  rule 
in  the  center  of  the  cervical  cord  and  that,  as  it  progresses,  it  must  always 
involve  at  first  the  gray  matter  of  the  posterior  and  anterior  horns  on  one 
or  both  sides,  is  the  reason  why  the  group  of  symptoms  always  occurs  in  a 
way  that  is  generally  very  characteristic,   although  it  may  show  some  varia- 


SYKKvTGOMYELIA  AND   HYDEOMYELUS 


1031 


tions.  It  is  seen  especially  in  men  in  youth  and  middle  age  (between  twenty 
and  forty). 

The  clinical  symptoms  of  syringomyelia  of  the  cervical  cord  develop  very 
gradually,  and  almost  always  begin  in  the  upper  extremities — one  arm  usually 
being  affected  before  the  other.  The  symptoms  observed  in  such  cases  may  best 
be  classed  in  three  groups :  1.  Motor  weakness  and  muscular  atrophy.  These 
symptoms  are  dependent  upon  the  involvement  of  the  anterior  horns  in  the  pro- 
cess. The  atrophy  affects  with  especial  preference  the  small  muscles  of  the 
hand  (interossei,  thenar  muscles),  and  also  the  muscles  of  the  forearm,  the  del- 
toid, etc.  Fibrillary  twitchings  and  electrical  reaction  of  degeneration  are  often 
found.  The  tendon  reflexes  are  lost  or  else  exaggerated,  which  may  be  easily  ex- 
plained from  the  special  localization  of  the  process.  2.  Disturbances  of  sensibil- 
ity are  almost  invariably  associated  Avith  this  muscular  atrophy.  The  chief  cause 
of  these  is  always  the  involvement  of  the  posterior  horns  in  the  process.  The  dis- 
turbances of  sensibility  almost  always  have 
this  peculiarity,  that  the  sensibility  for  pain 
and  the  temperature  sense  are  at  first  always 
affected,  while  the  simple  sensibility  for  touch 
and  the  pressure  sense  may  remain  normal  for 
a  long  time  or  throughout  the  disease.  The 
fact  that  the  patient  is  insensible  to  the  influ- 
ence of  pain  or  heat  is  therefore  of  special  sig- 
nificance, because  it  may  frequently  lead  to 
wounds,  burns,  etc.,  on  the  hands  and  forearms, 
which  the  patient  may  often  never  notice,  and 
which  therefore  may  heal  badly.  The  disturb- 
ances of  the  temperature  sense  may  affect 
either  the  sensibility  to  cold  or  the  sensibility 
to  heat,  or  both  at  once.  3.  The  third  group 
of  symptoms  is  made  up  of  peculiar  trophic 
changes.  The  above-mentioned  external  in- 
juries, caused  by  the  analgesia,  naturally  play 
a  large  part  in  this  connection  (felons,  bullae, 
phlegmon,  etc.) ;  *  but  we  must  also  assume 
special  trophic  disturbances  to  explain  many 
processes,  especially  the  peculiar  thickening  of 
the  bones  sometimes  observed,  the  atrophy  of 
the  fingers,  etc.     In  many  patients  there  may 

thus  develop  a  very  peculiar  and  characteristic  deformity  of  one  or  both  hands,  of 
-which  the  accompanying  cut  (Fig.  161)  gives  a  good  idea.  The  hand  and  fingers 
are  thickened,  and  some  fingers  are  shortened  by  atrophy  of  the  phalanges.  The 
most  striking  abnormal  vaso-motor  and  secretory  disturbances  may  also  occur. 

In  many  cases  the  symptoms  remain  confined  almost  entirely  to  the  upper 
■extremities.  They  progress  so  slowly  that  many  patients  are  able  to  do  a  certain 
amount  of  work  for  a  long  time ;  but  finally  changes  may  also  appear  in  the  legs, 
■either  simple  paresis  and  spastic  conditions  or  symptoms  similar  to  those  in  the 
arms  already  described.  These  arise  only  when  the  process  involves  the  gray 
matter  of  the  lumbar  cord.     On  the  other  hand,  the  disease  may  extend  upward 


Fig.  161. — Syringomyelia  of  the  cervical 
cord.  ]Jetoriiiit3-  of  the  hand,  atro- 
phy of  the  interossei  and  of  the  adduc- 
tor pollicis.    (Personal  observation.) 


*  The  so-called  MorvarCs  disease  is  nothinn^  but  syrineromyelia,  in  which  these  trophic  and  inllam- 
matory  change.s  are  especially  marked.  [The  larffe  number  of  cases  coming  under  Morvan's  observa- 
tion in  a  small  district  in  Brittany  suggest,  however,  that  Morvan's  disease  may  be  rather  an  infectious 
neuritis,  possibly  due  to  lepro.sy,  and  therefore  distinct  from  a  syringomyelia  with  marked  trophic  dis- 
turbances.— K.] 


1032  DISEASES    OE   THE   XEEVOUS    SYSTEM 

from  tlie  cervical  cord,  and  then  very  characteristic  bulbar  symptoms  may  ensue. 
The  commonest  bulbar  disturbances  are :  partial  loss  of  sensation  in  the  region 
of  the  trig-eminus,  unilateral  paralysis  of  the  hypoglossus  with  unilateral  atrophy 
of  the  tongue,  paralysis  of  one  vocal  cord,  unilateral  paralysis  of  the  accessory 
(weakness  and  atrophy  of  one  trapezius  and  stemo-cleido-mastoid),  paralysis  of 
the  soft  palate,  facial  paralysis,  abducens  paralysis,  etc.  In  many  cases  such  bul- 
bar symptoms  are  much  more  prominent  than  the  spinal  symptoms.  Abnormal- 
ities in  the  pupils  and  the  fissura  palpebrarum  are  seen  in  a  few  eases,  even  where 
the  gliosis  is  limited  to  the  cervical  cord,  and  are  to  be  explained  by  an  involve- 
ment of  the  so-called  eilio-spinal  center. 

It  is  a  remarkable  fact  that  syringomyelia  is  very  often  associated  with  a  more 
or  less  pronounced  kyphoscoliosis  of  the  spine.  We  are  of  the  opinion  that  the 
kyphoscoliosis  is  not  due  to  the  syringomyelia,  but  that  it  is  also  an  expression 
of  abnormal  conditions  of  development  and  growth  in  the  vicinity  of  the  medul- 
lary tube. 

The  course  of  syringomyelia  is  very  chronic,  yet  always  unfavorable.  Death 
finally  ensues  from  some  intercurrent  disease,  general  weakness,  pyelo-nephritis,. 
or,  as  we  have  seen,  from  amyloid  disease  of  the  kidneys  due  to  many  suppurative 
processes. 

The  diagnosis  of  typical  cases  of  syringomyelia  of  the  cervical  cord  is  not  dif- 
ficult if  we  once  know  the  type.  A  careful  examination  of  the  sensibility  prevents 
us  from  mistaking  it  for  spinal  muscular  atrophy.  Any  combination  of  muscular 
atrophy  in  the  hands  with  analgesia  and  disturbances  of  the  temperature  sense 
must  awaken  the  suspicion  of  syringomyelia,  as  must  all  unusual  trophic  disturb- 
ances occurring  in  the  hands,  etc.  If  the  three  groups  of  symptoms  mentioned 
above  co-exist,  we  can  be  almost  sure  of  our  diagnosis.  Only  exceptionally  can 
other  processes  in  the  cervical  cord  (such  as  compression  following  caries,  as  we 
have  ourselves  seen)  produce  a  similar  picture  and  give  rise  to  confusion.  The 
differential  diagnosis  between  syringomyelia  and  leprosy  may  be  more  difficult,^ 
as  the  latter  sometimes  gives  rise  to  a  very  similar  type  of  disease;  but  in  such 
eases  the  special  endemic  conditions,  the  peculiar  changes  in  the  skin,  and  finally 
the  discovery  of  the  specific  bacillus,  may  enable  us  to  make  a  correct  decision. 

There  is  no  special  treatment  for  syringomyelia.  The  treatment  must  be 
symptomatic.  We  should  remember,  when  there  is  analgesia,  to  warn  the  patient 
of  the  possibility  of  injury. 


CHAPTEE   XV 

SPINA    BIFIDA 

(Bi/drorrhachis.     Myelocele.     Meningocele) 

We  give  the  name  of  spina  bifida  to  a  congenital  fissure-formation  on  the  pos- 
terior side  of  the  vertebral  arches,  due  to  anomalies  of  development,  and  associ- 
ated with  a  hernia-like  protrusion  of  the  sac  of  the  dura.  The  most  frequent  seat 
of  the  malformation  is  in  the  sacral  and  lumbar  regions.  Only  rarely  is  the 
tumor  so  great  as  to  hinder  the  birth  of  the  child.  Children  afflicted  with  spina 
bifida  are  usually  born  normally,  and  not  till  afterwards  do  we  find  the  tumor  in 
the  sacral  region ;  its  size  may  be  from  that  of  a  small  nut  to  that  of  the  fist  or 
larger.  The  skin  above  the  tumor  is  sometimes  entirely  normal,  but  in  other 
cases  very  tense  and  reddened.  If  we  have  an  opportunity  to  examine  the  tiimor 
carefully  post  mortem,  we  usually  find  beneath  the  skin  the  protruded  sac  of  the 
dura,  and  beneath  it  the  arachnoid.    Only  rarely  is  the  dura  also  fissured,  so  that 


SECONDAEY  DEGENEEATIONS  I^t  tHE  SPIRAL  COED  1033 

the  sac  is  formed  exclusively  of  the  arachnoid.  It  is  filled  with  a  clear  fluid 
which  is  precisely  identical  with  the  cerebro-spinal  fluid.  In  rare  cases  there  is 
also  a  dilatation  of  the  central  canal,  hydromyelus ;  then  the  substance  of  the 
cord  is  atrophied  to  a  greater  or  less  extent,  and  the  central  canal  communicates 
directly  with  the  cavity  of  the  spina  bifida.  In  other  cases  the  condition  of  the 
cord  is  normal;  sometimes  its  lower  end  is  adherent  to  one  spot  of  the  sac.  We 
must  refer  to  the  text-books  of  pathological  anatomy  in  regard  to  the  many  fur- 
ther details  of  the  anatomy  and  the  history  of  development. 

In  regard  to  the  clinical  symptoms  of  spina  bifida,  the  condition  of  most  chil- 
dren at  first  is  perfectly  normal,  apart  from  the  malformation.  The  tumor  itself 
usually  feels  tense.  If  we  exert  pressure  on  it  with  the  hand,  we  can  often  force 
part  of  its  contents  back  into  the  vertebral  canal.  This  causes  an  increase  of  the 
cerebral  pressure,  and  we  notice,  besides  the  lessening  of  the  spina  bifida,  a 
marked  expansion  of  the  fontanelles,  and  also  the  appearance  of  somnolence, 
contractions,  and  changes  in  the  pulse  and  respiration,  which  demand  a  speedy 
interruption  of  this  rather  dangerous  experiment.  If  such  symptoms  do  not 
appear  at  all,  we  can  conclude  that  the  sac  is  completely  constricted  and  closed. 

Only  rarely,  however,  does  the  child's  condition  remain  normal.  The  tumor 
usually  shows  a  slow  growth,  and  the  results  of  pressure  on  the  spinal  cord 
or  on  the  cauda  equina  gradually  appear.  Paralysis,  anaesthesia,  vesical  dis- 
turbances, bed-sores,  etc.,  develop,  and  these  symptoms  finally  lead  to  death.  Still 
more  frequently  the  sac  bursts,  or  its  walls  inflame,  and  this  becomes  fatal  from 
the  onset  of  a  purulent  meningitis. 

The  prognosis  of  most  cases  of  spina  bifida  is  accordingly  to  be  regarded  as 
unfavorable,  unless  we  succeed  in  curing  the  disease  by  surgical  treatment.  Ee- 
covery  has  been  brought  about  in  many  cases  by  methodical  compression  of  the 
sac,  and  by  puncture,  with  evacuation  of  the  fluid  and  a  subsequent  injection  of 
a  solution  of  iodine  to  obtain  an  obliteration  of  the  sac ;  but,  on  the  other  hand, 
the  operative  treatment  of  spina  bifida  is  attended  with  many  dangers,  including 
liability  to  meningitis,  so  that  we  note  frequent  bad  results  as  well  as  the  favor- 
able ones.  We  can  not  here  go  into  the  details  of  the  surgical  methods  for  the 
cure  of  spina  bifida;  they  can  be  found  in  full  in  the  text-books  of  surgery. 


CHAPTEE   XVI 
SECONDARY    DEGENERATIONS    IN    THE    SPINAL    CORD 

Although  the  secondary  degenerations  in  the  spinal  cord  are  chiefly  interest- 
ing merely  from  an  anatomical  point  of  view,  we  must  briefly  describe  them, 
because,  in  the  first  place,  a  clinical  significance  has  been  ascribed  to  them  in  cer- 
tain quarters,  and  also  because  the  study  of  secondary  degeneration  has  been  the 
starting-point  of  all  our  present  knowledge  as  to  the  systemic  diseases  of  the 
spinal  cord. 

1.  Secondary  Degeneration  in  the  Spinal  Cord  after  Cerebral  Lesions. — We 
already  know  (compare  page  834)  that,  every  lesion  of  the  great  motor  ganglion- 
cells  in  the  anterior  cornua  of  the  spinal  cord,  and  every  permanent  break  in  con- 
duction in  the  motor  nerves  themselves,  is  followed  by  a  secondary  degeneration 
of  the  peripheral  portion  of  the  motor  fibers.  We  assume  as  the  reason  for  this, 
as  we  have  seen,  a  "  trophic  influence  "  of  the  said  ganglion-cells  on  the  motor 
fibers  arising  from  them,  so  that  the  latter  degenerate  when  the  conduction  of 
that  trophic  influence  is  interrupted,  or  when  the  trophic  ganglion-cells  them- 


1034 


DISEASES    OF   THE    I^EKVOUS    SYSTEM 


selves  are  destroyed.  Precisely  analogous  conditions  exist  for  the  first  great  por- 
tion of  the  motor  conducting  tract,  the  lateral  pyramidal  tract,  from  the  cortex 
cerebri  to  the  anterior  horns  of  the  spinal  cord  (vide  Fig. 
137,  page  986).  The  great  ganglion-cells  of  the  motor 
portion  of  the  cortex  cerebri  also  exert  a  trophic  influence 
on  the  motor  fibers  arising  from  them,  which  extends  to 
the  end  of  these  fibers — that  is,  up  to  but  exclusive  of 
large  motor  ganglion-cells  of  the  spinal  cord.  This  atro- 
phic influence  may  be  understood  if  we  regard  the  gan- 
glion-cell and  its  corresponding  nerve-fiber  as  forming  one 
complete  unit  and  properly  only  a  single  cell,  a  neurone, 
and  that  therefore  the  process  of  the  cell  body  (the  "  nerve- 
fiber  ")  can  not  possibly  lead  an  independent  existence 
when  separated  from  the  "  ganglion-cell " — that  is,  from 
the  nucleus  of  the  cell  body.  If  therefore  there  be  disease 
situated  in  the  motor  portion  of  the  cortex  cerebri  itself, 
or  in  any  part  of  the  motor  tract  in  the  brain  (the  motor 
fibers  of  the  corona  radiata,  the  internal  capsule,  the  crus, 
or  the  pons),  by  which  disease  the  conduction  is  inter- 
rupted— if  there  be  disease  there,  we  repeat,  a  secondary 
descending  degeneration  of  the  motor  fibers  ensues  in  the 
whole  portion  below,  down  to,  but  exclusive  of,  the  anterior 
horns  of  the  gray  matter.  The  secondary  descending  de- 
generation of  the  pyramidal  tract  is  found  correspondingly 
in  the  crus,  in  the  pons,  and  in  the  pyramid  of  the  same 
side  on  which  the  focus  of  disease  in  the  brain  is  situated. 
From  this  point  we  can  trace  the  main  part  of  the  degen- 
eration below  the  decussation  of  the  pyramids  farther 
down  the  lateral  column  of  the  spinal  cord  on  the  opposite 
side  (secondary  degeneration  of  the  lateral  crossed  pyram- 
idal tract)  (see  Fig.  162),  while  in  many  cases  besides 
we  find  a  slighter  secondary  degeneration  in  the  anterior 
column  of  the  spinal  cord  on  the  same  side  (secondary 
degeneration  of  the  anterior  uncrossed  pyramidal  tract). 
As  we  know  from  Flechsig's  investigations,  the  relative 
amounts  of  the  crossed  lateral  fibers,  and  the  anterior 
fibers  that  remain  uncrossed,  vary  in  individual  cases 
within  certain  limits.  In  the  cases  where  no  anterior 
pyramidal  tract  exists — that  is,  where  all  the  motor  fibers 
pass  over  to  the  lateral  column  of  the  opposite  half  of  the 
spinal  cord  in  the  decussation  of  the  pyramids — of  course 
a  descending  degeneration  in  the  anterior  column  is  wholly 
wanting.  We  must  add,  however,  that  in  some  cases  a 
small  number  of  fibers  seem  to  proceed  uncrossed  in  the 
lateral  column,  so  that  accordingly  we  may  also  have  a 
slight  secondary  descending  degeneration  in  the  lateral 
pyramidal  tract  of  the  same  (affected)  side  (Pitres). 

2.  Secondary  Degeneration  in  the  Spinal  Cord  in 
Transverse  Affections  of  the  Spinal  Cord  itself. — If  a 
lesion  be  situated  in  any  part  of  the  spinal  cord,  by  which 
more  or  less  of  its  transverse  section  is  affected,  the  in- 
terruption of  conduction  in  these  fibers  is  also  followed  by 
the  appearance  of  secondary  degenerations  which  may  be 
made  out  both  in  a  descending  and  in  an  ascending  direc- 


FiG.  162.— Secondary  de- 
scending degeneration 
of  the  pyramidal  tracts 
in  a  primary  lesion  of 
the  left  half  of  the 
cerebrum.  The  lateral 
pyramidal  tract  of  the 
right  half  of  the  cord  is 
degenerated  down  to 
the  lowest  part  of  the 
lumbar  region  (1-8)  ; 
the  anterior  pyramidal 
tract  of  the  left  half  of 
the  cord  is  degenerated 
to  the  beginning  of  the 
lumbar  enlargement 
(1-6). 


SECONDAEY  DEGENERATIONS  IN  THE  SPINAL  COED  1035 


tion  (see  Eig.  163).  It  is  most  frequently  transverse  myelitis,  compression  of  the 
spinal  cord,  and  tumors  of  the  cord,  which  give  rise  to  secondary  degenerations. 
The  latter,  however,  of  course,  are  never  due  to  the  sort  of  lesion,  but  only  to  its 
seat,  and  to  the  interruption  of  conduction  caused  by  it. 

The  secondary  descending  degeneration  affects  the  pyramidal  tract  in  a  fash- 
ion precisely  analogous  to  that  which  we  have  also  learned  to  recognize  in  sec- 
ondary degenerations  after  cerebral  lesions;  but  since  the  primary  affection 
usually  affects  the  pyramidal  tract  on  both  sides,  the  descending  secondary  de- 
generation of  course  develops  in  both  lateral  pyramidal  tracts,  and  also  in  the 
anterior  pyramidal  tracts,  if  they  exist  below  the  point  of  lesion.  In  general  the 
area  of  the  descending  degeneration  of  the  pyramidal  tract  is  larger  in  transverse 
diseases  of  the  spinal  cord  than  it  is  in  lesions  of  the  brain.  The  principal  reason 
of  this  is  that  lesions  of 'the  brain  hardly  ever  destroy  com- 
pletely all  the  motor  fibers  belonging  to  one  half  of  the 
body.  Furthermore,  in  a  transverse  lesion  of  the  cord 
certain  other  small  systems  of  fibers  of  uncertain  signifi- 
cance also  degenerate  downward:  among  these  are  a  small 
zone  of  fibers  lying  internally  to  the  lateral  cerebellar  tract 
and  Gowers's  tract  (vide  infra)  and  extending  to  the  an- 
terior border  of  the  cord  near  the  anterior  pyramidal  tract 
(Lowenthal's  "  iniermedian  fasciculus  of  the  aniero-lateral 
column  ")>  and  also,  very  constantly,  a  small  comma-shaped 
fasciculus  in  the  middle  of  each  posterior  column,  formed 
probably  of  descending  collaterals  of  the  fibers  of  the  pos- 
terior columns  (the  so-called  Schultze's  comma,  Fig.  163), 
which  we  can  not  usually  trace  very  far  downward. 

The  secondary  ascending  degeneration,  developing  up- 
ward from  the  primary  point  of  disease,  affects  several 
systems  of  fibers  which  conduct  centripetally,  the  so-called 
columns  of  Goll  (the  internal  portion  of  the  posterior  col- 
unan's),  and  also  two  systems  of  fibers  in  the  outer  border 
of  the  lateral  columns.  The  degeneration  of  the  posterior 
columns  is  most  extensive  immediately  above  the  point  of 
interruption  and  gradually  decreases  upward  (Fig.  163). 
We  can  readily  understand  this  degeneration  if  we  remem- 
.ber  that  the  fibers  of  the  posterior  columns  are  the  ascend- 
ing fibers  of  the  posterior  roots,  which  have  their  origin  in 
the  cells  of  the  spinal  ganglia.  Since  the  new  fibers  from 
the  posterior  roots  which  enter  higher  up  are  always  ex- 
ternal to  the  fibers  coming  from  the  lower  roots,  the  degen- 
eration must  be  limited  more  and  more,  as  it  ascends  com- 
pletely, to  the  region  of  the  columns  of  Goll.  A  secondary 
ascending  degeneration  in  the  posterior  columns  also  fol- 
lows division  of  the  posterior  roots,  and  therefore,  of  course,  injuries  of  the 
Cauda  equina.  The  secondary  ascending  degeneration  in  the  lateral  columns  is 
made  up  of  a  smaller  posterior  and  a  broader  anterior  portion.  The  former  is  the 
lateral  cerebellar  tract  discovered  by  Flechsig;  its  fibers  arise  from  the  cells  of 
Clarke's  columns  in  the  lower  dorsal  cord,  and  therefore  they  must  degenerate 
when  separated  from  these  cells.  The  fibers  may  be  traced  upward  into  the 
corpus  restiforme,  and  then  to  the  cerebellum.  The  bundle  of  fibers  anterior 
to  the  lateral  cerebellar  tract,  which  also  degenerate  upward,  is  distinct  from 
the  lateral  cerebellar  tract  in  its  development  and  its  origin.  It  probably  arises 
from  cells  of  the  posterior  horns,  and  is  called  Gowers'  tract  or  the  antero-lateral 
ascending  tract.    Its  termination  and  significance  are  still  unknown. 


Fig.  163.— Secondary  as- 
cending and  descend- 
ing degeneration  in  a 
transverse  affection  of 
the  upper  dorsal  re- 
gion. The  columns  of 
Goll  and  the  direct 
cerebellar  tracts  are 
degenerated  upward. 
The  lateral  pyramidal 
tracts  are  degenera- 
ted downward. 


1036  DISEASES    OF    THE   NEEYOUS    SYSTEM 

Although  no  clinical  sigTiificance  at  all  can  be  attributed  to  secondary  as- 
cending degeneration,  the  theory  first  advanced  by  the  French  observers- 
(Charcot  and  others)  prevails  almost  universally,  that  secondary  descending- 
degeneration  causes  definite  clinical  symptoms.  The  secondary  contractures 
and  the  increase  of  the  tendon  reflexes  in  the  paralyzed  limbs,  occurring  in 
hemiplegia,  are  especially  referred  to  this.  We  shall  see  in  a  later  section, 
that  this  theory  is  by  no  means  proved,  and  is  even  improbable,  so  that,  in 
our  opinion,  the  secondary  descending  degeneration  also  has  no  material  clin- 
ical significance. 

3.  Secondary  Degeneration  in  the  Spinal  Cord  after  Amputations. — If  we  ex- 
amine the  spinal  cord  of  persons  who  have  had  an  arm  or  a  leg  amputated  some 
time  before  their  death,  we  sometimes  find  that  the  entire  corresponding  half  of 
the  cord  is  smaller;  but  the  diminution  of  the  posterior-  column  on  that  side  is 
the  most  marked.  On  careful  microscopic  examination  we  can  detect  a  slight 
but  evident  loss  of  fibers  in  the  region  of  the  column  of  Goll — that  is,  in  the 
median  portion  of  the  posterior  columns.  We  can  also  discover  a  slighter  loss  of 
fibers  in  the  column  of  Goll  on  the  other  side  (opposite  to  the  amputation).  We 
can  not  enter  into  a  more  detailed  description  here  of  this  condition,  which  is 
of  interest  theoretically,  but  which  need  not  be  considered  practically  and  which,, 
furthermore,  is  in  many  respects  not  fully  explained. 


CHAPTEK   XVII 

UNILATERAL    LESION    OF    THE    SPINAL    CORD 

{Brown-Sequard''s  Spinal  Paralijsift) 

Unilateral  lesion  is  not  a  definite  disease  of  the  spinal  cord,  but  a  peculiar 
group  of  symptoms,  which  occurs  whenever  an  interruption  of  conduction  is 
produced  by  any  affection  in  one  lateral  half  of  the  spinal  cord.  Since  the  symp- 
toms in  these  cases  were  first  carefully  studied  clinically  and  experimentally  by 
Brown- Sequard,  we  often  call  the  type  of  disease  in  question  "  Brown-Sequard's 
paralysis."  We  see  this  paralysis  in  its  purest  form  in  injuries  of  the  spinal 
cord.  Almost  perfectly  exact  sections  of  one  lateral  half  of  the  spinal  cord 
have  been  produced  by  stabs  from  a  knife,  a  sword,  etc.  Tumors  and  syph- 
ilitic affections  especially,  and  more  rarely  central  gliosis,  multiple  sclerosis, 
hsematomyelia,  compression  of  the  cord  in  caries  or  cancer  of  the  vertebrae, 
etc.,  may  also,  during  a  certain  period  of  their  course,  cause  the  symptoms  of 
a  more  or  less  sharply  defined  unilateral  lesion. 

The  peculiar  condition  of  the  symptoms  in  unilateral  lesion  is  easily  explained 
by  a  consideration  of  the  course  of  the  fibers  in  the  spinal  cord.  In  the  accom- 
panying diagram  (see  Fig.  164)  the  motor  fibers  from  the  anterior  roots  are 
marked  v,  the  sensory  fibers  from  the  posterior  roots,  h.  As  is  well  known,  the 
sensory  fibers,  h,  pass  at  once  into  the  opposite  half  of  the  spinal  cord,  and  accord- 
ingly decussate  with  the  corresponding  sensoiy  fibers  of  the  other  side.*  The 
motor  fibers,  v,  however,  pass  upward  uncrossed  on  the  side  on  which  they  enter 
the  spinal  cord,  and  mainly  in  the  lateral  column.  If  now,  for  example,  there  be 
situated  on  the  right  half  of  the  spinal  cord  at  a  a  lesion,  e.  g.,  a  section  of  one 

[*  More  recent  investigations  by  Mott  render  this  theory  of  immediate  decussation  somewliat  doubt- 
ful, and  unilateral  lesion  may  not  always  present  tlie  group  of  symptoms  described  below. — K.] 


imiLATEEAL  LESION  OF  THE   SPINAL   CORD 


103Y 


lialf  the  cord,  the  conduction  of  those  motor  fibers  which  come  from  the  right  side 
is  interrupted,  as  well  as  the  conduction  of  those  sensory  fibers  which  come  from 
the  left  side.  From  this  it  follows  that  there  must  be  motor  paralysis  on  the  same 
side  of  the  body  as  the  lesion  in  the  spinal  cord,  and  some  degree  of  anaesthesia 
on  the  other  side  of  the  body.  If  the  affection  be  situated  in  the  dorsal  or  lumbar 
cord,  the  leg  on  the  corresponding  side  is  paralyzed,  and  the  leg  on  the  other  side 
is  anaesthetic.  If  the  lesion  be  situated  in  the  cervical  cord,  above  the  entrance  of 
the  nerves  for  the  upper  extremities,  the  arm  and  the  leg  on  the  side  of  the  lesion 
are  both  paralyzed  (spinal  hemiplegia),  while  the  arm  and  the  leg  on  the  other 
side  are  anaesthetic,  but  possess  normal  mo- 
tility; but  strictly  unilateral  disease  of  the 
lowest  end  of  the  cord  (the  sacral  cord  and 
conus  terminalis)  may  not  give  rise  to  the 
picture  of  a  Brown-Sequard's  unilateral 
lesion,  because  at  this  level  no  full  decussa- 
tion of  sensory  fibers  has  taken  place.  At 
most  we  find  a  flaccid  atrophic  paralysis  in 
one  leg  with  a  disturbance  of  sensation  on 
the  same  side,  and  an  anaesthesia  of  the 
5crotum,  perineum,  and  penis  on  the  other 
side,  because  the  sensory  fibers  for  this  re- 
gion enter  the  lowest  part  of  the  cord,  and 
therefore  have  their  decussation  the  lowest. 
On  more  careful  examination,  further 
conditions  of  physiological  interest  appear. 
The  sensibility  on  the  side  of  the  motor  pa- 
ralysis is  usually  not  wholly  normal.  In 
the  first  place,  we  sometimes  find  an  evi- 
dent diminution  of  the  muscular  sense  (the 
perception  of  passive  movements),  and  in 
the  second  place  the  cutaneous  sensibility 
is  not  always  normal,  but  there  is  some- 
times a  pronounced  hyperaesthesia  for  all, 
or  at  least  for  some,  of  the  forms  of  irrita- 
tion. Slight  pricks  are  very  painful,  and 
tickling  the  soles  of  the  feet  is  felt  with 
abnormal  strength.  Above  the  hyperaes- 
thetic  territory  in  the  skin  we  usually  find 
a  narrow  anesthetic  zone  (Fig.  165,  h),  and 
above  this  at  times  again  a  narrow  hyper- 
aesthetic  strip  (see  Fig.  165,  c).  The 
anaesthetic  zone  is  easily  explained.  It 
of    the    lesion    in    the    spinal    cord — that 


Fig.  164. — (From  Erb.)  Schematic  representa- 
tion of  the  course  of  the  main  tracts  in  the 
cord,  represented  for  a  single  pair  of  roots. 
V.  Anterior  roots,  h.  Posterior  roots.  1. 
Paths  for  motor  and  vaso-motor  conduc- 
tion. 2.  Paths  for  muscular  sense.  3.  Paths 
for  cutaneous  sensibility  on  the  right. 
1'.  2',  3'.  The  same  paths  on  the  left.  The 
arrows  indicate  the  direction  of  physiologi- 
cal conduction. 


corresponds    precisely    to    the    level 
is,    to    those    sensory    fibers    coming 


from  the  same  side,  which  are  immediately  involved  as  soon  as  they  enter 
the  cord;  but  a  satisfactory  explanation  is  entirely  lacking  for  the  appear- 
ance of  the  hyperaesthesia  on  the  paralyzed  side,  and  for  the  origin  of  the 
uppermost  narrow  hyperaesthetic  zone.  The  reflexes,  especially  the  tendon  reflexes, 
are  usually  increased  on  the  paralyzed  side.  There  is  often  a  vigorous  ankle 
clonus,  a  symptom  which  must  be  explained  by  the  loss  of  the  reflex  inhibitory 
influences  coming  from  above.  Definite  statements  are  lacking  as  to  the  condition 
of  the  cutaneous  reflexes.  The  cremasteric  and  abdominal  reflexes  are  often 
absent  on  the  paralyzed  side,  just  as  in  cerebral  hemiplegia  (q.  v.).  In  some 
cases  ataxia  has  been  observed  on  the  side  of  the  lesion,  instead  of  paralysis ;  this 
is  apparently  due  to  an  affection  of  the  posterior  column  on  that  side.     Finally, 


1038 


DISEASES    OF    THE    NERVOUS    SYSTEM 


we  often  find  on  the  side  of  the  lesion  the  signs  of  a  vaso-motor  paralysis,  espe- 
cially a  marked  rise  in  the  cutaneous  temperature,  even  2°  (1°  C),  or  more. 

On  the  other  side,  opposite  the  lesion,  the 
motility  is  normal.  The  disturbance  of  sensi- 
bility affects  the  sensibility  to  pain  and  tem- 
perature chiefly,  while  the  sensibility  to  touch 
is  usually  wholly  or  almost  wholly  retained. 
The  muscular  sense  (the  perception  of  passive 
movements)  is  not  affected,  in  contrast  to  the 
paralyzed  side  (vide  supra).  Above  the  anaes- 
thetic region  we  also  find  frequently  a  narrow 
hypersesthetic  zone  (see  Fig.  165,  c).  The  re- 
flexes are  usually  normal,  or  a  little  increased. 
The  statements  just  made  in  regard  to  the 
sensory  disturbances  agree  well  with  the  rest 
of  our  knowledge  as  to  the  sensory  conducting 
tracts.  We  know  that  only  the  posterior  root- 
fibers  which  enter  the  posterior  gray  matter 
decussate  in  the  cord  (page  799),  and  that 
these  fibers  serve  chiefly  to  conduct  impres- 
sions of  pain  and  temperature  (compare  page 
1031).  The  anaesthesia  in  unilateral  lesions 
therefore  affects  chiefly  these  two  qualities  of 
sensibility.  The  muscular  sensations  are  con- 
ducted by  fibers  which  ascend  uncrossed  in  the 
posterior  columns.  The  disturbance  of  the 
muscular  sense  is  therefore  manifested,  as  has 
been  said,  upon  the  paralyzed  side.  There  are 
apparently  so  many  ways  of  conduction  open 
for  simple  tactile  sensations  that  these  are 
only  rarely  much  diminished. 

If  other  spinal  symptoms  (disturbances  of 
micturition  and  defecation,  neuralgic  pains, 
muscular  atrophy,  changes  in  the  electrical 
excitability,  etc.)  are  associated  with  the 
sjTnptom-complex  just  described,  these  symp- 
toms are  dependent  upon  the  special  localiza- 
tion of  the  disease ;  for  we  must  take  special 
note  that  the  clinical  picture  of  a  unilateral- 
lesion  may  not  be  perfectly  distinct,  but  we. 
can  often  recognize  only  a  few  prominent 
features. 

We  need  add  nothing  as  to  the  prognosis  and  treatment  of  unilateral  lesion, 
because,  of  course,  they  are  governed  entirely  by  the  form  of  the  primary  disease. 


Fig.  165. — Schematic  representation  of 
the  chief  symptoms  in  unilateral  le- 
sion of  the  left  dorsal  cord.  (After 
Erb.)  The  oblique  shading-  sig-nifies 
motor  and  vaso-motor  paralysis  ;  the 
vertical  shading  signifies  cutaneous 
anaesthesia  :  the  dots  signify  cutane- 
ous hyperaesthesia. 


PROGRESSIVE   BULBAR   PARALYSIS  1039 


IV.— THE   DISEASES   OF   THE    MEDULLA   OBLONGATA 


CHAPTER  I 


PROGRESSIVE    BULBAR    PARALYSIS 

(  Glosso-lab io-lury II geal  Paralysis) 

DucHENNE  in  1860  described  for  the  first  time  in  complete  detail  the  symptoms 
of  a  disease  to  which  Wachsmiith  subsequently  gave  the  name  of  progressive  bul- 
bar paralysis.  Duchenne  did  not,  however,  recognize  the  true  seat  of  the  disease, 
and  it  was  not  until  1870  that  Charcot  in  France,  and  E.  Leyden  in  Germany, 
were  enabled  to  confirm  the  suggestion  of  Wachsmuth  that  the  lesion  is  a  progres- 
sive degeneration  and  atrophy  of  the  nuclei  in  the  medulla  oblongata.  Since  then 
our  knowledge  of  the  disease  has  rapidly  increased,  both  from  the  clinical  and  the 
anatomical  standpoints;  and  Kussmaul  and  others  have  thoroughly  investigated 
its  relations  to  two  other  closely  allied  forms  of  disease- — amyotrophic  lateral 
sclerosis  and  progressive  muscular  atrophy. 

.3itiology. — We  have  scarcely  any  positive  information  about  the  cause  of  the 
disease.  Heredity  seems  in  general  of  slight  importance ;  but  some  observations 
indicate  that  the  disease  may  also  occur  in  families,  so  that  we  must  probably 
assume  in  the  last  instance  that  the  special  cause  of  the  affection  is  usually  a 
congenital  abnormality  of  the  system  of  neurones  which  later  become  diseased. 
In  some  cases  its  origin  is  ascribed  to  catching  cold,  emotional  excitement,  trau- 
matic influences,  or  excessive  bodily  exertion.  Perhaps  it  is  sometimes  occa- 
sioned by  excessive  use  of  the  muscles  to  which  the  disease  is  chiefly  confined,  as 
in  playing  on  wind-instruments ;  but  in  many  instances  no  possible  external  cause 
can  be  found.  Men  seem  somewhat  more  liable  to  be  attacked  than  women.  The 
disease  hardly  ever  appears  until  middle  or  old  age — that  is,  after  thirty-five. 
Only  a  few  cases  have  been  observed  in  childhood. 

Clinical  History. — The  symptoms  are  almost  always  very  slow  in  their  devel- 
opment. There  may  be  mild  premonitory  symptoms — such  as  painful  sensations 
in  the  back  of  the  neck.  Then  there  is  a  very  gradual  appearance  of  difficulty 
in  articulation.  Many  words  are  pronounced  indistinctly.  The  first  trouble  is 
noticed  especially  with  letters  in  the  utterance  of  which  the  tongue  plays  an  es- 
sential part:  E,  R,  L,  S,  G  (hard),  K,  D,  T,  and  N.*  It  is  easily  seen  that  the 
derangement  is  not  aphasic.  There  is  no  forgetting  or  confounding  of  the  words 
or  letters ;  but  the  innervation  of  the  tongue  has  become  impaired.  Long  before 
the  ordinary  movements  of  this  member  are  visibly  embarrassed,  the  patient  has 
lost  the  ability  to  make  those  more  delicate  manipulations  of  it  which  are  essen- 
tial to  normal  speech.  This  disturbance  of  articulation  is  termed  articulatory 
disturbance  of  speech  (alalia  or  anarthria). 

By  the  time  this  has  become  somcAvhat  marked,  it  is  usually  possible  to  detect, 
on  close  examination,  that  the  tongue  is  beginning  to  atrophy.  It  seems  flabby, 
thin,  and  less  rounded.  Here  and  there  its  surface  presents  furrows  and  depres- 
sions ;  and  often  the  individual  fasciculi  exhibit  active  fibrillary  contractions. 

[  *  Except  as  otherwise  specified,  the  letters  and  words  used  as  examples  her6  and  later  on  are  to  be 
given  the  ordinary  English  pronunciation. — K.] 


1040  DISEASES    OE    THE    I^^EEVOUS    SYSTEM 

Just  as  in  progressive  muscular  atrophy,  the  impairment  of  motion  usually 
keeps  equal  pace  '^  with  the  atrophy.  The  greater  the  atrophy,  the  less  is  the 
mobility.  Finally  it  becomes  quite  impossible  to  project  the  tongue  from  the 
mouth  or  move  it  from  side  to  side.  The  tongue  lies  flat  and  limp  on  the  floor  of 
the  mouth.  Its  surface  is  often  diversified  with  furrows  and  depressions,  contain- 
ing much  desquamated  epithelium  or  the  like.  Evidently  any  great  impairment 
of  motility  in  the  tongue  hinders  not  only  speaking,  but  also  chewing  and  swal- 
lowing. The  org'an  can  no  longer  bring  out  such  portions  of  the  food  as  get 
between  the  cheeks  and  the  teeth,  nor  can  it  push  the  bolus  backward  within  the 
grasp  of  the  pharyngeal  constrictors. 

Even  before  the  atrophy  of  the  tongue  becomes  extreme,  analogous  disturb- 
ances usually  appear  in  neighboring  groups  of  muscles.  As  a  rule,  the  muscles  of 
the  lips  are  affected  next  after  the  tongue.  The  fii'st  thing  the  patient  notices  is 
a  peculiar  feeling  of  stiffness  or  tension  in  the  lips.  Movement  becomes  gradually 
more  and  more  difficult;  and  the  patient  becomes  unable  to  pucker  his  lips  so 
as  to  whistle.  Speech  is  also  noticeably  interfered  with,  for  now  all  those  letters 
the  pronunciation  of  which  demands  labial  movements  are  very  imperfectly  artic- 
ulated, and  at  last  they  can  not  be  uttered  at  all.  These  are  O,  A  (long),  P,  F,  B, 
M,  and  V;  and  also  the  sound  of  double  O,  as  in  tool.  It  also  becomes  gradually 
evident  that  the  lips  atrophy.  They  grow  thin,  with  sharp  edges  and  wrinkled 
skin.    Fibrillary  contractions  are  not  infrequently  visible. 

This  atrophy  of  the  lips  (orbicularis  oris)  is  followed  by  atrophy  and  paresis 
of  some  of  the  other  muscles  of  expression  supplied  by  the  lower  division  of  the 
facial  nerve.  The  general  facial  expression  of  a  patient  with  bulbar  paralysis 
thus  comes  to  bear  a  very  characteristic  stamp :  the  mouth  remains  half  open,  and 
seems  to  be  broadened,  the  corners  of  the  mouth  are  drawn  down,  and  the 
lower  lip  hangs  down,  so  that  the  whole  aspect  is  persistently  lachrymose.  Even 
in  laughing,  the  lower  half  of  the  face  relaxes  comparatively  little;  while  the 
region  supplied  by  the  upper  division  of  the  facial  nerve,  and  the  movements  of 
the  eyeball,  remain  as  a  rule  perfectly  normal. 

The  third  group  of  muscles  affected  are  those  of  the  pharynx  and  larynx. 
The  soft  palate  becomes  paretic,  and  produces  further  trouble  in  swallowing. 
Quite  often  the  liquid  ing'esta  are  regurgitated  throug'h  the  nose.  The  voice 
hecomes  nasal.  The  production  of  many  sounds,  and  in  particular  of  B  and  P, 
is  now  impossible,  since,  in  addition  to  the  labial  paresis,  a  portion  of  the  essen- 
tial current  of  air  escapes  through  the  nostrils.  This  explains  why  the  letters 
mentioned  can  sometimes  be  pronounced  better  if  the  nose  be  compressed.  The 
paralysis  of  the  constrictors  of  the  pharynx  impedes  deglutition  more  and  more, 
till  the  impairment  of  nutrition  becomes  extreme. 

The  enfeebled  action  of  the  laryngeal  muscles  is  betrayed,  in  the  earlier 
stages  of  the  disease,  by  a  certain  weakness  and  monotony  in  speaking.  Modula- 
tions of  the  voice,  and  the  production  of  the  hig'her  notes,  as  in  singling,  are  no 
long-er  possible.  If  the  inneiwation  of  the  larynx  becomes  still  more  impaired,  it 
becomes  a  very  serious  matter.  If  the  arytsenoid  cartilages  do  not  press  together 
firmly  on  swallowing,  the  entrance  to  the  larj-nx  is  inadequately  closed,  and  food 
is  often  swallowed  the  wrong  way.  Liquid  and  even  solid  ingesta  get  into  the 
larynx,  and  excite  a  violent  cough;  or,  being  inhaled  into  the  air-passages,  they 
cause  bronchitis  or  lobular  pneumonia.     The  paralysis  may  reach  such  a  degree 

*  At  the  commencement  of  the  disease  the  paralysis  may  possibly  seem  greater  than  the  atrophy, 
so  far  as  the  latter  can  be  detected.  Nor  would  it  be  impossible  for  a  primary  lesion  of  the  nuclei  of 
nerves  to  result  in  a  paralysis  before  the  secondary  descending  degeneration  had  become  completely 
developed,  or  for  the  degeneration  to  begin  in  the  corresponding  central  neurones.  On  the  other 
hand,  it  must  be  borne  in  mind  that  numerous  individual  fibers  in  the  lip  or  tongue  might  be  already 
atrophied  before  the  eye  or  the  touch  could  appreciate  any  change  in  bulk. 


PEOGRESSIYE  BULBAR  PARALYSIS         1041 

that  the  voice  is  at  best  a  hoarse  whisper.  With  the  laryngoscope  we  can  see  that 
the  vocal  cords  are  paralyzed.  The  inability  to  close  the  glottis  tightly  is  ex- 
tremely unfavorable,  for  it  renders  the  patient  unable  to  cough  vigorously.  Mu- 
cous accumulations  may  therefore  come  to  be  the  source  of  extreme  dyspnoea. 

The  catalogue  of  symptoms  is  not  yet  ended.  As  we  have  seen,  the  muscular 
atrophy  of  the  tongue  and  lips  can  invariably  be  detected.  That  of  the  pharyn- 
geal and  laryngeal  muscles  can  not  be  demonstrated  during  life,  although  it  is  to 
be  found  post  mortem.  Inasmuch  as  the  process  is  one  of  genuine  degeneration 
with  consequent  atrophy,  the  affected  fibers  ought  to  give  the  reaction  of  degener- 
ation to  electricity;  but  this  is  difficult  of  actual  proof,  just  as  it  is  in  progressive 
muscular  atrophy,  because  numerous  healthy  fibers  lie  side  by  side  with  the 
degenerated  ones.  Still,  in  an  advanced  case,  careful  examination  will  usually 
bring  out  an  evident  degenerative  reaction  here  and  there  in  the  tongue  and  lips. 

The  disturbance  of  reflex  action  is  often  striking.  Usually  the  reflexes  are 
g'reatly  diminished  or  even  absent,  so  that  one  can  tickle  the  root  of  the  tongue 
and  the  epiglottis  without  causing  the  patient  to  gag.  In- a  few  instances  the 
facial  muscles  exhibit  an  increase  of  tendon  reflex,  as  can  be  shown  by  tapping 
upon  the  tendons,  the  periosteum  of  the  jaws,  or  the  bridge  of  the  nose.  This 
behavior  reminds  one  of  the  condition  of  the  muscles  in  amyotrophic  lateral 
sclerosis  (q.  v.). 

Exceptionally,  still  other  muscular  groups  are  involved.  Of  such  disturbances, 
the  most  frequent  is  in  the  region  supplied  by  the  motor  branch  of  the  trigeminus, 
impairing  mastication.  The  impairment  of  these  muscles  now  combines  with  the 
labial  and  lingual  atrophy  to  render  chewing  almost  impossible.  In  very  rare 
•cases  the  ocular  muscles  are  also  involved,  with  resulting  ptosis  and  strabismus. 

All  the  symptoms  thus  far  enumerated  are  exclusively  motor.  Sensation  is 
perfect  to  the  end.  The  sensibility  of  the  skin  of  the  face  and  of  the  mucous 
membrane  of  the  tongue  and  mouth,  as  well  as  the  sense  of  taste,  are  unimpaired. 
Disturbances  of  sensation  in  the  distribution  of  the  trigeminus,  and  more  or  less 
■deafness,  have  been  reported  in  one  or  two  cases ;  but  there  is  some  doubt  about 
the  observations.  It  does,  however,  seem  certain  that  secretory  and  vaso-motor 
derangements  are  frequent.  Salivation  deserves  especial  mention.  In  many 
<3ases  of  bulbar  paralysis  it  is  a  constant  symptom,  so  that  the  patient  is  obliged 
to  keep  a  pocket-handkerchief  to  his  mouth,  to  catch  the  fluid  as  it  dribbles  away. 
This  is  due,  to  a  certain  extent,  to  the  fact  that  the  secreted  saliva  can  not  be 
swallowed,  and,  as  the  lips  do  not  shut  tightly,  it  naturally  escapes  from  the 
mouth;  but  volumetric  examinations  have  rendered  it  pretty  certain  that  the 
amount  of  saliva  is  abnormally  large.  The  explanation  of  this  has  not  been 
■determined.  !N^or  as  yet  do  we  know  much  about  the  vaso-motor  disturbances. 
Many  patients  complain  of  a  feeling  of  heat  and  "boiling  "  in  the  head.  We 
may  also  mention  in  this  connection  that  occasionally,  toward  the  close  of  the 
■disease,  the  pulse  becomes  very  rapid  (140-160).  This  is  probably  due  to  paralysis 
of  the  vagus. 

The  course  of  the  disease  is  invariably  protracted.  The  order  in  which  the 
symptoms  appear  is,  as  a  rule,  that  in  which  they  have  just  been  described.  The 
atrophy  and  paresis  appear  first  in  the  tongue,  then  in  the  lips  and  the  neighbor- 
ing muscles  of  the  face,  and  lastly  in  the  muscles  of  the  soft  palate,  pharynx,  and 
larynx.  Still,  there  may  be  some  deviation  from  this.  Usually  the  progress  of 
the  disease  is  very  gradual.  There  may  be  an  apparent  arrest  of  the  trouble;  or 
less  often  there  are  quite  sudden  exacerbations.  When  all  the  different  symptoms 
are  well  developed,  the  clinical  picture  is  unusually  characteristic.  The  peculiar 
immobility  of  expression ;  the  broad,  slightly  gaping  mouth,  with  the  atrophied 
lips ;  the  almost  unintelligible  speech,  low,  monotonous,  and  labored ;  and  the 
inability  to  swallow — these  often  betray  the  disease  at  once.  The  last  stage  of 
66 


1042 


DISEASES    OF    THE   l^EEVOUS    SYSTEM 


the  illness  is  the  more  distressing,  in  that  the  intelligence  remains  to  the  end 
entirely  unclouded. 

The  entire  duration  of  the  disease  is  usually  several  years — perhaps  two  to  five. 
If  death  is  not  caused  by  some  intercurrent  trouble,  it  is  brought  about  in  one  of 
three  ways :  either  through  inanition,  due  to  the  increasing  difficulty  of  degluti- 
tion; or  through  pulmonary  complications — namely,  bronchitis,  lobular  pneu- 
monia, or  gangrene,  as  a  result  of  food  passing  down  the  trachea ;  or  through  sud- 
den asphyxia  or  cardiac  failure. 

Pathology.  Nature  of  the  Disease,  and  its  Appearance  as  a  Symptom  of 
Progressive  Muscular  Atrophy  or  of  Amyotrophic  Lateral  Sclerosis. — If  we  seek 
the  anatomical  lesion  corresponding  to  the  group  of  symptoms  above  depicted,  we 
shall  find,  on  microscopic  examination  of  the  nervous  system,  in  all  cases  of  this 
description,  a  typical  disease  of  the  medulla  oblongata.  The  ganglionic  nuclei 
and  the  nerves  (compare  the  accompanying  anatomical  diagram.  Fig.  166),  corre- 
sponding to  those  muscles  which  we  have  found  to  undergo  atrophy  in  bulbar 
paralysis,  present  distinct  evidences  of  degeneration.  This  is  most  readily  dem- 
onstrated in  the  nucleus  of  the  hypoglossus.  The  ganglionic  cells  have  some  of 
them  entirely  disappeared,  while  others  are  greatly  atrophied.  The  connective 
tissue  is  increased  in  amount,  and  the  walls  of  the  blood-vessels  traversing  the 
nucleus  are  thickened.  In  the  earlier  stages  there  are  often  many  cells  which 
contain  granules  of  fat.    The  same  changes,  though  perhaps  less  pronounced,  are 


^22r.  IS. -a. 


Fig.  166.— The  position  of  the  nuclei  of  the  cranial  nerves.  The  medulla  oblongata  and  the  pons  are  sup- 
posed to  be  transparent.  The  nuclei  of  origin  (motor)  are  black,  the  terminal  nuclei; (sensory)  are. red. 
(From  Edinger.) 


exhibited  by  the  common  nucleus  of  the  vagus  and  accessorius,  that  of  the  facial, 
and  sometimes  also  that  of  the  glosso-pharyngeal  nerve.  The  other  nuclei  are 
perfectly  normal.  We  never  find  a  diffuse  "  inflammation,"  but  in  every  case  a 
primary  degeneration  of  the  nuclei,  which  spreads  no  farther. 

Starting  from  these  nuclei,  the  degeneration  and  atrophy  may  be  seen  to 
extend  into  the  nerve-fibers  which  issue  from  them.  The  roots  of  the  hypo- 
glossus, vagus,  accessory,  and  facial  nerves  can  often  be  seen  by  the  naked  eye  to 
be  diminished  in  size  and  of  a  gray  color.  The  microscope  always  shows  a  partial 
atrophy  of  their  fibers.  Finally,  there  is  a  corresponding  atrophy  of  muscles  of 
the  tongue,  lips,  and  other  parts.  "We  need  not  enter  into  detail,  for  the  histo- 
logical conditions  are  precisely  those  seen  in  the  muscles  of  the  trunk  and  ex- 
tremities in  the  spinal  form  of  progressive  muscular  atrophy. 

Thus  we  find  progressive  bulbar  paralysis  perfectly  analogous  with  progressive 
muscular  atrophy.    The  motor  nuclei  in  the  medulla  oblongata  are  the  motor  and 


PEOGEESSIVE   BULBAE   PAEALYSIS  1043 

trophic  centers  of  the  bulbar  nerves  and  of  the  muscles  which  these  nerves  supply. 
The  relation  is  precisely  the  same  as  exists  between  the  anterior  cornua  of  the 
spinal  cord  on  the  one  hand,  and  the  spinal  nerves  and  the  muscles  which  they 
innei-vate  on  the  other.  In  both  diseases  there  is  a  degenerative  atrophy  of  the 
individual  neuro-muscular  elements,  the  so-called  neurones  (consisting  of  nerve- 
cells  and  peripheral  nerve-fibers),  and  their  corresponding  muscular  fibers.  In 
both  diseases  the  atrophy  and  the  functional  disability  of  the  muscles  keep  pace 
with  each  other,  and  in  both  the  affection  is  limited  strictly  to  the  motor  tract, 
sensibility  suffering  no  impairment  whatever.  Certain  questions  about  bulbar 
paralysis  are  as  unsettled  as  similar  ones  about  progressive  muscular  atrophy. 
It  is  uncertain  whether  the  primary  degenerative  process  is  limited  to  the  bulbar 
nuclei,  and  the  degeneration  of  the  nerves  and  muscles  is  to  be  regarded  as  sec- 
ondary; or  whether  the  entire  motor  apparatus,  from  the  ganglionic  cell  to  the 
muscular  fiber,  is  simultaneously  attacked ;  or,  finally,  whether  the  atrophy  begins 
in  the  muscle  and  involves  the  corresponding  nerve-fiber  and  nerve-cell  only  in 
its  further  progress.  We  think  it  improbable  that  these  points  will  be  cleared 
up  verj^  speedily.    Their  solution  would  seem  to  be  only  of  theoretical  interest. 

We  certainly  must  recog'nize,  however,  the  essential  identity  of  progressive 
bulbar  paralysis  and  progressive  muscular  atrophy.  The  resemblance  becomes 
even  more  striking  if  we  consider  that  very  frequently  both  diseases  are  present 
simultaneously.  Often,  after  a  case  of  progressive  muscular  atrophy  has  lasted 
for  some  time,  the  symptoms  of  bulbar  paralysis  also  appear.  On  the  other 
hand,  an  illness  may  begin  with  bulbar  symptoms,  and  later  on.  be  complicated  by 
atrophy  of  the  muscles  of  the  extremities — almost  always  seen  first  in  the  arms. 
If  cases  of  this  sort  come  to  aiitopsy,  we  find  a  combination  of  the  anatomical 
lesions  of  both  diseases;  in  addition  to  the  degeneration  of  the  nuclei  in  the 
medulla  oblongata,  there  is  marked  atrophy  of  the  ganglionic  cells  in  correspond- 
ing places  in  the  anterior  gray  cornua  of  the  spinal  cord. 

Progressive  bulbar  paralysis  has  as  close  a  relation  to  amyotrophic  lateral  scle- 
rosis (vide  page  986)  as  to  progressive  spinal  muscular  atrophy.  Amyotrophic 
lateral  sclerosis  is  at  first  situated,  as  a  rule,  only  in  the  portions  of  the  motor 
conducting  system,  including  the  pyramidal  tracts,  which  supply  the  extremities ; 
but  finally  there  is  very  often  an  involvement  of  the  motor  bulbar  nuclei — that  is, 
bulbar  paralysis  sets  in.  It  seems  justifiable,  therefore,  to  say  that  these  three 
diseases — progressive  bulbar  paralysis,  progressive  spinal  muscular  atrophy,  and 
amyotrophic  lateral  sclerosis — differing  as  they  do  in  the  localization  of  their 
lesions,  are  yet  closely  allied.  They  are  to  be  regarded  as  manifestations  of  one 
morbid  process  which  is  probably  essentially  the  same  in  its  pathology  and  aeti- 
ology. We  do  not  know  the  special  cause  of  this  process  of  degeneration.  In 
many  cases,  although  perhaps  not  in  all,  we  must  finally  assume  a  congenital 
weakness  of  the  affected  nerve  territory.  Such  a  defective  nerve  territoiy  suc- 
cumbs prematurely  to  the  injurious  influences  which  either  are  associated  with 
the  normal  functions  themselves  or  act  upon  them  from  without  in  some  other 
fashion.  At  any  rate,  there  is  always  a  primary  chronic  degeneration  of  portions 
of  the  main  motor  conducting  tract,  in  one  or  another  area  and  varying  extent.  If 
we  accustom  ourselves  to  regard  these  three  groups  of  symptoms  as  really  identi- 
cal, we  shall  be  less  puzzled  by  the  slight  variations  which  different  cases  may 
present  than  if  we  attempt  to  differentiate  the  disorders  too  nicely  on  account  of 
unessential  variations. 

Diagnosis. — The  diagnosis  of  a  typical  case  of  progressive  bulbar  paralysis  has 
no  difficulties,  if  we  only  hold  firmly  to  the  definition  of  the  disease  and  its  symp- 
toms as  above  depicted.  Upon  careful  examination  of  the  other  muscles,  and  con- 
sideration of  the  course  of  the  disease  as  a  whole,  we  shall  be  able  in  each  case  to 
determine  whether  the  bulbar  trouble  is  the  sole  disease,  or  merely  a  part  of  a 


104:4  DISEASES    OF   THE    NEEVOUS    SYSTEM 

more  extended  degeneration  of  the  motor  tract.  If  there  are  no  symptoms  but 
those  referable  to  the  medulla  oblongata,  we  must  bear  in  mind  that  the  phe- 
nomena of  genuine  progressive  bulbar  paralysis  may  be  closely  simulated  by  other 
bulbar  diseases.  The  acute  troubles,  such  as  thrombosis  or  haemorrhage,  although 
they  produce  similar  symptoms,  can  easily  be  differentiated  by  the  manner  of 
their  appearance,  contrasting  with  the  invariably  slow  development  of  genuine 
bulbar  paralysis.  It  is,  however,  much  more  difficult  to  eliminate  gradually  form- 
ing tumors  situated  in  the  medulla  oblongata  or  its  vicinity.  Here  prolonged 
observation  is  frequently  needed,  until  finally  such  phenomena  appear  as  are  for- 
eign to  typical  bulbar  paralysis.  Such  symptoms  are  disturbances  of  sensation 
and  invasion  of  the  upper  division  of  the  facial,  the  nerves  of  special  sense,  and 
the  ocular  muscles.  The  same  is  true  of  that  rare  trouble,  diffuse  sclerosis  of  the 
medulla  oblongata. 

It  should  also  be  mentioned  that  bilateral  cerebral  trouble  may  occasion  so 
complete  a  paralysis  of  the  tongue  and  lips,  according  to  Lepine  and  others,  as  to 
simulate  bulbar  paralysis.  Such  cases  have  been  termed  "  glosso-labio-pharyngeal 
paralysis  of  cerebral  origin,"  or  pseudo-bulbar  paralysis.  Indeed,  in  rare  in- 
stances, a  similar  group  of  symptoms  seems  to  be  referable  to  unilateral  cerebral 
disturbances.  This  is  explained  by  assuming  that  the  muscles  involved  upon  both 
sides  receive  at  least  a  portion  of  their  motor  nervous  fibers  from  the  same  hemi- 
sphere. And  yet  in  most  of  these  cases  of  pseudo-bulbar  paralysis  the  exclusion 
of  the  genuine  disease  is  possible,  because  certain  variations  from  the  typical 
course  of  the  disease  are  pronounced  enoug'h  to  set  us  right.  Thus  there  is  an 
apoplectic  onset  or  repeated  apoplectiform  attacks.  The  paralysis  is  not  perfectly 
symmetrical.  There  is  also  paralysis  of  the  extremities  on  one  or  both  sides.  The 
lips  and  tongue  react  normally  to  electricity  without  much  atrophy,  or  there  are 
marked  signs  of  mental  weakness.  In  most  cases  there  is  an  extensive  arterio- 
sclerosis at  the  bottom  of  the  whole  morbid  process,  for  the  sclerosis  of  the  cere- 
bral arteries  often  leads  to  multiple  foci  of  softening  or  to  multiple  haemorrhages. 

Prognosis  and  Treatment. — Despite  th,e  unfavorable  prognosis  of  progressive 
bulbar  paralysis,  we  must  at  least  try  to  check  the  progress  of  the  disease.  Elec- 
tricity may  perhaps  be  regarded  as  the  most  promising  means  to  employ.  To  in- 
fluence the  seat  of  the  trouble,  galvanization  is  chiefly  used.  The  poles  are  applied 
to  the  two  mastoid  processes,  every  day  if  possible,  for  two  or  three  minutes,  and 
the  current  is  repeatedly  reversed.  We  may  also  galvanize  the  sympathetic 
nerve  and  the  affected  muscles  of  the  lips  and  tongue.  Upon  the  muscles  the 
faradic  current  may  also  be  tried.  When  deglutition  begins  to  be  impaired,  it  is 
an  excellent  thing  to  excite  the  action  of  swallowing,  by  galvanism.  For  this  the 
anode  is  placed  upon  the  nape  of  the  neck,  and  the  cathode  upon  one  side  of  the 
larynx.  At  every  cathodic  closure  (IvaS),  or  every  time  that  the  cathode  is 
passed  across  the  side  of  the  larynx,  there  is  a  reflex  act  of  deglutition.  The  cur- 
rent should  be  of  medium  strength. 

It  may  be  well  to  prescribe  further  a  resort  to  treatment  by  baths,  or  the 
"  cold-water  cure  "  may  be  cautiously  tried,  but  we  should  not  expect  either  of 
these  procedures  to  have  any  special  influence  on  the  disease.  The  same  internal 
remedies  are  recommended  as  in  the  chronic  diseases  of  the  cord,  especially  argen- 
tic nitrate,  ergotine,  and  potassic  iodide.  For  salivation,  atropine  may  prove 
beneficial,  in  pills  of  tftt  of  a  grain  (gramme  0.0005),  three  or  four  to  be  taken 
daily. 

The  way  of  giving  nourishment  is  important  if  deglutition  is  impaired.  We 
should  try  carefully  to  avoid  having  the  food  go  down  the  wrong  way,  lest  pul- 
monary complications  ensue.  It  is  therefore  wise  not  to  defer  the  use  of  the  stom- 
ach-tube too  long,  •  through  which  we  may  introduce  milk,  eggs,  wine,  and  the 
various  infant  foods. 


EAEER   EOEMS    OF   CHRONIC   BULBAR   PARALYSIS       1045 

In  the  distressing  close  of  the  disease,  narcotics  must  be  exhibited  to  lessen 
the  patient's  suffering,  at  least  as  far  as  we  can. 


CHAPTER   II 


THE  RARER  FORMS  OF  CHRONIC  BULBAR  PARALYSIS,   PROGRESSIVE 
OPHTHALMOPLEGIA    AND    ASTHENIC    BULBAR    PARALYSIS 

1.  Progressive  Ophthalmoplegia 

As  we  have  seen,  the  form  of  chronic  bulbar  paralysis  described  in  the  pre- 
vious chapter  as  "  typical,"  is  practically  limited  in  its  effects  to  the  distribution 
of  the  hypoglossus,  the  labial  division  of  the  facial,  and  the  pharyngeal  muscles. 
Possibly  the  reason  it  extends  no  farther  is  merely  that  death  is  so  speedy.  But 
there  are  a  few  rare  cases  where  the  chronic  degenerative  process  comes  to  in- 
volve other  motor  nuclei,  together  with  the  corresponding  nerve-fibers  and  muscles. 
Of  course  the  clinical  phenomena  of  these  cases  vary  from  the  ordinary ;  and  yet 
there  is  no  real  reason  to  distinguish  them  from  common  bulbar  paralysis,  par- 
ticularly as  all  sorts  of  transitional  forms  are  to  be  observed.  Thus,  we  have  our- 
selves noticed  that  there  is  sometimes  a  symmetrical  and  slowly  progressive 
paresis  of  the  upper  division  of  the  facial,  and  in  particular  of  that  portion  which 
supplies  the  cheek,  complicating  the  glosso-pharyngeal  paralysis.  In  other  cases 
we  have  seen  the  degeneration  attack  from  the  start  the  entire  distribution  of 
the  facial,  gradually  producing  a  complete  "  diplegia  facialis.'^  Sometimes,  also, 
the  ordinary  symptoms  of  bulbar  paralysis  are  accompanied  by  disturbances  in 
the  area  of  distribution  of  the  ocular  nerves,  probably  the  result  of  degeneration 
of  the  corresponding  nerve-nuclei  (see  Fig.  166,  page  1042). 

What  seems  very  remarkable  is  that  the  process  may  be  confined  entirely  to 
the  ocular  muscles.  A.  von  Graefe  named  this  condition  progressive  ophthalmo- 
plegia. Another  name  is  "  anterior  bulbar  paralysis."  In  this  form  a  bilateral 
paralysis  of  all  the  external  ocular  muscles  progresses  with  extreme  slowness  and 
is  perfectly  symmetrical.  The  movements  of  the  eye  are  therefore  impaired  in  all 
directions.  Diplopia  is  never  present.  The  pupil  reacts  to  light,  and  almost 
always  the  power  of  accommodation  is  preserved.  Finally  both  eyeballs  become 
absohitely  motionless,  and  there  is  a  well-marked  though  incomplete  ptosis.  There 
is,  beyond  a  doubt,  a  progressive  degeneration  of  the  nuclei  and  fibers  of  the  cor- 
responding nerves — that  is,  the  abducens  and  motor  oculi;  but  with  these  the 
process  may  stop,  spreading  no  farther.  We  have  ourselves  lately  met  with  a 
patient  who  presented  total  bilateral  ophthalmoplegia,  in  whom  the  condition  had 
existed  without  the  slightest  change  for  fifteen  years.  Besides  the  oculo-motor 
paralysis  the  muscles  of  the  face  (Fig.  167)  and  even  those  of  the  body  are  some- 
times involved.  On  the  other  hand,  in  a  few  cases  the  process  seems  to  be  lim- 
ited to  only  a  part  of  the  oculo-motor  nerves  (as  the  abducens). 

The  diagnosis  of  genuine  progressive  ophthalmoplegia  is  usually  easy,  if  we 
hold  strictly  to  the  definition  of  the  disease  as  a  degeneration  of  the  motor  nuclei 
and  nerves  exclusively  (that  is,  completely  analogous  to  progressive  spinal  mus- 
cular atrophy  and  bulbar  paralysis).  We  shall  thus  avoid  confusing  it  with  those 
cases  in  which  progressive  ophthalmoplegia  occurs  as  one  s.\Tnptom  of  a  compli- 
cated morbid  process  of  quite  a  different  sort.  Thus  we  must  bear  in  mind  par- 
ticularly that  tabes  and  general  paralysis  may  lead  to  complete  ophthalmoplegia. 
To  these  cases  may  be  added  those  that  follow  sji)hilitic  infection.     Multiple 


1046 


DISEASES    OE    THE    XEEYOUS    SYSTE:^: 


sclerosis  may  also  lead  to   almost   coBiplete   ophthalmoplegia;  and.  finally,   the 
same  symptom-complex  has  been  observed  as  a  post-diphtheritic  nervous  disease. 

The  progressive  ophthalmoplegias  which  develop  after  birth  are  also  to  be 
distinguished  from  the  congenital  defects  in  the  movements  of  the  eyes.     Com- 


FiG.  .167. — Progressivi 


jplithalmoplegia.     l'aral\>i>  uf  both  eyeballs  with  bilateral  ptosis.    'Weakuess  of 
both  I'acial  uerves.    lErlangen  Medical  Clinique.; 


plete  external  ophthalmoplegia  (that  is,  paralysis  of  all  the  external  ocular  mus- 
cles) has  been  repeatedly  obser\-ed  as  a  congenital  condition,  and  also  congenital 
bilateral  abducens  paralysis,  congenital  ptosis,  etc.  Autopsies  of  such  cases  are 
still  lacking.  There  are  probably  defective  conditions  of  the  corresponding  nerve- 
nuclei,  and  perhaps  of  the  nerves  or  muscles  also. 


2.  Asthenic  Bulbar  Paralysis.     Pseudo-paralytic  Myasthexia 

We  will  speak  at  this  point  of  a  very  remarkable  and  peculiar  type  of  disease, 
the  milder  forms  of  which  were  first  described  by  Erb,  and  the  severe  and  fatal 
forms  by  Oppenheim.  The  symptoms  of  the  affection  consist  of  ptosis,  paresis  of 
the  facial  muscles,  and  disturbances  of  mastication,  swallowing,  and  talking.    On 


EARER   FORMS    OF   CHRONIC   BULBAR   PARALYSIS       1047 

more  careful  observation  it  is  seen  that  these  symptoms  are  only  in  part  uniform 
and  persistent,  but  that  they  are  due  chiefly  to  an  extremely  rapid  fatigue  and 
exhaustion  of  the  affected  muscles  (Goldflam).  Such  a  patient  can,  for  instance, 
utter  a  few  sentences  quite  plainly,  but,  if  he  continues  to  talk,  his  speech  grows 
more  indistinct  and  inarticulate,  and  finally  it  becomes  an  incomprehensible 
lalling-.  The  same  thing  is  seen  in  chewing  and  swallowing:  the  first  mouthfuls 
are  chewed  and  SAvallowed  in  quite  the  normal  fashion,  but  in  a  few  minutes  it 
becomes  wholly  impossible  to  take  any  more  food.  Besides  these  "  bulbar  "  symp- 
toms, which  at  first  are  the  most  striking,  we  also  see  very  similar  symptoms  in 
the  muscles  of  the  extremities ;  usually  the  same  rapid  fatigue  progressing  to  the 
most  complete  failure  of  their  function.  One  of  our  patients,  if  she  had  pre- 
viously rested,  could  go  up  a  flight  of  stairs  very  well,  but  on  the  second  attempt 
she  had  to  take  hold  of  the  banisters,  and  the  third  or  fourth  attempt  failed  com- 
pletely on  account  of  the  complete  muscular  weakness  that  ensued. 

As  Jolly  has  found,  we  can  detect  this  same  abnormal  fatigue  by  continued 
faradic  stimulation  of  the  muscles. 

This  clinical  condition  permits  us  to  draw  the  conclusion  that  there  is  no 
permanent  and  complete  atrophy  or  degeneration  of  the  motor  apparatus  as  a 
basis  for  the  clinical  symptoms;  and,  in  fact,  in  those  cases  in  which  death  finally 
ensued  (in  one  or  two  years)  from  choking,  insufiSciency  of  respiration,  etc.,  the 
autopsies  have  thus  far  been  wholly  negative  (hence  the  term  "  bulbar  paralysis 
without  anatomical  lesion").  This  is  also  the  reason  why  in  this  affection  de- 
cided improvement  or  even  complete  recovery  may  occur  after  the  disease  has 
continued  for  several  months,  if  the  functional  impairment  of  the  affected  nerve 
territory  again  disappears.  In  order  to  express  this  distinction  between  the 
bulbar  paralyses  due  to  coarse  anatomical  changes  and  the  merely  functional 
disease  now  in  question,  we  have  proposed  for  the  latter  the  name  of  "  asthenic 
bulbar  paralysis.''  We  must,  however,  note  that  the  disease  is  not  limited  exclu- 
sively to  the  territory  of  the  bulbar  nerves,  although  the  bulbar  disturbances  are 
usually  most  prominent  in  the  clinical  picture.  On  the  other  hand,  there  are 
apparently  some  eases  where  the  abnormal  fatigue  and  the  consequent  symptoms 
occur  only  in  the  extremities,  without  any  implication  of  the  bulbar  muscles. 
For  this  condition  the  name  proposed  by  Jolly,  "  pseudo-paralytic  myasthenia," 
is  more  suitable. 

From  what  has  been  said  above,  the  prognosis  is  to  be  regarded  as  not  abso- 
lutely unfavorable,  but  recurrences  are  to  be  dreaded  even  when  recovery  has 
apparently  set  in.  The  treatment  is  first  of  all  to  provide  the  greatest  physical  rest 
and  care  for  the  patient.  If  it  is  difficult  to  take  food,  nourishment  must  be  given 
cautiously  by  the  a?sophageal  tube.  We  may  try  mild  massage  and  galvaniza- 
tion of  the  muscles,  and  central  galvanization  of  the  spinal  cord  and  medulla 
oblongata.  Internally  we  have  given  strychnine,  arsenic,  and  phosphorus,  without 
any  perceptible  benefit.  On  the  hypothesis  that  the  trouble  was  perhaps  de- 
pendent upon  some  chemical-toxic  influence,  the  cautious  use  of  sweating  has 
also  been  recommended. 

[Family  Periodic  Paralysis.— Goldflam  has  described  a  peculiar  affection, 
first  carefully  studied  by  Westphal,  Avhich  merits  brief  mention.  It  consists  of 
recurring  attacks  of  paralysis,  most  marked  in  the  legs,  associated  with  loss  of 
reflex  and  electrical  excitability,  without  mental  or  sensory  symptoms  and  with 
intervals  of  perfect  health.  Thirty-five  out  of  fifty-three  cases  occurred  in  three 
families,  but  the  families  showed  no  special  signs  of  nervous  degeneracy.  The 
attacks  are  apt  to  begin  at  puberty,  and  they  are  also  apt  to  come  on  during  sleep 
after  some  unusual  muscular  exertion.  The  frequency  of  the  attacks  varies 
greatly,  from  one  or  two  in  a  lifetime  to  several  times  a  week.  The  average  dura- 
tion of  the  individual  attack  is  from  ten  to  forty-eight  hours.     The  attacks  begin 


1048  DISEASES    OF    THE    NERVOUS    SYSTEM 

somewiiat  gradually,  usually  in  the  legs,  and  they  may  increase  to  complete  paraly- 
sis of  all  the  muscles  of  the  limbs,  body,  and  neck.  The  cranial  nerves  are  rarely 
involved.  The  deep  reflexes  are  abolished,  and  the  plantar  reflex  is  often  absent. 
There  is  a  quantitative  diminution  of  electrical  reactions,  sometimes  amounting 
to  complete  abolition,  but  there  is  no  reaction  of  degeneration.  The  mechanical 
irritability  of  muscles  and  nerves  is  also  lost.  In  two  cases  the  heart  became 
enlarged  during  the  attack.  The  sphincters  are  not  affected.  The  pathology  is. 
wholly  unknown.  Goldflam  believes  that  the  trouble  is  in  some  way  connected 
with  the  muscular  dystrophies.  The  prognosis  is  good  so  far  as  life  is  concerned,, 
but  the  attacks  usually  recur  through  life.     Treatment  is  unavailing. — K.] 


CHAPTER  III 
ACtTTE    AND    APOPLECTIFORM    BULBAR    PARALYSIS 

1.    HAEMORRHAGE   INTO    THE    MeDULLA    OBLONGATA   AND   THE   PoNS 

HEMORRHAGE  into  the  medulla  oblongata  and  the  pons  is  much  more  frequent 
than  into  the  spinal  cord,  but  it  is  much  rarer  than  cerebral  haemorrhage.  As  to 
its  production,  the  same  views  are  held  as  will  be  considered  in  detail  under  cere- 
bral haemorrhage,  in  the  next  section.  In  the  first  place,  there  is  probably  always 
some  disease  of  the  blood-vessels — that  is,  atheroma  or  miliary  aneurism — and 
then  some  factor  productive  of  increased  arterial  tension.  There  may  be  cardiac 
hypertrophy,  nephritis,  excessive  bodily  exertion,  or  alcoholism.  Now  and  then 
injuries  of  the  occiput  are  followed  by  an  effusion  into  the  medulla.  It  is  not  rare 
to  have  secondary  and  usually  small  ecchymoses  in  acute  inflammation  of  the 
spinal  cord  (vide  infra),  and  in  purulent  meningitis,  or  in  connection  with  new 
growths  which  are  richly  vascular. 

The  anatomical  conditions  produced  by  bulbar  haemorrhage  are  so  completely 
analogous  with  those  of  cerebral  haemorrhage  that  the  reader  may  safely  be 
referred  to  the  succeeding  section  about  these  also.  The  size  of  the  lesion  varies 
greatly.  Bleeding  extensive  enough  to  affect  the  greater  part  of  a  transverse  sec- 
tion is  more  frequent  in  the  pons  than  in  the  medulla  oblongata.  If  the  blood 
is  poured  out  close  under  the  floor  of  the  fourth  ventricle,  as  has  been  repeatedly 
observed,  it  may  break  into  the  ventricle.  If  death  be  not  speedy,  the  blood  is- 
mostly  absorbed,  and  in  its  place  develops  either  an  "  apoplectic  scar  "  or  an  apo- 
plectic cyst. 

There  may  be  slight  prodromata,  but  the  real  symptoms  of  bulbar  haemorrhage 
are  very  sudden.  There  is  almost  always  a  pronounced  apoplectic  seizure.  The 
patient  has  a  shock,  falls  down,  and  becomes  dizzy  or  even  unconscious.  In  other 
cases  there  may  be  headache,  vomiting,  tinnitus  aurium,  and  clonic  spasms,  or 
even  a  typical  epileptiform  attack. 

In  most  cases  death  is  speedy,  if  not  immediate.  This  is  probably  due  in  every 
instance  to  grave  lesions  of  the  respiratory  and  circulatory  centers,  rendering 
continued  existence  impossible.  Sometimes  the  initial  symptoms  abate,  where- 
upon the  local  results  of  the  lesion  become  appreciable. 

The  first  characteristic  feature  of  bulbar  paralyses  now  manifests  itself,  that 
disturbances  are  particularly  great  in  the  distribution  of  the  bulbar  nerves, 
while  in  cerebral  apoplexy  they  never  appear  in  the  same  way.  Another  point 
is,  that  these  paralytic  symptoms  are  combined  with  paralysis  of  the  extremities 
in  a  peculiar  way,  as  a  result  of  the  anatomical  relations.     For  the  same  reason. 


ACUTE  AND  APOPLECTIFOKM  BULBAR  PARALYSIS   104^ 


the  order  of  the  paralysis  in  the  extremities  may  also  be  peculiar.  Of  the  bulbar 
paralyses  we  may  mention  more  or  less  complete  paralysis  of  the  tongue,  and  a 
consequent  difficulty  in  articulation  (anarthria)  ;  frequent  inability  to  swallow; 
and  paralysis  in  the  distribution  of  the  accessorius,  facial,  and  trigeminus.  If 
there  is  a  lesion  of  the  pyramidal  tracts  in  the  pons  or  medulla,  we  have  paralysis 
of  the  extremities  in  addition  to  the  specific  bulbar  symptoms.  If  the  haemor- 
rhage be  extensive,  all  four  extremities  may  be  more  or  less  completely  paralyzed ; 
but  in  most  instances  the  paralysis  is  unilateral.  In  the  larger  number  of  hsemor- 
rhages  into  the  pons  there  is  crossed  paralysis.  The  paralysis  of  the  extremi- 
ties is  upon  one  side,  and  that  of  the  facial  is  on  the  other  side.  This  is  a  great 
aid  to  diagnosis.  It  is  easy  to  see  how  this  happens  if  we  bear  in  mind  that 
the  cerebral  fibers  of  the  facial  cross  at  a  point  certainly  much  higher  than  the 
decussation  of  the  pyramids,  in  which  latter  place  the  motor  fibers  of  the  ex- 
tremities cross.  Now  a  haemorrhage  may  be  situated  in  one  side  of  the  pons, 
above  the  decussation  of  the  pyramids  but  below  that  of  the  facial.  This  would 
occasion  (vide  Fig.  168,  y)  a  paralysis  of  the  facial  on 
the  same  side  with  the  lesion,  and  of  the  extremities  upon 
the  opposite  side;  but  if  the  lesion  be  higher,  above  the 
place  where  the  facial  crosses  over,  all  the  paralytic  symp- 
toms would  be  on  the  opposite  side  of  the  body  (vide 
Fig.   168,   x). 

In  other,  rarer  instances  we  observe  similar  combina- 
tions; only  some  other  bulbar  nerve  replaces  the  facial, 
such  as  the  hypoglossus  or  abducens.  In  a  few  cases  the 
lesion  is  at  the  very  decussation  of  the  pyramids.  This 
is  extremely  rare  in  haemorrhage,  though  somewhat  more 
frequent  in  troubles  of  a  difl^erent  nature.  The  result 
may  be  that  the  motor  fibers  for  one  extremity  are  cut  off 
before  they  cross,  and  those  of  the  other  extremity  after 
they  have  crossed.  Thus  is  produced  the  rare  phenome- 
non of  a  crossed  hemiplegia — i.  e.,  paralysis  of  the  arm 
on  one  side  and  of  the  leg  on  the  other. 

Disturbances  of  sensation  in  the  skin  of  the  paralyzed 
extremities  sometimes  result  from  trouble  in  the  pons, 
but  they  are  very  seldom  extreme,  and  they  can  not  be 
made  available  for  making  out  the  exact  locality  of  the 
haemorrhage,  since  the  course  of  the  sensory  fibers  through 
the  upper  extremity  of  the  spinal  cord  is  still  almost  un- 
known. The  anaesthesia  sometimes  observed  in  the  distribution  of  the  trigeminus 
is  of  more  value,  as  this  may  be  due  to  a  lesion  of  the  nucleus  or  root  of  the 
nerve. 

There  are  other  symptoms,  which  are  indeed  rare,  but  Avhich  bear  an  impor- 
tant relation  to  certain  nervous  centers  of  the  medulla.  Thus,  there  may  be 
marked  respiratory  disturbance;  the  pulse  may  become  rapid  or  irregular;  there 
may  be  vaso-motor  derangement,  as  shown  by  a  rise  of  the  cutaneous  temperature 
and  by  a  subjective  sensation  of  warmth;  and  occasionally  there  are  temporary 
albuminuria  and  glycosuria.  The  temperature  of  the  body  is  generally  normal  at 
first,  or  nearly  so;  but  in  case  of  a  fatal  termination  it  often  rises  greatly,  even 
to  107.5°  (42°  C.)  or  higher. 

As  to  the  prognosis  of  bulbar  haemorrhage,  speedy  death  has  been  repeatedly 
observed,  as  we  have  said.  If  the  immediate  effects  be  successfully  withstood,  the 
prospect  becomes  more  favorable.  The  effusion  is  gradually  absorbed,  the  symp- 
toms of  compression  abate,  and  there  is  a  steady  progress  toward  comparatively 
good  or  even  perfect  health..   More  often,  however,  some  of  the  paralytic  symp- 


FiG.  168.— Diapfram  of  focal 
diseases  in  the  pons. 
L.  Left.  R.  Right.  P. 
Pons.  Mo.  Medulla  ob- 
longata. DP.  Decussa- 
tion of  the  pyramids. 
E.  Fibers  to  the  ex- 
tremities. F.  Facial 
fibers.  X.  Lesion  in  the- 
upper  half  of  the  pons. 
y.  Lesion  in  the  lower 
half  of  the  pons. 


1050  DISEASES    OF   THE   ITEEVOUS    SYSTEM 

toms  remain  stationary,  either  in  the  distribution  of  the  bulbar  nerves  (the 
lingual  or  pharyngeal),  or  in  the  extremities,  as  shown  by  persistent  hemiplegia. 
If  this  latter  be  the  case,  the  subsequent  contractures  and  other  symptoms  are  the 
same  as  in  ordinary  cerebral  hemiplegia. 

The  diagnosis  of  bulbar  haemorrhage  is  based  upon  the  apoplectic  onset,  and 
upon  the  presence  of  specific  bulbar  symptoms,  such  as  disturbance  of  speech  and 
of  deglutition,  and,  most  characteristic  of  all,  if  it  occur,  a  crossed  hemiplegia. 
The  differential  diagnosis  between  embolism  and  haemorrhage  can  hardly  ever  be 
made  -with  certainty  (vide  infra). 

The  treatment,  not  only  of  the  seizure  but  of  the  persistent  paralysis,  should 
conform  to  the  principles  which  will  hereafter  be  set  forth  in  describing  the 
treatment  of  cerebral  haemorrhage.  If  the  bulbar  nerves  present  obstinate  symp- 
toms, we  must  employ  the  same  means  as  in  chronic  bulbar  paralysis,  the  most 
effective  being  electricity. 

2.  Embolism  and  Thrombosis  of  the  Basilar  Artery 

The  medulla  and  pons  receive  their  blood  chiefly  from  branches  of  the  anterior 
spinal,  vertebral,  and  basilar  arteries.  These  branches  penetrate  the  anterior 
median  fissure  and  then  proceed  to  the  nerve-nuclei.  A  far  smaller  portion  of 
the  circulation  flows  through  the  "  arteries  of  the  roots."  These  are  minute  off- 
shoots of  the  lateral  branches  of  the  basilar  and  vertebral  arteries,  which  enter 
the  cord  at  the  roots  of  the  nerves  and  penetrate  to  the  corresponding  nuclei. 
According  to  Duret,  the  nuclei  of  the  hypoglossal  and  accessory  nerves  are  sup- 
plied from  the  anterior  spinal  and  vertebral  arteries ;  those  of  the  vagus,  glosso- 
pharyngeal, and  auditory  nerves  by  branches  of  the  upper  end  of  the  vertebral 
arteries;  and  the  nuclei  of  the  facial,  trigeminus,  and  the  three  nerves  to  the 
ocular  muscles  by  branches  of  the  basilar.  There  may  be  individual  exceptions  to 
these  rules.  Occlusion  by  embolism  or  thrombosis  of  the  arteries  just  named 
must  occasion  a  secondary  softening  in  corresponding  portions  of  the  medulla, 
and  it  is,  therefore,  a  not  very  infrequent  cause  of  apoplectic,  or  at  least  very 
rapidly  developing,  bulbar  paralysis. 

The  causes  of  thrombosis  or  embolism  in  the  arteries  just  mentioned  are  the 
same  as  we  shall  consider  minutely  when  treating'  of  cerebral  softening.  Emboli 
are  most  frequent  in  cardiac  disease.  They  occur  only  in  the  vertebral  arteries, 
oftenest  in  the  left  one,  and  are  never  primary  in  the  basilar  artery;  but  an 
embolus  may  be  enlarged  by  thrombosis  after  lodging  in  one  of  the  vertebral  arter- 
ies, and  then  block  up  the  basilar.  Thrombosis  is  of  more  frequent  occurrence, 
and  results  from  chronic  changes  in  the  arteries,  mainly  atheroma  or  syphilitic 
endarteritis.  The  latter  disease,  one  favorite  locality  for  which  is  the  basilar 
artery,  is  the  commonest  cause  of  acute  softening  of  the  pons. 

The  anatomical  condition  is  likewise  similar  to  that  in  cerebral  softening 
(q.  v.).  In  the  region  which  is  deprived  of  arterial  blood  by  the  occlusion  of  the 
afiluent  vessel,  the  acute  anaemia  entails  necrosis  and  disintegration  of  tissue.  A 
spot  of  "  softening  "  results,  made  up  mainly  of  vestiges  of  nervous  tissue  and 
numerous  cells  filled  with  granules  of  fat. 

When  the  basilar  artery  is  blocked  up,  the  symptoms  appear  very  suddenly. 
There  is  either  an  apoplectic  seizure,  or  at  least  a  very  rapid  development  of  pa- 
ralysis (occupying  only  a  few  days).  The  symptoms  of  the  first  onset  are,  in  all 
essential  points,  those  of  bulbar  or  even  of  cerebral  apoplexy.  Although  there  is 
usually  no  marked  loss  of  consciousness  in  apoplectic  bulbar  paralysis,  yet  no 
great  diagnostic  significance  can  be  assigned  to  its  absence.  The  siidden  obstnic- 
tion  of  the  basilar  artery  produces  such  a  disturbance  of  the  circulation  even  in 
anterior  portions  of  the  brain  as  may  suspend  consciousness.  In  some  few  in- 
stances this  circulatory  derangement  may  even  give  rise  to  choked  disk,  as  seen 


ACUTE  AND   APOPLECTIFOEM  BULBAE  PAEALYSIS   1051 

by  the  ophthalmoscope.  Often  there  are  noticeable  respiratory  and  cardiac  symp- 
toms, such  as  Cheyne-Stokes  respiration,  and  rapid  pulse. 

If  death  be  not  immediate,  and  we  are  therefore  enabled  to  make  out  the  symp- 
toms due  to  the  local  disturbance,  we  usually  observe  the  same  phenomena  as  have 
just  been  described  under  bulbar  hsemorrhage.  There  is  sometimes  paralysis  of 
all  the  extremities,  but  usually  there  is  trouble  only  upon  one  side.  Then  we 
have  the  characteristic  crossed  hemiplegia.  The  facial  nerve  or  the  nerves  of  the 
ocular  muscles  may  be  paralyzed.  It  has  repeatedly  happened  that  the  paralysis 
seemed  at  first  much  greater  upon  one  side,  but  after  a  few  days  changed  over  to 
the  opposite  one.  This  must  be  due  to  changes  in  the  circulation;  the  thrombus 
grows  larger,  or  a  collateral  circulation  is  developed.  The  specific  bulbar  symp- 
toms are  the  familiar  ones  of  all  bulbar  derangements — namely,  lingual  paralysis 
with  resulting  difficulty  in  articulation,  pharyngeal  paralysis,  and  rarely  deafness, 
as  a  result  of  lesion  of  the  acoustic  center.  Of  course,  the  severity  and  extent 
of  all  these  symptoms  must  vary  according  to  the  location  and  size  of  the  spot  of 
softening. 

The  prognosis  of  cases  of  this  sort  is  almost  always  unfavorable.  Death 
results  in  a  few  days  at  latest.  It  is  often  ushered  in  by  a  high  temperature. 
Exceptionally,  there  is  a  transition  into  a  chronic  form. 

We  need  say  nothing  about  treatment,  except  that  the  same  remedies  are 
employed  as  in  other  acute  bulbar  diseases. 

3.  Acute  iNFLAMaiATORY  Bulbar  Paralysis 

(Acute  Jjulhar  Myelitis.     Midtiple  Bulbar  Neuritis) 

"  Acute  bulbar  paralysis,"  in  the  stricter  sense  of  the  term,  means  a  form  of 
disease  where  marked  symptoms  of  bulbar  derangement  appear  acutely — that  is, 
within  a  few  days  or  weeks.  The  anatomical  lesion  is  probably  an  acute  inflam- 
mation of  the  medulla  oblongata.  It  is  a  rare  disorder,  and  its  aetiology  is  doubt- 
ful. There  are  usually  mild  prodromata :  vertigo,  headache,  and,  in  one  case  of 
our  o"\\ai,  painful  sensations  in  the  back  of  the  neck.  Evident  bulbar  symptoms 
very  quickly  follow.  Usually  the  first  of  these  is  dysphagia.  ISTot  only  is  deglu- 
tition impaired,  but  the  paresis  of  the  soft  palate  and  of  the  laryngeal  muscles 
allows  liquids  to  enter  the  nostrils  or  the  larynx.  The  tongue  also  becomes  grad- 
ually paralyzed,  speech  becomes  indistinct,  and,  if  the  soft  palate  be  involved, 
nasal. 

Sometimes  the  extremities  also  become  iDaretic,  as  a  result  of  the  extension  of 
the  disease  to  the  region  of  the  pyramids ;  but  in  many  instances  the  extremities 
remain  unaffected  to  the  end.  Paralyses  of  the  facial  nerve  and  of  the  ocular 
muscles  are  somewhat  more  frequent.  The  temperature  is  sometimes  a  little  ele- 
vated (100°-102°,  38°-39°  C),  but  not  always.  The  pulse  is  almost  invariably 
rapid ;  in  our  patient  it  was  148. 

The  prognosis  is  apparently  always  bad.  Often  death  takes  place  in  four  to 
eight  days,  or  it  may  be  not  till  the  end  of  two  or  three  weeks.  It  is  invariably 
preceded  by  all  the  tokens  of  paralysis  of  respiration.  In  our  case  there  was  well- 
marked  paralysis  of  the  diaphragm  at  the  end. 

As  yet,  few  autopsies  have  been  reported.  Generally  the  medulla  presents  no 
macroscopic  changes.  Exceptionally,  it  can  be  seen  to  be  softened  and  mottled 
Avith  minute  htemorrhages.  The  microscope  detects  abundant  evidence  of  inflam- 
mation :  granule-cells,  infiltration  with  nuclei  around  the  blood-vessels,  thicken- 
ing of  the  walls  of  some  of  the  blood-vessels,  small  extravasations,  swollen  axis- 
cylinders,  etc.  It  should  also  be  borne  in  mind  that  precisely  similar  clinical 
phenomena  seem  often  to  be  referable  to  peripheral  changes,  such  as  multiple 
neuritis  affecting  the  bulbar  nerves. 

The  treatment  of  acute  bulbar  paralysis  is,  of  course,  almost  hopeless.     In 


1052  DISEASES    OF    THE   l^ERVOUS    SYSTEM 

early  stages  we  should  apply  counter-irritation  to  the  nape  of  the  neck;  and  we- 
might  prescribe  mercurial  inunction.  It  might  be  well  to  employ  the  con- 
stant current,  applied  at  the  back  of  the  neck,  and  also  in  such  a  manner  as  to- 
excite  the  movements  of  deglutition.  We  found  injections  of  strychnine  useless^ 
Toward  the  end,  narcotics  are  indispensable. 


CHAPTER   lY 
COMPRESSION    OF    THE    MEDULLA 

Acute  compression  and  other  injuries  of  the  medulla  are  due  most  frequently 
to  fracture  or  dislocation  of  the  atlas  and  axis.  As  is  well  known,  dislocation  of 
the  axis,  or  backward  dislocation  of  the  atlas,  usually  causes  instant  death. 

Gradual  compression  is  seen  in  chronic  disease  of  the  bones  around  the  me- 
dulla, in  caries  and  tumors  of  the  occiput  and  of  the  first  two  vertebrae.  Enchon- 
droma  of  the  base  of  the  skull;  new  growths  of  the  sphenoid,  at  its  junction 
with  the  occipital ;  tumors  of  the  dura ;  and  sometimes  even  tumors  of  the  cere- 
bellum— may  all  excite  by  their  pressure  the  gravest  bulbar  symptoms.  We 
should  also  mention  aneurism  of  the  vertebral  artery  at  its  upper  end,  and  of  the^ 
basilar,  as  capable  of  doing  similar  harm.  In  all  these  cases  the  main  cause  of 
disturbance  is  undoubtedly  the  mechanical  pressure,  either  directly  destroying- 
the  nervous  tracts  or  interrupting  the  transmission  of  nervous  influences ;  but 
the  circumstances  may  be  further  complicated  by  hsemorrhages,  and  sometimes 
perhaps  by  inflammation  of  the  medulla  itself. 

The  clinical  phenomena  of  gradual  bulbar  compression  resemble  those  of  spinal 
compression,  in  that  they  usually  begin  with  symptoms  of  irritation  in  the  distri- 
bution of  those  nerves  the  roots  of  which  are  first  affected.  There  are  neuralgia 
of  the  trigeminus,  twitching  of  the  facial  muscles,  tinnitus  aurium,  etc.  If  the 
compression  becomes  greater,  there  are  more  serious  bulbar  symptoms :  disturb- 
ances of  speech  and  deglutition,  paralysis  of  the  tongue,  soft  palate,  face,  and 
very  likely  motor  (paretic  or  ataxic)  and  sensory  symptoms  in  the  extremities- 
Usually  we  also  see  general  cerebral  symptoms,  such  as  vertigo,  headache,  vomit- 
ing, and  sometimes  epileptiform  convulsions. 

We  can  not,  of  course,  draw  up  a  definite  and  rigid  list  of  symptoms,  since- 
both  the  individual  symptoms  and  the  general  course  of  the  disease  exhibit  great 
variations  according  to  the  way  in  which  the  compression  is  brought  about.  The- 
diagnosis  can  be  made  in  those  cases  only  where  some  setiological  factor  such  as 
trauma  or  caries  of  the  vertebrae  is  known  to  exist.  Aneurism  of  the  vertebral 
artery  is  said  by  Moser  sometimes  to  give  rise  to  a  loud  systolic  murmur  heard 
between  the  mastoid  process  and  the  spine.  In  all  other  cases  we  can  seldom  do 
more  than  surmise  the  truth.  Slow  compression  is  distinguished  from  genuine- 
progressive  bulbar  paralysis  chiefly  by  the  course  it  pursues — that  is,  there  are 
initial  symptoms  of  irritation — by  the  greater  complexity  of  the  clinical  phenom- 
ena, such  as  sensory  lesions  and  hemiplegia,  and  sometimes  by  the  asymmetry  of 
certain  symptoms.  If  the  anterior  part  of  the  medulla  is  compressed  in  the  region 
of  the  pyramids,  there  may  for  a  time  be  no  bulbar  symptoms,  but  merely  motor- 
symptoms  in  the  extremities.     These  are  chiefly  paretic  or  spastic. 

The  prognosis  is  almost  always  bad,  as  can  be  inferred  from  the  nature  of  the- 
causative  disease.  Death  is  brought  on  either  by  inhalation-pneumonia,  or  by 
paralysis  of  respiration.  Treatment  must  be  purely  symptomatic,  and  should  fol- 
low the  same  rules  as  in  progressive  bulbar  paralysis. 


HEMATOMA   OF   THE   DURA   MATEE  1053 


v.— THE   DISEASES   OF    THE    BRAIN 


SECTION  I 

Diseases  of  the  Cerebral  Meninges 
CHAPTER   I 

HEMATOMA    OF    THE    DURA    MATER 

{Internal  HmnorrJiagic  Pachymeningitis) 

Etiology  and  Pathology. — Hasmatoma  of  the  dura  mater  is  the  name  given 
to  effusions  of  blood  found  on  the  inner  surface  of  the  dura  mater.  These  effu- 
sions are  of  considerable  area,  but  of  moderate  thickness,  and  are  usually  encap- 
sulated. There  has  been  much  discussion  as  to  their  mode  of  origin,  and  views 
still  differ.  One  is  that  the  haemorrhage  is  the  primary  lesion,  and  that  the 
connective-tissue  membranes  are  developed  only  by  the  organization  of  the  clot. 
This  conception  was  originally  the  prevailing  one,  but  was  opposed  by  Virchow, 
who  was  led  by  the  results  of  his  own  investigations  to  maintain  that  the  haemor- 
rhage was  always  secondary.  The  primary  process  he  believed  to  be  a  peculiar 
sort  of  inflammation — "  hsemorrhagic  pachjTueningitis."  This  gave  rise  to  a  new 
growth  of  richly  vascular  connective  tissue,  into  which  the  haemorrhage  took 
place.  Of  late,  however,  the  tendency  is  again  to  regard  the  hsemorrhage  as  the 
initial  change,  at  least  in  certain  cases,  and  to  refer  it  to  an  affection  of  the  walls 
of  the  blood-vessels  which  diminishes  their  power  of  resistance. 

The  mildest  forms  of  internal  pachymeningitis  present  a  delicate  membrane 
upon  the  inner  surface  of  the  dura  mater,  quite  easily  separable,  of  a  reddish 
■color,  and  dotted  with  numerous  red  and  brownish  spots.  These  spots  are  due  to 
minute  haemorrhages  and  collections  of  haematoidine.  The  membrane  itself  is  a 
■delicate  interstitial  tissue,  traversed  by  numerous  wide  capillaries. 

In  more  advanced  cases  the  thickening  is  much  greater.  There  are  usually 
several  layers,  the  newest  and  most  superficial  being  nearest  the  brain.  The  old- 
est, which  is  in  apposition  with  the  dura  mater,  is  composed  of  connective  tissue 
that  has  already  become  rather  firm  and  fibrous.  It  is  evident  from  this  lamellar 
structure  that  the  whole  process  goes  on  by  fits  and  starts.  The  clinical  course  of 
the  disease  will  be  seen  from  what  follows  to  agree  well  with  such  a  view.  The 
■effusions  are  sometimes  very  extensive,  even  larger  than  a  hen's  egg,  and  exercise 
no  slight  pressure  upon  the  underlying  cerebral  parenchyma.  The  ha3morrhage 
always  takes  place  inside  the  mass,  or  between  its  layers.  The  effusion  may,  how- 
ever, break  through  the  innermost  layer,  so  that  the  blood  flows  into  the  arach- 
noideal  spaces ;  this  is  known  as  "  intermeningeal  apoplexy." 

The  favorite  location  of  the  haematoma  is  the  parietal  region.  It  is  some- 
times found  at  the  base  of  the  brain,  in  the  posterior  or  middle  fossa.  Occasion- 
ally the  haematoma  is  bilateral. 

Haemorrhagic  pachymeningitis  is  not  a  rare  disease.  It  is  sometimes  found  to 
exist  in  a  moderate  degree  in  chronic  cardiac,  renal,  or  pulmonary  cases,  which 
■come  to  autopsy.  Usually  there  have  been  no  special  symptoms,  the  lesion  being 
■discovered  incidentally.     It  has  been  found  in  like  manner  in  connection  with 


105i  DISEASES    OF   THE   XEEVOUS    SYSTEM 

a  great  many  acute  infectious  diseases,  such  as  typhoid  fever  and  small-pox.  It  is 
a  more  important  and  more  frequent  complication  in  other  chronic  cerebral  dis- 
eases, in  particular  such  as  induce  marked  atrophy  of  the  brain  as  a  -n-hole.  It  is 
especially  common  in  general  paralysis  of  the  insane  and  in  other  forms  of  de- 
mentia. In  the  apparently  primary  hgemorrhagic  pachymeningitis  chronic  alco- 
holism is  the  commonest  and  most  important  causal  factor.  In  hard  drinkers  it  is 
not  very  unusual  for  the  hfematoma  to  be  so  extensive,  if  it  occurs  at  all,  as  to 
cause  grave  cerebral  derangement.  Very  likely  changes  in  the  vascular  '«"alls, 
such  as  atheroma  and  fatty  degeneration,  contribute  an  important  part  to  the  re- 
sult in  such  patients.  Injury  is  a  second  important  cause.  We  have  seen  a  case 
of  hsematoma  of  the  dura  with  a  fatal  termination  in  a  patient  "who  some  months 
before  had  received  very  severe  blows  on  the  head  in  a  fight.  Hsematoma  may  also 
occur  in  all  diseases  where  there  is  a  general  hfemorrhagic  diathesis.  Thus  it  is 
seen  in  pernicious  anaemia,  leukaemia,  and  scurvy.  Here  certainly  the  haemor- 
rhage is  the  primary  event. 

As  might  be  inferred  from  the  tetiological  factors  enumerated,  the  disease  is 
found  chiefly  in  advanced  life,  and  much  oftener  in  men  than  in  women. 

Symptoms. — Xot  infrequently  a  hsematoma  of  the  dura  is  found  post  mortem, 
which  had  during  life  been  entirely  unsuspected.  Either  the  haemon-hage  was 
not  extensive  enough  to  cause  any  symptoms,  or  the  brain  exercised  that  remark- 
able tolerance  which  it  sometimes  shows  even  when  there  are  wide-reaching 
lesions ;  or  such  symptoms  as  may  have  existed  escaped  particular  notice,  in  the 
severity  of  the  more  general  symptoms  (of  typhoid  fever  or  some  similar  disease). 
But  in  other  cases  hsemorrhagic  pachymeningitis  excites  grave  symptoms,  al- 
though they  are  seldom  so  characteristic  as  to  reveal  the  diagnosis ;  for  individual 
cases  vary  greatly,  according  to  the  size  of  the  haemorrhages,  their  location,  and 
the  frequency  of  their  recurrence. 

Almost  always  the  beginning  of  the  disease  is  rather  sudden.  It  may  even  be 
like  an  apoplectic  seizure.  The  symptoms  are  referable  partly  to  the  general 
effect  of  the  haemorrhage  upon  the  brain,  and  partly  to  the  exact  locality  of  the 
haemorrhage.  The  more  general  symptoms  comprise  headache,  impairment  of 
intelligence  (that  is,  stupor  or  even  complete  coma),  slow  or  irregular  pulse,  vom- 
iting, and  contracted  pupils — all  being  symptoms  of  cerebral  compression.  Xow 
and  then  we  even  find  choked  disk.  Other  phenomena  are  added  to  the  above 
when  the  heematoma  occupies  its  usual  position,  upon  one  side  and  in  the  neigh- 
borhood of  the  motor  cortical  region,  or  central  convolutions.  The  hemiplegia 
symptoms  are  not  infrequent,  such  as  hemiparesis,  and,  from  the  irritation  which 
the  effusion  produces  in  the  motor  centers,  twitchings  and  convulsions  in  one  half 
of  the  body.  Sometimes  these  symptoms  are  limited  to  a  single  extremity  or  to 
the  distribution  of  the  facial  nerve.  Aphasia  has  been  repeatedly  obseiTed  when 
the  haemorrhage  was  near  the  island  of  Eeil.  If  the  effusion  increases,  the  motor 
disturbance  becomes  correspondingly  aggravated,  and  it  may  become  bilateral. 
Sensation  is  usually  little  impaired. 

The  further  course  of  the  disease  varies  greatly  in  different  cases.  In  the 
worst  cases  there  is  speedy  death,  usually  ushered  in  by  deep  coma.  In  others,  the 
first  symptoms  are  followed  by  improvement,  although  mild  indications  of  cere- 
bral pressure  persist,  such  as  headache  or  vertigo,  or  else  local  symptoms,  such  as 
hemiparesis.  It  is  possible  for  the  effused  blood  to  be  absorbed,  and  complete  re- 
covery to  ensue;  but  usually  new  haemorrhages  and  corresponding  s^^nptoms 
arise.  It  is  precisely  this  appearance  of  the  symptoms  in  separate  attacks,  this 
frequent  recurrence  of  severe  cerebral  disturbances,  that  is  characteristic  of  hsem- 
atoma of  the  dura  mater.  As  already  intimated,  the  way  in  which  the  anatomical 
lesions  develop  explains  this  perfectly.  Thus  the  disease  may  drag  on  for  months 
and  years,  sometimes  improving-  and  sometimes  getting  worse  again.     Then  some 


PUEULENT   MENINGITIS  1055 

attack  at  last  proves  fatal.  Arrest  and  actual  improvement  are  still  possible  even 
in  the  later  stages,  although  often  the  features  of  the  case  have  meanwhile  under- 
gone essential  alteration  because  of  the  progress  of  some  causative  disease.  In 
general,  the  clinical  phenomena  of  hsematoma  of  the  dura  are  often  complicated 
and  obscured  by  the  co-existence  of  the  primary  disease. 

The  diagnosis  is  therefore  difficult.  The  main  points  may  be  recapitulated  as 
follows:  First,  the  existence  of  setiological  factors,  such  as  alcoholism,  previous 
injury,  or  chronic  cerebral  disease;  second,  the  sudden  onset,  and  also  the  abrupt 
appearance  of  further  symptoms,  the  alternation  of  rapid  aggravation  and  im- 
provement ;  and  third,  the  existence  of  symptoms  which  experience  has  taught  us 
to  refer  mainly  to  the  cortex  of  the  brain,  namely,  unilateral  convulsions,  mono- 
plegic  paresis  and  contractures,  and  contracted  pupils.  Nevertheless,  frequent 
errors  in  diagnosis  can  not  be  avoided. 

Treatment. — The  possibility  of  therapeutic  interference  being  successful  is 
very  small.  In  apoplectic  shocks,  ice  to  the  head  is  useful ;  and  if  the  patient  be 
robust,  it  may  also  be  advisable  to  use  local  depletion,  by  leeches  on  the  temples  or 
behind  the  ears.  It  is  also  customary  to  prescribe  some  such  drug  as  senna  or 
calomel  for  "  intestinal  depletion." 

If  the  first  onset  is  successfully  withstood,  the  main  points  in  the  further 
treatment  are  general  hygienic  and  dietetic  directions,  so  as  to  guard  as  far  as 
possible  against  fresh  haemorrhages.  Alcohol  and  excessive  bodily  or  mental 
exertion  should  be  forbidden.  Of  course,  paralysis  or  other  persistent  disturb- 
ances may  call  for  special  attention. 


CHAPTEE   II 


PURULENT    MENINGITIS 

{Purulent  Cerebral  Leptomeningitis.     Meningitis  of  the  Convexity) 

.Sltiology. — Purulent  inflammation  of  the  dura  mater  has  no  clinical  impor- 
tance, for  it  is  very  rare,  and  occurs  only  as  the  result  of  the  extension  of  disease 
from  neighboring  parts.  We  shall  accordingly  consider  below  purulent  inflam- 
mation of  the  pia  mater  only.  One  important  variety  of  this  disease  has  already 
been  discussed  (see  page  111  ei  seq.)  as  one  of  the  infectious  diseases,  under  the 
name  of  epidemic  cerebro-spinal  meningitis.  There  we  saw  also  that  the  occa- 
sional sporadic  cases  of  primary  or  "  idiopathic  "  meningitis  are  probably  identi- 
cal setiologically  with  those  of  epidemic  meningitis.  In  all  other  instances,  puru- 
lent meningitis  is  a  secondary  disease — that  is,  the  specific  pus  coccus  (usually 
the  streptococcus  pyogenes),  which  excites  the  purulent  inflammation,  originates 
in  some  other  organ  primarily,  and  affects  the  meninges  only  secondarily.  We 
should,  therefore,  seek  most  carefully  in  every  case  of  purulent  meningitis,  at 
the  bedside  and  more  particularly  at  the  autopsy,  to  discover  the  way  by  which 
the  pathogenic  virus  reached  the  meninges.  We  have  no  right  to  say  that  the 
case  is  one  of  primary  meningitis,  strictly  so  called,  until  we  have  made  a  most 
careful  examination  with  a  negative  result.  From  a  clinical  standpoint,  it  is  true 
that  many  cases  of  secondary  meningitis  do  seem  as  if  they  were  primary,  be- 
cause not  infrequently  the  real  primary  disease  excites  insignificant  symptoms, 
or  perhaps  no  symptoms  at  all. 

Secondary  purulent  meningitis  is  due  most  frequently  to  disease  of  the  cranial 
bones,  and  in  particular  to  disease  of  the  petrous  portion  of  the  temporal  bone, 
with  the  auditory  apparatus  therein  contained.     If  we  consider  the  anatomical 


1056  DISEASES    OF   THE   NEEVOUS    SYSTEM 

jelations  of  the  middle  and  internal  parts  of  the  ear,  we  can  easily  understand 
■why  inflammation  in  them  is  not  infrequently  followed  by  meningitis.  Usually 
it  is  a  caries  of  the  petrous  portion  of  the  temporal  bone,  itself  due  to  an  otitis 
media,  which  leads  to  an  irruption  into  the  cranial  cavity.  This  is  especially  apt 
to  take  place  through  the  thin  vault  of  the  tympanic  cavity.  It  may  also  extend 
from  the  mastoid  cells,  or  by  direct  propagation  along  the  sheaths  of  the  acoustic 
or  facial  nerves,  or  along  the  vessels  which  lie  in  the  petroso-squamous  suture. 
The  dura  is  first  attacked,  and  then  the  pia.  In  many  instances,  the  neighboring 
venous  sinuses  (transverse,  cavernous,  and  superior  petrosal)  transmit  the  in- 
flammation, being  first  attacked  by  a  suppurative  thrombo-phlebitis.  Again,  ex- 
ceptionally, a  purulent  inflammation  in  the  upper  part  of  the  nasal  cavity  or  in 
the  orbital  cavity  (panophthalmitis)  may  lead  to  meningitis. 

Another  and  frequent  source  of  meningitis  is  found  in  the  various  in- 
juries of  the  cranium.  In  the  great  majority  of  these  cases  there  is  an  open 
wound,  admitting  infectious  agents  which  are  suspended  in  the  air.  The  suppura- 
tion often  commences  in  the  spongy  texture  of  the  diploe,  thence  extending  to  the 
dura  and  pia,  either  directly  or  by  way  of  a  purulent  thrombosis  of  some  sinus 
into  which  the  veins  of  the  diploe  enter.  It  was,  indeed,  often  afiirmed  in  the 
past  that  we  could  have  a  traumatic  purulent  meningitis  without  any  open 
wound ;  but  this  is  not  easily  explained,  according  to  our  present  views  as  to  the 
origin  of  purulent  inflammations.  There  are  probably  in  every  case  small  wounds 
■of  the  skin,  which  are  perhaps  overlooked.  The  statements  are  also  to  be  rejected 
that  the  heat  of  the  sun's  rays,  striking  upon  an  uncovered  head,  may  excite 
purulent  meningitis.  In  most  cases  of  fatal  sunstroke  we  find  marked  hyperaemia 
of  the  meninges,  but  no  inflammation. 

Meningitis  may  have  an  intra-cranial  origin;  it  is  sometimes  the  sequel  of 
■cerebral  abscess,  ^o  matter  what  starts  the  abscess,  if  it  extends  to  the  surface 
of  the  brain,  it  causes  a  more  or  less  extensive  purulent  meningitis  at  that  point. 
An  abscess  may  burst  into  one  of  the  lateral  ventricles,  and  the  infection  be  car- 
Tied  from  that  point  to  the  pia  at  the  base  of  the  brain. 

All  the  cases  thus  far  contemplated  allow  of  the  explanation  that  the  inflam- 
mation reaches  the  meninges  by  direct  extension;  but  there  is  another  group  of 
<3ases  where  the  agent  that  infects  the  pia  mater  originates  at  some  distant  part  of 
the  body,  and  is  probably  conveyed  by  the  blood  or  lymph  currents.  These  cases 
are  often  termed  metastatic  meningitis. 

Of  this  sort  is  the  secondary  meningitis  seen  in  connection  with  genuine  lobar 
pneumonia,  a  combination  already  discussed  (see  page  215).  The  meningitis  is 
also  sometimes  a  complication  of  empyema,  rarely  of  pyemia  and  septicaemia,  or 
ulcerative  endocarditis,  and  very  rarely  of  typhoid  fever  and  the  acute  exanthe- 
mata (small-pox,  scarlet  fever),  and  of  acute  articular  rheumatism.  In  each  case 
we  must,  of  course,  determine  whether  the  meningitis  may  not  have  a  connecting 
link  between  itself  and  the  primary  disease,  such  as  otitis  in  scarlatina,  or  sec- 
ondary empyema  in  typhoid  fever. 

Pathology. — For  the  pathological  anatomy  of  purulent  meningitis,  we  may 
refer  mainly  to  the  statements  made  on  page  112,  under  epidemic  meningitis,  for 
the  lesions  are  similar.  The  only  way  to  determine  whether  a  meningitis  is  sec- 
ondary or  primary  is  by  finding  or  failing  to  find  disease  in  neighboring  or  remote 
parts,  for  example,  pneumonia.  The  seat  of  the  meningitis  will  vary  according 
to  that  of  the  primary  inflammation,  if  there  be  any.  If  the  meningitis  is  due  to 
caries  of  the  petrous  bone  or  to  an  injury  of  the  skull,  the  purulent  exudation  is 
usually  most  abundant  in  the  immediate  neighborhood  of  the  primary  lesion, 
hetween  the  pia  and  arachnoid.  Thence  it  gradually  extends  along  the  surface  of 
the  brain,  sometimes  chiefly  on  the  convexity  and  sometimes  at  the  base.  But  in 
general  it  may  be  said  that  both  the  secondary  and  the  metastatic  varieties  of 


PURULEISrT   MENINGITIS  1057 

mening-itis  as  a  rule  affect  the  convexity,  although  this  is  by  no  means  invariably 
the  case.  This  rule  explains  why  these  cases  are  sometimes  termed  mening-itis  of 
the  convexity,  in  contrast  to  tubercular  meningitis,  which  latter,  as  we  shall  find, 
has  a  preference  for  the  base  of  the  brain,  and  hence  is  called  basilar  menin- 
gitis. The  spinal  pia  mater  is  sometimes  simultaneously  attacked,  but  not  so 
constantly  as  in  primary,  or  epidemic  meningitis.  The  brain  is  almost  always 
ittvolved — the  inflammation  extends  along  the  vessels  which  dip  from  the  pia 
mater  into  the  cerebral  parenchyma.  It  is  not  a  rare  thing  to  find  minute  ab- 
scesses or  ecchymoses  in  the  interior  of  the  brain.  The  whole  parenchyma  is  usu- 
ally moist,  03dematous,  and  of  a  doughy  consistency.  The  meningeal  exudation 
exerts  upon  the  brain  a  pressure  which  gives  rise  to  important  symptoms;  by  it 
the  superficial  cerebral  convolutions  are  often  considerably  flattened.  The  lateral 
ventricles  almost  always  contain  more  or  less  sero-pus. 

Clinical  History. — So  varied  are  the  primary  diseases  which  may  entail  a  men- 
ingitis, that  it  is  hardly  possible  to  make  a  sketch  of  the  disease  which  would  suit 
all  cases.  If  the  meningitis  comes  on  during  the  course  of  pyemia,  pneumonia, 
or  some  other  severe  illness,  its  proper  symptoms  are  often  inextricably  confused 
with  those  of  the  primary  trouble;  and  when  the  skull  or  the  brain  has  been 
mechanically  injured,  it  is  very  hard  to  determine  whether  a  meningitis  has  been 
excited,  because  the  trauma  may  of  itself  produce  such  serious  effects.  The  fol- 
lowing description,  therefore,  applies  chiefly  to  cases  of  apparently  primary  men- 
ingitis, or  to  cases  where  the  meningitis,  although  secondary,  is  well  marked. 

The  beginning  in  such  cases  may  be  sudden,  or  it  may  be  somewhat  insidious. 
Sometimes  the  grave  symptoms  appear  almost  at  43nce,  accompanied  by  a  chill  and 
high  fever.  Sometimes  there  are  for  a  time  indefinite  and  more  or  less  ambigu- 
ous prodromata,  but  almost  always  it  is  the  headache  which  first  attracts  atten- 
tion. This  grows  worse  with  more  or  less  rapidity,  and  almost  always  becomes 
very  violent.  Exceptionally  it  may  be  insignificant.  Not  infrequently  it  varies 
considerably,  being  much  worse  at  some  hours  or  on  some  days  than  on  others. 
The  location  of  the  pain  is  sometimes  frontal,  sometimes  occipital,  and  sometimes 
over  the  whole  head.  Next  in  prominence  to  the  headache,  particularly  in  the 
later  stages  of  the  disease,  is  the  mental  disturbance.  The  patient  complains  of 
vertigo,  becomes  dull  and  stupid,  or  begins  to  wander.  The  delirium  may  be  ex- 
tremely violent,  but  usually  there  is  depression  rather  than  exaltation,  and  the 
stupor  merges  into  coma.  That  the  headache  still  continues  may  be  inferred  from 
the  frequent  raising  of  the  hand  to  the  head  and  the  grimace  of  pain  whenever 
the  head  is  moved,  until  finally  the  coma  becomes  so  profound  that  even  these 
reflex  actions  cease. 

Usually  these  general  cerebral  symptoms  are  attended  by  others  referable  to 
the  particular  locality  affected.  The  neck  is  rigid.  This  is  most  marked  when 
the  posterior  fossa  and  the  medulla  are  affected.  Then  there  are  all  sorts  of 
paralytic  or  irritative  symptoms  in  the  distribution  of  the  cranial  nerves,  mainly 
due  to  lesions  of  the  nerves  where  they  emerge  from  the  base  of  the  brain ;  there 
is  derangement  of  the  oculo-motor  nerves,  as  shown  by  paralysis  or  nystagmus ;  the 
pupils  are  unequal,  or  are  contracted  or  dilated,  and  do  not  react  to  light;  there 
is  paresis  of  the  facial,  or  trismus,  or  grinding  of  the  teeth.  All  these  symptoms 
may  be  equally  pronounced  in  other  forms  of  meningitis.  Sometimes  we  can 
detect  optic  neuritis  with  the  ophthalmoscope.  Other  symptoms  are  due  to  cere- 
bral disturbance,  often  apparently  located  chiefly  in  the  cortex.  Thus  there  may 
he  twitchings  of  individual  muscles,  or  even  genuine  convulsions  in  one  or 
more  limbs,  or  paralysis  of  one  extremity  or  of  half  the  body.  Sometimes  the 
autopsy  explains  these  phenomena,  but  often  we  fail  to  find  any  marked  ana- 
tomical lesion  to  correspond  to  them,  and  are  obliged  to  ascribe  them  to  circu- 
latory or  functional  derangement. 
67 


1058  DISEASES    OF    THE    XEEVOUS    SYSTEM 

Of  the  remaining-  symptoms,  the  fever  is  most  important.  Almost  always  the 
temperature  is  decidedly  elevated,  not  infrequently  reaching  104°  or  105°  (40°— 
40.5°  C).  The  fever  is,  however,  very  irregular.  There  may  be  repeated  chills- 
with  great  elevations  of  temperature.  The  pulse  is  generally  rapid,  and  ofteiL 
somewhat  irregular.  Exceptionally  it  is  less  frequent  than  normal,  because  of 
cerebral  compression.  Vomiting  is  not  a  rare  symptom,  particularly  at  firsts 
There  is  almost  invariably  constipation,  and  the  abdomen  is  often  tense  and  con- 
cave. The  urine  is  scanty,  and  often  contains  a  trace  of  albumen.  Secondary 
diseases  are  sometimes  found  post  mortem,  such  as  lobular  pneumonia,  due  to- 
inhalation  of  food  during  the  comatose  state. 

The  entire  course  of  the  disease  occupies  only  a  few  days  in  very  acute  cases, 
and  scarcely  ever  exceeds  a  week  or  ten  days.  The  termination  is  almost  sure- 
to  be  fatal.  In  the  few  cases  of  recovery  which  have  been  reported  the  diagnosis 
is  doubtful.  In  most  instances  deep  coma  precedes  death,  though  sometimes  it  is- 
ushered  in  by  convulsions.  There  is  often  a  great  rise  of  temperature  (107.5°, 
42°  C,  or  higher)  before  the  close  of  life. 

Diagnosis. — The  diagnosis  of  purulent  meningitis  is  sometimes  pretty  evi- 
dent ;  but  it  may  be  very  obscure,  so  that  we  can  not  always  avoid  confounding  it. 
with  other  severe  acute  diseases,  such  as  typhoid  fever,  pyaemia,  and  general 
tuberculosis.  In  general  the  most  characteristic  symptoms  of  any  variety  of  men- 
ingitis are  intense  headache,  rapid  onset  of  grave  cerebral  disturbances,  delirium 
and  insensibility,  stiffness  of  the  neck,  and  disturbances  in  the  distribution  of 
the  cranial  nerves  (especially  impaired  motion  of  the  eyeball  and  optic  neuritis)- 
These  last,  although  often  slight,  are  generally  present ;  and  in  connection  witk 
these  separate  symptoms  we  must  also  always  consider  the  whole  course  of  the 
disease  and  any  setiological  factors  which  may  exist.  Typhoid  fever  is  excluded 
by  its  usually  slower  onset,  the  greater  delay  in  the  appearance  of  grave  cerebral 
symptoms,  the  rose-spots,  the  greater  size  of  the  spleen,  the  characteristic  stools, 
and  the  peculiar  fever-curve.  It  may  also  be  of  importance  in  diagnosis  that  iiL 
typhoid  fever  there  is  usually  no  leucocytosis  of  the  blood,  since  in  purulent 
meningitis  the  number  of  leucocytes  in  the  blood  is  increased.  Severe  septic- 
and  pysemic  diseases,  including  ulcerative  endocarditis,  likewise  excite  cerebral 
disturbances  which  might  be  misleading,  but  these  diseases  are  to  be  recognized 
by  their  aetiology  (external  wounds,  abortion,  etc.),  cutaneous  ecchymoses,  septic 
retinitis,  swelling  of  the  joints,  and  repeated  rigors.  Uraemia  may  also  simulate 
meningitis.  Sometimes  the  character  of  the  urine,  and  the  predominance  of  con- 
■vulsions,  will  set  us  right,  but  not  always.  "We  may  state  in  conclusion  that  every- 
one who  sees  many  cases  must  (like  ourselves)  repeatedly  have  met  with 
patients  presenting  the  symptoms  of  a  severe  and  acute  cerebral  affection  appar- 
ently primary,  without  demonstrable  cause,  and  seeming  to  justify  a  diagnosis 
of  meningitis,  but  yet  yielding  post  mortem  no  signs  of  disease  beyond  "  hyper- 
semia,"  "  oedematous  swelling,"  and  similar  changes  of  only  secondary  importance. 
We  are  as  yet  wholly  unable  to  explain  such  cases. 

Granting  that  meningitis  exists,  what  variety  is  present  ?  The  aetiology  is  a 
great  help  in  answering  this  question.  We  should  endeavor  to  learn  whether- 
there  has  been  traumatism  or  some  old  ear  trouble.  It  is  well  to  employ  the  aural 
speculum.  We  can  not  say  that  a  patient  has  epidemic  meningitis  unless  several 
cases  occur  simultaneously,  although  herpes  is  very  characteristic,  as  it  appears 
only  exceptionally  in  other  varieties.  [Lumbar  puncture  may  sometimes  be  of 
assistance  in  the  diagnosis. — K.]  Usually  tubercular  meningitis  also  can  be 
diagnosticated  only  by  means  of  the  aetiology.  Its  symptoms,  of  course,  are  in 
almost  all  particulars  identical  with  those  of  purulent  meningitis.  Sometimes, 
however,  tubercles  can  be  detected  in  the  choroid  by  means  of  the  ophthalmoscope- 
For  further  particulars  see  the  next  chapter. 


TUBERCULAE   MENII^GITIS  1059 

Prognosis.— The  prognosis  of  purulent  meningitis  is  almost  invariably  wtiolly 
unfavorable,  as  follows  from  what  has  been  said  above.  In  the  reported  cases 
of  recovery  from  meningitis  the  diagTiosis  must  be  determined  with  the  greatest 
caution,  but  it  is  not  impossible  that  sporadic  cases  of  epidemic  diplococcus  men- 
ingitis may  terminate  favorably.  We  may  also  state  that  sometimes  in  severe 
infectious  diseases  "  meningitic  "  symptoms  may  appear  which  lead  us  to  fear 
the  worst,  but  which  finally  disappear.  In  acute  purulent  inflammation  of  the 
middle  ear,  especially  in  the  young,  meningitic  symptoms  (headache,  stupor) 
sometimes  set  in,  which  also  seem  threatening,  but  which  disappear.  It  is,  of 
course,  usually  impossible  to  determine  positively  the  anatomical  processes  in 
such  cases. 

Treatment. — The  treatment  of  the  different  forms  of  meningitis  varies  but 
little.  Locally,  the  favorite  remedies  are  ice  applied  to  the  head,  which  should 
be  shaved  if  practicable,  and  local  depletion  by  means  of  leeches  behind  the  ears 
or  on  the  temples.  Many  physicians  recommend  cutting  off  the  hair  and  rubbing 
in  antimonial  ointment,  or  applying  ethereal  tincture  of  iodine.  We  have  never 
tried  this.  Cool  baths  with  douching  can  not  be  employed  unless  the  patient  can 
be  moved  without  too  much  pain.  For  violent  pain  or  great  restlessness  we  must 
use  narcotics.  The  best  is  morphine  subcutaneously.  We  can  not  hope  for  much 
benefit  from  other  internal  remedies,  such  as  iodide  of  potassium  or  calomel. 

Prophylaxis  demands,  above  all,  prompt  recourse  to  the  otologist  for  aural 
trouble  of  any  kind,  and  strictly  antiseptic  treatment  of  all  injuries  of  the  skull. 
Even  in  cases  of  meningitis  that  have  already  begun,  surgical  interference 
(trephining  the  mastoid,  etc.)  may  perhaps  often  check  the  advance  of  the  inflam- 
mation and  lead  to  recovery. 


CECAPTER  III 

TUBERCULAR  MENINGITIS 

{Basilar  Meningitis) 

etiology. — Tuberculosis  of  the  leptomeninges  is  always  a  secondary  affec- 
tion— a  sequel  to  previously  existing  tubercular  disease  of  some  other  organ. 
Why  the  pia  mater  should  be  so  often  singled  out  for  secondary  infection  with 
the  tubercular  virus,  or  what  path  that  virus  traverses  to  reach  the  pia, 
we  can  hardly  say.  We  can  merely  state  what  the  other  tubercular  diseases 
are,  which,  as  experience  shows,  entail  tubercular  meningitis  most  frequently. 
These  primary  affections  may  be  of  themselves  productive  of  grave  clinical 
phenomena,  the  meningitis  merely  adding  to  the  complexity  of  the  pic- 
ture. Again,  the  primary  trouble  may  not  have  betrayed  itself  at  all,  or  its 
symptoms  may  have  been  long  ago  arrested,  so  that  the  meningitis  seems  to  be 
a  primary  disease.  In  some  cases  even  the  most  careful  examination  will  fail  to 
detect  the  origin  of  the  trouble. 

Tubercular  meningitis  is  oftenest  a  sequel  to  pulmonary  tuberculosis.  It  may 
appear  as  a  terminal  complication  in  cases  of  advanced  phthisis,  or  it  may  come 
on  while  the  signs  of  pulmonary  disease  are  as  yet  very  slight.  Next  in  order  as  a 
causative  affection  comes  tubercular  pleurisy.  This  origin  is  not  infrequent.  As 
we  have  already  seen,  most  cases  of  apparently  primary  pleurisy  are  due  to  tuber- 
cle. This  statement  is  supported  by  the  fact  that  it  is  not  very  exceptional  for  the 
symptoms  of  tubercular  meningitis  to  supervene  suddenly  upon  what  had  seemed 
to  be  genuine  convalescence  from  pleurisy.  In  children,  and  sometimes  in  adults, 
the  virus  may  be  carried  to  the  meninges  from  cheesy,  tubercular,  bronchial  or 


1060  DISEASES    OF   THE   NERVOUS    SYSTEM 

mesenteric  glands,  or  from  tubercular  or  "  fungous  "  disease  of  the  bones  or 
joints.  Another  danger  to  adults  is  tubercular  disease  of  the  genito-urinary 
apparatus.  It  should  also  be  noticed  that  a  single  large  tubercle  in  the  brain  may 
lead  to  miliary  tuberculosis  of  the  meninges.  In  short,  we  see  that  it  is  not 
impossible  for  any  tubercular  infiltration,  wherever  situated,  to  communicate 
infection  either  to  the  meninges  alone  (in  some  remarkable  way),  or  simul- 
taneously to  them  and  many  other  organs.  In  this  latter  case,  where  in  all  proba- 
bility the  blood  carries  the  virus  through  the  system,  the  meningitis  is  merely 
a  part  of  a  general  miliary  tuberculosis  (see  page  261),  while  in  the  former  case 
the  reason  why  the  meninges  are  exclusively  or  primarily  affected  depends  upon 
the  special  form  of  the  infection;  but  we  are  almost  wholly  ignorant  of  the  way 
by  which  the  tubercle  bacilli  reach  the  meninges.  We  are  ourselves  disposed  to 
suspect  that,  in  many  cases  at  least,  the  infectious  material  first  enters  the 
arachnoid  sac  of  the  spinal  cord  through  the  lymph  sheaths  of  the  nerves  (e.  g., 
the  intercostal  nerves),  and  thence  extends  upward  to  the  base  of  the  brain. 

We  sometimes  hear  the  attack  ascribed  to  such  causes  as  over-exertion,  mental 
exciteraent,  traumatism,  etc.;  but  we  need  hardly  say  that  these  can  not  be 
properly  regarded  as  setiological  factors,  and  that  usually  they  are  merely  coin- 
cidences. Age,  however,  does  have  an  influence;  children  are  much  oftener  at- 
tacked than  adults,  although  the  latter  also  are  liable  to  the  disease. 

Pathology. — As  in  tuberculosis  of  serous  membranes,  so  in  tuberculosis  of  the 
pia,  there  are  two  effects  of  infection  to  be  distinguished  from  each  other :  (1) 
the  development  of  the  specific  new  growth — that  is,  of  miliary  tubercles;  and  (2) 
the  inflammation.  The  relative  degree  of  these  two  varies.  Sometimes  the 
tubercles  are  very  abundant  and  the  inflammatory  exudation  comparatively 
scanty;  and  in  other  cases  the  inflammation  is  considerable,  although  relatively 
few  tubercles  are  discoverable.  The  tubercles  are  usually  found  in  greatest 
number  along  the  course  of  the  larger  blood-vessels,  and  therefore  chiefly  in  the 
furrows  and  clefts  of  the  surface  of  the  brain,  in  the  fissure  of  Sylvius,  at  the 
chiasma,  the  pons,  the  medulla,  and  the  cerebellum.  And,  in  general,  the  base  of 
the  brain  is  usually  more  affected  than  the  convexity — hence,  as  we  have  said,  the 
name  of  "  basilar  meningitis."  There  are,  however,  exceptions  to  this  rule.  We 
very  often  find  that  the  region  supplied  by  one  or  more  arteries  suffers  above 
other  parts;  this  must  be  due  to  the  manner  of  infection.  The  inflammatory 
lesions  consist  of  hypersemia,  usually  well  marked,  and  a  sero-gelatinous  exuda- 
tion of  variable  amount.  That  this  exudation  is  partly  cellular  can  always  be 
proved  by  the  microscope,  and  often  even  macroscopically  from  the  great  cloudi- 
ness of  the  pia;  but  still  we  seldom  find  enough  to  justify  us  in  calling  the  pro- 
cess one  of  genuine  purulent  inflammation.  Small  haemorrhages  into  the  pia  are 
quite  often  found.  The  brain  itself  is  usually  flattened  from  the  pressure  of  the 
meningeal  exudation.  Often  the  inflammation  involves  the  brain-substance 
itself,  as  shown  microscopically  by  tubercles,  inflammatory  changes,  and  capillary 
haemorrhages.  The  ventricles  usually,  although  not  invariably,  contain  a  hydro- 
cephalic effusion.  This  led  earlier  observers  to  term  the  disease  "  acute  hydro- 
cephalus." The  effusion  is  serous,  but  generally  turbid  from  cellular  constituents, 
and  not  infrequently  tinged  with  blood.  The  choroid  plexus  is  engorged,  and  it 
may  present  tubercles.  The  spinal  cord,  in  the  majority  of  cases,  shares  in  the 
tubercular  disease.  Here,  too,  we  find  infiammation  of  the  pia  and  miliary 
tubercles. 

Clinical  History. — Tubercular  meningitis  almost  always  begins  with  a  pro- 
dromal stage,  which  is  often  brief,  but  which  may  last  one  or  two  weeks,  or  even 
longer.  The  patient  may  be  apparently  well  (vide  supra)  until  this  comes  on,  or 
he  may  have  already  shown  signs  of  some  other  tubercular  affection.  He  noAv 
feels  somewhat  ill  at  any  rate,  and  begins  to  complain  of  headache,  worse  at  some 


TUBERCULAE   MENINGITIS  1061 

times  than  at  others.  There  is  anorexia  and  very  often  constipation.  Another 
frequent  prodrome  is  an  attack  of  vomiting,  which  may  or  may  not  recur.  Sleep 
is  disturbed,  either  by  the  headache  or  by  a  certain  general  restlessness.  We  have 
occasionally  met  with  cases  where  the  illness  began  with  pronounced  mental  dis- 
turbance. The  patient  became  irrational  and  said  and  did  queer  things,  and  then 
a  few  days  later  there  appeared  distinctive  meningeal  symptoms.  In  two  pa- 
tients, who  were  hard  drinkers,  the  disease  began  just  like  delirium  tremens. 

'  After  an  initial  period  of  variable  duration,  the  general  health  becomes  more 
and  more  impaired.  The  headache  increases.  The  patient  takes  to  his  bed,  begins 
to  be  delirious,  and  soon  presents  well-marked  symptoms  of  grave  brain  trouble. 
Intelligence  becomes  more  and  more  impaired.  The  patient  is  sleepy,  and  he  can 
be  roused  imperfectly  by  the  voice,  if  at  all.  At  the  same  time  he  is  usually  quite 
restless  at  first,  grasping  at  invisible  objects  in  the  air,  picking  the  bed-clothes, 
and  continually  moving  his  legs.  The  delirium  may  be  low  or  noisy ;  the  patient 
may  keep  up  a  constant  singing,  screaming,  or  whistling.  The  persistence  of 
the  headache  even  in  this  stage  is  shown  by  the  facial  contortions  and  complaints 
of  the  sufferer,  whenever  there  is  a  temporary  approach  to  consciousness.  There 
is  also,  as  a  rule,  decided  tenderness  in  the  nape  of  the  neck  on  pressure,  fre- 
quently accompanied  by  great  stiffness  of  the  neck.  Sometimes  there  is  stiffness 
of  the  entire  spinal  column,  and  pain  in  the  same.  This  is  certainly  due  to  the 
coincident  spinal  meningitis. 

Another  group  of  symptoms  in  the  distribution  of  the  cranial  nerves  are  iden- 
tical with  those  seen  in  other  forms  of  meningitis.  Ptosis  is  not  infrequent, 
on  one  or  both  sides,  due  to  paresis  of  the  motor  oculi.  There  is  strabismus, 
either  internal  or  external.  Symptoms  of  irritation  of  the  nerves  governing  the 
movements  of  the  eye  are  very  frequent,  especially  in  the  early  stages  of  the  dis- 
ease. Thus  we  see  slow  involuntary  lateral  movements  of  the  eyeballs,  and  some- 
times nystagmus.  The  pupils  are  often  unequal;  they  may  be  enlarged  or  con- 
tracted, and  often  they  undergo  marked  and  repeated  variations  in  size.  The  re- 
action of  the  pupils  to  light  is  usually  sluggish,  and  it  may  be  absent.  With  the 
ophthalmoscope  we  find  not  infrequently  neuritis,  or  choked  disk.  In  some  in- 
stances, but  not  in  all,  we  find  also  tubercles  in  the  choroid,  which,  of  course, 
greatly  assists  diagnosis.  Sometimes  there  is  occasional  twitching  in  the  distribu- 
tion of  the  facial  nerve,  or  a  slight  tonic  contraction,  or  again  paresis  on  one  side. 
The  natural  explanation  of  all  these  phenomena  is  that  the  nerve-trunks  are  inter- 
fered with  at  the  base  of  the  brain,  either  by  the  pressure  of  the  exudation  or 
by  participation  in  the  inflammatory  process,  or  by  the  minute  hsBmorrhages 
which  sometimes  take  place  into  the  sheath  of  the  nerves. 

Disturbances  in  the  extremities  may  be  caused  by  various  lesions.  Motor 
symptoms  of  irritation  are  apparently  referable  for  the  most  part  to  changes  in 
the  cortex  of  the  brain.  We  see  occasional  twitching  of  larger  or  smaller  groups 
of  muscles,  or  rarely  convulsions.  These  latter  may  be  unilateral,  or  limited 
to  a  single  extremity.  Sometimes  there  is  well-marked  paresis  of  one  half  the 
body  or  paralysis  of  one  limb,  or  there  may  be  aphasia,  although  it  is  only  in  a 
part  of  the  cases  that  we  find  post  mortem  any  lesion  which  explains  these  symp- 
toms. In  most  cases,  however,  there  is  a  particularly  large  collection  of  tubercles 
in  certain  places  upon  the  cortex  cerebri,  occasioning  a  local  compression  or  an 
inflammatory  oedema,  which  in  its  turn  excites  the  phenomena  mentioned.  Some- 
times the  brain-substance  itself  is  found  in  a  state  of  red  softening  underneath 
these  spots.  Another  not  very  rare  symptom  is  a  peculiar  stiffness  of  the  limbs, 
due  either  to  direct  irritation  or  to  reflex  action.  The  reflexes  in  the  lower  ex- 
tremities are  generally  exaggerated  at  first,  but  later  on  become  diminished,  and 
finally  abolished.  The  reflexes  upon  one  side  may  be  more  vigorous  than  upon  the 
other.     As  to  sensation,  it  is  hard  to  reach  definite  conclusions,  because  of  the 


1062  DISEASES    OF   THE   IsTeeVOIJS    SYSTEM 

patient's  stupor.  Sometimes  there  is  well-marked  cutaneous  hypersesthesia,  prob- 
ably referable  to  an  implication  of  the  spinal  cord  in  the  process. 

The  behavior  of  the  pulse  and  temperature  is  interesting.  The  temperature 
is  usually  elevated,  but  often  only  to  a  slight  extent — that  is,  varying  between 
100.5°  and  102°  (38°.and  39°  C).  Often  the  temperature  falls  quite  low,  only  to 
rise  again,  the  alternations  being  at  irregular  intervals.  Exceptionally  the  tem- 
perature may  remain  high  (104°  F.,  40°  C.)  most  of  the  time.  Toward  the  end 
there  is  usually  a  decided  change  in  temperature,  either  upward  or  downward. 
In  many  instances  there  is  a  very  low  temperature  before  death ;  in  two  cases  we 
have  seen  a  temperature  of  87.8°  (31°  C).  Or  the  temperature  may  rise  to  106° 
(41°  C.)  or  higher  just  before  death.  The  pulse  is  often  abnormally  slow  in  the 
early  stages  of  the  disease,  even  numbering  only  40  to  60  beats  per  minute.  This 
is  referable  without  doubt  to  the  increased  intra-cranial  pressure.  Later  on  the 
pulse  becomes  small  and  rapid.  The  transition  may  be  very  sudden.  The  vagus 
is  at  first  irritated,  and  then  paralyzed.    The  pulse  is  often  irregular. 

Respiration  is  generally  moderately  accelerated.  If  the  breathing  is  very 
deep  and  rapid,  we  should  always  think  of  simultaneous  miliary  tuberculosis  of 
the  lungs.  Toward  the  close  of  the  disease  the  respiration  often  assumes  the 
Cheyne-Stokes  type  :  there  is  a  long  pause,  followed  by  very  superficial  and  gentle 
respiration,  which  gradually  grows  deeper  and  deeper,  then  diminishes  again, 
and  is  succeeded  by  another  complete  pause.  This  symptom  is  always  raost  omi- 
nous, for  it  indicates  that  the  excitability  of  the  respiratory  center  is  already 
greatly  impaired. 

Symptoms  referable  to  still  other  organs  are  few.  Vomiting  is  rare  in  the 
later  stages  of  the  disease.  The  abdomen  often  presents  a  "  boat-shaped  "  concav- 
ity, as  the  result  of  tonic  muscular  contraction,  and  is  hard  and  tense.  There  is 
almost  always  constipation.  The  spleen  may  be  somewhat  enlarged.  The  urine 
sometimes  contains  a  trace  of  albumen.  On  account  of  the  drowsiness,  it  is  usu- 
ally voided  in  the  bed  or  retained  in  the  bladder.  Almost  invariably  there  is  rapid 
marasmus. 

The  entire  duration  of  tubercular  meningitis  varies  somewhat,  chiefly  because 
of  the  varied  length  of  the  first  stage.  When  the  disease  is  once  fully  developed, 
the  illness  seldom  lasts  more  than  three  to  ten  days  longer.  Frequently  the 
illness  is  divided  into  three  stages :  1.  The  stage  of  cerebral  irritation,  with  head- 
ache, stiff  neck,  vomiting,  and  delirium;  2.  The  stage  of  cerebral  compression, 
due  chiefly  to  the  hydrocephalus,  and  causing  drowsiness,  slowness  of  the  pulse, 
paralysis  of  the  oculo-motor  nerves,  hemiplegia,  etc. ;  and  3.  The  paralytic  stage, 
presenting  deep  coma,  relaxation  of  the  previously  contracted  muscles,  accelerated 
pulse,  and  marked  variations  of  temperature.  Such  a  division  is  too  diagram- 
matic to  correspond  accurately  to  the  real  phenomena,  but  it  will,  nevertheless, 
often  aid  us  in  getting  a  general  idea  of  the  course  of  the  disease. 

The  termination  of  tubercular  meningitis  seems  to  be  inevitably  fatal. 
Sooner  or  later  the  patient  loses  consciousness  completely,  his  pulse  grows  very 
small  and  rapid,  his  respirations  irregular  and  intermittent  (Cheyne-Stokes),  his 
temperature,  as  we  have  said,  either  rises  high  or  falls  far  below  normal,  and, 
finally,  death  is  ushered  in  by  a  paralysis  of  all  the  vital  functions.  A  few 
physicians  have  reported  eases  of  recovery ;  but  was  the  diagnosis  correct  ?  While 
we  would  by  no  means  absolutely  deny  that  recovery  from  tubercular  meningitis 
might  occur,  it  would  certainly  be  very  difficult  to  prove,  in  any  particular  in- 
stance, that  such  a  thing  had  happened. 

Tubercular  Menin^tis  in  Children. — The  disease  is  so  prone  to  attack  chil- 
dren that  it  seems  desirable  to  subjoin  a  few  remarks  about  the  peculiarities  of 
the  affection  as  observed  in  them. 

Often  the  little  patient  is  pale  and  weakly,  with  tubercular  antecedents;  but 


TUBERCULAR   MENINGITIS  1063 

sometimes  apparently  healthy  and  vigorous  children  are  attacked.  Tubercular 
meningitis  may  be  the  sequel  of  measles,  whooping-cough,  or  some  other  disease, 
which  has  occasioned  the  development  of  the  tubercular  process.  Usually  the 
severer  symptoms  are  preceded  by  a  rather  long  prodromal  stage  (a  week  or  ten 
-days),  which  often  does  not  forebode  the  severity  of  the  disease  that  is  begin- 
ning. The  child  looks  pale,  has  a  poor  appetite,  grows  thin,  is  restless  in  his  sleep, 
is  out  of  humor  and  cries  during  the  day,  is  often  tired  and  sleepy,  does  not  play 
naturally,  the  tongue  is  coated  and  the  bowels  constipated.  The  second  stage  is 
generally  ushered  in  by  headache  and  vomiting.  The  headache  is  not  very  often 
violent;  but  children  complain  with  remarkable  frequency  of  pain  in  the  abdo- 
men and  chest.  The  cause  of  this  symptom  is  unknown.  The  pulse  is  almost 
invariably  slow,  often  somewhat  irregular  and  whirring  (that  is,  as  if  it  trembled 
l)eneath  the  finger),  and  it  frequently  undergoes  surprisingly  rapid  changes  in 
rate — for  example,  varying  twenty  or  more  beats  inside  of  a  few  hours.  Very 
early  the  child  becomes  dull  and  drowsy.  Frequently  it  emits  a  peculiar  deep 
sigh,  or  that  sudden  loud  scream  or  "  cephalic  cry  "  which  physicians  long  ago 
learned  to  recognize  and  fear.  The  symptoms  referable  to  the  cranial  nerves  and 
"the  nervous  disturbances  in  the  limbs  are  similar  to  those  seen  in  adults.  Strabis- 
mus is  almost  constant.  Very  often  there  are  trismus,  and  a  distinctly .  audible 
grinding  of  the  teeth,  most  distressing  to  the  by-standers.  Trousseau  laid  weight 
upon  the  appearance  of  red  spots  (taches  cerehrales)  upon  the  skin  after  it  has 
laeen  mechanically  irritated;  but  these  have  no  diagnostic  value.  They  are  due 
to  increased  reflex  action,  and  are  seen  in  all  sorts  of  acute  diseases.  The  fever 
is  irregular  throughout  and  generally,  as  in  adults,  not  very  high,  100°  to  102° 
'(38°-39°  C).    Respiration  is  usually  rapid,  and  often  is  irregular. 

The  change  from  bad  to  worse  is  almost  always  announced  by  a  rapid  increase 
in  the  pulse-rate,  to  160  or  200.  The  child  becomes  completely  comatose.  Very 
often  there  are  repeated  epileptiform  convulsions,  either  universal  or  affecting 
single  extremities.     Death  is  iisually  preceded  by  a  decided  rise  in  temperature. 

Diagnosis. — When  the  symptoms  are  pronounced,  the  diagnosis  of  meningitis 
is  easy,  and  we  have  merely  to  determine' just  what  variety  is  before  us.  That 
the  disease  is  due  to  tuberculosis  is  never  to  be  ascertained  by  means  of  the 
meningeal  symptoms  themselves,  but  is  rendered  possible  only  by  the  aetiology, 
if  that  be  discoverable.  Here,  as  in  all  tubercular  diseases,  we  have  chiefly  to  re- 
gard (1)  heredity  and  (2)  the  evidence  of  previoiis  or  existing  tubercular  affec- 
tions in  other  parts  of  the  body.  Under  this  second  head  are  to  be  considered 
scrofula,  diseases  of  the  bones  and  joints,  pulmonary  tuberculosis,  pleurisy,  and 
tuberculosis  of  the  genitals  or  of  the  choroid.  If  our  search  be  unsuccessful,  we 
may  sometimes  get  a  hint  of  the  truth  from  the  general  appearance  of  the  pa- 
tient :  for  example,  he  may  be  pale,  or  narrow-chested.  And,  again,  the  absence 
of  trauma,  aural  disease,  or  epidemic  meningitis  will  make  tuberculosis  more 
probable. 

In  its  early  stages,  or  when  it  varies  from  the  usual  course,  tubercular  meniu- 
■gitis  may  be  very  difficult  to  diagnosticate.  This  is  particularly  true  when  the 
patient  is  a  child.  The  early  malaise  and  vomiting  are  treated  as  "  ordinary 
gastric  catarrh  "  until  the  grave  cerebral  symptoms  disclose  the  mistake  in  diag- 
nosis. In  such  cases  we  should  be  carefxil  not  to  disregard  the  initial  slowness 
and  irregularity  of  the  pulse.  This  alone  should  make  our  prognosis  guarded. 
The  fever  may  be  prominent  at  the  commencement,  and  tempt  us  to  call  the  case 
one  of  incipient  typhoid  fever;  and.  indeed,  the  correct  diagnosis  is  often  impos- 
sible until  the  disease  develops  further.  In  regard  to  this,  see  the  preceding 
chapter  on  purulent  meningitis,  whore  the  exclusion  of  severe  septic  diseases  and 
•of  urfemia  is  also  considered. 

Before  the  autopsy  we  must  remain  in  great  uncertainty  as  to  the  number 


1064  DISEASES    OF   THE   NEKVOUS    SYSTEM 

and  distribution  of  the  tubercles,  the  existence  of  a  large  effusion  into  the  lateral 
ventricles,  etc.  We  are  often  amazed  at  the  post-mortem  examination  by  the 
apparent  insignificance  of  the  lesions.  Paralysis  of  the  cranial  nerves  (eyes, 
face)  implies  that  the  base  of  the  brain  is  gravely  affected.  If  such  symptoms  are 
absent,  and  there  are  mental  disturbances,  and  symptoms  of  motor  irritation  dis- 
played in  the  extremities,  we  are  led  to  infer  meningitis  of  the  convexity.  If  the 
nervous  disorder  be  mainly  unilateral,  we  may  assume  that  one  hemisphere  is 
more  affected  than  the  other. 

Treatment.— However  hopeless  the  prospect,  we  are  nevertheless  bound  to 
employ  all  the  remedies  at  our  command,  as  in  other  forms  of  meningitis.  Above 
all,  we  should  be  thorough  in  applying  ice  to  the  head,  and  we  may  also  try  in- 
unctions of  iodoform  ointment  to  the  shaven  scalp,  and  lukewarm  baths,  with 
douching.  The  inunction  of  mercurial  ointment  (especially  on  the  head,  neck, 
and  back)  has  also  been  recommended.  The  most  common  internal  remedies  are 
calomel — half  a  grain  to  a  grain  (gramme  0.03-0.05)  for  a  child  every  two  hours — 
and  infusion  of  senna.  Iodide  of  potassium  may  also  be  freely  given,  fifteen 
grains  daily  to  a  child,  and  two  or  three  times  as  much  to  an  adult.  Whether 
it  does  any  good  is  extremely  doubtful.  If  the  patient  is  very  restless,  narcotics 
are  indispensable.  Stimulants  are  often  given  in  the  last  stage  of  the  disease, 
but  generally  without  effect. 

About  prophylaxis,  we  need  merely  refer  to  the  general  statements  on  page 
254,  in  regard  to  prophylaxis  from  the  various  tubercular  diseases. 


CHAPTER   IV 
THROMBOSIS    OF    THE    CEREBRAL    SINUSES 

iEtiology  and  Pathology. — The  sinuses  of  the  dura  mater  sometimes  present 
a  thrombosis,  under  circumstances  similar  to  those  which  induce  the  sanie  process 
in  other  veins.  The  most  frequent  occasion  for  such  thrombosis  is  marasmus, 
however  brought  about,  with  the  accompanying  feebleness  of  circulation.  This 
is  the  explanation  of  those  not  very  rare  cases  found  among  wretched  and  ill- 
nourished  children  in  the  first  year  of  life,  and  also  in  patients  with  phthisis, 
cancer,  etc.  We  must  note  in  particular  that  in  severe  anasmic  conditions  (espe- 
cially in  chlorosis)  sinus  thrombosis  is  comparatively  common. 

Half  way  between  marantic  thrombosis  and  the  inflanunatory  variety  imme- 
diately to  be  described,  come  those  cases  which  are  seen  in  typhoid  fever  and 
other  severe  acute  infectious  diseases.  Here  the  specific  virus  apparently  plays 
an  important  part  (just  as  in  thrombosis  of  the  femoral  vein),  although  very 
likely  the  cardiac  weakness  also  promotes  the  thrombosis. 

Genuine  inflammatory  thrombosis  (thrombophlebitis) — that  is,  thrombosis  in 
connection  with  real  phlebitis  of  the  sinus — is  almost  always  due  to  the  extension 
of  inflammation  from  some  neighboring  part.  The  most  fruitful  cause  is  sup- 
puration in  the  petrous  portion  of  the  temporal  bone,  the  result  of  otitis  or  caries. 
This  spreads  to  the  walls  of  the  transverse  or  petrosal  sinuses,  which  are  close  by. 
Also  wounds,  necrosis,  or  other  affections  of  other  cranial  bones  may  excite  throm- 
bosis ;  likewise,  although  seldom,  deep-seated  inflammation  of  the  soft  parts  of  the 
head  and  face,  large  furuncles  or  erysipelatous  abscesses,  may  produce  the  same 
result.  The  reason  why  sinus  thrombosis  may  arise  from  the  causes  last  men- 
tioned lies  in  the  fact  that  the  external  veins  of  the  skull  are  also  connected  with 
the  sinuses  of  the  dura  mater  by  means  of  the  emissary  veins  of  Santorini.     It  is 


THROMBOSIS    OF   THE    CEEEBRAL    SINUSES  1065 

easy  to  understand  that  purulent  thrombophlebitis  of  the  cerebral  sinuses  is 
often  found  associated  with  purulent  meningitis  or  brain  abscess. 

Thrombosis  due  to  marasmus  is  most  frequently  found  in  the  superior  longi- 
tudinal and  transverse  sinuses,  while  the  inflammatory  variety  usually  occupies 
either  the  transverse,  petrosal,  or  cavernous  sinuses.  Of  course  the  thrombus 
may  grow  out  from  its  original  sinus  into  neighboring  ones.  Important  clinical 
symptoms  are  caused  by  secondary  venous  stasis  in  the  veins  which  empty  into 
the  occluded  sinus.  These  symptoms  are  most  pronounced  when  the  longitudinal 
sinus  is  affected ;  objectively,  we  find  the  meningeal  veins  which  lie  on  the  surface 
of  the  brain  distended  and  tortuous;  and  often  there  are  extensive  meningeal 
ecchymoses.  Even  the  cerebral  parenchyma  beneath  shows  distinct  evidence  of 
passive  congestion,  and  minute  capillary  haemorrhages  have  been  repeatedly 
found  in  it. 

Symptoms. — In  some  instances  moderate  thrombosis  of  the  cerebral  sinuses 
has  been  found  post  mortem,  although  there  had  been  no  symptom  suggesting  it 
before  death.  In  other  cases  the  thrombosis  does  excite  undeniable  cerebral  dis- 
order, but  the  symptoms  are  so  general  and  ambiguous  that  the  most  we  can  do 
is  to  suspect  the  existence  of  the  clot  without  being  at  all  certain  about  it.  Sinus 
thrombosis  in  marantic  children  usually  causes  coma,  stiffness  of  the  neck  and 
back,  strabismus,  nystagmus,  and  sometimes  clonic  spasms  in  the  face  and  limbs. 
The  symptoms  in  adults  are  similar,  comprising  headache,  drowsiness,  occasion- 
ally delirium,  sometimes  coma,  and  varying  symptoms  of  irritation  or  of  paraly- 
sis in  the  distribution  of  the  cranial  nerves  (nystagmus,  strabismus,  trismus) 
and  in  the  extremities.  But  even  all  these  symptoms  are  insufiicient  to  make 
the  diagnosis  certain.  They  must  be  re-fenforced  by  certain  other  phenomena 
more  distinctly  referable  to  the  peculiar  circulatory  disturbances  occasioned 
by  the  thrombosis.  Occlusion  of  the  cavernous  sinus  sometimes  excites  well- 
marked  symptoms  of  stasis  in  the  ophthalmic  veins.  Thus  the  retina  may  be 
seen  through  the  ophthalmoscope  to  be  passively  congested,  there  is  oedema  of 
eyelids  and  the  conjunctiva,  the  eyeball  is  unusually  prominent,  and  the  frontal 
vein  is  distended.  In  case  of  an  inflammatory  thrombosis,  the  periphlebitic  swell- 
ing may  cause  symptoms  in  the  distribution  of  the  neighboring  nerves,  especially 
paresis  of  the  oculo-motor  or  abducens,  or  trigeminal  neuralgia.  In  thrombosis 
of  the  transverse  sinus  an  oedematous  swelling  is  occasionally  seen  behind  the 
ear,  near  the  mastoid  process.  If  the  clot  projects  into  the  petrosal  sinus  or  even 
actually  into  the  internal  jugular,  the  lower  part  of  this  vein  collapses.  And  inas- 
much as  the  external  jugular  can  empty  itself  with  unusual  ease  into  the  unfilled 
internal  jugular  vein,  the  external  jugular  is  also  affected  and  becomes  less 
prominent  upon  the  affected  than  upon  the  normal  side.  Sometimes  it  is  even 
possible  to  feel  the  thrombus  in  the  internal  jugular.  Such  thrombosis  causes 
pain  and  swelling  in  the  neck  on  the  affected  side.  When  the  superior  longi- 
tudinal sinus  is  blocked  up,  there  are  symptoms  of  nasal  engorgement  (epistaxis). 
and  distention  of  the  veins  about  the  temples,  which  veins  are  connected  with  the 
longitudinal  sinus  by  emissary  veins.  We  must  confess,  however,  that  all  these 
special  symptoms  are  comparatively  rare,  and  often  difficult  of  demonstration 
even  when  present. 

Primary  thrombosis  of  the  transverse  sinus  with  extension  of  the  clot  into  the 
venfe  magnse  Galeni,  thus  causing  internal  hydrocephalus,  has  been  repeatedly 
observed  in  the  chlorotic.  The  clinical  picture  consists  of  the  rapid  onset  of 
severe  cerebral  symptoms  (headache,  vomiting,  somnolence),  which  rapidly  pro- 
gress to  deep  sopor  and  lead  to  death  in  a  few  days.  When  unilateral  paralysis 
and  symptoms  of  motor  irritation  occur  (choreic  twitchings,  ei)ileptiform 
attacks),  they  are  due  in  part  to  hfemorrhages  from  stasis  in  the  brain  substance. 

The  symptoms  become  more  complex  where  there  is  a  suppurative  phlebitis, 


1066  DISEASES    OF   THE   NERVOUS    SYSTEM 

because  there  are  usually  pysemic  symptoms  as  the  disease  progresses.  Thus, 
there  may  be  rigors  and  high  fever,  pulmonary  abscess,  suppurative  arthritis,  etc. 
We  have  already  mentioned  the  combination  of  thrombosis  of  a  sinus  with  puru- 
lent meningitis  or  brain  abscess. 

The  prognosis  is  almost  always  bad,  both  because  of  the  nature  of  the  causa- 
tive disease  and  because  of  the  grave  cerebral  derangement  or  the  secondary 
pyaemia.  Spontaneous  recovery  may  occur,  but  it  is  rare.  The  nervoiis  symptoms 
may  last  at  times  only  a  week  or  two,  but  they  may  extend  over  several  months. 

Treatment  in  most  cases  must  be  purely  symptomatic.  Only  when  a  purulent 
sinus  thrombosis  follows  ear  disease  can  surgical  interference  give  very  satisfac- 
tory results.  The  details  of  such  treatment  are  to  be  found  in  the  text -books  of 
operative  aural  surgery. 


SECTION  II 

Diseases  of  the  Brain-Substance 

CHAPTER  I 

DISTURBANCES    OF    CIRCTJLATION    IN    THE    BRAIN 

{Cerebral  Hyperamia.     Cerebral  Aiuemia) 

It  is  presumable  that  so  sensitive  an  organ  as  the  brain  is  much  influenced 
even  by  slight  disturbances  of  circulation ;  but  as  yet  we  have  comparatively  little 
knowledge  of  the  production  and  character  of  such  disturbances,  their  very  exist- 
ence being  very  difficult  to  demonstrate.  There  are  many  instances  where  marked 
cerebral  symptoms  justify  the  assumption  that  the  brain  is  in  some  abnormal 
condition,  where  yet  there  are  many  arguments  against  any  marked  ana- 
tomical lesion.  Here  we  surmise  that  there  is  some  circulatory  derangement, 
although  we  have  no  actual  and  direct  arguments  to  rely  upon.  For  example, 
we  refer  to  this  cause  certain  cases  of  headache,  of  sensations  of  pressure  in  the 
head,  of  vertigo,  of  general  hypersesthesia,  and  of  that  protean  and  nevertheless 
easily  distinguishable  disease  known  as  cerebral  neurasthenia  (q.  v.).  At  present, 
however,  we  can  not  determine  how  far  circulatory  disturbances  are  actually  con- 
cerned in  these  cases,  or  of  what  kind  they  are,  or  whether  there  may  not  be 
purely  functional  disease  of  the  brain  entirely  independent  of  changes  in  the 
blood-vessels. 

Certain  groups  of  cerebral  symptoms,  which  come  on  in  paroxysms,  seem  the 
most  clearly  referable  of  all  to  circulatory  disturbance.  There  can  hardly  be  a 
doubt  that  the  phenomenon  known  as  fainting  or  syncope  is  due  to  sudden  cere- 
bral ansemia.  As  is  well  known,  fainting  is  usually  the  result  of  a  clearly  demon- 
strable cause.  Frequent  and  familiar  causes  are  emotional  excitement,  terror, 
unusual  psychical  impressions  (like  the  sight  of  blood),  the  influence  of  great 
heat,  or  great  physical  strain,  as  by  long  standing.  The  condition  of  the  stomach 
has  certainly  a  great  influence  in  many  cases.  There  are  many  persons  who,  if 
they  go  long  beyond  the  usual  time  without  eating  (particularly  if  they  go  with- 
out breakfast),  are  very  liable  to  syncope.  Some  individuals  are  especially  sub- 
ject to  fainting  fits.  Such  persons  are  often  slight  and  anaemic  (for  example, 
convalescents),  but  some  are  in  appearance  robust  and  vigorous.  Many  children 
are  subject  to  fainting. 

The  immediate  cause  of  the  cerebral  anaemia  in  all  these  cases  is  doubtful. 
Mental  excitement  is  usually  supposed  to  lead,  in  fainting,  to  a  contraction  of  the 


DISTUEBANCES    OF   CIRCULATIOISt   IN    THE   BRAIN       1067 

minute  cerebral  arteries.  It  is  not,  however,  impossible  that  in  these  cases  also,  as 
in  others,  sudden  cardiac  weakness  is  one  factor,  although,  if  so,  it  is  strange 
that  we  never  see  a  trace  of  cyanosis.  Where  the  attack  is  apparently  connected 
with  unusual  conditions  of  the  abdominal  organs  we  are  reminded  of  the  relations 
of  the  splanchnic  nerve  to  the  heart  (Goltz's  experiment  of  beating  the  belly  of  a 
frog),  and  of  the  possibility  that  the  brain  might  be  left  anaemic  if  the  abdominal 
vessels  suddenly  dilated  and  absorbed  a  large  proportion  of  the  whole  blood- 
supply. 

The  symptoms  of  an  ordinary  fainting  fit  are  known  to  every  one.  There  are 
usually  certain  prodromata.  The  person  begins  to  "  feel  badly."  Dizziness  comes 
on,  the  senses  are  confused,  the  patient  gapes,  the  ears  ring,  there  are  spots  be- 
fore the  eyes  or  total  darkness,  the  floor  seems  to  move,  and  surrounding  objects 
begin  to  spin  around.  All  this  is  almost  always  accompanied  by  nausea,  and 
sometimes  there  is  actual  vomiting.  If  the  person  can  lie  down  promptly  the 
attack  is  sometimes  averted  without  complete  loss  of  consciousness.  Otherwise 
there  is  unconsciousness  for  a  time  varying  from  some  minutes  to  even  a  half- 
hour  or  longer.  What  is  most  noticeable,  even  in  the  beginning  of  the  attack, 
is  the  pallor  which  overspreads  the  face  and  often  becomes  extreme,  and  is 
the  visible  expression  of  the  coincident  cerebral  anaemia.  Very  often  the  face 
and  body  are  bathed  in  cold  perspiration.     The  pulse  is  usually  small  and  rapid. 

There  is  no  real  danger  in  an  ordinary  attack.  The  most  important  therapeu- 
tic measure  is  to  lay  the  patient  horizontal  as  soon  as  possible,  to  favor  the 
return  of  blood  to  the  brain.  Mild  stimulants  should  also  be  employed;  the  face 
should  be  sprinkled  with  cold  water,  the  temples  rubbed  with  vinegar  or  cologne- 
water  ;  brandy  or  wine  should  be  administered.  We  can  overcome  a  tendency  to 
fainting  fits  only  by  strengthening  the  constitution. 

The  results  of  chronic  cerebral  anaemia  are  observable  when  the  cerebral  con- 
dition is  part  of  excessive  general  anaemia.  Almost  all  cases  of  chlorosis,  per- 
nicious anaemia,  and  acute  anaemia  from  loss  of  blood  (as  in  ulcer  of  the  stomach) 
display  most  plainly  the  symptoms  of  cerebral  anaemia.  The  phenomena  are 
essentially  the  same  as  in  syncope,  only  less  in  degree.  Consciousness  is  main- 
tained, except  in  the  worst  cases.  A  sort  of  persistent  drowsiness,  however, 
often  attended  by  frequent  gaping,  is  one  of  the  most  constant  symptoms.  The 
patient  is  most  distressed,  as  a  rule,  by  loud  tinnitus  aurium,  persistent  nausea, 
and  sometimes  by  obstinate  headache.  All  these  symptoms  are  aggravated,  and 
often  increase  to  an  actual  attack  of  fainting,  if  the  patient  sits  up  in  bed,  and 
are  least  marked  when  he  lies  as  quietly  as  possible  in  a  horizontal  position. 
The  treatment  of  this  condition  is  of  course  identical  with  that  of  the  causative 
disease  and  the  general  anaemia. 

Cerebral  hyperaemia,  like  cerebral  anaemia,  may  be  either  chronic  or  paroxys- 
mal. Of  the  chronic  variety  we  know  almost  nothing.  It  seems  doubtful,  to  say 
the  least,  whether  there  is  really  a  "  general  plethora,"  or  whether  the  headaches 
and  vertigo  of  which  "  full-blooded  "  persons  complain  are  due  to  hyperaemia  of 
the  brain.  ISTor  have  we  any  direct  proof  that  the  cerebral  symptoms  resulting 
from  chronic  poisoning  (alcohol,  tobacco,  etc.),  or  from  persistent  mental  over- 
exertion, are  brought  about  by  hyperaemia,  as  some  assume,  rather  than  by  func- 
tional disorder  of  the  nervous  elements  themselves. 

These  conditions,  which  are  called  attacks  of  "  cerebral  congestion  "  or  "  rush 
of  blood  to  the  head,"  are  often  referred  to  the  sudden  onset  of  cerebral  hyperae- 
mia. There  is  a  more  or  less  sudden  appearance  of  general  excitement,  with  a 
sensation  of  warmth  in  the  head  and  neck,  strong  pulsation  of  the  carotids,  a  red 
face,  general  hyperaesthesia  and  irritability,  headache,  vertigo,  tinnitus,  spots  be- 
fore the  eyes,  and  nausea.  An  attack  lasts  half  an  hour  to  an  hour.  In  severe 
cases  there  may  be  maniacal  excitement,  or  there  may  be  stupor  and  drowsiness 


1068  DISEASES    OF   THE   NERVOUS    SYSTEM 

and  other  symptoms  of  lowered  intellectual  activity,  resembling  a  slight  apoplectic 
attack  (see  a  later  chapter).  The  special  cause  of  such  attacks,  however,  is  usu- 
ally obscure.  It  is,  indeed,  very  probable  that  in  these  attacks  vaso-motor  dis- 
turbances play  a  part  (dilatation  of  the  cerebral  vessels  from  vascular  paralysis 
or  from  irritation  of  the  vaso-dilator  nerves)  ;  but  it  is  very  questionable  whether 
these  vascular  changes  are  really  the  primary  diseased  state,  rather  than  the 
result  of  some  other  different  morbid  condition.  Possibly  we  have  to  do  some- 
times with  epileptic  states,  or  more  frequently  with  one  manifestation  of  general 
nervousness,  neurasthenia  or  hysteria  (q.  v.)  with  primary  mental  disturb- 
ances  (anxious  ideas,  etc.). 

In  treating  "  congestion  "  we  should  keep  the  patient  as  quiet  as  possible,  with 
head  and  shoulders  raised;  and,  secondly,  we  should  endeavor  to  draw  the  blood 
away  from  the  brain.  This  purpose  will  be  served  by  hot  foot-baths,  sinapisms 
applied  to  the  chest  and  the  calves,  and  such  purgatives  as  senna  or  colocynth. 
It  is  also  beneficial  to  apply  cold  to  the  head.  In  a  severe  ease  it  is  proper  to  put 
leeches  to  the  temples  or  the  mastoid  processes. 

To  prevent,  as  far  as  possible,  the  recurrence  of  the  attacks,  we  must  have 
regard  to  the  whole  mental  and  physical  constitution  of  the  patient.  We  may 
mention,  as  of  chief  importance,  diet  (no  alcohol)  and  a  course  at  some  watering- 
place,  or  cold-water  treatment. 


CHAPTER   II 


OENERAL    PRELIMINARY    REMARKS    UPON    THE    LOCALIZATION 
OF    CEREBRAL    DISEASES 

( Topical  Diagnosis  of  Cerehfal  Lesions) 

The  physiological  relations  of  the  brain  are  such  that  the  symptoms  of  cere- 
bral disease  are  determined  to  a  greater  extent  by  the  locality  than  by  the  nature 
of  the  lesion.  If,  for  example,  there  arises  at  any  place  a  break  in  the  con- 
tinuity of  the  cerebral  motor  tract,  the  result,  as  we  already  know  (see  page  831), 
is  hemiplegia  upon  the  opposite  side  of  the  body.  The  result  is  precisely  the 
same,  whether  the  interruption  be  due  to  a  haemorrhage,  an  abscess,  a  new 
growth,  or  an  embolic  softening.  If  in  any  way  the  function  of  the  motor  fibers 
is  suspended,  then  the  necessary  sequence  in  every  case  is  a  paralysis  of  definite 
extent  and  definite  characteristics.  Much  the  same  may  be  said  of  many  other 
symptoms  which  appear  when  there  is  a  lesion  of  one  or  more  definite  places,  but 
which  are  never  referable  to  a  special  abnormal  process,  regardless  of  the  portion 
of  brain  thereby  affected. 

However  self-evident  these  simple  statements  may  appear,  it  required  a  long 
time  for  them  to  gain  universal  acceptance  among  physicians.  The  chief  cause 
of  this  was  the  conception  entertained  by  the  older  physiologists  in  regard  to 
the  functions  of  the  brain.  Flourens,  in  1842,  taught  that  functionally  all  parts  of 
the  cerebrum  were  alike,  and  therefore  any  one  part  could  act  vicariously  for  any 
other ;  and  this  view  had  numerous  adherents  among  physicians,  as  well  as  physi- 
ologists. It  was  nevertheless  experience  at  the  bedside  and  the  autopsy-table 
which  first  led  to  observations  and  discoveries  irreconcilable  with  this  view. 
Above  all,  it  was  the  lesions  found  in  aphasia  which  forced  men  to  localize  one 
particular  cerebral  symptom  as  due  to  an  aftection  of  one  particular  spot  in  the 
brain.  In  1861  Broca  announced  that  the  appearance  of  aphasia  is  always  due  to 
a  lesion  of  the  left  third  frontal  convolution;  and  this  was  the  starting-point 
of  the  doctrine  of  localization  in  general.  Nine  years  later  (1870)  appeared  the 
famous  treatise  of  Fritsch  and  Hitzig  detailing  successful  attempts  at  excitation 


THE   LOCALIZATION    OF    CEREBRAL   DISEASES  1069 

of  the  surface  of  the  brain  in  animals,  and  thus  overthrowing  the  old  idea  that 
the  gray  cortical  substance  could  not  be  irritated.  It  was  shown  that  excitation 
of  certain  places  in  the  cortex  is  followed  by  muscular  contractions  in  well-defined 
portions  of  the  opposite  side  of  the  body,  so  that  we  are  justified  in  assuming  the 
existence  of  a  number  of  cortical  centers,  which  are  quite  limited  in  extent. 
These  results  were  soon  confirmed  by  numerous  observations  in  cerebral  pa- 
thology in  man;  and  to-day  our  information  about  the  motor  functions  of 
the  cerebral  cortex  forms  the  best-known  portion  of  the  doctrine  of  cerebral 
localization.  Of  late  years  successful  work  has  been  done  in  this  exceedingly 
difiicult  field  by  Meynert  and  Flechsig  among  anatomists;  Ferrier,  Munk,  Goltz, 
and  other  physiologists ;  and  such  pathologists  as  Charcot  and  his  pupils,  ISToth- 
nagel,  Wernicke,  Hughlings  Jackson,  Horsley,  and  others.  It  is  true  that  we 
are  only  just  beginning  to  know  something  about  the  subject.  There  are  numer- 
ous contradictory  views  asserted,  and  numerous  questions  unanswered.  The  fol- 
lowing summary,  therefore,  is  to  be  regarded  merely  as  expressing  the  prevailing 
opinions  now  existing.  Much  in  it  will  surely  be  altered  in  the  course  of  time; 
but  still  this  doctrine  of  special  localization  of  the  various  cerebral  functions 
marks  out  in  general  outlines  the  only  foundation  upon  which  we  can  hope  to 
erect  a  system  of  cerebral  pathology  and  diagnosis.  In  the  following  sketch  we 
shall,  for  practical  reasons,  put  the  results  of  clinical  observations  upon  man  in 
the  foreground,  and  merely  speak  incidentally  of  the  corresponding  experimental 
achievements.  This  will  be  the  quickest  way  to  gain  acquaintance  with  the 
practical  points  in  the  diagnosis  of  what  Griesinger  called  the  "focal  diseases"; 
and  then,  when  we  take  up  the  separate  varieties  of  cerebral  disease,  we  shall 
have  these  general  remarks  to  refer  to. 

1.  The  Motor  Region  of  the  Cortex  Cerebri 

Clinical  observation  and  the  results  of  experiment  both  teach  that  a  part 
of  the  cerebral  cortex  is  distinct  from  the  rest,  inasmuch  as  it  is  the  exclusive 
seat    of   motor   functions.      This    "  motor    region "    (vide    Figs.    169    and    170) 


Fig.  160.— Lateral  aspect  of  the  brain  (from  Ecker).    The  pyri  and  lobules  are  in  Roman  type,  the  sulci 

and  fissures  in  italics. 


1070 


DISEASES    OF   THE   NERVOUS    SYSTEM 


is  made  up  chiefly  of  the  two  central  convolutions  (gyri  centrales  anterior  et 
posterior,  in  Fig.  169),  and  the  paracentral  lobule  (vide  Fig.  171),  which  lies  on 
the  median  surface  of  the  cerebrum.  To  a  slight  degree  the  motor  region  also 
embraces  the  neighboring  portions  of  the  frontal  convolutions  and  the  upper 
parietal  convolutions.    It  is  also  anatomically  different  from  the  other  regions  of 


Fig.  170. — Lateral  aspect  of  the  brain  (after  Ecker).  The  motor  region  of  the  cortex,  consisting  of  the 
anterior  and  posterior  central  convolutions,  as  well  as  of  the  paracentral  lobule  shown  in  Fig.  li'l,  is 
shaded. 


the  cortex,  as  Betz  was  the  first  to  point  out,  for  it  alone  possesses  certain  large 
pyramidal  ganglion-cells,  which  must  certainly  be  regarded  as  the  same  motor 
ganglion-cells  from  which  the  fibers  of  the  pyramidal  tract  arise  (vide  supra,  page 
829).  However  extensive  the  destructive  processes  which  attack  other  parts  of 
the  surface  of  the  brain,  provided  they  do  not  involve  these  particular  convolu- 
tions, they  cause  no  paralytic  symptoms;  while  all  diseases  which  destroy  any 
considerable  portion  of  the  "  motor  "  region  inevitably  result  in  a  motor  disturb- 
ance on  the  opposite  side  of  the  body. 

We  can  distinguish  still  further  in  different  regions  of  the  cortex  special 
centers  for  the  various  groups  of  muscles,  but  we  must  take  special  note  that  the 
individual  centers  are  not  sharply  distinguished  from  one  another,  but  that  they 
overlap.  Thus  the  different  centers  which  are  associated  have  an  intimate  con- 
nection, which  also  seems  necessary  physiologically.  The  center  for  the  move- 
ments of  the  facial  muscles  (facial  region),  lies,  as  it  would  seem,  at  the  lower 
end  of  the  central  convolutions,  and  particularly  of  the  anterior  central  convolu- 
tion. Near  by,  probably  somewhat  lower,  is  found  the  center  for  the  movements 
of  the  tongue.  This  center  probably  extends  to  the  foot  of  the  third  frontal  con- 
volution, so  that  on  the  left  side  it  is  accordingly  in  close  proximity  to  the  special 
motor-speech  center  (vide  infra).  The  center  for  the  movements  of  the  arm  lies 
somewhat  higher  than  the  center  for  the  facial,  occupying  roughly  the  middle  por- 
tion of  the  anterior  and  probably  the  posterior  central  convolutions.  The  center 
for  the  lower  extremity  is  found  partly  in  the  uppermost  portions  of  the  central 


THE    LOCALIZATION    OF    CEEEBRAL   DISEASES 


1071 


convolutions,  but  apparently  lies  for  the  most  part  in  the  paracentral  lobule.  The 
center  for  the  movements  of  the  trunk  probably  lies  in  front  of  the  leg  center  in 
the  most  posterior  portion  of  the  upper  frontal  convolution  and  also  on  the 
median  surface  of  that  convolution  (the  so-called  marginal  gyrus,  the  median 
portion  of  the  upper  frontal  convolution). 

Within  these  great  cortical  centers  for  the  chief  portions  of  the  body  (leg, 
arm,  face,  tongue)  there  is  a  much  more  accurate  localization  for  individual 
groups  of  muscles,  and  perhaps  even  for  individual  muscles.  This  fact  has  been 
established  especially  by  the  interesting  experiments  of  excitation  of  the  cortex 
of  monkeys  by  Ferrier,  Horsley,  and  others.  Pathological  observations  and 
occasional  attempts  at  excitation  of  the  cortex  which  have  been  practiced  on  man 
after  trephining  or  in  extensive  cranial  defects  arising  from  injury  or  disease, 
have  shown  that  the  conditions  in  man  are  in  general  quite  the  same  as  in  the 
higher  apes.    Within  the  leg  center  lie  special  centers  for  the  toes  and  foot,  chiefly 


Fig.  171. — Aspect  of  the  median  surface  of  the  cerebrum,  which  is  shown  when  the  two  hemispheres  are 
separated  from  each  other  by  a  sag:ittal  section.  B.  Corpus  callosum.  The  differences  in  the  type 
have  the  same  meaning-  as  in  Fig.  169.  The  paracentral  lobule,  as  a  part  of  the  motor  region  of  the 
cortex,  is  shaded.  (Copied  from  Eckee,  only  the  paracentral  lobule  is  made  more  sharply  prominent 
than  in  the  original.) 

above  and  especially  in  the  posterior  central  convolution.  Then  come  the  centers 
for  the  movements  of  the  knee,  and  then  those  for  the  movements  of  the  hip. 
In  the  paracentral  lobule  are  found  chiefly  the  centers  for  the  thigh  and  the 
pelvic  and  glutseal  muscles.  Within  the  arm  center  and  for  the  most  part  above 
— that  is,  toward  the  leg  center — are  the  centers  for  movements  of  the  shoulder 
and  elbow.  Farther  downward  come  the  centers  for  the  movements  of  the  hand 
and  fingers,  chiefly  in  the  anterior  central  convolution.  The  separate  position  of 
the  center  for  the  thumb  is  especially  noticeable ;  this  is  in  the  posterior  central 
convolution,  adjoining  the  centers  for  the  facial  muscles.  Farther  downward 
lie  the  centers  for  the  upper  facial  territory  above  the  centers  for  the  muscles  of 
the  mouth  and  lips.  In  the  lowest  part  of  the  central  convolutions  and  in  the 
adjacent  portions  of  the  two  lower  frontal  convolutions  lie  the  motor  centers  for 
movements  of  mastication  (the  centers  for  closing  the  mouth  are  said  to  lie  above 
those  for  opening  the  mouth),  and  for  the  movements  of  the  tongue  and  vocal 
cords.  The  exact  position  of  these  centers  in  man  is  not  yet  definitely  known. 
The  centers  for  the  associated  movements  of  the  eyes  to  one  side  seem  to  be  quite 
scattered.     We  elicit  these  movements  (usually  coincident  with  a  corresponding 


1072 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


turning  of  the  head)  on  irritation  of  the  posterior  portion  of  the  frontal  lobe 
adjoining  the  region  of  the  centers  for  the  arm  and  face;  but,  on  the  other  hand, 
pathological  observations  favor  the  existence  of  a  center  for  associated  movements 
of  the  eyes  in  the  region  of  the  angular  gyrus  (vide  infra).  This  multiple  locali- 
zation is  perhaps  explained  by  the  fact  that  the  movements  of  the  head  and  eyes 
are  closely  associated  both  with  all  complicated  activities  of  the  hand  and  with 
the  functions  of  sense  (listening,  looking  at  objects).  The  diagram  on  page 
1073  (Eig.  173),  from  a  drawing  by  C.  K.  Mills,  gives  a  review  of  all  these 
details. 

The  topical  diagnosis  of  diseases  in  the  motor  region  of  the  cerebral  cortex 
is  based  upon  the  following  considerations : 

In  the  first  place,  we  have  already  remarked  (page  831)  that  the  relative  posi- 
tions of  the  motor  centers  for  the  face,  arm,  and  leg  are  such  as  to  allow  readily 
of  isolated  paralysis  of  any  one  of  these  portions  of  the  body— that  is,  "  mono- 


FiG.  172. — (Drawn  according  to  Ecker.)  Explanation  of  the  topographical  relations  between  the  surface  of 
the  brain  and  the  skull,  c.  Fissure  of  Rolando.  i?C.  and  VC.  Posterior  and  anterior  central  convolu- 
tions. S.  Si  and  Sn.  Fissure  of  Sylvius.  P^  P^.  Upper  and  lower  parietal  lobes.  O.  Occipital  lobe. 
Cb.  Cerebellum.     T.  Temporal  lobe.    F.  Frontal  lobe. 


plegia."  In  fact,  we  already  possess  a  long  series  of  observations  where  circum- 
scribed lesions  in  the  motor  area  of  the  cortex  produced  paralysis  of  one  side  of 
the  face,  or  of  one  arm  or  leg,  and  of  no  other  part.  Such  paralysis  is  termed 
monoplegia  of  the  face,  the  arm,  or  the  lower  extremity.  It  follows,  from  what 
has  been  said,  that  even  during  life  we  can  state,  with  considerable  accuracy, 
the  spot  on  the  surface  of  the  brain  where  the  disease  must  be  situated.  Still 
more  frequently,  a  combined  paralysis  of  two  portions  of  the  body  is  to  be  ob- 
served as  a  result  of  cortical  lesion;  the  commonest  is  a  simultaneous  paralysis 
of  the  arm  and  face ;  more  rarely  we  see  the  arm  and  leg  paralyzed  together.  On 
the  other  hand,  we  may  feel  certain,  from  the  position  of  the  motor  centers,  that 
no  single  center  of  disease  could  paralyze  simultaneously  the  leg  and  the  face, 
while  the  arm  escaped  injury.  As  a  matter  of  fact,  no  such  combination  has  ever 
been  observed.  It  is  also  worthy  of  note  that  the  muscles  that  always  act 
bilaterally    (frontal   muscles,   muscles    of   mastication,    eye    muscles,   vocal-cord 


THE    LOCALIZATION    OF    CEREBEAL   DISEASES 


1073 


muscles,  etc.)  have  also  a  bilateral  innervation.     A  unilateral  focus  of  disease 
in  any  center,  therefore,  does  not  cause  paralysis  of  these  muscles. 

Besides  this  limitation  of  the  paralysis  to  one  portion  of  the  body  just  dis- 
cussed, localized  disease  of  the  cortex  has  another  very  characteristic  feature.  In 
it  the  symptoms  of  irritation  of  the  motor  centers  are  noticeably  frequent.  There 
are  tonic  and  clonic  spasms,  which,  like  the  paralysis,  not  infrequently  affect 
one  arm,  or  the  arm  and  half  the  face.  Sometimes,  hovpever,  they  involve 
the  entire  half  of  the  body.  These  paroxysmal  spasms  are  termed  "  cortical 
epilepsy,"  partial  epilepsy,  or  Jacksonian  epilepsy;  for  the  movements  are  just 
the  same  as  in  genuine  epilej)sy.  Numerous  cases  of  disease  have  taught  us 
thai  such  circumscribed  epileptiform  attacks  occur  only  in  affections  of  the  motor 
cortex.    They  furnish  still  more  definite  information  as  to  the  precise  locality  of 


Fig.  173. — Localization  in  the  cerebral  cortex. 


the  lesion;  for  spasms  in  the  distribution  of  the  facial  nerve  imply  that  mainly 
the  lovrer  third  of  the  central  convolutions  is  affected;  of  the  arm,  the  middle 
third ;  and  of  the  leg,  the  upper  portions  of  the  same.  If  we  have  the  opportunity 
to  observe  such  attacks  of  partial  cortical  epilepsy  accurately,  we  can  almost 
always  determine  that  the  twitching  begins  in  quite  a  limited  muscular  terri- 
tory— for  example,  in  the  face,  the  thumb,  etc.  The  attack  often  begins  with 
a  slight  sensory  aura  (parsesthesia  in  the  part  of  the  body  affected)  ;  then  fol- 
lows a  tonic  muscular  contraction  which  soon  passes  into  a  decided  clonus.  From 
this  point  the  twitchings  extend,  and  always  in  the  order  corresponding  to  the 
local  arrangement  of  the  different  centers  which  lie  next  to  one  another.  It  is 
therefore  always  of  importance  in  diagnosis  to  determine  in  what  group  of 
muscles  the  twitchings  begin,  because  we  can  thus  decide  that  the  corresponding 
cortical  center  is  the  chief  seat  of  the  morbid  affection.  In  the  muscles  inner- 
vated bilaterally  (the  frontal  muscles,  the  eye  muscles,  the  muscles  of  mastication, 
etc.)  the  convulsions  also  occur  bilaterally.  In  very  severe  attacks  the  spasm 
finaliy  involves  the  other  half  of  the  body,  the  irritation  being  conveyed  through 
the  fibers  of  the  corpus  callosum  to  the  corresponding  cortical  motor  centers  of  the 
68 


1074  DISEASES    OF   THE   NEEVOUS    SYSTEM 

other  hemisphere.  The  twitchings  usually  persist  the  longest  in  the  muscles  first 
affected.  In  the  attacks  of  circumscribed  cortical  epilepsy  there  is  no  disturbance 
of  consciousness,  but  if  the  convulsion  extends  to  both  halves  of  the  body,  there  is 
usually  loss  of  consciousness,  or  at  least  a  decided  clouding  of  consciousness.  The 
individual  attacks  last  only  a  short  time — about  one  or  two  minutes.  After  they 
cease  there  usually  remains  a  very  transitory  motor  weakness  or  even  complete 
paralysis  in  the  muscles  most  affected,  which  is  in  a  degree  the  indication  of  ex- 
haustion of  the  affected  center.  Temporary  disturbances  of  speech  are  often 
associated  with  right-sided  Jacksonian  epilepsy.  The  relation  of  convulsions  to 
permanent  paralysis  varies  greatly.  Often,  for  example,  when  there  is  haemor- 
rhage into  the  central  convolutions,  violent  unilateral  convulsions  come  on 
simultaneously  with  the  paralysis.  In  the  case  of  tumors  and  other  lesions 
which  develop  slowly,  partial  epileptiform  spasms  will  often  appear  quite  a  long 
time  before  there  are  persistent  symptoms  of  paralysis.  Finally,  it  is  not  rare 
for  epileptiform  attacks  to  occur  repeatedly  in  regions  that  are  already  paralytic. 
Either  of  the  occurrences  described  in  the  two  preceding  sentences  are  particu- 
larly strong  evidence  that  the  cortex  cerebri  is  diseased.  Besides  the  pronounced 
epileptic  attacks,  disease  of  the  motor  region  of  the  cortex  may  give  rise  to  less, 
violent  symptoms  of  motor  irritation,  such  as  occasional  twitching,  rhythmical 
twitching,  tonic  contraction,  etc. 

About  the  condition  of  sensation  when  there  is  cortical  paralysis  we  know  as- 
yet  very  little.  The  experimental  researches  of  Munk  and  the  anatomical  inves- 
tigations of  Elechsig  and  others  have  led  to  the  conclusion  that  the  termination 
of  the  sensory  tract  of  the  lemniscus,  the  so-called  sensory  sphere,  is  in  part  in 
the  same  cortical  region  as  the  motor  cortical  centers.  We  might,  therefore,  he- 
inclined  to  suppose  that  a  disturbance  of  sensation  would  invariably  accompany 
cortical  paralysis  in  man  also,  but  about  this  point  clinical  observations  do  not 
yet  give  perfectly  harmonious  results.  From  our  own  experience,  however,  we 
believe  that  we  can  say  that  sensory  disturbances  are  far  more  common  than  was- 
formerly  supposed.  It  is  a  remarkable  fact,  however,  that  the  sensibility  for  pain 
and  temperature  is  hardly  ever  affected,  but  the  disturbances  involve  the  simple 
sensations  of  touch  and  especially  the  stereognostic  sense  (recognition  of  objects 
by  touch,  see  page  795).  Disturbances  of  the  muscular  sense  and  ataxic  disturb- 
ances have  also  been  repeatedly  observed  in  diseases  of  the  motor  cortical  region.. 

2.  The  other  Parts  of  the  Cortex  Cerebri,  except  the  Center  for  Speech 

1.  Frontal  Convolutions.- — Unilateral  disease  of  the  anterior  portion  of  the' 
brain  may  be  quite  extensive  without  causing  notable  disturbance  of  any  kind. 
Certflinly  the  greatest  part  of  the  upper  two  frontal  convolutions  have  no  motor 
functions.  It  is,  however,  maintained  that  the  posterior  portion  contiguous  to 
the  anterior  central  convolution,  called  the  foot  of  the  frontal  convolutions,  does; 
contain  motor  centers.  We  have  stated  above  (page  1071)  that  the  motor  centers 
for  the  muscles  of  the  trunk  are  situated  in  the  upper  frontal  convolution,  espe- 
cially on  its  median  aspect.  This  is  the  reason  why  a  decided  swaying  of  the 
trunk  in  walking  and  in  standing  (just  as  in  cerebellar  ataxia,  vide  infra)  has- 
been  repeatedly  observed  in  diseases  of  the  frontal  lobe,  especially  in  tumors. 
The  third  (lowest)  frontal  convolution  on  the  left  side  has,  as  we  shall  soon  see,. 
an  undoubted  connection  with  the  motor  processes  of  speech. 

There  is  a  quite  generally  accepted  opinion  that  the  cortex  of  the  frontal  por- 
tion of  the  brain  is  to  be  regarded  as  the  "  seat  of  the  higher  psychical  functions.''^ 
Some  few  cases  are  on  record  where  extensive  bilateral  lesions  of  these  parts  had 
for  their  only  manifestations  mental  symptoms  (loss  of  mental  functions,  changes 
in  character,  the  so-called  morbid  wittiness,  Witzelsticht,  etc.)  without  any  other 
disturbances.     In  general  paralysis  also,  and  in  other  forms  of  dementia,  the  pre- 


THE   LOCALIZATION^   OF   CEEEBRAL   DISEASES 


1075 


dominance  of  atrophy  in  the  frontal  lobe  is  very  striking,  so  that  it  is  actually 
very  probable  that  the  frontal  lobe  has  a  close  relation  to  the  higher  mental 
processes.  Nevertheless,  we  can  not  emphasize  too  much  the  fact  that,  at  present, 
we  have  no  certain  knowledge  about  the  precise  form  of  this  relation  or  of  the 
nature  of  the  physical  functions. 

2.  Parietal  Convolutions. — We  know  but  little  about  the  fimctions  of  the 
cortex  of  the  parietal  lobe,  and  the  symptoms  which  might  indicate  disease  of 
that  portion  of  the  cerebrum.  According  to  Elechsig,  a  large  part  of  the  sensory 
tract  of  the  tegmentum  ends  in  the  parietal  cortex.  We  might  therefore  expect 
decided  disturbances  of  sensibility  in  diseases  of  the  parietal  lobe,  but  unequivocal 
clinical  and  anatomical  evidence  in  support  of  this  hypothesis  is  still  almost 
wholly  lacking.  Observations  on  the  occurrence  of  motor  disturbances  in  diseases 
of  the  parietal  cortex  are  somewhat  more  numerous.  Centers  for  associated 
movements  of  the  eyes  seem  to  be  situated  in  this  region  (in  the  angular  gyrus). 
In  diseases  of  this  region  we  may  often  observe  an  interesting  symptom  of  irrita- 
tion, the  so-called  "  conjugate  deviation  " — 

that  is,  the  simultaneous  turning  of  the  head 
and  eyes  to  one  side.  The  angular  gyrus  is 
also  said  to  contain  a  center  for  the  ocular 
portion  of  the  facial  (orbicularis  oculi  mus- 
cle) and  the  levator  palpebrse  superioris ; 
but  of  course  these  statements  have  not  been 
universally  accepted. 

3.  Occipital  Convolutions. — The  clinical 
and  experimental  investigations  of  the  last 
few  years  have  all  shown  that  the  occipital 
portion  of  the  cerebrum  contains  the  cortical 
center  for  visual  sensations.  It  is  here,  in  all 
probability,  that  the  fibers  of  the  optic  nerve 
terminate  in  the  cortex  cerebri.  A  glance 
at  the  accompanying  diagram  (Fig.  174) 
will  make  it  easy  to  understand  the  disturb- 
ances  of  vision   which   result   from   lesions 

of  the  occipital  lobe.  L  represents  the  left  eye  and  R  the  right,  CTi  the  optic 
chiasma,  where,  as  is  now  certain,  some  of  the  fibers  of  the  optic  nerves  cross  to 
the  opposite  side.  The  fibers  (distinguished  by  a  broken  line)  from  the  outer 
or  temporal  half  of  each  retina  extend,  without  crossing,  into  the  correspond- 
ing optic  tract  {Tract,  opt.),  while  those  from  the  inner  or  nasal  half  of 
the  retina  cross  over  in  the  chiasma.  The  right  occipital  lobe,  for  example, 
comes  in  this  way  to  receive  the  fibers  from  the  outer  half  of  the  right 
retina  and  from  the  inner  half  of  the  left.  If  the  right  occipital  lobe  becomes 
disorganized,  then  the  images  formed  upon  the  parts  of  the  retinas  just  named, 
belonging  to  the  left  half  of  the  field  of  vision,  are  unperceived.  With  each  eye 
the  patient  sees  only  such  objects  as  lie  in  the  right  half  of  his  field  of  vision, 
and  is  blind  to  all  that  lies  upon  his  left.  This  sort  of  visual  disturbance,  where 
each  eye  becomes  blind  to  the  same  "  homonymous  "  portions  of  the  field  of  vision, 
is  termed  hemianopsia,  or  hemiopia.  A  lesion  of  the  right  occipital  lobe  causes, 
therefore,  left-sided  hemianopsia,  and,  vice  versa,  destruction  of  the  left  occipi- 
tal lobe  entails  right-sided  hemianopsia.* 


Fig.  174. — Diagram  of  the  course  of  the  optic 
fibers  in  the  chiasma. 


[*  When  hemianopsia  is  due  to  a  lesion  between  the  chia.sma  and  the  pulvinar  and  crenieulate 
body  (second  optic  neurone,  vide  infra,  page  1089),  tlie  pupil  does  not  react  when  light  is  thrown  on 
the  blind  half  of  the  retina,  although  it  does  react  when  light  is  thrown  on  the  sound  half  (  Wernicke's 
'•  heniiopic  pupillary  reaction").  When  hemianopsia  is  due  to  a  lesion  between  these  ganglia  und  the 
cuneus  (third  optic  neurone)  this  heiuiopic  reaction  does  not  occur.— K.] 


1076  DISEASES    OF    THE   NEEVOUS    SYSTEM 

The  anatomical  evidence  is  still  very  contradictory  as  to  the  precise  localiza> 
tion  of  the  visual  center.  Disturbances  of  vision  are  found  most  constantly 
in  diseases  of  the  cuneus  and  the  first  occipital  convolution.  In  this  region  the 
sensations  of  light  as  such  seem  therefore  to  take  their  rise.  In  diseases  of  the 
medullated  layers  of  the  occipital  lobes  and  their  vicinity  (angular  gyrus) — that 
is,  of  the  connecting  tracts  between  the  occipital  cortex  and  other  cortical  regions 
— ^we  sometimes  observe  the  interesting  symptom  of  so-called  "  soul  blindness  " 
(Munk).  This  disturbance  is  when  the  patient  can  still  see  objects,  but  can  not 
recognize  what  they  signify.  He  no  longer  knows  what  to  do  with  them,  or  he 
uses  them  in  the  most  utterly  wrong  way.  He  no  longer  recognizes  his  acquaint- 
ances by  their  appearance,  but  only  by  the  sound  of  their  voice.  In  diseases  of 
the  left  occipital  lobe  the  connections  between  the  optic  impressions  and  ideas 
of  language  may  sometimes  be  solely  affected;  then  there  develop  optic  aphasia 
and  alexia;  the  patient  recognizes  objects,  but  he  can  not  name  them.  He  can  not 
read  or  copy,  but  he  can  write  very  well  spontaneously  and  from  dictation  (com- 
pare the  following  section). 

4.  Temporal  Convolutions. — The  relation  of  the  temporal  lobe  to  hearing  is 
apparently  analogous  with  that  of  the  occipital  lobe  to  vision.  Destruction  of  the 
posterior  half  of  the  superior  temporal  convolution,  according  to  some  obseWa- 
tions,  is  apparently  capable  of  causing  actual  deafness  in  the  opposite  ear;  but 
the  trouble  usually  disappears  in  a  very  short  time.  Each  auditory  nerve  is  there- 
fore probably  connected  with  both  temporal  lobes.  It  is  much  more  certain  than 
these  observations  of  actual  disturbance  of  hearing,  that  diseases  of  the  [left] 
superior  (first)  temporal  convolution  cause  so-called  word  deafness  ("  soul  deaf- 
ness ")^that  is,  the  loss  of  comprehension  of  spoken  language.  We  will  return 
again  to  this  condition,  which  is  usually  associated  with  motor  aphasia. 

We  may  observe,  in  conclusion,  that  the  olfactory  nerve  probably  ends  in  the 
gyrus  uneinatus  and  the  parts  adjacent  (Fig.  171,  page  1071),  so  that  we  may 
assume  that  that  is  the  center  for  smelL 

[The  sensori-motor  centers  in  the  Rolandic  region,  and  the  special  centers  for 
vision,  hearing,  and  smell  which  have  just  been  described,  occupy  only  about  one 
third  of  the  area  of  the  cerebral  cortex.  Flechsig  has  found  that  the  fibers  con- 
nected with  these  areas  assume  their  myeline  sheaths  at  an  early  period  of 
foetal  life,  while  the  fibers  connected  with  other  regions  become  myelinized  much 
later.  These  other  regions  he  regards  as  association  centers,  and  believes  that 
they  are  especially  concerned  in  the  higher  intellectual  functions.  The  anterior 
association  centers,  embracing  the  anterior  portions  of  the  frontal  convolutions 
and  the  gyrus  rectus,  are  supposed  by  him  to  be  the  chief  centers  for  ideas  of 
personality.  The  posterior  association  centers  include  the  prsecuneus,  the 
parietal  convolutions  (except  the  posterior  central  convolution),  all  portions  of 
the  occipital  cortex  except  the  visual  area,  and  all  portions  of  the  temporal  cortex 
except  the  auditory  and  olfactory  areas.  These  centers  are  supposed  to  be  the 
centers  for  ideas  referring  to  the  external  world.  The  island  of  Reil  and  the 
parts  adjacent  form  the  middle  association  center.  Flechsig's  hypotheses  have 
been  strongly  opposed,  especially  on  the  anatomical  side.  It  is  doubtful  whether 
the  projection  and  the  association  centers  in  the  cortex  can  be  so  definitely  dis- 
tinguished, but  the  hypotheses  thus  advanced  have  also  some  clinical  and  patho- 
logical support,  and  they  present  a  rich  field  for  further  investigation. — K.] 


THE    LOCALIZATION    OF    CEREBEAL   DISEASES  1077 

3.  The  Centers  of  Speech,  and  the  Disturbances  of  Speech 

{ Ap]ta>sia  and  Allied   Condition^) 

The  Various  Forms  of  Aphasia,  and  their  Anatomical  Localization. — As  we 

remarked  at  the  very  begiiuiing-  of  this  chapter,  the  peculiar  derangements  of 
speech  observed  in  many  cerebral  diseases  were  the  first  symptoms  which  were 
found  to  be  caused  by  a  distinctly  localized  cerebral  lesion.  .For  the  better  under- 
standing of  this  extremely  interesting  subject,  it  is  necessary  that  we  should 
enter  somewhat  minutely  into  the  processes  connected  with  normal  speech. 

Incitement  to  speech — that  is,  to  the  oral  expression  of  our  thoughts  to  others 
— comes  either  from  an  internal  impulse  or  from  external  causes  which  excite 
this  impulse.  Speech  always  requires  internal  mental  activities — the  presence  of 
ideas  and  their  transformation  into  that  which  we  wish  to  communicate  by 
speech.  Where  there  are  no  conceptions  there  can  be  no  words.  The  demented 
person  is  silent,  because,  like  the  newborn  infant  or  the  brute,  he  has  nothing  to 
say;  but,  on  the  other  hand,  the  impulse  to  speak  must  also  be  present.  In 
melancholic  insanity  we  sometimes  observe  persistent  loss  of  speech,  not  from 
any  lack  of  something  to  say,  but  because  there  is  no  incitement  to  the  act,  or 
because  inhibitory  influences  immediately  repress  any  tendency  to  utter  words. 
If  we  take  for  granted  that  the  mental  material  for  speech  exists,  then  the  trans- 
formation of  this  material  into  actual  speech  is  a  result  of  the  following'  compli- 
cated processes,  the  disturbance  of  which,  individually,  produces  the  various 
forms  of  aphasia. 

In  the  first  place,  the  speaker  must  be  acquainted  with  the  word  which  ex- 
presses the  mental  conception.  If,  for  instance,  he  wishes  to  tell  another  the 
name  of  some  animal,  he  must  know  the  appropriate  word — "  dog,"  "  sparrow," 
"  frog-."  This  knowledge,  which,  as  far  as  our  mother  tongue  is  concerned,  we 
all  acquired  in  childhood,  may,  as  experience  shows,  be  lost  again  in  case  of  cere- 
bral disease.  Just  as  we  may  ourselves  forget  a  word  momentarily,  or  as  any 
healthy  person  may,  at  the  sight  of  an  animal  that  is  perhaps  rather  rare,  be 
"  unable  at  the  minute  to  think  of  its  name,"  so  in  disease  one  may  forget  all  or 
a  greater  or  less  number  of  words.  Such  a  patient  sees  a  dog,  and  knows  well 
enough  that  it  is  an  animal  possessed  of  such  and  such  qualities,  but  he  has 
forgotten  its  name.  The  association  between  the  conception  "  dog,"  and  like- 
wise between  the  perception  of  a  dog  by  the  eye,  and  the  appropriate  vocal  repre- 
sentation "  dog,"  is  lost.  This  condition  is  termed  amnesic  or  sensory  aphasia, 
because  it  is  due  to  complete  or  partial  loss  of  the  memory  for  words.  The 
patient  knows  perfectly  well  what  he  wishes  to  say,  but  the  words  escape  him.  At 
the  same  time,  in  cases  of  pure  amnesic  aphasia,  the  power  of  repetition  is  unim- 
paired. As  soon  as  we  say  "  dog  "  to  the  patient,  he  repeats  the  word  perfectly 
well;  and  sometimes  he  also  perceives  that  this  is  really  the  correct  word;  bvit  in 
other  instances,  although  the  word  is  correctly  repeated,  the  patient  does  not 
become  conscious  of  its  meaning  {vide  infra  "word  deafness  "). 

If  we  examine  cases  of  amnesic  aphasia  more  carefully  we  may  notice  by  what 
special  sensory  perceptions  the  memory  of  the  lost  word  can  be  eventually  called 
back.  Although  the  mere  idea  alone  does  not  call  the  proper  word  back  to  con- 
sciousness, the  sensory  perception  (so  far  as  we  have  to  do  with  external  objects) 
may  often  by  association  recall  the  corresponding  word.  It  is,  of  course,  most 
frequently  the  visual  perception  which  recalls  the  memory  of  the  word.  If  this 
association  also  fails  we  speak  of  an  optic-amnesic  aphasia.  In  other  cases 
auditory  impressions  (e.  g.,  the  ticking  of  a  watch,  the  note  of  a  musical  instru- 
ment) may  restore  the  recollection  of  the  proper  word,  or,  in  other  cases  still, 
sensations  of  touch,  taste,  or  smell.  All  these  associations  between  given  percep- 
tions and  the  corresponding  verbal  representations  may  be  destroyed  at  the  same 


1078  DISEASES    OF   THE   ^^EEVOUS    SYSTEM 

time  or  one  by  one,  or  they  may  be  partially  retained.  Sometimes  it  is  only 
by  the  simultaneous  action  of  different  sensory  impressions — e.  g.,  perceptions 
of  sig'ht  and  touch — that  the  idea  of  the  word  can  again  be  recalled  to  con- 
sciousness. 

Of  great  interest  are  certain  cases  where  there  is  only  partial  amnesia.  These 
have  been  repeatedly  observed.  Thus  a  patient  forgot  nothing  but  his  own  name, 
remembering  all  other  words  perfectly;  or  the  loss  of  words  may  be  confined  to 
but  one  language,  the  patient  being  still  able  to  express  himself  tolerably  well  in 
another  tongue.  In  a  case  observed  by  Graves,  the  patient  still  knew  the  initial 
letter  of  all  words ;  if,  for  example,  he  saw  a  cow,  he  would  know  that  the  corre- 
sponding word  began  with  C,  and  would  look  under  C  in  a  dictionary  till  he  found 
the  word. 

Among  the  amnesic  disturbances,  we  may  also  class  the  dissolution  of  closely 
associated  sequences  of  words,  as  are  found,  for  example,  in  the  order  of  numbers, 
in  the  names  of  the  days  of  the  week,  the  names  of  the  months,  familiar  prayers, 
etc.  Although  such  sequences  of  words  which  have  been  practiced  from  childhood 
may  on  the  one  hand  (vide  infra)  greatly  facilitate  the  pronunciation  of  the  indi- 
vidual words,  on  the  other  hand  the  connection  often  becomes  so  loose  that  the 
patient  may  repeat  the  whole  list  very  well  after  any  person,  but  he  can  not  recite 
it  spontaneously.  Such  tests  often  show  most  interesting  peculiarities.  Thus  we 
have  repeatedly  noticed,  for  example,  that  aphasic  patients  can  repeat  the  names 
of  the  days  of  the  week  very  well  in  their  ordinary  sequence,  but  that  it  is  very 
hard  to  say  them  backward.  Many  patients  find  great  difficulty  in  counting 
backward. 

If  the  memory  for  words  be  retained,  the  next  requisite  for  speaking  is  the 
transfer  of  the  word  image  into  such  action  of  the  muscles  of  our  organs  of  speech 
as  is  calculated  to  produce  the  word  in  question  as  an  actual  sound.  This  motor 
process  is  so  complicated  that  an  extremely  accurate  co-ordination  of  movements 
is  demanded  for  the  correct  pronunciation  of  the  word.  Man  therefore  possesses 
a  separate  center,  in  which  this  transfer  of  the  word  image  into  the  motor  pro- 
cesses of  speech  takes  place.  If  this  center  be  diseased,  there  again  results  a  loss, 
or  at  least  a  greater  or  less  impairment,  of  speech.  The  patient  is  in  this  case 
well  aware  of  the  word  he  wishes  to  say,  but  he  can  not  pronounce  it.  He  has, 
if  we  may  use  the  expression,  forgotten  the  movements  that  are  essential  to 
speaking.  His  tongue  and  lips  are  not  really  paralyzed,  but  the  patient  no  longer 
knows  how  to  make  use  of  them  for  talking.  He  has  reverted  to  the  condition  of 
childhood,  before  he  had  learned  to  talk.  The  patient  often  makes  the  greatest 
effort  to  speak.  The  word  he  wishes  to  utter  "  keeps  hovering  before  him  " ;  he 
moves  his  mouth  in  the  most  striking  manner,  but  brings  out  only  an  occasional 
sound,  and  that  incorrect.  This  commonest  form  of  speech  disturbance  is  known 
as  ataxic  aphasia.  Of  course  it  is  equally  impossible  for  the  patient  to  repeat 
a  word  after  some  one  else.  He  keeps  his  eyes  fixed  on  the  mouth  of  the  speaker, 
and  endeavors  to  imitate  the  motions  of  his  mouth,  but  he  is  either  partially  or 
totally  unable  to  reproduce  the  sound. 

Ataxic  aphasia  exhibits  many  degrees  of  intensity.  On  the  one  hand  there  are 
cases  of  complete  aphasia,  where  the  patient  can  utter  only  such  separate  sounds 
as  "  a,"  "  e,"  etc.  And,  on  the  other  hand,  there  are  also  mild  cases  where  there 
are  merely  errors  in  pronunciation.  Such  cases  may  best  be  termed  "  ataxic  " 
aphasia.  The  patient  pronounces  many  words  correctly,  but  with  others  there 
are  such  mistakes  as  the  transposition  of  individual  letters,  the  misplacement  or 
omission  of  letters,  or,  finally,  the  adding  on  of  letters.  For  example,  he  will 
say  thens  instead  of  then,  widow  instead  of  window,  dipter  instead  of  dipper,  hefd 
instead  of  held,  wrelster  instead  of  wrestler,  and  belnow  instead  of  below.  This 
mildest  form  of  ataxic  disturbance  is  termed  "  stumbling  over  syllables  "   (Sil- 


THE   LOCALIZATION   OF    CEREBRAL   DISEASES  1079 

hernstolpern),  or  "literal  ataxia."  Patients  sometimes  affix  the  same  inappro- 
priate termination  to  many  words 5  for  example,  a  woman  used  to  count:  "  onen, 
twoen,  threen,  fouren,  fiven,"  etc.  In  most  instances  the  patient  can  pronounce 
some  words  tolerably  well,  others  only  imperfectly  and  with  difficulty,  and  still 
others  not  at  all.  Usually  the  patient  gradually  learns  a  few  common  words  and 
expressions  (e.  g.,  "  good  morning  ")  by  means  of  persistence  in  repeating  them 
as  they  are  uttered  by  another,  so  that  he  pronounces  them  better  and  better. 
What  is  very  remarkable,  and  not  so  very  rare,  is  that  a  patient  will  be  able  when 
in  a  passion  to  pronounce  a  word,  such  as  an  expression  of  anger,  an  oath,  or  an 
exclamation,  perfectly  well,  because  it  is  done  to  a  certain  extent  involuntarily, 
while  he  can  not  utter  the  same  words  if  he  wishes  to  say  them.  One  patient 
under  our  observation  always  said  "  well,"  in  answer  to  the  question,  "  How  are 
you  ?  "  but  she  was  wholly  unable  to  repeat  the  word  "  well  "  by  itself  when  asked 
to  do  so.  Association  also  often  exerts  an  appreciable  influence ;  for  example,  a 
patient  who  finds  it  absolutely  impossible  to  pronounce  "  six,"  utters  it  with 
perfect  distinctness  if  he  begins  to  count  from  one,  in  the  ordinary  way,  up 
to  six.  When  patients  have  at  last  managed  to  say  the  right  word,  they  some- 
times stick  to  it — that  is,  they  continue  to  repeat  this  word  when  they  should  say 
something  else.  In  many  severe  cases  of  motor  aphasia  the  whole  capacity  for 
speech  is  limited  to  a  few  syllables  or  a  few  brief  phrases,  which  always  appear 
as  soon  as  the  patient  makes  any  attempt  to  speak  (so-called  monophasia). 

A  patient  of  our  own  could  for  a  long  time  utter  nothing  but  the  meaningless 
words,  "  selher  sag  ich  ndmlich  selher^'  (self  say  I  namely  self).  The  entire 
verbal  thesaurus  of  another  (female)  patient  whom  we  saw  consisted  of  the 
meaningless  sounds  "  bibi  "  and  "  eibibi."  Still  a  third  could  say  only  "  tinne, 
tinne."  The  patient  is  quite  well  aware  that  what  he  says  is  wrong,  but,  despite 
all  his  efforts,  every  attempt  to  speak  excites  these  same  sounds.  It  produces  a 
comical  impression  to  see  the  patient  use  the  same  invariable  word,  with  all  sorts 
of  facial  expression.  Thus  the  woman  mentioned  above  begged  for  things,  with 
"  bibi,"  in  a  coaxing  tone,  while  sometimes  she  would  give  vent  to  violent  anger 
with  a  loud  "  bibibibi." 

Amnesic  (sensory)  aphasia  may  also  vary  greatly  in  degree.  It  is  only  rarely 
observed  in  its  pure  form,  but  it  is  usually  associated  with  motor  aphasia.  The 
amnesic  (sensory)  aphasia  does  not  always  consist  of  the  complete  loss  of  memory 
of  words,  but  very  often  merely  of  a  disturbance  of  the  firm  bond  of  association 
between  ideas  and  their  corresponding  words.  Patients  with  sensory  aphasia 
therefore  very  often  confuse  their  words  or  form  entirely  false  and  senseless 
words  (so-called  paraphasia).  Such  a  patient  may  talk  a  long  while  without 
conveying  any  idea  to  the  listener,  inasmuch  as  he  says  "  brush "  instead  of 
"  bed,"  or  "  gove  "  instead  of  "  give,"  etc.  It  is  a  very  interesting  fact  that  in 
paraphasia  the  influence  of  certain  associations  are  often  manifest.  The  patient, 
for  instance,  utters  a  wrong  word  which  has  a  certain  resemblance  in  sound  to 
the  right  one,  begins  with  the  same  syllable,  etc.  Purely  ideal  associations  some- 
times also  play  a  part;  thus  one  of  our  patients  called  a  white  handkerchief 
"  snow,"  etc. 

The  aphasic  disturbances  thus  far  described  all  refer  to  the  power  of  speech — 
that  is,  to  the  uttering  of  ideas  aloud,  but  we  now  come  to  the  description  of 
the  disturbance  in  the  understanding  of  speech,  which  is  often  associated  with 
this  or  which  in  rare  cases  may  occur  by  itself.  This  disturbance  consists  of  the 
patient's  inability  to  understand  the  Avords  spoken  to  him,  although  he  can 
hear  them  well.  The  word  when  heard  no  longer  excites  in  his  consciousness 
the  appropriate  idea.  The  patient  is  not  really  deaf,  for  he  hears  everything, 
but  he  no  longer  understands  what  he  hears,  and  he  has  forgotten  what  the  words 
signify.    The  vernacular  sounds  to  him  as  a  foreign  language,  of  which  he  knows 


1080  DISEASES    OF    THE    NEEVOUS    SYSTEM 

nothing  or  of  which  he  has  learned  but  little,  would  to  a  well  man.  This  con- 
dition is  best  termed,  according  to  Kussmaul,  "  word  deafness  "  or  "  soul  deaf- 
ness." Wernicke  also  calls  word  deafness  "  sensory  aphasia,"  which  does  not 
seem  to  us  to  be  quite  correct,  since  word  deafness — that  is,  the  defective  under- 
standing of  speech — is  not  identical  with  the  inability  to  speak  in  consequence  of 
the  loss  of  ideas  of  speech  (amnesic  or  sensory  aphasia  in  the  stricter  sense). 
Amnesic  aphasia  and  word  deafness  are  of  course  very  often  associated  from  allied 
reasons,  but  it  may  very  well  be  the  case  that  a  patient  has  forgotten  the  word 
for  an  idea,  but  that  he  at  once  recognizes  its  significance  as  soon  as  he  hears 
it.  Word  deafness  is  in  a  certain  sense  a  higher  degree  of  verbal  amnesia.  A 
healthy  person  often  can  not  find  the  word  for  an  idea  in  a  foreign  language,, 
but  the  idea  comes  to  him  at  once  if  he  hears  the  word.  It  is  much  harder  tO' 
speak  a  foreign  language  than  to  understand  it. 

Slighter  degrees  of  word  deafness  are  very  often  (we  might  say  almost  always) 
associated  with  motor  aphasia.  We  must,  however,  search  for  thera  carefully, 
preferably  by  giving  the  patient  certain  commands  (to  point  to  certain  objects, 
or  parts  of  the  body,  to  perform  certain  acts),  avoiding  any  suggestive  help  by 
signs  or  expression,  and  seeing  whether  he  understands  what  is  said  and  acts 
accordingly.  We  may  also  test  him  by  holding  an  object  in  front  of  him  and 
calling  it  by  various  wrong  names  and  then  finally  giving  it  the  correct  name. 
We  thus  see  whether  the  patient  gives  any  sign  of  recognizing  the  correct  name 
or  not.  The  detection  of  word  deafness  is  usually  limited,  however,  to  concrete 
nouns,  certain  verbs  or  adjectives,  but  it  is  hardly  practicable  to  examine  for 
word  deafness  for  any  other  words  (many  abstract  words,  adverbs,  etc.),  espe- 
cially when  the  patient  is  also  aphasic.  We  very  often  notice,  therefore,  that 
aphasic  patients  understand  very  well  the  usual  brief  questions  directed  to  them, 
but  that  they  are  quite  unable  to  follow  with  complete  understanding  any  long 
speech,  anything  that  is  read  to  them,  etc.  They  often  fail  to  understand  be- 
cause the  rapidity  of  perception  is  much  impaired.  We  have  seen  patients  who 
understood  any  question  or  sentence  only  after  the  words  had  been  repeated 
several  times.  In  such  patients  we  also  see  at  times  a  decided  failure  of  memory 
of  the  actual  words.  If  we  repeat  to  them  any  long  sentence,  they  can  repeat 
only  the  first  four  or  five  words  correctly,  while  they  have  wholly  forgotten  the 
end  of  the  sentence,  or  at  best  they  have  retained  the  sense  but  not  the  sound  of 
the  words.  We  can  readily  understand  how  this  actual  weakness  of  memory, 
or  abnormally  easy  fatigue  of  memory,  may  have  an  inhibitory  influence  on  the 
understanding  of  speech. 

The  list  of  disturbances  occurring  in  aphasia  is  by  no  means  exhausted  by  the 
examination  of  the  motor  power  of  speech  as  such  and  of  the  understanding  of 
words  when  heard.  Word  and  idea  are  jet  closely  associated  with  two  other 
modes  of  expression,  which  are  brought  about  not  by  the  ear  but  by  the  eye.  We 
mean  the  movements  of  mimetic  expression  (or  the  language  of  signs  in  the  ordi- 
nary sense  of  the  word)  and  then  the  far  more  important  written  or  printed 
optical  signs — letters,  script,  numbers,  etc.  Here  also  we  find  the  close  associa- 
tions between  signs  and  ideas  on  the  one  hand  and  signs  and  sounds  on  the  other. 
These  associations  may  be  loosened  or  wholly  lost,  and  then  there  follow  a  series 
of  further  morbid  symptoms  which  are  often  to  be  observed  as  existing  with 
aphasia. 

The  disturbances  of  movements  of  mimetic  expression  ("  amimia ")  have 
not  a  very  great  practical  significance,  but  they  often  show  many  interesting 
features.  We  are  often  surprised  to  see  how  incapable  aphasic  patients,  who 
can  not  speak,  are  in  giving  expression  to  their  thoughts,  desires,  etc.,  by  signs. 
They  sometimes  employ  signs  in  a  way  that  is  quite  contrary  to  their  usual  mean- 
ing.   Thus  we  have  often  seen  patients  nod  their  heads  when  they  clearly  wished 


THE   LOCALIZATION    OF    CEREBRAL   DISEASES  1081 

to  deny  something.  The  understanding  of  signs  made  by  others  may  also  be 
much  diminished. 

Agraphia,  the  disturbance  of  the  power  of  expression  in  writing,  is  far  more 
important  than  amimia.  We  can  also  distinguish  here  a  pure  motor  (ataxic) 
and  an  amnesic  agraphia. 

By  motor  (ataxic)  agraphia  we  understand,  of  course,  not  the  inability  to 
write  on  account  of  any  paralysis  of  the  arm,  but  the  inability  to  unite  the  dif- 
ferent letters  correctly  to  make  up  the  written  word.  The  patient  is  also  unable 
to  copy  a  word  put  before  him,  but  he  can  often  do  this  well  when  he  can  not  write 
spontaneously  or  from  dictation.  Then  there  is  writing  amnesia  (amnesic 
agraphia).  In  such  cases  also  we  often  see  interesting  relations  of  association, 
since  the  patient  may  write  a  wrong  word  which  in  sound  or  idea  is  somewhat 
like  the  word  desired.  The  entire  manner  of  writing  in  such  cases  is  often  notice- 
able. The  patient  holds  his  pencil  or  his  pen  with  peculiar  awkwardness;  he 
writes  a  very  small  hand,  or  the  letters  gradually  grow  smaller,  etc. 

Alexia  has  the  same  relation  to  agraphia  that  word  deafness  has  to  aphasia. 
Alexia  is  word  blindness — that  is,  the  defective  understanding  of  written  speech, 
the  inability  to  read.  This  disturbance  is  plainly  allied  to  soul  blindness  above 
described  (page  1076),  but  alexia  may  very  well  exist  without  special  soul  blind- 
ness, since  only  the  association  between  the  written  signs  and  the  corresponding 
idea  has  been  lost.  Patients  with  pure  alexia  can  neither  read  nor  copy  what  is 
written,  but  they  are  able  to  write  very  well  spontaneously  or  from  dictation. 
Speaking  accurately,  we  miist  distinguish  between  reading  aloud  and  reading  to 
one's  self.  The  printed  word  Avhen  seen  may  excite  the  idea,  although  it  can  not 
be  pronounced  aloud.  On  the  other  hand,  many  patients  can  read  aloud  without 
understanding  what  is  read  or  pronounced. 

In  conclusion  we  may  mention  briefly  an  interesting  disturbance  which  is  also 
closely  related  to  aphasia — the  disturbance  in  the  power  of  musical  expression 
I  amusia] .  In  these  cases  the  most  varied  morbid  symptoms  may  occur,  which 
refer  both  to  the  perception  and  to  the  reproduction  of  musical  tones.  The  asso- 
ciations between  ideas  of  tone  and  the  printed  notes  may  be  loosened  or  wholly 
lost.  The  examination  of  the  relations  existing  between  words  and  tones  as  they 
exist  in  singing  is  also  very  interesting.  We  have  often  seen  aphasic  patients 
who  could  not  repeat  the  words  of  a  familiar  song,  but  who  could  at  once  utter  the 
correct  words  plainly  if  they  sang  it. 

From  all  that  has  been  said  we  can  see  how  extremely  manifold  and  in  how 
many  varying  combinations  the  special  symptoms  of  aphasia  may  occur.  Only 
a  careful  and  thorough  study  of  each  individual  case  of  aphasia  will  insure  an 
exhaustive  review  of  all  the  disturbances  present. 

The  Anatomical  Changes  occurring  in  Aphasia. — As  has  already  been  men- 
tioned, aphasia  was  the  first  cerebral  symptom  which  could  be  referred  to  disease 
of  any  definite  part  of  the  brain.  The  whole  "  topical  diagnosis  "  of  diseases  of 
the  brain  has  therefore  started  from  aphasia.  As  early  as  1825  Bouillaud  affirmed 
that  disease  of  the  anterior  lobes  of  the  brain  is  alone  capable  of  producing  dis- 
turbances of  speech.  In  1836  another  French  physician.  Mare  Dax,  pointed  out 
for  the  first  time  that  only  lesions  of  the  left  half  of  the  brain  cause  aphasia ;  and 
in  1861  Broca  was  able  at  last  to  declare  that  the  "  center  for  speech  "  lies  in  the 
left  third  frontal  convolution  ("  Broca's  convolution  ").  This  law  has  since  been 
confirmed  by  hundreds  of  autopsies,  but  it  applies  only  to  true  motor  aphasia.  If 
there  is  motor  aphasia,  we  may  with  certainty  assume  that  there  is  disease  of  the 
posterior  portion  of  the  left  third  frontal  convolution.  It  is  in  this  region,  there- 
fore, that  those  complicated  processes  of  motor  co-ordination  which  are  essential 
to  the  utterance  of  a  word  take  place.  A  second  important  and  positive  fact  we 
owe  to  Wernicke :  if  there  is,  either  with  motor  aphasia  or  alone,  word  deafness — 


1082  DISEASES    OE   THE   XERYOUS    SYSTEM 

that  is,  a  defective  understanding  of  spoken  language — we  may  from  this  fact 
ahnost  always  conclude  that  there  is  disease  of  the  left  upper  (first)  temporal 
convolution  (and  especially  its  posterior  portion).  In  this  part  of  the  brain,  then, 
is  the  connection  between  the  heard  word  and  the  corresponding  idea.  Among 
other  localizations  we  may  mention  that  pronounced  motor  agraphia  probably 
points  to  a  lesion  of  the  foot — that  is,  of  the  posterior  portion— of  the  second  left 
frontal  convolution.  Pure  alexia  (word  blindness)  has  been  observed  especially 
in  focal  diseases  of  the  left  lower  parietal  lobe  (region  of  the  angular  gyrus)  and 
the  neighboring  parts  of  the  occipital  lobe. 

The  anatomical  localizations  of  the  different  forms  of  amnesic  aphasia  can 
be  determined  less  accurately  because  in  such  cases  there  may  be  various  possible 
interruptions  between  the  various  centers  of  perception  and  the  speech  centers 
("  conduction  aphasia,"  "  subcortical  aphasia  ").  Since,  however,  the  tracts  lead- 
ing to  the  motor-speech  center  probably  pass  through  the  neighborhood  of  the 
island  of  Eeil,  we  may  expect  that  amnesic  aphasia  would  occur  most  frequently 
in  destruction  of  this  region;  but,  from  reasons  that  are  easily  understood,  foci 
of  disease  in  other  situations  may  also  give  rise  to  such  "  conduction  aphasias." 
As  soon  as  amnesic  aphasia  is  associated  with  defective  understanding  of  speech 
(soul  deafness),  we  may  almost  always  assume  a  lesion  in  the  vicinity  of  the 
upper  temporal  convolution. 

j^o  general  rules  can  be  laid  down  as  to  the  prognosis  and  course  of  aphasia, 
inasmuch  as  everything  must  of  course  depend  upon  the  nature  of  the  disease 
which  excites  the  aphasia.  In  the  aphasias  due  to  cerebral  htemorrhage  or  cere- 
bral embolism  {vide  infra), -which  are  the  most  common,  we  very  often  observe 
that  the  disturbances  are  very  marked  at  first,  but  that  they  gradually  diminish 
or  wholly  disappear.  On  the  other  hand,  there  are  also  cases  of  almost  complete 
motor  aphasia,  which  may  persist  for  years  until  the  death  of  the  patient.  [When 
aphasia  occurs  in  childhood  it  usually  disappears  completely,  perhaps  because  the 
other  hemisphere  of  the  brain  becomes  educated. — K.] 

In  regard  to  treatment  we  can  here  mention  only  one  thing,  that  methodical 
training  in  the  form  of  actual  lessons  in  speaking  or  writing  may  sometimes  be 
of  some  service.  In  motor  aphasia  we  may  give  lessons,  just  as  to  deaf-mutes, 
by  assisting  the  new  practice  of  the  necessary  muscular  movements  by  visual 
impressions,  while  in  verbal  amnesia  methodical  training*  of  the  memory  is 
necessary  for  a  new  "  impression  "  of  the  forgotten  word.  Of  course  all  such 
training  demands  much  tact  and  patience  on  both  sides. 

[Dejerine's  Views  on  Aphasia. — The  doctrines  of  Dejerine  and  his  pupils 
have  acquired  so  much  importance  in  the  study  of  aphasic  disturbances,  and  these 
doctrines  differ  so  much  from  the  views  expressed  above,  that  it  seems  advisable 
to  give  a  brief  synopsis  of  them. 

According  to  Dejerine  there  are  only  three  centers  for  images  of  language : 
Broca's  center,  for  motor  images  of  articulation,  at  the  foot  of  the  left  third 
frontal  convolution ;  Wernicke's  center,  for  auditory  images  of  words,  in  the  pos- 
terior part  of  the  first  and  second  left  temporal  convolutions ;  and  the  center  for 
visual  images  of  words  in  the  angular  gyrus.  These  three  centers  form  the 
''  zone  of  language,"  and  surroiuid  the  extremity  of  the  fissure  of  Sylvius  like  a 
horseshoe  (see  Fig.  173,  page  1073).  They  are  connected  with  one  another  and 
also  with  the  adjacent  sensori-motor  (especially  that  part  which  contains  centers 
for  the  lips,  tongue,  and  larynx),  visual,  and  auditory  centers. 

The  zone  of  language  may  be  affected  by  disease  in  two  ways:  (1)  The  lesion 
may  destroy  a  part  of  the  zone  or  its  intrinsic  fibers ;  or  (2)  it  may  isolate  a  part 
of  the  zone  from  the  adjacent  cortex.  In  the  first  case — aphasia  from  lesion  of 
the  zone  of  langiiage,  true  aphasia,  or  cortical  aphasia — internal  language  as  a 
whole  and  all  the  forms  of  language  will  be  affected  to  a  greater  or  less  extent, 


THE   LOCALIZATION    OF   CEREBRAL   DISEASES  1083 

although  the  dominant  clinical  phenomena — motor  aphasia,  word  deafness,  word 
blindness — will  vary  with  the  seat-of  the  lesion.  The  idea  of  the  word  is  affected, 
and  this  gives  rise  to  a  considerable  degree  of  mental  impairment. 

In  true  motor  aphasia  from  destruction  of  Broca's  center  the  patient  may 
utter  an  occasional  word  (vide  supra,  page  1079),  but  he  is  unable  to  do  more  than 
that.  He  has,  moreover,  lost  the  idea  of  the  word  so  completely  that  he  can 
not  even  indicate  the  number  of  syllables  of  which  it  is  composed,  and  he  is 
wholly  unable  to  write  spontaneously  or  from  dictation,  except  that  he  can  often 
write  his  name  or  some  very  familiar  word.  The  co-existence  of  agraphia  is 
characteristic  of  this  form  of  motor  aphasia.  There  is  no  marked  word  deafness, 
although  the  spontaneous  evocation  of  auditory  images  is  affected  and  the  patient 
has  difficulty  in  comprehending  rapid  speech.  Word  blindness  is  less  marked, 
and  in  copying  the  patient  will  copy  print  as  script.  In  true  word  deafness  from 
destruction  of  Wernicke's  center  the  patient  may  seem  deaf,  confused,  or  even 
demented,  although  the  mental  failure  is  much  less  than  at  first  it  appears.  There 
is  inability  to  understand  what  is  said,  and  the  loss  of  all  auditory  images  de- 
prives the  motor  center  of  any  regulator,  so  that  the  patient  uses  wrong  words, 
or  even  mere  jargon — paraphasia  or  jargonaphasia.  There  is  usually  some  word 
blindness  and  the  patient  becomes  unable  to  write,  or  else,  on  account  of  the  loss 
of  the  idea  of  the  word,  he  may  write  nonsense  or  jargon — ^jargonagraphia. 
When  he  copies  he  usually  makes  a  servile  copy,  copying  print  as  print  and  script 
as  script.  In  true  word  blindness  there  is  also  complete  agraphia,  and  some 
degree  of  word  deafness  and  paraphasia.  In  these  sensory  forms  of  true  aphasia 
there  is  less  likely  to  be  any  paralysis,  owing  to  the  situation  of  the  affected 
centers. 

When  the  zone  of  language  is  still  intact,  but  when  the  lesion  has  simply 
cut  off  the  connections  of  its  centers  with  other  centers,  we  find  the  condition 
which  Dejerine  calls  pure  aphasia,  or  sub-cortical  aphasia.  In  these  cases  inter- 
nal language  is  unaffected,  the  idea  of  the  word  is  retained,  and  there  is  never 
agraphia.  The  symptoms  are  referable  solely  to  the  affected  center.  With  pure 
motor  aphasia  the  patient  can  write  normally  and  can  tell  the  number  of  sylla- 
bles in  a  word.  With  pure  word  deafness  the  only  symptoms  are  inability  to 
understand  what  is  said  and  to  write  from  dictation.  With  pure  word  blindness 
there  is  also  right  homonymous  hemianopsia,  and  the  patient  copies  in  a  slavish 
manner,  but  there  is  no  agraphia ;  he  can  write  normally,  both  spontaneously  and 
from  dictation.  In  no  form  of  pure  aphasia  is  there  any  mental  impairment. 
Dejerine  furthermore,  does  not  believe  that  there  is  any  special  writing  center 
at  the  foot  of  the  second  left  frontal  convolution  or  anywhere  else;  for  there  is 
agraphia  in  every  case  of  lesion  of  the  zone  of  language,  and  the  agraphia  is  mani- 
fested not  only  by  inability  to  write  with  either  hand,  but  by  inability  to  produce 
words  intelligently  by  arranging  lettered  blocks  or  by  the  use  of  the  type- 
writer.— K.] 

4.  The  Centrum  Ovale,  Internal  Capsule,  Central  Ganglia,  and  Region  of  the 

Corpora  Quadrigemina 

Centrum  Ovale. — The  white  substance  of  the  hemispheres  is  made  up,  so  far 
as  we  know  at  present,  both  of  commissural  fibers,  Avhich  connect  the  various 
cortical  centers  together,  and  of  fibers  which  proceed  downward  from  the  centers 
of  the  cortex  and  connect  these  centers  with  peripheral  parts  of  the  body  (corona 
radiata).  As  to  the  symptoms  caused  by  diseases  which  destroy  the  commissural 
fibers,  there  is  hardly  anything  known.  We  can  only  surmise  that  in  case  of 
disturbances  of  association,  such  as  we  have  studied  imder  aphasia  and  kindred 
disorders,  we  should  consider  lesions  of  commissural  fibers,  as  of  those  connect- 
ing together  the  temporal  and  frontal  lobes,  the  occipital  and  frontal  lobes,  etc. 


1084  DISEASES    OF   THE   NEEVOUS    SYSTEM 

A  break  in  the  continuity  of  the  fibers  of  the  corona  radiata  must  of  course  result 
in  the  same  symptoms  as  if  the  corresponding  center  were  itself  destroyed.  This 
explains  why  circumscribed  lesions  of  the  centrum  ovale,  if  they  involve  the 
motor  fibers  of  the  corona  radiata,  which  proceed  from  the  central  convolutions 
(and  only  if  they  do  this),  cause  hemiplegia,  or,  if  very  limited,  monoplegia. 
In  an  analogous  manner,  disease  of  the  white  substance  of  the  occipital  lobe  may 
entail  hemianopsia;  of  the  temporal  lobe,  auditory  disturbances,  such  as  word 
deafness.  More  than  once,  quite  extensive  disease  of  the  white  substance  of  the 
frontal  lobe  on  one  side  has  been  discovered  post  mortem,  although  no  symptoms 
whatever  had  been  caused  by  it.  Only  when  the  coronal  fibers  which  proceed  from 
the  left  third  frontal  convolution  are  involved  in  disease  is  motor  or  ataxic 
aphasia  inevitable. 

Internal  Capsule. — The  most  important  facts  relating  to  the  functions  of  the 
internal  capsule,  as  far  as  at  present  known,  have  been  already  stated.  In  par- 
ticular, it  was  pointed  out  that  through  the  posterior  limb  of  the  internal  cap- 
sule, in  a  comparatively  narrow  space,  passes  the  pyramidal  tract  on  its  way  from 
the  central  convolutions  to  the  crura  cerebri  (see  Fig.  95,  page  829).  Here, 
then,  even  a  very  limited  focal  disease  must  lead  to  complete  hemiplegia  on  the 
opposite  side  of  the  body.  Clinical  experience  also  shows  that  the  largest  number 
of  cases  of  persistent  hemiplegia  are  occasioned  by  disease  in  this  spot.  The 
arrangement  of  the  fibers  in  this  region  is  such  that  the  fibers  for  the  face  are 
for  the  most  part  anterior,  the  fibers  for  the  arm  next,  and  the  fibers  for  the  leg 
posterior.  In  a  brilliant  experimental  study  Horsley  and  Beevor  have  shown  that 
in  monkeys  the  different  motor  portions  of  the  internal  capsule  can  be  separately 
irritated  in  a  much  more  exact  fashion.  They  found  in  these  experiments  that 
the  motor  fibers  of  the  internal  capsule  showed  the  following  arrangement  from 
before  backward:  opening  the  eyes,  associated  movements  of  the  head  and  eyes 
to  one  side,  tongue,  angle  of  the  mouth,  shoulder,  elbow,  wrist,  fingers,  thumb, 
trunk,  hip,  ankle,  great  toe,  other  toes. 

The  sensory  tract  (compare  page  799,  and  Fig.  95,  page  829)  lies  at  the  pos- 
terior extremity  of  the  internal  capsule,  and  apparently  includes  not  only  the 
fibers  for  cutaneous  sensation,  but  also  for  the  organs  of  special  sense.  Com- 
plete disorganization  of  this  spot  ought  therefore  to  cause,  in  the  opposite  half 
of  the  body,  not  only  anaesthesia  of  the  skin,  but  also  simultaneously  a  corre- 
sponding impairment  of  smell,  taste,  and  hearing,  and  hemianopsia — in  short,  a  so- 
called  complete  cerebral  hemiansesthesia.  Still,  in  regard  to  this  very  point  we 
are  rauch  in  need  of  further  and  definite  observations. 

Certain  practical  conclusions  in  regard  to  diagnosis  can  be  deduced  from  the 
preceding  facts.  A  purely  motor  hemiplegia,  unattended  by  impairment  of  sen- 
sation, implies  a  lesion  that  does  not  involve  the  posterior  portion  of  the  internal 
capsule;  but  probably  this  portion  is  also  affected,  when  there  is  not  only  pa- 
ralysis, but  considerable  sensory  disturbance.  The  sensory  disturbance  does  not 
invariably  extend  to  all  the  senses ;  quite  often  there  is  nothing  but  cutaneoiis 
anaesthesia. 

Lesions  in  the  neighborhood  of  the  internal  capsule  may  also  cause  symptoms 
of  irritation  of  the  tracts  which  pass  through  the  internal  capsule.  Thus  unilat- 
eral symptoms  of  motor  irritation  in  particular  have  frequently  been  observed  in 
the  form  of  choreic  twitchings  (so-called  post-hemiplegic  chorea,  vide  infra),  and 
unilateral  symptoms  of  sensory  irritation  (pain,  parsesthesia)  may  also  be  caused 
sometimes  by  lesions  in  the  vicinity  of  the  posterior  portion  of  the  internal  cap- 
sule (Edinger). 

Central  Ganglia;  Caudate  Nucleus  (Corpus  Striatum  proper).  Lenticular 
Nucleus,  and  Optic  Thalamus. — Before  the  course  of  the  pyramidal  tract  had 
been  accurately  determined,  ordinary  cases  of  cerebral  hemiplegia  were  almost 


THE   LOCALIZATION   OF   CEKEBRAL   DISEASES  1085 

universally  ascribed  to  lesions  of  the  central  ganglia,  and  in  particular  of  the 
caudate  and  lenticular  nuclei.  At  present,  however,  observations  seem  to  force 
one  to  the  conclusion  that  a  comple'te  hemiplegia  can  be  produced  only  by  a  cutting 
off  of  the  pyramidal  tract.  There  are,  indeed,  numerous  cases  of  hemiplegia  pre- 
senting circumscribed  disease  of  the  central  ganglia ;  but  they  can  probably  all  be 
explained  by  supposing  either  that  the  pyramidal  tract,  as  it  lies  in  the  contiguous 
internal  capsule,  is"  directly  involved  in  the  disease,  or  that  its  functions  are  sus- 
pended by  the  indirect  effects  of  the  neighboring  lesion — for  instance,  by  the 
pressure  it  exercises.  Accordingly,  we  find  that  circumscribed  lesions  of  the 
central  ganglia  in  the  neighborhood  of  the  internal  capsule  generally  produce  a 
temporary  hemiplegia— that  is,  the  paralysis  gradually  improves  as  the  indirect 
influence  of  the  focal  disease  upon  the  internal  capsule  ceases.  Chronic  and  in- 
curable hemiplegia,  however,  ,if  due  to  a  lesion  anywhere  in  this  region,  always 
implies  an  actual  lesion  of  the  pyramidal  tract  in  the  internal  capsule.  In  regard 
to  hemiansesthesia,  also,  the  facts  seem  to  be  quite  analogous.  It  was  formerly 
held  that  this  phenomenon  was  especially  connected  with  a  lesion  of  the  optic 
thalamus,  the  reason  being  that  the  sensitive  fibers  lie  so  close  to  the  thalamus 
in  the  posterior  extremity  of  the  internal  capsule  that  they  become  themselves 
involved. 

About  the  symptoms  which  lesions  of  the  central  ganglia  directly  produce 
little  is  definitely  known.  The  results  of  both  clinical  observation  and  experiment 
are  quite  contradictory,  and  in  repeated  instances  quite  extensive  disorganization 
of  these  parts  has  existed  without  producing  any  symptoms  to  speak  of  during 
life.  In  particular,  it  should  be  borne  in  mind  that  softening  may  occur  in  the 
lenticular  and  caudate  nuclei,  and  yet  not  a  trace  of  hemiplegia  be  observable.  It 
seems  probable  also  that  the  optic  thalamus  has  nothing  to  do  with  voluntary 
motion ;  but  apparently  it  has  some  importance  for  movements  of  mimetic  expres- 
sion (Bechterew,  ISTothnagel).  In  hemiplegics  we  sometimes  see  that  the  lower 
half  of  the  face  on  one  side  can  not  be  moved  voluntarily,  but  it  is  moved  very 
actively  in  emotional  expression,  such  as  laughing  or  crying.  In  such  cases  we 
can  decide  that  the  thalamus  is  intact,  while  in  lesion  of  the  thalamus  the  con- 
trary is  observed — the  affected  half  of  the  face  can  be  moved  voluntarily,  but 
it  remains  completely  rigid  in  emotional  expression.  As  to  sensory  functions, 
there  is  only  one  which  the  optic  thalamus  is  certainly  known  to  possess :  the 
central  termination  of  some  fibers  of  the  optic  nerve  lies  in  its  posterior  por- 
tion (the  so-called  pulvinar),  while  other  fibers  go  to  the  corpus  geniculatum  ex- 
ternum. Destruction  of  the  posterior  part  of  the  thalamus  accordingly  produces 
complete  hemianopsia  (vide  page  1075)  of  the  opposite  side.  The  thalamus  is  also 
very  probably  connected  with  other  centripetal  fibers  from  the  lemniscus,  but  we 
do  not  know  positively  whether  these  are  sensory  or  co-ordinating  fibers,  and 
pathology  has  not  yet  taught  us  as  to  the  functions  of  the  thalamus  in  this 
regard.  Focal  disease  of  the  thalamus  has  repeatedly  occasioned  post-hemiplegic 
symptoms  of  irritation  ("post-hemiplegic  chorea,"  vide  supra),  as  is  easily  to 
be  explained  from  the  propinquity  of  the  pyramidal  tract.  According  to  recent 
experiments,  the  lenticular  nucleus  contains  centers  for  regulating  heat.  The 
striking  changes  in  temperature  sometimes  seen  in  cerebral  affections  may  often, 
therefore,  be  brought  into  possible  relation  to  diseases  of  the  lenticular  nucleus, 
but  accurate  observations  are  still  almost  wholly  lacking. 

Corpora  Quadrigemina  and  Crura  Cerebri.— Diseases  of  the  corpora  quadri- 
gemina  are  infrequent,  and  usually,  when  they  do  occur,  they  are  merely  a  part 
of  more  extensive  lesions  of  the  brain.  They  are  therefore  very  rarely  considered 
from  a  diagnostic  point  of  view. 

The  anterior  tubercles  are  certainly  connected  with  the  fibers  of  the  optic 
nerve.    If  both  of  the  anterior  tubercles  be  destroyed,  total  blindness  is  inevitable. 


1086  DISEASES    OF   THE   NEEVOUS    SYSTEM 

while  if  only  one  be  disorganized,  hemianopsia  is  to  be  anticipated.  Still,  these 
symptoms  are,  of  course,  too  ambiguous  ever  to  be  regarded  as  pathognomonic  of 
localized  disease  of  the  anterior  corpora  quadrigemina.  Another  point  to  be  con- 
sidered, whenever  the  corpora  quadrigemina  are  diseased,  is  the  position  of  the 
nuclei  of  the  nerves  which  preside  over  the  motions  of  the  eyeball,  and  in  particu- 
lar of  the  oculo-motor  and  trochlear  nerves.  This  explains  why  unilateral,  or  even 
bilateral,  paralysis  of  the  oculomotorius  has  been  repeatedly  observed  in  connec- 
tion with  lesions  of  the  corpora  quadrigemina,  as  have  also  more  rarely  nystag- 
mus and  immobility  of  the  pupil.  It  is  also  worthy  of  note  that  in  diseases  in 
the  region  of  the  corpora  quadrigemina,  especially  of  the  posterior  corpora,  ataxia 
of  the  body,  similar  to  cerebellar  ataxia,  has  been  repeatedly  observed  (Noth- 
nagel).  This  ataxia  is  in  all  probability  due  to  a  disturbance  of  the  superior 
cerebellar  peduncle  coming  from  the  corpus  dentatum  of  the  cerebellum,  which 
after  decussating  goes  to  the  red  nucleus  (nucleus  ruber.  Fig.  86,  page  798),  be- 
neath the  corpora  quadrigemina,  and  is  further  connected  with  the  cerebrum.  If 
we  have  to  do,  therefore,  with  an  ophthalmoplegia  affecting  both  eyes,  but  not  com- 
pletely symmetrical,  and  manifesting  itself  especially  by  symptoms  of  paralysis 
of  the  oculo-motor  and  trochlear  nerves  (more  rarely  the  abducens),  and  if  this 
ophthalmoplegia  is  associated  with  an  uncertain,  staggering  gait,  we  must  con- 
sider disease  of  the  corpora  quadrigemina.  Of  course  a  similar  association  of 
symptoms  may  also  occur  in  tumors  of  the  cerebellum.  The  posterior  corpora 
quadrigemina  and  the  median  geniculate  bodies  are  connected  with  the  acoustic 
nerve,  so  that  in  diseases  of  this  region  we  may  expect  disturbances  of  hearing. 
Should  the  crura  cerebri  become  involved  in  the  disease,  the  resulting  symp- 
toms are  often  very  characteristic  of  the  locality  affected ;  there  is  paralysis  of  one 
side  of  the  body  (arm,  leg,  facial  nerve),  and  at  the  same  time  a  crossed  paralysis 
(that  is,  one  situated  upon  the  opposite  side)  of  the  motor  oculi.  A  glance  at  Fig. 
96  (page  830)  will  explain  this  phenomenon.  Thus,  a  circumscribed  lesion  on  the 
right  side  would  destroy  the  fibers  of  the  third  nerve  (III)  on  that  side,  and 
therefore  produce  a  right-sided  paralysis  of  the  oculo-motor  nerves,  and  at  the 
same  time,  if  extensive  enough,  the  lesion  would  involve  the  pyramidal  fibers  of 
the  right  crus,  and  thus  occasion  left  hemiplegia.  That  disease  of  the  tegmentum 
would  lead  to  sensory  disturbances  or  sometimes  ataxia  may  be  taken  for  granted. 
Diseases  of  the  tegmental  region  and  its  vicinity  therefore  cause  a  clinical  pic- 
ture which  is  composed  of  hemiplegia,  tactile  hemianesthesia  (or  hemiataxia), 
and  crossed  oculo-motor  paralysis  of  the  opposite  side. 

5.  The  Cerebellum 

Quite  extensive  destruction  of  the  cerebellum  may  take  place  without  any 
symptoms  to  indicate  it.  In  such  cases,  however,  the  disease  is  almost  invariably 
confined  to  the  hemispheres ;  but,  if  the  central  portion  or  vermiform  process  be 
attacked  to  any  great  extent,  peculiar  symptoms  almost  always  result,  pointing  in 
many  instances  with  considerable  certainty  to  disease  of  the  cerebellum.  In 
some  cases,  however,  disease  limited  to  the  cerebellar  hemispheres  may  cause 
pronounced  cerebellar  symptoms. 

There  are  two  especially  characteristic  symptoms — a  peculiar  uncertainty  of 
gait  (cerebellar  ataxia),  and  troublesome  vertigo. 

Cerebellar  ataxia  affects  the  trunk  and  lower  extremities.  Both  standing 
and  locomotion  are  chiefly  interfered  with.  When  the  patient  is  lying  in  bed  he 
can  move  his  legs  almost  as  well  as  ever,  and  with  normal  vigor;  but  as  soon  as 
he  gets  up,  the  characteristic  motor  disturbances  become  very  evident.  Even 
while  standing  still,  the  whole  body  can  usually  be  plainly  seen  to  sway  back  and 
forth.  This  becomes  more  marked  if  the  patient  brings  his  heels  together.  If  he 
stands  with  his  legs  widely  apart,  the  trouble  is  less  noticeable.    Closing  the  eyes. 


THE   LOCALIZATION   OF    CEKEBRAL   DISEASES  1087 

as  a  rule,  does  not  aggravate  the  swaying,  inasmuch  as  the  cutaneous  and  mus- 
cular sensibility  of  the  lower  limbs  remains  normal  in  uncomplicated  cerebellar 
disease.  When  the  patient  tries  to  walk,  he  sways  and  totters,  precisely  as  if 
he  were  deeply  intoxicated,  but  usually  in  a  very  different  way  from  that  seen  in 
tabes  dorsalis.  Instead  of  the  uniform  stamping  and  pitching  gait  of  the  latter, 
cerebellar  ataxia  causes  a  real  staggering  of  the  whole  body,  so  that  in  severe 
cases  the  patient  loses  entirely  the  ability  to  walk  straight,  but  seems  to  fall 
forward,  as  it  were,  in  a  zigzag  line,  now  to  the  right  and  now  to  the  left.  Some- 
times, but  by  no  means  invariably,  it  is  noticed  that,  in  walking,  the  body  sways 
principally  in  one  particular  direction,  either  forward,  backward,  or  to  one 
side.  Such  peculiarities,  however,  do  not  enable  us,  with  our  present  knowledge, 
to  determine  with  certainty  just  what  position  in  the  cerebellum  the  lesion 
occupies.  The  most  we  can  do  is  to  surmise,  in  such  a  case,  that  the  middle 
peduncles  of  the  cerebellum  (vide  infra)  are  involved.  It  is  worthy  of  note  that, 
with  few  exceptions,  the  ataxia  does  not  involve  the  upper  extremities.  Many  a 
patient  who  can  scarcely  walk  unaided  is  still  able  to  perform  the  most  delicate 
manipulations  with  his  hands.  This  shows  that  it  is  only  in  maintaining  the 
bodily  equilibrium — essential  to  standing  and  locomotion — that  the  function 
of  the  cerebellum  is  important. 

As  already  stated,  this  cerebellar  ataxia  is  in  most  cases  attended  with  pro- 
nounced vertigo.  There  is  not,  however,  a  complete  correspondence  between  the 
locomotor  disturbance  and  the  dizziness.  Exceptionally  one  symptom  may  be 
present  without  the  other.  The  vertigo  is  usually  felt  only  when  the  patient 
is  erect,  standing  or  moving  about,  and  is  very  seldom  felt  when  he  lies  quietly 
in  bed.  Cerebellar  vertigo  is  usually  a  true  vertigo  or  turning  sensation :  the 
patient  feels  as  if  he  himself  or  the  surrounding  objects  were  revolving.  The 
feeling  of  vertigo  may  be  constantly  present  or  it  may  conae  on  in  severe  individ- 
ual paroxysms.  The  cause  of  the  vertigo  is  probably  to  be  looked  for  in  a  dis- 
turbance of  those  tracts  which  go  to  the  cerebellum  through  the  corpus  restiforme 
as  a  continuation  of  the  vestibular  nerve. 

Little  definite  is  known  about  other  symptoms  of  disease  in  the  cerebellum. 
True  ataxia  of  the  legs  (as  in  tabes)  is  also  seen  at  times;  but  in  such  cases 
we  usually  have  to  do  with  the  distant  action  of  the  disease  on  the  tract  of  the 
lemniscus.  The  patellar  reflex  has  sometimes  been  found  absent  in  cerebellar 
disease.  This  symptom  also  is  probably  always  dependent  upon  co-existing  dis- 
turbances of  the  spinal  cord.  In  some  cases  intention  tremor  has  been  found  in 
the  arms;  in  others  hemiparesis  of  the  extremities  on  the  side  of  the  disease 
(corresponding  to  the  results  of  Luciani's  experiments  on  animals).  The  signifi- 
cance of  all  these  symptoms  is  still  doubtful.  We  will  return  later  to  certain  spe- 
cial symptoms,  especially  those  occurring  in  tumors  of  the  cerebellum. 

We  must  add  in  conclusion  a  few  words  about  diseases  of  the  middle  cerebellar 
peduncles  (crura  cerebelli  ad  pontem).  Those  peculiar  symptoms  known  as  forced 
movements,  and  forced  positions  are  usually  referred  to  an  irritation  of  these 
peduncles  on  the  ground  of  physiological  experiments.  Forced  positions  are 
when  the  patient  always  lies  upon  one  particular  side  in  bed,  whether  he  is  per- 
fectly conscious,  or  in  a  state  of  complete  unconsciousness.  If  he  is  put  in  any 
other  posture,  he  at  once  involuntarily  reassuraes  his  former  position.  ISTot  infre- 
quently this  forced  position  of  the  trunk  is  accompanied  by  a  corresponding 
forced  position  of  the  head  and  eyeballs,  while  the  extremities  are  seldom  affected. 
Genviine  forced  moA^ements  are  seen  far  less  often.  They  produce  either  often- 
repeated  rotations  of  the  body  on  its  longitudinal  axis,  or,  if  the  patient  be  able 
to  walk  at  all,  involuntary  circular  movements  ("circus  movements  "),  etc.  Ac- 
cording to  the  statements  of  Russell,  the  forced  movements  in  disease  of  the  right 
middle  cerebellar  peduncle  are  in  the  direction  "  of  a  corkscrew  screwed  into  a 


1088  DISEASES    OF    THE    NERVOUS    SYSTEM 

cork,"  and,  in  disease  of  the  left  peduncle,  the  direction  "  of  a  corkscrew  screwed 
out  of  a  cork."  It  must  be  said,  however,  that  the  symptoms  of  forced  positions 
and  forced  movements  are  on  the  whole  rare  and  of  doubtful  value  in  diagnosis ; 
for  in  some  cases  of  cerebral  disease  the  same  symptoms  have  been  observed  with- 
out any  discoverable  affection  of  the  middle  cerebellar  peduncle.  On  the  other 
hand,  in  two  cases  of  tumor  of  the  middle  cerebellar  peduncle  with  autopsy  we 
failed  to  find  any  forced  movements. 


For  convenient  reference  we  subjoin  a  summary  of  the  most  important  facts 
bearing  upon  the  localization  of  cerebral  diseases. 

1.  The  most  frequent  cause  of  ordinary  hemiplegia  is  a  lesion  of  the  pyramidal 
tract  in  the  posterior  limb  of  the  internal  capsule.  If  the  hemiplegia  be  persist- 
ent, then  this  tract  is  actually  destroyed;  if  temporary,  the  tract  has  been  func- 
tionally deranged  for  a  time  by  focal  disease  in  neighboring  parts  of  the  brain. 

2.  Monoplegic  cerebral  paralysis  is  usually  due  to  affections  of  the  cortex  of 
the  brain — that  is,  the  central  convolutions  and  the  paracentral  lobule.  Mono- 
plegia of  the  face  and  tongue  is  the  result  of  lesions  in  the  lower  extremity  of  the 
anterior  central  convolutions.  Monoplegia  of  the  arm  is  referable  principally  to 
some  lesion  of  the  middle  third  of  the  anterior  central  convolutions.  Monoplegia 
of  the  lower  extremity  imijlies  some  affection  of  the  upper  portion  of  the  anterior 
central  convolutions  and  the  paracentral  lobule. 

3.  Hemiplegia  or  monoplegia,  if  associated  with  epileptiform  convulsions 
affecting  either  one  half  or  one  particular  portion  of  the  body,  are  almost  always 
caused  by  cortical  lesions.  These  same  symptoms  of  motor  irritation  without 
accompanying  paralysis  are  likewise  to  be  ascribed  to  some  irritation  of  the  above- 
mentioned  regions  of  the  cortex. 

4.  Hemiplegia  with  crossed  paralysis  of  the  oculo-motor  nerve  indicates  a 
lesion  of  the  crus  cerebri.  Co-existing  tactile  hemiansesthesia  implies  that  the 
tegmentum  is  involved. 

5.  Hemiplegia  with  crossed  facial  paralysis  implies,  with  great  certainty,  that 
the  lesion  is  situated  in  the  pons. 

6.  Post-hemiplegic  chorea  (vide  infra)  seems  to  occur  especially  when  there 
is  focal  disease  in  the  neighborhood  of  the  posterior  part  of  the  internal  capsule. 

Y.  Hemiansesthesia  of  the  skin  and  of  the  organs  of  special  sense,  associated 
with  hemianopsia,  is  due  chiefly  to  lesions  of  the  most  posterior  portion  of  the 
internal  capsule. 

8.  Hemianopsia  may  be  due  to  a  lesion  of  the  occipital  lobe  (cuneus).  Prob- 
ably, also,  a  lesion  of  the  posterior  extremity  of  the  internal  capsule  may  cause  it, 
in  which  case  it  is  usually  associated  with  hemiansesthesia.  Finally,  it  may  be 
produced  by  affections  of  the  pulvinar  of  the  optic  thalamus,  of  one  lateral  genicu- 
late body,  of  one  of  the  anterior  corpora  quadrigemina,  or  of  one  of  the  optic 
tracts. 

9.  Genuine  motor  aphasia  indicates  disease  of  the  foot  of  the  third  left  frontal 
convolution. 

10.  Word  deafness  (loss  of  understanding  of  speech)  is  due  to  disease  of  the 
first  left  temporal  convolution ;  word  blindness  (loss  of  understanding  of  writing) 
is  due  to  disease  of  the  left  lower  parietal  lobe  (angular  gyrus). 

11.  Difficulty  in  articulation  implies  disease  of  the  medulla,  as  does  also  dys- 
phagia. 

12.  Staggering  gait  and  vertigo  are  the  most  constant  symptoms  of  cerebellar 
disease,  but  they  may  also  occur  in  diseases  of  the  corpora  quadrigemina  and  of 
the  frontal  lobe  {vide  supra).  Forced  positions  and  forced  movements  perhaps  in- 
dicate lesions  of  the  crura  cerebelli  ad  pontem. 


CEKEBEAL   H^^MOEEHAGE  1089 

As  an  appendix,  we  may  add  a  very  brief  review  of  the  course  of  the  most  im- 
portant conducting  tracts : 

1.  Chief  Motor  Tract. — (a)  First  central  neurone:  Ganglion-cells  in  the 
motor  cortex  of  the  brain,  axis-cylinder  processes  through  the  corona  radiata,  pos- 
terior limb  of  the  internal  capsule,  crusta  of  the  crus  cerebri,  decussation  in  the 
pyramids,  postero-lateral  column  of  the  spinal  cord,  terminal  arborization  in  the 
anterior  horns  (for  the  motor  cranial  nerves  previously  in  their  nuclei).  (&) 
Second  peripheral  neurone:  Ganglion-cells  in  the  anterior  horns  (or  in  the  nuclei 
of  the  motor  cranial  nerves),  axis-cylinder  processes  in  the  anterior  root  and  the 
peripheral  nerve,  terminal  arborization  in  the  muscular  fibers. 

2.  Chief  Centripetal  (Sensory  and  Co-ordinating)  Tract. — (a)  First  (periph- 
eral) neurone:  Ganglion-cells  in  the  spinal  ganglion,  axis-cylinder  processes 
partly  in  the  peripheral  sensory  nerve  [modified  protoplasmic  processes],  partly 
in  the  posterior  root;  terminal  arborization,  partly  in  the  posterior  horns  (sen- 
sory fibers),  partly,  after  passing  through  the  posterior  columns  of  the  cord,  in 
the  nuclei  of  the  columns  of  Goll  and  Burdach  (co-ordinating  fibers),  (h)  Second 
neurone :  Ganglion-cells  in  the  posterior  horns  or  in  the  nuclei  of  the  columns  of 
Goll  and  Burdach,  axis-cylinder  processes  through  the  antero-lateral  columns, 
inter-olivary  layer,  lemniscus  tract  of  the  medulla  and  pons,  tegmentum  of  the 
crus  cerebri,  posterior  portion  of  the  internal  capsule.  Terminal  arborization 
in  part  in  the  optic  thalamus,  (c)  Third  neurone:  Ganglion-cells  in  the  optic 
thalamus,  axis-cylinder  processes  to  the  cerebral  cortex  (central  convolutions, 
parietal  lobe). 

3.  Chief  Optic  Tract. — First  peripheral  neurones  lie  wholly  in  the  retina,  and 
the  ganglion-cells  of  the  second  neurones  are  also  in  the  retina,  axis-cylinder  pro- 
cesses through  the  nerve  and  optic  tract  (partial  decussation!)  to  the  lateral 
geniculate  body,  the  anterior  corpora  quadrigemina,  and  the  pulvinar  of  the 
optic  thalamus,  where  the  terminal  arborization  takes  place.  Third  neurones 
from  the  cells  of  the  parts  mentioned  through  the  posterior  portion  of  the  inter- 
nal capsule  [and  the  optic  radiations  of  Gratiolet]  to  the  cortex  of  the  occipital 
lobe. 

4.  Chief  Acoustic  Tract. — The  ganglion-cells  of  the  peripheral  neurone  lie  in 
the  cochlear  ganglion  of  the  cochlea,  the  axis-cylinder  processes  in  the  cochlear 
nerve,  termination  in  the  ventral  acoustic  nucleus.  Here  the  second  neurone 
begins,  whose  axis-cylinder  process  goes  in  the  trapezoid  body  and  the  strise  acous- 
ticse  (?),  and  then  in  the  lateral  lemniscus  to  the  posterior  corpora  quadrigemina 
and  the  median  geniculate  body.  Here  probably  a  third  neurone  begins,  which 
ends  mainly  in  the  cortex  of  the  temporal  lobe.  The  acoustic  fibers  also  run  partly 
crossed  and  partly  uncrossed,  so  that  each  auditory  nerve  is  connected  with  both 
hemispheres. 


CHAPTEE   III 
CEREBRAL    HAEMORRHAGE 

.3]tiology. — The  cause  of  cerebral  haemorrhage  should  always  be  sought  in 
some  disease  of  the  coats  of  the  minute  cerebral  arteries.  Cerebral  haemorrhage 
occurs  most  frequently,  therefore,  in  persons  who  suffer  from  general  arterio- 
sclerosis, find  especially  from  arterio-sclerosis  of  the  cerebral  arteries;  but  other 
forms  of  disease  of  the  walls  of  the  blood-vessels,  fatty  and  hyaline  degeneration, 
and,  in  particular,  syphilitic  endarteritis,  may  give  rise  to  cerebral  haemorrhage. 
Tn  1868  it  was  first  shown  by  Charcot  and  Boui^hnrd  that  in  many  cases  of  large 
69 


1090  DISEASES    OF   THE   IS'ERVOUS    SYSTEM 

cerebral  hsemorrhage  there  are  miliary  aneurisms  of  the  small  atheromatous  arter- 
ies of  the  brain  substance,  some  one  of  which  has  burst  and  allowed  the  blood  to- 
escape.  All  later  investigators  have  confirmed  their  statements  about  the  occur- 
rence and  importance  of  these  miliary  aneurisms.  The  aneurisms  may  attain  a 
diameter  of  a  millimetre  or  more.  They  usually  appear  like  spindle-shaped  dilata- 
tions of  the  entire  circumference  of  the  vessel,  although  sometimes  the  bulging  is- 
confined  to  one  side  of  it.  Inasmuch  as  the  intra-cerebral  arteries  possess  almost 
no  true  adventitia,  it  is  easy  to  see  that  these  vessels  are  especially  predisposed  to 
aneurismal  dilatation  (especially  in  the  form  of  a  so-called  dissecting  aneurism). 

Most  of  the  circumstances  which  come  under  our  consideration  as  favoring 
the  development  of  cerebral  hsemorrhage  have  also  a  close  relation  to  arterio- 
sclerosis. Age  plays  a  specially  important  part.  Although  exceptionally  a 
younger  individual  may  be  attacked,  the  majority  of  svifferers  are  over  fifty  years 
old — that  is,  at  the  time  of  life  when  arterio-sclerosis  usually  becomes  most  fully 
developed.  Again,  cerebral  htemorrhage  is  decidedly  more  frequent  in  men  than 
in  women,  which  is  also  true  of  atheroma.  Alcoholism,  syphilis,  and  gout  are  also 
reckoned  among  the  setiological  factors  of  both  disorders,  and  in  both  a  hereditary 
predisposition  is  not  very  rarely  demonstrable.  What  is  called  the  "  apoplectic 
habit  "  also  deserves  brief  mention.  Although  there  is  no  variety  of  constitution 
which  exempts  its  possessor  from  the  possibility  of  cerebral  haemorrhage,  yet  it 
can  not  be  denied  that  often  the  victims  of  apoplexy  do  exhibit  a  certain  "  habit.'^ 
Such  persons  are  not  very  tall,  but  are  corpulent,  broad-chested,  with  a  short, 
thick  neck  and  round  face ;  and  they  have  not  been  disinclined  to  the  pleasures 
of  the  table  and  the  bottle.  Such  persons  often  sufier  at  the  same  time  from 
emphysema,  moderate  hypertrophy  of  the  heart,  and  general  arterio-sclerosis,  as 
the  condition  of  the  radial  and  temporal  arteries  may  disclose  even  during  life. 

Granting,  therefore,  that  disease  of  the  arteries,  and  sometimes  more  particu- 
larly miliary  aneurisms  resulting  from  chronic  endarteritis  of  the  smaller  cere- 
bral arteries,  must  be  regarded  as  the  chief  cause  of  cerebral  hsemorrhage,  then, 
on  the  other  hand,  the  question  suggests  itself  whether  an  abnormal  elevation  of 
the  blood-pressure  may  not  have  some  part  in  determining  the  haemorrhage.  If 
the  coats  of  the  arteries  be  normal  the  greatest  increase  of  pressure  would  not 
be  able  to  cause  rupture  of  the  vessels ;  but  if  the  wall  of  the  artery  is  diseased, 
or  if  aneurisms  have  already  been  developed,  then  there  can  be  no  doubt  that  a 
persistent  or  even  a  temporary  elevation  of  the  blood-pressure  must  favor  the 
bursting  of  the  vessels.  In  this  sense  a  cerebral  haemorrhage,  occurring  in  pa- 
tients with  certain  forms  of  cardiac  hypertrophy  (contracted  kidney,  idiopathic 
hypertrophy,  etc.),  combined  with  disease  of  the  vessels,  may  be  referred  in  part 
to  the  increased  arterial  tension ;  but  it  is  most  of  all  with  regard  to  many  excit- 
ing causes,  which  are  immediately  followed  by  a  cerebral  haemorrhage,  that  in- 
creased blood-preSsure  assumes  great  importance.  Here  it  is  temporary.  Cere- 
bral haemorrhage  may,  for  example,  follow  excessive  muscular  exertion,  the  inges- 
tion of  a  large  amount  of  .food,  indulgence  in  alcohol,  taking  a  cold  bath,  violent 
mental  excitement,  etc.  An  apparently  slight  injury  is  especially  to  be  consid- 
ered. In  all  such  cases,  however,  the  change  in  the  arteries  is  a  necessary  pre- 
requisite. 

It  should  be  mentioned,  in  conclusion,  that  cerebral  haemorrhage  is  sometimes 
merely  the  expression  of  a  general  hasmorrhagic  diathesis,  as  we  find  it  in 
leukaemia,  pernicious  anaemia,  and  those  affections  which  are  called,  in  a  stricter 
sense,  haemorrhagic  diseases,  such  as  scurvy  and  purpura  hemorrhagica.  The 
grave  infectious  diseases,  including  septicaemia,  typhus  or  typhoid  fever,  and 
small-pox,  may  occasion  haemorrhage  into  the  brain  as  well  as  into  other  organs. 
The  haemorrhages  are  generally,  however,  from  capillary  vessels,  and  are  very 
rarelv  extensive. 


CEKEBRAL  HEMORRHAGE  1091 

Pathology. — Arterio-sclerosis  and  miliary  aneurisms  do  not  develop  in  all  the 
cerebral  arteries  with  equal  frequency,  and  accordingly  we  find  certain  regions 
particularly  liable  to  cerebral  hasmorrhage,  being  very  much  oftener  affected  by 
it  than  others.  These  regions  seem  also  to  be  the  ones  where  the  arterial  blood- 
pressure  is  relatively  the  highest."  Hemorrhage  takes  place  by  far  the  most 
frequently  from  the  branches  of  the  artery  of  the  fissure  of  Sylvius.  The  large 
central  ganglia  in  the  neighborhood  of  the  lateral  ventricles,  the  optic  thalamus, 
caudate  and  lenticular  nuclei,  and  also  the  adjacent  white  matter  of  the  internal 
capsule  and  centrum  ovale,  are  therefore  usually  affected  by  the  haemorrhage. 
Hemorrhages  in  other  portions  of  the  brain  are  much  less  frequent — such  as 
haemorrhages  into  the  convolutions,  the  pons,  the  cerebellum,  the  crura  cerebri,  or 
the  medulla.  If  the  blood  escapes  into  the  neighborhood  of  a  ventricle,  it  may 
burst  into  the  latter.  Likewise,  in  rare  instances,  an  effusion  of  blood  in  the 
cortex  may  make  its  way  out  upon  the  surface  of  the  brain. 

An  extensive  collection  of  blood  in  one  of  the  hemispheres  may  exercise  so 
decided  a  pressure  upon  surrounding  parts  that  the  results  of  increased  tension 
upon  the  affected  side  are  at  once  recognized  when  the  skull  is  opened.  The  dura 
on  that  side  is  more  tightly  stretched,  the  f  alx  is  crowded  over  to  the  opposite  side, 
the  convolutions  on  the  convexity  seem  flattened,  and  the  furrows  are  shallow. 
Exceptionally,  when  there  is  a  very  large  effusion  reaching  nearly  to  the  surface, 
we  may  even  detect  fluctuation. 

On  cutting  through  the  brain-substance  we  find  the  seat  of  haemorrhage,  and 
are  enabled  to  determine  its  position  and  extent.  Its  size,  of  course,  varies  con- 
siderably in  different  cases ;  it  may  be  small,  or  it  may  occupy  a  large  part  of  an 
entire  hemisphere.  The  wall  of  the  effused  mass  is  made  up  of  ragged  and  torn 
cerebral  tissue,  and  the  mass  itself  contains  dehris  of  the  nervous  elements  entan- 
gled in  the  coagulated  blood.  The  blood-clots  are  almost  always  very  dark-colored 
when  fresh.  Later  on,  the  mass  changes  to  a  chocolate-colored  or  more  brownish- 
yellow  pulp,  composed  of  the  disintegrated  remnants  of  the  nervous  substance 
and  the  clotted  blood.  The  microscope  reveals,  particularly  in  the  immediately 
surrounding  tissues,  numerous  fatty  granular  cells.  These  are  white  blood- 
corpuscles  which  have  absorbed  the  fat  resulting  from  the  decomposition  of  the 
myeline  substance.  There  is  also  always  an  abundance  of  haematoidine  crystals, 
due  to  the  disintegration  of  the  red  blood-globules.  At  a  greater  distance  from  the 
effusion  the  tissues  present  a  yellowish  tinge,  from  the  imbibition  of  such  blood- 
pigment  as  has  reached  them  in  a  state  of  solution;  and  there  is  also  usually  an 
oedematous  softening  of  the  parts  not  too  far  removed  from  the  hsemorrhagic  focus. 

If  the  patient  survive,  the  mass  is  gradually  absorbed.  It  slowly  diminishes 
in  size,  and  the  surrounding  parts  tend  to  reassume  their  normal  relations.  The 
final  result  in  many  cases  is  a  cavity  filled  with  serous  fluid  and  bounded  by 
smooth  walls.  This  "  apoplectic  cyst "  remains  stationary.  In  some  instances, 
however,  and  particularly  if  the  effusion  be  rather  small,  the  walls  approach  each 
other  as  more  and  more  of  the  fluid  is  absorbed;  there  is  a  great  hyperplasia  of 
connective  tissue;  and  so,  finally,  there  is  nothing  left  but  a  so-called  apoplectic 
scar,  usually  of  a  yellow  color,  due  to  vestiges  of  the  blood-pigment.  The  position 
and  dimensions  of  the  permanent  lesion  determine,  of  course,  the  question  of  sec- 
ondary descending  degeneration  (vide  page  1033),  as  well  as  the  nature  and  extent 
of  the  persistent  clinical  symptoms. 

Clinical  History. — The  symptoms  of  cerebral  haemorrhage  agree  closely  with 
the  anatomical  lesions  just  described.     The  vascular  disease  responsible  for  the 

[*  Mendel  has  found  that  the  normal  blood-pressure  in  the  lenticulo-striate  arteries,  which  are 
most  prone  to  rupture,  is  much  higher  than  it  is  in  the  cortical  and  many  other  small  artei'ies  of  the 
brain. — K.] 


1092  DISEASES    OF   THE   N'EEVOUS    SYSTEM 

JiEemorrliage  (arterio-sclerosis,  miliary  aneurisms)  in  many  cases  excites  no  mor- 
bid symptoms;  bnt,  on  the  other  hand,  we  often  find  that  persons  attacked  by  a 
cerebral  haemorrhage  have  suffered  much  from  vertigo,  headache,  etc.,  for  more  or 
less  time  before  the  shock.  Such  symptoms  are  undoubtedly  due  to  the  disease  of 
the  cerebral  blood-vessels  and  to  the  slight  disturbances  of  the  circulation  thus 
produced. 

As  soon  as  the  vessel  wall  or  an  aneurism  bursts,  however,  and  blood  escapes 
into  any  part  of  the  brain-substance,  there  is  immediately  seen  a  group  of  grave 
cerebral  symptoms,  collectively  termed  an  apoplectic  attack,  or  "  shock."  As  the 
blood  escapes  under  a  pressure  nearly  equal  to  the  general  arterial  pressure,  and 
doubtless  much  greater  than  that  to  which  the  soft  substance  of  the  brain  is  nor- 
mally exposed,  the  affected  portion  of  the  brain  is  at  once  subjected  to  a  consid- 
erable increase  of  tension,  which  is  transmitted  for  various  distances  in  all  direc- 
tions. It  need  not  be  said  that  the  destructive  influence  of  the  hsemorrhage,  which 
is  probably  manifested  by  a  compression  of  the  nervous  tissue  itself  and  also 
more  especially  by  a  compression  of  the  blood  and  lymph  channels  and  a  conse- 
quent disturbance  of  the  circulation,  may  vary  exceedingly,  and  that  therefore 
the  symptoms  are  by  no  means  equally  severe  in  all  cases.  The  larger  the  rent 
in  the  blood-vessel,  and  the  more  rapid  and  abundant  the  consequent  haemorrhage, 
the  worse  is  the  apoplectic  attack.  Bleeding  from  larger  vessels  is  therefore  usu- 
ally attended  by  graver  symptoms  than  from  the  minute  arterial  twigs.  An  ex- 
tensive cerebral  hgemorrhage  sometimes  causes  the  patient  to  fall  down  suddenly 
in  complete  unconsciousness,  while  smaller  haemorrhages  may  occasion  only  a 
temporary  attack  of  vertigo  and  slight  cloudiness  of  intellect.  If  the  tear  in  the 
wall  of  the  artery  be  very  small  and  narrow,  permitting  the  blood  to  escape  but 
slowly,  then  there  may  be  no  sudden  attack  at  all,  the  phenomena  requiring  a  cer- 
tain length  of  time  for  their  development. 

There  is  also  an  important  relation  between  the  location  of  the  haemorrhage 
and  the  severity  of  the  apoplectic  attack.  The  chief  symptom  of  these  cases  is 
loss  of  consciousness  (about  which  we  shall  soon  speak  at  length)  ;  and  as  this 
is  certainly  due  to  an  interruption  of  the  functional  activity  of  the  cerebral 
cortex,  it  is  plain  that  the  nearer  the  cortex  is  to  the  haemorrhagic  focus,  the 
more  apt  are  the  symptoms  to  be  serious.  It  is  confirmatory  of  this  that  haemor- 
rhage into  the  more  deeply  situated  portions  of  the  brain,  the  crura  cerebri 
or  the  pons,  quite  often  occasions  comparatively  slight  symptoms.  But  there 
is  a  fact  about  the  circulation  in  the  brain  that  often  causes  the  shock  from 
haemorrhage  into  the  brain-stem  to  be  greater  than  the  shock  following  hgemor- 
rhage into  the  cortex  or  the  white  substance  of  the  hemispheres.  This  fact 
is  that  the  brain-stem  has  comparatively  much  larger  arteries  than  the  other 
parts  just  mentioned,  which  contain  only  minute  blood-vessels.  Fiirthermore,  as 
Buret  and  Heubner  have  shown,  the  blood-vessels  are  so  distributed  that  the 
arterial  tension  in  the  brain-stem  is  not  a  little  higher  than  in  the  other  portions. 
This  renders  intelligible  the  clinical  phenomenon  that  hemorrhages  in  the  terri- 
tory of  the  main  arteries,  besides  being,  as  we  have  said,  the  most  frequent  of  any, 
produce  apoplectic  symptoms  even  when  the  effusion  is  comparatively  small; 
while  sometimes  hsemorrhages  of  about  the  same  size  in  the  cortex  or  white  sub- 
stance may  not  be  noticed. 

The  clinical  phenomena  of  the  apoplectic  attack  will  now  be  considered  in 
detail.  The  onset  is  sometimes  absolutely  without  warning,  but  in  other  cases  it 
is  preceded  for  a  greater  or  less  length  of  time  by  certain  prodromata.  These  are 
either  the  result  of  the  disturbance  of  circulation  caused  by  the  disease  of  the 
blood-vessels  in  the  brain,  and  then,  as  already  stated,  they  comprise  occasional 
headache,  vertigo,  tinnitus  aurium,  spots  before  the  eyes,  languor,  and  muscular 
weakness ;  or  they  are  caused  by  minute  haemorrhages,  which  seem  not  inf re- 


CEKEBEAL  ELEMOKEHAGE  1093 

quently  to  precede  a  greater  one.  In  such  a  case,  the  friends  state  that  of  late 
the  patient  has  had  one  or  more  slight  and  brief  attacks,  characterized  by  f aint- 
ness,  temporary  trouble  in  speaking,  sudden  but  temporary  weakness  of  an  arm 
or  leg,  and  similar  symptoms.  The  prodromata  may  extend  over  several  days 
or  even  weeks  and  months  preceding  the  severe  attack. 

In  other  cases  there  are  no  such  premonitory  symptoms.  The  apoplexy  occurs 
unexpectedly  and  suddenly.  In  the  midst  of  apparently  vigorous  health  the 
patient  sinks  down  "  as  if  he  had  been  struck."  In  still  other  cases  there  are 
indeed  no  prodromata,  but  the  symptoms  do  not  at  first  appear  in  all  their  sever- 
ity, and  occupy  some  hours  or  even  a  whole  day  in  their  gradual  development. 
This  is  due  to  a  slow  and  gradually  increasing  haemorrhage,  and  is  termed  a  slow 
or  delayed  apoplectic  attack.  The  patient  grows  confused,  anxious,  and  delirious 
(a  case  of  our  own  had  pronounced  hallucinations  of  sight)  ;  the  arm  and  leg  on 
one  side  become  paretic,  and  gradually  more  and  more  completely  paralyzed ;  and 
after  a  few  hours  complete  unconsciousness  comes  on. 

The  attack  may  be  rapidly  fatal.  In  such  cases  the  abnormal  pressure  prob- 
ably involves  the  medulla  oblongata  and  paralyzes  the  cardiac  and  respiratory 
centers  there  situated.  Usually,  however,  there  is  merely  a  complete  loss  of  con- 
sciousness, more  or  less  rapidly  developed.  Sometimes  the  patient  has  time  to 
lie  down.  He  usually  sinks  back  in  his  chair  or  falls  to  the  floor,  and  becomes 
deeply  comatose.  The  face  is  often  noticeably  flushed,  and  the  pulse  full  and 
tense,  but  not  infrequently  somewhat  slow,  because  of  the  increased  cerebral 
pressure.  The  respirations  are  deep,  noisy,  stertorous,  and  likewise  often  slow. 
The  relaxed  cheeks  and  lips  are  often  drawn  deeply  in  at  every  inspiration,  and 
puffed  out  at  every  expiration.  The  temperature  is  usually  subnormal  at  flrst, 
later  regaining  the  normal,  or  even  a  higher  point.  In  a  rapidly  fatal  case,  how- 
ever, the  temperature  remains  depressed  till  death.  It  is  not  very  rare  in  severe 
cases  to  observe  a  peculiar  position  of  the  head  and  eyes,  both  being  turned  in  the 
same  direction.  This  phenomenon  is  termed  by  Prevost  conjugate  deviation 
(^deviation  conjuguee)  of  the  eyes  and  head.  It  is  generally  temporary,  and  is 
said  by  Landouzy  to  be  connected  principally  with  a  lesion  of  the  lower  parietal 
lobule  (see  also  page  1075).  There  is  no  perfectly  constant  relation  between  the 
lateral  deviation  and  the  half  of  the  brain  affected.  The  most  common  condition 
is  that  the  eyes  are  directed  toward  the  affected  hemisphere,  and  so  to  a  certain 
extent  "  look  toward  the  lesion  "  and  away  from  the  paralyzed  side  of  the  body. 
The  pupils  present  no  constant  peculiarities.  Often  they  are  of  normal  size.  In 
other  cases  they  are  contracted,  dilated,  or  unequal.  'No  deflnite  diagnostic  con- 
clusions can  be  drawn  from  them.  In  the  worst  cases  the  pupils  will  not  react  to 
light;  in  other  cases  they  react,  but  often  sluggishly. 

During  the  deep  apoplectic  coma  the  extremities  generally  lie  completely 
motionless  and  limp.  In  the  worst  cases  reflex  action  is  wholly  suspended;  but 
sometimes  the  vigorous  thrust  of  a  pin  or  the  pinching  of  the  skin  will  excite  an 
occasional  slow  reflex  twitch,  or  a  motion  as  if  to  ward  off  the  tormentor. 
Whether  the  apoplexy  has  caused  hemiplegia  at  all,  and  if  so  in  what  place,  can 
not  always  be  easily  determined  during  the  initial  coma.  Still,  it  is  often  to  be 
observed,  even  now,  that  one  angle  of  the  mouth  hangs  down  lower  than  the 
other,  and  that  the  corresponding  cheek  is  more  puffed  out  during  expiration 
than  is  the  other;  that  the  extremities  of  one  side  are  much  heavier  and  fall 
much  more  limply  than  those  on  the  opposite  side  of  the  body,  and  that  the  reflex 
action  and  defensive  movements  are  almost  absent  upon  one  side  (the  paralyzed 
side),  while  they  can  be  clearly  demonstrated  on  the  other. 

In  contrast  to  the  usual  laxness  of  the  arms  and  legs  during  the  apoplectic 
coma  is  the  tonic  rigidity  sometimes  seen  in  the  extremities,  particularly 
on  the  side  opposite  to  the  haemorrhage.     This  symptom  seems  to  be  especially. 


1094  DISEASES    OE   THE   NEEVOUS    SYSTEM 

although  not  exclusively,  connected  with  a  bursting  of  the  escaping  blood 
into  a  lateral  ventricle.  It  is  rather  exceptional  for  cerebral  hgemorrhage  to 
be  attended  with  general  or  unilateral  epileptiform  convulsions — a  symptom 
which,  as  we  have  seen,  is  referable  to  irritation  of  the  motor  regions  of  the 
cortex. 

It  should  be  mentioned  that  in  many  cases  of  cerebral  haemorrhage  the  urine 
passed  after  the  attack  has  been  found  to  contain  small  amounts  of  albumen  or 
sugar.  This  symptom  is  usually  ascribed  to  compression  of  the  medulla  from  the 
effusion.  There  is  usually  retention  of  urine;  in  other  cases  there  is  involun- 
tary micturition. 

A  certain  number  of  patients  never  awake  from  the  initial  coma.  Death  may 
not  be  immediate,  but  they  remain  completely  unconscious;  the  respirations 
become  more  rapid  and  irregular  (sometimes  of  the  Cheyne-Stokes  character), 
and  there  is  a  rattling  in  the  throat,  because  mucus  and  saliva  run  down  into  it; 
the  pulse,  which  was  at  first  retarded,  now  becomes  accelerated;  the  face  grows 
paler  and  more  and  more  sunken ;  the  eyes  are  deep  in  their  sockets ;  the  cornea 
becomes  opaque;  and  at  last,  after  the  coma  has  lasted  some  hours,  or  even 
one  or  two  days,  death  occurs,  often  attended  by  a  considerable  rise  in  tem- 
perature. 

This  termination  is,  however,  by  no  means  the  usual  one.  More  frequently 
the  patient  survives  the  attack.  The  bleeding  ceases,  the  clot  contracts,  and 
begins  to  be  disintegrated  and  absorbed.  At-  the  same  time  the  pressure  exerted 
upon  surroixnding  parts  grows  less  and  less,  the  more  distant  parts  of  the  brain 
gradually  recover  from  the  shock,  and  consciousness  slowly  returns.  The  patient 
begins  to  open  his  eyes  when  he  is  spoken  to  in  a  loud  tone ;  he  raises  his  hand  to 
his  head,  sighs,  and  yawns;  gradually  the  intellect  clears  up,  he  tries  to  talk,  or 
to  express  himself  by  signs ;  memory  returns,  and  he  recognizes  those  about  him 
once  more.  Exceptionally,  recovery  is  interrupted  by  a  fresh  and  perhaps  a 
fatal  relapse.  This  may  result  from  a  renewal  of  the  hemorrhage.  Generally, 
however,  improvement  persists,  the  patient  fully  regains  his  consciousness  at  the 
end  of  a  few  days,  and  it  now  becomes  possible  for  the  first  time  to  "  estimate  the 
damage." 

The  symptoms  thus  far  described  belong  to  severe  apoplectic  attacks.  Therc^ 
are  also,  as  we  have  said,  eases  of  all  degrees  of  mildness,  as  regards  the  first  onset. 
In  these  there  is  no  deep  and  persistent  coma.  The  patient  loses  consciousness 
only  temporarily,  if  at  all.  He  is  seized  with  vertigo,  or  with  sudden  headache, 
and  is  for  a  time  stupefied.  ISTausea  and  vomiting  are  of  frequent  occurrence, 
just  as  in  ordinary  syncope.  Yet  cases  presenting  these  comparatively  slight 
early  symptoms,  and  with  few  even  of  these,  may  exhibit  the  genuine  focal  symp- 
toms referable  to  the  hsemorrhage,  such  as  hemiplegia,  in  all  their  severity.  These 
latter  phenomena  must  now  be  considered. 

We  term  the  symptoms  of  loss  of  function  directly  dependent  upon  the  destruc- 
tion of  a  definite  portion  of  the  brain  the  direct  focal  symptoms  of  cerebral  haem- 
orrhage. Where  the  haemorrhage  takes  place  we  have  seen  that  a  larger  or  smaller 
extent  of  the  brain-substance  is  completely  destroyed  by  the  sudden  and  forcible 
escape  of  the  blood.  The  dimensions  of  this  lesion  are  represented  later  by  the 
apoplectic  scar  or  cyst,  and  its  position  by  the  nature  and  extent  of  the  persistent, 
and  for  the  most  part  irreparable,  loss  of  function  (Ausfallserscheinungen).  But 
there  are,  in  addition  to  these  direct  symptoms,  other  indirect  focal  symptoms, 
which  outlast  the  apoplectic  shock,  and  vary  with  the  locality  of  the  haemorrhage. 
These  do  not,  however,  correspond  to  the  territory  actually  destroyed.  They  are 
due  to  the  influence  exerted  for  a  certain  length  of  time  by  the  haemorrhagic  focus 
upon  the  immediate  surrounding  structures.  The  pressure  of  the  effusion,  the 
disturbance  of  circulation  resulting  from  it,  the  collateral  oedema,  and  perhaps 


CEREBRAL   HAEMORRHAGE 


1095 


also  the  imbibition  of  the  soluble  products  of  disintegration  of  the  apoplectic 
focus,  are  the  chief  factors  in  exciting  these  indirect  symptoms.  They  do,  indeed, 
outlast  the  initial  shock,  but  are  nevertheless  temporary,  vanishing  sooner  or 
later,  at  the  end  of  several  days  or  weeks,  or  even  months.  If  the  apoplectic  shock 
is  over  and  if  the  symptoms  still  exhibited  have  been  minutely  determined,  yet  we 
are  unable  to  say,  at  first,  whether  the  existing  focal  symptoms  are  direct  or  indi- 
rect. We  can  decide  about  this  only^  after 
further  observation.  If  the  early  symptoms 
■disappear  within  the  next  few  days  or  weeks, 
or  after  the  first  two  or  three  months,  we 
can  then  affirm,  retrospectively,  that  they 
were  indirect.  Such  as  outlast  the  first  six 
months  are  to  be  regarded  as  direct,  and  as 
not  destined  to  improve  much.  From  a 
practical  point  of  view  this  distinction  is  of 
extreme  importance.  We  shall  revert  to  the 
subject  when  considering  the  course  of  cere- 
bral  apoplexy. 

A  minute  description  of  all  the  focal 
symptoms  which  might  occur  after  cerebral 
lisemorrhage,  and  of  the  light  thus  thrown 
upon  the  location  of  the  haemorrhage,  need 
not  be  attempted  here,  for  it  would  neces- 
sitate a  repetition  of  all  the  facts  enumer- 
ated in  the  preceding  chapter.  It  is  only 
requisite  to  describe,  in  detail,  the  chief 
and  by  far  the  raost  frequent  results  of  a 
cerebral  hasmorrhage  —  ordinary  cerebral 
hemiplegia  (see  Fig.  175). 

It  has  been  mentioned  that  most  of 
these  haemorrhages  occur  near  the  lateral 
ventricles.  Hence,  in  a  majority  of  in- 
stances, the  motor  pyramidal  tract,  as  it  tra- 
verses the  internal  capsule,  is  either  direct- 
ly destroyed  or  at  least  indirectly  affected. 
Consequently,  most  patients  who  survive  the 
apoplectic  shock  present  a  paralysis  of  that 
half  of  the  body  which  is  opposite  the  seat 
of  hsemorrhage.  On  minute  examination 
we  usually  find,  in  the  first  place,  that  even 
in  the  distribution  of  the  facial  nerves  there 
is  a  distinct  difference  between  the  two 
sides,  the  lower  division  of  the  facial 
(which  supplies  the  muscles  of  the  cheek, 
nose,  and  mouth)  being  evidently  para- 
lyzed on  one  side,  while  its  upper  division 
is  entirely,  or  almost  entirely,  intact.  The 
side  as  well  as  on  the  other,  or  only  a  little  less  on  the  paralyzed  side  than 
on  the  sound  side;  but  if  the  patient  tries  to  dilate  his  nostrils,  or  alter  the 
shape  of  his  mouth,  or  whistle,  or  blow,  or  talk,  etc.,  the  paralysis  becomes  evi- 
dent. Often,  indeed,  while  the  face  is  quiet,  it  can  be  noticed  that  one  naso- 
Inbinl  fold  is  obliterntcd,  or  thnt  one  comer  of  the  mouth  droops.  It  is  an  in- 
teresting fact  that  the  paresis  of  the  lower  division  of  the  facial  is  much  more 
noticeable  during  voluntary  efforts,  as  in  showing  the  teeth,  than  when  the  patient 


Fig.  175. — Patient  with  right  hemiplegia. 
(Personal  ob.servation.) 


(going  to  the  eyes  and   forehead) 
forehead  can  be  wrinkled  on   one 


1096  DISEASES    OF   THE   NERVOUS    SYSTEM 

smiles  involuntarily.  A  patient  will  sometimes  try  in  vain  to  draw  back  the  cor- 
ner of  his  mouth,  then  begin  to  laugh  at  his  own  awkwardness,  and  thereupon 
open  his  mouth  in  an  almost  perfectly  normal  manner.  We  have  seen  above,  in 
the  chapter  on  cerebral  localization,  that  this  condition  can  probably  be  explained 
by  the  relation  of  the  optic  thalamus  to  the  movements  of  mimetic  expression. 
The  difference  in  the  behavior  of  the  upper  and  the  lower  part  of  the  face  in  cere- 
bral hemiplegia  is  probably  connected  with  the  fact  that  the  muscles  supplied  by 
the  upper  division  (frontalis,  corrugator  supercilii,  and  to  a  certain  extent  the 
orbicularis)  are  very  seldom  exercised  upon  one  side  alone,  but  always  bilaterally. 
Perhaps  both  sides  receive  nervous  fibers  from  each  cerebral  hemisphere,  so  that, 
if  a  single  center  be  intact,  it  alone  answers  for  the  muscles  on  both  sides.*  In  the 
distribution  of  the  lower  division  of  the  facial,  also,  ordinary  cases  of  cerebral 
hemiplegia  present  almost  always  a  more  or  less  marked  paresis,  and  only  excep- 
tionally a  complete  paralysis. 

There  is  quite  often  a  slight  impairment  of  the  hypoglossus  in  addition  to  the 
paresis  of  the  facial  nerve.  If  the  patient  puts  out  his  tongue,  its  tip  deviates 
toward  the  paralyzed  side.  This  is  a  result  of  paresis  of  one  of  the  genio-hyo- 
glossi.  When  both  these  muscles  contract,  they  may  be  said  to  push  the  tongue 
forward.  If  this  thrust  be  more  vigorous  on  one  (the  healthy)  side,  the  tongue  is 
deflected  toward  the  other  (paralyzed)  side.  In  ordinary  cerebral  hemiplegia  this 
is  almost  always  the  sole  way  in  which  the  movements  of  the  tongue  can  be  seen 
to  be  impaired.  Sometimes,  however,  the  slight  paresis  of  half  of  the  tongue, 
combined  with  the  facial  paresis,  entails  a  noticeable  difficulty  in  articulation. 
This,  to  be  sure,  is  only  exceptionally  great,  and  is  often  appreciated  by  the 
patient  alone,  who  is  conscious  that  an  effort  is  required  in  order  to  speak. 

The  soft  palate  is  rarely  much  affected.  It  may,  however,  hang  rather  lower 
down  on  the  paralyzed  than  on  the  affected  side,  and  move  less.  The  uvula  is 
inclined  sometimes  toward  the  healthy  and  sometimes  toward  the  paralyzed  side.. 
There  are  no  special  disturbances  of  function  as  a  result  of  these  changes. 

The  trapezius  is  the  only  muscle  of  the  trunk  which  is  ordinarily  much 
affected  in  cerebral  hemiplegia.  As  a  result  of  the  paresis  of  this  muscle,  the 
shoulder  sags  and  it  can  not  be  raised  as  high  as  on  the  normal  side.  If  the  pa- 
tient tries  to  take  a  very  deep  breath,  it  is  in  some  cases  possible  to  see  that  the 
paralyzed  side  lags  behind  a  little  in  respiration,  which  is  due  to  a  paresis  of  the 
respiratory  muscles  on  that  side.  It  is  perhaps  due  to  this  that  the  pulmonary 
diseases  which  attack  hemiplegic  patients  frequently  develop  in  the  lung  on  the 
affected  side,  where  respiration  is  deficient. 

The  most  important  element  in  the  hemiplegia  is  the  paralysis  of  the  extrem- 
ities. Immediately  after  the  haemorrhage  it  is  often  so  complete  that  even  the 
slightest  voluntary  motion  in  the  affected  arm  and  leg  is  impossible.  Other  cases, 
however,  exhibit  only  a  more  or  less  severe  paresis  (hemiparesis)  from  the  first; 
or  the  complete  paralysis  at  any  rate  is  confined  to  certain  groups  of  muscles,  the- 
others  still  retaining  vestiges  of  their  normal  contractility.  Even  when  there  is 
total  hemiplegia  at  first  some  of  the  muscles  almost  always  regain  a  certain 
amount  of  their  old  power  later  on  (vide  infra). 

The  behavior  of  the  reflexes  is  comparatively  constant  in  nearly  all  cases  of 
cerebral  hemiplegia.  In  general  the  rule  is  that  the  tendon  reflexes  are  increased 
on  the  paralyzed  side,  but  that  the  skin  reflexes  are  diminished.    The  increase  of 

*  There  is  a  remarkable  general  rule  which  should  be  mentioned  here,  and  which  is  perhaps  to  he 
explained  in  the  same  way,  namely,  that  those  muscles  which  are  usually  called  into  play  in  pairs  are 
never  completely  paralyzed  in  cerebral  hemipleiria.  Furthermore,  it  is  impossible  for  us  to  contract 
most  of  these  singly,  on  one  side  alone,  or  at  least  not  without  special  practice :  this  applies,  for 
instance,  to  the  corrugator  supercilii,  the  frontalis,  the  motores  oculi,  and  the  muscles  of  mastication 
and  respiration. 


CEKEBRAL   HEMORRHAGE  1097 

the  tendon  reflexes  is  an  almost  constant  symptom.  Only  when  the  sj'mptoms  of 
the  initial  shock  are  very  severe,  there  may  at  first  be  no  tendon  reflexes  whatever. 
In  all  eases  of  any  duration  they  are,  with  few  exceptions,  exaggerated,  and  usu- 
ally very  much  so.  In  the  arm  we  find  very  lively  periosteal  reflexes  on  tapping 
the  lower  end  of  the  radius  and  the  ulna  (see  page  840),  also  on  striking  the  ten- 
dons of  the  biceps  and  triceps,  the  clavicle,  etc.  In  the  leg  the  increase  of  the 
patellar  reflex  is  most  noticeable ;  but  there  is  often  a  lively  Achilles  reflex  also, 
an  increase  of  the  adductor  reflexes,  etc.  This  increase  of  the  tendon  reflexes  is 
by  no  means  limited  to  the  affected  side ;  it  can  almost  always  be  detected  on  the 
sound  side  also,  although  to  a  lesser  degree.  Many  have  expressed  the  opinion 
that  the  increased  tendon  reflex  upon  the  paralyzed  side  is  a  result  of  the  sec- 
ondary degeneration  of  the  pyramidal  tracts  in  the  spinal  cord.  In  our  judgment 
this  view  is  entirely  unfounded,  inasmuch  as  the  exaggeration  of  the  tendon  reflex 
often  appears  within  a  few  days,  or  even  a  few  hours,  after  the  apoplectic  attack — 
that  is,  before  a  secondary  degeneration  in  the  spinal  cord  is  to  be  thought  of.  We 
would  rather  seek  to  explain  the  phenomenon  as  being  due  to  the  suspension  of 
certain  reflex  inhibitory  influences  because  of  the  cerebral  lesion. 

There  is  very  often  found,  particularly  in  cases  of  long  standing  affected  with 
well-marked  contractures,  an  increase  of  "  direct  mechanical  excitability  "  in  the 
paralyzed  muscles,  such  that  a  tap  upon  them  causes  them  to  contract  vigorously. 
We  are  of  the  opinion  that  a  part  of  these  contractions  are  of  reflex  origin  and  are 
due  to  the  mechanical  irritation  of  the  fascia  of  the  muscles  (fascial  reflex). 
There  is  also  the  direct  mechanical  irritation  of  the  nerves  of  the  muscles. 

The  skin  reflexes  in  hemiplegia  behave  in  precisely  the  opposite  way  from  the 
tendon  reflexes,  being  almost  invariably  decidedly  diminished  on  the  paralyzed 
side.  In  the  paralyzed  arm  it  is  usually  impossible  to  excite  any  skin  reflex  what- 
ever; and  in  the  corresponding  leg  there  is  either  no,  or  at  any  rate  a  greatly 
diminished  reflex.  The  difference  in  certain  other  skin  reflexes,  especially  the 
abdominal  and  cremaster  reflexes  (page  839)  is  still  more  evident  than  in  the 
plantar  reflex.  [The  plantar  reflex,  however,  is  often  manifested  by  extension  of 
the  great  toe — the  Babinski  reflex. — K.]  These  reflexes  are  almost  always  much 
diminished  or  wholly  absent  on  the  paralyzed  side,  while  they  can  be  elicited  on 
the  sound  side  in  normal  strength,  a  distinction  which  is  not  infrequently  of 
service  in  determining  the  seat  of  the  hemiplegia  when  the  patient  is  stupid  or 
even  quite  unconscious.  There  is  often  a  marked  difference  in  the  conjunctival 
reflex  also.  On  the  paralyzed  side  we  can  touch  the  eyeball  with  the  finger  or  the 
head  of  a  pin  without  causing  an  immediate  reflex  closure  of  the  eye,  as  is  the 
case  on  the  healthy  side.  It  is  not  easy  to  explain  the  striking  behavior  of  all  the 
skin  reflexes  in  cerebral  hemiplegia,  especially  the  peculiar  contrast  between  them 
and  the  tendon  reflexes.  It  is  ordinarily  assumed  that  certain  inhibitory  influ- 
ences for  the  tendon  reflexes  are  lost  through  the  cerebral  disease,  while  the 
inhibition  of  the  skin  reflexes  is,  on  the  contrary,  put  into  a  state  of  irritation. 
This  explanation  is  evidently  forced  and  unsatisfactory,  and  thus  the  suspicion  is 
not  wholly  unwarranted  that  these  skin  reflexes,  contrary  to  the  physiological 
theories  thus  far  generally  accepted,  have  their  reflex  arcs  not  in  the  spinal  cord, 
but  much  higher  up  in  the  brain.  The  absence  of  certain  skin  reflexes  in  cerebral 
hemiplegia  is  accordingly  due  to  a  direct  injury  of  the  reflex  path.  Of  course  it 
must  be  emphasized  that  further  studies  upon  this  important  point  are  extremely 
necessary. 

Sensation  is  but  little  impaired  in  most  cases  of  cerebral  hemiplegia,  but  on 
careful  examination  we  often  find  a  decided  blunting  of  sensibility  for  simple 
contact,  although  the  sensibility  to  pain  and  temperature  and  the  muscular  sense 
are  retained.  Slight  parsesthesia  is  not  infrequently  complained  of  on  the  affected 
side,  especially  at  first.    Pain  in  the  paralyzed  parts  is  not  uncommon.    It  is  often 


1098  DISEASES    OE   THE   NEEVOUS    SYSTEM 

to  be  referred  to  special  peripheral  conditions  (contractures,  etc.),  but  sometimes 
there  is  apparently  an  irritation  of  the  central  sensory  tracts  (Edinger).  Any 
marked  disturbance  of  sensation  indicates,  as  has  been  seen  (conapare  page  1084), 
that  the  posterior  extremity  of  the  internal  capsule  is  involved.  Such  cases  are 
rare.  In  them  we  may  observe  a  complete  cerebral  hemiangesthesia  combined  with 
the  hemiplegia.  According  to  Gowers,  a  temporary  hemianopsia  is  often  present 
directly  after  the  occurrence  of  a  cerebral  haemorrhage.  We  have  seen  the  initial 
hemianopsia  combined  with  associated  paralysis  of  the  ocular  muscles.  It  is  also 
not  uncommon  to  find  hemiplegia  associated  with  permanent  hemianopsia ;  but  as 
yet  little  is  known  about  the  pathological  anatomy  of  such  cases.  The  most  likely 
thing  would  seem  to  be  some  lesion  of  the  fibers  of  the  optic  nerve  in  the  internal 
capsule  or  in  the  pulvinar  of  the  optic  thalamus.  The  muscular  sense  is  not  usu- 
ally affected  in  hemiplegia.  [The  stereognostic  sense  (vide  page  795)  is  not  in- 
frequently affected. — K.] 

Turning  now  to  the  further  course  of  hemiplegia,  we  find  a  new  group  of  im- 
portant symptoms.  First  of  all  should  be  considered  the  changes  in  the  paralyzed 
muscles.  If  the  hemii^legia  be  incomplete,  even  from  the  start,  almost  the  normal 
degree  of  motility  may  in  a  comparatively  brief  period  be  regained  by  the  affected 
side.  At  most  there  will  persist  a  certain  slight  amount  of  weakness  and  stiffness ; 
and  even  this  will  gradually  diminish.  From  what  has  been  already  said,  it  is 
evident  that  in  these  cases  the  initial  paresis  is  an  indirect  focal  symptom,  and 
accordingly  vanishes  as  soon  as  the  effusion  ceases  to  affect  the  tissues  not  im- 
mediately involved. 

Even  where  there  is  a  complete  hemiplegia  it  is  exceptional  for  this  con- 
dition to  remain  unabated  throughout  the  entire  region  affected.  After  a  fcAv 
weeks,  or  even  a  few  days,  one  part  and  another  of  the  paralyzed  half  of  the 
body  begin  to  recover  their  former  motility.  The  improvement  goes  on  slowly, 
and  in  the  most  favorable  cases  the  paralysis  may  for  the  most  part  have  vanished 
at  the  end  of  some  months.  Usually,  however,  the  improvement  advances  only  to 
a  certain  point,  and  the  condition  then  attained  remains  stationary.  We  now 
find  the  ordinary  characteristic  typical  "  hemiplegic,"  who  can  be  recognized  at  the 
first  glance  by  the  practiced  eye.  The  most  noteworthy  phenomenon  in  such  cases 
is  this,  that,  in  spite  of  many  individual  differences  in  the  final  recovery  of  cer- 
tain movements  and  also  in  the  permanence  of  the  paralysis  of  other  groups  of 
muscles,  there  is  still  a  very  striking  regularity  and  uniformity.  There  is  one 
chief  fact  which  is  very  noteworthy,  that  almost  invariably  the  leg  regains  greater 
power  of  movement  than  the  arm.  In  regard  to  the  condition  of  the  individual 
groups  of  muscles,  moreover,  we  almost  always  find  the  same  manifestations.  As 
has  been  shown  chiefly  through  the  interesting  investigations  of  Wernicke  and 
L.  Mann,  the  permanent  paralysis  in  cerebral  hemiplegia,  or  the  return  of  motion, 
never  relates  to  individual  muscles,  but  always  to  whole  groups  of  muscles  whose 
functions  are  closely  connected.  In  the  upper  extremity  there  is  usually  perma- 
nent paralysis  of  all  the  muscles  that  rotate  the  arm  outward  (supinators  of  the 
forearm,  outward  rotation  of  the  upper  arm.  by  the  infra-spinatus  and  teres  minor, 
and  fixation  and  outward  rotation  of  the  shoulder-girdle  by  the  lower  portion  of 
the  trapezius  and  the  rhomboidei),  and  of  those  that  raise  the  upper  arm  (deltoid, 
serratus),  and  also  paralysis  of  the  movements  at  the  elbow,  especially  of  exten- 
sion, of  opening  the  hand  (extensors  of  the  fingers,  fixation  of  the  wrist  by  the 
flexors),  and  of  opposition  of  the  thumb  (opponens,  abductor  brevis).  On  the 
other  hand,  inward  rotation  of  the  arm  and  closure  of  the  hand  are,  as  a  rule,  pre- 
served. The  patient  can  therefore  not  take  hold  of  an  object  on  account  of  the 
difficulty  of  opening  the  hand,  but  he  can  hold  firmly  what  he  has  once  grasped. 
Fine  movements  of  the  hand,  however,  are  much  impaired  on  account  of  the  dis- 
turbances in  the  movement  of  the  thumb.    In  the  leg  the  flexors  of  the  loAver  leg 


CEREBRAL   HAEMORRHAGE  1099 

and  the  dorsal  extensors  of  the  foot  usually  remain  permanently  paretic,  and 
also  the  abductors  and  inward  rotators  of  the  hip,  while  the  ilio-psoas,  the  quadri- 
ceps extensor,  and  the  plantar  flexors  of  the  foot  often  regain  their  power  of  mo- 
tion. The  return  of  mobility  in  the  ilio-psoas  and  quadriceps  is  therefore  of 
great  practical  significance,  because  by  it  the  patient  is  enabled  to  walk  again. 
Of  course  the  patient  needs  the  help  of  a  cane,  and  the  gait  remains  slow  and  la- 
bored, but  the  advantage  of  independent  locomotion  is  extremely  great.  The  gait 
of  the  hemiplegic  is  very  characteristic  and  is  always  of  the  same  type.  The 
affected  leg  has  the  toe  turned  slightly  outward,  it  is  moved  forward  slowly,  drag- 
ging on  the  ground,  in  a  slight  curve  whose  convexity  is  outward.  We  can  not 
state  with  certainty  the  reason  for  these  facts  just  mentioned — that  both  the  im- 
provement and  the  permanent  paralysis  almost  always  involve  regularly  the  same 
definite  groups  of  muscles.  The  muscles  which  regain  the  power  of  motion  are 
probably  those  which  can  be  most  easily  innervated  from  the  healthy  hemisphere 
on  the  same  side  of  the  body. 

It  is  improbable,  although  of  course  not  impossible,  that  fibers  when  once 
destroyed  can  undergo  regeneration ;  but  the  fact  above  mentioned  is  of  the  great- 
est practical  consequence,  that  hemiplegic  symptoms  can  not  improve  materially 
after  the  first  six  months. 

The  permanently  paralyzed  muscles  become  very  often  contractured  later  on. 
The  appearances  produced  exhibit  considerable  uniformity.  The  arm,  which 
suffers  more  from  paralysis  than  the  leg,  is  also  usually  more  contracted.  The 
fingers  are  almost  invariably  flexed;  the  forearm  contracted  in  a  position  of 
pronation,  and  usually  flexed  rather  than  extended ;  and  the  upper  arm  adducted 
(the  pectoralis  major  being  chiefly  affected).  These  contractures  correspond  ex- 
actly to  the  natural  positions  which  the  paralyzed  arm  almost  always  assumes  if 
left  to  itself,  either  from  gravity  or  as  a  result  of  any  remaining  power  of  move- 
ment. The  contractures  are  almost  always  found  in  the  same  groups  of  muscles 
which  suffer  relatively  the  least  loss  of  power  in  hemiplegia  (vide  supra).  Since 
the  position  once  acquired  from  the  paralysis  of  the  antagonistic  muscles  can  not 
be  altered,  so-called  passive  contractures  appear  in  the  permanently  shortened 
muscles.  The  correctness  of  this  theory  is  favored  by  the  fact  that  the  deformity 
can  to  a  certain  extent  be  prevented  by  the  persistent  use  of  passive  motion,  which 
renders  any  permanent  shortening  of  the  muscle  impossible.  ISTevertheless,  Char- 
cot and  his  pupils,  including  Bouchard,  hold  an  entirely  different  opinion — 
namely,  that  the  contractures  are  due  to  the  secondary  degeneration  of  the 
pyramidal  tract.  In  defense  of  their  position  no  fact  can  be  adduced,  save  that 
fatal  cases  exhibiting  hemiplegic  contractures  do  invariably  present  the  secondary 
degeneration  mentioned ;  but  of  course  this  is  no  proof  that  the  two  things  have 
any  causative  relation  to  each  other.  A  contracture  occurs  only  in  connection 
with  persistent  paralysis ;  a  persistent  paralysis  is  never  seen  unless  the  pyramidal 
tract  be  destroyed ;  and  if  it  be  destroyed,  a  secondary  degeneration  must  result. 
The  contractures  and  the  secondary  degeneration  are  therefore  two  sequelae,  inde- 
pendent of  each  other.  That  the  degeneration  should  "  irritate "  the  fibers, 
and  thus  excite  muscular  contractions,  is  extremely  improbable ;  for,  according  to 
all  analogy,  fibers  which  are  undergoing  degeneration  can  not  be  stimulated,  and 
can  not  therefore  transmit  any  sort  of  stimulus  to  the  paralyzed  muscles. 

If  the  contractures  become  marked  in  the  lower  limb,  they  may  involve  either 
the  extensors  or  flexors,  which  depends  in  the  main  upon  accidents  of  position, 
etc.  At  the  ankle  we  almost  always  find  a  contracture  of  the  muscles  of  the  calf, 
because  the  dorsal  extensors  of  the  foot  are  paralyzed  and  the  foot  falls  into  a 
position  of  plantar  flexion  from  its  own  weight.  The  fact  that  the  muscular  tonus 
is  increased  on  the  paralyzed  side  (analogous  to  the  increase  of  the  tendon  re- 
flexes) is  a  circumstance  which  is  not  whollj'  without  influence  on  the  strength 


1100  DISEASES    OE   THE   NEEVOUS    SYSTEM 

of  tlie  contracture.  We  may  mention  liere  the  fact  brought  forward  by  Hitzig 
that  many  contractures  are  slight  in  the  morning,  when  the  patient  wakes  from 
sleep,  and  become  more  marked  after  he  has  begun  to  move. 

Among  other  symptoms  we  will  mention  first  the  interesting  associated  move- 
ments, which  are  of  frequent  occurrence  in  hemiplegics.  The  chief  explanation 
of  them  is  that  the  patient  can  no  longer  innervate  the  different  paretic  groups 
of  muscles  with  ease.  In  order  to  do  so,  it  is  always  necessary  to  make  a  forcible 
associated  movement  of  the  leg,  when  the  patient  is  endeavoring  with  all  his 
energy  to  move  his  arm,  and  vice  versa.  If  the  patient  tries  to  raise  the  arm  at 
the  shoulder,  he  flexes  his  forearm  at  the  same  time.  The  coramon  associated 
movement  in  the  foot  (dorsal  extension  from  contraction  of  the  tibialis  anticus) 
on  flexing  the  hip  and  knee,  which  was  first  described  by  the  author,  is  especially 
striking.  'Not  infrequently  the  patient  is  quite  unable  to  extend  the  foot  dorsally 
as  an  isolated  movement,  but,  if  he  draws  the  whole  leg  up  to  the  trunk,  there  is 
then  always  a  simultaneous  marked  dorsal  extension  of  the  foot.  Associated 
movements  also  occur  on  the  sound  side  on  movements  of  the  affected  side,  and  it 
is  said  that  the  opposite  condition  has  also  been  observed. 

Another  peculiar  phenomenon  must  be  mentioned  here.  It  is  what  Weir 
Mitchell  has  termed  post-hemiplegic  chorea.  Some  time  after  the  paralysis  begins 
the  parts  affected  by  it  exhibit  involuntary  movements,  Reminding  one  of  chorea 
or  athetosis  (vide  page  836).  Sometimes  these  movements  are  continuous,  some- 
times they  occur  only  as  associated  movements  in  connection  with  voluntary 
motions  of  the  paralyzed,  or  even  of  the  sound,  side.  Hemiplegia  due  to  cerebral 
haemorrhage  very  seldom  exhibits  this  phenomenon.  It  is  said  to  occur  chiefly 
in  focal  disease  of  the  posterior  extremity  of  the  internal  capsule,  and  of  the 
optic  thalamus  (irritation  of  the  adjacent  pyramidal  tract?).  It  is  much  com- 
moner in  cerebral  infantile  paralysis  (vide  infra). 

It  is  interesting  to  observe  the  trophic  and  vaso-motor  changes  in  the  paralyzed 
parts.  At  first  the  skin  may  be  somewhat  redder  and  warmer  on  the  paralyzed 
than  on  the  sound  side.  ISTothnagel  has  shown  that,  even  in  the  distribution  of 
the  cervical  sympathetic,  symptoms  of  vaso-motor  paralysis  occur.  They  are  partly 
temporary  and  partly  persistent,  and  comprise  increase  of  temperature  and  color 
in  the  paralyzed  side  of  the  face,  swelling  of  the  eyelids,  and  contraction  of  the 
pupil;  but  they  are  usually  slight.  We  very  frequently  find,  especially  on  the 
back  of  the  hands,  more  or  less  puffiness,  which  is  likewise  usually  regarded  as  of 
vaso-motor  origin.  It  should,  however,  be  considered  that  the  natural  movements 
of  any  part  of  the  body  greatly  promote  the  nervous  and  lymphatic  circulation, 
and  that  the  quietude  of  paralysis  may  therefore  have  much  to  do  with  the  oedema. 
In  hemiplegia  of  some  duration  the  extremities  upon  the  paralyzed  side  are  always 
cooler  than  normal,  and  the  hand  in  particular  is  very  often  deeply  cyanotic. 
The  skin  sometimes  becomes  harsh  and  fissured,  and  often  is  thickened.  The  in- 
ternal surface  of  the  hand,  in  case  of  contracture,  is  frequently  quite  damp  with 
perspiration. 

Among  the  specific  trophic  symptoms  of  hemiplegia  Charcot  includes  "  acute 
malignant  decubitus."  This  sometimes  develops  with  extreme  rapidity  within  a 
few  days  after  the  shock,  and  usually  occupies  the  buttock  on  the  affected  side. 
There  appears  a  circumscribed  redness  with  the  formation  of  vesicles,  which  is 
soon  succeeded  by  a  deep-reaching  necrosis  of  the  soft  parts.  We  have  ourselves 
never  met  with  this  in  a  case  which  has  been  properly  nursed,  and  we  can  not 
therefore  help  thinking  that  its  development  is  not  wholly  due  to  trophic  disturb- 
ance, but  to  pressure  and  to  the  penetration  of  septic  matter  below  the  skin.  Of 
course,  patients  long  confined  to  bed  with  hemiplegia  are  as  liable  to  bedsores  as 
are  any  others  similarly  situated. 

If  the  hemiplegia  has  existed  for  some  time,  we  almost  always  find  the  para- 


CEREBRAL   ELEMORRHAGE  1101 

lyzed  muscles  more  or  less  atrophied  in  comparison  with  those  on  the  sound  side. 
On  microscopic  examination  we  also  find  an  evident  atrophy  of  the  individual 
fibers,  but  this  atrophy,  -as  a  rule,  is  not  so  extreme  as  in  peripheral  or  polio- 
myelitic  paralyses  (see  page  834).  Furthermore,  the  atrophy  is  always  "simple," 
not  "  degenerative,"  and  accordingly  the  f  aradic  and  galvanic  excitability  of  the 
paralyzed  muscles  is  completely  preserved,  even  if  the  muscles  are  very  much 
atrophied.  The  electrical  excitability  does  not  even  show  a  slight  quantitative 
diminution,  as  careful  examinations  have  taught  us.  In  some  cases,  even  in 
ordinary  hemiplegia,  the  atrophy  of  certain  muscles  (for  example,  the  interossei, 
the  thenar  muscles,  the  deltoid,  etc.)  may  come  on  unusually  early  and  become 
extremely  marked,  so  that  we  may  speak  of  a  "  cerebral  muscular  atrophy."  In 
such  cases  certain  trophic  influences  actually  seem  to  be  especially  manifest. 
The  joints  of  the  paralytic  extremities,  and  in  particular  the  knee  and  shoulder, 
may  exceptionally  become  inflamed.  The  arthritis  is  sometimes  acute,  and  some- 
times more  of  a  chronic  variety.  Its  cause  is  not  evident.  Charcot  thinks  that 
it  is  probably  a  neurotrophic  symptom,  and  he  is  of  the  same  mind  with  regard  to 
the  rarely  seen  swellings  of  the  peripheral  nerve-trunks  of  the  paralyzed  side 
("  hypertrophic  neuritis  "). 

Mental  symptoms  are  rare,  except  the  initial  loss  of  consciousness.  There  is 
sometimes,  however,  a  persistent  general  uneasiness  of  mind,  accompanied  by 
great  excitability  and  wakefulness.  In  a  large  number  of  cases  of  persistent 
hemiplegia  there  finally  come  on,  in  the  course  of  years,  constantly  increasing 
indications  of  mental  weakness.  The  patient  grows  dull  and  forgetful.  Very 
often  he  exhibits  a  peculiar  tendency  to  weeping,  bursting  into  tears  at  the  slight- 
est provocation;  but  frequently  he  is  subject  to  quick  alternations  of  feeling, 
weeping  and  laughing  in  the  same  minute.  The  patient  sometimes  becomes 
eventually  confused,  excited,  etc.  All  such  pronounced  conditions  are  usually 
dependent  upon  the  general  cerebral  atrophy  that  comes  from  arterio-sclerosis. 

The  general  nutrition  is  often  good  for  a  long  time.  Sometimes  there  is  even 
a  decided  tendency  to  corpulence.  In  other  cases,  and  especially  in  the  bedridden, 
marasmus  gradually  comes  on  and  hastens  the  fatal  termination,  particularly  if 
there  be  some  intercurrent  trouble,  such  as  a  bedsore  or  bronchitis. 

We  have  detailed  the  peculiarities  of  hemiplegia  somewhat  minutely,  because 
the  statements  will  apply  in  the  main  to  all  cases  of  cerebral  hemiplegia,  no  mat- 
ter in  what  place  the  pyramidal  tract  is  interrupted  or  by  what  sort  of  a  lesion. 
It  is  needless  to  enter  into  the  diverse  symptoms  which  are  caused  by  diversity 
in  the  exact  location  of  the  haemorrhage.  The  hemiplegia  itself  is  the  same, 
whether  the  effusion  be  in  the  cortex,  internal  capsule,  crus  cerebri,  or  pons.  It 
is  easy  to  infer  from  the  preceding  chapter  what  the  accessory  symptoms  are 
which  would  enable  us  to  localize  the  trouble.  We  need  mention  here  only  the 
frequent  combination  of  right  hemiplegia  and  aphasia.  This  occurs  when  there 
is  a  large  effusion  in  the  left  hemisphere,  extending  from  the  internal  capsule  to 
the  neighborhood  of  the  third  frontal,  or  possibly  the  uppermost  temporal  con- 
volution (compare  page  1077  et  seq.). 

Diagnosis. — The  diagnosis  of  cerebral  haemorrhage  rests  on  the  sudden  onset 
of  the  apoplectic  symptoms,  and  on  the  later  symptoms  (if  there  be  any)  of  im- 
pairment of  the  cerebral  functions.  The  diagnosis  can  scarcely  ever  be  made 
with  absolute  certainty,  for  cerebral  embolism  may  exhibit  almost  identical  phe- 
nomena:  the  differential  diagnosis  between  the  two  will  be  given  in  the  following 
chapter.  Occasionally  there  may  be  danger  of  mistaking  other  cerebral  affections 
for  a  haemorrhage,  such  as  meningitis  and  tumors.  The  same  may  be  said  of  a 
suddenly  developed  uraemia,  and  of  constitutional  sepsis.  In  these  cases  the  rapid 
onset  of  grave  cerebral  symptoms  of  a  general  nature,  such  as  unconsciousness, 
simulates  the  apoplectic  coma. 


1102  DISEASES    OE    THE   Is^EEVOUS    SYSTEM 

Prognosis. — The  first  question  is,  whether  the  patient  will  survive  the  initial 
shock.  The  answer  depends  upon  the  severity  of  the  early  symptoms.  The 
deeper  and  more  persistent  the  unconsciousness,  the  more  deficient  the  respiration 
and  pulse,  the  less  the  prospect  of  recovery;  but  we  can  never  decide  absolutely. 
[A  steady  rise  of  temperatuTe  or  a  very  high  temperature  is  also  of  bad  omen. 
— K.]  If  the  patient  have  withstood  the  first  onset  and  be  hemiplegic,  then  the 
possibility  of  improvement  hinges  on  the  question  whether  the  paralysis  is  a  direct 
or  an  indirect  focal  symptom.  Inasmuch  as  there  are  no  means  of  knowing  about 
this  at  first,  we  must  speak  very  guardedly.  [The  early  appearance  of  ankle 
clonus  or  greatly  exaggerated  patellar  reflex  is  apt  to  portend  permanent  paraly- 
sis with  contractures. — K.]  It  should  never  be  forgotten  that  the  haemorrhage 
may  recur.  The  predisposing  disease  of  the  blood-vessels  renders  individuals 
who  have  had  one  stroke  liable  to  be  visited,  sooner  or  later,  by  another. 

Treatment. — The  treatment  of  the  apoplectic  shock  demands,  first  of  all,  rest 
in  bed,  with  the  head  and  shoulders  elevated.  To  avoid  bedsores  it  is  very  impor- 
tant to  maintain  cleanliness,  and  to  watch  attentively  that  portion  of  the  skin 
which  is  pressed  against  the  bed  by  the  weight  of  the  body.  An  ice-bag  should 
be  put  upon  the  head,  and  particularly  over  that  side  on  which  the  hsemorrhage 
is  supposed  to  be.  Bleeding  was  formerly  universally  practiced,  but  of  late  its 
usefulness  is  doubted.  It  is  at  most  indicated  only  when  the  deep  congestion  of 
the  face,  the  violent  pulsation  of  the  carotids,  and  the  full,  slow  pulse  show  in- 
creased arterial  tension.  In  such  a  case,  if  the  patient  seem  otherwise  robust,  we 
may  bleed  at  the  commencement  of  an  attack,  in  the  hope  of  checking  the  flow  of 
blood  by  lowering  the  intra-arterial  pressure.  In  similar  conditions  experience 
shows  that  the  local  abstraction  of  blood  from  the  temples  is  sometimes  advan- 
tageous. The  bowels  should  be  well  emptied  by  enemata,  and  later  on  by  drastic 
purgatives.  If  the  respiration  and  pulse  fail,  we  may  try  stimulants  (ether,  cam- 
phor) . 

[Horsley  and  Spencer  have  found,  by  experiments  on  animals,  that  if  the  in- 
ternal carotid  be  tied  the  bleeding  from  the  divided  lenticulo-striate  artery  is 
checked.  Horsley  therefore  suggests  that  in  the  very  earliest  stage  of  cerebral 
hgemorrhage  ligature  or  compression  of  the  internal  carotid  may  check  the  bleed- 
ing, and  prevent  the  formation  of  a  large  clot  and  extensive  destruction  of  the 
brain.  TMs  procedure  has  been  tried  with  some  benefit  in  one  or  two  cases  of 
ingravescent  hsemorrhage. 

Where  there  is  much  diificulty  in  respiration  during  the  period  of  coma,  relief 
may  sometimes  be  obtained  by  turning  the  patient  upon  the  side. — ^K.] 

Wlien  the  patient  is  safely  over  the  shock,  our  resources  for  aiding  him  in  the 
further  stages  of  his  trouble  are  very  limited.  As  long  as  headache  and  symptoms 
of  fever  persist,  the  application  of  ice  to  the  head  should  be  kept  up,  and  other 
disturbances  should  be  treated  symptomatically.  For  uneasiness  and  wakeful- 
ness, small  doses  of  morphine  or  chloral  are  given.  Treatment  of  the  hemiplegia 
must  be  deferred  for  the  first  three  or  four  weeks,  until  all  the  initial  symptoms  of 
irritation  are  over.  Then  electricity  plays  the  chief  role.  Local  galvanization 
should  be  tried,  the  current  being  made  to  pass  transversely  through  the  head, 
with  as  much  regard  as  possible  to  the  position  of  the  haemorrhagic  focus ;  the 
current  should  be  feeble,  and  the  application  should  occupy  two  or  three  minutes. 
With  this  may  be  combined  galvanization  of  the  sympathetic  nerve  on  the  side  of 
the  ha3morrhage ;  nor  should  galvanization  (stroking  with  the  cathode)  and  fara- 
dization of  the  paralyzed  muscles  and  nerves  be  neglected.  If  favorable  changes 
take  place,  it  is,  however,  uncertain  how  much  should  be  ascribed  to  treatment; 
since,  as  has  already  been  stated,  there  is  often  improvement  without  treatment. 
Passive  movements  and  massage  of  the  paralyzed  limbs  are  very  important  as 
a  prophylaxis  against  contractures.     They  should  be  commenced  promptly,  and 


CEEEBEAL  EMBOLISM   AND   THEOMBOSIS  1103 

be  continued  methodically.  Massage,  and  later  on  systematic  and  appropriate 
gymnastic  exercises,  may  contribute  much  to  the  restoration  of  voluntary  motions. 
The  same  object  is  also  promoted  by  rubbing  with  spirits  of  camphor,  chloroform 
liniment,  etc. 

Internally,  potassic  iodide  is  frequently  given,  out  of  regard  for  its  "  absorb- 
ent "  properties.  We  may  also  try  the  effect  of  strychnine ;  it  is  most  adapted  for 
cases  of  some  duration. 

As  to  baths,  they  should  not  be  too  warm— that  is,  not  over  90°-93°  (26°-27° 
E.).  Moderately  warm  baths,  medicated  with  common  salt  if  it  seems  desirable, 
and  employed  three  or  four  times  a  week,  seem  to  be  beneficial.  If  it  be  thought 
best  to  send  the  patient  to  a  regular  bathing-place,  Wildbad,  Eagatz,  Teplitz, 
Wiesbaden,  Oeynhausen,  ISTauheim,  etc.,  may  be  chosen.  At  the  first-mentioned 
places  too  hot  baths  should  be  avoided. 

Hemiplegic  paralysis  often  lasts  so  long  that  the  physician  must  repeatedly 
change  the  details  of  treatment,  so  as  to  support  the  courage  and  patience  of  the 
sufferer.  Particular  care  should  be  given  to  regimen,  in  order  that  any  recur- 
rence of  the  haemorrhage  may,  if  possible,  be  avoided.  The  diet  should  be  simple ; 
any  large  amount  of  alcohol  should  be  forbidden;  and  there  should  be  no  severe 
bodily  exertion  or  mental  excitement. 


CHAPTEE   IV 

CEREBRAL  EMBOLISM  AND  THROMBOSIS  (ENCEPHALO-MALACIA) 

{Softening  of  the  Brain  from  Embolism  or  Thrombosis) 

.Sltiology  and  Pathology. — Occlusion  of  the  cerebral  arteries  is  one  of  the 
most  frequent  injuries  inflicted  by  embolism.  Usually  the  emboli  originate  in  the 
left  side  of  the  heart,  from  thrombi  in  the  left  auricle,  or  from  the  thrombotic 
deposits  which  form  in  chronic  endocarditis  (mitral  or  aortic  disease)  upon  the 
valves  of  the  left  ventricle.  Chronic  arterio-sclerosis  may  also  lead  to  thrombosis 
in  the  larger  arteries,  particularly  the  aorta;  and  in  case  the  cerebral  arteries 
themselves  are  extensively  atheromatous,  the  larger  vessels  at  the  base  of  the 
brain  may  furnish  material  for  embolism  of  the  smaller  cerebral  arteries. 

Thrombosis  of  the  arteries  of  the  brain  is  always  due  to  primary  disease  of  the 
blood-vessels,  the  most  common  cause  being  the  chronic  arterio-sclerosis  just  men- 
tioned. Wherever  the  atheroma  has  altered  the  normal  structure  of  the  intima, 
deposits  of  fibrine  may  take  place.  Their  development  is  further  promoted  by 
the  subnormal  elasticity  of  the  arteries,  and  by  the  occasional  narrowing  of  their 
lumen;  for  thus  the  flow  of  blood  is  rendered  slow,  if  not  even  completely 
checked.  It  is  easy  to  understand  that  thrombosis  and  embolism  may  each  give 
rise  to  the  other.  From  every  thrombus  an  embolus  may  be  detached ;  and  every 
firmly  lodged  embolus  may  form  a  nucleus  for  thrombosis. 

I^ext  to  arterio-sclerosis,  the  most  frequent  cause  of  a  cerebral  thrombus  is 
syphilitic  endarteritis.  In  the  chapter  on  cerebral  syphilis  this  subject  will  be 
minutely  considered.  Whether  thrombi  ever  form  here  independently  of  disease 
of  the  vessels  is  doubtful.  An  apparently  spontaneous  thrombosis  is  now  and 
then  seen  in  patients  who  are  cachectic  or  severely  ill  (cancer,  grave  t;sTphoid 
fever,  etc.).  Such  cases  are  explained  either  by  the  existing  cardiac  weakness, 
or  perhaps  by  an  abnormal  tendency  of  the  blood  to  coagulate. 

In  whatever  part  of  the  arterial  system  complete  occlusion  has  been  produced 
by  an  embolus  or  thrombus,  the  results  depend  upon  the  possibility  or  impossi- 


1104  DISEASES    OF    THE    NERVOUS    SYSTEM 

bility  of  blood  reaching  by  collateral  channels  the  region  thus  deprived  of  its 
ordinary  supply.  If  the  collateral  circulation  prove  efficient,  no  harm  is  done ;  if 
not,  the  tissues  must  perish  and  undergo  "  softening."  It  is  thus  a  matter  of  the 
greatest  practical  import  that  the  perforating  arteries  of  the  brain-stem,  and  par- 
ticularly the  branches  of  the  middle  cerebral  artery  in  the  fissure  of  Sylvius, 
which  supply  the  great  central  ganglia  and  internal  capsule,  are  all  "  terminal," 
in  Cohnheim's  sense — that  is,  they  form  few  anastomoses  with  neighboring  ves- 
sels. 'Now,  the  middle  cerebral  artery  and  its  branches  are  known  from  experience 
to  be  peculiarly  liable  to  embolism,  above  other  cerebral  arteries.  Hence  we  see 
why  the  region  they  supply  suffers  so  severely  and  so  very  frequently  from  emboli. 
It  is  noteworthy  that  the  left  middle  cerebral  artery  is  more  frequently  plugged 
by  emboli  than  is  the  right.  In  the  centrum  ovale  and  cortex  there  is  more  op- 
portunity for  collateral  compensation  than  in  the  central  ganglia ;  but  even  here 
the  supply  of  blood  often  proves  insufficient,  as  is  shown  by  the  not  infrequent 
occurrence  of  spots  of  softening  in  the  cortex  and  the  white  substance  of  the  cere- 
brum. On  the  other  hand,  embolic  foci  are  much  rarer  in  the  crura  cerebri,  pons, 
and  cerebellum. 

The  various  steps  in  the  process  which  begins  with  embolic  or  thrombotic 
occlusion  and  ends  in  softening  of  the  brain-substance  are  essentially  the  same  as 
occur  in  other  organs  (compare  chapter  on  pulmonary  embolism,  page  273).  The 
tissues  which  are  deprived  of  their  arterial  blood  perish,  become  disintegrated, 
and  are  transformed  into  a  soft  homogeneous  mass.  Into  the  empty  portion  of  the 
artery,  beyond  the  embolus,  blood  flows  in  the  reversed  direction  from  the  veins, 
and,  if  the  anatomical  relations  permit,  from  the  minute  arteries  in  the  neighbor- 
hood; but  the  supply  is  not  sufficient  to  nourish  the  tissues.  The  walls  of  the 
blood-vessels  become  abnormally  permeable  and  delicate,  so  that  some  red  glob- 
ules invade  the  disintegrating  region  by  diapedesis,  and  others  in  the  way  of 
minute  but  genuine  ecchymoses.  Actual  infarctions  are,  however,  never  formed 
in  the  brain,  perhaps  because,  as  Weigert  suggests,  the  nervous  structures  swell  so 
much  as  to  exclude  any  large  amount  of  blood;  but  the  little  punctiform  ecchy- 
moses are  in  many  instances  so  abundant  that  the  whole  softened  spot  seems  dis- 
tinctly reddish  or  yellowish.  This  red  or  yellow  softening  is  also  due  in  part  to 
the  tissues  being  stained  by  the  dissolved  pigment  of  disintegrated  blood-glob- 
ules. If  the  discoloration  be  not  very  striking,  then  we  speak  of  a  white  soft- 
ening. 

Fresh  foci  of  softening  are  seen  through  the  microscope  to  be  composed  of 
drops  of  myeline,  bits  of  swollen  nerve-fibers,  numerous  fatty  granular  cells,  and 
free  fat  globules.  The  time  required  for  these  changes  is  one  or  two  days.  If 
within  that  period  a  compensatory  collateral  circulation  is  set  up,  the  nervous 
structures  may  be  restored  and  resume  their  functional  activity.  If  not,  the  tis- 
sues perish  and  become  disintegrated.  The  white  blood-corpuscles  and  leucocyte? 
(and  possibly  also  the  endothelial  cells  of  the  blood-vessels,  and  the  neuroglia  and 
ganglion-cells)  absorb  the  fatty  detritus  thus  made,  and  come  to  form  the  fatty 
granular  cells  above  mentioned.  If  the  patient  live,  the  dead  and  disintegrated 
tissue  is  gradually  absorbed,  and  it  may  even  finally  be  replaced  by  a  cyst  not 
differing  in  appearance  from  those  which  occur  after  cerebral  hfemorrhage.  A 
minute  focus  of  softening  may  also  be  replaced  at  times  by  indurated  cicatricial 
tissue.  If  portions  of  the  surface  of  the  brain  become  softened,  quite  a  deep  de- 
pression often  results.  This  is  filled  up  in  part  with  serous  fluid  and  in  part  by 
hyperplasia  of  the  pia  mater.  Sometimes  the  convolutions  are  still  recognizable 
in  places;  but  they  are  atrophied,  of  a  yellowish  color,  and  of  a  greatly  increased 
consistency,  due  to  the  growth  of  cicatricial  tissue. 

Clinical  History. — The  occurrence  of  cerebral  embolism  is  attended  with 
almost  precisely  the  same  sort  of  shock  as  is  cerebral  haemorrhage.     We  do  not 


CEREBRAL   EMBOLISM    AXD    THROMBOSIS  1105 

aieed  to  enter  into  the  particulars  again  here,  but  will  refer  to  the  preceding  chap- 
ter (vide  page  1091).  In  embolism^  also,  the  intensity  of  the  shock  varies  from 
transitory  confusion  of  intellect  or  slight  vertigo  to  the  deepest  persistent  coma. 
One  chief  factor  in  determining  the  nature  of  the  case  is  the  size  of  the  occluded 
artery;  another  is  its  position,  according  as  the  embolism  has  taken  place  in 
the  hemispheres  or  toward  the  base  of  the  brain.  In  general,  however,  the  shock 
of  embolism,  especially  the  loss  of  consciousness,  is  not  often  so  severe  and  long 
continued  as  that  of  hsemorrhage ;  and  embolism  does  not  so  frequently  give  rise 
to  symptoms  of  cerebral  compression,  including  slowing  of  the  pulse.  The  tem- 
perature does  not  usually  show  the  decline  which  is  seen  in  fresh  cerebral  haem- 
orrhage, but  moderate  fever  sets  in  as  a  rule  in  the  course  of  a  few  days.  On  the 
other  hand,  epileptiform  convulsions  are  seen  more  often  in  embolism  than  in 
haemorrhage.  Embolism  again  may  have  a  rather  slow  onset,  where  there  is  at 
&st  a  small  embolus  and  this  becomes  the  nucleus  of  a  gradually  formed 
thrombus. 

It  is  not  easy  to  explain  why  there  should  be  a  shock  at  all  in  case  of  embolism. 
Perhaps  the  main  reason  is  the  diminution  of  pressure  which  the  embolism  occa- 
sions in  the  region  directly  affected  and  in  its  neighborhood.  The  portion  of 
the  artery  beyond  the  plug  becoming  empty  not  only  causes  a  draught  upon 
the  blood  and  lymph,  but  subjects  all  the  soft  surrounding  structures  to  a  dim- 
inution of  tension  and  to  a  certain  amount  of  strain  (Wernicke).  It  is  not 
impossible,  however,  that  the  disturbance  of  circulation  occasioned  in  the  sur- 
Tounding  blood-vessels,  including  the  capillaries  of  the  cortex,  by  sudden  em- 
bolism of  a  good-sized  artery  is  of  itself  enough  to  account  for  the  symptoms 
of  shock. 

With  regard,  also,  to  the  persistent  symptoms  of  embolism  we  may  be  equally 
hrief,  inasmuch  as  they  very  closely  resemble  those  which  follow  a  cerebral  haem- 
orrhage. As  has  been  said,  it  is  only  when  a  compensatory  collateral  circulation 
is  developed  within  the  first  forty-eight  hours  that  the  early  symptoms  of  focal 
disturbance  can  entirely  vanish.  After  this  period,  the  tissues  which  have  been 
deprived  of  their  normal  blood-supply  must  undergo  necrosis;  although  there  is 
still  room  for  hope  that  some  of  the  symptoms  will  prove  indirect,  and  therefore 
capable  of  improvement,  so  that  embolic  hemiplegia,  like  that  from  haemorrhage, 
may  improve  decidedly  in  the  course  of  the  first  few  weeks. 

Inasmuch  as  the  middle  cerebral  artery  is  by  far  the  most  frequent  seat  of 
cerebral  embolism,  and  inasmuch  as  this  artery  supplies  the  internal  capsule  as 
vpell  as  the  great  central  ganglia,  the  most  frequent  focal  sjTnptom  of  embolism 
of  the  brain  is  ordinary  cerebral  hemiplegia,  all  the  features  of  which  have  been 
depicted  in  the  preceding  chapter.  Aphasia  is  associated  with  it  with  comparative 
frequency,  for,  as  already  mentioned,  the  left  middle  cerebral  artery  is  especially 
apt  to  suffer.  Less  frequent  is  paralysis  of  a  single  member,  due  to  cortical  embo- 
lism, or  an  occipital  lesion  with  hemianopsia. 

Where  softening  is  the  result  of  thrombosis,  the  symptoms  are  but  seldom 
abrupt  in  their  onset.  Usually  the  focal  symptoms  and  the  more  general  ones 
(such  as  unconsciousness)  are  developed  rather  gradually.  This  is  most  often 
seen  in  so-called  senile  softening  of  the  brain,  a  disorder  almost  always  caused  by 
sclerosis  of  the  cerebral  arteries.  The  various  symptoms  generally  come  on  under 
cover  of  repeated  relapses  and  fresh  aggravations  of  the  disease.  A  severe  initial 
shock  seldom  occurs ;  but  almost  invariably  there  is  a  gradual  and  progressive 
dementia. 

The  further  course  and  the  final  termination  of  cerebral  softening  vary  as  do 

those  of  cerebral  haemorrhage.     Embolism  of  a  larger  artery  may  cause  speedy 

death.     If,  however,  the  first  shock  passes   away,  the   impairment  of  function 

which  may  be  left  behind  may  last  for  years  without  seriously  affecting  the  gen- 

70 


1106  DISEASES    OF    THE   JSTERVOUS    SYSTEM 

eral  health.  There  is  always  danger  of  a  recurrence  when  the  source  of  the  em- 
bolism continues  unchanged,  as  in  cardiac  disease  or  atheroma. 

Diagnosis. — Both  the  onset  and  the  persistent  focal  symptoms  are  so  much 
alike  in  hsemorrhage  and  embolism  that  in  many  cases  it  is  utterly  impossible  to 
decide  which  caused  the  apoplexy  and  hemiplegia.  The  following  are  factors  in 
making  a  differential  diagnosis,  if  one  can  be  made :  1.  It  is  very  important  to  find 
whether  there  be  any  source  for  an  embolus.  Thus,  if  the  patient  have  valvular 
cardiac  disease  (particularly  mitral),  embolism  is  more  probable  than  hsemor- 
rhage. 2.  A  young  person  is,  on  the  whole,  more  apt  to  have  embolism  than  haem- 
orrhage. At  a  later  period  of  life  one  is  about  as  probable  as  the  other.  3.  When 
the  shock  is  severe  and  persistent,  with  red  face,  strong  pulsation  of  the  carotids, 
and  signs  of  cerebral  compression  (slow  pulse),  we  should  think  of  hsemorrhage 
rather  than  embolism,  in  which  latter  the  initial  symptoms  are  sometimes  com- 
paratively slight  (vide  supra).  4.  Finally,  it  is  sometimes  possible  to  obtain  sup- 
port for  a  diag-nosis  of  cerebral  embolism  by  demonstrating  embolism  elsewhere, 
as  in  the  fundus  oeuli,  by  means  of  the  ophthalmoscope. 

In  rare  instances,  also,  tumors  of  the  brain,  into  the  substance  of  which  haem- 
orrhage takes  place,  may  induce  symptoms  closely  simulating  a  primary  apoplec- 
tic shock,  as  may  also  abscesses  which  have  been  previously  latent,  and  then  sud- 
denly burst  into  a  ventricle.    In  such  cases  a  correct  diagnosis  is  seldom  possible. 

Softening  due  to  a  thrombus  is  the  most  readily  diagnosticated  in  those  cases 
where  there  is  cerebral  syphilis  (q.  v.).  Senile  softening  is  inferred  from  the  age 
of  the  patient,  the  signs  of  general  arterio-sclerosis,  the  abrupt  advances  of  the 
disease  from  mildness  toward  severity,  and  the  developing  dementia. 

For  the  prognosis  and  treatment  of  cerebral  embolism  we  may  refer  simply  to 
what  was  said  in  the  preceding  chapter. 


CHAPTER   V 


INFLAMMATION    OF    THE    BRAIN 

(Acute  and  Chronic  Encephalitis) 

1.  Abscess  of  the  Brain  (Suppurative  Encephalitis) 

IEii\o\o^. — In  most  cases  of  cerebral  abscess  it  is  possible  to  demonstrate 
with  certainty  that  infectious  material  capable  of  exciting  suppuration  has  pene- 
trated to  the  encephalon.  This  is  particularly  true  of  those  not  very  rare  ab- 
scesses which  follow  injuries  of  the  scalp,  cranium,  or  brain  (traumatic  abscess 
of  the  brain).  Here  the  wound  is  probably  almost  always  an  open  one,  affording 
free  ingress  to  the  infection.  In  the  rare  cases  of  traumatic  cerebral  abscess, 
apparently  without  any  open  wound,  small  injuries  of  the  skin  have  probably  been 
overlooked.  It  is  not  essential  that  the  bones  should  be  injured,  however,  for 
experience  shows  that,  even  where  the  soft  parts  alone  are  wounded,  suppuration 
may  extend  to  the  brain.  The  manner  in  which  this  extension  takes  place  deter- 
mines the  question  whether  a  suppurative  meningitis  (q.  r.)  or  an  abscess  shall 
be  developed.  K"ot  infrequently  we  find  the  two  combined.  Another  source  of 
traumatic  cerebral  abscess  is  foreign  bodies  which  penetrate  into  the  brain  (for 
instance,  through  the  orbit),  and  thus  carry  septic  matter  into  the  very  substance 
of  the  organ. 

Besides  traumatic  causes,  any  existing  sufipuration  in  neighboring  parts  may, 
by  direct  extension,  occasion  cerebral  abscess.    The  same  processes  are  prominent 


INTLAMMATION   OF   THE   BRAIX  llOY 

in  this  connection  which  we  have  already  found  to  excite  purulent  meningitis 
{vide  page  1055) — particularly  suppuration  in  the  middle  ear  and  in  the  petrous 
bone  (chronic  purulent  otitis  media,  caries  of  the  petrous  bone).  As  a  rule,  the 
suppuration  attacks  the  brain  by  contiguity,  after  the  disease  of  the  bone  extends 
to  the  dura,  and  this  becomes  infected.  In  rare  cases  extra-dural  abscesses  are 
also  formed.  If  the  thin  roof  of  the  tympanic  cavity  is  broken  through,  the  ab- 
scess usually  forms  in  the  temporal  lobe,  while  suppuration  in  the  mastoid  usually 
leads  to  cerebellar  abscess.  The  excitants  of  suppuration  may  also  reach  the  brain 
along  the  lymph-sheaths  of  the  acoustic  and  facial  nerves  or  by  means  of  the  peri- 
vascular lymph-sheaths  and  veins.  About  one  third  of  all  abscesses  of  the  brain 
are  due  to  purulent  ear  disease.  The  danger  of  the  development  of  a  cerebral 
abscess  arises  especially  when  the  discharge  of  pus  is  checked  by  the  growtli  of 
granulations,  by  the  formation  of  cholesteatoma,  etc.,  and  also  in  acute  exacerba- 
tions of  chronic  purulent  otitis.  Abscesses  of  the  frontal  lobe,  following  suppura- 
tive processes  in  the  nasal  cavity  and  the  ethmoid,  are  much  less  common. 

In  yet  a  third  class  of  cases  the  morbific  agents  are  conveyed  from  foci  of 
disease  situated  in  distant  parts  of  the  body.  These  are  metastatic  or  embolic 
abscesses.  They  occur,  for  instance,  in  pyaemia  and  ulcerative  endocarditis. 
Abscesses  of  this  sort,  however,  are  usually  small,  and  seldom  are  conspicuous  in 
modifying  the  grave  general  disease.  Of  more  importance  are  cerebral  abscesses 
connected  with  certain  suppurative  affections  of  the  lungs  and  pleura.  These  are 
not  so  very  rare.  They  are  oftenest  associated  with  fetid  bronchitis,  pulmonary 
gangrene,  and  empyema.  Purulent  meningitis  (q.  v.)  may  occur  in  the  same  way. 
There  can  be  no  doubt  that  virus  is  in  some  way  conveyed  to  the  brain,  but  just 
how  is  not  yet  known. 

In  some  few  cases  of  cerebral  abscess  no  certain  aetiology  can  be  made  out. 
To  these  the  term  idiopathic  is  applied.  We  met  with  several  of  them  just  at  the 
time  of  an  epidemic  of  cerebro-spinal  meningitis ;  and  it  therefore  seems  reason- 
able to  suspect  that  possibly  many  apparently  spontaneous  cerebral  abscesses  are 
referable  to  the  same  poison  as  is  epidemic  meningitis.  In  other  cases  we  have 
to  do  with  other  forms  of  infection. 

From  the  variety  of  exciting  causes,  it  is  evident  that  in  cerebral  abscess 
the  special  variety  of  the  purulent  infection  is  not  always  the  same.  We  find 
streptococci  or  staphylococci  most  frequently  in  the  pus  of  an  abscess,  or  under 
some  circumstances  the  pneumonia  diplococci. 

Pathology. — The  pathological  anatomy  of  abscess  of  the  brain  is  precisely  the 
same  as  that  of  abscesses  in  other  organs.  The  size  varies  from  minute  foci 
hardly  as  large  as  a  lentil  to  extensive  cavities  occupying  nearly  the  whole  of 
one  lobe.  The  traumatic  and  otitic  brain  abscesses  are  usually  single,  but  meta- 
static abscesses  are  not  infrequently  found  in  considerable  numbers.  The  pus  is 
usually  greenish  yellow.  It  may  be  odorless  or  offensive.  Sometimes  remnants  of 
the  destroyed  ("  melted  ")  nervous  tissue  and  red  blood-globules  are  mixed  with 
it.  The  walls  of  the  abscess  often  bulge  out  irregularly.  The  cerebral  paren- 
chyma around  the  abscess  for  a  greater  or  less  distance  exhibits  white  softening. 
This  softening  is  due  partly  to  the  pressure  and  partly  to  the  spread  of  the  in- 
flammation. An  abundance  of  granular  cells  is  generally  to  be  found  in  the  tis- 
sues near  the  abscess. 

If  the  abscess  be  very  large  and  reach  nearly  to  the  surface  of  the  brain,  it  may 
sometimes  be  recognized  externally  by  a  distinct  bulging  and  perceptible  fluctua- 
tion. The  convolutions  on  the  surface  of  the  affected  hemisphere  are  almost  al- 
ways flattened.  If  the  abscess  extends  completely  to  the  surface  of  the  brain,  pii- 
rulent  meningitis  is  excited.  The  complication  of  cerebral  abscess  with  purulent 
phlebitis  and  sinus  thrombosis  has  also  been  quite  frequently  observed.  Abscesses 
which  are  centrally  situated  not  infrequently  burst  into  a  lateral  ventricle.     An 


1108  DISEASES    OF   THE   NERVOUS    SYSTEM 

abscess  of  long  standing  may  finally  become  encapsulated — that  is,  become  encased 
in  a  smooth,  firm  layer  of  connective  tissue,  which  prevents  further  extension  of 
the  process.  The  pus  inside  gradually  becomes  thick  and  cheesy.  Apparently, 
however,  it  is  very  seldom  entirely  absorbed,  and  a  new  acute  outbreak  of  inflam- 
mation, excited,  for  example,  by  an  injury,  is  always  among  the  possibilities. 

Clinical  History. — Small  abscesses,  and  even  large  ones,  may  for  a  long  time 
have  scarcely  any  symptoms.  This  is  particularly  true  of  apparently  idiopathic 
abscesses,  and  of  those  which  develop  very  slowly  and  insidiously  after  appar- 
ently insignificant  injuries  of  the  head  or  in  connection  with  chronic  inflamma- 
tion of  the  middle  ear,  etc.  There  is  sometimes  a  long  "  period  of  latency  "  or  a 
longer  period  of  indefinite  mild  precursory  symptoms  (occasional  headache,  ver- 
tigo, general  malaise,  a  slight  elevation  of  temperature,  etc.)  preceding  the  onset 
of  severe  cerebral  symptoms. 

In  abscesses  following  more  extensive  injuries,  the  symptoms  are  more  vio- 
lent from  the  start;  this  is  also  true  of  many  abscesses  which  develop  acutely 
and  enlarge  rapidly.  The  symptoms  can  hardly  be  distinguished  from  acute 
meningitis.  The  patient  is  dull,  or  grows  delirious;  he  has  violent  headache, 
vomiting,  symptoms  of  motor  irritation  (general  or  limited  convulsions),  and 
fever.  Sometimes  the  temperature  repeatedly  rises  to  a  high  point.  Definite 
focal  symptoms  (hemiplegia  or  monoplegia,  partial  cortical  epilepsy,  aphasic 
disturbances,  hemianopsia,  etc.)  may  manifest  themselves  according  to  the  spe- 
cial situation  of  the  abscess.  The  loss  of  consciousness  becoraes  more  and  more 
complete;  and  in  a  comparatively  brief  time  (one  or  two  weeks)  there  may  be 
profound  coma  and  death.  Rarely  the  violent  symptoms  abate,  and  the  acute 
passes  into  a  chronic  stage. 

The  symptoms  of  cerebral  abscess,  when  it  pursues  a  chronic  course,  may  be 
divided  into  (1)  the  general  symptoms  and  (2)  the  focal  symptoms,  resulting  from 
the  special  position  of  the  abscess.  There  is  no  other  localized  cerebral  disorder 
in  which  the  focal  symptoms  are  so  often  absent,  either  for  a  long  time  or  even 
throughout  the  illness.  This  is  partly  because  the  abscesses  are  often  situated  in 
parts  of  the  brain,  injury  to  which  does  not  occasion  any  demonstrable  focal 
symptoms.  Such  localities  are  the  white  matter  of  the  frontal  lobe,  the  hemi- 
spheres of  the  cerebellum,  etc.  A  second  reason  is  that  an  abscess  is  not  ver^'' 
apt  to  excite  indirect  focal  symptoms  by  its  influence  upon  the  parts  around  it. 

Among  the  general  symptoms,  the  most  important  is  a  persistent,  deeply  situ- 
ated, dull  headache.  Eor  a  long  time  it  may  be  the  only  symptom,  especially 
when  the  abscess  is  gradually  developed  after  an  injury  to  the  head  or  after  aural 
disease  of  long  standing.  The  pain  is  referred  mainly  to  the  seat  of  the  abscess ; 
but  the  exceptions  to  this  rule  are  not  infrequent.  The  skull  is  sometimes  espe- . 
cially  sensitive  to  percussion  in  the  vicinity  of  the  abscess;  but  we  should  not 
lay  too  much  stress  upon  this  symptom.  Another  frequent  symptom  besides 
headache  is  vertigo;  and  there  may  also  be  vomiting,  either  after  meals  or 
entirely  independently  of  food.  Another  valuable  symptom  in  diagnosis  is  the 
irregular  fever,  sometimes  slight,  and  sometimes  exhibiting  great  elevations  with 
intervals  between  them;  but  in  many  cases  also,  particularly  where  the  abscess 
is  encapsulated,  there  may  be  no  fever  whatever.  The  pulse  is  often  slow.  An 
important  diagnostic  point  is  that  choked  disk  and  optic  neuritis  may  occur  in 
abscess  of  the  brain,  but  they  develop  far  less  frequently  and  only  exceptionally 
do  they  reach  so  high  a  degree  as  in  tumors  of  the  brain  (q.  v.). 

The  general  health  may  be  but  slightly  disturbed.  Usually,  however,  there  is 
decided  indisposition.  The  patient  is  pale,  has  no  appetite,  loses  flesh,  and 
sometimes  shows  slight  mental  changes  (a  melancholy  condition,  temporary  con- 
fusion, etc.). 

As  to  the  focal  symptoms,  little  need  here  be  added  to  what  is  contained  in 


INFLAMMATION  OF  THE  BEAIN  1109 

Chapter  II  of  this  section.  Abscesses  involving  the  motor  region  of  the  cortex 
have  been  repeatedly  found  to  cause  limited  epileptiform  attacks  and  monoplegie 
paralysis.  It  is  particularly  characteristic  that,  as  the  abscess  grows,  one 
symptom  of  paralysis  is  added  to  another,  and  that  often  the  advance  of  the 
paralysis  is  ushered  in  by  epileptiform  convulsions.  Abscesses  in  the  occipital 
lobe  have  repeatedly  been  observed  to  cause  hemianopsia,  and  abscesses  in  the 
temporal  lobe  word  deafness ;  and  these  facts  have  been  used  in  making  a  diag- 
nosis of  the  location  of  abscesses.  Abscesses  in  the  cerebellum  may  remain  unsus- 
pected for  a  long  while;  but  in  other  cases  characteristic  cerebellar  symptoms 
(staggering  gait,  vertigo)  may  be  evident  as  well  as  severe  general  symptoms. 

The  duration  of  chronic  cerebral  abscess  varies  greatly.  In  most  cases  it  lasts 
for  months;  and  sometimes  it  has  certainly  lasted  for  years.  Particularly  when 
the  abscess  gives  rise  to  no  symptoms,  or  merely  to  slight  and  indefinite  ones 
referable  to  the  head,  it  may  last  a  very  long  time.  It  is  quite  often  the  case  that 
there  are  separate  attacks  of  the  severe  symptoms,  such  as  headache,  vomiting, 
and  fever,  and  that  in  the  intervals  of  variable  duration  between  these  paroxysms 
the  patient  feels  pretty  well. 

The  final  termination  of  cerebral  abscess,  unless  there  is  surgical  interven- 
tion, is  almost  always  fatal.  Recovery  is  not  impossible,  but  it  has  been  seen  with 
certainty  in  only  a  very  few  instances.  Death  either  comes  on  gradually,  when, 
as  the  abscess  grows  larger,  all  the  symptoms  become  correspondingly  aggra- 
vated; or  it  may  happen  quite  suddenly.  Sometimes  it  is  brought  about  by  the 
abscess  bursting  into  a  lateral  ventricle,  or  by  the  supervention  of  meningitis. 
Often  a  cerebral  abscess  terminates  in  a  sudden  and  unexpected  death,  where 
no  immediate  cause  for  the  event  can  be  found. 

Diagnosis. — Although  it  is  often  possible  to  make  a  correct  diagnosis  of  cere- 
bral abscess,  yet  there  is  usually  a  good  deal  of  difiiculty  in  arriving  at  such  a 
conclusion,  and  entire  certainty  is  seldom  attainable.  The.most  important  points 
in  diagnosis  are :  (1)  The  demonstration  of  some  caiise,  such  as  trauma,  chronic 
otitis,  fetid  pulmonary  diseases,  or  empyema.  (2)  The  presence  of  general  cere- 
bral symptoms,  such  as  headache,  vertigo,  and  vomiting;  and  the  fact  that  these 
are  sometimes  better  and  sometimes  worse.  To  aid  in  excluding  tumor,  we  have 
(3)  the  febrile  symptoms  frequently  caused  by  abscess,  but  rare  in  case  of  tumor; 
and  (4)  the  rarity  of  optic  neuritis,  which  is  very  frequently  occasioned  by 
tumors.  The  focal  symptoms,  if  there  be  any,  are  not  characteristic.  They 
grow  worse  by  fits  and  starts  in  tumor  just  as  in  abscess.  One  fact,  however,  is 
of  value,  namely,  that  while  tumors  (vide  infra)  frequently  cause  disturbances  in 
the  area  of  distribution  of  the  nerves  at  the  base  of  the  brain  (such  as  paralysis 
of  the  oculo-motor),  an  abscess  does  this  only  exceptionally.  It  is  often  quite 
impossible  to  make  a  diiferential  diagnosis  between  acute  abscess  and  purulent 
meningitis,  unless  focal  symptoms  are  developed,  which  indicate  the  existence  of 
an  abscess. 

The  timely  recognition  of  an  abscess  of  the  brain  following  purulent  otitis  is 
of  the  greatest  practical  importance.  It  is  important  to  know  that  cerebral 
symptoms  (headache,  vomiting,  vertigo,  stupor,  etc.)  may  also  occur  from  reten- 
tion of  pus  in  the  middle  ear,  and  that  they  may  disappear  completely  after 
evacuation  of  the  pus  by  paracentesis  of  the  membrana  tympani.  If  Ave  find  no 
retention  of  pus  in  the  ear,  however,  we  must  suspect  an  abscess  of  the  brain, 
if  any  persistent  cerebral  symptoms  arise.  Since  such  abscesses  of  the  brain  are 
most  frequently  situated,  as  we  have  said,  in  the  temporal  lobe  or  in  the  cere- 
bellum, we  should  pay  special  attention  to  the  localizing  symptoms  of  these  por- 
tions of  the  brain.  Abscesses  in  the  left  temporal  lobe  may  be  diagnosticated  with 
the  greatest  relative  certainty  by  the  discovery  of  aphasic  disturbances,  word 
deafness,  verbal   amnesia,   optic   aphasia,   etc.    (Oppenheim).     Deep-seated   ab- 


1110  DISEASES    OF   THE   NEKVOUS    SYSTEM 

scesses  may  also  cause  liemiparesis,  hemianopsia,  ataxia,  and,  by  pressure  on  the 
base  of  the  brain,  paresis  of  the  oculo-motor  or  abducens.  Otitic  abscesses  of  the 
cerebellum  cause  occipital  pain,  slight  stiffness  of  the  neck,  vertigo,  and  an  un- 
certain gait ;  but  not  infrequently  definite  cerebellar  symptoms  are  absent.  The 
general  cerebral  symptoms  (headache,  vomiting,  disturbances  of  the  sensorium, 
etc.)  are  the  same  in  otitic  abscesses  of  the  brain  as  in  other  varieties  of  abscess. 
We  may  also  consider  the  local  tenderness  of  the  skull  on  percussion,  usually 
above  the  upper  border  of  the  ear.  In  other  cases,  however,  the  diagnosis  of  otitic 
abscess  of  the  brain  is  very  difficult,  especially  if  we  can  find  no  pronounced  focal 
symptoms.  We  often  can  not  avoid  confounding  it  with  extra-dural  abscess, 
purulent  meningitis,  sinus  thrombosis,  etc.  The  presence  of  meningitis  can 
sometimes  be  established  by  lumbar  puncture. 

Treatment.- — The  only  possible  way  in  which  to  cure  an  abscess  is  by  opera- 
tion; the  skull  is  trephined  and  the  abscess  laid  open.  The  earlier  and  the  more 
accurately  the  diagnosis  of  abscess  can  be  made,  the  more  favorable  is  the  out- 
look for  the  patient.  With  the  present  antiseptic  modes  of  procedure,  the  dangers 
of  an  oj)eration  are  slight,  and  the  series  of  successful  results  that  have  already 
been  obtained  urgently  demand  further  surgical  intervention.  Many  a  life  can 
be  saved  by  timely  surgical  interference,  especially  in  abscesses  of  the  brain 
following  chronic  ear  disease.  For  particulars  we  must  refer  to  special  works 
on  surgery. 

If  operation  be  not  justifiable,  nothing  but  purely  symptomatic  treatment  is 
left  us.  Ice  to  the  head,  narcotics,  potassic  bromide,  electricity,  and  sometimes 
also  the  local  abstraction  of  blood,  are  the  main  remedies  beyond  general  hygienic 
measures. 

2.  Acute  and  Chronic  Non-suppnrative  Encephalitis 

While  the  spinal  cord  is  quite  frequently  affected  by  idiopathic  circumscribed 
inflammation  (transverse  myelitis),  analogous  cerebral  disease  is  much  more 
exceptional.  The  scanty  information  which  we  possess  upon  the  subject  is  as 
follows : 

1.  Idiopathic  (Inflammatory)  Softening-  of  the  Brain. — In  rare  instances 
there  are  found  in  the  brain  quite  extensive  foci  of  softening,  the  pathological 
anatomy  of  which  is  almost  identical  with  that  of  embolic  softening,  and  yet  the 
afferent  blood-vessels  do  not  furnish  any  explanation  of  the  cotidition.  They  have 
accordingly  been  termed  "  foci  of  inflammatory  softening."  The  mode  of  their 
production  is  unknown.  The  symptoms  resemble  closely  those  of  softening  from 
thrombosis. 

2.  Curable  Form  of  Encephalitis. — In  certain  cases  pronounced  symptoms  of 
focal  disease  exist  for  a  time,  and  suggest  a  tumor  or  the  like;  but  after  some 
months,  or  even  a  still  longer  time,  the  symptoms  gradually  abate,  and  finally 
there  is  complete  recovery.  Such  cases  are  usually  explained  by  assuming  that 
there  has  been  a  localized  eneephalitic  process,  capable  of  a  restoration  to  the 
normal  state.  The  nature  of  the  symptoms,  as  we  have  observed  them,  would 
seem  to  imply  that  the  lesion  is  generally  in  the  neighborhood  of  the  cortex, 
for  there  is  usually  paresis  of  some  part  of  the  body,  often  associated  with 
certain  symptoms  of  irritation  and  impairment  of  speech.  Possibly  the  recovery 
of  these  cases  may  be  assisted  by  electricity  and  potassic  iodide.  It  is  always 
hazardous,  however,  to  class  such  affections  as  "  encephalitis,"  since  we  can 
hardly  ever  exclude  absolutely  other  affections   (especially  syphilis). 

3.  Diffuse  Cerebral  Sclerosis. — Diffuse  sclerosis  of  the  brain  is  a  peculiar  dis- 
ease, which  is  usually  classed  as  a  chronic  inflammation.  The  whole  brain  may 
be  involved,  or  the  disease  may  be  conflned  chiefly  to  a  large  part  of  one  hemi- 
sphere.    There  is  a  very  marked  increase  in  the  consistency  of  the  brain-sub- 


INFLAMMATION   OF   THE   BRAIN 


1111 


stance,  so  that  it  cuts  like  a  tough  piece  of  leather.  The  microscope  reveals  in 
many  cases,  but  not  in  all,  diffuse  hyperplasia  of  the  neuroglia.  In  a  case  which 
we  recently  examined  there  was  a  decided  atrophy  of  the  nervous  fibers  lying  in 
the  white  substance  of  the  brain. — The  disease  is  rare,  and  its  characteristic 
symptoms  can  not  yet  be  stated  absolutely.  They  are  developed  slowly.  The 
most  constant  among  them  seem  to  be  hemiplegia  or  paraplegia  without  much 
change  in  sensation;  symptoms  of  motor  irritation,  such  as  epileptiform  convul- 
sions (sometimes  general  and  sometimes  uni- 
lateral), tremor,  or  single  twitchings,  which 
may  be  rhythmical  or  like  those  of  chorea; 
and,  lastly,  dementia.  When  both  hemispheres 
are  involved,  there  are  usually  marked  spastic 
symptoms  in  the  lower  limbs. 

The  disease  has  been  observed  especially  in 
children  and  also  in  elderly  people.  Alcohol- 
ism and  hereditary  syphilis  seem  to  be  among 
the  causes,  but  nothing  definite  is  known 
upon  this  point.  Transitional  forms  between 
diffuse  sclerosis  and  pseudo-sclerosis  apparent- 
ly occur  (vide  page  959).  Treatment  can  be 
only  symptomatic. 

4.  The  Acute  Encephalitis  of  Children. 
Cerebral  Paralysis  of  Children.  (Spastic 
Infantile  Hemiplegia  of  Benedict.) — Chil- 
dren not  infrequently  suffer  from  a  definite 
form  of  hemiplegia,  which  deserves  a  brief 
special  description. 

The  patient  is  usually  between  one  and 
four  years  of  age.  The  symptoms  almost  al- 
ways begin  acutely.  Having  been  previously 
healthy,  the  child  is  suddenly  attacked  with 
malaise  and  fever.  Very  often  there  is  nausea 
and  vomiting,  speedily  or  at  once  followed 
by  grave  cerebral  symptoms.  There  is  stupor, 
and  convulsions  are  particularly  frequent. 
This  condition  may  last  but  one  or  two  days; 
or  it  may  continue,  perhaps  with  unabated 
severity,  for  two  or  three  weeks.  Then  the 
acute  symptoms  abate,  and  the  child  recovers 
comparatively  fast ;  but  it  is  noticed  by  the 
parents  to  be  paralyzed;  and  this  paralysis 
seldom  entirely  disappears,   although  it  may 

diminish.     Sometimes  the  paralysis  follows  the  convulsions,  without  any  other 
definite  encephalitic  symptoms. 

If  such  children  come  under  observation  after  the  paralysis  has  lasted  some 
time,  as  is  usually  the  case,  their  condition  is  generally  as  follows :  The  cranial 
nerves,  as  a  rule,  are  but  little  affected.  The  main  change  is  in  the  extremities  of 
one  side;  and  the  arm  is  almost  always  worse  than  the  leg.  The  affected  parts 
betray  an  arrest  of  development,  more  or  less  impairment  of  motion,  in  many 
eases  a  marked  exaggeration  of  the  tendon  reflexes,  and  almost  invariably  con- 
tractures of  more  or  less  severity  (compare  Fig.  176).  The  muscles,  although 
generally  somewhat  atrophied,  never  exhibit  the  reaction  of  degeneration.  Sen- 
sation, as  a  rule,  is  unimpaired;  but  on  careful  examination  we  sometimes  find 
in  the  paralyzed  arm  a  slight  diminution  of  the  sensibility  to  touch,  and  especially 


infantile    paralysis. 
(Personal  observa- 


1112  DISEASES    OF   THE   NEEVOUS    SYSTEM 

a  loss  of  the  ability  to  recognize  objects  by  the  aid  of  the  sense  of  feeling  whert 
the  eyes  are  closed  (see  page  795).  Permanent  hemianopsia  may  also  be  asso- 
ciated with  the  heraiplegia.  Symptoms  of  motor  irritation  are  found  upon  the- 
affected  side  with  striking  frequency;  the  commonest  are  athetoid  movements 
(hemiathetosis,  hemichorea)  ;  and  associated  movements  are  also  not  infrequent^ 
The  constant  movements  of  the  fingers  resulting  from  the  athetosis  sometimes 
render  the  articulations  so  lax  that  it  is  possible  to  make  the  fingers  assume  an 
angle  of  ninety  degrees  or  even  less  with  the  back  of  the  hand,  at  the  metacarpo- 
phalangeal joint.  The  child  may  keep  making  motions  with  its  paretic  arm  while 
walking.  It  is  not  very  rare  for  epilepsy  to  develop  later.  There  are  con- 
vulsive attacks,  which  usually  begin  on  the  paralyzed  side,  but  which  may  later 
affect  the  whole  body.  With  right  hemiplegia  we  sometimes  see  co-existing  dis- 
turbances and  a  defective  development  of  speech.  The  intellectual  development 
of  many  such  children  is  tolerably  normal.  Others,  however,  are  more  or  less 
demented,  or  betray  defective  moral  sense. 

The  whole  course  of  the  disease  suggests  very  strongly  an  acute  encephalitis. 
The  process  is  probably  in  most  cases  limited  more  or  less  completely  to  the- 
motor  region  of  the  cortex,  and  hence  it  has  been  called  "  polio-encephalitis."  *  It 
reminds  one  forcibly  of  the  acute  poliomyelitis  of  children,  with  a  difference 
merely  in  the  localization  of  the  disturbance.  It  is  not  impossible  that  the  two 
diseases  have  a  very  similar,  if  not  identical,  aetiology.  They  can  hardly  be  differ- 
entiated in  their  initial  stage ;  but  when  further  developed  they  can  not  be  con- 
founded, becaiise  the  cerebral  disease  causes  unilateral  paralysis,  leaves  the  elec- 
trical reactions  unimpaired,  and  frequently  causes  exaggeration  of  the  tendon 
reflex.  It  deserves  mention  that  precisely  similar  phenomena  may  be  presented 
by  children  during  recovery  from  measles,  scarlet  fever,  pneumonia,  and  other 
acute  infectious  diseases. 

The  pathological  conditions  of  the  early  stage  have  not  yet  been  studied.. 
Long  after  the  process  has  run  its  course,  the  affected  portion  of  the  cerebrum- 
presents  marked  atrophy  with  cicatricial  contraction.  If  the  cortex  has  been 
affected  we  find  a  cicatricial  depression,  a  loss  of  substance,  a  so-called  poren- 
cephaly. At  these  places  the  pia  is  thickened.  Sometimes  limited  cystic  forma- 
tions are  found.  The  pyramidal  tract  exhibits  a  secondary  descending  degen- 
eration. It  is  thus  evident  that  the  process  is,  from  an  anatomical  point  of  view, 
precisely  like  the  atrophy  of  the  anterior  cornua  occasioned  by  poliomyelitis. 

Of  course  not  all  the  hemiplegias  arising  in  childhood  are  due  to  an  encepha- 
litis, for  in  not  a  few  eases  infantile  hemiplegia  may  be  due  to  embolic  softening, 
and  perhaps  sometimes  to  haemorrhage.  In  some  cases  it  is  often  hard  to  decide- 
whether  we  should  regard  a  cerebral  infantile  paralysis  as  the  result  of  a  pre- 
vious encephalitis  or  of  some  other  form  of  cerebral  disease;  but  it  seems  to  us 
highly  probable  that  a  large  part  at  least  of  the  very  peculiar  infantile  hemi- 
plegias must  have  their  special  cause,  which  we  have  assumed  to  be  encephalitis. 
The  chief  thing  to  be  considered  in  the  diagnosis  is  the  peculiar  onset  of  the 
disease  with  fever,  convulsions,  etc.,  in  a  child  who  was  previously  perfectly 
healthy.  This  distinguishes  encephalitic  paralysis  from  hemiplegia  existing 
since  birth  (congenital  defect,  injury  at  birth).  [There  is  really  little  patho- 
logical evidence  of  acute  polioencephalitis  in  children.  Sachs  and  Osier,  from 
the  study  of  a  large  number  of  cases,  find  that  the  cause  of  the  paralysis  is  almost 
always  haemorrhage  or  embolic  softening. — K.] 

The  treatment  at  first  is  to  be  governed  by  the  same  rules  as  in  the  initial 
period  of  acute  poliomyelitis   (q.v.).     The  hemiplegie  symptoms  which  persist 

[*  This  name,  lio-wever,  has  been  previously  applied  by  Wernicke  to  that  form  of  external  ophthal- 
moplegia due  to  changes  in  the  nerve  nuclei  in  the  pons  (vide  page  1045). — K.] 


INSOLATION  1113 

after  the  first  few  months  will  never  improve  much.  The  most  we  can  do  will  be 
by  means  of  electricity,  massage,  and  cold  baths  with  friction  ("cold  rubbing"). 
For  the  epileptic  attacks  large  doses  of  bromide  of  potassium  are  decidedly  bene- 
ficial.    This  may  be  combined  with  chloral,  belladonna,  etc. 

5.  Acute  Haemorrhagic  Encephalitis  in  Adults. — Cases  of  acute  haemor- 
rhagic  encephalitis  certainly  occur  in  adults.  They  have  been  observed  either 
as  a  sequel  of  other  acute  diseases  (especially  influenza)  or  as  a  primary  acute 
disease.  In  such  cases  very  severe  cerebral  symptoms  (headache,  loss  of  ^con- 
sciousness, hemiplegia)  come  on  quite  suddenly  and  lead  to  a  speedy  death  with 
high  fever.  The  autopsy  shows  several  hgemorrhagic-encephalitic  foci,  usually 
confined  to  one  hemisphere.  The  brain  substance  is  yellow  and  softened,  very 
oedematous,  and  studded  with  numberless  little  capillary  haemorrhages.  Milder 
curable  cases  of  acute  encephalitis  also  seem  to  occur  in  adults. 


CHAPTEE   VI 
INSOLATION.      SUNSTROKE.     HEAT    PROSTRATION.      THERMIC    FEVER 

[.ffitiology  and  Pathology. — Under  exposure  to  undue  heat,  either  in  the 
direct  rays  of  the  sun,  or,  during  hot  weather,  in  engine-rooms,  laundries,  and 
the  like,  marked  effects  may  be  produced  on  the  human  organism,  manifesting 
themselves  in  a  widely  different  manner  in  different  cases.  The  liability  to  these 
effects  is  much  greater  with  us  than  in  most  portions  of  Europe  or  in  Great  Bri- 
tain, and  is  enhanced  by  a  moist  atmosphere  which  tends  to  prevent  evaporation 
from  the  surface  of  the  body.  Attacks  may  come  on  at  night  and  under  cover  as 
well  as  by  day.  While  excessive  heat  is  the  sole  and  sufiicient  exciting  cause  of 
the  changes  and  symptoms  to  be  described,  exhaustion  due  to  muscular  exertion 
or  other  cause  plays  a  very  important  secondary  role.  A  vigorous  person,  how- 
ever, of  regular  and  temperate  habits,  can  stand  much  greater  heat  and  exertion 
than  an  individual  who  is  debilitated  or  addicted  to  the  use  of  stimulants.  The 
frequency  of  attacks  after  a  full  meal  has  been  noted.  Those  newly  arrived  in 
the  country  are,  other  things  being  equal,  more  likely  to  succumb  than  natives  or 
those  who  have  become  accustomed  to  the  climate.  That  high  temperature  due 
to  solar  or  artificial  heat,  or  a  combination  of  the  two,  is  the  prime  causative  con- 
dition, has  been  clearly  shown  by  experiments  on  animals.  There  is  practically 
nothing  to  add  to  the  researches  of  H.  C.  Wood. 

Pathological  Anatomy. — In  cases  of  sudden  death  from  shock  there  are  no 
constant  and  peculiar  lesions.  The  blood  is  dark,  imperfectly  coagulated,  and 
collected  in  the  veins ;  ecchymoses  are  frequently  found. 

After  death,  due  chiefly  to  abnormally  high  temperature — that  is  to  say,  in 
cases  of  thermic  fever — the  heart,  and  especially  the  left  ventricle,  is  firmly  con- 
tracted from  post-mortem  coagulation  of  its  myosine ;  the  lungs  are  apt  to  be 
much  engorged  with  dark  fluid  blood,  and  they  may  be  the  seat  of  haemorrhage ;  ex- 
travasation of  blood  under  the  skin  is  more  or  less  marked,  and  haemorrhage  into 
and  about  the  cervical  sympathetic  ganglia  has  also  been  observed.  The  mem- 
branes of  the  brain  and  cord  are  often  greatly  congested,  and  there  may  be  evi- 
dences of  beginning  meningitis.  The  blood-corpuscles  are  crenated  and  show 
a  diminished  tendency  to  the  formation  of  rouleaux.  Rigor  mortis  is  marked 
and  early  in  the  voluntary  muscles  as  well  as  in  the  heart,  and  is  attributable  to 
the  same  cause.  Parenchymatous  degeneration  of  the  organs  is  sometimes 
found. 


1114  DISEASES    OF    THE   NERVOUS    SYSTEM 

Symptoms  and  Course. — The  onset  of  the  attack  is  usually  sudden,  though 
there  may  be  slight  premonitions,  such  as  dizziness,  pain,  or  uncomfortable  sensa- 
tions in  the  head. 

It  will,  perhaps,  add  to  clearness  to  distinguish  three  leading  forms  of  attack, 
it  being  understood  that  nature  does  not  always  classify  cases  as  sharply  as  is 
done  here.  The  first  of  these  comprises  cases  of  heat  prostration,  denoted  by 
faintness,  syncope,  nausea,  and  sometimes  vomiting,  with  marked  muscular  and 
general  weakness.  The  surface  of  the  body  is  cool,  the  pulse  rapid  and  feeble. 
The  great  majority  of  these  cases  are  mild,  and  the  symptoms  pass  away  more  or 
less  quickly  on  placing  the  patient  in  the  recumbent  posture  in  a  relatively  cool 
and  quiet  place  with  free  ventilation.  After  a  few_  hours  the  patient  can  be  re- 
moved to  his  home,  and  in  a  day  or  two  he  has  recovered  perfectly,  except  for  some 
sensitiveness  to  heat  or  the  sun's  rays.  There  may  be  transient  insensibility,  or, 
on  the  other  hand,  the  case  may  terminate  fatally  very  soon  from  general  exhaus- 
tion and  cardiac  failure. 

The  second  form  includes  cases  with  respiratory  as  well  as  circulatory  failure, 
due  especially  to  the  exhaustion  of  the  nerve  centers  presiding  over  these  func- 
tions. Under  this  head  comes  cases  of  true  sunstroke — patients  suddenly  losing 
consciousness  while  exposed  to  the  sun.  The  skin  is  cold  and  the  pulse  is  feeble ; 
death  may  quickly  ensue  or  recovery  may  follow,  especially  if  prompt  and  suit- 
able treatment  be  instituted.  The  after-effects  of  the  attack  may  be  very  slow  to 
pass  away,  and  may  never  disappear  entirely. 

The  most  striking  characteristic  of  the  third  form  is  the  great  increase  in  the 
temperature — a  symptom  which  has  given  rise  to  the  term  thermic  fever.  In  this 
form  premonitions  are  more  conmion  than  in  the  others.  The  thermometer  may 
register  110°  or  even  more;  the  skin  is  burning  hot  and  generally  dry;  the  pulse 
is  slow  and  full,  or  quick  and  jerking;  the  respiration  is  quickened,  sighing,  or 
even  stertorous;  the  pupils  at  first  are  usually  contracted;  there  may  be  great 
restlessness;  coma  and  convulsions  sometimes  occur;  vomiting  is  common;  and, 
toward  the  close  of  life,  the  sphincters  are  sometimes  relaxed.  A  fatal  result  is 
due  to  apnoea  and  asthenia  combined.  What  was  said  with  regard  to  recovery 
from  the  second  form  holds  good  also  for  the  third. 

Diagnosis. — This  is  seldom  difiicult.  The  circumstances  under  which  the 
attack  comes  on  are  generally  patent;  and  the  hyperpyrexia,  if  present,  is  dis- 
tinctive. Acute  alcoholism  and  meningitis  are  the  chief  affections  which  might 
lead  to  error. 

Prognosis. — The  mortality  rate  of  the  severer  forms  of  the  disease  is  very 
high,  but  the  prognosis  depends  much  on  the  possibilities  of  securing  prompt  and 
skillful  treatment.  Under  this  many  a  case  recovers  from  a  seemingly  desperate 
condition.  The  tediousness  and  imperfection  of  recovery  have  been  already 
alluded  to.  For  long  periods  in  some  cases  the  mental  and  physical  powers  are 
much  impaired,  and  great  care  has  to  be  exercised  as  regards  exertion,  high  tem- 
perature, and  the  sun's  rays.    Insanity  is  sometimes  a  sequel. 

Treatment. — In  the  first  place,  much  may  be  done  by  preventive  measures  to 
obvipte  the  necessity  for  any  treatment.  A  regular  and  temperate  life  will  do 
much;  and  special  precautions  of  an  obvious  nature  should  be  taken  during  hot 
weatber  by  those  whose  occupations  involve  a  liability  to  exhaustion  and  exposure 
to  unusxial  bent.  It  would  be  well  if  it  were  generally  known  that  there  is  com- 
paratively little  danger  of  sunstroke  so  long  as  perspiration  is  free.  Many  an 
attack  might  be  averted  by  noting  the  activity  of  the  skin  and  seeking  rest  and 
shelter  as  sweating  diminishes.  A  considerable  responsibility  rests  upon  militia 
surgeons  and  others  in  similar  positions  during  hot  weather. 

Mild  cases  of  heat  prostration  seldom  require  other  measures  than  those 
already  indicated  in  describing  the  symptoms.    If  there  be  nausea,  and  it  seem  de- 


TUMORS  OF  THE  BRAIN  1115 

sirable  to  give  stimulants,  they  are  better  given  under  the  skin  or  by  the  rectum. 
The  clothing  should  be  loosened;  the  cold  douche  and  other  refrigerating  meas- 
ures are  not  indicated  unless  there  is  fever,  and  they  should  then  be  used  with 
caution. 

For  true  sunstroke,  treatment  should  be  active  and  energetic,  the  indications 
being  to  reduce  the  temperature  of  the  overheated  centers  and  to  stimulate  their 
activity.  If  a  cool  or  shady  spot  be  near  at  hand,  the  patient  should  be  removed  to 
it  and  largely  stripped  of  clothing;  if  not,  no  time  should  be  lost  before  resort- 
ing to  the  cold  douche  on  the  head  and  body  while  stimulants  are  administered 
by  enema  or  subcutaneously.  External  stimulation  by  mustard  or  flagellation, 
and  purgative  enemata,  are  said  to  be  sometimes  useful.  The  use  of  cold  exter- 
nally should  not  be  prolonged  in  these  cases  unless  there  is  fever.  Nervous  ex- 
haustion is  the  prominent  symptom,  and  all  depressing  measures  are  out  of 
place. 

The  case  is  widely  different  with  the  third  form  of  the  attack.  Here  the  imme- 
diate danger  is  from  the  hyperpyrexia,  which  must  be  combated  by  rubbing  the 
patient  with  ice,  placing  him  in  a  tub  of  water  with  lumps  of  ice,  or  similar  meas- 
ures, until  the  temperature  in  the  rectum  is  reduced  nearly  but  not  quite  to  the 
norraal  point.  In  the  application  of  the  refrigerating  measures  the  head  must  not 
be  neglected.  The  sole  indication  at  first  is  the  reduction  of  the  temperature. 
Antipyrine  subcutaneously  has  been  given  in  a  few  cases  in  the  Boston  City  Hos- 
pital, and  also  in  Brooklj^n,  with  good  results.  After  a  reduction  of  the  tempera- 
ture, any  symptoms  of  collapse  or  exhaustion  demand  stimulants. 

With  regard  to  the  employment  of  bloodletting  there  is  considerable  differ- 
ence of  opinion.  That  cases  occur  in  which  this  procedure  is  indicated  is  un- 
doubtedly true,  but  they  are  exceptional;  they  are  characterized  by  the  evi- 
dences of  great  cerebral  congestion  without  hyperpyrexia. 

The  subseqvient  management  of  convalescents  from  any  form  of  sunstroke  is 
often  very  important.  Prolonged  rest,  and  sometimes  change  of  climate,  may  be 
demanded.  A  symptomatic  and  common-sense  treatment  is  in  place.  It  has 
seemed  to  the  editor  that  quinine,  especially  in  solution  with  a  moderate  excess  of 
sulphuric  acid,  is  distinctly  useful  in  those  suffering  from  mild  or  moderate  after- 
effects of  undue  heat.] 


CHAPTER   VII 
TUMORS    OF    THE    BRAIN 

Mtiology. — The  precise  causes  which  lead  to  the  development  of  tumors  in  the 
brain  are  no  more  definitely  laiown  than  in  regard  to  other  organs.  The  new 
growths  are  usually  formed  insidiously  and  gradually  without  ascertainable  cause 
in  persons  previously  healthy.  We  are  therefore  disposed  at  the  present 
time  to  assume  that  there  is  some  abnormal  embryonic  predisposition  of  the  tis- 
sues which  acts  as  the  special  cause  of  the  subsequent  new  growth.  A  circum- 
stance which  deserves  mention  is  that  sometimes  the  first  symptoms  come  on 
immediately  or  a  short  time  after  some  injury  to  the  head.  Especially  in  cases 
of  sarcoma  arising  from  the  periosteum,  the  meninges,  etc.,  is  a  traumatic  ori- 
gin (that  is,  the  "  setting  free  "  of  a  predisposition  to  tumor  by  the  injury)  very 
probable,  although,  of  course,  hardly  ever  quite  certain.  Glioma  is  also  re- 
ferred at  times  to  a  traumatic  cause. 

Most  cerebral  tumors  are  found  in  persons  in  youth  or  middle  life.  Certain 
forms  of  tumor,  however,  particularly  solitary  tubercles,  are  comparatively  fre- 


1116  DISEASES    OF   THE   l^TEEVOUS    SYSTEM 

quent  in  children.    Sex  seems  to  exert  a  decided  influence  :  men  are  much,  oftener 
affected  than  women. 

Varieties  of  Cerebral  Tumor.* — The  most  important  forms  of  tumor  seen  in 
the  brain  are  as  follows : 

1.  Glioma. — Glioma  is  a  kind  of  tumor  peculiar  to  the  central  nervous  system, 
but  seen  much  oftener  in  the  brain  than  in  the  spinal  cord  {vide  page  1024). 
Apparently  the  new  growth  always  originates  in  the  neuroglia,  which  is  the  con- 
nective-tissue framework  of  the  true  nervous  matter.  As  seen  under  the  micro- 
scope, a  glioma  is  made  up  of  fibers  and  cells,  the  latter  being  like  the  normal 
cells  of  the  neuroglia,  while  the  fibers  seem  to  consist  mainly  of  the  numerous 
cell-processes.  Whether  the  ganglion-cells  also  take  an  active  part  in  the  new 
growth  has  not  yet  been  proved.  It  is  characteristic  of  gliomata  that  they  are 
seldom  sharply  defined,  but  shade  off  gradually  into  the  healthy  tissue.  The 
affected  portion  of  the  brain  is  usually  enlarged,  but  yet  maintains  pretty  nearly 
its  original  shape.  On  cross-section,  the  parts  that  have  undergone  "  gliomatous 
degeneration  "  present  a  yellowish  or  reddish-gray  surface.  It  is  usually  rather 
soft,  and  almost  always  is  very  vascular.  This  great  vascularity  is  not  without 
clinical  importance,  for  variations  in  the  fullness  of  the  blood-vessels,  and,  above 
all,  sudden  haemorrhages  into  the  interior  of  the  new  growth,  which  not  infre- 
quently occur,  may  produce  marked  symptoms. 

Gliomata  are  most  frequent  in  the  white  substance  of  the  cerebral  hemi- 
spheres, but  they  are  also  found  in  the  central  ganglia,  cerebellum,  and  else- 
where.    They  are  usually  single,  seldom  multiple. 

2.  Sarcoma. — It  is  very  seldom  that  any  form  of  sarcoma  originates  in  the 
brain-substance.  It  usually  begins  in  the  connective  tissue  of  neighboring  parts, 
in  the  dura  mater,  the  periosteum  of  the  cranium,  or  the  cranium  itself  (osteo- 
sarcoma). The  sarcoma  is  found  most  frequently  at  the  base  of  the  skull,  in  the 
form  of  a  circumscribed  tumor  of  varying  consistency,  and  by  pressing  upon 
neighboring  parts,  or  by  involving  them  in  the  diseased  process,  it  may  cause 
the  gravest  disturbances.  Histologically,  we  have  here  such  varieties  as  round- 
celled  or  spindle-celled  sarcoma,  fibro-sarcoma,  etc. 

3.  Gumma  and  Solitary  Tubercle. — Both  gumma  and  solitary  tubercle  are 
very  prone  to  attack  the  brain.  We  shall  revert  to  gumma  in  the  chapter  on 
cerebral  syphilis.  Solitary  tubercles  may  grow  to  the  size  of  a  cherry  or  larger. 
They  may  be  single  or  multiple,  and  may  occupy  any  part  of  the  brain.  They 
are  found  most  freqiiently  in  the  cortex,  and  in  the  cerebellum  and  pons. 

Solitary  tubercles  and  gummata,  upon  cross-section,  have  a  yellowish,  cheesy 
appearance,  and  are  usually  distinctly  defined.  Histologically,  they  are  composed 
of  granulation  tissue.  It  was  formerly  no  easy  matter  to  distinguish  gumma 
from  tubercle  in  all  cases;  but  now  certainty  is  attainable  by  determining  the 
presence  of  tubercle  bacilli  in  the  latter. 

4.  Carcinoma. — Carcinoma  completes  the  list  of  such  cerebral  tumors  as  have 
much  clinical  importance.  It  is  almost  always  secondary  in  the  brain.  It  has 
been  our  experience  that  secondary  cancer  of  the  brain  is  associated  principally 
with  primary  cancer  of  the  breast,  or  of  the  lungs  and  pleura ;  which  fact  bears  a 
remarkable  analogy  to  the  occurrence  of  secondary  cerebral  abscess  after  primary 
empyema,  pulmonary  gangrene,  etc. 

5.  Among  the  rarer  varieties  of  tumor  is  psammoma,  which  usually  starts 
from  the  meninges,  is  hard,  generally  comparatively  small,  and  therefore  often 
harmless,   and  contains  calcareous  matter,  so  that   it   grates  under  the   knife. 

*  From  a  clinical  standpoint,  the  term  "  cerebral  tumor"  usually  is  meant  to  include  also  such 
tumors  as  originate  in  the  neighborliood  of  the  brain  (as  in  the  base  of  the  skull),  if  they  finally 
involve  the  brain  itself. 


TUMOES  OF  THE  BEAK^  1117 

The  calcareous  deposits  are  found  in  the  form  of  roundish  objects,  which  are 
composed  of  flat  cells  which  lie  ov^r  one  another  like  the  coats  of  an  onion. 
Psammoma  is  probably  of  endothelial  origin.  Cholesteatoma,  which  has  a  sheen 
like  mother-of-peai"l,  has  also  been  observed  in  rare  instances,  and  also  angio- 
sarcoma, angioma,  etc.  The  not  very  rare  growths  arising  from  the  hypophysis 
cerebri  ("  struma  of  the  pituitary  giaud ")  remind  us  of  adenomata  in  their 
structure. 

6.  In  addition  to  the  true  tumors  we  may  mention  the  cysts  of  the  brain. 
They  develop  in  very  rare  cases  without  known  cause  (perhaps  as  a  sequel  to 
cranial  injuries?),  they  may  grow  to  the  size  of  an  apple,  and  may  cause  pre- 
cisely the  same  clinical  symptoms  as  a  tumor  of  the  brain. 

The  General  Symptoms  of  Cerebral  Tumors. — As  is  the  case  with  all  focal 
diseases  of  the  brain,  some  of  the  symptoms  of  cerebral  tumors  are  connected  with 
the  special  localization  of  the  new  growth.  There  are  definite  focal  symptoms, 
varying  with  the  part  destroyed,  or  at  any  rate  functionally  impaired,  and  it  is 
from  these  symptoms  alone  that  we  are  enabled  to  determine  the  position  of  the 
tumor.  But,  in  addition  to  these  focal  symptoms,  there  are  certain  general  symp- 
toms common  to  almost  all  cerebral  tumors  of  any  size.  They  are  in  large  part 
referable  to  the  general  compression  of  the  brain  due  to  the  enlargement  of  the 
new  growth.  In  the  first  place,  numerous  clinical  facts  indicate  that  whenever 
there  is  a  tumor  of  any  great  size,  a  large  part  of  the  entire  encephalon  is  sub- 
jected to  pressure;  and,  secondly,  the  anatomical  appearances  of  almost  every 
brain  affected  by  a  large-sized  tumor  lead  to  the  same  conclusion.  The  convolu- 
tions are  flattened  and  obliterated,  the  dura  mater  is  crowded  against  the  crani- 
um, and  perhaps  thinned  or  even  perforated  because  of  the  persistent  pressure,  or, 
on  the  other  hand,  thickened  as  a  result  of  chronic  inflammation.  ISTow  and 
then  the  effects  of  pressure  are  visible  even  in  the  bones  of  the  skull :  they  are 
worn  thin,  or  even  perforated,  or  their  sutures  are  loosened.  Another  result  of 
the  general  intracranial  tension,  through  its  effect  upon  the  venous  trunks  of 
the  brain,  is  serous  effusion  into  the  ventricles  (internal  hydrocephalus),  which 
occurs  very  frequently.  The  largest  effusions  are  caused  by  tumors  in  the  pos- 
terior cerebral  fossa,  which  directly  compress  the  vense  Galeni. 

The  symptoms  of  cerebral  tumors,  referable  to  the  effects  of  general  compres- 
sion, are  as  follows : 

1.  Headache  is  one  of  the  earliest  and  most  constant  symptoms.  It  is  usually 
persistent,  although  subject  to  temporary  exacerbations  and  intermissions.  The 
patient  describes  it  as  dull,  deeply  seated,  and  stupefying.  Although  it  affects  the 
whole  head,  it  is  sometimes  (not  invariably)  referred  mainly  to  the  neighborhood 
of  the  tumor.  It  is  particularly  true  of  persistent  occipital  headache  that  it  indi- 
cates a  new  growth  in  the  posterior  fossa.  Sometimes  also  it  is  possible,  by  tap- 
ping upon  the  skull,  to  find  an  especially  tender  region.  Considerable  caution, 
however,  should  be  used  in  drawing  diagnostic  conclusions  from  such  observa- 
tions. The  headache  usually  lasts  to  the  close  of  the  disease,  and,  even  after  the 
patient  has  become  completely  comatose,  the  persistence  of  the  pain  is  still  evi- 
dent from  his  low  groans  and  the  way  in  which  his  hand  seeks  his  head. 

2.  Next  in  frequency  to  headache  are  disttirhances  of  the  sensorium  and  intel- 
ligence. Even  the  facial  expression  may  be  somewhat  characteristic,  being  pe- 
culiarly languid,  apathetic,  and  dull.  The  patient  talks  slowly,  often  having  to 
think  a  long  time  before  knowing  what  to  sa5\  Memory  becomes  impaired, 
especially  with  regard  to  the  most  recent  events.  The  interest  of  the  patient  in 
those  about  him,  and  the  things  he  used  to  care  for,  grows  less  and  less.  He  has 
a  sleepy,  dazed  look,  and  grows  careless  and  untidy.  There  is  sometimes  pro- 
nounced somnolence.  Of  course,  individual  cases  present  various  deviations  from 
this  outline ;  but  in  general,  all  cases  are  a  good  deal  alike,  although  the  degree  of 


1118  DISEASES    OF   THE   NEEVOUS    SYSTEM 

mental  disturbance  may  vary  from  the  slighter  forms  of  stupor  to  the  highest  de- 
grees of  mental  weakness.  We  occasionally  see  other  forms  of  mental  disttixb- 
ance  in  tumors  of  the  brain,  such  as  melancholy,  hallucinatory  confusion,  states  of 
excitement,  abnormal  attempts  at  wit  (Witzelsucht),  etc.  In  such  cases,  however, 
local  disturbances  (especially  in  the  frontal  lobe)  are  probably  to  be  taken  into 
account. 

If  unusual  fullness  of  the  blood-vessels,  a  hgemorrhage  into  the  new  growth,  or 
some  similar  cause,  induces  a  sudden  temporary  increase  of  tension,  there  may  be 
such  marked  symptoms  as  syncope  or  an  apoplectiform  shock. 

3.  Other  general  cerebral  symptoms  are  vertigo,  slowing  of  the  pulse,  and 
vomiting.  If,  however,  vertigo  be  a  very  prominent  symptom,  it  implies  that  the 
cerebellum  is  especially  encroached  upon  by  the  tumor.  The  retardation  of  the 
pulse  is  a  frequent  symptom,  and  not  without  diagnostic  value.  It  has  already 
been  mentioned  as  one  result  of  general  compression  of  the  brain,  in  connection 
with  cerebral  haemorrhage.  The  rate  may  be  put  at  about  50  to  60,  or  even  lower. 
The  pulse  is  also  sometimes  slightly  irregular.  Cerebral  vomiting  may  be  one  of 
the  earliest  and  most  troublesome  symptoms.  It  frequently  occurs  independently 
of  the  ingestion  of  food,  especially  in  the  morning,  and  is  not  infrequently  asso- 
ciated with  dizziness. 

4.  Epileptiform  convulsions  are  sometimes  excited  by  cerebral  tumors,  al- 
though many  patients  are  free  from  them.  Such  attacks  in  all  probability  origi- 
nate invariably  in  the  cortex  of  the  cerebrum,  and  it  is  therefore  natural  that 
they  should  be  seen  most  frequently  (as  they  are)  in  connection  with  tumors  in 
the  cerebral  hemispheres.  This  rule,  however,  is  not  without  exceptions.  If  the 
convulsions  are  not  general,  but  are  unilateral  or  confined  to  distinct  portions  of 
the  body,  they  are  to  be  regarded  rather  as  focal  than  as  general  symptoms,  and 
they  may  be  utilized  to  determine  the  position  of  the  lesion  {vide  page  1073).  A 
certain  amount  of  information  in  the  same  direction  may  also  be  obtained  from 
those  attacks  which  begin  unilaterally  or  in  one  particular  limb,  and  then  quickly 
involve  the  entire  body. 

6.  Optic  neuritis  ("  choked  disk  ")  is  one  of  the  most  important  and  common 
general  objective  symptoms  of  cerebral  tumor,  occurring  in  about  eighty  per  cent, 
of  all  cerebral  tumors.  We  should  therefore  never  omit  to  make  an  ophthal- 
moscopic examination  of  the  fundus  oculi  in  a  case  of  chronic  cerebral  disease. 
Some  differences  of  opinion  yet  exist  in  regard  to  the  special  pathology  of  optic 
neuritis ;  but  we  may  regard  it  as  extremely  probable  that  the  main  factor  in  its 
production  is  the  purely  mechanical  one  of  general  compression  of  the  brain. 
This  opinion  is  supported  especially  by  the  fact  that  even  a  marked  choked  disk 
may  disappear  completely  in  a  short  time,  if  a  lessening  of  the  intracranial 
pressure  be  brought  about  by  trephining  the  skull  and  causing  an  abundant  dis- 
charge of  cerebro-spinal  fluid.  The  original  view  of  Von  Graefe  was  that  the 
increased  intracranial  pressure  obstructs  the  venous  return  through  the  vena 
centralis  retinae  into  the  cavernous  sinus.  The  opinion  which  prevails  at  present 
is  that  advanced  by  Schmidt  and  Manz — namely,  that  the  increased  tension  forces 
the  cerebro-spinal  fluid  into  the  lymph-sheath  of  the  optic  nerve  (Schwalbe),  and 
that  the  "  hydrops  vagince  nervi  optici"  thus  produced  compresses  the  nerve 
and  the  blood-vessels  which  traverse  it.  [Leber  and  Deutschmann  have  shown 
pretty  conclusively  that  the  increased  pressure  is  not  the  chief  cause  of  optic 
neuritis.  It  favors  its  production,  but  probably  there  must  be  the  presence  of 
some  irritant  as  well,  in  order  to  produce  the  inflammation.— K.]  At  any  rate, 
optic  neuritis  is  not  a  focal  symptom.  The  tumor  occasioning  it  may  have  any 
position,  if  only  it  gives  rise  to  general  compression  of  the  brain. 

Disturbances  of  vision  may  be  entailed  by  optic  neuritis,  but  they  are  not  a 
necessary  consequence  of  neuritis ;  the  patient  may  have  amblyopia,  defects  in 


TUMORS  OF  THE  BRAIN  1119 

the  field  of  vision,  or  even  total  blindness.  Only  in  a  few  instances  has  amblyopia 
been  one  of  the  earliest  symptoms  of  cerebral  tumor,  so  that  the  patient  has 
applied  first  of  all  to  an  oculist.  Usually  the  sight  is  preserved  for  quite  a  long 
time,  in  spite  of  the  abundant  objective  evidences  of  optic  neuritis.  The  latter 
consist  of  swelling  of  the  disk,  marked  distention  and  tortuosity  of  the  veins, 
possibly  haemorrhages  (from  passive  congestion),  and  cloudiness  of  the  disk, 
although  the  retina  still  exhibits  its  normal  transparency.  It  is  not  until  the 
long-continued  congestion  impairs  nutrition  to  such  an  extent  as  to  cause  atrophy 
of  the  optic  nerve  that  vision  is  much  impaired. 

6.  General  loss  of  flesh  and  strength  may  sometimes  appear  comparatively 
early  in  cases  of  tumor  of  the  brain.  It  is  due  in  large  part  to  the  small  amount 
of  food  taken,  vomiting,  and  wakefulness ;  but  it  is  not  impossible  that  the  grave 
cerebral  disorder  itself  exerts  a  direct  and  unfavorable  influence  upon  all  the 
processes  of  nutrition.  There  is  in  most  cases,  also,  a  tendency  to  obstinate  con- 
stipation. 

7.  In  conclusion  we  may  mention  that,  on  examination  of  the  spinal  cord  of 
persons  who  have  died  of  cerebral  tumor,  degenerative  chajages  have  been  found 
in  the  posterior  columns  and  posterior  roots  (Dinkier,  Mayer,  and  many  others), 
besides  the  ordinary  secondary  descending  degenerations.  These  changes  are 
probably  a  consequence  of  the  increased  cerebral  pressure  and  the  stasis  of  cere- 
bro-spinal  fluid  thus  occasioned,  and  thus  they  may  be  classed  among  the  "  gen- 
eral symptoms  "  of  tumor.  As  a  rule  they  have  no  clinical  significance ;  but  an 
otherwise  inexplicable  loss  of  patellar  reflex  may  perhaps  often  be  referred  to 
these  secondary  changes  in  the  spinal  cord. 

Tumors  in  the  Different  Parts  of  the  Brain  and  their  Focal  Symptoms. — The 
symptoms  above  discussed  indicate  the  existence  of  a  tumor,  but  not  its  particular 
location.  Other  phenomena  are  necessary  to  enable  us  to  localize  the  disease, 
but  it  is  not  exceptional  to  have  none  but  the  general  symptoms.  Tumors  in  the 
white  matter  of  the  frontal  lobe,  or  tumors  of  the  corpus  striatum  or  optic  thala- 
mus, as  well  as  others,  may  run  their  course  without  any  focal  symptoms ;  but 
most  cases  afford  evidence  which  points  with  more  or  less  certainty  to  the  exact 
position  of  the  tumor.  Almost  all  of  these  focal  symptoms  have  already  been 
fully  discussed  in  Chapter  II  of  this  section,  and  their  interpretation  follows  the 
rules  for  all  focal  lesions  of  the  brain.  We  may  therefore  be  brief  here.  It  is 
necessary  only  to  emphasize  the  fact  that  with  regard  to  cerebral  tumors,  as  well 
as  other  lesions,  focal  symptoms  should  be  divided  into  the  direct  and  the  indirect. 
Direct  focal  symptoms  are  the  immediate  result  of  the  destruction  of  nervous  tis- 
sue by  the  new  growth,  while  the  indirect  symptoms  are  excited  by  the  pressure  ex- 
erted by  the  tumor  upon  the  parts  closely  surrounding  it.  This  pressure  varies 
with  the  amount  of  blood  in  the  vessels  of  the  new  growth,  and  therefore  the  indi- 
rect symptoms  may  undergo  temporary  exacerbations  and  remissions.  An  inter- 
mediate position  is  occupied  by  those  focal  symptoms  which  occur  in  many  cases 
as  the  result  of  certain  anatomical  changes  secondary  to  the  new  growth.  TsTot 
infrequently  there  is  white  softening  of  the  substance  of  the  brain  around  the 
tumor  proper.  Probably  this  condition  is  generally  the  result  of  a  compression 
of  the  minute  blood-vessels  surrounding  the  new  growth,  but  sometimes  it  is  the 
sequel  of  an  obliterative  endarteritis  (Friedlander).  The  latter  cause  is  espe- 
cially operative  when  the  tumor  is  a  gumma  or  a  solitary  tubercle.  In  vascular 
new  growths  also,  especially  in  gliomata,  haemorrhages  may  occur  which  may 
often  exert  a  destructive  influence  over  a  greater  territory  than  the  new  growth 
itself. 

1.  Tumors  of  the  Cerebral  Hemispheres. — Tumors  in  the  vicinity  of  the 
central  motor  convolutions  are  especially  important,  because  thoy  give  the  best 
opportunity   for   an    accurate    topical    diagnosis    and    surgical   treatment.      The 


1120  DISEASES    OF    THE   NERVOUS    SYSTEM 

first  focal  symptoms  are  usually  attacks  of  partial  epilepsy,  such  as  have  already 
been  described  in  detail  (page  1073).  Monoplegia  gradually  sets  in,  which  may 
gradually  develop  to  complete  hemiplegia.  At  first  there  is,  for  example,  a 
brachio-facial  or  a  crural  monoplegia,  and  later  the  paralysis  attacks  the  leg 
or  the  arm  on  the  same  side.  The  precise  peculiarities  of  cortical  spasms  and 
paralyses  have  been  described  above  (see  page  1072).  On  careful  examination, 
disturbances  of  the  tactile  and  stereognostic  senses  can  often  be  discovered  in 
the  paralyzed  limbs.  Ataxia  and,  with  tumors  of  the  left  hemisphere,  disturb- 
ances of  speech  may  also  occur.  Tumors  which  involve  the  temporal  lohes  cause 
soul  deafness  or  amnesic  (sensory)  aphasia.  Tumors  of  the  occipital  lohe  may 
be  recognized  by  the  occurrence  of  disturbances  of  vision  (soul  blindness,  hemian- 
opsia). In  tumors  of  the  frontal  lohe  Bruns  and  others  have  repeatedly  observed 
a  striking  disturbance  of  the  gait  (a  staggering  gait,  a  tendency  to  fall  to  one 
side  or  backward,  similar  to  cerebellar  ataxia).  This  is  probably  connected 
with  a  disturbance  of  the  motor  centers  for  the  muscles  of  the  trunk,  which  are 
situated  in  tbe  frontal  lobe.  Tumors  of  the  brain  not  very  infrequently  arise  in 
the  corpus  callosum,  but  these  can  hardly  ever  be  diagnosticated  with  certainty. 
Characteristic  focal  symptoms  are  lacking;  there  are  usually  only  the  general 
symptoms  of  a  tumor  and  especially  deep  disturbances  of  consciousness  (stupor, 
somnolence,  loss  of  intelligence,  etc.). 

2.  Tumors  at  the  Base  of  the  Brain. — The  base  of  the  brain  is  a  favorite 
seat  of  new  growths.  The  symptoms  are  in  a  raajority  of  cases  quite  character- 
istic. Some  of  the  tumors  spring  from  the  base  of  the  skull;  among  these  are 
many  sarcomata  and  syphilitic  growths  ("gummatous  periostitis").  Other  tu- 
mors originate  in  the  meninges,  especially  the  dura ;  and  still  others  from  the 
brain  itself.  Of  these  last,  it  is  remarkable  that  some  spring  from  the  pituitary 
gland.  The  exact  starting  point  is  very  seldom  of  much  clinical  importance,  for 
all  the  parts  mentioned  are  in  such  close  proximity  to  one  another  that  there  is 
no  great  difference  in  the  symptoms  produced.  We  can  decide  merely  that  there 
is  a  tumor  in  this  or  that  place  at  the  base  of  the  brain. 

Tumors  at  the  base  of  the  brain  owe  their  characteristic  clinical  stamp  to  the 
frequency  with  which  the  cranial  nerves  at  the  base  are  involved.  The  anatom- 
ical relations  are  such  that  these  nervous  trunks  are  often  compressed  by  the  new 
growth  or  actually  incorporated  in  it.  Of  the  symptoms  thus  occasioned,  the 
most  frequent  is  paralysis  of  the  motores  oculi  (oculo-motor  and  abducens).  This 
is  at  first  usually  unilateral,  but  it  may  later  affect  both  sides.  If  one  of  the  optic 
tracts  be  involved,  hemianopsia  may  result,  and  pressure  upon  one  optic  nerve  may 
produce  unilateral  choked  disk  with  unilateral  disturbance  of  vision.  Tumors  of 
the  pituitary  gland  are  especially  prone  to  cause  symptoms  referable  to  the  optic 
nerve  at  an  early  period  (compare  also  page  902).  Lesions  of  the  trigeminus 
not  infrequently  cause  disturbances  of  sensation  in  the  face,  and  occasionally 
also  paralysis  of  the  muscles  of  mastication.  The  trunk  of  the  facial  often 
suffers.  The  facial  paralysis  thus  occasioned  throws  considerable  light  upon  the 
diagnosis,  for  the  frontal  muscle  and  the  orbicularis  oculi  are  involved  (compare 
page  862),  and  there  is  usually  to  be  found  in  the  paralyzed  muscles  the  reaction 
of  degeneration,  showing  that  the  paralysis  is  peripheral.  We  have  therefore 
reason  to  assume  that  the  lesion  is  situated  at  the  base  of  the  cranium,  rather  than 
in  the  brain  itself.  Tumors  arising  from  the  posterior  fossa  at  the  base  of  the 
brain  cause  pressure  paralysis  of  the  lower  cranial  nerves  (hypoglossus,  accessory) 
and  sometimes  pronounced  bulbar  symptoms  (disturbances  of  swallowing  and  ar- 
ticulation) from  pressure  on  the  medulla.  As  might  naturally  be  expected,  vari- 
ous degrees  and  forms  of  paralysis  in  the  extremities  are  often  found  in  combina- 
tion with  all  the  above-mentioned  disturbances  of  the  cranial  nerves.  Such  condi- 
tions are  most  frequent  when  the  crus  cerebri,  with  its  pyramidal  tract,  is  affected. 


TUMOES  OF  THE  BRAIN  1121 

There  is  no  need  of  enumerating  all  the  possible  varieties  of  symptoms.  We 
must  consider  them  all  carefully  in  each  individual  case,  and  then,  by  bearing 
in  mind  the  anatomy  of  the  parts,  we  shall,  in  a  majority  of  instances,  be  enabled 
to  determine  with  some  approach  to  accuracy  the  place  at  the  base  of  the  brain 
where  the  new  growth  must  be.  Sometimes  we  may  be  led  into  error  by  tumors 
which,  though  situated  in  the  brain-substance  and  at  a  comparative  distance,  yet 
by  their  pressure  give  rise  to  indirect  symptoms  referable  to  the  cranial  nerves 
at  the  base. 

3.  Tumors  in  the  Neighborhood  of  the  Third  Ventricle. — Tumors  sometimes 
develop,  which  are  situated  in  a  central  position  in  the  interior  of  the  brain, 
especially  in  the  neighborhood  of  the  third  ventricle,  and  therefore  give  rise  to 
few  well-marked  focal  symptoms.  Besides  the  general  symptoms  of  tumor  (amau- 
rosis from  optic  neuritis,  stupor,  headache,  vomiting)  there  is  general  weakness 
of  the  extremities,  often  associated  with  spastic  rigidity,  which  is  usually  only 
a  little  more  developed  on  one  side  than  on  the  other.  As  a  rule,  therefore,  it  is 
hard  to  make  an  accurate  topical  diagnosis. 

4.  Tumors  of  the  Cerebellum. — Cerebellar  tumors  are  comparatively  frequent, 
and  they  can  usually  be  diagnosticated  with  considerable  certainty.  The  charac- 
teristic focal  symptoms  of  all  cerebellar  diseases  have  already  been  fully  de- 
scribed above  (see  page  1086).  We  will  recall  here  in  particular  the  feeling  of 
vertigo  and  the  staggering  gait.  But  cerebellar  tumors  generally  occasion  also 
very  strongly  pronounced  general  symptoms — namely,  headache,  mainly  occipital ; 
sometimes  a  spasmodic  and  persistent  stiffness  of  the  neck ;  vomiting ;  and  visual 
disturbances,  due  mainly  to  the  frequent  existence  of  optic  neuritis.  Analogous 
to  this  last  symptom  would  seem  to  be  disturbances  in  other  nerves  of  special 
sense.  Thus,  when  the  general  intracranial  pressure  is  elevated,  the  acoustic 
and  olfactory  nerves  seem  liable  to  passive  congestion.  Tumors  in  the  posterior 
fossa  have  several  times  been  found  to  occasion  bilateral  anosmia  and  deafness ; 
and  they  should  always  be  considered  when  such  a  condition  is  found.  Cere- 
hellar  tumors  not  infrequently  as  they  continue  to  grow  exert  pressure  upon 
the  pons  and  medulla,  and  thus  special  clinical  symptoms  may  arise :  symptoms 
of  paralysis  or  irritation  on  the  part  of  the  posterior  cranial  nerves,  nystagmus, 
hemiparesis,  hemi ataxia,  etc. 

5.  Tumors  in  the  pons,  the  crura  cerebri,  and  the  medulla  are  to  be  judged 
according  to  the  general  rules  for  the  localization  of  cerebral  diseases. 

We  may  also  observe,  by  way  of  an  appendix,  that  repeated  attempts  have  been 
made  of  late  to  make  use  of  percussion  of  the  skull  as  an  aid  in  the  diagnosis 
of  the  seat  of  a  cerebral  tumor.  Over  a  tumor  which  is  not  too  deeply  seated 
the  bones  of  the  skull  are  said  to  give  sometimes  on  percussion  a  note  which  is 
not  wholly  dull  but  rather  tympanitic.  A  sort  of  "  cracked-pot "  resonance  has 
also  been  observed.  Percussion  of  the  skull,  however,  can  hardly  claim  great 
practical  significance,  since  the  interpretation  of  the  results  is  too  uncertain. 
[A  few  attempts  have  also  been  made  to  employ  the  Rontgen  rays  to  reveal  the 
situation  of  the  tumor,  but  the  results  thus  far  have  not  been  very  definite. 

In  view  of  the  increasing  importance  of  the  focal  diagnosis  of  tumors  of  the 
hrain,  it  has  seemed  advisable  to  insert  the  following  brief  summary  of  the  focal 
symptoms  of  tumors  in  different  parts  of  the  brain : 

Prefrontal  Region. — Marked  mental  impairment  (abnormal  attempts  at  wit 
[Witzelsucht]  ?)  ;  symptoms  of  invasion  of  the  central  region  (Jacksonian  epi- 
lepsy, aphasia)  ;  staggering  gait ;  disturbances  of  smell. 

Central  Region. — Jacksonian  epilepsy;  monoplegia;  tactile  hyposesthesia  and 
loss  of  stereognostic  sense;  motor  aphasia. 

Posterior ParietalRegion. — Word-blindness;  disturbance  of  muscularsense(?)  ; 
homonymous  hemianopsia. 
71 


1122  DISEASES    OF    THE   NERVOUS    SYSTEM 

Occipital  Region. — Homonymous  hemianopsia;  soul-blindness. 

Temporo-Sphenoidal  Region. — Often  a  latent  region.  Word-deafness,  if  the 
left  side  be  affected;  disturbances  of  taste,  smell,  and  hearing. 

Corpus  Callosum. — Often  a  latent  region.  Progressive  hemiplegia,  often  bi- 
lateral from  invasion ;  mental  disturbances. 

Optica-striate  Region. — Hemiplegia;  contracture.  In  posterior  part,  hemi- 
ansesthesia,  homonymous  hemianopsia,  post-hemiplegic  chorea,  athetosis. 

Crus  Cerebri. — Crossed  paralyses  of  the  oculo-motor  nerve  and  limbs. 

Corpora  Quadrigemina. — Oculo-motor  paralyses ;  reeling  gait ;  blindness  (  ?)  ; 
deafness  (?). 

Pons  and  Medulla. — Crossed  paralyses  of  face  and  limbs,  or  tongue  and  limbs. 
Other  cranial  nerve  lesions. 

Cerebellum. — Marked  cerebellar  ataxia;  marked  vertigo  and  vomiting. 

Base,  Anterior  Fossa. — Mental  impairment;  disturbances  of  smell  and  vision; 
exophthalmus. 

Base,  Middle  Fossa. — Disturbance  of  vision ;  oculo-motor  disturbances ;  hemi- 
plegia. 

Base,  Posterior  Fossa. — Trigeminal  neuralgia;  neuro-paralytic  ophthalmia; 
paralyses  of  face  and  tongue;  disturbance  of  hearing;  crossed  paralyses. 

Hypophysis. — Disturbance  of  vision,  especially  bitemporal  hemianopsia;  ocu- 
lo-motor disturbances;  acromegaly. 

It  also  is  of  importance,  in  cases  which  may  come  to  operation,  to  determine 
whether  the  growth  be  cortical  or  subcortical.  Seguin  has  given  certain  rules- 
which,  however,  are  not  absolute.  "  In  favor  of  a  strictly  cortical  or  epicortical 
lesion  are  these  symptoms,  none  of  them  having  specific  or  independent  value: 
localized  clonic  spasm;  epileptic  attacks  beginning  by  local  spasm,  followed  by 
paralysis ;  early  appearance  of  local  cranial  pain  and  tenderness ;  increased  local 
cranial  temperature.  In  favor  of  subcortical  location  of  a  tumor :  local  or  hemi- 
paresis  followed  by  spasm;  predominance  of  tonic  spasm;  absence,  small  degree, 
or  very  late  appearance  of  local  headache  and  of  tenderness  on  percussion;  nor- 
mal cranial  temperature." — K.] 

General  Course  of  Cerebral  Tumors. — The  symptoms  of  these  growths  almost 
always  cover  a  long  period  of  time.  Exceptionally  a  tumor  remains  latent  till  a 
haemorrhage  or  some  similar  event  takes  place  in  it,  giving  rise  to  sudden  and 
grave  symptoms,  and  possibly  to  an  equally  sudden  termination.  The  rule  is, 
however,  for  the  phenomena  to  develop  gradually.  According  to  the  location  of 
a  new  growth,  either  the  general  or  the  focal  symptoms  may  come  first  into 
prominence.  They  generally  occur  in  the  order  named.  First  of  all  is  an  ill- 
defined,  deeply  seated  headache,  and  by  degrees  all  the  other  general  and  focal 
symptoms  follow  after.  The  symptoms  may  vary  repeatedly  and  greatly  in 
severity,  a  fact  due  mainly  to  the  varying  pressure  of  the  tumor  on  neighboring- 
parts.  Repeated  mention  has  already  been  made  of  the  sudden  exacerbations 
which  may  come  on,  especially  in  case  of  the  vascular  gliomata. 

The  entire  duration  of  the  disease  is  usually  at  least  some  months,  and  may  be- 
one  or  two  years  or  more.  The  termination  is  almost  invariably  unfavorable. 
Death  may  be  rather  sudden,  or  it  may  not  come  till  after  a  long  period  of  wretch- 
edness. Fortunately,  however,  the  lameness,  blindness,  and  marasmus  are  fre- 
quently made  less  terrible  to  the  patient  because  of  his  mental  debility.  Recovery 
is  possible  only  when  the  growth  is  syphilitic.  It  is  indeed  possible  that  solitary- 
tubercles  may  also  end  favorably,  but  the  matter  is  still  in  doubt. 

Diagnosis. — The  main  points  in  support  of  a  diagnosis  of  cerebral  tumor  would 
be  the  gradual  onset  and  continuous  slow  increase  of  the  general  symptoms  above 
detailed — namely,  headache,  vertigo,  vomiting,  convulsions,  dementia,  etc.  The 
most  constant  of  these  symptoms  is  the  headache.    They  all  indicate  the  develop- 


TUMOKS    OF   THE   BRAIN  1123 

ment  of  some  chronic  brain  trouble,  a  tumor  being  the  most  probable  if  there  be 
no  definite  aetiology  to  suggest  some  other  process,  such  as  traumatism  resulting 
in  abscess,  or  syphilis.  Much  stress  may  also  be  laid  on  the  optic  neuritis,  since 
this,  as  we  have  said,  is  much  less  often  seen  in  other  chronic  brain  diseases 
(abscess  or  softening)  than  in  tumor. 

The  general  symptoms  indicate  that  a  tumor  of  the  brain  exists ;  but,  in  order 
to  learn  the  position  of  that  tumor,  we  have  to  rely  mainly  upon  the  focal  symp- 
toms. Their  gradual  development  and  the  way  in  which  one  new  symptom  is 
slowly  added  to  another,  also  give  further  ground  for  the  opinion  that  some 
continuously  progressive  disease  exists,  and  most  probably  a  cerebral  tumor.  Of 
diseases  with  a  similar  course,  abscess  is  recognized  especially  by  the  slighter 
symptoms  of  general  intracranial  pressure  and  by  the  absence  of  optic  neuritis, 
frequently  by  febrile  symptoms,  and  by  its  aetiology  (trauma,  purulent  otitis). 
Inflammatory  and  thrombotic  softening,  if  they  come  on  slowly,  usually  produce 
less  general  disturbance  than  do  tumors;  they  hardly  ever  cause  optic  neuritis, 
and  (unless  of  syphilitic  origin)  are  much  rarer  before  middle  age  than  tumors 
of  the  brain.  Sclerosis  sometimes  simulates  cerebral  tumor ;  but  here  also  there 
is  no  choked  disk;  the  disease  lasts  much  longer  (five  or  ten  years,  or  naore), 
and,  inasmuch  as  the  sclerosis  is  usually  multiple,  there  is  frequently  too  great 
a  complexity  of  symptoms  to  warrant  the  assumption  of  one  solitary  lesion. 
[We  must,  however,  bear  in  mind  that,  in  about  one  seventh  of  the  cases,  tumors 
also  are  multiple. — K.] 

Certain  rare  cases  of  chronic  circumscribed  meningitis  can  not  be  differen- 
tiated from  a  tumor.  They  generally  occur  at  the  base,  lead  to  a  considerable 
thickening  of  the  tissues,  and  they  may  simulate  all  the  symptoms  of  a  new 
growth  in  this  region.  Occasionally,  also,  chronic  hydrocephalus  is  confounded 
with  tumor  of  the  brain.  We  met  with  a  case  of  dropsy  of  the  fourth  ventricle 
which  presented  during  life  a  perfect  picture  of  tumor  of  the  cerebellum. 

As  to  the  nature  of  a  new  growth,  we  can  not  go  beyond  surmises.  If  the 
focal  symptoms  indicate  that  the  tumor  is  in  the  substance  of  the  brain  itself,  our 
first  thought  would  be  of  a  glioma,  because  it  is  by  far  the  commonest  sort  of 
growth  in  that  situation;  and,  as  has  been  stated,  certain  peculiarities  in  the 
course  of  the  disease  (especially  if  new  symptoms  add  themselves  abruptly)  would 
make  glioma  probable.  If,  on  the  other  hand,  the  tumor  be  at  the  base,  it  is 
most  apt  to  be  sarcoma,  which  is  the  most  frequent  form  of  new  growths  here. 
When  symptoms  referable  to  the  optic  nerve  occur  noticeably  early,  a  tumor  of 
the  pituitary  gland  is  to  be  thought  of.  In  all  cases,  and  especially  .in  tumors  at 
the  base  of  the  brain,  we  should  bear  in  mind  the  possibility  of  syphilis.  The 
previous  history  and  the  entire  body  of  the  patient  should  be  closely  searched 
with  this  point  in  mind ;  its  therapeutic  importance  need  not  be  dwelt  on. 

One  special  form  of  tumor  deserves  a  brief  mention  here — namely,  large 
cerebral  tubercles.  The  growth  may  be  single  or  solitary,  or  it  may  be  multiple. 
It  is  seen  chiefly  in  childhood,  and  any  chronic  cerebral  disorder  in  a  child  should 
suggest  the  possibility  of  such  a  growth.  It  is  rendered  all  the  more  probable  by 
the  co-existence  of  the  signs  of  tuberculosis  elsewhere,  as  in  the  lymph-glands, 
lungs,  or  bones.  The  syinptoms  are  analogous  to  those  produced  by  other  tumors. 
Among  the  most  frequent  phenomena  are  headache  and  convulsions.  The  latter 
are  often  unilateral.  There  may  also  be  all  sorts  of  focal  symptoms,  according  to 
the  locality  of  the  lesion. 

Prognosis. — Except  gumma ta,  all  tumors  of  the  brain  have  a  very  unfavor- 
able prognosis.  It  is  said  that  in  very  rare  instances  tubercular  growths  have 
been  arrested  or  cured ;  but  in  practice  we  can  never  rely  upon  any  such  result. 
In  all  other  cases  recovery  is  next  to  impossible.  The  time  intervening  between 
the  appearance  of  the  first  symptoms  and  death  varies  greatly,  as  has  been  said. 


1124  DISEASES    OF   THE   NEEVOUS    SYSTEM 

We  should  therefore  be  very  cautious  in  predicting  the  duration  of  the  illness.  It 
seldom,  however,  exceeds  one  or  two  years,  and  sudden  death  without  any  warn- 
ing may  occur  at  any  time. 

[Tubercular  growths  are  occasionally  found  at  autopsies,  which  have  become 
encapsulated,  and  have  apparently  existed  for  years  without  causing  symptoms. 
In  some  cases,  especially  with  tubercular  growths  in  children,  the  symptoms 
diminish  and  the  patient  may  live  for  years,  suffering  only  from  the  blindness, 
etc.,  caused  by  the  growth.  Other  cases  may  present  only  mild  symptoms,  and 
the  patient  may  lead  a  fairly  comfortable  life  for  years. — K.] 

Treatment. — Inasmuch  as  the  nature  of  the  tumor  can  not  be  determined  with 
absolute  certainty  Jn  any  instance,  antisyphilitic  treatment  should  always  be 
tried.  Forty  to  seventy-five  grains  of  mercurial  ointment  (grm.  3-5)  should  be 
used  by  inunction,  and  thirty  to  seventy-five  grains  (grm.  2-5)  of  potassic  iodide 
should  be  given  internally  each  day.  If  the  new  growth  be  syphilitic,  much  bene- 
fit may  be  obtained  in  this  way.  It  must  be  confessed  that  the  treatment  is  gener- 
ally of  little  avail,  because  the  tumors  are  not  of  a  syphilitic  character ;  although 
it  may  be  that  iodide  of  potassium  sometimes  has  a  temporary  good  effect 
upon  other  forms.  A  long-continued  course  of  arsenic  has  also  been  recom- 
mended, in  order  to  check  the  growth  of  the  tumor.  This  remedy  should  be  used 
especially  in  those  cases  where  there  is  a  suspicion  of  sarcoma  or  solitary 
tubercle. 

Of  late  years  many  attempts  have  been  made  to  reraove  tumors  of  the  brain 
by  surgical  measures.  In  this  respect  the  special  favorable  conditions  of  the 
individual  case  are  chiefly  to  be  considered.  If  we  are  able  to  make  an  approx- 
imately certain  diagnosis  of  a  tumor  on  the  surface  of  the  brain,  especially  in 
the  motor  cortex,  surgical  interference  is  warranted,  and  in  some  cases  it  has 
been  attended  with  decided  success,  either  permanently  or  at  least  for  a  time. 
Since  there  is  no  outlook  for  the  patient's  recovery  without  an  operation,  we 
should  make  an  attempt  at  operation  in  every  case  where  the  tumor  can  appar- 
ently be  diagnosticated  with  certainty  and  localized  in  the  motor  region  of  the 
cortex.  We  should,  of  course,  never  undertake  an  operation  with  too  great  ex- 
pectations, since  errors  in  diagnosis  and  unforeseen  complications  and  incidents 
only  too  often  arise.  When  there  are  marked  general  symptoms  of  pressure 
(headache,  somnolence,  optic  neuritis)  it  may  be  well  worth  while,  as  a  practical 
measure,  to  advise  simple  opening  of  the  skull  without  further  interference. 
In  some  cases  the  lessening  of  intracranial  pressure  that  ensues  has  a  very  favor- 
able effect,  at  least  upon  these  general  pressure  symptoms  of  tumor. 

Beyond  what  has  jiist  been  indicated,  treatment  must  be  symptomatic.  The 
headache  is  combated  with  ice-bags,  narcotics,  antipyrine,  etc.;  the  convulsions 
require  bromide  of  potassium  or  the  inhalation  of  chloroform;  the  vomiting  is 
lessened  by  rest  in  bed,  opium,  and  bits  of  ice.  The  general  care  and  nursing 
of  the  patient  are  very  important,  so  that  bedsores  and  the  like  may  be  avoided 
if  possible. 

APPEl^DIX 

HYDATIDS  OF  I'HE   BRAIN 

It  was  stated  on  page  510  that  the  cysticercus  cellulosa3,  which  originates 
from  the  tfenia  solium,  may  occur  in  great  numbers  in  the  brain.  The  cysticerci 
most  frequently  occupy  the  pia  mater,  but  generally  project  downward  into  the 
cortex  of  the  brain.  The  meninges  not  infrequently  exhibit  signs  of  chronic 
inflammation,  and  may  present  hsemorrhages,  which  are  not  always  minute.  If 
there  are  numerous  cysticerci  in  the  neighborhood  of  the  ventricles,  a  varying 
degree  of  internal  hydrocephalus  usually  develops.     The  individual  cysticerci  are 


CEREBEAL  SYPHILIS  1125 

usually  enveloped  in  a  capsule  of  connective  tissue,  but  they  may  be  entirely  de- 
void of  such  a  covering. 

No  characteristic  clinical  sketch  of  hydatids  in  the  brain  can  be  drawn,  be- 
cause the  symptomatology  of  each  case  differs  according  to  the  number  and  posi- 
tion of  the  parasites.  Sometimes  cj^sticerci  produce  absolutely  no  symptoms,  and 
are  discovered  incidentally  at  the  autopsy.  In  other  instances  they  cause  a  long 
and  tedious  illness.  Epileptiform  convulsions  seem  to  be  the  most  frequent  symp- 
tom, and  these  must  be  due  to  the  position  of  the  cysticerci  in  the  cortex  of  the 
brain.  They  may,  like  true  epileptic  attacks,  come  on  only  at  certain  times  when 
the  general  condition  is  otherwise  good ;  or  permanent  general  cerebral  symptoms 
may  also  appear,  such  as  persistent  headache,  vertigo,  and  mental  disorder.  In 
a  case  recently  under  our  observation  the  symptoms  consisted  solely  of  parox- 
ysmal headache  and  uncontrollable  vomiting.  The  diagnosis  of  suspected  tumor 
was  made.  The  autopsy  showed  a  cysticercus  the  size  of  a  cherry  in  the  fourth 
ventricle  with  secondary  hydrocephalus.  Other  cases  have  shown  merely  mental 
disturbances  (confusion),  staggering  gait,  vertigo,  etc.,  so  that  the  disease  has 
been  repeatedly  confounded  with  hysteria.  Special  focal  symptoms  are  only 
rarely  present  with  cysticerci  of  the  brain.  It  is  a  fact  of  great  practical  signifi- 
cance that  death  may  not  infrequently  come  on  suddenly  and  unexpectedly  in 
cysticerci  of  the  brain.  We  have  seen  several  such  cases  in  persons  who  pre- 
viously had  not  complained  of  feeling  at  all  ill,  or  wno  had  complained  merely 
of  slight  headache,  etc.  In  such  cases  the  cysticerci  are  usually  in  the  third  or 
fourth  ventricle,  and  probably  cause  sudden  pressure  upon  the  medulla. 

The  diagnosis  can  never  be  made  with  absolute  certainty.  The  presence  of 
cysticerci  in  the  brain  may  be  suspected  when  the  above-mentioned  severe  symp- 
toms occur  in  a  butcher  or  other  person  who  is  from  his  calling  especially  exposed 
to  infection,  or  who  is  known  to  have  had  or  still  to  have  a  tapeworm,  or  in  whom 
cysticerci  have  been  demonstrated  in  some  other  part  of  the  body,  such  as  the  skin. 

We  know  of  no  remedy  capable  of  destroying  the  cysticerci.  Treatment,  there- 
fore, can  be  only  symptomatic.  [In  a  few  cases,  chiefly  in  Australia,  the  cysticerci 
have  been  successfully  removed  by  surgical  interference. — K.] 


CHAPTER    VIII 
CEREBRAL    SYPHILIS 

.Sltiology. — The  importance  of  syphilis  as  an  setiological  factor  in  many 
chronic  diseases  of  the  nervous  centers  has  been  repeatedly  adverted  to  in  pre- 
ceding chapters ;  but,  as  we  have  already  stated,  the  influence  of  syphilis  upon  the 
genesis  of  these  diseases  is  shown  in  two  essentially  different  ways.  In  one  case 
there  is  a  probable  toxic,  so-called  post-syphilitic  degenerative  process  of  certain 
tracts  of  fibers  and  ganglion-cells  (tabes,  general  paralysis)  ;  in  the  other  case 
there  is  the  formation  of  true  tertiary  syphilitic  ("  gummatous  ")  new  growths. 
Only  this  latter  form  of  syphilitic  cerebral  disease  will  be  spoken  of  here. 

As  a  rule,  genuine  cerebral  syphilis  develops  in  the  later  stages  of  the  whole 
syphilitic  process,  but  sometimes  cerebral  symptoms  come  on  by  the  end  of  the 
first  year  from  the  date  of  the  initial  lesion.  Usually  the  interval  is  several 
years,  and  it  may  be  ten  or  even  twenty  years  after  the  beginning  of  the  disease, 
before  the  first  signs  of  the  cerebral  trouble  develop.  We  therefore  class  cere- 
bral syphilis  generally  among  the  "  tertiary  symptoms  "  of  syphilis. 

Liability  to  the  disease  does  not  seem  to  be  influenced  essentially  by  age  or 


1126  DISEASES    OF   THE   NEEVOUS    SYSTEM 

sex,  except  so  far  as  pertains  to  the  general  distribution  of  syphilis.  Even 
hereditary  syphilis  has  been  proved  to  cause  diseases  of  the  nervous  system.  But 
it  can  not  be  denied  that  a  predisposition  to  cerebral  syphilitic  disease  is  often 
engendered  by  those  influences  which  are  apt  to  promote  cerebral  disease  in  gen- 
eral. Just  as  the  position  of  syphilitic  cutaneous  lesions  is  often  determined  by 
external  irritation  at  some  one  place  on  the  skin,  so  the  disease  seems  more  liable 
to  attack  a  brain  which  is  exposed  to  certain  unfavorable  conditions  than  one 
which  is  perfectly  normal  and  vigorous.  Such  conditions  are  inherited  tendency 
to  nervous  diseases,  various  injurious  mental  influences,  poisons,  in  a  broad  sense, 
and  traumatism.  It  need  hardly  be  said  that  even  a  previously  sound  brain  does 
not  enjoy  immunity  from  the  affection. 

Pathology. — As  far  as  has  yet  been  ascertained,  there  are  two  chief  forms 
assumed  by  syphilis  in  the  brain:  (1)  a  circumscribed,  broad,  flat  syphilitic  new 
growth  like  a  tumor  (gumma,  syphiloma),  and  (2)  a  disease  of  the  arteries  of  the 
brain,  which  is  usually  quite  extensive.  There  is  no  essential  difference  underly- 
ing these  two  varieties.  They  may  also  occur  in  combination  with  each  other. 
The  disease  of  the  blood-vessels  is  really  a  syphilitic  new  growth  affecting  the 
walls  of  the  arteries. 

The  syphilitic  new  growths  are  yellowish  or  grayish-red,  and  frequently 
cheesy  in  the  center.  Their  most  frequent  seat  is  the  dura  mxater  or  the  sub- 
arachnoid space  whence  they  spread  to  the  brain-substance  or  the  neighboring 
vessels  and  nerves ;  but  exceptionally  they  may  originate  in  the  substance  of  the 
brain  itself.  Histologically  they  are  made  up  of  granulation  tissue  of  varying 
degrees  of  vascularity,  presenting  yellow  spots  usually  visible  to  the  naked 
eye.  These  spots  are  of  firmer  consistency  than  the  rest  of  the  growth,  and  have 
undergone  coagulation-necrosis  (have  become  cheesy).  In  the  brain  substance 
itself  circumscribed,  wedge-like  gummata  may  sometimes  develop,  which  closely 
resemble  solitary  tubercles ;  but  the  extensive,  flat  syphilitic  new  growths  arising 
from  the  meninges  (meningitis  gummosa)  are  of  much  greater  clinical  impor- 
tance. These  are  found  most  frequently  at  the  base  of  the  brain,  especially  devel- 
oping from  the  region  of  the  chiasma,  or,  more  rarely,  on  the  lateral  portions  of 
the  brain  (fissure  of  Sylvius)  or  on  the  convexity.  In  these  more  extensive  new 
formations  of  tissue  we  usually  find  all  the  different  stages  of  the  process  to- 
gether, fresh  granulation  tissue,  cheesy  places,  and  finally  the  transition  into 
contracting  cicatricial  connective  tissue  (scar  formation). 

The  syphilitic  disease  of  the  arteries  was  first  fully  appreciated  by  Heubner, 
who  has  described  it  accurately.  It  is  usually  most  pronounced  in  the  arteries  of 
the  base  of  the  brain,  and  especially  in  the  middle  cerebral  artery  and  its  branches. 
Even  the  unaided  eye  detects  a  grayish  opacity  in  the  arteries.  They  feel  firm 
and  stiff,  and  on  cross-section  their  walls  are  found  to  be  thickened,  either  uni- 
formly or  in  some  places  more  than  in  others.  This  causes  no  inconsiderable  nar- 
rowing of  the  lumen,  or  even  its  obliteration,  particularly  if  the  last  gap  be  closed 
by  the  formation  of  a  thrombus.  The  microscope  shows  that  the  new  growth 
originates  chiefly  in  the  intima  of  the  vessel,  where  there  is  a  hyperplasia  of  the 
endothelium,  and  a  gradual  transformation  of  it  into  a  firm  connective  tissue. 
But  the  adventitia  also  undergoes  a  gradual  thickening  of  considerable  extent. 
Syphilitic  endarteritis  presents  no  distinctive  histological  characteristics.  Entire 
certainty  that  the  inflammation  is  syphilitic  can  be  attained  only  by  discov- 
ering other  evidences  of  syphilis,  either  in  the  brain  or  elsewhere,  or  from  the 
personal  history  and  the  previous  course  of  the  disease. 

The  great  clinical  importance  of  syphilitic  endarteritis  is  due  to  its  cutting  off 
the  normal  supply  of  blood  from  the  regions  supplied  by  the  diseased  arteries.  If 
the  occlusion  be  complete,  cerebral  softening  is  inevitable,  as  in  ordinary  embo- 
lism and  thrombosis  of  cerebral  arteries;  and,  inasmuch  as  the  middle  cerebral 


CEEEBRAL  SYPHILIS  1127 

artery  is  particularly  liable  to  the  disease,  syphilitic  softening  is  most  often  found 
in  the  region  supplied  by  this  vessel. 

Clinical  History. — The  variety  of  the  pathological  processes  and  of  their  loca- 
tion produces  a  corresponding  variety  in  the  symptoms  of  cerebral  syphilis ;  but 
certain  types,  already  described  in  the  main  by  Heubner,  may  be  distinguished, 
and  in  many  cases  these  present  a  picture  which  is  very  characteristic  of 
cerebral  syphilis. 

1.  Basal  Gummatous  Meningitis.  Basal  Cerebral  Syphilis. — The  development 
of  a  flat  syphilitic  new  growth  spread  over  the  base  of  the  brain,  whose  anatom- 
ical relations  have  been  briefly  described  above,  causes  a  form  of  disease  which  in 
many  respects  agrees  with  that  of  tumors  of  the  base  of  the  brain  (vide  supra, 
page  1120),  but  which  also  often  shows  certain  characteristic  peculiarities.  The 
flrst  symptoms  consist  of  persistent  headache,  sometimes  growing  worse  at  night, 
vertigo,  vomiting,  and  a  certain  mental  dullness,  which  rarely,  however,  reaches 
such  a  high  degree  of  stupor  as  is  so  often  see  in  genuine  tumors  of  the  brain. 
States  of  marked  maniacal  excitement  also  occur  at  times.  The  patient  often 
has  an  intense  and  striking  polydipsia  and  polyuria.  To  these  symptoms  are  soon 
added  others,  which  are  due  to  the  invasion  of  the  different  basal  cranial  nerves 
by  the  morbid  process.  The  optic  nerve  and  the  motor  nerves  of  the  eye  (espe- 
cially the  oculo-motor)  are  almost  always  among  the  first  to  be  affected.  Disturb- 
ances of  vision  (limitation  of  the  visual  field,  in  some  cases  hemianopsia,  blind- 
ness of  one  or  both  eyes),  changes  in  the  pupils,  disturbances  of  motion  of  the 
eyeballs  or  eyelids,  may  now  become  manifest  in  various  ways.  Optic  neuritis 
or  choked  disk  may  occur,  but  in  general  the  ophthalmoscopic  changes  are  de- 
cidedly less  frequent  in  cerebral  syphilis  than  in  genuine  tumors  of  the  brain. 
It  is  a  very  characteristic  circumstance  that  all  the  different  symptoms  on  the 
part  of  the  cranial  nerves  (especially  the  changes  in  the  visual  field,  as  Oppen- 
heim  has  shown)  may  show  great  variations,  which  are  undoubtedly  connected 
with  changes  in  the  pressure  from  cicatricial  contraction,,  etc.  Of  the  other 
cranial  nerves,  the  facial,  acoustic,  olfactory,  and  trigeminus  are  most  readily 
affected,  but  we  should  always  make  a  very  complete  examination  in  every  way 
in  order  to  estimate  correctly  the  extent  of  the  process. 

The  further  course  of  the  disease  may  vary  very  much.  In  fresh  cases,  which 
are  recognized  and  treated  in  time,  there  may  be  decided  improvement,  and  even 
complete  recovery  or  at  least  an  arrest  of  the  morbid  process ;  but,  on  the  other 
hand,  the  symptoms  may  increase.  If  there  is  also  syphilis  of  the  arteries  (vide 
infra),  there  may  be  a  slowly  developing  hemiplegia,  hemiplegia  following  apo- 
plexy, epileptic  states,  bulbar  symptoms,  etc. — in  short,  a  complicated  form  of 
cerebral  disease,  which  is  no  longer  capable  of  any  material  change. 

2.  Gummatous  Meningitis  and  the  Formation  of  Syphiloma  on  the  Convexity 
of  the  Brain  and  in  the  Vicinity  of  the  Fissure  of  Sylvius. — In  this  somewhat 
less  frequent  localization  of  the  syphilitic  new  growth  prodromata  similar  to  those 
just  enumerated  precede  the  severer  symptoms.  Then  appear  violent  partial  or 
general  epileptiform  convulsions.  These  often  come  on  very  suddenly,  and  they 
:nay  recur  at  considerable  intervals  or  in  quick  succession.  There  are  usually  still 
other  symptoms  of  cortical  disturbance,  especially  paresis  of  one  limb  or  even  of 
one  half  the  body ;  very  frequently  slight  disturbances  of  speech  (stumbling  over 
syllables),  referable  to  the  cortex,  and  indications  of  mental  impairment.  Optic 
neuritis  as  a  rule  is  not  present.  Many  of  these  cases  reach  a  fatal  termination 
comparatively  early.  The  epileptiform  convulsions  become  more  and  more  fre- 
quent, and  unconsciousness  increases  to  deep  coma  ending  in  death.  But  in  cases 
of  precisely  this  type  prompt  and  energetic  treatment  may  accomplish  a  great  deal. 

3.  Cerebral  Syphilis  Involving  the  Cerebral  Arteries  Chiefly. — A  third  com- 
mon and  important  variety  of  cerebral  syphilis  is  characterized  chiefly  by  syphi- 


1128  DISEASES    OF   THE   NERVOUS    SYSTEM 

litic  arteritis.  ISTot  infrequently  there  is  a  prodromal  stage,  wliicli  is  sometiraes 
only  slight;  then,  as  a  result  of  the  occlusion  of  some  vessel,  which  often  occurs 
quite  suddenly,  there  is  a  pronounced  apoplectic  attack,  followed  in  most  cases 
by  hemiplegia.  The  intensity  of  the  initial  shock  may  vary  greatly;  sometimes 
there  is  only  a  slight  dizziness,  sometimes  there  is  a  coma  that  lasts  for  days. 
Sometimes  the  shock  is  succeeded  by  a  peculiar  condition  of  mental  confusion 
and  dullness,  which  may  persist  for  weeks.  In  severe  cases,  death  is  speedy, 
and  is  usually  ushered  in  by  a  great  rise  of  temperature.  Other  patients  improve 
more-  or  less  rapidly,  especially  under  proper  treatment. 

Apoplectic  attacks  of  this  sort  may  recur  after  temporary  improvement  has 
taken  place,  and  may  be  associated  with  all  sorts  of  nervous  symptoms. 

4.  Complicated  Cases  of  Cerebrospinal  Syphilis. — C omhination  of  Gumma- 
tous Syphilis  and  Syphilitic  Degeneration  of  the  Nerves  (Tabes,  General  Paraly- 
sis).— Besides  the  three  types  of  cerebral  syphilis  already  described  there  are  also 
many  cases  which  belong  in  part  to  one  of  the  types  mentioned,  but  which,  on 
the  other  hand,  exhibit  much  more  complicated  symptoms  on  account  of  the  far 
greater  extent  of  the  anatomical  changes.  In  the  first  place  we  will  mention  the 
combination  of  cerebral  and  spinal  symptoms.  The  latter  are  often  due  to  gum- 
matous spinal  meningitis  also,  which  is  very  often  situated  in  the  cervical  region 
of  the  cord,  and  which  may  lead  to  paraplegia,  brachial  paresis,  symptoms  of 
unilateral  lesion  (vide  page  1036),  shooting  root  pains,  vesical  disturbances,  etc. 
With  these  symptoms,  all  of  whose  varying  details  it  is  impossible  to  speak  of  here, 
are  not  infrequently  associated  cerebral  symptoms,  which,  for  their  part,  corre- 
spond to  the  conditions  above  described.  A  considerable  number  of  eases  whicli 
have  been  studied  anatomically  of  late  are  also  of  especial  interest.  In  these 
cases  the  symptoms  of  gummatous  syphilis  were  associated  with  genuine  tabes, 
or  in  other  cases  cerebral  symptoms  ensued,  which  were  of  the  type  of  general 
paralysis  (weakness  of  memory,  a  peculiar  disturbance  of  speech,  twitching 
of  the  facial  muscles,  paralytic  attacks,  etc.).  In  such  cases  the  multiplicity 
of  possible  details  is  inexhaustible ;  but  the  characteristic  peculiarity  of  the 
type  lies  in  this  regular  irregularity,  which  often  admits  a  positive  recognition 
of  syphilis  of  the  nervous  system  and  is  also  capable  of  a  clinical  and  anatomical 
interpretation,  with  proper  consideration  of  the  nature  of  the  disease. 

Diagnosis. — The  most  important  diagnostic  criteria  have  already  been  men- 
tioned in  the  description  of  the  symptoms.  Here,  too,  the  diagnosis  is  first 
topical  and  then  etiological  and  anatomical.  The  distinction  between  syphilis 
and  genuine  tumors  is  the  most  difficult.  Absence  of  optic  neuritis,  a  marked 
variability  in  the  severity  of  the  symptoms,  and  multiplicity  of  symptoms,  espe- 
cially the  combination  of  symptoms  demanding  different  localizations,  are  in  favor 
of  syphilis.  The  discovery  of  a  previous  syphilitic  infection  is,  of  course,  always 
important.  We  can  not  here  describe  in  detail  the  methods  of  determining 
this  fact.  The  history  of  the  patient,  as  well  as  previous  specific  affections — 
such  as,  in  women,  miscarriages,  abortions,  etc.-^and  the  objective  signs  on 
other  parts  of  the  body,  are  the  two  sources  of  information.  There  may  be 
scars  on  the  skin  or  mucous  membranes,  enlarged  glands,  ulcers,  tibial  periostitis, 
or  changes  in  the  testicles.  Age  is  also  important:  thus  an  apoplectic  attack 
in  a  young  person  would  suggest  syphilis,  because  the  other  causes  of  siTch  an 
attack  operate  chiefly  upon  the  aged.  The  results  of  treatment  often  throw 
considerable  light  upon  the  diagnosis.  As  there  is  nothing  to  lose  and  much 
perhaps  to  gain,  we  should  always  give  specific  remedies  in  doubtful  cases.  If 
they  prove  successful,  the  diagnosis  of  syphilis  receives  strong  confirmation. 

Prognosis  and  Treatment.^ — There  are  few  severe  and  dangerous  diseases 
in  which  timely  and  appropriate  treatment  is  attended  with  so  much  success  as 
that  achieved  in  many  cases  of  cerebral  syphilis.     In  order,  however,  both  to 


PEOGEESSIVE  GENEEAL  PAEALYSIS  OF  THE  INSANE  1129 

understand  the  favorable  results  and  not  to  be  misled  by  the  failures,  we  need 
to  gain  a  clear  idea  of  the  way  in  which  antisyphilitic  remedies  can  be  of  benefit. 
They  can  accomplish  this  only  by  causing  the  dissipation  and  absorption  of  the 
new  growth — that  is,  the  gumma  or  the  swelling  of  the  intima.  If  this  be 
effected,  the  surrounding  parts  are  of  course  relieved  from  pressure,  and  the 
circulation  becomes  unimpeded.  If  the  tissues  still  retain  functional  power, 
they  resume  their  duties  and  all  symptoms  of  disease  vanish.  But  when  the 
tissues  have  already  been  considerably  impaired  by  the  compression,  or  by  the 
scanty  blood-supply,  the  results  are  quite  different.  Even  then  the  degenerated 
nerve  trunks  at  the  base  of  the  brain  may  gradually  become  regenerated ;  but  such 
parts  of  the  true  cerebral  parenchyma  as  have  undergone  softening  have  lost 
their  functional  capacity  forever.  In  such  cases,  antisyphilitic  treatment  is 
unavailing. 

It  is  therefore  obvious  that  the  first  essential  of  success  is  to  begin  treatment 
as  early  as  possible.  The  sooner  a  correct  diagnosis  is  reached,  the  sooner  will 
existing  symptoms  be  relieved,  and  further  danger  be  averted.  The  method  of 
treatment  which  will  probably  accomplish  all  that  can  be  accomplished,  and  in 
the  shortest  possible  time,  is  energetic  mercurial  inunction.  At  least  a  drachm 
(grammes  3-5)  of  mercurial  ointment  must  be  rubbed  in  every  day  at  first,  accord- 
ing to  the  ordinary  method.  We  should  not  venture  to  restrict  the  diet  unless  the 
patient  be  well  nourished  and  "  full  blooded."  If  he  be  anaemic  and  feeble,  a 
generous  regimen  is  demanded.  Usually  the  internal  administration  of  iodide 
of  potassium  is  combined  with  the  inunctions ;  we  should  give  thirty  to  forty-five 
grains  (grammes  2-3),  or,  in  severer  cases,  even  a  drachm  or  a  drachm  and  a  half 
(grammes  4-6),  daily  [In  this  country  iodide  of  potassium  is  given  much  more 
freely.  In  cases  where  syphilis  is  suspected,  we  may  safely  begin  with  doses  of 
thirty  grains  (grammes  2)  three  times  a  day.  If  the  symptoms  be  urgent,  the  dose 
should  be  rapidly  increased  until  the  patient  takes  three  or  even  four  drachms 
(grammes  10-15)  three  times  a  day.  If  the  patient  have  syphilis,  the  danger  of 
iodism  seems  less.  The  drug  must  be  given  in  large  amounts  of  water,  and  it 
is  better  borne  if  given  in  Vichy  or  Giesshubler  water.  Sometimes  the  stomach 
will  not  tolerate  the  extreme  doses. — K.]  The  same  remedy  should  also  be  given 
afterward,  for  a  long  time,  in  smaller  doses.  When  there  is  no  benefit  at  all 
after  twenty  or  thirty  inunctions,  there  is  little  prospect  of  any  appreciable 
improvement.  In  favorable  cases,  the  mercury  often  begins  to  produce  some 
effect  after  the  fifth  or  sixth  inunction ;  and  it  may  cause  astonishingly  rapid 
improvement.  Potassic  iodide  alone  is  sufficient  for  the  milder  cases  only,  where 
there  is  merely  headache,  trigeminal  neuralgia,  or  paralysis  confined  to  the 
motores  oculi.  In  many  cases  it  may  be  desirable  from  other  reasons  to  carry 
out  the  treatment  at  some  health-resort  rather  than  at  home  (Aix,  Tolz,  Hall  in 
Upper  Austria,  Wiesbaden,  etc.).  These  resorts  are  also  suitable  for  after-treat- 
ment or  for  repeated  courses  of  treatment,  but  the  treatment  by  drugs  is  always 
much  more  important  than  the  baths. 


CHAPTEE   IX 

PROGRESSIVE    GENERAL    PARALYSIS    OE    THE    INSANE 

{Paralytic  Demerdia.     Paretic  Dementia.     General  Paresis) 

Preliminary  Remarks. — Although  the  description  of  mental  diseases  is  not 
a  part  of  the  plan  of  this  bonk,  we  must  nevertheless  make  an  exception  of  one 
disease  of  the  sort,  namely,  the  so-called  progressive  general  paralysis  of  the 


1130  DISEASES    OF   THE   NERVOUS    SYSTEM 

insane,  or  paralytic  dementia,  whicli  in  medical  parlance  is  often  abbreviated 
into  "  general  paralysis."  We  consider  it  advisable  to  make  this  exception,  be- 
cause a  great  part  at  least  of  the  symptoms  of  general  paralysis  are  purely  of  a 
physical  nature,  and  also  because  a  knowledge  of  this  disease,  which  is  so  com- 
mon and  so  fatal  in  its  results,  is  of  the  greatest  importance  for  the  general  prac- 
titioner. 

We  must  thank  the  French  alienists  Boyle  (1822)  and  Calmeil  (1826)  for  the 
first  clinical  descriptions  of  general  paralysis,  by  which  it  was  more  sharply 
differentiated  than  previously  from  the  diseases  which  resemble  it.  A  more 
accurate  knowledge  of  the  different  symptoms,  and  the  anatomical  changes  to 
which  the  morbid  symptoms  must  be  referred,  has,  however,  only  of  late  years 
been  rendered  possible  by  the  introduction  of  better  methods  of  investigation. 
Accordingly,  we  must  now  say  that  general  paralysis  is  a  disease  which  may 
attack  the  most  diverse  portions  of  the  whole  central  nervous  system  * — the  brain 
and  spinal  cord — at  the  same  time  or  successively,  although  we  can,  of  course, 
make  out  certain  rules  as  to  the  predisposition  of  individual  portions  to  disease, 
and  as  to  the  order  of  the  symptoms.  General  paralysis  begins  most  frequently  in 
those  regions  of  the  cerebrum  which  have  an  immediate  relation  to  the  regular 
course  of  the  psychical  and  certain  psycho-motor  processes.  Mental  and  motor 
symptoms  accordingly  form  the  introductory  features  of  the  disease  in  most 
cases.  More  extensive  regions  of  the  central  nervous  system  are  gradually  in- 
volved in  the  morbid  process,  which  goes  hand  in  hand  with  a  progressive  degen- 
eration of  all  the  higher  intellectual  faculties,  while  at  the  same  time  many  physi- 
cal disturbances  dependent  upon  nervous  changes  constantly  increase. 

lEtiologj. — General  paralysis  is  a  common  disease,  and  apparently  demands  a 
heavier  quota  from  the  better  and  more  highly  educated  classes  than  from  the 
lower  classes.  We  may  assume  that,  on  the  average,  one  tenth  of  all  patients 
committed  to  the  insane  asylums  are  general  paralytics.  In  most  patients  the 
beginning  of  the  disease  falls  in  the  period  between  the  thirtieth  and  fiftieth  year. 
The  disease  is  much  rarer  in  advanced  life.  In  young  people  under  twenty  it  has 
hardly  ever  been  observed.  [Over  one  hundred  cases  of  juvenile  general  paralysis 
have  been  reported,  almost  always  in  victims  of  hereditary  syphilis. — K.]  There 
is  no  doubt  that  the  male  sex  is  much  more  frequently  affected  than  the  female, 
but  the  number  of  cases  of  general  paralysis  among  women  is  not  very  small. 

What  is  the  special  cause  of  general  paralysis?  A  generally  acceptable  an- 
swer can  not  be  given;  but  the  theory  is  constantly  gaining  ground,  and  we 
agree  to  it,  from  our  own  experience,  that  by  far  the  most  important  causal  factor 
is  a  previous  syphilitic  infection.  Such  an  infection  can  be  made  out  in  at 
least  seventy-five  per  cent,  of  all  cases.  In  this  regard  precisely  the  same 
conditions  exist,  and,  of  course,  the  same  difficulties  in  the  interpretation  of 
this  relation  are  to  be  considered,  as  we  have  previously  mentioned  in  the 
account  of  the  dependence  of  tabes  dorsalis  on  syphilis  (see  page  961),  a  circum- 
stance which  again  is  not  without  significance,  since  the  most  intimate  points  of 
connection  are  to  be  found  between  tabes  and  general  paralysis  (vide  infra).  If 
we  consider  that  general  paralysis  depends  upon  a  previous  syphilis,  we  have 
an  easy  explanation  of  most  of  the  other  peculiarities  in  the  onset  of  the  disease, 
especially  the  above-mentioned  influence  of  age  and  sex,  the  decidedly  common 
occurrence  of  the  disease  in  persons  in  certain  callings — -such  as  artists  and  offi- 
cers— the  frequency  of  the  disease  in  large  cities  in  distinction  from  its  rarer 
occurrence  in  the  country,  etc. 

*  At  present  hardly  anything  is  known  in  regard  to  a  primary  implication  of  the  peripheral  nerves 
in  the  general  process.  The  principle  of  such  an  implication  would  be  very  readily  understood  in 
view  of  the  almost  regular  occurrence  of  degeneration  of  the  peripheral  nerves  in  tabes. 


PROGRESSIVE  GENERAL  PARALYSIS  OF  THE  INSANE   1131 

Besides  the  setiological  factors  named,  whicli,  in  our  opinion,  are  the  most 
important,  all  other  "  causes  "  of  general  paralysis  may  well  be  regarded  as  merely 
predisposing.  Mental  over-exertion  has  the  greatest  significance,  especially  if  it 
be  associated  with  psychical  irritation.  In  merchants,  civil  officers,  etc.,  who 
suffer  from  general  paralysis,  such  a  previous  over-exertion  can  often  be  made  out. 
In  some  cases  injury  to  the  head  or  insolation  is  claimed  to  be  the  cause.  Heredi- 
tary predisposition  to  nervous  diseases  plays  perhaps  a  certain  part  in  the  origin 
of  general  paralysis,  but  by  no  means  a  very  large  one. 

Clinical  History.— General  paralysis  usually  begins  so  slowly  and  gradually 
that  a  definite  period  for  its  beginning  can  hardly  ever  be  given.  In  addition,  it 
is  often  clear,  at  a  time  when  the  disease  is  already  fully  developed,  that  certain 
early  symptoms,  whose  nature  was  at  first  not  correctly  recognized,  ought  to  have 
been  regarded  as  the  initial  symptoms. 

The  first  symptoms  of  the  disease  in  the  psychical  domain  usually  consist  of 
the  gradual  appearance  of  a  change  in  the  whole  nature  and  in  the  mental  indi- 
viduality of  the  patient ;  wherein,  however,  the  mental  disturbance  usually  shows 
from  the  start  the  character  of  weakness — that  is,  of  a  lessened  capability  of 
mental  exertion.  The  patient's  ordinary  mental  work  no  longer  goes  on  as  easily 
as  before.  His  memory  is  uncertain,  and  there  are  marked  forgetfulness  and 
inattentiveness,  which  were  previously  quite  impossible  for  him  to  exhibit.  The 
patient  is  often  disorderly  in  his  dress,  and  violates  the  ordinary  social  rules  of 
decency  and  morality.  Since  his  judgment  as  to  the  value  and  significance  of 
things  is  uncertain,  he  commits  purposeless  actions,  wastes  money,  commits 
crimes,  is  dissolute,  etc.  In  these  respects,  too,  the  increasing  mental  dullness 
often  appears,  since  the  patient  becomes  incapable  of  any  higher  intellectual,  aes- 
thetic enjoyment,  and  since  the  sway  of  nobler  feeling  finally  becomes  feeble, 
and  unable  to  exert  any  lasting  influence  upon  his  actions.  Besides  all  these  signs 
of  beginning  mental  weakness,  we  often  notice,  on  the  other  hand,  an  abnormal 
irritability.  The  patient  easily  becomes  agitated,  or  gets  angry;  but  these  moods 
rapidly  pass  away  without  leaving  a  lasting  impression.  We  easily  understand 
how  this  change  in  the  whole  personality  of  the  patient  must  distress  and  alarm 
his  family,  since  the  relatives  at  first  can  not  understand  at  all  why  the  patient  is 
now  "  so  difFerent  from  what  he  was." 

In  the  first  period  of  the  disease  a  subjective  feeling  of  illness  is  frequently 
present.  The  patient  himself  notices  that  his  mental  capacity,  especially  his 
memory,  is  diminished,  and  he  very  often  becomes  extremely  anxious  on  this 
account.  It  frequently  happens  that  certain  subjective  sensations  are  also  no- 
ticed, a  feeling  of  confusion  in  the  head,  pressure  in  the  head,  dizziness,  rheuma- 
toid pains,  etc.  The  sleep  is  disturbed,  as  a  rule,  and  also  the  appetite  and  the 
digestion.  If  such  a  patient  comes  to  the  physician  with  his  complaints,  it  un- 
'fortunately  only  too  often  happens  that  he  is  in  the  beginning  regarded  as 
"  neurasthenic,"  and  is  treated  accordingly. 

Careful  observation,  however,  may  usually  even  now  discover  the  disease  with 
certainty.  The  beginning  mental  disturbance  is  usually  more  apparent  to  the 
family  than  to  the  physician,  who  has  not  known  the  patient  before  and  who  sees 
him  only  cursorily,  but  it  is  apt  to  become  manifest  on  a  somewhat  more 
searching  examination  of  the  patient.  We  generally  succeed  best  by  making 
the  patient  reckon ;  he  often  makes  the  greatest  mistakes  in  simple  examples  in 
multiplication;  especially  does  he  fail  in  mental  arithmetic,  etc. 

Certain  motor  symptoms,  however,  which  usually  come  on  in  the  early  stages 
of  the  disease,  are  of  the  greatest  diagnostic  significance,  especially  peculiar  dis- 
turbances of  speech  and  handwriting.  The  paralytic  disturbance  of  speech  shows 
itself  first  in  the  form  of  stumbling  over  syllables  (Silbernstolpern) ,  or  literal 
ataxia.     The  individual  sound  (in  distinction  from  bulbar  paralysis)  can  be  pro- 


1132  DISEASES    OF    THE    NERVOUS    SYSTEM 

nounced  quite  correctly,  but  the  combination  of  different  sounds  in  tlie  whole 
word  causes  increasing  difficulties.  It  is  a  good  plan,  in  order  to  recognize  the 
first  beginnings  of  this  symptom,  to  have  the  patient  pronounce  a  few  difficult 
words,  such  as  "  third  riding  artillery  brigade,"  "  representative  government," 
"  initiative,"  "  electricity,"  etc.  We  often  hear  "  artralleriry "  instead  of 
"  artillery,"  and  like  blunders.  In  the  later  stages  of  the  disease  the  speech  is 
sometimes  almost  wholly  incomprehensible.  We  also  observe  other  more  compli- 
cated aphasic  disturbances,  such  as  paraphasia,  persistent  repetition  of  the  same 
word,  etc.  In  such  cases  the  patients  are  sometimes  no  longer  able  to  read  any 
sentence  correctly.  They  at  times  put  in  entirely  different  words,  so  as  to  make 
utter  nonsense;  but  they  do  not  notice  it  themselves.  The  abnormal  associated 
movements  of  the  facial  muscles  on  speaking  are  also  often  to  be  observed,  and  are 
very  characteristic.  The  voice  of  general  paralytics  often  loses  its  power  of 
modulation  and  becomes  weak  and  rough — symptoms  which  depend  upon  a  de- 
fective innervation  of  the  vocal  cords.  The  change  in  the  handwriting,  to  be 
observed  in  general  paralytics,  is  even  more  characteristic  than  the  disturbance 
of  speech  (see  Fig.  lYY).     This  is  at  first  purely  of  a  motor  nature;  the  letters  are 


'c/j^^^ufiS^i''^^^  ^^'^^^^2<^^^a4-t>^^ 


Fig.  177.— Examples  of  handwriting  in  general  paralysis.  Attempts  made  by  patients  in  the  Danvers 
Insane  Hospital  to  write  "God  save  the  Commonwealth  of  Massachusetts."  Besides  the  motor  dis- 
turbance, the  frequent  omission  of  certain  letters  will  be  noticed,  e.  g.,  "  Masschuetts  "  for  "  Massachu- 
setts."   In  3  and  4  the  handwriting  is  almost  wholly  illegible. 

uncertain,  irregular,  and  tremulous.  A  psychical  factor,  however,  also  shows 
itself;  single  letters  are  omitted,  the  dot  on  the  i  and  the  marks  of  punctuation 
are  forgotten,  the  patient  ceases  to  keep  on  the  lines,  or  leave  a  free  margin,  etc. 
As  the  disease  advances,  the  disturbance  in  the  handwriting  gradually  increases, 
so  that  the  writing  may  finally  become  wholly  illegible,  and  may  consist  merely 
of  senseless  scratches. 

Besides  the  changes  in  the  speech  and  the  handwriting,  Avhich  we  have  just 


PROGEESSIVE  GENERAL  PARALYSIS  OF  THE  INSANE  1133 

briefly  described,  other  physical  disturbances  are  often  quite  early  symptoms,  and 
prove  in  how  many  parts  of  the  nervous  system  at  once  the  disease  may  begin  its 
work  of  destruction.  The  condition  of  the  pupils  especially  is  of  importance  in 
diagnosis.  They  are  often  unequal,  and  also  show  a  reflex  immobility  (see  page 
972)  in  a  large  number  of  cases,  especially  in  those  in  which  other  tabetic  symp- 
toms develoiD  (vide  infra).  Transitory  ocular  paralyses  are  at  times  early  symp- 
toms. Not  infrequently  we  find  quite  early  changes  in  the  tendon  reflexes,  very 
often  a  decided  increase  of  the  patellar  reflex,  or,  in  other  cases,  absence  of  the 
patellar  reflex,  which  latter  has  a  much  more  positive  value  in  diagnosis — it  is 
almost  invariably  a  tabetic  symptom  (vide  infra). 

The  association  of  reflex  immobility  of  the  pupils  with  an  increase  of  the 
patellar  reflex  is  not  uncommon.  In  the  distribution  of  the  sensory  nerves  we 
may  mention  as  repeatedly  observed  symptoms,  neuralgia,  attacks  of  migraine, 
and  finally  optic  atrophy,  the  latter  usually  as  one  symptom  of  a  co-existing 
tabes. 

We  can  not  give  a  generally  applicable  account  of  the  further  course  of  general 
paralysis,  since  it  may  differ  decidedly  in  this  respect.  In  what  follows  we  can 
point  out  only  the  main  features  of  the  different  types  of  the  disease,  and,  in 
particular,  we  will  sketch  very  briefly  the  groups  of  mental  symptoms. 

We  often  say  that  those  cases  belong  to  the  "  classical  form  "  of  general  paraly- 
sis where  an  initial  "  stage  of  depression  "  with  a  melancholy  tendency  is  followed 
by  a  second  stage  of  "  maniacal  exaltation."  This  is  the  stage  where  the  de- 
lusions, which  are  already  quite  pronounced,  assume  more  and  more  the  character 
of  "  grand  ideas,"  and  thus  exhibit  the  "  delusions  of  grandeur  "  which  have  for  a 
long  time  been  generally  regarded  as  ominous.  The  first  signs  are  often  found  in 
the  patient's  statements  that  he  is  now  much  better,  that  he  is  "  very  well,"  that 
he  feels  "  very  strong,"  etc.  These  delusions,  however,  often  assume  gradually  a 
more  exaggerated  form;  the  patient  considers  himself  enormously  rich,  he  owns 
thousands  of  palaces,  millions  of  dollars,  has  made  the  greatest  inventions,  con- 
siders himself  the  Emperor  Napoleon,  Christ,  a  "  higher  God,"  etc.  Any  judg- 
ment as  to  the  absurdity  of  these  ideas,  and  as  to  the  sad  contrast  between  his 
claims  and  the  reality,  has  already  become  impossible  to  him ;  but,  of  course,  there 
are  even  now  occasional  remissions  in  this  condition,  when  the  patient  is  clearei 
and  recognizes  temporarily  the  morbid  character  of  his  delusions. 

We  must  not  think,  however,  by  any  means,  that  the  delusion  of  grandeur  is 
necessarily  an  invariable  symptom  in  general  paralysis.  In  many  cases  (the  so- 
called  "  depressive  "  form  of  general  paralysis)  the  initial  melancholic-hypochon- 
driacal  condition  continues.  The  delusions  that  appear  possess  the  same  color- 
ing; the  patient  claims  that  he  can  no  longer  eat,  that  he  is  poisoned,  that  he 
has  lost  his  head  or  an  arm,  that  he  is  very  small  ("  delire  micromaniaque  "),  etc. 
Sometimes  acute  and  severe  conditions  of  anxiety  come  on.  In  other  cases,  again 
(the  agitated  or  maniacal  form  of  general  paralysis),  there  are  states  of  violent 
excitement,  in  which  the  patient  raves  loudly,  cries,  and  tries  to  destroy  whatever 
falls  in  his  way.  Such  states  sometimes  alternate  with  delusions  of  grandeur. 
Finally,  we  see  cases  of  patients — and  this  is  the  most  frequent  form — who,  in 
their  mental  relations,  present  simply  the  symptoms  of  a  mental  enfeeblement 
gradually  increasing  to  complete  dementia,  without  ever  showing,  in  any  notable 
form,  states  of  excitement,  the  development  of  delusions,  etc. 

While  the  intellectual  life  progresses  to  utter  ruin  in  the  ways  just  stated, 
the  physical  disturbances  of  the  disease,  as  a  rule,  gradually  advance  from  bad 
to  worse.  In  many  cases  ataxia  of  the  extremities  develops,  and  also  loss  of 
sensibility  and  vesical  disturbances — in  short,  the  symptoms  of  tabes.  In  these 
cases  the  tendon  reflexes  are  almost  alwa.ys  lost,  and  the  pupils  are  often  immobile. 
In  other  rarer  cases,  however,  there  is  actual  paralysis,  first  in  the  lower  and  then 


1134  DISEASES    OF   THE   NEEVOUS    SYSTEM 

in  the  upper  extremities.  In  these  cases  the  tendon  reflexes  are  often  increased, 
so  that  the  picture  of  "  spastic  paralysis  "  develops.  Again,  in  other  cases  bulbar 
symptoms  appear,  such  as  disturbances  in  swallowing  or  masticatory  paralysis, 
and  also  ocular  paralyses,  usually  as  a  part  of  the  tabetic  symptom-complex,  etc. 

Peculiar  attacks,  which  are  among  the  commonest  and  most  characteristic 
symptoms  of  general  paralysis,  are,  however,  of  special  interest,  and  sometimes 
even  of  marked  importance  in  diagnosis.  These  "  paralytic  attacks "  in  their 
milder  degrees  sometimes  appear  even  in  comparatively  early  stages  of  the  dis- 
ease. Then  they  usually  consist  of  attacks  of  vertigo,  an  obscuring  of  conscious- 
ness, or  even  a  loss  of  consciousness,  coming  on  quite  suddenly,  and  lasting  from 
a  few  minutes  to  half  an  hour  or  more,  and  they  are  not  infrequently  associated 
with  mild  hemiplegic  or  monoplegic  symptoms.  We  very  often  see,  besides  the 
vertigo,  a  temporary  feeling  of  weakness  in  the  right  arm,  associated  with  a 
marked  aphasic  disturbance  of  speech.  To  this  there  is  often  added  some  slight 
twitching  in  the  affected  extremities  or  in  the  face.  In  the  further  course  of  the 
disease  the  attacks  usually  increase,  and  are  termed  apoplectiform  or  epileptiform 
paralytic  attacks,  according  as  the  conditions  of  paralysis  or  spasm  predominate. 
The  epileptiform  attacks  may  often  be  repeated  with  great  frequency — thirty  or 
forty  attacks  a  day  or  more — during  which  time  the  patient  remains  in  an  uncon- 
scious state.  If  the  patients  gradually  return  to  consciousness,  sometimes  only 
after  a  week  or  two,  we  very  often  see,  as  a  result  of  such  severe  attacks,  a 
permanent  impairment  of  the  general  condition,  an  increase  of  the  dementia,  etc. 

The  other  organs,  apart  from  the  nervous  system,  are  only  secondarily  impli- 
cated in  the  morbid  process.  It  may  be  mentioned  briefly  here  that  formerly,  for 
a  long  time,  stress  was  laid  upon  certain  changes  in  the  pulse,  the  pulsus  tardus 
especially  being  thought  to  be  characteristic ;  but  the  numerous  investigations  of 
the  pulse  have  so  far  not  given  us  any  significant  or  sure  results. 

The  temperature  as  a  rule  is  approximately  normal,  or  often  somewhat  sub- 
normal, but  very  marked  changes  in  the  temperature  occur  in  connection  with 
the  paralytic  attacks — sometimes  elevations  and  sometimes  very  deep  declines. 

The  whole  duration  of  the  disease  is  in  some  cases  only  a  few  months  (the 
"  galloping  "  form  of  general  paralysis),  usually  it  is  two  or  three  years,  and  some- 
times much  more.  The  most  rapidly  fatal  form  is  that  in  which  there  is  very 
soon  a  marked  emaciation  and  a  rapid  loss  of  strength  as  a  result  of  the  sleepless- 
ness, the  constant  unrest,  and  the  refusal  of  food.  In  other  cases  death  ensues 
from  the  gradual  and  general  loss  of  strength,  or  in  a  paralytic  attack ;  or,  finally, 
as  is  frequently  the  case,  from  the  onset  of  secondary  conditions,  such  as  severe 
bedsores,  pyelo-cystitis,  tuberculosis,  intestinal  diseases,  etc. 

Pathological  Anatomy  and  Nature  of  the  Disease. — Considering  the  great 
difficulty  of  an  accurate  microscopic  examination  of  the  brain,  it  is  not  strange 
that  our  knowledge  of  the  pathological  anatomy  of  general  paralysis  is  still  very 
defective.  If  we  except  occasional  immaterial  changes  in  the  skull,  such  as 
hyperostoses  and  the  like,  or  in  the  meninges,  such  as  hs?.matoma  of  the  dura  or 
secondary  thickening  of  the  pia  over  atrophied  portions  of  the  brain,*  the  first 
striking  and  at  any  rate  most  important  anomaly  seems  to  be  the  atrophy  of  the 
brain  which  affects  chiefly  the  anterior  half,  especially  the  frontal  lobes.  In  this 
region  the  convolutions  are  very  much  diminished,  and  the  fissures  are  wide; 
the  weight  of  the  anterior  portion  of  the  brain  may  be  reduced  to  one  fourth  or 
one  third  of  the  normal.  If  we  examine  the  convolutions  microscopically  we  find 
that  the  diminution  of  the  whole  organ  depends  chiefly  upon  a  loss  of  nervous 
elements.     The  cortex  usually  shows  the  greatest  changes.     In  fresh  cases  we 

*  [An  adhesion  of  the  pia  mater  to  the  brain  substance  is  very  characteristic.  This  adhesion  may  be 
so  firm  that  bits  of  the  cortex  are  torn  away  on  endeavoring  to  separate  the  pia  from  the  brain. — K.] 


PROGEESSIVE   GEXEEAL  PARALYSIS   OF  THE  D^SAXE     1135 

sometimes  see  the  signs  of  a  mild  "  inflammation  " — that  is,  we  find  vascular  dila- 
tation and  little  disseminated  foci  of  round  cells  about  the  vessels,  but  the  changes 
in  the  nervous  elements  themselves  are  far  more  important,  and  consist  essen- 
tially of  a  degenerative  atrophy.  We  must  mention  especially  that  in  the  cortex 
of  the  frontal  lobes,  especially  marked  in  the  straight  convolution  and  in  the 
island  of  Reil,  and  also  in  other  portions,  we  can  make  out  with  certainty,  by  the 
aid  of  good  methods  of  examination,  a  very  considerable  loss  of  the  fine  medullary 
nerve-fibers,  mainly  those  which  run  parallel  with  the  surface,  and  hence  are 
termed  "  association-fibers  "  (Tuczek)  ;  but  signs  of  degeneration  and  atrophy  are 
very  often  to  be  seen  in  the  ganglion-cells  themselves.  The  destruction  of  the 
nervous  elements  is  regarded  by  many  investigators  as  secondary,  since  they  lay 
the  chief  stress  upon  the  marked  changes  in  the  interstitial  tissue,  numerous 
spider-cells,  or  thickening  of  the  vascular  walls,  which  are  almost  always  to  be 
found  in  old  cases,  and  hence  they  speak  of  an  interstitial  encephalitis  (Mendel). 
We  ourselves,  with  Tuczek,  Wernicke,  and  others,  are  much  more  inclined  to  the 
theory  that  we  have  to  do  mainly  with  a  primary  process  of  degenerative  atrophy 
of  the  nerve-fibers  and  nerve-cells,  to  which  the  increase  of  the  connective  tissue 
is  only  a  secondary  addition. 

The  anatomical  affection  in  general  paralysis,  moreover,  is  by  no  means  limited 
to  the  cerebral  cortex.  We  can  often  make  out  the  loss  of  fibers  in  the  deeper 
parts  also,  in  the  white  substance,  and  the  central  ganglia.  The  co-existing 
changes  in  the  spinal  cord,  first  accurately  described  by  Westphal,  and  since  then 
recognized  as  almost  constant,  are  of  especial  interest.  They  usvially  consist  of 
fascicular  systemic  degeneration  of  the  lateral  columns  (the  pyramidal  tract),  or 
the  posterior  columns.  A  large  part  of  the  physical  disturbances  of  general  para- 
lytics, such  as  tabetic  symptoms  or  spastic  paralysis  (vide  supra),  are  certainly 
due  not  to  the  cerebral  disease,  but  to  these  accompanying  changes  in  the  spinal 
cord. 

Accordingly,  we  believe  that,  on  the  basis  of  our  present  knowledge,  we  can 
best  conceive  the  nature  of  general  paralysis  in  the  following  way :  By  the  action 
of  certain  injurious  influences,  which  usually  seem  to  stand  in  some  connection 
with  syphilis  (see  page  961),  there  is  a  gradually  progressive  destruction  of  nerve- 
tissue  in  the  most  diverse  portions  of  the  nervous  system.  The  clinical  symptoms 
must  naturally  differ  according  to  the  significance  and  function  of  the  affected 
fibers  or  cells.  As  a  rule,  certain  cortical  regions  of  the  cerebrum  are  first  dis- 
eased. The  disturbances  of  speech  are  probably  dependent  upon  the  loss  of  fibers 
in  the  left  island  of  Reil,  the  disturbances  of  intelligence  upon  the  destruction  of 
fibers  in  the  cortex.  We  may  also  make  out  corresponding  anatomical  changes, 
either  cerebral  or  spinal,  as  an  explanation  of  the  later  motor,  tabetic,  and 
other  symptoms ;  but  in  many  cases  the  order  in  which  the  different  sections  are 
affected  varies  considerably.  We  have  seen  in  a  previous  section  (see  page  976) 
that  the  whole  process  may  begin  with  a  spinal  disease,  especially  tabes  dorsalis, 
to  which  the  paralysis  is  "added"  later;  but  we  must  understand  that  the  two 
conditions  are  wholly  analogous  to  and  co-ordinate  with  each  other.  Both  are 
parts  of  the  same  degenerative  process,  which  can  accomplish  its  work  of  de- 
struction in  the  most  diverse  regions  of  the  nervous  system. 

ISTo  coarse  anatomical  lesions  can  be  made  out,  as  a  rule,  to  explain  the  para- 
lytic attacks,  but  it  is  very  probable  that  they  depend,  at  least  in  great  part,  upon 
the  changes  in  the  motor  central  convolutions. 

Diagnosis. — Since  the  diagnosis  of  beginning  general  paralysis  is  of  the  great- 
est practical  importance,  we  will  once  more  mention  briefly  all  those  symptoms 
which  are  especially  to  be  considered  in  diagnosis :  Striking  alteration  in  the 
nature  and  the  behavior,  rapid  and  motiveless  change  in  the  disposition,  dis- 
turbances of  memory,  loss  of  intelligence  (failures  in  reckoning,  etc.),  the  char- 


1136  DISEASES    OF   THE   NERVOUS    SYSTEM 

acteristic  changes  in  the  speech  and  handwriting,  and  finally  the  co-existing 
somatic  symptoms:  inequality  of  the  pupils,  immobility  of  the  pupils,  loss,  or, 
more  rarely,  increase  of  the  tendon  reflexes,  and  mild  paralytic  attacks,  such  as 
vertigo,  disturbance  of  speech,  temporary  disturbance  of  motion  in  one  arm,  etc. 

We  would  also  mention,  as  especially  common  and  disastrous  mistakes,  that 
the  symptoms  of  general  paralysis  are  often  misunderstood  at  first,  and  are  re- 
garded as  the  signs  of  immorality,  the  failure  of  the  sense  of  duty,  etc.  It  also 
frequently  happens  that  general  paralysis  is  at  first  regarded  as  simple  neuras- 
thenia or  hypochondriasis,  and  treated  accordingly. 

As  a  rule,  general  paralysis  can  be  certainly  distinguished  from  other  organic 
nervous  diseases  by  careful  attention;  but  of  course  we  must  add  that  in  some 
cases  cerebral  tumors,  gummatous  processes,  and  especially  certain  cases  of  multi- 
ple sclerosis,  may  show  a  type  of  disease  very  like  general  paralysis.  We  should 
also  remember  that  gummatous  syphilis  may  be  combined  with  genuine  par- 
alytic symptoms  (vide  page  1128). 

Prognosis. — The  prognosis  of  general  paralysis,  like  that  of  all  chronic  degen- 
erative conditions  of  the  central  nervous  system,  is  wholly  unfavorable.  At  pres- 
ent we  know  of  only  a  small  and  decreasing  number  of  (doubtful)  recoveries,  but 
there  are  many  cases  where  there  is  a  temporary  improvement  in  the  condition,  a 
"  remission,"  sometimes  of  a  considerable  degree  and  lasting  a  long  time.  The 
earlier  the  patient  comes  under  proper  care  and  treatment  the  sooner  may  we  hope 
for  such  a  favorable  turn.  Of  course,  as  we  have  said,  relapses  of  the  disease  al- 
most always  come  on  later.  Those  cases  especially  are  to  be  regarded  as  un- 
favorable in  which  frequent  paralytic  attacks  come  on  early,  in  which  other 
physical  symptoms,  especially  of  a  spinal  nature,  soon  set  in,  and  in  which  the 
whole  nutrition  of  the  body  rapidly  suffers. 

Treatment.— -As  soon  as  the  disease  is  recognized,  the  first  and  imperatively 
necessary  injunction  must  be  to  remove  the  patient  from  all  physical  and  intel- 
lectual exertion  as  well  as  from  all  mental  excitement.  The  patient  must  there- 
fore, if  possible,  withdraw  from  business,  which  up  to  that  time  he  may  have  tried 
to  carry  on.  His  methods  of  life  and  his  diet  must  be  regulated,  and  every  excess 
must  be  forbidden.  For  the  cases  which  even  at  first  are  associated  with  states 
of  great  mental  excitement,  the  commitment  to  a  proper  asylum  is  often  most 
urgently  to  be  recommended,  while  for  cases  that  during  their  course  show  simple 
mental  weakness,  care  at  home  is  often  sufficient.  Only  by  a  timely  recognition 
of  the  disease  and  by  adopting  the  appropriate  measures  can  the  patient's  relatives 
be  spared  the  many  disagreeable  experiences  which  would  otherwise  undoubtedly 
ensue. 

In  regard  to  the  treatment  of  the  disease  itself,  we  should  advise  inunction 
with  mercurial  ointment,  especially  if  we  can  discover  a  previous  syphilitic  infec- 
tion. As  a  rule,  we  ought  not  to  expect  much  success  from  this  any  more  than 
in  tabes  (see  page  978),  but  we  may  perhaps  check  the  advance  of  the  disease. 
We  should  therefore  try  the  antisyphilitic  treatment  chiefly  in  the  initial  stages 
of  the  disease,  and  also  in  the  cases  where  the  suspicion  that  there  is  also  gum- 
matous syphilis  is  justified.  We  may  combine  the  internal  use  of  iodide  of 
potassium  with  the  inunction. 

Furthermore,  we  should  try  tepid  baths,  with  cool  sponging,  and  also  a  cautious 
application  of  electricity  (galvanization  of  the  head  and  spinal  cord),  and  pre-' 
scribe  internal  remedies,  especially  ergotine.    We  need  not  go  more  fully  here  into 
the  numerous  symptomatic  details. 


CHKONIC   HYDEOCEPHALUS  113Y 

CHAPTEE   X 
CHRONIC    HYDROCEPHALUS 

j5]tiology  and  Patholog-y. — Eepeated  mention  has  been  made  in  preceding 
chapters  of  the  occurrence  of  dropsy  in  the  ventricles  as  a  sequel  to  other  cerebral 
diseases,  such  as  meningitis  and  tumors.  Besides  this  "  secondary  hydro- 
cephalus," a  collection  of  fluid  in  the  ventricles  may  be  a  symptom  of  an  appar- 
ently idiopathic  primary  disease.  This  is  observed  most  of  all  in  the  newborn, 
or  at  least  in  young  children. 

Little  is  known  with  certainty  about  the  causes  of  chronic  hydrocephalus.  The 
assumption  is  very  frequently  made  that  the  condition  is  the  result  of  an  inflam- 
mation of  the  ependyma  of  the  ventricle,  which  itself  occurs  either  before  birth  or 
very  soon  after,  but  the  autopsy  often  fails  to  support  this  idea.  Our  knowledge 
is  equally  uncertain  as  to  the  existence  of  a  stasis  due  to  mechanical  obstruction 
(obliteration  of  the  foramen  of  Magendie,  etc.).  Syphilis,  drunkenness  in  the 
progenitors,  etc.,  have  been  regarded  as  predisposing  causes;  whether  justly  or 
not,  is  uncertain.  It  has  been  repeatedly  observed  that  the  disease  has  attacked 
several  children  of  a  single  family. 

The  most  important  physical  sign  of  hydrocephalus  in  children  is  enlargement 
of  the  head.  The  circumference  of  the  skull  may  even  in  the  first  year  of  life  be 
sixty  to  eighty  centimetres.  Usually  the  frontal  bones  and  the  parietal  eminences 
are  especially  prominent.  The  cranium  becomes  gradually  almost  as  thin  and 
translucent  as  paper.  The  fontanelles  and  sutures  gape  widely.  The  brain  is 
flattened  out,  so  as  to  seem  almost  like  a  bag,  filled  with  the  hydrocephalic  fluid. 
In  well-marked  cases  the  entire  thickness  of  the  hemispheres  is  frequently  not 
more  than  an  inch.  The  space  within,  containing  the  serous  effusion,  represents 
the  enormously  distended  ventricles,  particularly  the  lateral  ventricles,  although 
the  third  and  foiirth  ventricles  are  quite  often  distended  also.  The  walls  of  the 
ventricles  are  often  strewn  with  minute  granulations,  or  they  present  a  reticular 
liypertrophy.  The  hydrocephalic  fluid  usually  has  the  appearance  of  colorless 
serum,  and  contains  a  very  slight  amount  of  albumen,  if  any.  The  specific  grav- 
ity is  about  1004  to  1006.  The  amount  of  fluid  may  be  a  quart  or  more;  but,  of 
•course,  there  is  a  great  variation  in  this  respect  in  different  cases. 

Congenital  hydrocephalus  is  often  associated  with  other  peculiarities  or  de- 
fects in  the  structure  of  the  brain,  which  we  can  not  mention  here. 

Clinical  History. — Sometimes  a  child  is  born  with  hydrocephalus  so  far  devel- 
oped as  to  occasion  dystocia.  Usually,  however,  the  parents  notice  nothing  pecul- 
iar about  the  child  for  some  weeks.  Then  they  are  alarmed  by  the  gradual  swell- 
ing of  the  head.  As  a  basis  for  determining  abnormal  size,  we  may  mention  that 
under  normal  conditions  the  circumference  of  the  head  at  birth  is  about  thirty-five 
to  forty  centimetres,  at  the  end  of  a  year  about  forty-five  centimetres,  and  from 
that  age  to  puberty  there  is  a  gradual  approach  to  a  circumference  of  about  fifty 
centimetres.  The  possible  dimensions  in  chronic  hydrocephnlus  have  been  already 
stated.  The  increase  in  circumference  is  often  quite  rapid,  amounting  in  a 
fortnight  or  three  weeks  to  one  or  two  centimetres.  Usually  the  swelling  is  tol- 
erably symmetrical ;  but  sometimes  the  greater  increase  is  in  the  antero-posterior 
diameter,  making  the  skull  dolichocephalic.  At  times  the  rate  of  expansion  may 
be  particularly  rapid,  and  then  at  other  times  it  may  seem  to  be  suspended.  That 
the  fontanelles  and  sutures  remain  widely  open  has  already  been  mentioned; 
sometimes  it  is  even  possible  to  get  fluctuation  through  them.  An  intravascular 
murmur  can  now  and  then  be  heard  in  the  head,  but  it  has  no  great  importance 
with  regard  to  diagnosis.     The  veins  are  often  so  greatly  distended  as  to  form 

72 


1138  DISEASES    OF   THE   NEEVOUS    SYSTEM 

a  bluish  network  underneath  the  scalp.  The  face  remains  small,  in  striking  con- 
trast with  the  great,  heavy  cranial  portion  of  the  head.  The  head  almost  always 
hangs  over  forward,  from  its  own  weight.  The  eyes  generally  look  down,  partly  be- 
cause the  roof  of  the  orbit  is  depressed,  and  partly  because  of  impairment  of  the 
nervous  supply  to  the  motores  oculi. 

A  very  important  symptom  is  the  defective  intellectual  development  of  hydro- 
cephalic children.  They  can  not  learn  to  talk  well,  if  at  all.  If  they  play,  it 
is  in  a  silly  manner.  They  can  not  concentrate  their  attention  upon  anything, 
and  they  are  heedless  and  dirty.  It  must,  however,  be  mentioned  that  sometimes, 
in  spite  of  considerable  hydrocephalus,  the  patient  now  and  then  evinces  an  unex- 
pected activity  of  mind — thus,  he  gradually  becomes  able  to  distinguish  the  differ- 
ent objects  and  individuals  about  him. 

There  is  almost  invariably  motor  disturbance  also.  The  legs,  more  rarely  the 
arms,  are  decidedly  paretic,  or  there  may  be  even  complete  paraplegia.  There  are 
iisually  spastic  symptoms  and  increased  tendon  reflexes.  Few  patients  learn  to 
walk  or  stand  alone.  The  arms  seldom  present  any  great  paresis,  but  their  move- 
ments often  betray  an  awkwardness  and  uncertainty  suggestive  of  ataxia.  It  is 
noteworthy  that  sensation  almost  always  remains  intact;  at  least  the  patient 
reacts  vigorously  to  the  prick  of  a  pin,  etc.  Of  the  special  senses,  sight  is  most 
frequently  affected ;  choked  disk  and  atrophy  of  the  optic  nerve  have  been  observed 
repeatedly.  Symptoms  of  motor  irritation  are  of  very  frequent  occurrence,  such 
as  general  convulsions  and  spasm  of  the  glottis.  General  nutrition  is  pretty  well 
maintained  in  many  cases,  but,  as  a  rule,  hydrocephalic  children  are  atrophic  and 
ill  developed. 

The  chronic  hydrocephalus  of  children  almost  always  terminates  unfavorably. 
Only  a  few  patients  survive  the  fifth  year,  although  now  and  then  striking  excep- 
tions occur.  Death  is  generally  the  result  of  marasmus;  or  a  convulsive  seizure 
may  prove  fatal.  The  possibility  of  recovery  has  not  yet  been  demonstrated.  The 
progress  of  the  disease  may,  however,  be  arrested,  and  the  child  continue  for  years 
in  statu  quo. 

Hydrocephalus  in  adults  is  a  very  rare,  chronic,  and  apparently  idiopathic  dis- 
ease. Its  cause  again  is  assumed  to  be  chronic  inflammation  of  the  ventricular 
ependyma  (so-called  meningitis  serosa  ventriculorum) .  The  symptoms  are  some- 
times very  like  those  of  a  tumor  of  the  brain  (with  predominant  general  symp- 
toms), and  sometimes  there  is  a  remarkable  absence  of  characteristic  cerebral 
disturbance,  except  that  spastic  paralysis  of  the  extremities  (compare  page  1012) 
is  gradually  developed. 

Diagnosis. — A  pronounced  case  of  congenital  hydrocephalus  can  be  recognized 
without  difiieulty,  inasmuch  as  the  excessive  size  of  the  head  betrays  the  disease 
upon  the  first  glance.  Less  extreme  cases  may  indeed  be  somewhat  obscure,  and 
we  have  especially  to  avoid  confounding  the  condition  in  question  with  rachitic 
enlargement  of  the  skull.  We  should  always,  therefore,  take  into  consideration 
the  intellectual  powers,  the  presence  or  absence  of  motor  disturbances,  and  other 
similar  symptoms,  as  well  as  the  cranial  peculiarities.  In  the  hydrocephalus  of 
adults  there  is  often  no  enlargement  whatever,  so  that  a  diagnosis  can  hardly  ever 
be  made  positively. 

Treatment. — Thus  far,  no  remedy  has  been  applied  with  success  in  chronic 
hydrocephalus.  The  following  may  be  tried:  Applications  of  mercurial  oint- 
ment and  of  tincture  of  iodine  to  the  scalp,  methodical  compression  of  the  skull, 
and  iodide  of  potassium  internally.  The  hydrocephalic  fluid  has  often  been  drawn 
off,  to  a  certain  extent,  by  tapping,  but  only  rarely  with  permanent  success,  and 
usually  with  merely  temporary  benefit,  if  any.  Quincke  was  the  first  to  suggest 
drawing  off  the  hydrocephalic  fluid  by  so-called  lumbar  puncture ;  that  is,  puncture 
of  the  vertebral  canal.     This  can  be  done  most  easily  in  the  region  of  the  second,. 


MENIERE'S  DISEASE  1139 

third,  or  fourth  lumbar  vertebra.     Some  favorable  results  from  this  method  have 
been   reported. 

Jn  most  eases  we  confine  ourselves  to  purely  symptomatic  treatment,  and  to 
recommending  intelligent  care  for  the  child. 


CHAPTEE   XI 

MENIERE'S    DISEASE 

(  Vertigo  ab  aure  Icesa.     Labyrinthine  Ve?'tigo) 

In  1861,  Meniere,  a  French  physician,  first  called  attention  to  a  peculiar  affec- 
tion which  may  be  apparently  primary  or  may  result  from  chronic  aural  disease 
and  which  is  characterized  mainly  by  excessive  vertigo  and  loud  tinnitus  aurium. 
At  first  the  symptoms  appear  in  distinct  paroxysms.  These  are  ushered  in  by  a 
shrill  ringing  in  the  ears,  which  is  often  compared  to  the  whistling  of  a  locomotive, 
and  which  is  perceived  in  but  one  ear.  At  the  same  time,  or  shortly  after,  comes  on 
a  very  pronounced  dizziness,  of  a  unique  sort.  The  patient  has  a  feeling  as  if  his 
whole  body  were  moving,  as  if  he  were  falling  forward  or  were  whirling  around. 
Consciousness  is  unimpaired,  but  the  patient  feels  wretched,  the  skin  is  pale  and 
cool,  and  the  face  is  bathed  in  cold  perspiration.  Frequently  there  is  vomiting 
toward  the  close  of  the  attack.  The  first  paroxysms  are  of  brief  duration.  As 
the  disease  progresses  the  attacks  become  more  and  more  frequent,  and  at  last 
the  vertigo  may  be  constant,  being  extremely  annoying  to  the  patient  and  perhaps 
confining  him  to  bed.  Even  now  there  are  occasional  paroxysmal  exacerbations 
of  the  disorder,  usually  ushered  in  by  the  shrill  tinnitus.  The  tokens  of  chronic 
aural  disease  on  one  side,  or  less  frequently  on  both  sides,  also  persist.  Some- 
times there  is  purulent  otorrhoea ;  often  the  aural  speculum  reveals  lesions  of 
the  drum  or  of  the  middle  ear ;  and  almost  invariably  there  is  more  or  less  deaf- 
ness on  the  affected  side.  This  condition  may  persist  for  years,  until  finally  it 
ceases  of  its  own  accord,  after  the  deafness  on  that  side  becomes  complete. 

The  apoplectiform  occurrence  of  Meniere's  symptom-complex  in  persons  whose 
ears  were  previously  healthy  is  especially  characteristic  and  interesting,  but  very 
rare.  The  disease  begins  suddenly,  or  at  least  very  acutely,  with  an  attack  of  ver- 
tigo or  with  loss  of  consciousness.  In  a  very  short  time  total  deafness  sets  in, 
with  extreme  tinnitus,  vertigo,  and,  as  we  have  seen  in  one  case,  a  very  unsteady 
gait  (as  in  cerebellar  ataxia).  In  such  cases  we  may  suspect  an  effusion  of  blood 
into  the  labyrinth ;  but  there  may  also  be,  perhaps,  an  acute  inflammatory  process. 
Later  the  symptoms  may  gradually  become  less  severe,  but  there  is  hardly  ever 
complete  recovery. 

We  possess  scanty  information  as  to  the  origin  of  these  subjective  phenomena. 
That  they  are  due  to  a  disease  of  the  internal  ear  (labyrinth)  can  scarcely  be 
doubted ;  and  it  is  further  probable  that  in  every  case  the  vestibular  nerve  and  the 
semicircular  canals  are  involved.  ISTumerous  experimental  investigations  have 
demonstrated  that  these  last-named  structures  bear  a  part  in  maintaining  the 
equilibrium  of  the  body.  Acquaintance  with  this  variety  of  vertigo  is  valuable 
to  a  nervous  specialist,  inasmuch  as  Meniere's  disease  has  been  more  than  once 
confounded  with  epilepsy  or  disease  of  the  cerebellum  and  other  parts  of  the 
brain.  On  the  other  hand,  of  course,  we  must  also  add  that  purely  neurasthenic 
and  hysterical  conditions  may  sometimes  simulate  the  type  of  Meniere's  disease 
very  perfectly,  so  that  a  correct  diagnosis  often  can  not  be  made  until  the 
patient  has  been  carefully  observed  for  a  long  time. 


1140  DISEASES    OE   THE   NEEVOUS    SYSTEM 

Treatment  is  not  wholly  unavailing.  Charcot  has  discovered  that  the  persist- 
ent use  of  quinine  gives  great  relief — at  least  in  many  cases — and  it  may  even  com- 
pletely cure  the  disease.  Eight  to  fifteen  grains  (gramme  0.5-1)  of  quinine 
should  be  given  daily,  in  two  or  three  doses,  and  continued  for  at  least  several 
weeks.  Persevering  galvanic  treatment  (anode  to  the  ear,  cathode  to  the  back  of 
the  neck)  also  seems  to  us  to  be  at  times  of  decided  service.  The  particulars  of 
such  special  treatment  of  the  ear  as  may  be  necessary  must  be  sought  elsewhere. 


EPILEPSY  1141 


VI.— NEUROSES   WITHOUT    KNOWN   ANATOMICAL 

BASIS 


CHAPTEK  I 

EPILEPSY 

{Fallwg  Sickness.     Morbus  sacer) 

Etiology. — Epilepsy  is  a  peculiar  disease  of  rather  frequent  occurrence,  the 
main  symptom  of  which  is  paroxysmal  loss  of  consciousness.  In  typical  cases 
the  unconsciousness  is  associated  with  violent  general  convulsions ;  but  there  are 
many  anomalous  and  rudimentary  forms  of  epilepsy  without  any  symptoms  of 
motor  irritation.  "  Genuine  epilepsy  "  is  a  functional  neurosis — that  is,  with  our 
present  means  of  investigation  we  can 'discover  no  constant  objective  lesion  of  the 
nervous  system  as  its  basis.  It  is,  indeed,  true  that  attacks  similar  to  those  of 
true  epilepsy  not  infrequently  occur  in  the  course  of  tumor,  syphilis,  and  other 
diseases  which  do  present  an  anatomical  lesion ;  but  such  attacks  are  merely  symp- 
tomatic, and  are  therefore  termed  "  epileptiform,"  in  distinction  from  the  genuine 
epileptic  paroxysms. 

Of  the  actual  causes  of  epilepsy  we  know  nothing.  We  are  acquainted  only 
with  certain  factors  which  are  favorable  to  the  development  of  the  disease,  and  are 
to  be  regarded,  therefore,  as  predisposing  or  exciting  causes.  Heredity  is  decid- 
edly the  most  important  of  these.  About  one  third  of  all  cases  of  epilepsy  occur 
in  persons  who  have  inherited  a  nervous  diathesis,  and  one  or  more  of  whose  blood- 
relations  have  suffered  from  diseases  of  the  nervous  system.  It  should  not  be 
understood  that  we  must  find  other  cases  of  genuine  epilepsy  in  the  family,  in 
order  to  establish  the  fact  of  congenital  predisposition.  The  question  is  merely 
whether  the  ancestors  have  exhibited  a  general  tendency  to  nervous  disease.  The 
more  accurate  and  careful  our  investigations,  the  oftener  do  we  find  among  the 
relatives  of  the  patient  instances  of  nervous  trouble — sometimes  genuine  epilepsy, 
sometimes  insanity,  hysteria,  or  general  "  nervousness."  Of  course  these 
"  nervous  families  "  present,  besides  those  that  are  actually  ill,  others  who  are 
more  or  less  peculiar  and  odd,  and  yet  others  gifted  with  extraordinary  talents, 
although  frequently  somewhat  ill-balanced.  It  is  said  that  the  children  of  parents 
who  are  related  to  each  other  are  somewhat  predisposed  to  epilepsy,  as  well  as  to 
other  nervous  diseases;  but  certainly  this  factor  is  very  rarely  of  importance. 
Perhaps  drunkenness  in  the  parents  is  somewhat  more  prejudicial  in  this  regard. 
It  is  said  to  have  been  repeatedly  observed  that  children  begotten  while  the  father 
was  intoxicated  became  epileptic. 

There  are  other  influences  which  are  assumed  to  have  setiological  importance, 
but  whether  justly  or  not  is  difficult  to  decide.  Alcoholic  excesses  can  seldom  act 
in  this  way  (although  epilepsy  is  said  to  attack  absinthe-drinkers  in  France  quite 
frequently).  Venereal  excesses  probably  have  still  less  importance.  It  should 
also  be  borne  in  mind  that  not  infrequently  excesses  in  these  directions  are  the 
result  of  neurotic  tendencies  already  existing.  Syphilis  has  no  direct  connection 
with  genuine  epilepsy.  Epileptiform  convulsions  may,  as  we  have  seen,  be  symp- 
tomatic of  syphilis,  being  due  to  the  cerebral  lesion  caused  by  this  latter  disease. 
Certain  factors  may  determine  the  onset  of  epilepsy,  although  they  can  not  be 


1142  DISEASES    OF   THE   iN'EEVOUS    SYSTEM 

said  to  cause  the  disease  (except  the  symptomatic  epilepsy  which  develops  after 
a  previous  encephalitis).  Such  are  over-exertion  of  mind  or  body,  repeated  emo- 
tional disturbance,  certain  general  conditions  of  the  system,  such  as  anaemia  or 
malnutrition,  on  the  one  hand,  and  plethora  on  the  other;  and,  in  particular, 
acute  febrile  diseases,  such  as  scarlet  fever,  measles,  and  gastric  diseases.  [The 
individual  attack  is  often  brought  on  by  some  disturbance  of  digestion  or  indis- 
cretion in  diet. — K.]  Another  important  point  is  that  the  first  attack  is  some- 
times brought  on  by  great  mental  excitement,  especially  fright.  But  here,  too, 
it  is  probable  that  the  terror  is  merely  the  exciting  cause,  a  tendency  to  the  disease 
already  pre-existing.  "We  must  also  be  on  our  guard  against  confounding  genuine 
epilepsy  with  the  convulsive  form  of  hysteria  (g.  v.),  which  very  frequently  de- 
velops after  fright. 

In  some  instances  there  is  an  evident  connection  between  epilepsy  and  a  pre- 
vious injury  to  the  skull  at  birth  or  from  a  fall,  or  blow,  etc.  At  a  certain 
interval  after  the  trauma,  attacks  begin  which  seem  precisely  like  those  of  genu- 
ine epilepsy.  This  is  known  as  "  traumatic  epilepsy."  These  are  not  cases  of  genu- 
ine epilepsy,  however,  inasmuch  as  there  is  really  some  anatomical  lesion  of  the 
cortex  cerebri  which,  in  some  way  as  yet  unknown,  causes  irritation  of  the  motor 
centers  of  the  cortex  (vide  infra).  It  is  often  the  case  that  this  variety  of 
epileptiform  attacks  is  peculiar  in  that  the  convulsions  are  at  first  unilateral,  or 
confined  to  a  single  limb,  corresponding  to  the  seat  of  the  injury  in  the  opposite 
cerebral  hemisphere. 

"  Eeflex  epilepsy  "  remains  to  be  mentioned.  This  name  is  applied  to  cases 
where  each  convulsive  attack  seems  to  be  excited  by  reflex  influences  originating 
in  some  remote  part  of  the  body.  Most  cases  have  followed  injury  of  peripheral 
neiwe  trunks  (retained  splinters,  or  scars),  and  have  ceased  upon  removal  of 
the  exciting  cause.  Other  causes  are  new  growths  in  the  nerves,  foreign  bodies 
in  the  ear,  otitis,  intestinal  parasites,  and,  apparently,  diseases  of  the  female 
sexual  organs.  It  seems  probable  that  sufferers  from  these  attacks  have  had 
a  tendency  to  disease  of  the  nervous  system.  "We  must  hesitate  to  rank  re- 
flex epilepsy  in  the  same  class  with  the  genuine  form.  The  whole  subject  of 
"  reflex  epilepsy  "  needs  a  new  and  thorough  investigation.  It  has  been  in  the 
past  so  often  confounded  with  hysterical  ("  traumatic-hysterical ")  attacks,  that 
we  are  personally  disposed  to  doubt  the  occurrence  of  any  real  reflex  epilepsy. 

Both  the  traumatic  and  the  reflex  varieties  of  epilepsy  have  repeatedly  been 
the  object  of  experimental  investigation.  Brown-Sequard  has  shown,  by  a  great 
number  of  experiments,  that  epilepsy  can  be  excited  in  rabbits  by  injuries  to  the 
medulla,  the  spinal  cord,  and  the  sciatic,  as  well  as  other  peripheral  nerves.  A 
certain  time  after  the  operation  the  animals  undergo  spontaneous  convulsive 
paroxysms.  These  occur  at  frequent  intervals  and  for  a  long  time,  and  they  may 
be  voluntarily  excited  at  any  time  by  irritation  of  a  certain  portion  of  the  skin 
called  the  "epileptogenous  zone."  An  interesting  observation  in  this  connection 
has  been  made  by  Brown-Sequard,  which  is  that  sometimes  the  progeny  of  these 
animals,  who  have  been  made  epileptic,  suffer  from  spontaneous  epilepsy.  West- 
phal  induced  epilepsy  in  guinea-pigs  by  blows  upon  the  skull.  Immediately  after 
the  blow  general  convulsions  occurred,  but  soon  entirely  ceased.  Aftei-ward,  how- 
ever, there  were  repeated  epileptiform  attacks.  "Westphal  thought  that  the  causa- 
tive lesion  in  these  instances  was  the  minute  haemorrhages  which  were  found  in 
the  upper  part  of  the  cervical  division  of  the  cord  and  in  the  medulla. 

These  and  other  experiments,  which  will  be  spoken  of  later,  interesting  as  they 
may  be  in  themselves,  have  contributed  absolutely  nothing  to  our  knowledge  of 
genuine  epilepsy.  In  regard  to  the  latter  we  have  nothing  left  but  to  assume  that 
there  is  a  congenital,  abnormal  predisposition  of  the  brain,  and  especially  of  its 
motor  centers,  but  the  nature  of  this  predisposition  is  still  wholly  unknown. 


EPILEPSY  1143 

[Various  writers  have  maintained  that  the  epileptic  attack  was  due  to  an  accu- 
mulation of  toxic  products  in  the  blood — in  many  cases  an  auto-intoxication  f  rora 
intestinal  disturbances.  An  increase  in  the  toxicity  of  the  urine  has  been  noticed 
before  the  attack,  and  the  attack  may  sometimes  be  provoked  by  the  ingestion  of 
certain  toxic  substances.  The  toxic  origin  of  the  trouble,  however,  is  not  yet  estab- 
lished.—K.] 

Clinical  History. — In  describing  the  symptoms  of  epilepsy,  we  shall  first  con- 
sider the  various  forms  of  the  epileptic  paroxysm,  and  then  describe  the  general 
course  of  the  disease. 

1.  The  fully  developed  epileptic  paroxysm  is  usually  described,  for  the  sake 
of  greater  clearness,  as  made  up  of  several  stages.  First  is  the  prodromal  stage, 
or,  according  to  Galen's  expression,  still  in  vogue,  the  stage  of  the  epileptic  aura 
(awra  =  breath).  Xot  infrequently,  however,  there  is  no  aura  whatever,  the  con- 
vulsions coming  on  without  warning;  but  in  many  cases  the  prodromata  are 
well  marked,  and  are  repeated  with  noticeable  regularity  and  similarity  before 
each  individual  attack,  although  the  different  cases  of  epileiDsy  differ  greatly  as 
to  the  special  phenomena  of  the  aura  occurring  in  each. 

The  best  manner  in  which  to  distinguish  the  various  forms  of  aura  is  accord- 
ing to  the  nature  of  the  nervous  phenomena,  whether  sensory,  motor,  vaso-motor, 
or  psychical.  Of  these  the  most  frequent  is,  beyond  a  doubt,  the  sensory.  Here 
we  have  peculiar  parsesthesise,  beginning  in  the  arm  or  leg,  or  perhaps  in  the 
region  of  the  heart  or  stomach,  and  thence  usually  "  m.ounting  to  the  head."  It 
is  seldom  that  the  peculiar  sensation  is  actually  like  a  "  breath  "  or  puff  of  air. 
The  aura  whicjjpitjroceeds  from  the  epigastrium  is  sometimes  associated  with  a 
very  disagreeable  feeling  of  oppression  and  anxiety,  and  often  also  with  nausea 
and  vomiting.  The  aura  may  be  referred  to  the  nei-ves  of  special  sense.  In  cer- 
tain instances  the  patient  perceives  an  unpleasant  odor,  which  he  likens  to  some 
familiar  one.  An  aura  of  taste  also  occurs,  but  it  is  very  rare.  An  optical  aura 
is  much  more  frequent,  consisting  of  a  subjective  sensation  of  color  or  light  (usu- 
ally a  sensation  of  red  appears  first),  of  an  apparent  increase  or  diminution  of  the 
size  of  surrounding  objects,  or  finally  of  actual  hallucinations  of  vision,  such  as 
beholding  all  sorts  of  human  or  brute  shapes.  An  auditory  aura  is  not  very 
rare :  it  produces  a  sudden  feeling  of  deafness  in  one  ear,  or  various  subjective 
sounds,  like  whistling,  humming,  roaring,  etc. 

The  motor  aura  takes  the  form  of  mild  premonitory  contractions,  affecting  the 
head,  face,  arm,  or  leg.  There  may  be  aphasic  disturbance  at  the  same  time ;  or 
we  may  observe  symptoms  of  irritation  of  the  unstriped  muscles  (strangling,  or 
a  desire  to  go  to  stool).  Sometimes  there  are  prodromal  vaso-motor  phenomena, 
where  the  aura  consists  of  a  sensation  of  cold  or  warmth,  often  associated  with 
excessive  pallor  or  redness  of  the  face  or  hands.  An  attack  may  be  ushered  in  by 
chilliness,  perspiration,  or  palpitation. 

Finally,  the  name  of  psychical  aura  is  applied  to  those  initial  symptoms  which 
consist  of  vertigo,  confusion  of  thought,  or  other  pronounced  disorders  of  con- 
sciousness. A  particularly  frequent  form  for  this  to  assume  is  excessive  mental 
uneasiness  and  excitement.  We  may  also  add  that  various  forms  of  aura  are  not 
infrequently  seen  in  combination. 

The  aura  lasts  sometimes  only  a  few  seconds.  It  may  persist  long  enough  for 
the  patient,  who  knows  from  experience  what  is  coming,  to  lie  down  or  take 
other  precautionary  measures  (vide  infra).  In  some  few  cases  the  aura  may  last 
hours,  and  even  days.  This  is  especially  true  of  the  psychical  variety.  Some- 
times the  aura  passes  away  without  being  succeeded  by  any  true  epileptic  fit ;  but 
it  is  usually  followed  by  the  second  stage  of  the  attack — the  convulsive  stage. 

The  convulsive  stage  of  the  epileptic  attack  almost  invariably  begins  abruptly. 
Perhaps  there  is  no  aura,  or  only  a  very  brief  one,  before  the  patient  falls  suddenly 


1144  DISEASES    OF    THE   In'ERVOUS    SYSTEM 

to  the  ground,  usually  on  his  face,  although  sometimes  on  the  side  or  back.  Con- 
sciousness is  entirely  suspended.  Insensibility  is  complete,  and  often  the  patient 
sustains  severe  injury  from  his  fall.  Some  patients  utter  a  loud  "  epileptic  cry  " 
at. the  commencement  of  the  attack,  but  they  are  already  entirely  unconscious. 

The  convulsive  attack  begins  with  a  brief  period  of  general  tonic  spasm  of  the 
muscles.  The  head  is  usually  strongly  extended,  the  teeth  are  pressed  firmly 
together,  the  trunk  is  curved  backward  in  opisthotonos,  the  extremities  are  ex- 
tended, and  the  fingers  are  clenched  over  the  flexed  thumb.  Inasmuch  as  the 
respiratory  muscles  participate  in  the  seizure,  breathing  stops,  and  the  original 
pallor  of  the  face  soon  gives  place  to  deep  cyanosis.  This  general  tonic  convul- 
sion ordinarily  is  but  brief,  perhaps  fifteen  to  thirty  seconds.  It  is  followed  by 
the  second  period  of  the  convulsive  stage — that  of  the  clonic  convulsions.  The 
facial  muscles  now  exhibit  the  most  violent  contortions;  the  eyeballs  roll,  or  oc- 
casionally present  a  conjugate  deviation  toward  one  side;  the  tongue  is  thrust 
out  and  retracted  convulsively;  the  head  beats  violently  against  the  floor;  and 
the  muscles  of  the  arms,  legs,  and  trunk  undergo  the  severest  clonic  spasms.  The 
pupils  are  probably  contracted  for  a  short  time  at  first,  but  during  the  convulsive 
stage  they  are  widely  dilated  and  do  not  react  at  all.  The  pulse  is  somewhat  accel- 
erated, but  not  greatly.  The  temperature  is  normal,  or  elevated  a  small  fraction 
of  a  degree.  The  cutaneous  reflexes  are  still  suspended  directly  after  an  attack ; 
but  the  tendon  reflexes  are  generally  somewhat  exaggerated,  although  sometimes- 
they  also  are  diminished  or  absent.  Not  infrequently  an  involuntary  dejection 
takes  place  during  the  flt,  or  the  bladder  is  emptied;  and  in  men  there  may  be  a 
seminal  emission.  During  these  violent  convulsions  the  body  is  often  severely 
injured.  The  tongue  is  frequently  bitten.  The  face,  which  is  usually  pale  at  the 
beginning  of  the  attack,  becomes  extremely  cyanotic.  The  veins  in  the  neck  are 
distended,  and  the  venous  stasis  is  so  extreme  that  sometimes  minute  hsemor- 
rhages  occur  into  the  conjunctiva,  the  skin  of  the  face,  and  other  parts. 

The  convulsive  stage  usually  lasts  several  minutes.  Then  the  contractions 
cease,  often  after  a  deep,  long-drawn  sigh;  and  the  patient  passes  into  the  third 
stage  of  post-epileptic  coma.  He  lies  unconscious,  but  his  respiration  grows 
quiet,  and  the  cyanosis  vanishes.  Gradually  the  coma  yields  to  slumber,  which 
may  persist  for  some  hours ;  but  some  patients  remain  only  a  very  brief  time  in 
this  stage,  and  recover  from  their  attack  with  surprising  rapidity.  It  is,  however, 
not  infrequently  the  case  that  for  some  days  after-pains  are  felt ;  there  are  head- 
ache, languor,  and  exhaustion,  and  mental  despondency  and  irritability.  For 
some  time  there  may  be  severe  pain  in  the  muscles,  particularly  those  of  the 
trunk.  There  may  be  slight  paresis  of  one  limb  or  one  side  of  the  body  after  an 
attack,  but  this  speedily  vanishes  again  in  cases  of  pure  epilepsy.  In  the  first 
urine  passed  after  the  seizure  is  often  found  a  trace  of  albumen,  and  perhaps  a  few 
hyaline  casts.  Not  infrequently  there  is  also  decided  polyuria  for  some  time  sub- 
sequent to  the  fit.  Almost  always  after  recovery  of  consciousness  there  is  no 
recollection  of  what  has  happened,  or  it  is  very  imperfect.  On  careful  investiga- 
tion we  often  find  that  the  memory  of  events  immediately  preceding  the  attack 
(for  fifteen  minutes  to  two  hours  before)  has  also  entirely  disappeared.  A 
student,  for  example,  who  had  an  epileptic  attack  at  the  author's  clinique,  later 
had  absolutely  no  knowledge  of  how  he  came  to  the  clinique  or  of  what  he  had 
seen  or  heard  there  before  his  attack.  In  a  few  cases  (especially  after  traumatic 
epilepsy)  this  retrograde  amnesia  may  extend  over  a  much  longer  period. 

2.  The  Milder,  Rudimentary  Forms  of  Epileptic  Seizure.  Petit  Mai. — Be- 
sides these  violent  paroxysms  just  delineated  ("  grand  mal "),  there  are  very  often 
witnessed  in  epilepsy  milder  attacks  of  so-called  "  petit  mal.'"  Sometimes  there 
is  only  a  transitory  dizziness,  or  slight  faintness,  or  perhaps  a  brief  loss  of  con- 
sciousness,  but  without   accompanying   symptoms   of   motor   irritation.     These 


EPILEPSY  1145 

milder  attacks  may  or  may  not  be  preceded  by  an  aura.  Cases  have  been  repeat- 
edly seen  where  the  patient  suddenly  pauses  in  the  midst  of  conversation,  card- 
playing,  piano-playing,  or  other  occupation,  stares  absently  for  a  moment,  and 
then,  with  equal  abruptness,  goes  on  with  what  he  was  doing,  as  if  nothing  had 
happened.  In  other  instances  the  patient  pursues  his  occupation  during  this 
brief  suspension  of  consciousness.  For  example,  if  seized  while  upon  the  street, 
he  walks  on  mechanically,  but  takes  the  wrong  turning,  or  goes  into  a  strange 
house,  when  suddenly  he  comes  to  himself  and  wonders  to  find  himself  where  he 
is.  Cases  of  "  sudden  somnolence  "  are  also  almost  all  of  them  ascribable  to  epi- 
lepsy. There  are  all  sorts  of  transitional  forms  between  the  slight  attack  of 
vertigo  and  the  typical  epileptic  fit.  Wot  infrequently  the  patient  falls  down 
unconscious,  but  he  has  only  a  slight  twitching  of  the  face  or  arm,  and  in  a  few 
minutes  is  entirely  himself  again.  Very  often,  especially  in  children,  the  attack 
consists  of  a  short,  piercing  cry,  loss  of  consciousness,  a  few  convulsive  movements 
of  the  arms — and  in  a  few  seconds  all  is  over.  Such  attacks  come  on  in  the  day- 
time and  often  in  the  night  as  well.  In  other  patients  the  attacks  consist  of  sud- 
den pallor,  springing  to  the  feet,  rushing  to  the  door,  the  ejaculation  of  some  short 
words,  etc.  In  short,  it  is  hardly  possible  to  describe  all  the  different  manifesta- 
tions of  the  rudimentary  and  atypical  epileptic  attacks;  but  persons  who  suffer 
from  such  slight  attacks  not  infrequently  have  perfectly  typical  and  fully  devel- 
oped epileptic  attacks  besides,  and  this  is  of  especial  importance  in  diagnosis. 

[The  medico-legal  bearings  of  epilepsy,  in  its  mild  as  well  as  in  its  severe  form, 
are  very  important,  but  they  can  be  only  alluded  to  here.] 

3.  Epileptoid  Conditions  (Epileptic  Equivalents).— Cases  of  petit  mal  are  gen- 
erally rudimentary  forms  of  the  typical  epileptic  paroxysm,  and  consist  merely 
of  a  simple  impairment  of  consciousness,  possibly  associated  with  slight  motor 
symptoms;  but  in  the  epileptoid  state  the  characteristic  features  of  the  typical 
epileptic  attack  are  quite  subordinate.  The  disturbance  is  paroxysmal,  and  it  can 
often  be  shown  to  be  connected  with  genuine  epileptic  seizures,  else  its  undoubted 
relation  to  epilepsy  would  never  have  been  recognized.  The  greatest  practical  im- 
portance attaches  to  the  "psychical  equivalents  of  epilepsy"  (Samt).  These  are 
attacks  of  mental  disturbance,  which  either  immediately  succeed  a  typical  epileptic 
fit  ("post-epileptic  insanity")  or  occur  independently.  These  attacks  are  mani- 
fested by  states  of  complete  mental  confusion,  in  which  the  patient  may  do  the 
strangest  things — may  strip  himself,  steal,  jump  into  the  water,  or  commit  incen- 
diarism. Besides  these  "  states  of  epileptic  confusion  "  there  are  also  attacks  of 
violent  psychical  excitement,  associated  with  terror,  frightful  hallucinations,  and 
resultant  maniacal  excitement.  Not  infrequently  the  patient  is  led  to  acts  of  vio- 
lence against  those  about  him.  In  the  young  the  attack  may  take  a  peculiar  form : 
the  child  runs  about  in  a  peevish  way,  collects  dll  sorts  of  things  together,  makes 
strange  motions,  etc.  We  have  also  frequently  seeia  in  children  brief  states  of  dis- 
turbed consciousness  of  sudden  onset,  with  dominant  ideas  of  apparent  anxiety, 
often  associated  with  some  twitching.  Many  cases  of  so-called  pavor  nocturnus 
are  certainly  epilepsy,  although  it  is  sometimes  not  easy  to  exclude  hysteria.  Nu- 
merous and  valuable  particulars  upon  this  subject,  and  a  consideration  of  its  great 
medico-legal  importance,  must  be  sought  in  text-books  on  insanity,  as  we  can  not 
discuss  them  further  here. 

Among  the  rarer  forms  of  epileptoid  attack  are  the  epileptoid  sweatings 
(Emminghaus),  a  spontaneous  outbreak  of  excessive  perspiration  in  epileptics, 
which  may  or  may  not  be  associated  with  impairment  of  consciousness,  and  also  at- 
tacks of  epileptic  tremor  (Fere),  procursive  epilepsy  (attacks  when  the  patient 
runs  impulsively  foi-ward),  etc. 

General  Course  of  the  Disease.— In  a  large  majority  of  cases  epilepsy  begins 
before  the  thirtieth  year.     Often  the  disease  appears  in  early  youth,  and  some- 


1146  DISEASES   OF  THE  NERVOUS   SYSTEM 

times  even  in  the  earliest  years.  Many  a  child  has  "  convulsions  from  teething," 
which  later  on  are  seen  to  have  been  epileptic.  It  is  only  in  rare  instances  that 
the  first  appearance  of  trouble  occurs  in  advanced  life. 

It  is  impossible  to  give  any  general  rule  as  to  the  frequency  of  the  paroxysms. 
Different  cases  differ  very  much.  There  are  persons  who  during  their  whole  life 
have  no  more  than  three  or  four  seizures,  at  intervals  of  ten  or  fifteen  years,  while 
in  most  cases  there  is  an  attack  every  two  to  eight  weeks.  In  severe  types  the  fits 
may  even  recur  daily.  One  very  often  sees  certain  variations  in  the  course  of  the 
disease;  at  some  periods  the  intervals  between  the  attacks  will  be  longer,  and 
at  others  shorter.  In  severe  cases  the  patient  may  have  for  several  days  very  fre- 
quent seizures,  so  that  he  does  not  regain  consciousness  at  all  between  them.  This 
is  termed  the  epileptic  state  {etat  de  mal,  status  epilepticus).  The  condition  is 
quite  rare.  It  is  often  fatal,  death  being  ushered  in  by  a  great  rise  of  tempera- 
ture. 

External  influences  sometimes  affect  the  frequency  of  epileptic  attacks.  Alco- 
holic or  sexual  excess,  [indiscretions  of  diet,]  mental  excitement,  and  physical 
over-exertion  almost  always  exert  a  malign  influence.  An  opposite  effect  is  often 
experienced  where  a  quiet  life  is  led,  with  every  attention  paid  to  hygiene  and  pure 
air.  In  women,  the  appearance  of  the  catamenia  is  not  infrequently  the  signal  for 
the  occurrence  of  an  attack.  In  many  instances  the  disease  begins  with  the  first 
establishment  of  menstruation.  Sometimes,  however,  epileptic  girls  grow  better 
when  they  arrive  at  puberty.  Pregnancy  sometimes  increases  and  sometimes 
diminishes  the  frequency  of  the  paroxysms.  Intercurrent  diseases  seem  frequently 
to  exert  a  beneficial  infiuence  upon  the  frequency  of  the  attacks. 

There  is  a  practical  distinction  between  diurnal  and  nocturnal  epilepsy.  Many 
l^atients  have  attacks  only  during  the  day,  while  others  again  have  them  only 
at  night.  A  case  of  pure  nocturnal  epilepsy  may  go  on  for  a  long  time  un- 
suspected, particularly  if  the  patient  sleeps  alone.  He  seldom  has,  on  the  next 
morning,  the  slightest  recollection  of  his  attack  during  the  night.  He  usu- 
ally perceives,  however,  from  a  confused  feeling  in  his  head,  or  from  certain  in- 
juries, such  as  a  bitten  tongue,  or  from  the  disordered  state  of  the  bed,  that 
something  must  have  happened  to  him  during  the  night.  In  some  cases  of  noc- 
turnal epilepsy  the  patient  wakes  up  out  of  sleep  before  he  enters  into  the  epi- 
leptic state  of  unconsciousness.  Probably  he  is  aroused  by  the  aura.  Besides 
cases  where  the  fits  occur  during  the  day  or  the  night  only,  mixed  forms  are  fre- 
quently seen. 

With  regard  to  the  occurrence  of  the  different  varieties  of  epileptic  seizure,  all 
sorts  of  combinations  are  possible.  Many  cases  never  have  any  but  the  typical 
convulsions ;  but  in  many  others  there  are  also  a  greater  or  less  number  of  attacks 
of  petit  mal.  The  latter  may  even  be  for  a  long  period  the  sole  indication  of  the 
disease.  Often  there  are  no  epileptoid  conditions  whatever,  while  in  other  in- 
stances the  "  psychical  equivalents "  are  the  most  prominent  feature  of  the 
disorder. 

During  the  interval  between  the  individual  attacks  many  epileptics  seem  per- 
fectly well,  both  physically  and  mentally.  They  are  not  infrequently,  to  be  sure, 
somewhat  peculiar  and  nervously  excitable,  or  again  dull  and  lethargic ;  but  this 
does  not  by  any  means  apply  to  them  all.  Many  epileptics,  and  particularly  such 
as  have  comparatively  infrequent  paroxysms,  are  very  capable;  and  history 
furnishes  numerous  examples  of  eminent  men  who  suffered  from  this  disease- — 
for  instance,  C?esar,  Mahomet,  Rousseau,  and  Napoleon  I. 

Much  effort  has  been  devoted  to  the  discovery  of  "  signs  of  physical  degener- 
acy "  in  epileptics.  Relying  upon  numerous  measurements,  Benedikt  believes 
that  a  majority  of  epileptics  exhibit  craniometric  anomalies,  such  as  asymmetry 
of  the  cranium,  macroeephalia,  or  steepness  of  the  vertex.     It  is  also  not  unusual 


EPILEPSY  1147 

to  meet  with,  anomalies  of  the  ears,  teeth,  or  hands  *  in  such  cases.  Indeed,  all 
peculiarities  of  this  sort  are,  in  general,  more  frequently  observed  in  neuropathic 
families  than  in  healthy  ones. 

When  the  disease  has  lasted  some  time,  and  particularly  if  the  attacks  come  at 
very  short  intervals,  the  general  condition  of  the  patient  often  undergoes  a 
gradual  but  marked  change.  This  rule  is  by  no  means  invariable.  The  mind 
becomes  more  and  more  affected;  the  intellect  grows  feeble;  memory  grows 
weaker,  and  occasionally  there  is  at  last  dementia.  In  such  cases  the  body  also 
suffers.  There  are  emaciation,  paresis,  tremor,  and  other  persistent  disturbances 
of  cerebral  origin. 

In  regard  to  the  duration  of  epilepsy,  it  must  be  termed  a  life-long  disease.  To 
be  sure,  it  is  no  rare  thing  for  the  paroxysms  to  cease  and  not  return  for  years. 
But  one  can  never  rest  satisfied  that  all  trouble  is  at  an  end;  some  cause  or  other 
may  excite  another  attack  after  a  long  interval.  In  general,  an  epileptic  has  a 
shorter  life-expectancy  than  healthy  persons,  especially  as  he  may  be  carried  off 
by  chronic  pulmonary  or  other  intercurrent  disease. 

The  prognosis  is  obvious  from  what  has  been  already  said.  The  individual 
seizure  is  only  exceptionally  dangerous  of  itself.  The  so-called  "  status  epilepti- 
cus  "  often  ends  fatally,  as  above  stated.  In  general,  those  cases  may  be  called 
the  most  favorable  where  the  separate  paroxysms  are  infrequent  and  mild;  but 
even  here  the  disease  may  suddenly  assume  an  aggravated  form.  With  regard 
to  the  distinction  between  nocturnal  and  diurnal  epilepsy,  the  nocturnal  is,  in 
our  opinion,  the  milder  of  the  two. 

Pathology. — The  very  fact  that  in  the  intervals  between  attacks  the  patient 
often  betrays  no  sign  of  disease,  shows  that  epilepsy  can  not  be  due  to  any  per- 
sistent macroscopic  lesion  of  the  tissues.  Indeed,  in  many  cases  nothing  is  found 
at  the  autopsy,  or,  at  most,  changes  which  can  not  be  regarded  as  essential,  such 
as  osteosclerosis  of  the  cranium  or  thickening  of  the  cerebral  meninges.  Epi- 
leptic subjects  who  were  during  life  decidedly  demented  usually  present  atrophy 
of  the  hemispheres.  Meynert  states  that  changes  in  the  pes  hippocampi  major  are 
noticeably  frequent  in  epilepsy;  but  these  changes  are  not  at  all  constant,  and 
their  significance  remains  to  be  established. 

We  must  therefore,  for  the  present,  be  content  to  assume  that  the  cause  of  the 
epileptic  seizure  is  an  intermittent  functional  condition  of  irritation.  A  natural 
question  is,  Where  shall  we  locate  this  irritation,  and  what  may  be  its  nature? 
The  opinion  was  long  current  that  the  medulla  oblongata  must  be  regarded  as  the 
true  seat  of  the  disease.  Schroder  van  der  Kolk  was  the  first  to  express  this 
opinion.  It  afterward  received  support  from  the  experimental  investigations  of 
Nothnagel,  who  demonstrated  that  irritation  of  a  particular  spot  ("  convulsive 
center")  in  the  pons,  in  rabbits,  invariably  excites  general  convulsions.  Never- 
theless, most  pathologists  have  now  abandoned  this  view,  because  experiment  and 
clinical  observation  indicate  with  increasing  distinctness  that  the  origin  of  epi- 
leptic convulsions  is  to  be  sought,  at  least  in  the  great  majority  of  cases,  in  the 
cerebral  cortex.  The  clinical  evidence  is  the  invariable  combination  of  con- 
vulsions and  impairment  of  consciousness ;  the  circumstance  that  the  milder  and 
the  masked  forms  of  epilepsy,  now  known  to  be  intimately  related  to  the  true 
epileptic  convulsions,  also,  almost  without  exception,  indicate  psychical  disturb- 
ance; that  attacks,  the  symptoms  of  which  are  perfectly  analogous  with  those  of 
epilepsy,  are  often  found  to  be  the  result  of  anatomical  lesions  of  the  cerebral 
cortex;  and,  finally,  that  these  conviilsions  in  man  and  the  convulsions  of  "  cortical 
epilepsy"  (vide  infra),  experimentally  produced  in  animals,  extend  over  the 
different    groups  of  muscles  in  a  way  which  corresponds  precisely  with  the  ana- 


*  We  have  seen  an  epileptic  wlio  had  six  tinsrers  on  each  hand. 


1148  DISEASES   OF  THE  NEEYOUS   SYSTEM 

tomical  position  of  the  different  motor  centers  in  the  cortex  (Hughlings  Jackson). 
For  example,  if  the  convulsion  begins  in  the  distribution  of  the  facial  nerve,  it 
extends  from  this  point  to  the  arm  before  it  affects  the  leg. 

^  There  is  also  experimental  evidence  that  epileptic  paroxysms  are  of  cortical 
origin.  A  great  number  of  obserA^ers  (Hitzig,  Ferrier,  Albertoni,  Luciani,  Franck, 
and  Pitres)  have  proved  that  electrical  irritation  of  the  motor  regions  of  the 
cortex  in  animals  will  produce  epileptiform  convulsions.  Unverricht  has  made 
some  of  the  latest  and  most  thorough  investigations  in  regard  to  this  point  upon 
dogs.  He  found  that  when  a  motor  center  is  stimulated  the  convulsions  spread 
from  the  corresponding  group  of  muscles  to  others  in  a  way  which  corresponds 
precisely  to  the  anatomical  position  of  the  separate  centers.  If  one  of  the  centers 
in  the  cortex  be  destroyed,  the  convulsions  of  the  corresponding  muscles  cease  at 
once.  This  proves  that  the  motor  centers  must  be  intact  in  order  to  render  the 
occurrence  of  epileptic  seizures  possible.  Just  how  the  stimulation  extends  from 
one  center  to  another  we  have  as  yet  no  certain  information.  Probably  it  travels 
horizontally  through  the  cortex. 

We  see,  therefore,  that  in  all  probability  the  seizures  in  man  also  originate  in 
the  cortex  of  the  brain.  The  phenomena  of  the  aura  are  likewise  referable  to 
some  stimulation  of  the  cortex,  probably  of  the  sensory  region  in  most  cases,  as  in 
the  optical  aura.  The  starting-point  of  the  irritation  is  probably  usually  in  the 
motor  cortex,  but  it  does  not  seem  impossible  that  an  irritation  developing  in  the 
posterior  cortical  regions  may  extend  secondarily  to  the  anterior  motor  portion  of 
the  cortex  (Unverricht).  The  manner  in  which  the  irritation  is  created  is  as  yet 
entirely  conjectural.  Kussmaul  and  Tenner  proved  that  epileptiform  convulsions 
can  be  excited  by  a  general  cerebral  ansemia ;  and  this  fact  was  the  main  founda- 
tion for  the  assumption  that  the  genuine  epileptic  convulsions  are  also  due  to  a 
temporary  cerebral  anemia,  caused,  it  may  be,  by  local  vaso-motor  constriction. 
Definite  proof  has  not  yet  been  furnished  on  this  point.  In  the  artificial  epilepsy 
which  Unverricht  produced,  and  that  also  which  Magnan  excited  by  absinthe,  the 
cortex  of  the  brain  was  not  strikingly  ansemic.  In  regard  to  the  occurrence  of 
the  attacks  in  true  genuine  epilepsy  we  can  therefore  provisionally  make  the  im- 
perfect assumption  that,  as  the  result  of  a  diseased  condition,  the  motor  cortex 
of  the  brain  has  lost  the  power  to  store  up  its  motor  energy  and  to  give  it  out 
again  in  normal  fashion,  and  that  therefore  there  arise,  from  time  to  time,  morbid 
"  discharges  of  energy "  and  an  outbreak  of  the  convulsive  movements  already 
described.  We  will  omit  a  further  discussion  of  this  theory,  since  we  would  soon 
be  lost  in  the  realm  of  mere  hypothesis. 

Diagnosis. — Most  cases  of  epilepsy  are  easily  recognizable.  It  needs  only  to  be 
borne  in  mind  that  epileptiform  convulsions  may  also  occur  as  a  symptom  of 
cerebral  diseases  which  do  have  an  anatomical  basis,  such  as  tumor,  abscess,  mul- 
tiple sclerosis,  and  hydatids.  As  a  rule,  however,  such  diseases  are  readily  distin- 
guished by  the  state  of  the  patient  between  the  seizures,  or  by  the  further  course 
of  the  illness.  It  should  also  be  understood  that  unilateral  convulsions,  or  such 
as  are  confined  to  a  single  member  (Jacksonian  epilepsy,  vide  supra,  page  1073), 
are  usually  not  true  epilepsy,  but  symptoms  of  some  circumscribed  affection  of  the 
cortex.  We  will  return  once  more  to  the  differentiation  from  hysterical  convul- 
sions in  the  chapter  on  hysteria.  Weight  should  be  laid  on  the  general  character 
of  the  attack,  the  complete  loss  of  consciousness  in  epilepsy,  the  dilatation  of  the 
pupils,  which  do  not  react  to  light,  the  initial  pallor  not  infrequently  observed, 
and  the  subsequent  cyanosis  of  the  face.  We  may  also  consider  the  character  of  the 
onset  and  the  duration  of  the  attack  (in  true,  genuine  epileptic  attacks  the  con- 
vulsive stage  seldom  lasts  longer  than  a  few  minutes),  the  biting  of  the  tongue, 
the  condition  of  the  patient  immediately  after  the  attack  (deep,  continued  sleep 
is  in  favor  of  epilepsy),  the  possibility  of  exciting  the  hysterical  attacks  volun- 


EPILEPSY  1149 

tarily  (by  suggestion,  by  pressure  on  a  "  hysterogenous  "  zone,  etc.),  which  we 
can  not  do  with  epileptic  attacks.  The  same  factors  (especially  the  condition  of 
the  pupils  and  the  biting  of  the  tongue)  are  the  chief  means  of  discovering 
simulated  epileptic  attacks. 

Treatment. — Although  no  remedy  is  capable  of  working  a  certain  and  perma- 
nent cure  of  epilepsy,  yet  a  favorable  influence  can  be  exerted  upon  the  disease  in 
many  ways,  so  as  to  lessen  the  frequency  and  severity  of  the  paroxysms,  and  to 
avert  many  of  their  evil  results. 

In  the  first  place,  regimen  is  of  great  importance.  Any  excessive  exertion  of 
mind  or  body  must  be  forbidden.  Temperance  must  be  exercised  in  eating  and 
drinking.  Alcohol,  strong  coffee,  and  tea,  can  be  used  only  moderately;  nor  is 
too  much  smoking  permissible.  The  diet  should  be  simple  and  unirritating,  and 
vegetable  rather  than  animal.  It  is  said  that  in  some  cases  decided  improvement 
has  been  brought  about  by  confining  the  patient  to  milk  and  vegetables.  In 
summer  the  patient  should  live  quietly  in  the  country  or  the  mountains.  We 
have  also  the  individual  constitution  to  consider:  a  weak  and  anaemic  person 
must  have  iron  and  abundant  nourishment;  and  a  full-blooded,  corpulent  indi- 
vidual should  drink  the  natural  aperient  waters,  and  live  abstemiously. 

Proceeding  to  the  treatment  of  the  disease  itself,  we  shall  only  rarely,  when 
dealing  with  "reflex"  epilepsy  (vide  supra),  have  to  consider  a3tiological  condi- 
tions. The  excision  of  old  sears,  the  extraction  of  foreign  bodies,  or  trephining  the 
skull,  where  the  disease  has  followed  an  injury,  are  said  to  have  brought  about 
permanent  recovery  in  a  few  cases.  We  should  also  deal  with  any  nasal  or  aural 
disease,  in  order,  by  rational  treatment  of  any  such  trouble,  to  exert,  if  possible,  a 
favorable  influence  upon  the  convulsive  attacks.  If  we  discover  any  intestinal 
worms  they  should  be  expelled.  In  genuine  typical  epilepsy  we  have  no  such  indi- 
cations to  fulfill,  and  we  must  have  recourse  to  such  treatment  as  experience  shows 
can  influence  favorably  the  outward  manifestations  of  the  disease. 

Among  these  remedies,  potassic  bromide  has  an  undisputed  right  to  the  first 
place.  It  should  be  the  first  remedy  tried  in  any  severe  case.  Apparently  it  acts 
by  directly  lowering  the  sensitiveness  of  the  motor  centers  of  the  cortex  to  irrita- 
tion. Rather  large  doses  are  requisite.  Beginning  with  about  one  drachm 
(grammes  4—5)  a  day,  we  may  find  it  advisable  to  increase  up  to  two  or  two  and  one 
half  drachms  (grammes  8-10).  It  may  be  prescribed  in  water  (1  to  10  or  15),  or  in 
powders  which  the  patient  himself  is  to  dissolve  in  water,  sweetened  if  desired. 
The  remedy  in  almost  all  cases  needs  to  be  used  for  months  and  years,  and  it  is 
therefore  often  advisable  for  the  patient  to  buy  a  half  pound  or  a  pound  at  a  time 
and  weigh  it  out  himself  into  the  proper  doses.  It  should  always  be  taken  in  a 
good  deal  of  water,  half  a  tumbler  or  more,  to  avoid  irritating  the  stomach.  The 
total  amount  for  the  day  is  usually  divided  into  two  or  three  portions;  but  the 
whole  may  be  dissolved  in  a  large  amount  of  water  (seltzer  water)  and  drunk 
gradually  through  the  day.  The  other  bromide  salts,  the  bromides  of  sodium  and 
ammonium  are  also  frequently  employed.  They  have  the  advantage  of  disturb- 
ing the  stomach  less  than  does  the  potassium  salt.  It  is  well  to  combine  the  various 
bromides.  Erlenmeyer  strongly  recommends  a  mixture  of  two  parts  each  of 
potassic  and  sodic  bromides  with  one  of  ammonic  bromide  in  so-called  "  bromine  " 
water. 

In  using  the  bromides,  persistence  is  necessary  for  at  least  months,  and  often, 
with  occasional  interruptions,  for  years,  if  benefit  is  to  be  obtained.  In  case  there 
are  unpleasant  symptoms  due  to  the  remedy,  such  as  excessive  acne,  a  bad  breath, 
muscular  lassitude  and  tremor,  cardiac  weakness,  dyspepsia,  impotence,  or  mental 
depression  and  weakness  of  memory,  we  must  diminish  the  dose,  or  even  omit  the 
medicine  for  a  time.  Many  patients  are  greatly  annoyed  by  pustules  due  to  the 
bromide;  this  can  sometimes  be  avoided  by  giving  Fowler's  solution  at  the  same 


1150  DISEASES   OF  THE  ]^EEVOUS   SYSTEM 

time.  If  the  attacks  are  decidedly  abated,  the  dose  may  be  gradually  diminished, 
to  be  increased  again,  however,  if  there  be  any  tendency  to  a  relapse. 

There  is  no  doubt  that  the  frequency  of  the  attacks  can  be  lessened  by  the 
continued  use  of  bromides.  This  action  is  of  course  manifest  only  in  those  cases 
where  the  individual  attacks  occur  rather  frequently'  (every  three  or  four  weeks 
or  oftener).  If  we  are  treating  epileptics  who  have  intervals  of  six  months  to 
a  year  or  more  between  the  individual  attacks,  it  is  hardly  possible  to  decide 
with  certainty  whether  the  bromide  treatment  has  any  efficacy,  and  the  long- 
continued  use  of  bromide  which  is  necessary  is  often  attended  by  unpleasant 
accompaniments.  We  are  therefore  usually  disposed  in  such  cases  to  abstain 
wholly  from  the  bromide  treatment.  Elechsig  recommends  combining  the  bromide 
treatment  with  the  use  of  opium.  "We  should  give  at  first  simply  the  extract  of  opi- 
um, beginning  with  two  and  a  half  grains  (gramme  0.15)  a  day,  and  gradually  in- 
creasing to  six  or  eight  grains  (gramme  0.25-0.35)  or  more,  always  divided  into 
two  or  three  doses  in  the  day.  After  using  opium  for  six  weeks  we  stop  it  abruptly 
and  begin  with  a  bromide  treatment,  continuing  about  two  months.  Whether 
this  method  has  any  special  advantages  can  be  told  only  after  longer  experience. 

Recourse  to  other  remedies  is  seldom  had,  unless  potassic  bromide  fails,  or  for 
some  cause  must  be  discontinued.  We  may  then  try  valerian  in  powder,  eight  to 
thirty  grains  (grammes  0.5-2)  several  times  a  day,  or  as  an  infusion.  It  is  a  very 
good  plan  to  give  patients  who  are  taking  bromide  a  cup  or  two  of  valerian  tea  at 
bedtime.  Belladonna  may  also  be  exhibited,  or  a  pill  of  atropine,  grain  t^-^ 
(gramme  0.0005),  three  to  five  times  a  day;  or  zinc  oxide  in  the  dose  of  one  to 
three  grains  (gramme  0.05-0.20),  perhaps  combined  with  one  fourth  of  a  grain  of 
extract  of  belladonna  [U.  S.  P.],  and  fifteen  grains  of  valerian,  as  a  powder,  three 
times  a  day,  and  finally  chloral  in  small  doses  (five  to  ten  grains  a  day,  grammes 
0.3-0.5,  divided  into  several  doses).  Combinations  of  the  bromide  salts  with  some 
one  of  the  remedies  mentioned  have  seemed  to  us  ver\'  advantageous  in  many  cases. 
We  have  sometimes  seen  a  decidedly  favorable  action  from  a  mixture  of  the  bro- 
mides with  small  doses  of  chloral  or  with  atropine,  especially  where  there  are  fre- 
quent rudimentary  attacks.  Bechterew  recommends  the  combination  of  bromides 
with  adonis  vemalis  (an  infusion  of  two  or  three  parts  of  adonis  vernalis  in  180 
parts  of  water,  to  which  eight  to  twelve  parts  of  bromide  are  added).  Many  rem- 
edies formerly  recommended  are  not  worth  mentioning,  as  they  are  wholly  in- 
efficacious. 

Electricity  is  apparently  beneficial  in  occasional  instances,  and  it  may  be  tried 
in  connection  with  other  remedies.  The  galvanic  current  should  be  cautiously 
applied  to  the  head  and  the  sympathetic  nerves.  Still  greater  benefit  is  some- 
times obtained  from  a  carefully  conducted  cold-water  cure.  Cold  sponging  with 
friction  at  night  helps  most  cases,  and  it  is  sometimes  very  advisable  to  send  the 
patient  in  summer  to  some  appropriate  establishment  for  cold-water  treatment. 
We  can  not  hope  for  any  benefit  from  the  surgical  treatment  of  epilepsy  except 
in  those  cases  where  the  epilepsy  is  symptomatic,  and  we  can  expect,  by  the  opera- 
tion, to  remove  or  render  harmless  some  actual  local  lesion  in  the  brain  (a  de- 
pression of  the  skull,  a  cicatrix,  a  cyst,  a  meningeal  adhesion,  etc.).  [In  some  cases 
of  Jacksonian  epilepsy  an  attempt  has  been  made  to  relieve  the  attacks  by  removing 
the  cortical  center  in  which  they  apparently  originate.  After  the  brain  is  exposed 
this  center  is  determined  by  faradization  of  the  cortex.  In  a  number  of  cases  the 
center  has  been  excised  even  when  there  was  no  macroscopic  evidence  of  disease. 
The  convulsions  have  often  ceased  for  a  time,  but  they  have  usually  returned 
later,  and  the  removal  of  the  cortex  is  apt  to  cause  permanent  paralysis. — K.] 

Treatment  during  the  Paroxysm. — In  most  cases  we  can  do  little  during  the 
seizure  except  to  take  such  precautionary  measures  as  common  sense  suggests. 
We  possess   no  means   of  suppressing   an   attack  when   once   under  way;   nor, 


INFANTILE  CONVULSIONS    (ECLAMPSIA  INFANTUM)     1151 

indeed,  is  it  often  dangerous.  In  individual  instances  the  patient  finds  out  from 
experience  some  method  to  cut  short  the  paroxysm  during  the  aura.  For 
instance,  there  are  cases  where  tightly  bandaging  or  vigorously  rubbing  the  part 
in  which  the  aura  originates  will  avert  the  convulsions.  A  number  of  cases  have 
also  been  known  where  the  ingestion  of  a  generous  quantity  of  common  salt  dur- 
ing the  aura  has  had  the  same  effect.  In  these  cases  the  aura  usually  starts  from 
the  epigastrium.  A  patient  of  our  own,  whose  attacks  began  with  a  feeling  of  rec- 
tal tenesmus,  maintained  that  she  could  almost  invariably  suppress  the  convul- 
sions by  promptly  going  to  stool,  if  she  had  time  and  opportunity.  It  was  for- 
merly a  frequent  manoeuvre  to  seek  to  ward  off  the  attack  by  compressing  the 
carotids ;  but  this  usually  fails.  Berger  recommends  the  inhalation  of  nitrate  of 
amyl  at  the  commencement  of  the  fit,  having  repeatedly  seen  benefit  follow  its  use. 

In  the  "  status  epilepticus,"  narcotics  are  the  most  deserving  of  trial,  and  in 
particular  chloroform  or  ether  given  by  inhalation,  and  the  internal  use  of  chloral 
(forty-five  to  seventy-five  grains  a  day,  grammes  3-5).  Amyl  nitrite  may  also 
be  of  service. 

[It  is  sometimes  desirable  to  withhold  the  knowledge  that  he  is  an  epileptic 
from  the  patient,  whose  ordinary  life  should  be  interfered  with  as  little  as  is 
possible. 

Especially  in  cases  characterized  by  headache  and  heat  in  the  head,  Brown- 
Sequard  finds  the  application  of  ice  directly  to  the  back  of  the  neck  and  between 
the  shoulders  useful.] 


APPENDIX 

INFANTILE  CONVULSIONS   (ECLAMPSIA  INFANTUM) 

Convulsions  in  childhood  are  of  such  frequency  and  importance  as  to  justify 
brief  special  mention  here. 

Every  practitioner  learns  from  daily  experience  that  the  young  are  especially 
predisposed  to  convulsions.  Probably  this  is  due  in  part  to  excessive  reflex  excita- 
bility of  the  brain  in  childhood.  .  Thus  children  not  infrequently  undergo  con- 
vulsions under  circumstances  in  which  adults  would  very  rarely  have  them. 
They  sometimes  are  seen  in  children  in  the  beginning  of  acute  febrile  diseases, 
such  as  pneumonia,  scarlet  fever,  measles,  febrile  sore  throat,  etc.  They  also  occur 
from  indigestion,  particularly  when  the  stomach  has  been  overloaded;  sometimes 
on  account  of  teething ;  or  because  of  intestinal  worms.  In  these  cases  they  are 
usually  regarded  as  of  reflex  origin,  although  they  may  possibly  be  due  to  the 
action  of  toxines  (especially  with  intestinal  worms). 

Convulsions  may  occur  in  very  early  life  without  ascertainable  cause.  In 
many  cases  they  are  really  the  commencement  of  epilepsy,  as  is  seen  afterward. 
Again,  they  may  be  due  to  some  actual  lesion  in  the  brain.  For  example,  if  one 
recalls  the  initial  stage  of  the  acute  poliomyelitis  and  acute  encephalitis  of  chil- 
dren (vide  pages  1015  and  1111),  it  will  not  seem  unlikely  that  many  rapidly  fatal 
cases  of  "  convulsions "  are  really  instances  of  the  diseases  mentioned.  This 
point  has  not  yet  been  at  all  satisfactorily  investigated  by  pathologists.  At  any 
rate,  it  does  not  seem  satisfactory  to  us  to  regard  the  "  oedema  of  the  meninges  " 
found  in  such  cases  as  an  independent  disease  and  the  sufficient  cause  of  death. 
Often  convulsions  occur  suddenly  in  children  and  then  cease,  never  to  recur,  with- 
out our  being  able  to  find  any  explanation  of  the  attack.  Experience  shows  that 
rachitic  children  are  especially  liable  to  suffer  from  eclampsia — possibly  because 
of  cranial  rachitic  changes  (?). 

The  symptoms  of  the  eclamptic  attacks  are  on  the  whole  analogous  with  those 


1152  DISEASES   OF  THE  NERVOUS   SYSTEM 

of  epileptic  paroxysms.  The  child's  eyes  become  staring  and  fixed,  and  there 
are  tonic  and  clonic  spasms  of  the  face,  trunk,  and  extremities.  Such  seizures 
may  continue  for  days  with  brief  intermissions.  In  such  cases  the  prognosis  is 
dubious,  particularly  if  the  child  be  weakly,  but  it  is  by  no  means  absolutely  bad. 
The  cause  and  the  significance  of  the  convulsions  can  seldom  be  determined 
immediately. 

Symptomatic  treatment  consists  of  applying  cold  to  the  head,  wet  packs,  sina- 
pisms on  the  chest  and  the  calves  of  the  legs,  and  perhaps  an  enema  (to  which 
vinegar  may  be  added.  These  measures  generally  answer  for  mild  cases.  If  the 
fits  are  very  frequent  and  violent,  we  may  allow  even  small  children  to  inhale 
chloroform,  often  with  great  advantage.  A  dessertspoonful  is  to  be  poured  upon 
a  handkerchief  and  administered  cautiously. 

Of  course,  we  must  also  try  to  discover  and  remove  the  cause  (acute  diseases, 
intestinal  worms).  The  attacks  due  to  overloading  the  stomach  usually  occur  in 
not  very  young  children,  and  are  apt  to  be  greatly  benefited  by  a  prompt  emetic  or 
purge. 

[A  bath  at  a  temperature  of  90°-95°,  while  cool  water  is  applied  to  the  head, 
seems  often  to  be  of  service ;  if  the  child  be  exhausted  by  diarrhoea,  the  cold  to  the 
head  should  be  omitted.  In  a  teething  child  it  can  do  no  harm,  and  it  sometimes 
has  a  very  marked  beneficial  effect  to  lance  the  gums  thoroughly.  Enemas  con- 
taining chloral  with  or  without  bromide  of  potassium  are  more  used  in  this  coun- 
try than  is  chloroform  by  inhalation. 

A  drop  of  nitrite  of  amyl  by  inhalation  is  said  by  Eustace  Smith  to  exert  a 
controlling  effect  on  the  muscular  movements.] 


CHAPTER   II 

CHOREA 

{Chorea  Minor.     Syden.hani's  Chorea.     St.   Vitus' s  Dance) 

.ffitiology. — Centuries  ago  the  name  chorea  (dance)  was  applied  mainly  to 
those  strange  states  of  "  dancing  mania  "  which  were  endemic  in  certain  places, 
being  due  to  excessive  mental  excitement  and  to  the  innate  propensity  to  imita- 
tion. The  specific  for  this  condition  was  held  to  be  a  pilgrimage  to  some  shrine 
of  St.  Vitus.  At  the  present  time,  however,  chorea  is  used  to  designate  a  perfectly 
definite  disease,  of  which  the  characteristic  symptom  is  the  appearance  of  certain 
peculiar  motor  phenomena  due  to  irritation  of  the  nervous  centers.  It  is  some- 
times called  chorea  minor,  in  contradistinction  from  what  was  formerly  termed 
chorea  major  or  magna.  This  latter  is,  however,  not  a  genuine,  independent  dis- 
ease, but  a  manifestation  of  hysteria  {q.  v.),  or  apparently  in  many  instances  of 
epilepsy. 

Chorea  proper  is  mainly  a  disease  of  childhood.  It  occurs  most  often  between 
the  fifth  and  fifteenth  years,  although  it  may  be  seen  both  earlier  and  later. 
There  is  a  slightly  greater  liability  to  it  in  girls  than  in  boys.  Hereditary  neuro- 
pathic tendencies  are  also  a  factor  in  its  aetiology,  but  not  a  very  important  one. 
(See  the  appendix  to  this  chapter  for  chronic  hereditary  chorea.) 

As  to  causation,  in  many  cases  nothing  definite  can  be  made  out.  Mental  ex- 
citement, as  from  fright,  seems  in  some  few  instances  to  favor  the  onset  of  the 
trouble.  It  is  also  certain  that  the  imitative  impulse  will  often  lead  to  choreic 
movements  in  healthy  children  who  come  in  contact  with  choreic  patients,  but  it 
is  doubtful  whether  this  "  imitative  chorea  "  can  be  regarded  as  true  chorea.     It 


CHOREA  1153 

seems  to  us  far  more  correct  in  such  cases,  which  are  very  amenable  to  psychical 
treatment,  to  speak  of  a  hysterical  chorea.  There  is  a  very  interesting  connection 
between  chorea  and  acute  articular  rheumatism.  Although  the  statement  of  cer- 
tain authors,  that  almost  every  case  of  acute  articular  rheumatism  in  children 
is  followed  by  chorea,  is  far  too  strong,  yet  this  sequence  is  comparatively  fre- 
quent. Chorea  is  sometimes  seen  also  in  children  who  have  a  mild  form  of 
chronic  rheumatism,  or  especially  in  such  as  have  valvular  cardiac  disease, 
whether  preceded  by  articular  rheumatism  or  not.  This  undoubted  and  close  con- 
nection existing  between  chorea,  articular  rheumatism,  and  valvular  heart  disease, 
indicates  the  possibility  that  in  true  chorea  there  is  an  intoxication  arising  from 
some  infection. 

Pregnancy  exerts  a  special  influence  upon  the  development  of  chorea  in  women. 
Chorea  gravidarum  is  most  frequent  in  comparatively  youthful  primiparte.  The 
nature  of  the  connection  between  chorea  and  pregnancy  is  still  utterly  obscure. 

Clinical  History. — Chorea  usually  begins  gradually,  and  without  any  special 
prodromata.  Sometimes,  however,  there  are  prodromal  symptoms,  chiefly  a  cer- 
tain mental  depression  and  irritability,  with  indisposition  to  intellectual  effort. 
There  may  be  slight  rheumatic  pains  or  anorexia,  and  other  evidences  of  constitu- 
tional disturbance. 

Ordinarily  the  peculiar  motor  disturbances  are  the  first  thing  to  attract  the 
attention  of  the  patient  or  its  parents.  There  are  involuntary  and  irrepressible 
movements  in  the  most  diverse  groups  of  muscles.  Both  single  contractions  and 
also  complicated  movements  occur,  independently  of  the  will,  and  in  all  parts  of 
the  body,  now  in  one  place,  now  in  another,  sometimes  in  a  single  member,  and 
sometimes  in  several  at  once.  The  movements  may  be  made  in  rapid  succession, 
or  may  be  separated  by  long  intervals  of  quiet.  The  facial  muscles  may  be 
involved,  causing  an  occasional  wrinkling  of  the  brow  or  distortion  of  the  mouth. 
When  there  is  marked  chorea  of  the  facial  muscles,  as  usually  happens  in  severe 
cases,  the  patients  often  make  the  strangest  grimaces,  sometimes  with  some  par- 
ticular expression  of  emotion  (laughter,  anger,  etc.).  The  eyes  also  may  take 
part  in  the  involuntary  movements,  being  moved  from  side  to  side,  or  opened 
and  closed.  The  pupils  are  frequently  dilated.  If  the  patient  be  asked  to  pro- 
trude his  tongue  and  keep  it  quiet,  it  will  often  be  involuntarily  withdrawn  into 
the  mouth  or  thrust  to  one  side.  The  tongue  may  even  be  sufficiently  affected 
to  impair  speech,  which  is  explosive  and  indistinct.  The  laryngeal  muscles  have 
also  been  observed  to  make  choreic  movements.  The  arms  are  frequently  the 
most  affected  of  any  part ;  they  are  twisted,  flexed,  elevated,  put  behind  the  back — • 
in  short,  moved  in  every  conceivable  way.  The  trunk  is  generally  but  little  dis- 
turbed in  the  milder  cases,  but  in  severe  ones  the  whole  body  participates.  The 
patient  stands  up,  lies  down  again,  turns  upon  his  side,  etc.  The  legs  are 
seldom  as  much  disturbed  as  the  arms  and  face,  but  slight  movements  of  the 
lower  limbs  are  very  frequent — the  foot  is  thrust  forward  or  extended,  the 
knee  is  flexed,  and  so  on.  In  general,  it  may  be  said  to  be  characteristic  of  chorea 
that  the  abnormal  motor  irritation  usually  affects  a  considerable  number  of 
muscles  simultaneously,  thus  exciting  all  sorts  of  combined  movements ;  and, 
secondly,  that  choreic  movements,  for  the  most  part,  are  not  short  twitches,  but 
take  place  in  a  manner  decidedly  similar  to  that  of  voluntary  movements. 

The  vigor  of  the  movements  varies  greatly  in  different  cases.  At  first  they 
may  be  too  slight  for  the  unpracticed  eye  to  catch.  Many  children  in  an  incipient 
stage  of  chorea  are  unjustly  punished  at  school  because  they  write  ill  or  do  not 
sit  quietly.  Many  cases  are  mild  throughout,  never  having  very  severe  disturb- 
ance. Others,  though  considerably  annoyed,  can  nevertheless  walk  or  stand 
alone.  In  the  severest  cases,  however,  the  whole  body  is  continually  in  active 
motion.  The  patient  throws  himself  about  in  bed,  and  all  the  extremities  exhibit 
73 


1154  DISEASES   OF  THE  NEEVOUS   SYSTEM 

constant  violent  and  irregular  movements.  The  ingestion  of  food  is  extremely- 
difficult,  sleep  is  disturbed,  and  the  patient's  flesh  and  strength  are  rapidly  and 
greatly  diminished. 

Eurther,  each  individual  case  presents  variations  in  severity  at  different  times. 
If  the  patient  be  left  quietly  to  himself,  the  contractions  are  comparatively  very 
slight.  As  soon  as  he  is  conscious  of  being  watched  or  as  soon  as  any  one  speaks 
to  him,  his  condition  usually  becomes  much  worse.  On  the  other  hand,  of  course,. 
the  movements  may  also  be  somewhat  influenced  by  the  will.  The  patient  some- 
times becomes  quieter  if  the  body  is  completely  supported  and  gently  restrained,. 
etc.     During  sleep  the  choreic  movements  usually  cease  altogether. 

In  many  cases  all  the  voluntary  muscles  are  involved;  but  sometimes  the  dis- 
ease is  limited  to  certain  groups  of  muscles.  Very  frequently  the  disturbance  is 
mainly  unilateral  (hemichorea) ;  the  opposite  side  of  the  body  then  exhibits  few 
involuntary  movements,  or,  it  may  be,  none.  As  already  stated,  the  face  and 
upper  extremities  are  often  more  affected  than  the  trunk  and  lower  limbs. 

These  motor  disturbances  often  constitute  the  sole  or  the  predominant  symp- 
tom of  chorea.  There  is  hardly  ever  muscular  weakness  or  paralysis.  It  is 
remarkable  how  little  feeling  of  fatigue  there  usually  is,  despite  the  incessant 
activity.  In  a  few  cases  only,  of  genuine  chorea,  have  we  seen  actual  paresis, 
affecting,  for  instance,  one  arm,  or  in  hemichorea  the  choreic  half  of  the  body. 
Sensation  is  unimpaired.  The  reflexes  do  not  exhibit  striking  peculiarities.  The 
tendon  reflexes  we  have  usually  found  normal,  more  rarely  very  weak  or  even  a  lit- 
tle increased.  There  may  be  isolated  spots  in  the  spinal  column  tender  on  pressure^ 
but  this  is  not  at  all  constant.  That  chorea  may  be  complicated  by  arthritis  and 
valvular  cardiac  disease  has  already  been  stated.  Some  caution  should  be  exer- 
cised in  making  a  diagnosis  of  cardiac  lesion  here,  for  experience  shows  that 
choreic  patients  are  apt  to  have  functional  murmurs  and  slight  irregular  cardiac 
action.  [Osier  has  found  that  the  endocarditis  of  chorea  is  very  apt  to  lead  to 
organic  valvular  disease.  Of  110  choreic  patients  that  he  examined  more  than 
two  years  after  the  attack,  54  presented  signs  of  organic  heart  disease. — K.]  The 
temperature  is  not  elevated,  in  spite  of  the  constant  muscular  contractions,  nor  is 
the  amount  of  urea  excreted  by  the  kidneys  increased. 

Slight  mental  disturbance  is  frequently  observed.  The  patient  is  often  rude, 
peevish,  capricious,  incapable  of  mental  exertion,  irritable,  and  inclined  to  tears. 
More  marked  mental  disturbances  (confusion,  hallucinations)  are  sometimes  met 
with  in  the  severer  cases,  especially  in  chorea  gravidarum.  [These  mental  dis- 
turbances sometimes  become  very  severe  (chorea  insaniens^ .  The  patient  becomes 
excited  and  delirious,  and  is  very  apt  to  die  in  a  few  weeks  of  general  exhaustion,, 
with  considerable  fever,  104^-105°  E. — ^K.] 

The  entire  process  generally  occupies  several  months.  In  mild  cases,  however, 
recovery  may  ensue  at  the  end  of  a  few  weeks,  while,  on  the  other  hand,  cases 
may  last  a  year  or  even  longer.  Variations  in  the  intensity  of  the  chorea  are 
often  witnessed.  These  are  sometimes  spontaneous,  and  sometimes  are  due  to 
outward  influences.  Even  when  the  disease  is  apparently  extinguished,  we  must 
be  prepared  for  a  possible  relapse.  The  disease  may  appear  repeatedly  in  the 
course  of  a  few  years,  in  such  a  way  that  it  is  not  easy  to  determine  whether  the 
different  attacks  are  relapses  or  new  illnesses.  The  protracted  cases  are,  as  a  rule, 
comparatively  mild;  and  many  cases  that  begin  with  great  violence  end  compara- 
tively early.  In  adults,  and  still  more  frequently  in  the  aged  (chorea  senilis), 
however,  the  chorea  sometimes  assumes  a  chronic  form  and  becomes  stationary. 

The  termination  of  chorea,  in  the  great  majority  of  cases,  is  favorable,  l^ow 
and  then  severe  cases  do  occur  which  end  in  death.  In  these  the  choreic  move- 
ments are  extremely  violent.  The  patient  is  tossed  about  in  his  bed,  and  can  eat 
little  and  sleep  none.     We  have  ourselves  observed  three  such  cases,  in  girls  four- 


OHOEEA  1155 

teen  to  seventeen  years  of  age,  which  proved  fatal  within  the  first  two  or  three 
weeks.  Two  died  from  general  exhaustion  and  collapse,  and  the  third  from 
gangrene  affecting  numerous  cutaneous  traumatic  lesions,  which  had  occurred 
despite  every  possible  precaution. 

Nature  of  the  Disease, — All  cases  of  genuine  chorea  thus  far  examined  by 
pathologists  have  failed  to  furnish  any  lesions  which  can  be  regarded  as  essential. 
In  the  three  cases  above  mentioned  the  autopsy  revealed  absolutely  nothing 
abnormal  in  the  central  nervous  system.  We  are  at  present,  therefore,  obliged  to 
classify  chorea  as  a  "  neurosis  "—that  is,  as  a  disease  that  produces  functional  dis- 
turbances, for  which  latter  there  is  no  anatomical  basis  known  to  us.  The  symp- 
toms themselves  show  that  the  disorder  must  affect  principally  some  motor  region 
of  the  nervous  system;  but  just  which  motor  region  is  involved  can  at  present 
only  be  conjectured.  It  seems  very  probable,  however,  that  the  true  seat  of  chorea 
is  to  be  sought  in  the  brain.  In  the  first  place,  the  frequent  occurrence  of  hemi- 
chorea  would  indicate  this;  as  would  also  the  fact  that  slight  mental  anomalies 
are  frequently  combined  with  chorea ;  and,  finally,  "  choreiform  "  movements  may 
occur  as  the  sole  symptom  of  undoubted  cerebral  disease,  as  in  post-hemiplegie 
hemichorea.  We  have,  however,  no  hint  as  to  whether  the  motor  regions  in- 
volved are  those  located  in  the  cortex,  or  others.  The  surmise  has  quite  often 
been  expressed  that  chorea  is  due  to  embolism  of  a  mild  type ;  but,  in  our  opinion, 
this  view  entirely  lacks  proof,  and  is  even  extremely  improbable.  As  has  been 
said  above,  we  believe  that  the  most  probable  theory  is  that  genuine  chorea  is  of 
toxic  and  usually  post-infectious  origin. 

Diag-nosis. — The  diagnosis  is  almost  always  easy,  and  it  can  often  be  made  at  a 
glance.  The  motor  symptoms  of  athetosis,  paralysis  agitans,  and  of  alcoholic, 
senile,  saturnine,  and  mercurial  tremor  are  so  characteristic  as  to  be  readily  dis- 
tinguished from  the  movements  of  chorea.  It  is  not  difficult  to  perceive  the 
difference  between  genuine  idiopathic  chorea  and  the  symptomatic  choreiform 
movements  occasioned  by  some  other  cerebral  lesion. 

Prognosis. — As  has  been  stated,  the  prognosis  of  ordinary  chorea  is  almost  in- 
variably favorable,  although  the  disease  may  prove  very  tedious.  The  possibility 
of  relapses  should  be  borne  in  mind.  The  prognosis  is  doubtful,  only  in  the  worst 
cases  of  acute  chorea,  where  there  is  great  and  rapid  failure  of  the  general 
health.  Chorea  gravidarum  must  also  be  regarded  as  of  far  more  serious  progno- 
sis than  the  ordinary  chorea  of  childhood. 

Treatment. — Even  in  mild  cases  the  patient  must  be  kept  from  school  and  at 
home,  in  order  to  avoid  all  unnecessary  excitement  from  ridicule  and  the  like. 
If  the  chorea  be  only  moderately  severe,  it  is  not  necessary  that  the  child  should 
be  in  bed;  we  may  even  allow  moderate  exercise  in  the  open  air.  Where  the 
motions  are  violent,  we  should  seek  to  guard  the  patient  from  self-injury  by  means 
of  pillows  and  cushions. 

Among  the  remedies  recommended  for  chorea,  the  chief  place  is  occupied  by 
arsenic  and  potassic  bromide.  Arsenic  in  particular  seems  often  to  be  of  value. 
We  give  Fowler's  solution  alone,  or  with  equal  parts  of  peppermint  water  or  com- 
pound tincture  of  cinchona ;  we  may  begin  with  five  drops,  in  water,  two  or  three 
times  a  day,  gradually  increasing  to  eight  or  ten  drops.  [In  severe  cases  larger 
doses  may  be  given.  It  should  be  pushed  up  to  twenty  drops  or  more,  stopping 
for  twenty-four  hours  if  symptoms  of  poisoning  appear,  and  beginning  again  at 
the  same  dose.  It  should  be  freely  diluted. — K.]  In  children  under  six,  the  dose 
should  be  made  somewhat  smaller.  If  the  child  be  anaemic,  iron  may  be  given 
in  addition ;  or,  if  there  be  great  restlessness  and  loss  of  sleep,  narcotics  may  also 
be  administered.  Antipyrine,  in  doses  of  seven  to  fifteen  grains  (grammes 
0.5-1)  several  times  a  day,  is  sometimes  of  decided  service  in  severe  cases.  We 
give  it  especially  in  cases  associated  with  rheumatism.     Many  observers  have  seen 


1156  DISEASES   OF  THE  NEKVOUS   SYSTEM 

good  results  from  sodic  salicylate,  fifteen  to  thirty  grains  three  times  a  day 
(grammes  1-2).  If  these  remedies  have  no  effect  we  may  also  try  bromide 
of  potassium  in  large  doses,  a  drachm  or  more  (grammes  3-5)  a  day.  In  severe 
chorea  we  have  seen  frequently  undoubted  benefit  from  the  bromides.  ISTumerous 
other  drugs  have  been  recommended :  oxide  of  zinc,  valerianate  of  zinc,  nitrate  of 
silver,  and  sulphate  of  copper.  The  efiicacy  of  all  these  remedies  is  doubtful  and 
at  present  they  are  very  rarely  used.  Eeiss  has  lately  recommended  physostigmine, 
one  sixth  to  one  third  of  a  grain  a  day  (gramme  0.001-0.002),  best  subcutaneously. 
[Sulfonal,  three  to  five  grains  (gramme  0.2-0.4)  three  times  a  day,  acts  well,  as 
an  adjuvant  to  arsenic,  in  cases  where  there  is  much  excitement.  Exalgine,  two 
or  three  grains  (gramme  0.1-0.2)  three  times  a  day,  has  also  been  recommended. — 
K.]  l^arcotics  should  be  employed  very  cautiously  in  chorea.  Although  chloral 
has  been  recently  recommended  for  grave  cases,  there  are  instances  known  where 
this  remedy  has  been  followed  by  unfortunate  results ;  but  we  may  try  the  contin- 
ued and  cautious  use  of  small  doses  of  chloral,  giving  to  children  two  to  five  grains 
(gramme  0.1-0.3),  and  to  adults  ten  to  fifteen  grains  (gramme  0.5-1)  daily,  or  a 
few  larger  doses  at  night. 

Hydrotherapeutics  of  a  mild  kind  do  good,  and  can  easily  be  carried  out  in 
most  instances.  Thus,  we  may  use  lukewarm  baths,  a  wet  pack,  or  gentle  spong- 
ing with  water  at  72°-82°  (18°-22°  R.)  to  great  advantage.  In  some  obstinate 
cases  sweating  seems  of  service.  We  have  also  repeatedly  seen  decided  benefit 
from  the  use  of  methodical  gymnastic  exercises,  consisting  of  regular  flexion  and 
extension  of  the  arms,  marching  in  time,  etc. 

Electricity  may  also  be  tried.  A  feeble  current  of  galvanic  electricity  is  ap- 
plied to  the  head  (in  the  region  of  the  motor  centers),  or  the  spinal  cord  is  gal- 
vanized. If  there  be  points  along  the  spinal  column  where  pressure  causes  pain, 
it  is  said  to  be  an  excellent  plan  to  apply  the  anode  to  them;  but  the  results  of 
electrical  treatment  are  seldom  very  brilliant. 

In  the  chorea  of  pregnancy,  which  sometimes  is  a  very  violent  disease,  the 
same  remedies  may  be  employed.  If  they  do  no  good,  artificial  delivery  may 
be  required ;  after  which,  as  we  can  attest,  there  may  be  a  rapid  abatement  of  all 
symptoms. 


APPEl^DIX 

CHRONIC  HEREDITARY  CHOREA.  ELECTRICAL  CHOREA.  PAEAJ^IYOCLONUS  (MYOCLONIA) 

1.  Chronic  Hereditary  Chorea  (Hunting'ton's  Chorea). — Chronic  chorea  also 
manifests  itself  by  severe  choreic  movements  of  the  body,  but  in  its  nature  it  is 
a  wholly  different  disease  from  ordinary  chorea.  It  is  notably  of  family  (generic) 
or  hereditary  occurrence.  The  symptoms  of  the  disease  begin  as  a  rule  between 
thirty  and  forty.  The  choreic  movements  gradually  become  more  severe  and 
increase  to  the  most  curious  and  strange  movements  of  the  face  and  the  whole 
body.  The  ability  to  walk  and  to  use  the  arms  in  eating,  dressing,  etc.,  is  retained 
for  a  long  time ;  but  every  action  is  accompanied  by  distressing  associated  move- 
ments and  twitchings  of  the  whole  body.  The  sensibility  and  the  other  nervous 
functions  are  unaffected,  but  mentally  we  notice  a  decided  but  gradual  failure  as 
time  goes  on,  which  may  increase  to  complete  dementia.  The  anatomical  basis 
of  this  remarkable  disease  is  still  unknown.  The  disease  is  incurable.  The 
remedies  used  in  ordinary  chorea  never  mitigate  the  symptoms. 

2.  Electrical  Chorea. — Henoch  gave  this  name  to  a  form  of  chorea  in  children 
which  differed  from  the  ordinary  chorea  by  the  much  quicker,  lightning-like  eon- 
tractions  coming  on  in  single  muscles   (especially  of  the  neck  and  shoulders). 


PARALYSIS  AGITANS  1157 

The  contractions  give  the  impression  that  the  muscles  have  been  put  in  contraction 
by  single  galvanic  shocks.  They-  come  on  at  rather  long  intervals  of  three  to 
five  minutes.  The  same  name,  "  electrical  chorea,"  has  also  been  given  to  a  pe- 
culiar disease,  said  to  be  endemic  in  Lombardy,  which  was  first  described  by 
Dubini,  and  which  is  therefore  known  by  the  name  of  "  Dubini's  disease."  In  this 
affection  also  muscular  twitchings  occur,  usually  beginning  in  one  arm  and  grad- 
ually involving  all  the  extremities.  After  several  weeks  or  months  paralysis  and 
muscular  atrophy  set  in,  and  not  infrequently,  it  is  said,  epileptiform  convulsions 
and  fever.     Nothing  definite  is  known  as  to  the  anatomical  changes. 

3.  Paramyoclonus  Multiplex  (Myoclonia). — This  name  was  first  used  by 
Friedreich  for  a  case  observed  by  him,  in  which  there  were  clonic  spasms  in  sym- 
metrical groups  of  muscles  of  the  arms  and  legs,  which  came  on  in  paroxysms 
without  any  disturbance  of  consciousness.  There  was  also  a  considerable  increase 
of  the  tendon  reflexes.  Such  cases  have  since  been  described  in  considerable  num- 
bers, but  undoubtedly  very  different  morbid  conditions  have  been  confounded  with 
one  another.  We  can  regard  as  genuine  paramyoclonus — that  is,  as  a  specific  dis- 
ease sui  generis — only  those  cases  where  lightning-like  contractions  come  on  in 
single  muscles,  often  without  any  visible  effect  of  movement.  The  muscles  of  the 
trunk  and  extremities  are  most  frequently  involved.  This  peculiar  morbid  condi- 
tion is  on  the  one  hand  most  closely  allied  to  electrical  chorea  mentioned  above, 
while,  on  the  other  hand,  according  to  our  own  experience,  it  has  a  decidedly  close 
relation  to  the  different  forms  of  Uc  convulsif  (clonic  facial  spasm,  clonic  ac- 
cessory spasm,  q.  v.).  A  large  number  of  the  cases  described  as  myoclonia  or 
paramyoclonus,  however,  are  undoubtedly  to  be  classed  as  hysteria  {vide  infra). 

Unverricht  and  others  have  described  a  special  form  of  myoclonia.  It  is  char- 
acterized by  its  occurrence  in  various  members  of  one  family,  by  the  extension 
of  the  twitchings  to  the  lingual  and  pharyngeal  muscles,  and  by  its  complication 
with  epileptic  attacks. 


CHAPTER   III 

PARALYSIS    AGITANS 

( Sliahing  Palsy.     ParMnison's  Disease) 

^tiolog-y. — In  1817  Parkinson  described  for  the  first  time  a  disease  which  he 
named  "  shaking  palsy."  It  is  not  of  very  frequent  occurrence,  and  as  yet 
little  has  been  ascertained  with  regard  to  its  setiology.  In  most  cases  it  develops 
very  gradually,  without  any  demonstrable  cause.  It  almost  always  attacks  elderly 
persons,  being  very  rare  before  the  thirty-fifth  year.  Sex  does  not  seem  to  exert 
any  great  predisposing  influence.  Hereditary  neuropathic  tendencies  can  indeed  be 
traced  in  some  instances,  but  they  are  certainly  of  less  potency  in  paralysis  agitans 
than,  for  instance,  in  epilepsy.  Special  exciting  causes  have  sometimes  been  ob- 
served, such  as  catching  cold,  violent  emotional  excitement,  and  traumatic  inflxi- 
ences  (blows,  falls,  injuries,  etc.).  Berger  reports  two  cases  where  the  first  symp- 
toms appeared  after  an  acute  febrile  disease  (typhoid  fever). 

Clinical  History.- — Paralysis  agitans  has  two  characteristic  symptoms,  viz.,  (1) 
peculiar  evidences  of  motor  irritation,  evinced  by  tremor,  and  (2)  a  condition  of 
stiffness  and  persistent  shortening  of  certain  muscles,  consequent  upon  which  is  a 
series  of  peculiar  motor  phenomena. 

The  trembling  is  generally  the  earliest  symptom  to  attract  the  patient's  atten- 
tion. It  usually  begins  in  the  hands,  especially  in  the  right  hand,  and  then 
gradually  involves  the  arm  and  leg  on  the  same  side,  next  the  other  arm  and 


1158 


DISEASES   OF  THE  NEEVOUS   SYSTEM 


leg,  and  finally,  in  well-marked  cases,  the  entire  body.  The  form  of  tremor  is 
very  characteristic.  There  are  rapid,  uniform,  oscillatory  movements  of  varying 
extent.  The  tremor  is  usually  greatest  in  the  hands  and  arms.  At  the  same  time 
the  thumbs  and  half-flexed  fingers  exhibit  a  movement  which  suggests  spinning 
or  pill-rolling.  The  forearm  is  generally  flexed  and  extended  in  rapid  alterna- 
tion, but  it  is  always  very  difficult  to  determine  just  what  muscles  contract.     With 

regard  to  the  trunk,  it  is  often  a  question  whether  its 
tremor  is  of  independent  origin,  or  due  merely  to  the 
motion  of  the  extremities.  Charcot  states  that  the 
head  and  the  facial  muscles  are  never  implicated,  but 
there  is  doubt  about  this  point.  "We  ourselves,  as  well 
as  other  observers,  have  repeatedly  seen  independent 
tremor  of  the  head.  As  to  the  face,  the  muscles  about 
the  chin  seem  to  suffer  chiefly. 

The  trembling  of  paralysis  agitans  is  almost  con- 
tinuous. It  may,  indeed,  cease  for  a  moment  in  a 
limb,  but  only  to  recur  immediately.  The  quieter  the 
patient  is  in  mind  and  body,  the  less  violent  are  the 
movements.  If  he  is  excited,  or  begins  to  speak,  or  is 
watched,  the  tremor  at  once  becomes  exaggerated,  and 
may  be  violent  enough  to  jar  the  whole  body  vehe- 
mently. Active  motion  does  not  intensify  the  tremor. 
On  the  contrary,  it  may  often  be  observed  that  the 
trembling  abates  when  the  muscles  undergo  vigorous 
voluntary  contraction,  as  when  a  weight  is  lifted,  or 
the  hand  of  another  is  firmly  grasped. 

The  second  symptom  is  almost  more  characteristic 
than  the  first.  It  consists  of  a  peculiar  rigidity  of  the 
rauscles.  We  generally  notice,  even  in  the  face,  a 
peculiar  tension  of  the  muscles.  This  often  produces 
a  stolidity  of  expression,  so  that  the  emotions  are  less 
clearly  depicted  than  upon  the  countenance  of  a 
healthy  person.  We  have  been  especially  impressed 
in  several  cases  by  the  infrequency  of  winking.  The 
head  gradually  becomes  more  and  more  flexed.  When 
the  disease  has  lasted  some  years,  the  chin  may  even 
rest  upon  the  sternum.  The  muscles  of  the  trunk  and 
extremities  also  stiffen  gradually,  and  lead  to  peculiar 
and  almost  pathognomonic  appearances.  The  body  is 
bent  over  forward;  the  arms  cling  to  the  trunk,  and  are  flexed  at  the  elbow  joint; 
the  fingers  are  flexed,  especially  at  the  metacarpo-phalangeal  joint;  the  thumbs 
rest  against  the  fingers,  as  if  holding  a  pen,  or  else  are  flexed  inward  upon  the 
palm;  and  the  legs  are  somewhat  bent  at  the  knee.  The  accompanying  picture 
(Fig.  178)  is  from  the  photograph  of  a  patient  who  was  for  a  long  time  under 
observation  at  the  clinique  in  Leipsic,  and  gives  a  good  representation  of  the 
characteristic  posture. 

The  stiffness  of  the  muscles  also  operates  to  impair  motion  in  various  ways. 
In  particular  all  movements  of  the  trunk  are  greatly  impeded.  In  advanced  cases 
the  patient  can  not  get  upon  his  feet,  if  he  is  lying  in  bed,  without  help.  Inas- 
much, however,  as  the  muscular  strength  usually  remains  good  (vide  infra),  he 
requires  to  exert  but  a  slight  traction  upon  some  helping  hand  in  order  to  attain 
an  erect  posture.  On  the  other  hand,  the  patient  is  often  utterly  unable  to  turn 
in  bed  from  one  side  to  the  other.  In  severe  cases,  therefore,  it  is  often  neces- 
sary to  alter  the  patient's  position  several  times  in  a  night,  especially  as  lying  long 


Fig.  1?'^  — Lbdrdcteribtic  position 
of  the  body  m  paralysis 
agitans. 


PAEALYSIS   AGITANS  1159 

in  one  attitude  makes  him  feel  very  uneasy.  If  the  patient  is  in  a  chair,  he  can 
not  get  up  of  himself,  because  it  is  impossible  for  him  to  bend  his  body  forward 
in  the  necessary  manner;  but  with  just  a  little  help  he  can  stand  up,  and  he  is  then 
able  to  walk  alone  or  even  to  run.  Then,  since  the  flexion  of  the  trunk  forward 
brings  the  center  of  gravity  forward  also,  and  the  trunk  can  not  be  sufficiently 
bent  backward,  he  is  apt  to  "  get  going,"  so  that  he  can  not  stop  until  he  brings 
up  against  a  post  or  a  wall.  If  such  a  patient,  with  a  considerable  degree  of 
anteflexion  and  rigidity  of  the  trunk,  is  slightly  pushed  from  behind,  he  will 
have  to  start  into  a  run  to  avoid  falling.  This  phenomenon  is  termed  "  propul- 
sion." A  push  backward,  which  brings  the  center  of  gravity  behind  the  point 
of  support,  is  very  likely  to  make  such  a  patient  fall,  as  he  will  seldom  succeed 
in  moving  backward  fast  enough  to  recover  his  balance  (retropulsion).  Both  pro- 
pulsion and  retropulsion  are  conceived  by  Charcot  to  be  "  forced  movements  " 
(see  page  836)  in  the  strict  sense  of  the  term.  "We  are,  however,  convinced,  as 
the  result  of  numerous  observations,  that  these  phenomena  can  in  every  case  be 
explained  simply  by  the  mechanical  conditions  arising  from  displacement  of  the 
center  of  gravity  and  the  muscular  rigidity.  Again,  the  reason  why  many  pa- 
tients are  prone  to  keep  their  arms  behind  them  as  they  walk  is  that  such  a  posi- 
tion contributes  slightly  toward  bringing  the  center  of  gravity  farther  back- 
ward. 

The  movements  of  the  extremities  are  less  impaired  than  those  of  the  trunk, 
but  they  often  betray  a  certain  slowness  and  stiffness.  The  strength  of  the 
muscles  may  be  preserved  for  a  long  while,  but  often  there  is  at  last  evident 
paresis.  Even  in  the  early  stages  of  the  disease  the  muscles  may  become  easily 
fatigued.  The  impairment  of  facial  expression  has  already  been  referred  to.  In 
many  cases  the  muscles  of  the  eye  also  seem  to  participate  in  the  rigidity,  making 
it  difficult  for  the  eye  in  reading  to  follow  rapidly  along  each  line,  or  to  pass  from 
the  end  of  one  line  to  the  beginning  of  the  next.  [The  voice  is  often  affected; 
the  patient  talks  in  a  high-pitched  monotone. — K.] 

The  muscular  rigidity  is  almost  more  characteristic  of  paralysis  agitans  than 
is  the  tremor.  Indeed,  there  would  seem  to  be  cases,  as  we  have  ourselves  ob- 
served, where,  at  least  for  a  time,  the  posture  of  the  patient  is  typical,  and  yet 
there  is  no  trembling.  Such  cases  might  be  called  paralysis  agitans  sine  agiia- 
tione.  In  uncomplicated  cases  all  other  nervous  functions  remain  perfectly 
normal.  Sensation  is  never  impaired.  Sometimes  some  pain  is  felt  at  the  com- 
mencement of  the  disease,  particularly  in  the  shoulders.  There  is  no  striking 
disturbance  of  reflex  action  or  of  the  bladder.  In  a  few  cases  of  paralysis  agi- 
tans, cerebral  and  mental  symptoms  have  been  observed ;  but  they  are  so  rare  that 
it  is  impossible  to  say  whether  they  belong  to  the  disease  or  are  merely  accidental 
complications.  It  is  also  noteworthy  that  many  patients  complain  of  a  subjective 
feeling  of  excessive  warmth.  The  internal  temperature  is  normal ;  but  it  is  said 
that  the  temperature  of  the  surface  of  the  body  is  frequently  somewhat  elevated. 
Sometimes  there  is  a  tendency  to  excessive  perspiration.  [Mosse  and  Baiial  have 
found  that  the  excretion  of  urea  and  the  total  excretion  of  phosphoric  acid  is  in- 
creased in  paralysis  agitans,  but  that  the  excretion  of  imperfectly  oxidized  phos- 
phoric acid  is  diminished,  thus  showing  that  there  is  increased  combustion. — K.] 

The  disease  runs  a  very  chronic  course,  perhaps  for  twenty  years  or  more. 
From  the  first,  it  keeps  on  slowly  but  gradually  developing.  The  symptoms 
rarely  exhibit  marked  alterations  of  mildness  and  severity,  but  for  long  periods 
the  progress  of  the  disease  may  be  apparently  arrested.  Recovery  has  never  yet 
been  observed.  The  final  and  fatal  termination  is  not  brought  about  by  the  dis- 
ease itself,  but  is  due  to  some  intercurrent  affection  or  to  general  marasmus.  The 
original  of  the  picture  on  the  opposite  page  came  to  a  pitiable  end  by  tumbling  face 
downward  into  a  puddle  of  water.     He  could  not  get  up,  and  was  drowned. 


1160  DISEASES   OF  THE  NEEVOUS   SYSTEM 

Nature  of  the  Disease.— The  true  nature,  of  the  disease  is  unknown.  Inas- 
much as  the  disorder  is  purely  a  motor  one,  the  corresponding  lesions  must  be 
sought  somewhere  in  the  motor  system.  As  yet,  however,  post-mortem  examina- 
tions of  the  nervous  system,  even  with  the  microscope,  have  revealed  no  charac- 
teristic changes ;  at  least  we  can  ascribe  no  significance  to  the  statements  in  this 
respect  made  by  some  observers.  We  must,  therefore,  confess  that  we  have  even 
had  a  doubt  whether  it  is  justifiable  to  claim  that  paralysis  agitans  is  an  affection 
of  the  nervous  system  at  all,  or  whether  it  may  not  possibly  be  of  purely  muscular 
origin.  Certainly  it  would  not  be  impossible  for  abnormal  processes  in  the  mus- 
cles to  excite  the  tremor  and  tonic  contraction.  But,  as  has  been  said,  there  is 
at  present  no  ground  for  deciding  this  question;  we  would  merely  suggest  it. 

[Gordinier  has  found  some  perivascular  sclerosis  in  the  posterior  portion  of 
the  spinal  cord,  with  pigmentation  and  degeneration  of  the  ganglion-cells  and 
some  dilatation  of  the  vessels.  He  thinks  the  symptoms  are  due  to  irritation  from 
an  increase  of  the  neuroglia  in  the  posterior  columns,  causing  excitability  of  the 
reflex  collaterals  of  the  posterior  nerve-roots  which  arborize  about  the  motor  cells 
in  the  anterior  horns.  This  causes  an  increased  discharge  of  energy,  which  gives 
rise  to  tremor  and  rigidity.  Other  observers  have  found  somewhat  similar 
changes  in  the  white  matter  of  the  cord,  and  also  in  the  gray  matter. — K.] 

Diagnosis. — Any  typical  case  of  paralysis  agitans  can  be  easily  and  certainly 
recognized,  often  at  the  first  glance.  The  important  factors  are  the  peculiar 
tremor,  the  characteristic  carriage,  and  the  rigidity  of  the  muscles  of  the  trunk 
and  extremities.  It  was  formerly  a  difiicult  matter  to  distinguish  between  paraly- 
sis agitans  and  multiple  sclerosis ;  but  to-day  the  peculiarities  of  the  two  diseases 
are  better  known,  and  confusion  is  seldom  possible.  The  character  of  the  tremor 
varies  in  the  two.  In  paralysis  agitans  it  persists  even  when  the  patient  is  quiet, 
and  it  is  decidedly  oscillatory.  The  motion  in  multiple  sclerosis  {q.  v.)  is  almost 
always  an  intention  tremor  only;  and,  what  is  of  still  greater  importance  in  dis- 
tinguishing between  them,  the  general  appearances  of  the  two  diseases  are  essen- 
tially unlike. 

Treatment. — As  has  already  been  implied  above,  we  possess  no  means  of  con- 
trolling the  disease.  In  most  cases,  therefore,  the  treatment  is  confined  to  general 
hygienic  measures.  Good  may  be  done  by  lukewarm  baths  of  considerable  dura- 
tion, and  by  gentle  massage  of  the  muscles.  Among  internal  remedies  Erb  has 
lately  recommended  hyoscine,  as  having  the  most  palliative  and  soothing  influ- 
ence. It  is  best  given  subcutaneously,  and  we  must  always  begin  with  very 
small  doses,  as  otherwise  unpleasant  symptoms,  such  as  vertigo,  headache,  etc.,  may 
arise.  We  inject  one  two-hundredth  to  one  one-hundredth  of  a  grain  (milligramme 
i~^)  in  aqueous  solution  (solution  of  hyoscine  muriate,  1  to  1,000,  seven  to 
fifteen  minims).  If  well  borne  we  can  cautiously  increase  the  dose.  [Atropine 
and  hyoscyamine  have  also  shown  good  results,  especially  when  given  subcu- 
taneously.— K.]  Arsenic,  ergotine,  potassic  bromide,  physostigmine,  and  curare 
may  also  be  tried.  Francotte  praises  the  action  of  sulphate  of  duboisine  (subcu- 
taneously or  in  pills  of  lio  grain,  gramme  0.0005,  three  to  six  times  a  day)  ;  this 
also  must  be  used  with  care.  If  electricity  is  to  do  any  good  at  all,  the  case  must 
be  a  recent  one.  It  is  said  that  in  some  instances  stretching  of  the  nerves  has 
diminished  the  tremor  considerably;  but  our  own  observations  would  not  lead  us 
to  recommend  the  procedure  in  this  disease. 


ATHETOSIS 


1161 


CHAPTER   IV 
ATHETOSIS 

In  1871  the  American  neurologist  Hammond  described  under  the  name  of 
athetosis  (ciSeros,  without  fixed  position)  a  peculiar  symptom  of  irritation  of  the 
motor  centers,  differing  in 
a  characteristic  manner 
from  all  other  forms  of 
involuntary  movements,  in- 
cluding the  epileptiform 
and  choreic.  The  move- 
ments of  athetosis  (see 
page  836)  are  often  very 
complicated  and  peculiar. 
The  part  affected  by  them 
is  in  continuous  unrest.  If 
the  facial  muscles  (usually 
those  of  the  lower  division 
of  the  facial  nerve)  and  the 
muscles  of  mastication  be 
attacked,  the  face  and 
mouth  are  constantly  being 
twisted  and  distorted.  If 
the  tongue  suffer,  as  in  one 
case  which  we  saw,  speech 
is  difficult  and  indistinct. 
If  the  muscles  of  the  back 
of  the  neck  be  implicated, 
the  head  is  usually  drawn 
backward  or  to  one  side, 
and  is  turned  and  twisted 
in  all  sorts  of  ways.  Most 
characteristic  of  all,  how- 
ever, are  the  movements  ex- 
hibited by  the  hand  and 
fingers  when  affected.  The 
fingers  are  incessantly  be- 
ing separated,  extended, 
flexed,  and  intertwined,  as- 
suming the  oddest  posi- 
tions. The  accompanying 
pictures  may  serve  to  il- 
lustrate this  (Fig.  179). 
The  character  of  the  move- 
ments reveals  that  the  in- 
terossei  must  be  chiefly 
involved.  It  is  a  very  fre- 
quent result  of  the  unceas- 
ing stretching  of  the  articu- 
lar ligaments  of  the  fingers 
that    at    last    the    articula- 

4.-^ 1  „  1         J      J.       Fig-  1'''9. — Example  of  the  position  of  the  fingers  in  the  movement 

tions      become      relaxed     to  'of  athetosis  (personal  observation). 


1162  DISEASES   OF  THE  NERVOUS   SYSTEM 

such  a  degree  as  to  permit  of  such  a  hyperextension  of  the  fingers,  as  it  is  impos- 
sible for  a  healthy  person  to  imitate.  The  arms  are  generally  less  severely  affected 
than  the  hands ;  and  in  the  lower  limbs  the  trouble  is  not  often  so  severe  as  in  the 
upper.     The  toes  may,  however,  exhibit  motions  analogous  to  those  of  the  fingers. 

Although  in  general  the  movements  are  continuous,  their  vigor  frequently 
varies.  Thus  they  almost  always  are  aggravated  if  the  patient  becomes  excited. 
During  sleep  they  generally  cease,  although  in  certain  instances  they  have  per- 
sisted even  then,  only  being  diminished.  When  voluntary  motions  are  made 
they  ordinarily  grow  feebler;  but  they  may,  on  the  contrary,  become  exaggerated, 
taking  the  form  of  sympathetic  movements. 

We  must  distinguish  between  genuine  idiopathic  athetosis  and  a  symptomatic 
form,  which  also  occurs. 

Symptomatic  athetosis  is  seen  in  various  nervous  diseases.  The  first  observa- 
tions reported  by  Hammond  were,  most  of  them,  made  in  cases  of  epilepsy,  or  in 
severe  psychoses,  and  the  like.  [In  Hammond's  original  case  the  athetosis  was 
symptomatic  and  due  to  a  lesion  involving  the  optic  thalamus,  the  lenticular 
nucleus,  and  the  most  posterior  portion  of  the  internal  capsule. — K.]  By  far  the 
most  frequent  source  of  the  phenomenon,  however,  is  hemiplegia,  producing  what 
is  known  as  post-hemiplegic  chorea,  or  better,  post-hemiplegic  hemiathetosis. 
This  is,  to  be  sure,  a  very  rare  sequel  to  the  ordinary  hemiplegia  of  elderly  per- 
sons, but  follows  rather  infantile  paralysis  of  cerebral  origin  (vide  page  1112). 
Some  traces  of  athetosis  are  seen  in  a  majority  of  the  cases  of  infantile 
hemiplegia. 

Idiopathic  athetosis  is  rare.  Here  the  peculiar  movements  are  the  chief,  if 
not  the  sole,  symptom  of  disease.  A  few  cases  of  this  sort  have  been  reported 
where  the  athetosis  began  without  known  cause,  and  usually  was  limited  to  some 
one  region.  It  attacked  elderly  individuals  who  were  previously  healthy.  Of  espe- 
cial importance  is  an  apparently  congenital  form  of  athetosis,  dating  from  the 
earliest  infancy.  Of  this  we  have  ourselves  seen  several  instances,  which  closely 
resembled  one  another.  The  condition  is  a  permanent  one,  not  progressive,  nor,  on 
the  other  hand,  capable  of  any  great  amelioration.  The  movements  are  almost  al- 
ways most  pronounced  in  the  face,  head,  and  fingers.  Other  nervous  disturbances, 
paralysis  or  impairment  of  sensation,  are  entirely  absent  or  are  associated  with 
the  athetosis  in  various  ways.  The  intelligence  of  the  patient  is  sometimes,  but 
not  always,  diminished. 

Of  the  nature  of  athetosis,  or  the  locality  or  nature  of  the  irritation,  we  possess 
no  information  as  yet.  It  is  extremely  probable  that  the  lesion  is  in  every  case  a 
cerebral  one.  Perhaps  it  is  in  the  cortex.  In  symptomatic  athetosis  we  find 
post  mortem  the  changes  caused  by  the  original  trouble.  In  idiopathic  athetosis 
no  changes  have  thus  far  been  reported.  In  a  case  of  our  own  which  came  to 
autopsy,  absolutely  nothing  abnormal  was  found  in  the  brain.  The  patient  was 
an  elderly  female,  who  displayed  typical  movements  of  the  arm  and  hand. 

It  is  not  yet  known  whether  recovery  is  possible.  A  certain  amount  of  im- 
provement sometimes  follows  the  administration  of  Fowler's  solution,  bromide 
of  potassium,  or  galvanism. 


CHAPTER   V 

TETANY 

(Intermittent  Tetanus.     Tetanilla) 

.ffitiology. — Tetany,  a  name  originating  with  Corvisart,  is  applied  to  a  pe- 
culiar neurosis,  characterized  mainly  by  paroxysmal  tonic  convulsions,  usually 


TETANY  1163 

painful,  in  certain  symmetrical  and  bilateral  groups  of  muscles.  The  disease 
attacks  by  preference  children  and.  young  adults  between  fifteen  and  thirty  years 
of  age.  The  physiological  processes  peculiar  to  the  female  sex  seem  to  have  an 
especial  tendency  to  excite  the  disorder.  It  is  comparatively  so  frequent  in 
nursing  women  that  Trousseau  has  called  it  "  contracture  des  nourrices.^'  It  is 
also  remarkable  that  tetany  is  especially  common  in  certain  occupations,  particu- 
larly in  cobblers  and  tailors. 

Among  exciting  causes,  catching  cold  deserves  particular  mention.  Hence  the 
earlier  observers  describe  the  disease  as  "  intermittent  contracture  of  rheumatic 
origin."  In  other  cases  the  disorder  has  appeared  as  a  sequel  to  other  acute  dis- 
eases, such  as  typhus  or  typhoid  fever,  small-pox,  and  intestinal  troubles.  A  very 
remarkable  fact  was  pointed  out  by  N.  Weiss — namely,  that  tetany  is  apt  to  follow 
operative  extirpation  of  goitre.  We  have  once  observed  attacks  of  tetany  in  a  pa- 
tient with  exophthalmic  goitre.  Its  occurrence  in  gastric  diseases  is  also  interest- 
ing, it  being  seen  especially  in  dilatation  of  the  stomach  due  to  cicatricial  stenosis 
resulting  from  ulcer  of  the  pylorus  with  hypersecretion  of  gastric  juice.  The  tet- 
any of  childhood  is  seen  chiefly  in  patients  with  dyspeptic  and  intestinal  symp- 
toms. All  these  observations  suggest  the  action  of  some  toxic  substance,  and  it  is 
therefore  worthy  of  note  that  attacks  precisely  like  tetany  have  been  observed  in 
different  intoxications  (ergotine,  alcohol,  chloroform).  In  chronic  alcoholic  sub- 
jects tonic  spasms  like  tetany  are  not  very  rare.  Reports  from  various  quarters 
indicate  that  tetany  may  sometimes  be  epidemic.  Most  cases  ordinarily  occur  in 
the  winter  and  spring  (February  and  March).  On  the  other  hand,  endemic  influ- 
ences also  seem  to  us  to  have  some  importance.  At  any  rate,  the  published  ac- 
counts would  seem  to  indicate  that  tetany  is  much  more  frequent  in  Heidelberg 
(Erb,  E.  Schultze),  Breslau  (Berger),  and  Vienna  (N.  Weiss),  than  in  Leipsic, 
for  instance,  where  it  is  one  of  the  very  rarest  nervous  diseases.  [It  is  also  very 
rare  in  America.  Crozer  Griffith  a  few  years  ago  was  able  to  collect  only  seventy- 
three  reported  cases,  while  forty  or  fifty  cases  have  been  treated  at  the  hospital 
in  Vienna  in  a  single  year. — K.] 

Erom  what  has  been  said  it  is  evident  that  we  should  probably  not  regard 
tetany  as  one  single  disease  £etiologically.  Just  as  we  distinguish  in  epileptic 
attacks  between  genuine  epilepsy  and  symptomatic  epileptic  (epileptiform)  con- 
vulsions, so  we  may  distinguish  between  "  idiopathic  "  and  symptomatic  tetany. 

Clinical  History. — The  paroxysm  of  tetany  usually  has  certain  prodromata, 
consisting  of  slight  general  discomfort  and  pain,  and  of  a  feeling  of  weakness  and 
stiffness,  most  marked  in  the  arms.  These  symptoms  last  some  hours  (at  least) 
before  the  true  convulsive  stage  begins.  The  extremities,  and  more  particularly 
the  fingers,  almost  always  suffer  first;  and  then,  after  the  arms,  the  lower  ex- 
tremities become  involved.  The  spasm  usually  affects  the  toes  before  it  seizes 
upon  the  other  parts  of  the  leg.  The  symptoms  are  almost  invariably  bilateral 
and  symmetrical.  Exceptionally,  the  disturbance  commences  in  the  leg,  or  is 
confined  to  one  side  of  the  body.  In  most  cases  the  flexor  muscles  are  pre- 
dominantly affected,  giving  rise  to  very  characteristic  postures.  The  fingers 
are  in  apposition  with  one  another,  and  placed  as  if  holding  a  pen,  or,  as  Trous- 
seau says,  as  if  the  hand  were  about  to  be  thrust  into  the  vagina,  during  labor; 
but  in  the  attack  the  fingers  may  also  be  closed  in  a  fist.  The  hands  are  flexed, 
the  elbows  are  also  slightly  flexed,  and  the  upper  arm  in  severe  cases  is  pressed 
against  the  chest.  In  the  lower  extremities,  the  toes  are  flexed,  and  the  feet  are 
in  the  posture  of  talipes  equinus.  The  muscles  of  the  thigh  are  less  frequently 
affected,  as  are  also  the  muscles  of  the  trunk,  the  muscles  of  mastication,  the 
facial  and  ocular  muscles,  and  the  diaphragm. 

The  intensity  of  the  tonic  spasm  is  very  great.  The  affected  muscles  feel  as 
hard  as  a  board,  and  are  usually  rather  sensitive  to  pressure.     The  attack  some- 


1164  DISEASES   OF  THE  lYERVOUS   SYSTEM 

times  continues  only  a  few  minutes,  but  not  infrequently  it  may  occupy  several 
hours  or  days.  Other  nervous  symptoms  are  less  prominent ;  the  most  noticeable 
are  parffisthesiaj,  tearing  pains,  etc.  Anaesthesia  is  very  rare.  The  reflexes 
are  generally  normal.  There  is  no  impairment  of  consciousness.  In  only  a  few 
cases  has  a  combination  of  tetany  and  hallucinatory  confusion  been  seen.  In  a 
few  instances  slight  oedematous  swelling  and  other  trophic  disturbances  have  been 
observed,  and  sometimes  profuse  perspiration.  The  temperature  is  normal,  or 
sometimes  subnormal  or  slightly  elevated  (100.5°  to  101°  [C.  38°-38.4°]),  and  the 
pulse  is  often  quite  rapid.     Polyuria  has  sometimes  been  observed. 

When  the  attack  ceases,  which  it  always  does  gradually,  and  never  suddenly, 
the  patient  feels  perfectly  well,  save  for  a  slight  pain  and  stiffness  in  the  mus- 
cles, but  all  the  muscles  often  feel  weak  and  uncertain  during  the  whole  period 
of  the  disease.  Even  in  the  interval  between  the  paroxysms  there  are  also  some 
few  objective  symptoms,  which  have  a  most  important  bearing  on  the  pa- 
thology of  tetany.  In  the  first  place,  the  peripheral  nerves  are  generally  abnor- 
mally sensitive  to  electricity  (especially  to  galvanism,  less  regularly  to  f  aradism) . 
The  complete  demonstration  of  this  fact  we  owe  to  Erb.  The  weakest  current  will 
frequently  produce  violent. contractions.  The  different  sensory  nerves  and  nerves 
of  special  sense  also  seem  often  to  exhibit  a  similar  abnormal  irritability  (Hoff- 
mann), and  finally  we  very  often  find  a  considerable  increase  in  the  mechanical 
irritability  of  nerves,  which  is  seen  with  especial  frequency  in  the  facial  (Chvostek, 
]Sr.  Weiss).  Thus,  if  the  face  be  vigorously  stroked  from  above  downward,  with 
the  finger  or  the  handle  of  a  percussion  hammer,  almost  all  the  muscles  contract 
energetically,  one  after  the  other.  Similar  contractions  are,  of  caurse,  obtained  by 
light  percussion  of  the  different  branches  of  the  facial.  The  direct  mechanical 
excitability  of  the  muscles,  on  the  other  hand,  is  not  increased  (F.  Schultze). 

Another  very  characteristic  symptom  was  discovered  by  Trousseau — "  Trous- 
seau's sign."  It  is  found  in  most  cases,  although  not  in  all,  and  is  this :  a  fresh 
paroxysm  can  at  any  time  be  artificially  excited  by  pressure  upon  the  larger 
arteries  and  nerves  of  the  ami  (particularly  the  median  nerve  and  the  brachial 
artery) .  It  is  not  definitely  known  how  compression  accomplishes  this ;  but  com- 
pression of  a  nerve  seems  to  be  the  main  point,  as  the  corresponding  experiments 
on  animals  show,  in  which  an  artificial  tetany  is  produced  by  extirpation  of  the 
thyroid.  Berger  found  that  mechanical  or  electrical  irritation  of  certain  painful 
points  situated  along  the  spinal  column  produces  the  same  result. 

The  frequency  of  the  attacks  varies  greatly  in  individual  cases.  As  a  rule, 
there  are  several  paroxysms  daily;  but  the  intervals  may  last  for  days,  or  again 
may  be  almost  inappreciable.  The  entire  duration  of  the  disease  is  generally  sev- 
eral weeks,  but  many  cases  last  for  months  or  even  years.  It  is  noteworthy  that 
when  the  paroxysms  grow  less  frequent  and  violent  there  is  also  a  gradual  diminu- 
tion in  the  hypersensitiveness  of  the  nerves  and  in  the  reaction  to  Trousseau's 
test.  As  long  as  these  symptoms  persist,  spontaneous  attacks  are  also  possible. 
Many  persons  seem  especially  disposed  to  tetany,  so  that  the  affection  repeatedly 
recurs  in  them. 

The  termination  of  tetany  is,  as  a  rule,  favorable,  but  in  some  cases  death 
results,  which  of  course  is  usually  due  to  complications.  In  children  the  dis- 
ease may  have  an  unfavorable  termination  if  the  spasms  involve  the  diaphragm  or 
the  laryngeal  muscles.  Nothing  definite  is  known  as  to  the  special  nature  of 
tetany.  ]^o  essential  or  positive  anatomical  lesions  have  yet  been  detected.  The 
symptoms  leave  us  in  doubt  whether  the  disease  affects  the  peripheral  nerves  or 
the  nervous  centers. 

Diagnosis. — The  diagnosis  is  not  difiicult  if  we  only  consider  carefully  the 
symptoms  presented,  the  nature  of  the  paroxysms,  and  the  other  phenomena  above 
enumerated.     It  is  of  fundamental  importance,  however,  after  determining  that 


TETANUS  1165 

the  attacks  are  tetany,  to  discover,  if  possible,  their  special  cause,  and  especially 
to  determine  whether  we  have  to  do  with  "  idiopathic  "  or  symptomatic  tetany. 
It  should  also  be  said  that  tonic  sp-asms,  like  tetany,  may  also  occur  in  the  hands 
in  hysteria.  The  peculiar  tonic  spasms  of  young  children  are  not,  in  our  opinion, 
to  be  regarded  indisputably  as  tetany;  a  special  form  has  already  been  described 
(^vide  page  881)  under  the  name  of  arthrogryposis.  This  is  characterized  by  per- 
sistent tonic  contracture,  not  paroxysmal,  and  most  pronounced  in  the  distribu- 
tion of  the  ulnar  nerve  on  both  sides.  In  such  cases  there  is  no  incerased  me- 
chanical irritability  of  the  nerves. 

Treatment. — The  main  treatment,  besides  general  hygienic  measures  (es- 
pecially rest  and  nursing)  and  the  consideration  of  all  discoverable  causes 
(gastric  and  intestinal  diseases,  chronic  intoxications,  excessive  work  with  the 
hands,  etc.),  is  electricity.  The  stabile  current  is  passed  upward  through  the 
nerves  affected;  the  galvanic  current  is  also  applied  to  the  spinal  cord,  and  the 
anode  is  applied  to  the  various  nerve-trunks,  with  the  cathode  on  the  sternum. 
This  last  procedure  sometimes  dissipates  a  spasm  actually  present.  Internal 
remedies,  such  as  bromide  of  potassium,  arsenic,  and  belladonna,  rarely  produce 
brilliant  results.  Tepid  baths,  and  the  cautious  use  of  cold  sponging,  with  friction 
and  massage,  may  be  tried.  The  internal  exhibition  of  thyroid  preparations  may 
sometimes  be  attended  with  good  results. 


CHAPTER   VI 

TETANUS 

(Zooh-jaw) 

Tetanus  is  an  acute  infectious  disease  whose  chief  symptom  consists  of  the 
occurrence  of  severe,  extensive,  tonic  ("  tetanic  ")  muscular  spasms.  The  specific 
cause  of  tetanus,  the  tetanus  bacillus,  was  first  discovered  by  ISFicolaier  in  garden 
earth.  Rosenbach  first  cultivated  the  same  bacilli  from  the  secretion  of  the 
wound  of  a  man  who  died  of  traumatic  tetanus.  Since  then  the  specific  signifi- 
cance of  the  tetanus  bacillus  has  been  positively  confirmed  beyond  any  doubt  by 
numerous  investigations.  These  bacilli  are  distinguished  by  a  little  head  (spur) 
at  one  end.  If  a  small  amount  of  these  bacilli  be  injected  under  the  skin  of 
mice,  the  most  violent  tetanic  spasms  ensue  in  the  animals  thus  treated.  Since 
the  development  of  the  bacteria  remains  limited  to  the  seat  of  the  wound  or  the 
injection,  it  is  a  priori  probable  that  the  spasms  are  not  excited  immediately  by 
the  bacilli,  but  by  a  chemical  poison  produced  by  them  during  life.  In  fact, 
Brieger  has  lately  succeeded  in  producing  several  alkaloid-like  substances  from 
tetanus-cultures,  so-called  toxines,  which  he  terms  tetanine,  tetanotoxine,  and 
spasmotoxine.  All  these  substances  are  violent  poisons,  and,  like  strychnine,  pro- 
voke the  most  violent  tetanic  spasms  in  the  animals  experimented  on. 

In  regard  to  the  method  of  infection  in  man,  it  occurs  by  far  most  frequently 
through  open  wounds  (operation  wounds,  or  small  accidental  injuries).  Since 
the  tetanus  bacilli  are  found  chiefly  in  the  soil,  we  can  readily  understand  that 
injuries  of  the  feet  in  persons  who  go  barefoot,  or  injuries  of  the  hands  in 
gardeners,  farmers,  etc.,  most  frequently  give  rise  to  tetanus.  Such  cases  were 
formerly  called  traumatic  tetanus,  in  distinction  from  rheumatic  tetanus,  follow- 
ing exposure  to  scA^ere  cold,  or  idiopathic  tetanus,  which  was  thought  to  occur  with- 
out any  discoverable  cause.  In  the  cases  last  mentioned  there  was  probably  some 
wound  infection  which  was  overlooked  (just  as  in  erysipelas)  on  account  of  the 


1166:  DISEASES  OF  THE  JSTERVOUS   SYSTEM 

smallness  of  the  wound.  It  of  course  would  not  be  impossible  for  the  infection 
sometimes  to  take  place  in  some  other  manner.  Tetanus  neonatorum  is  undoubt- 
edly an  ordinary  wound  tetanus,  almost  always  arising  from  an  infection  of 
the  umbilicus. 

In  Germany  [and  temperate  latitudes  generally]  tetanus  is  a  comparatively 
rare  disease.  Men  are  much  oftener  attacked  than  women.  Tetanus  is  much  more 
common  in  the  tropics  than  in  our  climate.  The  frequency  of  the  disease  in 
negroes  is  well  known.  Tetanus  is  also  not  equally  frequent  at  all  times.  En- 
demics and  epidemics  of  tetanus  have  often  been  observed,  especially  in  time  of 
war.  These  have  arisen  in  part  from  the  unfavorable  influence  of  certain  external 
conditions,  such  as  poor  care,  bad  weather,  sleeping  on  the  wet  ground,  etc. 

Clinical  History. — In  so-called  "  rheumatic  "  tetanus  the  symptoms  usually 
begin  soon  after  exposure  to  the  exciting  cause.  There  may  be,  however,  an  in- 
terval during  which  the  patient  feels  perfectly  well,  or  at  most  has  only  certain 
mild  and  indefinite  premonitory  symptoms,  such  as  languor  and  headache.  Simi- 
lar prodromata  may  occur  in  the  apparently  idiopathic  cases. 

Traumatic  tetanus  seldom  begins  immediately  after  the  injury  has  been 
received.  Several  days  or  even  weeks  may  intervene  previous  to  the  outbreak  of 
the  disease.  Here,  too,  there  may  be  mild  prodromata  for  a  brief  period  preceding 
the  graver  phenomena.  The  patient's  wound  presents  no  specific  appearances. 
Tetanus  may  be  associated  with  either  slight  or  severe  injuries,  whether  treated 
carelessly  or  kept  apparently  aseptic. 

The  symptoms  of  the  disease  proper  are  the  same  in  both  rheumatic  and 
traumatic  tetanus.  They  usually  begin  gradually.  Ordinarily,  the  first  thing 
noticed  is  a  feeling  of  rigidity  and  tension  in  the  muscles  of  the  face,  lower  jaw, 
and  back  of  the  neck.  The  stiffness  spreads  by  degrees  to  the  muscles  of  the  back 
and  abdomen.  The  disease  is  sometimes  completely  developed  in  a  few  hours,  but 
sometimes  not  till  after  several  days. 

The  persistent  tension  of  the  facial  muscles  gives  the  countenance  a  strange 
immobility.  The  brow  is  usually  wrinkled,  and  the  corners  of  the  mouth  are 
often  drawn  back  in  a  "  sardonic  grin,"  or  the  face  has  a  tearful  expression  from 
the  deepening  of  the  naso-labial  folds  and  the  drawing  down  of  the  corners  of 
the  mouth.  Most  prominent  of  all  is  the  tonic  spasm  of  the  masseters,  or  trismus. 
The  teeth  are  so  firmly  pressed  together  that  it  finally  becomes  impossible  to 
open  the  mouth  more  than  one  or  two  millimetres.  The  eyes  are  staring,  the 
pupils  usually  eontr:^cted.  The  muscles  at  the  back  of  the  neck  draw  the  head 
somewhat  backward,  but  in  many  cases  it  can  still  be  moved  quite  well,  although  in 
other  cases  it  is  fixed  by  the  spasm.  The  spinal  column  is  bent  forward,  so  that 
the  trunk  is  convex  anteriorly,  permitting  the  hand  to  be  passed  between  it  and 
the  bed — opisthotonos.  The  muscles  of  the  back  are  hard  and  contracted.  The 
epigastrium  and  the  anterior  part  of  the  abdomen  are  flat.  The  abdominal  mus- 
cles are  as  hard  as  a  board.  The  lower  limbs  may  be  rigidly  extended  at  the 
knee,  and  the  adductors  are  also  contracted,  but  as  a  rule  the  feet  and  toes  are 
free  from  spasm.  The  arms  generally  can  be  quite  freely  moved,  but  the  move- 
ments at  the  shoulder  are  usually  decidedly  impaired.  Convulsive  dysphagia,  as 
seen  in  hydrophobia  (g.  v.),  may  occur,  but  it  is  rare  {vide  infra). 

In  many  cases  the  continuous  tonic  spasm  is  occasionally  interrupted  by  sud- 
den and  irregular  paroxysms,  during  which  all  the  affected  muscles  become  still 
more  tense.  In  severe  cases  this  gives  the  whole  body  a  violent  shock,  and  makes 
the  opisthotonos  even  more  pronounced.  In  a  very  bad  case  the  paroxysms  are 
very  frequent;  in  a  mild  case  they  are  rare  or  almost  indistinguishable.  Some- 
times they  are  apparently  spontaneous,  and  sometimes  they  are  evidently  of  reflex 
origin,  being  superinduced  by  external  irritation.  In  severe  cases  the  cause  may 
be  comparatively  insignificant,  such  as  a  slight  jar  or  noise. 


TETANUS  1167 

If  there  are  other  nervous  derangements,  little  is  known  about  them — partly, 
no  doubt,  because  it  is  seldom  possible  to  make  an  extended  examination  of  the 
patient.  Sensation  is  said  to  have  been  impaired  in  some  instances,  but  in  others 
it  is  perfectly  normal.  The  muscles  affected  by  the  spasms  are  usually  the  seat 
of  severe  pain.  The  cutaneous  reflexes  are  almost  always  greatly  exaggerated. 
In  two  cases  which  we  saw  very  recently,  the  patellar  reflex  was  much  increased, 
and  in  one  there  was  distinct  ankle-clonus.  Paralysis  is  extremely  exceptional. 
There  is  often  profuse  perspiration.  The  forehead  is  usually  studded  with  many 
beads  of  sweat.     The  intellect  remains  perfectly  unclouded. 

There  is  a  special  form  of  tetanus  which  must  be  briefly  mentioned.  It  was 
first  described  by  E.  Eose,  and  is  called  "  hydrophobic  tetanus,"  or  "  cephalic 
tetanus."  It  occurs  only  in  connection  with  injuries  situated  in  the  distribution 
of  the  cranial  nerves — that  is,  in  the  face  and  head — and  is  characterized  in  most 
cases  by  violent  spasm  of  the  pharynx  and  CESophagus.  This  is  in  addition  to  the 
other  ordinary  phenomena  of  tetanus.  The  disease  in  many  ways  reminds  one  of 
hydrophobia.  Another  characteristic  point  is  that  in  most  cases  there  is  facial 
paralysis  on  the  injured  side. 

Tetanus,  as  a  rule,  gives  rise  to  no  disturbances  referable  to  the  internal  vis- 
cera. In  one  case,  however,  in  the  Leipsic  hospital,  croupous  pneumonia  and  acute 
nephritis  came  on  a  few  days  before  the  end.  Often  there  are  dyspnoea  and  a 
most  harassing  sense  of  thoracic  oppression — symptoms  due  mainly  to  the  convul- 
sive rigidity  of  the  muscles,  by  which  the  thorax  is  constantly  maintained  in  the 
position  it  normally  assumes  during  inspiration.  Expectoration  is  impeded ;  and, 
finally,  there  may  be  such  an  accumulation  of  secretions  in  the  mouth  and  air- 
passages  as  to  cause  a  secondary  diffuse  bronchitis,  or  an  inhalation  pneumonia. 
Another  occasional  source  of  extreme  dyspnoea  is  spasm  of  the  glottis. 

The  pulse  often  remains  normal  for  a  long  while,  but  it  is  usually  accelerated, 
not  infrequently  reaching  120  or  160  beats  a  minute  in  severe  cases.  Such  a 
pulse  is  small,  and  may  be  somewhat  irregular.  The  temperature  is  at  first  usu- 
ally normal,  or  slightly  elevated  (100°-102°  [38°-39°  C.]).  Later  it  is  almost  sure 
to  rise ;  and,  as  Wunderlich  pointed  out,  it  is  often  very  high  shortly  before  death 
— for  instance,  10Y°  to  111°  (42°-44°  C).  It  is  not  rare  for  the  temperature 
to  keep  on  rising  for  a  short  time  after  death.  'No  explanation  of  this  terminal 
elevation  of  temperature  has  yet  been  furnished.  It  can  not  be  the  result  of  the 
increased  production  of  heat  occasioned  by  the  muscular  spasm,  for  in  earlier 
stages  the  most  violent  convulsions  are  unattended  by  any  such  change.  Au- 
thorities are,  therefore,  inclined  to  assume  that  at  the  last  there  is  a  paralysis 
of  the  centers  which  regulate  the  warmth  of  the  body,  just  as  is  seen  in  other 
severe  nervous  disorders,  such  as  meningitis,  injury  to  the  cervical  portion  of 
the  cord,  and  uraemia. 

Interesting  observations  have  been  made  with  regard  to  tissue-metamorphosis 
during  tetanus.  The  excretion  of  urea  is  not  increased.  This  fact  agrees  well 
with  Voit's  view,  that  muscular  activity  has  no  relation  to  the  breaking  down 
of  albuminoids.  Senator  failed  to  find  any  increase  of  kreatine  and  kreatinine  in 
the  urine.  Probably  the  production  of  carbonic  dioxide  is  abnormally  large  in 
tetanus.  At  least,  physiological  considerations  would  strongly  indicate  this,  al- 
though it  has  not  yet  been  actually  demonstrated.  Occasionally  traces  of  albumen 
and  sugar  have  been  detected  in  the  urine.  There  is  usually  obstinate  constipa- 
tion, probably  due  to  the  persistent  rigidity  of  the  abdominal  muscles;  and, 
indeed,  micturition  is  not  a  little  impeded  from  the  same  cause. 

It  may  be  said,  in  regard  to  the  general  course  of  the  disease,  that  there  are 
severe  and  mild  forms  of  the  disease.  What  has  been  said  above  applies  mainly  to 
the  severe  form.  In  this,  all  the  symptoms  reach  their  extreme  violence  in  a  few 
days,  the  paroxysms  occur  in  quick  succession,  and  death  usually  takes  place 


1168  DISEASES   OF   THE   NervquS    SYSTEM 

within  a  week  or  two.  The  fatal  result  is  brought  about  by  the  suspension  of 
respiration  and  by  cardiac  failure.  Of  course,  the  extreme  difficulty  of  taking  an 
adequate  amount  of  food  has  an  unfavorable  influence.  The  bad  cases  seldom 
outlast  the  first  week.  If  they  do,  there  is  some  slight  hope  of  recovery;  the 
paroxysms  may  gradually  become  less  frequent  and  less  severe,  until  they  finally 
cease  altogether.  The  severer  form,  however,  so  rarely  ends  favorably  that  the 
prognosis  is  always  very  grave.  The  mild  form,  on  the  contrary,  usually  runs  a 
much  more  favorable  course.  In  it,  all  the  symptoms  are  from  the  first  much 
less  severe.  Often  there  is  only  more  or  less  trismus,  accompanied  by  no  marked 
spasm  in  the  muscles  of  the  trunk,  if  any  at  all.  There  is  little  constitutional 
disturbance.  The  temperature  is  normal,  and  the  prognosis  is  rather  favorable. 
The  disease  may  sometimes  drag  on  for  some  weeks,  but  it  often  ends  in  complete 
recovery.  It  must  not  be  forgotten,  however,  that  what  at  first  seems  a  mild  case 
may  develop  into  the  severe  form. 

The  anatomical  changes  in  the  nervous  system  in  fatal  cases  are  almost  wholly 
negative.  Further  investigations  are  necessary  to  determine  how  far  the  finer 
changes  in  the  motor  cells  of  the  spinal  cord,  which  have  repeatedly  been  found 
of  late,  are  of  pathological  significance.  Any  small  haemorrhages,  etc.,  have,  if 
they  be  present,  only  a  secondary  significance. 

Diagnosis. — In  most  cases,  tetanus  can  be  easily  recog-nized  from  the  peculiar 
convulsions  and  the  general  aspect  of  the  disease.  It  might  be  confounded  with 
acute  meningitis,  for  this  may  cause  rigidity  of  the  neck  and  back;  but  here 
there  are  usually  certain  cerebral  ssrmptoms  also  present,  such  as  headache  and 
impairment  of  consciousness;  and,  on  the  other  hand,  in  tetanus,  trismus  is  an 
almost  constant  phenomenon,  although  exceptional  in  meningitis.  Strychnine 
poisoning  produces  convulsions  similar  to  those  of  tetanus,  but  they  generally 
affect  the  extremities  in  a  more  marked  degree.  Hydrophobia  is  distinguished 
from  tetanus  by  the  aetiology,  the  absence  of  trismus,  the  predominance  of  the 
pharyngeal  convulsions,  and  the  greater  distinctness  of  the  individual  paroxysms. 
The  hysterical  conditions  similar  to  tetanus  can  usually  be  easily  distinguished 
from  genuine  tetanus  by  the  discovery  of  specific  hysterical  symptoms  (anaes- 
thesia, etc.). 

Where  trismus  is  the  only  symptom,  we  must  guard  against  mistaking  for 
tetanus  the  symptomatic  rigidity  of  the  jaws  which  occurs  with  severe  sore  throat, 
diseases  of  the  teeth,  or  inflammation  of  the  maxillary  articulation. 

Treatment. — Through  the  recent  bacteriological  investigations  the  treatment 
of  tetanus  seems  to  be  directed  into  entirely  new  channels.  Animals  may  be 
rendered  immune  to  tetanus  by  inoculation  with  attenuated  cultures  of  the 
specific  germs  just  as  they  can  be  to  many  acute  infectious  diseases.  The  blood 
serum  of  such  animals  then  contains  substances  ("  antitoxine  "  or  "  alexine  ") 
which  annul  the  action  of  the  tetanus  toxine  (Tizzoni,  Behring).  A  considerable 
number  of  experiments  upon  the  therapeutic  usefulness  of  the  tetanus  serum  have 
also  been  tried  on  man,  but  the  reports  upon  the  therapeutic  benefits  are  still  very 
contradictory.  It  is,  however,  not  only  justifiable,  but  virgently  desirable  to  inject 
the  tetanus  serum  as  early  as  possible  in  every  severe  case  of  tetanus  infection. 

If  the  physician  can  not  obtain  an  antitoxic  serum,  he  must  look  to  the 
methods  of  treatment  heretofore  employed.  We  have  ourselves  treated  all  the  cases 
we  have  seen  in  the  last  few  years  with  salicylic  acid  (eight  grains,  gramme  0.5, 
every  hour),  and  we  believe  that  we  have  repeatedly  seen  a  favorable  influence 
from  this  remedy.  Otherwise  narcotics  are  to  be  used.  Those  chiefly  recom- 
mended are  subcutaneous  injections  of  morphine,  opium  in  large  doses,  and 
chloral,  of  which  thirty  grains  (grammes  2)  should  be  given  two  or  three  times  a 
day,  and  the  amount  gradually  increased.  If  deglutition  be  very  difficult,  the 
chloral  may  be  given  by  enema.    Bromide  of  potassium  should  also  be  mentioned 


CONGENITAL   MYOTONIA  1169 

<at  least  two  and  a  half  to  four  drachms,  grammes  10-15,  daily),  and  calabar-bean 
(a  sixth  of  a  grain  of  extract  of  physostigmine,  gramme  0.01,  three  to  five  times 
a  day) .  The  above  remedies  diminish  the  irritability  of  the  nervous  centers.  In 
ourare  we  possess  a  means  of  lowering  the  excitability  of  the  terminations  of  the 
motor  nerves  in  the  muscles.  It  has  therefore  been  employed  by  many,  but  by 
few  with  success.  It  is  difficult  to  say  what  the  dose  of  curare  is,  inasmuch  as 
the  strength  of  different  samples  varies.  The  best  way  is  to  determine  the 
strength  of  the  solution  to  be  employed  by  experimenting  on  some  animal.  Usu- 
ally a  one-per-cent.  solution  of  curare  in  water  is  employed,  and  an  amount  equal 
to  one  quarter  of  the  contents  of  a  Pravaz's  syringe  is  injected,  the  dose  being 
gradually  and  cautiously  increased.  [Such  a  syringe  contains  about  thirteen 
minims    (0.8  gramme).] 

It  is  very  desirable  to  put  the  patient  by  himself  in  a  darkened  and  quiet 
chamber.  Nourishment  should  be  liquid,  and  lukewarm  stimulants,  such  as 
alcohol  and  camphor,  should  be  given  from  the  first.  Protracted  warm  baths 
may  be  given  cautiously.  We  know  from  personal  observation  that  such  baths 
are  very  grateful  to  some  patients. 

It  need  hardly  be  said  that  in  traumatic  tetanus  the  primary  wound  should 
receive  careful  attention.  Since,  according  to  recent  investigations,  the  tetanus 
bacilli  remain  limited  in  their  growth  to  the  seat  of  the  wound,  it  may  be  indi- 
cated in  the  beginning  of  tetanus,  if  possible,  to  amputate  the  wounded  part  or 
to  excise  the  wound.  Of  course,  from  present  experience,  Ave  can  not  promise  a 
successful  result. 


CHAPTER   YII 

CONGENITAL    MYOTONIA 

(  Thomxeii^  Di.iea-se) 

In  1876,  Thomsen,  a  Schleswig  physician,  described  a  peculiar  disease  which  up 
to  that  time  had  escaped  observation.  He  had  had  experience  of  it  in  himself  and 
numerous  members  of  his  own  family.  Thomsen  called  it  "  tonic  convulsions  of 
the  voluntary  muscles,"  an  appropriate  but  somewhat  clumsy  name,  for  which 
we  suggested  instead  "  congenital  myotonia."  Apparently  the  disease  is  very 
infrequent ;  but  a  considerable  number  of  cases  have  already  been  reported  in 
Oermany,  France,  and  Italy. 

The  disease  is  probably  always  congenital;  at  least,  the  symptoms  invariably 
date  from  the  earliest  infancy.  It  is  very  often  generic  and  hereditary;  and 
males  of  the  same  family  seem  to  suffer  oftener,  and  also  more  severely,  than  do 
females.  The  essential  symptom  of  myotonia  is  this :  whenever  any  voluntary 
muscle  has  been  inactive  for  a  time  and  is  then  made  to  contract,  it  falls  into 
a  state  of  more  or  less  persistent  contraction,  a  mild  sort  of  tetanus,  so  that  it 
•can  not  be  immediately  relaxed.  It  is  obvious  that  this  would  interfere  with  any 
series  of  motions,  and  make  voluntary  movement  difficult.  The  patient  is  not 
paralyzed  at  all,  but  he  has  a  feeling  of  great  resistance  to  be  overcome  in  per- 
forming any  act.  Quick  and  accurate  motions  are  often  out  of  the  question, 
so  that,  for  instance,  the  patient  can  not  perform  military  duty.  It  is  noteworthy 
that  the  stiffness  temporarily  disappears  after  the  patient  has  been  moving  his 
muscles  for  some  time.  On  going  up-stairs,  the  first  steps  are  often  very  stiff  and 
laborious,  while  succeeding  ones  grow  easier  and  easier.  Mental  excitement 
invariably  exerts  a  very  unfavorable  influence,  exaggerating  the  stiffness  of  the 
muscles. 

74 


IIYO  DISEASES  OF  THE  NEEVOUS   SYSTEM 

Upon  physical  examination,  the  observer  is  usually  struck  by  the  extraordinary 
development  of  the  muscles.  The  size  of  the  extremities,  in  particular,  almost 
deserves  the  term  "  genuine  muscular  hypertrophy,"  although  the  strength  is  not 
always  proportionately  great.  Certain  extremely  interesting  variations  in  the 
electrical  excitability  of  the  nerves  and  muscles  are,  however,  very  remarkable. 
These  were  first  studied  in  detail  by  Erb  and  given  the  name  of  "  myotonic  reac- 
tion." The  motor  nerves  show  quantitatively  a  normal  faradic  and  galvanic 
excitability.  All  single  shocks  give  short  contractions,  but  on  continued  excita- 
tion (faradic  current,  labile  galvanic  current),  a  very  characteristic  persistence 
of  the  contraction  occurs  after  the  cessation  of  the  irritation.  The  muscles  are 
very  easily  excited  by  f aradism,  and,  with  rather  strong  currents,  always  show 
the  above-mentioned  persistence  of  the  contraction.  When  the  current  is  applied 
continuously  peculiar  wave-like,  oscillating  muscular  contractions  occur.  On  gal- 
vanic excitation  of  the  muscles  a  slight  increase  of  excitability  is  manifest. 
With  rather  strong  currents  the  contractions  are  decidedly  slow,  tonic,  and 
also  persistent.  They  occur  only  on  closing  the  current,  not  on  opening.  Finally 
we  almost  always  see  in  the  muscles  a  very  remarkable  phenomenon,  discovered 
by  Erb :  rhythmical  wave-like  contractions  occur  in  the  muscles,  under  the  action 
of  a  stabile  current,  which  start  from  the  cathode  and  go  to  the  anode.  The  direct 
mechanical  excitability  of  the  muscles,  on  percussion,  is  usually  increased,  but 
this  does  not  apply  to  the  idio-muscular  contractions.  The  reflexes,  sensation, 
and,  indeed,  all  other  nervous  phenomena,  are  normal. 

These  facts  render  it  very  probable  that  the  cause  of  the  disease  is  to  be  sought 
in  the  muscle  itself,  and  that  myotonia  is  due  to  a  congenital  peculiarity  of  the 
muscular  system.  This  hypothesis  is  supported  especially  by  the  interesting  his- 
tological discoveries  of  Erb  on  excised  bits  of  muscle.  He  found  a  considerable 
increase  in  the  volume  of  the  individual  fibers,  whose  transverse  striation  was 
often  very  fine  and  indistinct,  at  times  the  formation  of  vacuoles  in  the  fibers,  a 
great  increase  of  nuclei,  and  a  moderate  increase  of  interstitial  connective  tissue. 
Nothing  is  known  at  present  in  regard  to  anatomical  changes  in  the  nervous 
system.  Erb  reports  that,  upon  microscopic  examination  of  minute  particles  of 
muscular  tissue  which  were  excised,  he  found  marked  hypertrophy  of  individual 
muscular  fibers,  and  an  increase  in  the  number  of  nuclei  in  the  sarcolemma. 

The  disease  persists  through  life.  The  patient  gradually  becomes  accustomed 
to  it,  and  learns  to  conceal  his  misfortune  as  much  as  possible.  There  may  be  no 
constitutional  disturbance.  Sometimes  there  is  melancholia.  Therapeutic  efforts 
have  not  yet  been  attended  with  much  success.  We  might  try  cold  sponging, 
with  friction,  gentle  massage,  and  methodical  exercise  of  the  muscles. 

[Eulenburg  describes  a  congenital  family  affection,  which  he  calls  congenital 
paramyotone,  allied  to  myotonia,  where  tonic  spasm  was  produced  by  cold.  Gow- 
ers  has  found  the  association  of  tonic  spasm  with  ataxia — ataxic  paramyo- 
tone.— K.] 


CHAPTEE    VIII 
CATALEPSY 


Formerly  catalepsy  was  regarded  as  a  special  form  of  disease,  but  at  present 
the  opinion  is  almost  universally  held  that  it  is  merely  a  symptom  of  several  differ- 
ent diseases.  As  was  mentioned  on  page  83Y,  "  cataleptic  rigidity  "  is  a  term  de- 
scriptive of  that  peculiar  condition  of  the  muscles  in  which  the  limbs  maintain 
involuntarily  any  position  into  which  the  observer  puts  them.    If  we  change  the 


CATALEPSY  UTl 

position  of  the  members  which  are  cataleptic,  the  patient  does  not  make  the 
slightest  effort  to  alter  the  posture  in  which  we  leave  them,  however  strange, 
awkward,  and  apparently  insupportable,  it  may  be.  The  limbs  may  be  moved  in 
this  way  almost  like  was,  and  they  are  therefore  said  to  exhibit  a  "waxy  flexi- 
bility." 

No  real  explanation  of  the  cataleptic  state  has  been  given.  We  have  not  yet 
advanced  beyond  the  study  of  the  circumstances  under  which  it  appears,  and  of 
the  associated  phenomena.  As  has  been  said,  the  tonic  muscular  spasm  of  cata- 
lepsy is  never  very  great,  being  little  more  than  sufficient  to  overcome  gravity  and 
maintain  the  limb  in  the  posture  given  to  it.  This  shows  that  there  must,  in  every 
case,  be  a  due  proportion  in  the  vigor  of  the  contractions  of  antagonistic  muscles ; 
and  this  relative  force  must  vary  with  every  change  of  position.  How  this  con- 
tinuous and  remarkable  regulation  of  motor  nervous  energy  takes  place  is  an 
unanswered  question.  Perhaps  reflex  action  has  something  to  do  with  it.  A 
further  interesting  point  is,  that  changes  of  position  induced  by  electrical  stimula- 
tion of  the  nerves  or  muscles  are  not  permanent ;  when  the  stimulus  ceases  to  act, 
the  limb  falls  back  into  its  old  place. 

Catalepsy  occurs  oftenest  as  a  symptom  of  hysteria  (see  the  following  chapter). 
In  this  case  it  is  usually  associated  with  other  disturbances,  chief  among  which 
are  impairment  of  consciousness  and  anaesthesia.  The  anaesthesia  is  especially 
marked  in  the  muscles.  For  example,  the  patient  will  stand  for  an  hour  with 
arms  extended,  and  yet  experience  not  the  slightest  sensation  of  weariness.  At 
last,  however,  the  arms  sink  slowly  down.  Closely  allied  to  hysterical  catalepsy 
is  hypnotic  catalepsy,  a  condition  which  can  be  artificially  produced  by  certain 
procedures  in  many  hysterical  subjects  at  will  (see  the  next  chapter).  Charcot 
has  reported  cases  where  the  lethargy  of  hypnotism  could  invariably  be  trans- 
formed into  catalepsy  by  opening  the  previously  closed  eyes.  These  cases  also 
presented,  in  addition  to  the  catalepsy,  the  strange  phenomenon  called  "  sugges- 
tion." If  the  patient  were  put  into  any  posture  associated  with  some  definite 
mental  conception  (such,  for  example,  as  the  attitude  of  prayer,  or  that  assumed 
in  terror,  or  to  express  detestation),  then  the  corresponding  thoughts  would  come 
into  the  mind,  as  a  hallucination,  but  with  all  the  vividness  of  reality.  Ample 
proof  of  this  was  visible  in  the  expression  of  the  face  and  in  the  whole  bearing 
of  the  subject.  An  analogous  fact  has  been  observed  by  Duchenne,  Lasegue,  and 
ourselves — namely,  that  sometimes  a  hysterical  person  can  be  brought  into  the 
cataleptic  state  by  artificial  closure  of  the  eyes  (compare  what  is  said  in  the  next 
chapter  about  hysterical  ansesthesia). 

Catalepsy  is  also  seen  in  many  psychoses,  particularly  in  certain  grave  forms 
of  melancholia  (melancholia  attonita,  katatonia),  and  sometimes  in  progressive 
general  paralysis.  (For  particulars  see  works  on  insanity.)  The  cataleptic  state 
may  also  develop  in  connection  with  grave  organic  cerebral  disease,  as  in  menin- 
gitis and  apoplectic  coma.  It  may  finally  be  mentioned  in  passing  that  quite  well- 
marked  catalepsy  is  sometimes  observed  in  young  children  of  one  or  two  years 
when  they  are  ill.  Probably  they  fall  into  a  sort  of  stupor;  or  often  it  seems 
that  they  are  rendered  hypnotic,  as  it  were,  by  the  presence  of  strangers. 

Catalepsy  has  been  regarded  as  a  special  disease  in  those  vers'  rare  cases  where 
otherwise  healthy  persons  are  liable  to  "  cataleptic  fits."  The  condition  comes  on 
suddenly,  unprovoked,  and  passes  off  spontaneously  after  a  variable  length  of 
time.  It  is,  however,  very  probable  that  such  of  these  cases  as  are  not  hysterical 
are  epileptoid,  and  deseiwe  to  be  classed  with  genuine  epilepsy. 

Progfiiosis  and  Treatment. — Since  catalepsy  is  a  symptom  of  so  many  different 
diseases,  it  is  impossible  to  make  any  general  statements  with  regard  to  prognosis 
or  therapeutics.  The  reader  may  gain  some  light  from  the  remarks  on  the  treat- 
ment of  hysteria  in  the  next  chapter. 


1172  DISEASES   OF  THE  NERVOUS   SYSTEM 

CHAPTEE   IX 
HYSTERIA 

etiology  and  Definition.— It  is  impossible  to  give  a  definition  of  hysteria  that 
shall  be  at  once  brief  and  accurate,  for  the  aspects  of  the  disease  are  so  manifold 
that  there  is  no  one  symptom  -which  can  be  called  pathognomonic  or  even 
universally  characteristic.  Hysteria  is  therefore  symptomatically  not  a  well- 
rounded  morbid  unit,  although  the  nature  of  all  those  pathological  conditions 
which  we  term  hysterical  may  very  well  be  regarded  from  a  single  point  of  view. 
Hysteria  thus  has  its  peculiarities  and  its  rules  like  any  other  disease.  Only 
because  its  laws  have  been  sought  elsewhere  than  where  they  really  are,  has  the 
claim  often  been  made  in  the  past  that  the  morbid  symptoms  of  hysteria  were 
subject  to  no  law. 

The  fundamental  condition  for  a  right  understanding  of  hysteria  seems  to  be 
that  we  should  free  ourselves  from  the  old  untenable  idea  that  hysteria  is  a  "  gen- 
eral functional  disease  of  the  Avhole  nervous  system,  where  now  this  and  now  that 
portion  of  it  may  be  disturbed  in  its  functions."  We  regard  hysteria  as  a  disease 
which  relates  to  the  cerebral  activity  immediately  associated  with  the  psychical 
processes — that  is,  one  may  say,  with  a  psychosis,  but  in  the  broader  sense  of  the 
word;  the  disturbance  affects  not  only  the  normal  course  of  the  psychical  pro- 
cesses, but  also  their  association  with  the  purely  corporeal  processes  of  innerva- 
tion. We  therefore  call  any  symptom  hysterical  which  is  due  to  a  disturbance  of 
the  normal  relations  between  the  processes  of  our  consciousness  and  our  cor- 
poreity. Between  our  ideas  of  volition  and  our  muscles,  as  between  the  excitations 
of  our  sensory  nerves  and  our  consciousness,  there  exist  under  normal  conditions 
very  definite  and  very  well  ordered  connections.  If  there  comes  a  loosening,  a 
displacement,  a  false  estimate  in  these  connections,  it  gives  rise  to  a  "  nervous  " 
disturbance  of  motion  or  sensation,  a  "  hysterical "  symptom ;  but  the  starting- 
point  of  the  disturbance  always  lies  ultimately  in  the  psychical  domain.  If, 
for  example,  the  idea  of  volition  suffers  a  morbid  change  in  the  sense  that  it 
can  no  longer  arouse  a  corporeal  motor  excitation  in  any  muscular  territory, 
a  "  hysterical "  paralysis  follows.  If  the  consciousness  turns  permanently  from 
definite  sensory  impressions  that  come  to  it,  we  have  to  do  with  a  hysterical 
anaesthesia.  Later  deductions  will  prove  more  plainly  this  characteristic  psycho- 
genetic  origin  of  all  hysterical  symptoms. 

In  the  meantime  we  may  add  to  what  has  been  said  the  following  characteristic 
features  of  hysterical  affections : 

1.  All  hysterical  disturbances,  no  matter  how  severe  the  functional  nervous 
derangement  attributable  to  them,  are  without  visible  anatomical  basis.  The  best 
proof  of  this  is  the  fact  that  any  hysterical  affection,  however  severe,  may  some- 
tiraes  develop  and  then  may  recover  completely  in  a  very  short  time. 

2.  The  hysterical  affection  is  very  often  most  intimately  associated  with 
discoverable  causes  of  a  psychical  nature.  N'ot  only  is  its  appearance  and  incipi- 
ency  most  closely  linked  with  emotional  excitement,  but  later  on  the  mind  is  the 
main  if  not  the  only  channel  through  which  causes  can  operate  to  change  the  con- 
dition of  the  patient,  whether  favorably  or  unfavorably. 

3.  It  is  therefore  evident  that  the  origin  of  all  hysterical  disturbances  must  be 
sought  in  the  most  central  portions  of  the  nervous  system — those  regions  which 
are  most  directly  concerned  in  the  mental  processes.  Hysterical  phenomena  are, 
however,  exhibited  in  all  parts  of  the  nervous  system,  so  far  as  these  depend  upon 
psychical  processes  or  may  be  altered  by  them.  The  symptoms  of  hysteria  are 
therefore  more  manifold  than  those  of  almost  any  other  disease.     Although  so 


HYSTEEIA  1173 

manifold,  certain  symptoms  predominate  with,  such  frequency  as  to  be  character- 
istic of  hysteria,  and  therefore  to  be  regarded  as  especially  valuable  in  diagnosis. 
Eollowing  Charcot,  we  term  such  symptoms  "  hysterical  stigmata."  These  symp- 
toms are  most  constantly  present,  and  therefore  they  can  easily  be  found  at  any 
time. 

4.  Besides  the  permanent  symptoms — the  "  stigmata  "■ — we  see  in  many  cases 
of  hysteria  peculiar  nervous  attacks.  These  are  also  highly  characteristic  of 
hysteria,  since  they  come  on  in  forms  which  are  seen  in  no  other  disease ;  but  there 
are  also  patients  who  suffer  from  hysteria  who  nevertheless  are  never  visited 
by  attacks.  The  possibility  of  the  occurrence  of  an  attack  is,  however,  always 
present.  Very  often  the  attacks  are  provoked  by  easily  discoverable  psychical 
causes. 

After  this  brief  introduction,  turning  to  the  special  aetiology,  psychical  causes, 
as  has  been  said,  are  of  first  importance.  In  numerous  instances  hysteria  comes 
on  as  an  immediate  sequel  to  violent  emotional  excitement  or  to  a  "  psychical 
trauma,"  if  we  may  use  such  an  expression.  Hysterical  convulsions  or  paralysis 
may  be  excited  by  great  terror  or  violent  anger  or  any  unusual  agitation.  Here 
the  efficient  psychical  cause  is  often  hidden  by  some  attendant  circumstance. 
If,  for  example,  a  patient  falls  into  the  water,  or  gets  burned,  or  tumbles  down- 
stairs, and  thereupon  develops  hysteria,  the  mistake  is  often  made  of  ascribing 
the  subsequent  nervous  disease  to  catching  cold,  or  to  the  injury  received, 
although  really  it  was  the  mental  excitement  which  produced  it.  The  various 
physical  injuries  (falls,  blows,  burns,  etc.)  play  a  far  greater,  and  perhaps  the 
greatest,  part  in  the  genesis  of  hysterical  conditions.  In  such  cases  it  is  not 
the  physical  injury  itself,  but  the  terror  it  causes,  or  rather  the  whole  disturbance 
of  consciousness  due  to  the  trauma  (terror,  anxiety  about  the  consequences, 
fright,  etc.),  which  produces  the  hysterical  symptoms.  These  nervous  affections 
produced  by  physical  injury  (traumatic  hysteria,  traumatic  neuroses)  are  of 
such  great  practical  importance  that  we  will  devote  special  consideration  to  them 
later. 

What  is  very  remarkable  in  such  cases  is  that  the  special  attendant  circum- 
stances of  the  psychical  disturbance  often  influence  the  localization  of  the  hys- 
terical phenomena :  that  part,  to  which  attention  was  particularly  directed  at  the 
time,  not  infrequently  becomes,  later  on,  the  seat  of  the  nervous  disturbance.  In 
hysterical  joint-affections  (page  821)  the  cause  not  infrequently  proves  to  have 
been  an  injury  to  the  particular  joint  now  suffering  from  hysteria.  A  young 
girl,  who  was  awakened  at  night  by  the  smoke  of  her  burning  mattress,  and  who 
had  a  severe  laryngitis  from  inhaling  the  vapors,  exhibited  later  an  indubitably 
hysterical  paralysis  of  the  vocal  cords.  In  the  case  of  another  girl,  who  in  jump- 
ing from  a  carriage  fell  upon  her  side,  we  afterward  saw  hemiansesthesia  of  the 
same  side.     Many  such  instances  could  be  cited. 

Certain  hysterical  cases,  therefore,  have  for  their  obvious  cause  a  single  occa- 
sion of  mental  agitation;  but  in  many  others  the  disease  is  not  thus  abruptly 
excited.  As,  in  poisoning,  we  can  distinguish  between  the  sudden  action  of  a 
large  dose  and  chronic  cases  where  minute  amounts  of  poison  are  absorbed  daily 
for  a  long  period,  so  hysteria  may  come  on  not  only  after  a  single  violent  shock, 
but  also  as  the  final  consequence  of  psychical  influences  insignificant  in  them- 
selves, but  potent  because  of  their  frequent  repetition  or  persistency.  It  is  in 
cases  of  this  sort  that  the  causes  do  not  become  evident  to  the  physician  until  he 
has  gained  the  entire  confidence  of  his  patient ;  for  the  root  of  the  trouble  is  often 
entwined  about  the  most  private  affairs.  Anxiety,  sorrow,  disappointed  expecta- 
tions, abandoned  hopes,  and,  in  brief,  everything  which  can  depress  and  over- 
whelm the  mind — these  are  factors  which  may  at  last  excite  the  functional  nerv- 
ous derangements  of  hysteria. 


1174  DISEASES   OF  THE  NEKVOUS   SYSTEM 

Finally,  we  must  state  that  hysteria  may  often  develop  without  any  specially 
noticeable  cause.  We  see  this  particularly  in  young-  people  with  a  marked 
hereditary  nervous  taint.  Here  the  ordinary  daily  demands  upon  a  central 
nervous  system,  which  had  originally  an  abnormally  weak  constitution,  sometimes 
suffice  to  disturb  in  a  measure  its  normal  equilibrium. 

This  leads  us  to  a  second  extremely  important  point  in  the  eetiology  of  hysteria. 
The  blow  which  brings  a  feeble  body  to  the  ground  rebounds  without  effect  from  a 
massive  frame.  Exactly  the  same  may  be  said  of  the  "  blows "  to  which  the 
nervous  system  is  subjected.  Few  entirely  escape  these  influences,  but  there 
are  some  "  strong  natures  "  who  resist  the  psychical  assault  without  wavering, 
while  others  have  a  feebly  resistant  ("  inferior  ")  nervous  organization  and  are 
overpowered.  We  see,  therefore,  that  the  predisposition  of  different  individuals 
to  diseases  of  the  nervous  system  varies.  This  fact  is  a  very  important  one  in 
the  pathogenesis  of  all  functional  nervous  disorders.  In  what  this  predisposition 
consists  we  do  not  know,  being  acquainted  only  with  its  results  and  with  some 
of  its  causes. 

In  many  cases  this  predisposition  is  hereditary.  Hysteria  is  most  prominent 
among  those  neuroses  which  attack  different  members  of  a  family — one  suffering 
frora  one  disease  and  another  from  another  (vide  page  1141).  It  is  also  possible 
to  acquire  such  a  predisposition.  At  least  it  may  be  developed  and  fostered,  on  the 
one  hand,  or,  on  the  other,  checked  and  repressed.  In  these  directions  physical  as 
well  as  psychical  factors  are  of  importance.  Anything  which  weakens  the  con- 
stitution diminishes  the  resistant  power  of  the  nervous  system.  Among  psychical 
influences,  nothing  favors  the  development  of  hysterical  tendencies  more  effi- 
ciently than  does  a  bad  education.  Hysteria  is  often  ascribable  to  an  irritability 
and  feebleness  of  the  nervous  system  thus  engendered.  The  whims  of  the  child 
are  not  controlled,  its  will  is  not  strengthened,  or  its  energy  developed;  its 
imagination  is  unsuitably  and  excessively  stimulated,  or  its  intellectual  powers 
are  overtaxed  and  prematurely  ripened. 

It  is  well  known  that  hysteria  occurs  more  frequently  in  the  "  feebler  "  female 
sex  than  among  men;  but  it  is  by  no  means  a  rare  thing  for  men  to  exhibit 
hysterical  convulsions,  paralysis,  contracture,  or  other  well-marked  disturbances. 
Most  cases  occur  between  puberty  and  the  end  of  middle  life.  It  is  quite  common 
to  see  pronounced  hysteria  in  children,  especially  such  as  are  over  eight  or  ten 
years  old.  The  disease  very  frequently  begins  to  develop  a  year  or  two  previous 
to  puberty.  Nationality  and  race  also  seem  to  exert  some  influence — for  instance, 
the  severer  forms  of  hysteria  are  decidedly  more  frequent  in  France  than  in  Ger- 
many, but  severe  hysteria  is  by  no  means  rare  in  Germany.  The  Jewish  race  are 
particularly  subject  to  hysteria,  and  to  nervousness  in  general. 

One  matter  remains  to  be  considered  with  regard  to  aetiology,  to  which  a 
greatly  exaggerated  importance  was  formerly  ascribed.  It  is  the  influence  of  dis- 
ease of  the  sexual  organs.  The  very  name  "  hysteria  "  (va-repa  =  uterus)  reveals 
what  the  old  view  was,  namely,  that  hysteria  invariably  originated  in  disease  of 
the  female  genitals.  Not  to  speak  of  the  fact  that  the  disease  occurs  in  men  and 
children,  an  unprejudiced  consideration  of  the  matter  will  show  that  the  above 
assumption  is  entirely  groundless  even  in  regard  to  women.  A  large  number  of 
hysterical  women  present  no  anomaly  of  their  sexual  organs ;  and  even  if  the  lat- 
ter be  diseased,  we  are  not  justified  in  assuming  at  once  that  the  hysteria  is 
secondary  to  the  sexual  disorder.  In  these  cases,  also,  we  usually  find,  on  cnreful 
inquiry,  that  psychical  causes  have  been  at  work;  and  these  are  incomparably 
more  potent  in  exciting  hysteria  than  is  malposition  of  the  uterus  or  constriction 
of  the  cervical  canal.  It  is  true,  however,  that  disease  of  the  genital  organs 
may  depress  the  spirits  more  than  some  other  diseases  would,  and  so  indirectly 
promote  hysterical  disturbances.     In  the  same  indirect  way,  menstruation,  preg- 


HYSTERIA  1175 

nancy,  and  parturition  exert  an  important  influence  upon  the  development  and 
course  of  hysteria.  Sexual  excesses  or  total  abstinence  from  sexual  indulgence 
also  produce  their  effects  indirectly  through  the  mind. 

The  Symptoms  and  Manifestations  of  Hysteria 

Considering  the  great  differences  in  the  external  morbid  symptoms  under 
which  hysteria  may  manifest  itself,  it  is  not  easy  to  give  in  a  brief  summary  a 
comprehensive,  intelligible,  and  yet  accurate  description  of  its  clinical  manifesta- 
tions. We  believe  that  we  can  best  attain  this  end  by  speaking  first  of  the  most  im- 
portant and  most  frequent  of  the  single  symptoms  of  hysteria,  by  describing  next 
the  hysterical  attacks,  and  finally  by  trying  to  evolve  a  general  picture  of  the 
disease. 

1.  The  Hysterical  Stigmata,  especially  Sensory  Anaesthesia  and  Hyper- 
aesthesia. — In  every  case  where  the  diagnosis  of  hysteria  has  already  been  estab- 
lished or  where  it  is  to  be  confirmed,  we  must  examine  the  patient  for  certain 
symptoms,  which,  as  we  have  said,  are  very  common  in  hysteria,  and  in  part  so 
peculiar  to  it,  that  by  themselves  they  are  often  of  decisive  diagnostic  significance. 
These  symptoms  are  termed  "  hysterical  stigmata."  A  knowledge  of  them  is  the 
more  important  for  the  physician  in  that  we  often  detect  them  only  by  a  special 
examination  directed  to  that  end.  Patients  only  exceptionally  inform  us  as  to 
these  symptoms.  It  is  not  at  all  unusual  for  patients  to  have  no  inkling  of  their 
existence  until  after  an  examination. 

The  most  important,  because  the  commonest,  of  these  hysterical  signs  relate  to 
sensibility.  The  more  carefully  we  examine,  the  more  rarely  will  we  meet  with  a 
case  of  severe  hysteria  in  which  in  some  sensory  region  we  do  not  find  manifest 
disturbances,  especially  a  diminution  of  sensibility.  We  must  therefore  test 
accurately  not  only  the  sensibility  of  the  whole  surface  of  the  body,  but  also  the 
functions  of  all  the  special  senses  (sight,  hearing,  smell,  and  taste). 

The  sensory  disturbances  of  the  skin  must  first  be  mentioned.  Not  infre- 
quently we  find  a  diminution  of  sensibility  over  the  whole  surface  of  the  body, 
especially  a  more  or  less  complete  analgesia.  In  such  cases  we  can  stick  a  pin  in 
deeply  anywhere,  or  pierce  a  fold  of  skin  with  a  pin,  without  the  patient's  com- 
plaining of  pain.  As  is  well  known,  it  often  happens  that  hysterical  patients,  in 
order  to  appear  interesting  or  from  some  other  reason,  produce  upon  themselves 
deep  injuries  and  wounds ;  this  is  almost  always  connected  with  the  patient's  anal- 
gesia. Very  often,  however,  the  anaesthesia  is  not  general,  but  it  is  limited  to  a 
definite  region.  We  find  complete  anaesthesia  of  one  arm  or  leg,  or  we  find  on  the 
trunk  or  the  extremities  single  areas  of  anaesthesia,  in  which  the  anaesthetic  parts 
are  bounded  by  the  normally  sensitive  skin;  these  areas  may  take  all  possible 
forms,  and  may  often  be  very  peculiar.  The  sensibility  to  pain  is  almost  always 
the  most  disturbed,  even  when  the  other  forms  of  cutaneous  sensibility  may  be 
quite  unaffected,  but  changes  in  the  sensibility  to  temperature,  pressure,  etc.,  may 
also  occur.  It  may  be  added  that  in  the  severer  forms  of  anassthesia  the  deeper  parts 
may  also  be  insensitive,  so  that  the  so-called  muscular  sense  is  absent,  and  pa- 
tients with  their  eyes  shut  have  not  the  slightest  idea  of  the  position  of  the 
angesthetic  limbs.  [The  skin  reflexes  are  usually  diminished  or  absent  over  the 
anaesthetic  regions.  In  hemianaesthesia  the  gagging  reflex  from  irritating 
the  back  of  the  pharynx,  palate,  or  tongue,  may  be  absent  on  the  anaesthetic 
side.— K.] 

Besides  cutaneous  anaesthesia,  disturbances  in  the  sensibility  of  the  other  sen- 
sory organs  (other  "  sensory  anaesthesias  ")  are  among  the  commonest  signs  of 
hysteria.  Sometimes  the  patients  say,  when  asked,  that  they  see  indistinctly  and 
dimly.  If  we  examine  the  eyes  we  often  find  a  loss  of  visual  acuteness  and  a 
rapidly  induced  fatigue  on  using  them.     A  limitation  of  the  visual  field  is  the 


1176  DISEASES   OE  THE  ITERVOUS   SYSTEM 

most  characteristic  sign- — that  is,  an  aneesthesia  of  the  peripheral  portions  of  the 
retina.  The  degree  of  this  limitation  sometimes  shows  manifest  differences  for 
the  different  colors.  Hysterical  achromatopsia  is  a  common  symptom — that  is,  a 
partial  or  complete  loss  of  the  color  sense.  According  to  Charcot,  in  the  hysteri- 
cal the  perception  of  violet  usually  first  disappears,  then  green,  and  lastly  blue  and 
yellow;  but  we  must  not  hold  too  strictly  to  all  these  rules;  for,  although  the 
Erench  investigators  are  otherwise  deserving  of  great  praise  in  adding  to  our 
knowledge  of  hysteria,  in  this  respect  they  seem  decidedly  too  schematic,  and  to 
have  generalized  too  rashly.  Diminution  of  the  auditory  acuteness  in  one  or  both 
ears  is  also  not  imcommon.  Anaesthesia  of  smell  and  taste  is  still  more  common. 
Salt,  quinine,  vinegar,  sugar,  etc.,  either  excite  no  sensation  of  taste  at  all,  or  the 
tongue  is  anaesthetic  for  one  or  another  of  these  substances.  The  same  holds  for 
the  sense  of  smell.  All  these  symptoms  are  especially  important  in  diagnosis,  be- 
cause in  organic  diseases  they  seldom  reach  such  a  degree  as  in  hysteria. 

The  sensory  anaesthesias  above  described  may  of  course  be  combined  in  various 
ways  in  different  cases,  but  none  of  these  combinations  is  so  characteristic  and 
individual  as  hysterical  hemianesthesia,  a  symptom-complex  which  occurs  almost 
solely  in  hysteria,  and  is  therefore  of  distinct  diagnostic  value. 

Hysterical  hemiansesthesia  is  one  of  the  most  common  symptoms  of  profound 
hysteria.  It  must  often  be  sought  for,  inasmuch  as  the  patient  herself  frequently 
has  no  suspicion  of  its  existence  until  her  attention  is  called  to  it.  It  seems  just 
as  if  one  half  of  the  body  had  been  entirely  lost  to  consciousness ;  the  patient  does 
not  know  whether  it  is  or  is  not  capable  of  feeling. 

In  a  typical  and  fully  developed  case  the  hemiansesthesia  does  actually  affect 
just  one  half  of  the  body.  There  are  rudimentary  forms;  but  in  these  complete 
ones,  the  boundary  between  the  anaesthetic  parts  and  the  parts  retaining  normal 
sensitiveness  accurately  corresponds  to  the  median  line  of  the  body.  The  skin  on 
the  affected  side  is  entirely  insensible  to  the  prick  of  a  needle  or  to  heat.  Often 
it  seems  somewhat  blanched,  and  its  blood-vessels  seem  to  be  constricted ;  at  least 
the  skin  very  often  bleeds  surprisingly  little  if  wounded.  The  mucous  membranes 
upon  the  abnormal  side  are  all  equally  anaesthetic,  including  the  conjunctiva,  and 
the  corresponding  half  of  the  buccal  cavity  and  of  the  tongue.  The  deeper  parts, 
such  as  the  muscles  and  joints,  are  also  almost  invariably  anaesthetic.  The  patient 
can  no  longer  feel  in  what  position  the  limbs  of  the  affected  side  are ;  and  if  they 
are  moved  passively,  no  sensation  is  communicated  to  her.  The  organs  of  special 
sense  are  usually  involved.  Hearing  is  impaired  upon  the  affected  side ;  the  corre- 
sponding half  of  the  tongue  can  not  taste ;  the  corresponding  nostril  can  not  smell ; 
and  sight  upon  that  side  is  affected  in  a  peculiar  manner.  There  is  no  hemianopsia, 
but  a  total  amblyopia,  or  possibly  amaurosis.  If  the  amaurosis  be  not  complete,  we 
find  at  least  a  limitation  of  the  visual  field  and  the  signs  of  the  above-mentioned 
achromatopsia. 

Apart  from  other  hysterical  symptoms  with  which  hemiansesthesia  as  well  as 
all  the  other  sensory  anaesthesias  may  be  associated,  we  must  mention  here  one 
symptom  which  is  in  close  relation  to  anaesthesia,  and  which  was  first  described  by 
Duchenne  under  the  name  of  "  loss  of  muscular  sense  "  (perte  de  la  conscience 
musculaire).  The  patient,  whose  arm,  for  example,  is  anaesthetic,  can  not  move 
it  if  she  closes  her  eyes,  although  with  the  eyes  open  she  can  move  it  as  well  as  ever. 
When  the  eyes  are  shut  the  arm  remains  motionless  in  the  position  it  has  pre- 
viously occupied.  If  its  position  be  altered  by  passive  motion,  the  new  position  is 
maintained  with  equal  persistency.  There  is,  with  the  eyes  shut,  pronounced 
catalepsy.  Duchenne  referred  this  peculiar  symptom  to  the  loss  of  a  special 
sense  which  he  termed  "muscular  sense"  (conscience  musculaire).  According  to 
our  present  conception  of  hysteria  it  would  be  more  correct  to  regard  the  symptom 
as  purely  psychical. 


HYSTEEIA  1177 

[The  various  ana3Sthesias  and  many  other  symptoms  of  hysteria  might  often  be 
termed  more  properly  "  delusions  of  not-feeling."  Patients  with  hysterical  blind- 
ness, for  example,  when  prisms  are  placed  before  their  eyes,  so  that  they  imagine 
they  are  looking  with  the  sound  eye  when  they  are  really  looking  with  the  "  blind  " 
eye,  can  sometimes  see  very  well.  When  hypnotized  such  patients  can  recall  that 
they  have  been  touched  or  pricked  in  the  anaesthetic  area,  etc.  This  is  often  mis- 
taken for  deliberate  simulation,  but  it  is  really  another  instance  of  the  psychical 
nature  of  the  disease. — K.] 

The  much-discussed  and  peculiar  symptoms  of  transfer,  as  well  as  metal- 
loscopy  and  allied  symptoms,  will  be  mentioned  below. 

Thus  far  we  have  spoken  only  of  anaesthesia,  but  we  very  often  find  in  the  hys- 
terical certain  hypersesthetic  regions.  These  hypersesthesias  are  so  characteristic 
that  we  must  reckon  them  among  the  hysterical  stigmata,  and  must  therefore  look 
for  them  in  every  case.  Sometimes  the  physician's  attention  is  called  to  these 
places  because  they  are  the  seat  of  constant  slight  or  severe  pain.  In  other  cases 
the  tenderness  appears  only  upon  pressure.  The  hyper^esthesia  may  be  so  great 
that  the  patient  can  scarcely  bear  the  slightest  touch.  Of  course,  the  hyper- 
sesthesia  is  very  closely  connected  with  the  condition  of  the  patient's  attention. 
If  the  thoughts  be  diverted,  even  firm  pressure  is  often  not  at  all  noticed.  We  see 
clearly,  then,  that  we  usually  have  to  do  here  with  a  "  psychical  hypersesthesia." 

The  hyperffisthetic  spots  are  either  quite  extensive  or  quite  circumscribed,  or 
even  limited  to  one  definite  spot.  They  may  lie  near  to  or  in  the  midst  of  anses- 
thetic  areas.  They  are  relatively  rarest  in  the  extremities  and  more  common  on 
the  head  and  trunk,  especially  on  the  sternum,  on  the  sides  of  the  chest,  under  the 
mammse,  etc.  Most  common,  and  therefore  especially  characteristic,  is  the  hyper- 
sesthesia  of  the  vertebral  column,  and,  in  women,  of  the  lower  abdominal  region 
("  ovarian  pain,"  "  ovarie  ").  The  latter  term  is  convenient  but  by  no  means  cor- 
rect, since  really  we  have  only  a  tenderness  of  the  soft  parts  in  general,  which  is  at 
once  noticeable  on  deep  pressure,  and  we  do  not  have  solely  or  chiefly  a  tender- 
ness of  the  ovary.  We  usually  find  ovarie  only  on  one  side,  oftener  on  the  left 
than  on  the  right.  Analogous  symptoms  in  men — tenderness  in  the  groins  or  the 
testicles — are  less  common.  ITypersesthesia  of  the  vertebral  column,  hysterical 
"  spinal  irritation,"  is  even  more  important  for  diagnosis  than  ovarie.  The  hyper- 
sesthesia  affects  either  the  whole  spine  or  merely  single  portions  of  it,  often  only 
single  vertebrae.  It  may  attain  so  high  a  degree  that  the  slightest  touch  of  the 
skin  over  the  vertebrae,  or  somewhat  deep  pressure,  may  cause  the  liveliest  out- 
cries and  shrinking.     This  symptom  is  almost  pathognomonic  of  hysteria. 

The  relations  which  these  hyperaesthetic  regions  have  to  the  hysterical  attacks 
are  very  important,  and  they  have  therefore  procured  for  them  the  name  of  "  hys- 
terogenous  zones."  We  will  speak  further  on  this  point  in  describing  the  hysteri- 
cal attacks. 

Hyperaesthesia  in  other  sensory  regions — abnormal  sensitiveness  of  the  eye, 
ear,  etc. — also  occurs.  Thus  certain  cases  of  hysterical  blepharospfism  seem  to  be 
due  to  an  immoderate  sensitiveness  to  light.  Unusually  sharp  hearing  is  noted, 
especially  during  the  hysterical  attacks.  Here,  too,  belongs  the  aversion  of  many 
patients  to  certain  odors  and  flavors,  and  the  like. 

We  may  also  mention  in  this  place  hysterical  pains.  They  can  scarcely  be 
separated  strictly  from  hysterical  hyperaesthesia;  at  least,  almost  all  hysterical 
patients,  who  complain  of  pain  (in  the  back,  in  the  face,  in  the  arms  and  legs, 
and  very  often  "  all  over"!),  state  that  these  pains  are  increased  by  motion  and 
pressure.  The  more  the  patient's  general  disposition  is  disturbed,  the  more  he 
thinks  of  his  pain,  and  the  worse  it  becomes.  If  the  patient  is  busied  with  other 
things,  he  forgets  his  pain  entirely.  Suggestive  influences  (vide  infra)  are  of 
great  effect.     There  can  therefore  be  no  doubt  that    these  feelings  of  pain  are  of 


1178  DISEASES   OF  THE  i^ERVOUS   SYSTEM 

a  purely  psycliical  nature ;  they  are,  so  to  speak,  "  imaginary  pains,"  hallucina- 
tions of  pain.  Hysterical  pains  sometimes  become  very  important  because  they 
render  the  patient  inactive.  There  are  hysterical  patients  who  lie  the  whole  day 
on  the  sofa,  because  they  can  not  stir  a  limb  "  on  account  of  pain."  Mobius  and 
others  have  described  such  especially  pronounced  cases  under  the  name  of 
"  akinesia  algera."  In  oyr  opinion,  there  is  no  reason  for  wishing  to  make  a 
separate  disease  of  such  cases,  because  such  conditions  often  enough  occur  alone 
or  associated  in  various  ways  with  other  symptoms  in  severe  neurasthenia  and 
hysteria. 

2.  Hysterical  Paralysis. — Hysterical  paralysis  is  frequently  an  immediate 
sequel  to  some  violent  mental  excitement  (for  example,  "  paralysis  from  fright  ")  ; 
but  it  may  come  on  gradually.  Hysterical  paralysis  is  indubitably  of  central 
origin.  It  is  a  paralysis  of  the  will.  The  patient  has  lost  the  power  to  will  a 
contraction  of  the  affected  muscles.  One  always  has  the  feeling  that  the  patient 
could  move  the  paralyzed  limb  perfectly  well  if  she  only  desired  to;  but  she  can 
not  bring  the  will  to  bear  on  it,  and  this  inability  is  the  real  trouble.  It  also 
seems  a  remarkable  circumstance  that  hysterical  paralysis  often,  but  of  course 
not  always,  affects  only  certain  combined  movements.  Many  patients,  for  in- 
stance, can  move  their  legs  very  well  in  bed,  but  they  can  not  walk  a  step 
("abasia,"  vide  infra).  We  have  seen  a  hysterical  writing  paralysis;  the  right 
arm  was  not  paralyzed,  but  it  utterly  refused  to  make  any  attempt  to  write. 

The  extremities  are  most  frequently  paralyzed,  particularly  the  lower  limbs; 
but  hemiplegia  is  not  especially  rare.  A  very  common  manifestation  is  loss  of  the 
power  to  stand  or  walk.  The  patient  lies  in  bed  or  on  a  sofa,  and  sometimes  while 
thus  reclining  she  can  flex  and  extend  the  legs  very  well;  but  as  soon  as  she  is 
urged  to  stand  up  or  walk,  the  knees  double  up,  the  patient  begins  to  tremble,  the 
respiration  grows  rapid  and  convulsive,  and  there  is  not  the  slightest  effort  made 
to  move  the  legs.  In  France  the  names  "  astasia  "  and  "  abasia  "  are  used  for 
these  common  hysterical  symptoms.  If  only  one  leg  be  paralyzed,  the  gait  is 
often  very  peculiar  and  characteristic.  The  sound  limb  makes  long  strides,  while 
the  paralyzed  one  is  held  perfectly  rigid,  and  often  is  dragged  along  with  a  loud 
shuffling  sound.  The  arms  are  much  less  often  affected.  The  facial  muscles  are 
hardly  ever  paralyzed,  although  they  may  be  involved  in  hemiplegia.  We  once 
saw  hysterical  diplopia. 

In  regard  to  the  more  precise  form  of  the  paralysis,  both  flaccid  and  spastic 
paralyses  occur  in  hysteria.  In  many  cases  of  hysterical  paralysis  the  tendon 
reflexes  may  be  so  exaggerated — nay,  there  may  even  be,  as  we  have  repeatedly 
seen,  such  a  lively  ankle  clonus — that  one  is  at  first  disposed  to  think  of  actual 
spinal  paralysis.  In  other  cases,  as  in  paralysis  of  an  arm,  the  paralyzed  limb 
hangs  down  completely  flaccid.  The  paralyzed  parts  are  often  at  the  same  time 
completely  anaesthetic  (a  circumstance  which  may  often  be  distinctive  in 
diagnosis),  but  in  other  cases  they  are  normally  sensitive  or  even  hyperaBS- 
thetic. 

Hysterical  paralysis  of  the  vocal  cords  is  very  often  seen.  The  voice  is  gener- 
ally lost  suddenly,  and  the  patient  can  talk  only  in  a  whisper — hysterical  aphonia. 
On  laryngoscopic  examination,  we  are  often  struck,  at  the  outset,  by  the  anaes- 
thesia of  the  pharjmx  and  its  lack  of  reflex  excitability.  We  find  no  trace  of  any 
anatomical  lesion  of  the  cords,  but  merely  that  they  are  paretic.  The  glottis  can 
not  be  completely  closed,  and  sometimes  the  vocal  cords  actually  become  wider 
apart  upon  every  effort  at  phonation.  The  patient  then  speaks  exclusively  in  a 
whisper. — Hysterical  mutism  quite  rarely  follows  hysterical  aphonia.  The  pa- 
tients entirely  lose  voluntary  control  of  their  speech  apparatus,  and  finally  be- 
come completely  dumb.  We  will  also  mention  here  hysterical  stammering,  al- 
though it  should  more  properly  be  classed  with  the  spasmodic  hysterical  symp- 


HYSTERIA 


1179 


toms.  The  voluntary  quiet  innervation  of  the  muscles  of  articulation  is  affected, 
so  that  the  speech  is  altered  in  the  most  peculiar  waj,  by  needless  spasmodic  at- 
tendant movements,  grimaces,  etc'  We  have  very  often  observed  such  hysterical 
disturbances  of  speech  (stammering  or  mutism),  especially  in  children  {as  a  result 
of  fright).  A  loss  of  the  pov^er  of  vpriting  may  sometimes  be  associated  -with,  the 
dumbness  in  an  interesting  way. 

Hysterical  paralysis  of  deglutition  is  much  less  frequent  than  paralysis  of 
the  vocal  cords.  If  there  be  dysphagia,  it  is  often  not  an  easy  matter  to  determine 
whether  it  is  due  to  paralysis  or  to  spasm,  which  comes  on  at  any  attempt  to 
swallow. 

3.  Hysterical  Contractures. — Contractures  may  occur  as  isolated  phenomena, 
or  in  combination  with  other  symptoms,  such  as  anaesthesia  or  paralysis.  They 
are  caused  by  unusually  strong  tonic  muscular  contractions.  The  starting-point 
of  the  irritation  is  certainly  in  the  central  nervous  system.  Sometimes  the  con- 
tractures are  temporary,  but  often  they  are  characterized  by  their  intensity  and 
their  great  persistency.  The  extremities  suf- 
fer most  frequently,  although  the  trunk  or 
the  back  of  the  neck  may  be  affected.  In  the 
hands  and  feet,  especially  in  the  toes,  flexor 
contractures  predominate,  but  in  the  larger 
joints  extensor  contractures  are  the  rule. 
Although  many  varieties  occur,  single  forms 
of  contracture  are  especially  characteristic. 
As  an  example,  we  will  refer  to  the  accom- 
panying illustrations   (Figs.  180,  181). 

The  relations  of  hysterical  contractures 
to  the  articular  neuralgias  have  already  been 
mentioned  (page  821).  They  may  occur  in 
hemiplegic,  paraplegic,  or  monoplegic  form. 
They  often  follow  a  hysterical  convulsive  at- 
tack (vide  infra).  All  hysterical  contrac- 
tures disappear  completely  in  chloroform  nar- 
cosis, after  the  use  of  an  Esmarch  bandage, 
aiid  in  deep  sleep. 

4.  Vaso-motor  Disturbances.  Secretory 
Disturbances.  Symptoms  in  the  Internal 
Organs. — Besides  the  sensory  and  motor 
symptoms  just  described,  other  symptoms  oc- 
cur in  hysteria  which  fall  under  the  domain 
of  the  vaso-motor  and  secretory  nerves;  but 

in  our  opinion  we  should  cite  here  with  positiveness  only  those  symptoms  which 
we  find  to  be  dependent  directly  or  indirectly  upon  psychical  processes.  In  this 
domain,  however,  the  credulity  of  many  physicians  has  brought  to  light  a  mass 
of  apparently  wonderful  and  inexplicable  observations,  which  are  not  proof 
against  rigid  criticism. 

In  the  first  place  abnormal  anaemia  or  abnormal  fullness  of  the  vessels  (a  cool, 
pale  skin  in  the  one,  a  hot,  red  skin  in  the  other)  is  not  infrequent,  and  points 
to  vaso-motor  influ^ences.  Since  we  know  that  the  vascular  nerves  are  influenced 
in  a  high  degree  by  the  emotions,  we  can  probably  assume  a  central  origin  for 
these  symptoms.  Haemorrhages  from  internal  organs  are  harder  to  explain ;  they 
are  apparently  not  uncommon  in  hysteria,  and  they  have  often  been  referred 
to  "  nervous  vaso-motor  influences,"  but  in  our  opinion  we  must  be  extremely 
guarded  in  such  an  assumption.  We  most  frequently  see  hysterical  hsematemesis 
or  hysterical  haemoptysis — that  is,  the  evacuation  of  blood  from  the  mouth,  either 


Fig, 


.  180.— Hysterical  contracture.  (From 
Bourneville  and  Regnard's  Iconographie 
de  la  Salpetriere). 


1180 


DISEASES   OF  THE  NEEVOUS   SYSTEM 


with  cough  or  in  a  way  suggestive  of  choking.  Inexperienced  physicians  have 
thus  often  been  led  to  a  false  belief  in  dangerous  pulmonary  disease  or  gastric 
ulcer;  but  if  we  look  more  closely  we  shall  find  that  the  blood  evacuated  is  of  a 
clear  raspberry-red  color,  is  mixed  with  a  good  deal  of  mucus  and  saliva,  and  is 
of  a  thin  fluid  consistency.  The  whole  amount  is  seldom  more  than  two  or  three 
ounces  (grammes  50-80).     If  we  inquire  more  carefully  as  to  its  origin,  we  can 

usually  find  a  source  for  the  blood  in  the  gums 
or  in  the  oral  or  pharyngeal  mucous  membrane. 
There  are  often  spasmodic  chokings  or  hic- 
coughs, by  which  a  haemorrhage  of  the  mucous 
membrane  is  mechanically  produced.  It  is  also 
certain  that  in  many  cases  intentional  decep- 
tion on  the  part  of  the  patients  may  lie  at  the 
bottom  of  the  hasmorrhage.  We  must  be  ex- 
tremely cautious  in  haemorrhages  from  the 
genitals,  from  the  skin,  from  the  palms  in  the 
"  stigmatized,"  etc.  We  once  exposed  a  hysteri- 
cal woman  who  had  for  years  produced  the  most 
extensive  gangrenous  spots  upon  her  skin  by 
caustic  soda ! 

Finally,  among  the  vaso-motor  disturbances 
we  must  mention  one  symptom  whose  signifi- 
cance, in  our  opinion,  has  not  yet  been  satisfac- 
torily explained- — we  mean  hysterical  fever.  In 
severe  hysteria,  especially  at  the  time  of  severe 
attacks  and  psychical  disturbances,  other  ob- 
servers, and  we  ourselves,  have  repeatedly  seen 
high  febrile  temperatures,  106°  (41°  C.)  and 
more ;  and  these  temperatures  come  on  in  a  very 
irregular  manner.  In  none  of  the  eases  under 
our  own  observation,  however,  could  we  wholly 
exclude  the  possibility  of  simulation — that  is, 
of  producing  a  rise  of  the  mercury  by  rubbing 
and  pressing  on  the  thermometer.  In  all  the 
measurements  we  made  ourselves  in  the  rectum 
the  temperature  was  normal,  while  the  high 
fever  was  always  said  to  occur  in  our  absence. 
We  therefore  recommend  the  greatest  caution 
with  reference  to  this  point. 

Anomalies  of  the  secretory  and  excretory 
organs  have  also  been  met  with  in  hysteria. 
Many  patients  have  a  remarkably  dry  skin, 
while  others  sometimes  perspire  very  freely. 
The  secretion  of  saliva  is  subject  to  similar 
modifications.  Very  remarkable  observations 
have  been  made  in  a  few  cases  with  regard  to 
hysterical  ischuria;  for  days  only  a  very  small 
amount  of  urine  has  been  passed,  although  there  has  been  no  retention.  In  one 
case  of  this  sort,  observed  by  Charcot,  there  was  violent  vomiting  at  the  same 
time,  and  the  vomitus  was  said  to  contain  a  comparatively  large  amount  of  urea 
(vicarious  excretion).  Such  observations,  which  are  very  few  in  number,  are  at 
present  not  susceptible  of  an  exact  explanation,  but  the  suspicion  of  simulation 
does  not  seem  to  us  wholly  excluded.  Hysterical  polyuria  occurs  more  frequently 
than  ischuria.     A  large  amount  of  very  light-colored  urine  of  low  specific  gravity 


Fig.  181. --Contracted  position  of  the  left 
f oot  i  n  traumatic  hysteria.  (Personal 
observation.) 


HYSTERIA  1181 

is  excreted.  This  polyuria  is  in  raany  instances  merely  the  result  of  excessive 
ingestion  of  liquids.  Polydipsia  (excessive  thirst,  or  probably,  to  speak  more  cor- 
rectly, a  morbid  tendency  constantly  to  drink  water)  is  a  very  frequent  symptom 
in  hysteria,  particularly  at  the  close  of  a  fit. 

The  digestive  disturbances  which  many  patients  have  are  mainly  such  as  have 
already  been  discussed  on  page  463,  under  the  head  of  "  nervous  dyspepsia." 
Colicky  pains,  obstinate  constipation,  occasional  diarrhoea,  and  similar  symp- 
toms, are  by  no  means  rare.  Hysterical  vomiting,  especially,  often  plays 
a  very  great  part,  since  it  may  very  much  impair  the  patient's  nutrition.  In 
other  cases,  of  course,  the  patient's  well-nourished  appearance  is  in  striking  con- 
trast with  her  statement  that  she  "  has  to  vomit  everything  up  again."  Hys- 
terical tympanites  also  deserves  mention.  It  is  due  to  the  accumulation  of  a 
large  amount  of  air  and  gas  in  the  primse  vise.  This  may  be  in  part  the  result 
of  a  sort  of  paralysis  ("  atony  ")  of  the  muscular  coat  of  the  stomach  and  intes- 
tines, but  another  frequent  cause  is  the  swallowing  of  large  amounts  of  air. 
Perhaps  the  patient  does  this  on  purpose.  The  prominence  and  tension  of  the 
abdominal  walls  may  be  so  considerable  as  to  simulate  grave  diseases,  such  as 
peritonitis,  a  tumor,  or  pregnancy.  Doubts  of  this  sort  can  always  be  dispelled 
by  inducing  anaesthesia  with  chloroform.  It  is  possible  to  remove  the  gas  com- 
pletely in  a  short  time  by  pressing  upon  the  abdomen,  or  by  introducing  a  long- 
tube  through  the  rectum. 

Sometimes  there  are  symptoms  referable  to  the  genital  organs.  It  has  been 
already  pointed  out  that  too  much  prominence  was  formerly  given  to  the  influence 
of  sexual  diseases  in  exciting  hysteria.  It  is  also  true  that  nervous  derangements 
of  the  genital  organs,  as  of  all  the  other  organs,  may  be  among  the  symptoms  of 
hysteria.  Many  pains  and  hyperaesthetic  conditions  of  the  genital  organs  must 
in  particular  be  so  interpreted,  while  co-existing  disturbances  of  menstruation 
are  often  to  be  regarded  as  co-ordinate  symptoms.  We  can  also  readily  under- 
stand that  sexual  relations  often  influence  very  excitable,  hysterical  individuals 
to  no  slight  extent,  as  is  indeed  very  frequently  betrayed  by  the  character  of 
their  hallucinations  and  their  utterances  when  delirious. 

5.  General  Mental  and  Bodily  Constitution  of  the  Hysterical.— If  we  regard 
hysteria  as  a  disease  which  is  largely  psychical,  which  is  the  only  correct  view,  it 
will  not  seem  strange  if  the  whole  mental  constitution  and  nature  of  the  patient 
show  special  peculiarities.  In  many  cases,  therefore,  the  psychical  condition  of 
the  hysterical  is  so  characteristic  that  the  physician  can,  from  the  patient's  nature 
and  demeanor,  form  his  conclusions  as  to  the  form  of  her  disease. 

Hysterical  persons  are  irritable  and  emotional,  easily  depressed,  sensitive, 
whimsical,  and  subject  to  violent  extremes  of  feeling.  They  are  inclined  to  exag- 
gerate their  sufferings,  exact  a  great  deal  of  attention,  and  are  anxious  to  excite 
sympathy.  They  have  little  energy  or  force  of  will,  but  they  are  sly  and  obsti- 
nate in  carrying  out  any  pet  desire.  Again,  they  can  be  very  amiable  and  attrac- 
tive if  they  take  the  fancy.  They  are  often  shrewd  and  active  mentally,  but  hys- 
teria is  also  not  infrequently  seen  in  dull  and  stupid  persons. 

This  brief  sketch  represents  many  cases,  as  we  have  said,  but  not  all.  The 
patients  to  whom  it  refers  as  a  rule  present  no  very  great  disturbances,  but  com- 
plain merely  of  all  sorts  of  general  derangements,  sometimes  of  one  kind  and  some- 
times of  another,  and  yet  are  able  to  perform  their  daily  duties  tolerably  well.  A 
case  of  paralysis,  contracture,  or  other  important  localized  hysterical  trouble  may 
not  present  any  marked  mental  peculiarities.  Often,  of  course,  the  patient  conceals 
them  from  the  physician,  and  the  psychopathic  nature  of  the  whole  mental  con- 
stitution ("character  ")  is  finally  revealed  only  by  a  closer  acquaintance  with  the 
patient  and  her  previous  life. 

With  regard  to  the  general  physical  constitution  of  hysterical  subjects,  it  has 


1182  DISEASES  OF  THE  NERVOUS   SYSTEM 

already  been  mentioned  that  any  bodily  v/eakness  favors  the  development  of  the 
disease;  and  yet  hysteria  is  by  no  means  confined  to  the  ill-nourished,  weakly, 
and  anaemic.  On  the  contrary,  many  patients  seem  to  be  in  blooming  health  and 
well  nourished.  In  a  severe  case  of  hysteria,  however,  the  effects  of  the  disease 
on  general  nutrition  may  be  very  distinct.  Little  food  is  ingested,  sleep  is  dis- 
turbed, digestion  is  affected  {vide  infra),  and  the  bodily  health  is  gradually 
undermined. 

Hysterical  Attacks,  Conditions  of  Spasm,  etc. 

While  the  symptoms  thus  far  described  are  largely  of  a  permanent  character, 
paroxysmal  nervous  symptoms  are  also  very  common  in  hysteria.  The  diagnosis 
of  the  entire  morbid  condition  is  often  made  certain  by  the  onset  of  such  hysteri- 
cal attacks,  which  are  often  very  characteristic,  and  their  significance  is  readily 
perceived  by  the  experienced  physician.  There  are  some  cases  of  hysteria  which 
run  their  course  entirely  free  from  these  attacks,  and  present  only  certain  per- 
manent nervous  symptoms,  such  as  paralysis,  contractures,  ansesthesia,  etc.;  but 
there  are  also  other  patients  in  whom  the  hysterical  attacks  dominate  the  whole 
scene,  and  are  sometimes  the  only  manifestations  of  the  disease.  A  hysterical  at- 
tack is  not  infrequently  the  beginning  of  the  trouble,  especially  in  those  cases 
where  the  disease  is  excited  by  fright,  etc.,  and  where  the  attack  follows  immedi- 
ately upon  the  psychical  excitement. 

In  regard  to  the  severity  and  the  variety  of  the  hysterical  attacks,  they  are  so 
manifold  that  an  exhaustive  account  of  all  the  possibilities  can  not  here  be  given ; 
but  certain  features  and  details  are  so  common  in  them,  and  recur  so  often,  that  a 
consideration  of  them  is  often  in  itself  sufficient  for  a  correct  diagnosis. 

The  mildest  form  of  the  hysterical  attack  consists  of  the  development  of  a  feel- 
ing of  distress,  anxiety,  vertigo,  and  especially  of  a  loss  of  voluntary  control  of 
the  body.  The  patient  sinks  on  a  bed  or  chair,  closes  the  eyes,  and  becomes  inca- 
pable of  action  or  speech.  Mild  symptoms  of  motor  irritation  usually  ensue, 
most  commonly  an  acceleration  of  respiration,  general  tremor,  winking  of  the 
eyes,  etc.  Mild  spastic  symptoms  in  the  pharyngeal  muscles  and  the  diaphragm 
are  not  uncommon.  There  is  very  often  a  lively  palpitation  during  the  attack. 
The  face  is  sometimes  quite  red,  but  in  other  cases  pale. 

In  such  mild  attacks  any  impartial  observer  has  decidedly  the  impression  that 
the  patient  is  humoring  her  inclinations.  If,  therefore,  she  be  encouraged,  or  if 
cold  water  be  thrown  in  the  face  or  on  the  back  without  too  great  regard  for  her 
feelings,  she  usually  soon  regains  her  will-power  and  rapidly  recovers. 

In  an  unbroken  series  these  mildest  forms  of  attack  pass  over  into  the  severer 
types,  where  the  clouding  of  consciousness  is  greater  and  the  symptoms  of  motor 
irritation  are  more  severe.  Complete  loss  of  consciousness,  so  common  in  epi- 
lepsy, is  scarcely  ever  seen  in  hysterical  seizures,  but  there  is  very  often  a  marked 
clouding  of  consciousness,  and  in  the  severe  forms  morbid  alterations  of  con- 
sciousness {vide  infra).  If  hysterical  attacks  occur  which  resemble  those  of  epi- 
lepsy ("hystero-epilepsy  "),  we  must  think  of  the  possibility  of  a  combination  of 
the  two  diseases ;  but  usually  the  form  of  the  hysterical  convulsion  is  essentially 
different  from  that  of  the  epileptic.  In  severe  hysterical  convulsions  the  con- 
vulsive movements  are  more  varied,  more  extensive,  and  more  complicated  than  in 
epilepsy.  The  arms  make  thrashing  and  thrusting  movements,  and  often  appar- 
ently quite  well-co-ordinated  movements.  Patients  strike  the  bed,  and  sometimes 
their  own  bodies,  with  clenched  fists;  they  seize  objects,  such  as  the  bedclothes 
or  furniture,  and  cling  fast  to  them.  We  also  see  clonic  or  tonic  flexor  and  ex- 
tensor spasms  in  the  legs.  The  eyes  are  almost  always  rolled  up,  more  rarely 
they  converge  or  are  turned  to  one  side,  and  they  often  roll  about.  The  lids  are 
tightly  closed  or  occasionally  open.     There  is  almost  always  trismus,  and  there  is 


HYSTEEIA  1183 

often  grinding  of  the  teeth.  The  trunk  usually  twists  and  turns  the  most  of  any 
part  of  the  body.  The  patient  often  hits  her  head  violently  against  the  wall  or 
the  bed.  The  whole  body  may  assiome  positions  which  a  healthy  person  can 
scarcely  imitate  without  special  practice.  The  best  known,  and  in  fact  one  of  the 
commonest  and  most  characteristic,  is  the  arched  position  (arc  de  cercle),  of 
which  the  accompanying  illustration  (Fig.  182)  gives  an  idea. 

Many  patients  rest  for  a  time  on  the  floor  supported  only  by  the  head  and  toes. 
At  intervals  they  fling  or  roll  their  bodies  to  and  fro,  drum  on  the  floor  with  their 


Fig.  182. — Hysterical  arc  de  cercle  (Bourneville  and  Regnardj. 

legs,  throw  themselves  into  the  air,  etc.  Any  one  who  has  once  seen  such  a  "  grand 
hysterical  convulsion  "  will  never  forget  the  picture. 

A  different  but  yet  a  common  form  of  hysterical  convulsion  is  characterized  by 
a  pronounced  implication  of  the  respiratory  muscles.  The  attack  begins  with  a 
spasmodic  acceleration  of  respiration,  and  the  breathing  becomes  progressively 
shorter  and  more  rapid.  We  have  ourselves  counted  two  hundred  respirations  a 
minute.  Other  peculiar  spasms  of  the  respiratory  muscles,  which  occur  in  this 
way  only  in  hysteria,  are  also  common;  hiccough,  loud  sobbing,  grunting,  etc. 
The  muscles  of  the  pharynx  are  usually  implicated  in  producing  these  noises.  Of 
course,  all  these  spasmodic  conditions  may  be  joined  in  the  most  varied  ways  with 
spasms  of  the  trunk  and  the  extremities.  We  very  often  find  during  the  hysterical 
attacks  pronounced  cataleptic  states.  Tf  the  patient  lies  in  bed  with  the  eyes 
closed  and  without  marked  convulsions,  we  can  put  the  arms  and  legs  into  the 
strangest  positions  passively,  and  they  are  kept  there  for  a  long  time  (see 
Fig.  183). 

One  of  the  most  essential  factors  which  often  gives  the  most  characteristic 
stamp  to  the  grand  hysterical  attack,  is  the  relation  which  the  spasms  often  have 
to  certain  co-existing  abnormal  conditions  of  consciousness.  During  the  attack 
the  patient  is  usually  not  unconscious,  but  she  is  under  the  dominion  of 
morbid  delusions,  and  these  often  mirror  themselves  in  the  outAvard  movements. 
The  patient  is  wholly  dominated  by  a  definite  circle  of  ideas;  she  has  hallucina- 
tions, and  passes  through  some  frightful  or  exciting  event.  All  this  is  most 
strikingly  manifested  in  her  movements  and  her  expression.  Hence,  in  an  attack 
the  face  often  expresses  terror,  rage,  threatening,  concupiscence,  serenity,  etc. 
Very  often  the  internal  excitement  breaks  forth  in  words,  and  there  is  actual  hys- 
terical delirium,  the  most  marked  emotional  utterances,  etc.  We  often  observe, 
and  it  is  a  fact  of  especial  interest,  that  in  hysterical  attacks  which  have  come  on 
immediately  after  a  severe  fright,  or  some  exciting  event,  the  same  scene  to  some 
degree  is  rehearsed  over  in  the  patient's  consciousness  in  each  subsequent  attack. 
If,  for  example,  hysterical  attacks  come  on  in  a  nervous  child  who  has  been  at- 
tacked by  a  dog,  we  can  not  infrequently  recognize  again  the  cries  of  terror  at 


1184 


DISEASES   OF   THE   NERVOUS    SYSTEM 


the  approacli  of  the  dog  in  each  new  attack,  etc.  The  patients  often  talk  continu- 
ally to  themselves  during  the  attack,  usually  very  rapidly,  with  frequent  repeti- 
tions of  the  same  phrase  or  word.  We  can  often  succeed  in  giving  the  deliriiim  a 
definite  direction  by  questioning  the  patient,  or  converse  regularly  with  the  pa- 
tient during  an  attack,  but  usually  the  pure  motor  spasms  again  set  in,  or  persist 
for  some  time  in  atonic  form. 

We  can  not  go  further  into  the  numerous  details  of  the  symptoms  of  the  grand 
attack  {"  grand e  hysterie  "),  for  an  accurate  knowledge  of  which  we  must  thank 
the  observations  of  Charcot  and  the  school  of  La  Salpetriere  in  Paris  (Boumeville 
and  Eegnard,  P.  Richer).  The  descriptions  of  the  French  authors  apply  to  the 
grand  hysteria  not  infrequently  seen  in  Germany.  In  regard  to  the  whole  picture 
of  the  attack  the  French  neurologists  distinguish  several  periods  which  corre- 
spond in  general  with  the  above-described  conditions.  The  first  period  consists  of 
severe  epileptiform  convulsions  apparently  associated  with  loss  of  consciousness. 


Fig.  183. — Hj'sterical  attack  with  catalepsy".    (Personal  observation.) 


Then  comes  the  period  of  "contortions  and  grand  movements"  (clownismus), 
and  finally  the  period  of  plastic  positions  and  passionate  attitudes  (attitudes  pas- 
sionelles).  The  short  and  very  significant  expressions  of  this  scheme  are  of  prac- 
tical value,  but  according  to  our  experience  one  can  only  rarely  expect  sharply  de- 
fined "  periods  "  in  the  individual  case ;  the  grand  hysterical  attack  is  rather  com- 
posed in  the  most  varied  ways  of  the  different  symptoms  above  mentioned. 

There  remains  one  essential  trait  needed  to  complete  the  picture  of  the 
hysterical  attack,  and  that  is  the  "  suggestibility  "  of  the  patient,  which  is  so  pe- 
culiarly characteristic  of  hysteria.  By  "  suggestion  "  we  mean  the  artificial  pro- 
duction of  a  definite  psychical  state,  or  a  physical  state  dependent  on  the  mind, 
by  arousing  the  appropriate  ideas.  In  the  general  characteristics  of  the  mental 
constitution  of  many  hysterical  persons  we  have  already  had  to  point  out  how 
much  and  how  often  such  patients  let  themselves  be  dominated  by  their  imagina- 
tions. Suggestion  is  merely  the  artificial  fostering  of  this  psychical  peculiarity 
and  its  special  application.     The  more  we  try  to  foster  and  preserve  this  pecul- 


HYSTERIA  1185 

iarity,  the  more  v,  ^  leave  uncorrected  the  false  ideas  which  the  patients  have,  the 
better  we  succeed  at  last  in  making  the  patients  merely  a  shuttlecock  for  their 
ideas.  Hence  the  physician's  daily  experience  teaches  that,  as  suggestion  experi- 
ments are  repeated,  the  patients  more  easily  become  susceptible  to  them,  so  that 
finally  we  can  actually  "  do  everything  with  them."  There  can  scarcely  be  any 
difference  of  opinion  as  to  whether  such  an  experiment  is  entirely  justifiable, 
medically  and  morally;  and  even  the  fostering  of  suggestion  for  therapeutic  pur- 
poses is  a  two-edged  sword  whose  action  is  not  always  rigidly  within  the  physi- 
cian's control. 

Suggestion  is  most  easy  during  the  hysterical  attack  itself,  especially  in  those 
forms  where  the  patients  speak,  hear,  and  answer.  As  soon  as  we  give  the 
patients'  ideas  a  definite  direction,  and  tell  them  in  a  convincing  tone  that 
they  are  in  a  garden  or  a  wood,  picking  flowers  or  fruit,  that  they  are 
attacked,  bound,  lying  on  the  edge  of  a  precipice  or  the  water,  etc.,  we  see  in  their 
bearing  and  speech  that  they  think  they  are  actually  experiencing  all  these  con- 
ditions in  their  delirium  and  hallucinations.  The  emotional  utterances  of  fear, 
terror,  joy,  or  aversion  are  then  often  expressed  with  astonishing  art.  In  the 
same  way  we  can  suggest  paralyses,  contractures,  or  anaesthesias.  The  most 
interesting  feature  of  it  all  is,  that  when  the  attack  is  over  every  trace  of  recol- 
lection of  what  happened  during  it  is  lost.  The  same  patients  who  just  now  were 
so  much  excited  by  some  definite  idea,  a  few  seconds  later,  as  soon  as  the  attack 
has  ceased  of  itself  or  has  artificially  been  brought  to  an  end  (vide  infra),  know 
nothing  more  about  it.  They  have  not  even  a  vanishing  recollection  like  that  of  a 
dream  about  what  they  have  just  said  and  done,  even  if  it  be  expressly  described; 
but  it  is  still  more  remarkable  that  during  the  following  attack  they  often  re- 
member very  well  what  they  have  experienced  actually,  or  in  their  imaginations 
in  the  past  attack.  In  such  cases  we  can  truly  speak  of  "  double  conscious- 
ness." Processes  of  the  conscious  waking  life,  however,  often  remain  in  the  con- 
sciousness during  the  attack.  We  have  already  said  that  the  actual  event  (scene 
of  terror,  etc.)  which  has  given  rise  to  the  first  onset  of  the  attacks,  is  often  re- 
vealed anew  in  the  delirium  of  subsequent  attacks. 

Hypnotic  symptoms  are  closely  allied  to  the  processes  in  suggestion.  We  can 
not  give  here  a  complete  review  of  this  field,  which,  as  is  well  known,  has  been  so 
much  studied  of  late.  The  tendency  of  human  nature  to  mysticism  and  the  influ- 
ence of  suggestions,  which  may  be  potent  not  only  with  the  patients  but  oven 
with  the  investigating  physicians,  are  the  reasons  why  the  false  and  the  true  have 
often  been  mixed  in  the  study  of  hypnosis.  We  can  say  only  that  one  great  ad- 
vance is  now  generally  recognized,  and  that  is,  that  most  persons  of  scientific 
training  have  abandoned  the  hypothesis,  once  frequently  accepted,  of  a  special 
^'magnetic  power"  (animal  magnetism),  by  which  the  "  magnetizers  "  could  put 
their  "  mediums  "  into  the  "  magnetic  sleep  "  or  other  abnormal  conditions. 

Hypnosis  is  nothing  more  than  the  intentional  artificial  production  of  a  hys- 
terical attack,  or  a  hysterical  psychosis  by  suggestion — that  is,  by  the  action  of 
definite  ideas  on  the  person  to  be  hypnotized.  Therefore,  only  those  persons  can 
be  hypnotized  in  whom  these  ideas  have  a  strong  enough  influence.  N'o  man  can 
be  hypnotized  to  whom  the  nature  of  hypnosis  is  clear.  The  essential  feature  of 
all  hypnotic  procedures  is  merely  to  produce  in  the  most  lively  way  possible  the 
idea,  "  It  will  happen  as  the  hypnotizer  says."  All  other  things — the  fixation  of 
the  eyes  on  bright  objects,  the  vibrations  of  a  tuning-fork,  etc.— are  side  issues, 
and  serve  merely  to  support  the  suggestion.  In  all  easily  hypnotizable  persons 
the  mere  closure  of  the  eyes  and  the  remark,  "  Now  go  to  sleep,"  are  enough  to 
produce  the  hypnotic  sleep.  Patients  (and  here  we  may  actually  speak  of  "  pa- 
tients ")  reach  this  suggestibility,  of  course,  only  after  they  have  often  been  hyp- 
notized; for  the  oftener  the  same  action  of  an  idea  is  produced  the  more  easily 
75 


1186  DISEASES  OE  THE  ITEEVOUS   SYSTEM 

it  occurs — a  law  which  follows  also  from  many  other  experiments  in  the  psychical 
domain.  The  different  forms  of  hypnosis  are  not  distinguishable  from  the  various- 
hysterical  conditions.  Hypnosis  is  an  artificial  hysterical  symptom,  designedly 
produced,  and  from  this  alone  we  note  the  danger  of  all  hypnotic  experiments- 
if  they  are  practiced  by  the  ignorant.  In  this,  too,  it  has  often  been  showru 
that  we  can  not  become  free  again  from  the  spirits  which  we  call  up. 

The  Erench  physicians  (Richer)  distinguish  four  chief  forms  of  the  hypnotic 
state,  which  show,  however,  many  transitions :  1.  The  cataleptic  state,  in  whicK 
the  limbs  retain  all  the  positions  artificially  given  them  (see  the  previous  chap- 
ter). 2.  The  state  of  "  sug*gestion,"  of  artificially  produced  hallucinations.  If 
we  put  the  body  passively  into  certain  positions  corresponding  to  definite  acts, 
we  can  produce  in  the  patient  all  the  appropriate  ideas  with  the  distinctness  of" 
a  hallucination.  To  this  category  belong  the  well-known  hypnotic  exhibitions 
where  hypnotized  adult  men  dance  dolls,  eat  raw  potatoes  with  an  expression  of" 
enjoyment,  etc.  3.  The  lethargic  state,  that  is,  a  state  of  apparent  unconscious- 
ness, with  the  eyes  closed,  the  muscles  completely  relaxed,  and  a  marked  increase 
of  excitability  in  the  muscles  and  nerves.  A  light  pressure  or  a  slight  blow  on  a 
nerve,  such  as  the  facial,  suffices  to  put  all  the  muscles  supplied  by  it  into  a  tetanic- 
contraction  which  outlasts  the  irritation.  4.  By  certain  manipulations  (for  in- 
stance, rubbing  over  the  vertex)  we  can  change  the  lethargic  state  into  one  of 
hysterical  somnambulism.  The  patients  remain  half  unconscious,  but  answer 
automatically  questions  which  are  put  to  them,  obey  orders  given  to  them,  and 
sometimes  show  certain  sensory  hypersesthesias.  We  see  that  all  these  forms  are 
precisely  identical  with  the  different  forms  of  the  hysterical  attack.  Only  the- 
increased  mechanical  excitability  of  muscles  and  nerves  is  not  yet  fully  explained, 
but  the  reported  observations  upon  this  point  have  not  yet  been  absolutely  con- 
firraed.  It  is  especially  a  question  whether  suggestion — that  is,  ideas  which  lead  to- 
unconscious  muscular  contractions — may  not  also  play  a  part  here  ? 

We  have  thus  far  omitted  to  dwell  upon  an  important  point  in  the  description 
of  the  hysterical  attack — namely,  the  relation  to  it  of  "  hysterogenous  zones."" 
We  have  mentioned  above  how  often  in  hysterical  patients  certain  parts  of  the- 
body  (the  ovarian  region,  the  sides  of  the  chest,  etc.)  are  extremely  sensitive  to 
pressure.  It  is  by  no  means  uncommon  that,  in  spite  of  the  patient's  resistance, 
somewhat  longer  pressure  on  such  a  spot  may  excite  a  hysterical  attack.  On  the- 
other  hand,  we  sometimes  succeed  in  causing  an  existing  attack  to  cease  by  pres- 
sure on  the  same  zone.  We  are  of  the  opinion  that  in  these  manipulations  also 
ideas  become  potent  as  connecting  links;  for  we  may,  as  we  have  often  demon- 
strated in  the  clinique,  by  suggestive  persuasion  aloud  or  by  all  possible  procedures- 
excite  and  then  inhibit  attacks  in  hysterical  patients.  In  siich  cases  we  never- 
have  to  do  with  physiological  reflex  processes,  but  always  with  the  action  of  ideas 
suggested  to  the  patient. 

Einally,  we  must  add  that  there  are  also  milder  forms  of  hysterical  spasm- 
which  are  limited  to  a  definite  muscular  region,  and  are  not  associated  with  any 
marked  clouding  of  consciousness.  There  are,  for  example,  isolated  spasms  of  the 
muscles  of  the  neck,  isolated  respiratory  spasms  (spasmodic  cough,  etc.),  not  infre- 
quently associated  with  the  strangest  noises,  and  isolated  spasms  in  the  arms  and 
legs;  the  laryngeal  muscles  may  also  be  affected  (hysterical  spasm  of  the  glottis). 
Spasms  of  the  diaphragm  and  other  muscles  of  inspiration  are  quite  common 
under  the  form  of  hysterical  hiccough,  which  may  sometimes  last  in  the  severest 
way  for  days  and  weeks.  To  spasmodic  conditions  in  the  muscles  of  the  pharynx 
and  oesophagus  we  refer  the  well-kno-wn  symptom  of  so-called  globus  hys- 
tericus :  the  patients  feel  as  if  a  ball  were  moving  up  and  down  in  the  throat. 

We  sometimes  see  spasmodic  conditions  which  come  on  in  a  clonic  fashion,  or 
in  single  twitchings  in  this  or  that  muscular  territory;  sometimes  affect  sym- 


HYSTEKIA  1187 

metrical  groups  of  muscles ;  are  not  associated  with  disturbances  of  consciousness ; 
cease  during  sleep,  and  are  often  easily  cured  by  appropriate  mental  treatment. 
Such  conditions  have  often  been  falsely  called  paramyoclonus,  or  myoclonia  (q.  v). 
Among  the  forms  of  hysterical  spasm  we  may  also  reckon  the  peculiar  attacks, 
essentially  of  a  psychical  nature,  when  more  complicated  morbid  excitations  of 
volition  occur  with  or  without  the  ordinary  convulsive  movements.  In  such  at- 
tacks the  patients  begin  to  ejaculate  the  filthiest  words  of  abuse  (coprolalia), 
or  to  repeat  every  word  they  hear  (echolalia),  or  to  practice  peculiar  "  impulsive  " 
movements  (tearing  everything  to  bits,  etc.).  We  see  no  reason  to  regard  such 
conditions  as  a  special  disease  under  the  name  of  "  maladie  des  tics."  We  have 
repeatedly  observed  such  conditions  (especially  in  children)  which  were  undoubt- 
edly to  be  regarded  as  hysteria,  and  which  could  rapidly  be  made  to  disappear  by 
appropriate  psychical  treatment.  The  severer  forms  of  these  conditions  of  course 
belong  to  the  pronounced  hysterical  psychoses. 

General  Course  of  the  Disease. — Our  description  of  the  symptomatology  of 
hysteria  has  been  confined  to  the  most  important  and  frequent  phenomena;  and 
yet  even  this  meager  outline  shows  what  an  infinite  variety  of  shapes  the  disease 
assumes.  1.  In  one  class  of  cases  there  are  no  severe  symptoms  whatever.  The 
patient  merely  displays  the  general  mental  condition  characteristic  of  hysteria : 
she  is  easily  excited,  prone  to  make  much  of  her  ills,  has  all  sorts  of  symptoms, 
such  as  pain,  cephalic  symptoms,  palpitation,  dyspepsia,  and  dyspnoea,  and  these 
are  aggravated  by  mental  excitement,  while  at  other  times  they  may  so  nearly 
vanish  that  the  patient  does  not  appear  to  be  ill.  2.  A  second  class  of  cases  has 
more  severe  disturbance,  coming  on  after  some  unfavorable  psychical  or  other 
influence  (vide  supra).  The  patient  may  have  displayed  a  general  hysterical 
tendency  previously,  or  may  have  seemed  perfectly  well.  Here  we  may  observe 
all  the  symptoms  above  enumerated  and  described.  There  may  be  paralysis, 
spasm,  contracture,  ansesthesia,  or  parsesthesia.  The  individual  symptoms  may 
persist  obstinately  for  weeks  and  months;  but  again  they  may  vanish  suddenly 
or  give  place  to  other  disturbances.  Psychical  influences  are  unmistakably 
potent,  not  merely  in  the  incipient  stage  but  also  in  the  further  course  of  the 
disease.  Any  aggravation  of  the  symptoms  is  often  referable  to  emotional  ex- 
citement. This  is  particularly  true  of  the  hysterical  convulsions.  In  other 
cases,  of  course,  the  hysterical  attacks  come  on  apparently  quite  spontaneously, 
just  like  epileptic  states.  3.  The  third  class  comprises  the  most  severe  forais  of 
hysteria,  with  those  nervous  disturbances  briefly  outlined  above.  They  are  as 
complicated  as  they  are  puzzling,  and  form  manifold  combinations  with  all  the 
other  hysterical  phenomena,  including  anaesthesia,  contracture,  and  paralysis. 

The  entire  duration  of  the  disease  varies  greatly.  The  true  root  of  all  evil  is 
the  abnormal  excitability  of  the  nervous  system,  which  always  remains  in  un- 
stable equilibrium ;  and  often  it  is  not  possible  to  cure  this.  If  not,  the  trouble 
lasts  almost  indefinitely.  ISTew  manifestations  of  the  disease  succeed  to  periods  of 
apparently  perfect  health.  Usually  the  symptoms  do  not  abate  till  qi;ite  late  in 
life.  There  are,  however,  many  instances  of  complete  and  permanent  relief. 
This  favorable  termination  is  more  especially  to  be  hoped  for  where  the  patient 
comes  into  suitable  and  appropriate  conditions  of  life,  having  some  regular  occu- 
pation which  is  not  exposed  to  all  sorts  of  unfavorable  psychical  influences.  Many 
cases  of  hysterical  disturbance,  in  previously  healthy  children  or  young  adults,  and 
due  to  some  distinct  cause,  terminate  comparatively  soon,  and  never  recur.  It  is 
never  possible, however,  to  be  sure  that  there  will  be  no  relapse,  inasmuch  as  a  single 
appearance  of  hysteria  shows  unmistakably  that  the  nervous  system  is  abnormally 
vulnerable  to  external  impressions  and  the  mental  emotions  excited  by  them. 

Diagnosis. — An  experienced  physician  is  seldom  greatly  puzzled  by  hysterical 
affections.     Although  the  disease  may  at  first  simulate  some  grave  organic  disor- 


IISS  DISEASES   OF  TEffi  KEEYOUS   SYSTEM 

der,  a  careful  physical  examination  and  continued  observation  will  almost  invaria- 
bly disclose  tlie  true  character  of  the  ease.  In  the  first  place,  there  are 
never  any  such  symptoms  as  would  absolutely  prove  the  existence  of  some  organic 
lesion.  Eor  example,  we  never  find  marked  atrophy  or  loss  of  electrical  reaction 
in  connection  with  hysterical  paralysis.  "We  should  also  regard  the  whole  psychi- 
cal behavior  of  the  patient,  the  influence  exerted  upon  her  by  emotional  disturb- 
ances, the  disappearance  of  the  symptoms  when  the  attention  is  diverted,  and  the 
aetiology  of  the  illness — for  instance,  the  development  of  the  symptoms  after  some 
mental  excitement  or  emotion.  The  discovery  of  specific  hysterical  symptoms, 
the  so-called  hysterical  stigmata,  sensory  ansesthesia,  hysterogenous  zones,  etc., 
are  especially  important.  Many  symptoms  of  hysteria,  especially  hysterical  aba- 
sia, hysterical  aphonia,  hysterical  hypergesthesise,  certain  forms  of  spasm,  hemi- 
anesthesia, etc.,  are  in  themselves  so  characteristic  that  from  them  alone  a  correct 
diagnosis  can  usually  be  made  at  the  first  glance.  The  very  circumstance  that 
hysterical  affections  do  not  keep  to  the  laws  of  nervous  anatomy  and  nervous  phys- 
iology, and  that  they  often  can  not  be  brought  into  harmony  with  them,  is  of  im- 
portance in  their  recognition ;  but,  on  the  other  hand,  we  must  earnestly  warn  the 
physician  against  making  the  diagnosis  of  "  hysteria  "  too  readily.  Pronounced 
hysterical  symptoms  are  of  course  only  rarely  mistaken  by  an  experienced  physi- 
cian, but  very  often  all  sorts  of  symptoms  may  be  due  to  concealed  affections,  which 
can  not  be  positively  determined  (certain  cases  of  gastric  ulcer,  gall-stones,  renal 
calculi,  beginning  cerebral  diseases  [especially  multiple  sclerosis. — K.],  arterio- 
sclerosis, etc.),  and  these  symptoms  may  falsely  be  regarded  as  "hysterical,"  es- 
pecially when  we  are  actually  dealing  with  nervous  patients.  Repeated  careful 
objective  examination  and  observation  is  therefore  imperatively  necessary.  In 
doubtful  cases  the  diagnosis  can  sometimes  be  rendered  certain  only  by  the  result 
of  treatment.  In  doubtful  cases,  however,  the  physician  should  not  proceed  too 
roughly  or  too  rapidly,  since  he  may  only  too  easily  cause  harm. 

Since  an  investigation  of  hysterical  and  epileptic  attacks  is  of  especial  impor- 
tance, we  will  give  here  a  synopsis  of  the  most  important  distinguishing  features. 

Epileptic  Coxvtlsioxs  Hysterical  Coxvulsioxs 

1.  Sudden  fall  to  the  ground ;  often  con-  1.  Slow  sinking  to  the  ground :  no  exter- 
sequent  external  injuries.  nal  injuries. 

2.  Sudden  pallor  of  the  face.  Often  marked  2.  Xo  striking  pallor  of  the  face.  Xo 
cyanosis  later.  marked  cyanosis. 

3.  Pupils  dilated  :  do  not  react.  3.  Pupils  react. 

4.  Convulsions  according  to  the  nature  of  4.  Convulsions  consist  of  extensive  move- 
cortical  epilepsy  in  the  form  of  convulsive  ments.  striking  out  with  the  arms  or  legs, 
twitching.     Tongue  often  bitten.  twisting  of  the  body,  etc.   E-esi^irat cry  spasms. 

Xo  biting  of  the  tongue. 

5.  Often  one  initial  cry.  then  total  loss  of  5.  Hysterical  disturbances  of  conscious- 
consciousness.                     "                                       ness.  but  no  complete  loss  of  consciousness; 

spasmodic  and  continuous  cries,  laughter, 
weeping,  etc.  Talking  during  the  attack, 
emotional  disturbauces.  delirium,  etc. 

6.  Convulsions  rarely  last  longer  than  a  6.  Attack  may  last  from  half  an  hour  to 
few  minutes,  followed  by  deep  sleep.                     an  hour  or  more.     Patient  often  wakes  sud- 
denly. 

7.  Suggestive  and  hypnotic  procedures.  T.  The  attacks  may  easily  be  excited  arti- 
and  also  external  irritation  during  the  attack,  ficially  at  any  time  by  hypnotic  or  other  sug- 
without  any  influence.                                              gestive  procedures,  or  they  may  be  inhibited 

in  like  manner  (pressure  on  definite  parts  of 
the  body  or  the  like).  During  the  attack  the 
convulsions  may  be  influenced  or  even  wholly 
■  suppressed  by  sprinkling  with  water,  a  cold 
douche,  etc. 

8.  Other  hysterical  symptoms  are  absent.  8.  Other  hysterical  symptoms  mav  co-exist 

and  often  remain  after  the  attack  (hysterical 
hemiana^sthesia,  paralysis,  contractures,  etc.). 


HYSTEEIA 


1189 


Treatment. — What  has  been  said  about  the  aetiology  of  hysteria  at  once  sug- 
gests a  possible  method  of  prophylaxis.  A  watchful  eye  will  often  detect,  even  in 
childhood,  the  signs  of  abnormal  -nervous  excitability,  and  in  such  a  case  the 
parent  will  make  it  his  duty  to  impose  a  suitable  physical  and  mental  regimen, 
that  graver  disturbances  may  be  averted. 

If  hysteria  be  already  developed,  the  first  and  most  important  treatment  is 
mental.  There  could  be  no  greater  mistake  than  to  deride  the  patient  or  treat 
Jber  as  a  malingerer;  for  hysteria 
is  a  disease,  and  its  symptoms  are 
just  as  independent  of  any  con- 
scious volition  on  the  part  of  the 
patient  as  those  of  any  other  dis- 
ease. It  is,  however,  also  abso- 
lutely essential  to  carry  out  the 
moral  training,  which  the  physi- 
cian must  institute  with  all  the 
proper  strictness  and  energy,  be- 
cause in  this  way  alone  can  any 
good  be  accomplished.  Therefore 
an  absolutely  positive  diagnosis  is 
the  first  essential  in  the  success- 
ful treatment  of  hysteria.  If  the 
physician  is  in  doubt  as  to  the 
nature  of  the  trouble  (vide 
supra),  he  can  not  proceed  with 
necessary  inflexible  consistency, 
and  the  therapeutic  results  are 
seldom  satisfactory;  but  if  the 
diagnosis  is  assured,  then  there  is 
no  need  of  making  the  slightest 
concession  to  the  patient.  Some- 
times this  most  important  indica- 
tion can  be  fulfilled  only  after  the 
patient  has  been  withdrawal  from 
the  over-anxious  and  over-assidu- 
ous parents  or  relatives,  and  like 
unfavorable  influences.  In  such 
cases,  treatment  in  some  institu- 
tion vsdll  often  be  vastly  better 
than  the  best  care  at  home;  and 
our  own  experience  leads  us  to 
recommend  most  urgently  that 
the  eventful  necessity  of  removal 
to  an  asylum  should  be  constantly 
borne  in  mind  with  regard  to  ag- 
gravated cases.  Often  the  mere 
dread  of  removal  to  such  a  place 
has  a  favorable  mental  influence. 

Proper  moral  treatment  achieves  comparatively  the  best  results  where  there  is 
hysterical  paralysis.  "When  we  are  once  certain  that  the  paralysis  is  due  to 
hysteria,  the  patient  must  be  instructed  how  to  regain  by  practice  the  lost  power 
of  the  will  over  the  paralyzed  muscles.  If  the  paralysis  affect  the  lower  extremi- 
ties, as  it  usually  does,  the  patient  must  be  set  on  her  feet,  regardless  of  all  her 
opposition  and  complaints,  and  kindly  but  most  firmly  required  to  try  to  walk. 


Fig.  1S4.— Hysterical  abasia.    Exercise  in  walking. 
(Erlangen  Medical  Clinique.) 


1190  DISEASES  OF  THE  ISTERVOUS   SYSTEM 

Of  course,  at  first  she  must  be  well  supported  (see  Fig.  184).  This  exercise  raust 
be  methodically  gone  through  with  several  times  a  day.  Gradually  the  patient's 
gait  becomes  more  and  more  secure.  She  regains  confidence  in  her  own  ability, 
and,  having  once  begun  to  improve,  usually  makes  rapid  progress  toward  complete 
recovery.  Every  experienced  physician  can  recall  numerous  instances  where  hys- 
terical paralysis  which  had  lasted  weeks  and  months  was  cured  in  a  few  days  by 
this  mode  of  treatment.  Faradization  of  the  muscles,  cold  sponging,  with  fric- 
tion and  bathing,  are  excellent  adjuvants;  and  the  disagreeable  element  in  these 
procedures  of  itself  stimulates  the  patient  to  make  every  possible  exertion  to  re- 
gain the  use  of  her  limbs. 

When  there  is  hysterical  paralysis  of  the  vocal  cords,  a  similar  training  (ener- 
getic efforts  to  make  the  vocal  cords  tense  and  to  produce  a  loud  tone)  will  be 
found  both  practicable  and  efficient.  Electricity  is  also  of  great  value.  It  may 
be  applied  externally  or  within  the  larynx.  Often  the  patient,  terrified  by  the 
sudden  pain  it  causes,  recovers  her  voice  at  once.  The  same  holds  true  of  all 
hysterical  disturbances  of  speech  and  of  hysterical  dumbness  or  mutism. 

The  treatment  of  hysterical  contractures  consists,  first,  of  an  effort  to  relax 
the  contracture  by  massage  and  energetic  passive  motion.  Faradism  will  be 
found  of  assistance  here  also.  In  order  to  remove  the  contracture  permanently, 
the  patient  must  be  induced  to  exercise  the  muscles  regularly  by  making  voluntary 
movements.  We  sometimes  have  the  greatest  difficulty  in  getting  the  patient  to 
make  the  first  attempt  to  move.  In  such  cases  we  can  attain  our  end  only  by  great 
patience  and  perseverance  and  by  the  suggestive  aid  of  all  sorts  of  manipula- 
tions (galvanism  through  the  head,  etc.). 

The  treatment  of  hysterical  spasmodic  conditions  often  causes  greater  difficul- 
ties. The  main  thing  is  to  bring  the  patient  to  control  herself  at  the  beginning 
of  the  attack,  either  by  an  energetic  appeal,  by  diverting  the  attention,  etc.  In 
many  cases  a  sharp  sensory  irritation,  douching  with  cold  water,  or  a  bath  with 
cold  affusions,  acts  to  restore  the  energy  of  the  patient's  will  and  the  control 
over  the  muscles,  and  thus  to  check  the  spasms.  The  dread  of  the  repetition  of 
the  bath  does  its  part  in  restraining  the  patients  from  giving  themselves  up  unre- 
sistingly to  a  repetition  of  the  attack.  The  electric  current  (strong  faradism  dur- 
ing the  attack)  may  also  act  favorably  in  the  same  way.  The  action  of  such 
measures,  however,  often  gradually  weakens,  the  patients  become  accustomed  to 
the  cold  baths,  and  they  remain  without  effect. 

The  milder  varieties  of  hysterical  convulsion,  such  as  hysterical  hiccough  or 
cough,  are  often  controlled  by  a  stern  reproof.  It  is  precisely  in  these  cases  that 
the  moral  effect  of  transfer  to  some  institution  frequently  causes  the  abrupt  disap- 
pearance of  symptoms  which  have  lasted  for  months.  All  the  forms  of  hysterical 
spasm  occurring  in  children  especially  are  easily  removed  by  proper  treatment 
(especially  isolation  from  the  family!).  The  severe  hysterical  attacks,  on  the 
other  hand,  are  often,  of  course,  peculiarly  obstinate,  and  they  may  resist  for 
months,  and  even  years,  the  most  intelligent  treatment.  In  all  hysterical  spasms 
limited  to  certain  muscles  methodical  gymnastic  exercises  are  often  attended  by 
the  best  results.  We  inhibit  the  abnormal  motor  innervations,  and  direct  the 
will  into  other  well-regulated  paths:  regular  respiratory  exercises  in  respira- 
tory spasms,  gymnastic  exercises  with  the  arms  for  twitching  of  the  arms,  etc. 

Hysterical  anaesthesia  is  best  treated  with  the  f  aradic  wire-brush.  The  vigor- 
ous irritation  restores  the  anaesthetic  parts  to  the  domain  of  consciousness.  It 
should  be  said,  however,  that  these  cases  may  prove  obstinate  or  relapse. 

The  most  difficult  of  all  hysterical  cases  to  treat  are  those  where  the  symptoms 
are  not  strongly  pronounced,  but  where  there  is  a  general  hysterical  condition,  ex- 
pressing itself  in  a  multitude  of  nervous  derangements,  such  as  palpitation,  dys- 
pepsia, and  general  debility,  or  in  purely  subjective  symptoms,  or  in  emotional 


HYSTEEIA  1191 

"tendencies.  Such  patients  are  often  advanced  in  years,  so  that  little  is  to  be  hoped 
ior  from  moral  training;  and  their  circumstances  may  be  unfavorable  without 
our  being  able  to  remedy  the  situation.  Even  here,  however,  the  physician  may 
greatly  benefit  the  patient  by  means  of  psychical  influences,  if  he  once  gains  her 
■complete  confidence.  We  should  also  consider  all  such  remedies  as  invigorate  the 
Jiervous  system;  electricity  should  be  given,  either  in  the  form  of  general  faradi- 
sation, the  faradic  brush  applied  to  the  back  and  shoulders,  or  the  galvanic  cur- 
rent applied  to  the  spinal  column  and  the  sympathetic  nerve ;  and  of  still  greater 
importance  is  a  methodical  cold-water  treatment,  either  by  sponging,  bathing, 
•or  douches.  Such  patients  are  often  vastly  improved  by  sea-bathing  in  summer, 
or  by  going  to  the  mountains. 

The  numerous  internal  remedies  for  hysteria  are  also  of  more  use  in  these 
general  conditions  than  where  there  are  marked  nervous  disturbances  in  special 
parts  of  the  body.  In  the  latter,  internal  remedies  do  good  only  indirectly  and  in 
a  psychical  fashion  by  so-called  suggestion,  especially  if  the  patient  has  great 
confidence  in  the  virtues  of  the  medicine  or  in  the  physician  who  prescribes  it. 
This  is  the  explanation  of  the  frequent  cases  of  rapid  recovery  after  taking 
iomoeopathic  and  "  electro-homoeopathic  "  remedies,  and  those  still  more  marvel- 
ous cures  effected  by  means  of  holy  water  and  relics. 

Among  the  "  anti-hysterical "  agents  contained  in  our  medical  thesaurus,  asa- 
f oetida,  valerian,  and  castoreum  are  the  most  famous ;  but  probably  few  would  at 
the  present  day  claim  that  they  possess  any  specific  virtues.  Perhaps  the  prepara- 
tions of  valerian  are  the  most  useful  where  there  is  hysterical  excitement,  as 
■evinced  by  convulsions  or  palpitation.  Bromide  of  potassium,  arsenic,  and  other 
medicines  which  ordinarily  exert  a  favorable  influence  upon  the  nerves,  seldom 
accomplish  any  permanent  good  in  hysteria,  although  often  prescribed.  We  must 
Titter  an  urgent  warning  against  narcotics,  especially  morphine,  since  they  do  little 
good  and  there  is  great  danger  of  developing  the  morphine  habit  in  such  patients. 

If  hysteria  be  complicated  by  some  actual  organic  disease,  the  latter,  of  course, 
•demands  special  treatment.  Great  benefit  is  hoped  for  by  many  from  the  cure  of 
any  uterine  complaint  which  may  be  present.  Cases  are  actually  known  where 
grave  hysterical  disturbance  has  vanished  upon  dilatation  of  a  constricted  cervical 
canal  or  rectification  of  a  displacement;  but  there  are  numerous  other  instances 
•on  record  where  gynaecological  treatment  has  proved  entirely  unavailing.  There 
is  hardly  a  doubt  that,  in  the  successful  cases,  the  main  benefit  was  due  to  the 
mental  influence  of  the  treatment.  In  general  we  would  utter  an  urgent  warning 
against  needless  gynaecological  examinations  and  treatment  in  hysterical  subjects. 
The  patient's  condition  is  often  merely  made  worse  by  such  procedures. 

In  general,  we  may  certainly  maintain  that  all  methods  of  treatment  of  hys- 
teria are  efficient  only  when  associated  with  the  necessary  psychical  factor;  that 
is,  the  patient's  belief  in  the  efficacy  of  the  remedy,  or,  as  we  are  accustomed  to 
say  at  present,  with  suggestion.  Hence  any  prescription,  no  matter  how  sense- 
less it  seems,  may  have  the  greatest  effect  as  soon  as  the  patient  "  believes  in  it " 
— that  is,  as  soon  as  the  psychical  action  of  this  belief  is  manifest.  Hence  it 
follows  that  in  hysteria,  as  a  rule,  treatment  either  produces  rapidly  a  brilliant 
■success  or  it  has  no  effect  at  all. 

We  must  here  mention  two  methods  of  treatment  which  have  lately  been  much 
discussed — metallotherapy  and  treatment  by  hypnosis. 

In  regard  to  metallotherapy  a  French  physician,  named  Burq,  discovered  years 
ago  that  by  laying  plates  of  metal  upon  a  cutaneous  surface  affected  by  hysterical 
anaesthesia  a  remarkable  result  is  sometimes  produced.  Almost  at  once  sensation 
is  restored  to  the  immediate  region,  and  often  to  a  much  larger  area.  Most  of 
the  cases  have  been  those  of  hysterical  hemianaesthesia.  It  is  not  every  kind  of 
metal  which  will  prove  effective,  nor  will  the  same  kind  affect  all  patients.     It  is 


1192  DISEASES   OE  THE  XEKVOUS   SYSTEM 

said  that  iron  is  most  frequently  efficient;  but  sometimes  copper,  zinc,  or  gold  is 
required.  The  process  of  determining  the  metal  essential  to  each  individual  case 
Burq  called  "  metalloscopy  " ;  and  he  stated  that  this  metal  would  also  have  the 
same  effect  if  given  internally!  In  1876  a  committee  appointed  by  the  Paris 
Societe  de  Biologie  tested  these  statements,  at  least  with  regard  to  the  external 
application  of  metals — the  idea  of  their  internal  administration  having  been 
pretty  much  abandoned — and  confirmed  them.  Charcot  also  discovered  many 
remarkable  facts  of  a  similar  nature,  which  likewise  soon  received  universal  sub- 
stantiation. The  most  remarkable  of  these  phenomena  is  known  as  transfer. 
The  return  of  sensation  to  the  anaesthetic  area,  as  a  result  of  applying  a  metal 
plate,  is  accompanied  by  a  simultaneous  development  of  ansesthesia  upon  the 
opposite,  previously  normal  side,  in  an  exactly  corresponding  place.  Sometimes 
sensation  oscillates  from  one  side  to  the  other  and  back  again,  so  that  now. one 
half  of  the  body  and  now  the  other  is  .alternately  sensitive  or  ansesthetic.  If  the 
metal  be  placed  at  the  start  upon  the  normal  skin,  that  part  becomes  anaesthetic, 
while  the  corresponding  part  upon  the  opposite  side  of  the  body  regains  its  former 
normal  condition. 

It  has  also  been  discovered  that  other  hysterical  symptoms  exhibit  analogous 
phenomena.  Transfer  can  sometimes  be  observed  in  hysterical  amblyopia,  achro- 
matopsia, deafness,  loss  of  smell  and  taste,  contractures,  and  paralysis.  Such 
transfers  may  be  induced  by  various  means  other  than  metal  plates.  These  are 
classed  as  sesthesiogenous  remedies,  and  include  large  magnets,  feeble  galvanic 
currents,  and  static  electricity.  Vibrating  tuning  forks  and  sinapisms  have  also 
produced  similar  results.  Hence  it  seems  to  us  to  be  an  indubitable  conclusion 
that  the  whole  group  of  symptoms  just  described  has  no  peculiar  position. 
These  symptoms  are  simply  the  results  of  suggestion,  produced  in  this  case  again 
by  ideas.  The  similarity  of  the  test  as  performed  by  the  physician  produces  the 
similarity  of  the  symptoms  that  ensue. 

Of  late  the  treatment  of  hysteria  by  hypnosis  has  acquired  a  far  greater  prac- 
tical significance  than  metallotherapy ;  it  is  a  mode  of  treatment  which  has  been 
employed  most  extensively  by  the  "  school  of  ISTancy "  (Bernheim)  and  its  ad- 
herents. If,  during  hypnosis,  morbid  states  can  be  produced  by  suggestion,  it 
naturally  follows  that  morbid  states  can  also  be  cured  by  suggestion.  If  by  many 
well-known  successes  the  hypnotizing  physician  has  at  the  outset  acquired  the 
patient's  confidence,  as  relies  win  the  confidence  of  believers,  the  most  beautiful 
results  can  o^  course  be  attained  by  hypnosis.  There  is  no  special  peculiar  princi- 
ple in  the  hypnotic  treatment.  Any  other  efficient  mode  of  treating  hysteria 
rests  on  the  same  conditions  and  presumptions.  Hypnosis  has  only  the  one  great 
consequence,  that  it  is  artificially  produced  as  a  severe  abnormal  mental  state  in 
a  patient  who  previously  had  not  spontaneously  fallen  into  this  state.  In  that 
lies  the  sequel,  which  of  course  need  not  always  be  permanent,  but  which  often 
enough  has  been  most  severe :  the  attempt  to  hypnotize  a  patient  who  is  suffering 
from  a  slight  hysterical  affection  has  not  infrequently  been  followed  by  the  onset 
of  a  severe  hysterical  attack.  The  mischance  will  seldom  happen  to  the  physi- 
cians and  magnetizers  who  practice  hypnotism  as  a  specialty,  because  their 
psychical  influence  on  their  patients  is  usually  greater  from  the  outset;  but  we 
should  consider  it  a  misfortune  if  hypnosis  should  come  into  too  general  use. 
That  in  this  way  apparently  the  most  wonderful  cures  can  often  be  obtained,  is 
perfectly  well  established  and  not  at  all  surprising ;  but  the  same  cures  can  also 
be  obtained  in  other  ways,  without  running  the  risk  of  producing  first  that  of 
which  you  would  cure  your  patient,  for  to  hypnotize  means  to  make  temporarily 
hysterical  (see  page  1185).  Furthermore,  it  is  not  hard  to  prophesy  that,  as  the 
knowledge  of  the  peculiar  nature  of  hypnosis  becomes  general,  it  will  lose  its  halo 
with  the  patient,  and  with  that  it  will  lose  its  healing  power. 


NEUEASTHENIA  1193 


CHAPTEE   X 


NEURASTHENIA 

(]!\'ervous  DehiUty.     2sirvou»nesB) 

Concept  of  the  Disease  and  iEtiology. — The  name  of  neurasthenia  is  given 
to  a  nervous  symptom-coraplex  Avhich  comes  on  in  a  great  variety  of  ways.  Its 
cause  is  not  to  be  looked  for  in  an  organic  disease  but  in  a  merely  functional  dis- 
turbance of  the  nervous  substance.  The  nature  of  this  functional  disturbance  is 
ordinarily  characterized  by  the  two  symptoms  of  "  abnormal  irritahility  "  and  "  ah- 
normal  exhaustibility  " ;  but  the  phenomena  of  neurasthenia  and  its  allied  morbid 
states  are  by  no  means  wholly  exhaiisted  by  the  combined  concept  of  "  irrita'ble 
weakness."  "We  may  also  add  that  the  entire  nervous  system  does  not  by  any 
means  take  part  in  this  abnormal  functioning.  On  the  contrary,  the  more  care- 
fully we  study  and  analyze  the  symptoms  of  neurasthenia,  the  conviction  is  forced 
upon  us  here,  just  as  in  hysteria,  that  in  neurasthenia  we  have  to  do  essentially 
only  with  an  abnormal  mental  condition  of  the  sick  person,  and  that  the  countless 
physical  complaints  and  symptoms  of  the  neurasthenic  are  ultimately  to  be  re- 
ferred in  the  main  to  a  disturbed  ideational  life. 

ISTervousness  and  neurasthenia  are  brief  practical  terms  applied  to  certain 
forms  of  an  abnormal  mental  constitution.  In  by  far  the  greatest  number  of  all 
cases  this  abnormal  mental  constitution,  or  at  least  its  basis,  is  congenital.  IvTeu- 
rasthenia  of  course  does  not  always  show  itself  in  childhood,  although  it  does  often 
enough.  It  does  not  always  develop  to  the  same  degree,  varying  according  to  the 
action  which  various  external  influences  exert  in  making  it  more  or  less  promi- 
nent. We  can  only  rarely,  however,  wholly  dispense  with  the  ultimate  assumption 
of  a  definite  congenital  "  nervous  "  predisposition.  Of  course  we  must  admit  that 
neurasthenic  conditions  of  exhaustion  and  irritation  may  also  occur  under  the 
influence  of  persistent  mental  over-exertion  or  persistent  and  severe  mental 
irritation  in  persons  who  were  previously  "  perfectly  well " ;  but  in  general  we 
are  usually  inclined  to  attribute  to  these  factors  just  mentioned  merely  the 
role  of  exciting  causes;  for  every  nervous  system  does  not  succumb  to  the  same 
burden ;  one  endures  it  without  pennanent  harm,  while  another  breaks  down 
under  it. 

The  congenital  factor  in  the  onset  of  neurasthenia  is  shown  especially  by  a 
careful  regard  of  hereditary  conditions.  ISTervousness,  neurasthenia,  hysteria, 
degenerative  insanity — these  are  closely  associated  morbid  conditions,  at  the  basis 
of  which  lies  the  inherited  abnormal  mental  constitution,  and  these  conditions 
are,  therefore,  unfortunately  linked  together  in  many  families.  Where  the  laity, 
from  a  natural  dread  of  the  worst  forms,  are  disposed  to  believe  in  a  funda- 
mental distinction,  the  medical  eye  sees  only  quantitative  differences  in  a  long 
series  of  psychical  conditions,  which,  without  definite  boundaries,  join  the  nor- 
mal psychical  life  on  the  one  side  and  on  the  other  pass  into  pronounced  in- 
sanity. 

It  is  our  task  here  to  describe  merely  the  mild  neurasthenic  states,  which  far 
exceed  in  frequency  all  other  nervous  diseases.  If  it  has  been  imagined  that 
neurasthenia  is  a  modern  disease,  this  idea  is  incorrect.  It  is  as  old  as  our  definite 
knowledge  of  the  diseases  of  mankind,  and  if  the  increasing  frequency  of  neu- 
rasthenia is  often  ascribed  to  the  restless  haste,  the  unrest  and  the  excitement 
of  "  modern  "  life,  a  glance  at  the  history  of  past  centuries  with  their  horrors  and 
their  disorders  of  war  will  render  such  a  hypothesis  extremely  doubtful.  The 
name  "  neurasthenia  "  is  the  only  thing  that  is  new  or  modern.  This,  and  the 
better  insight  into  the  nature  of  the  disease,  we  owe  to  the  American  neurologist 


1194  DISEASES  OF  THE  NEEVOUS   SYSTEM 

Beard  (1880).*  It  is  also  true  that  all  the  exciting  causes  above  mentioned  are 
still  active  in  their  full  force  to-day,  and  that  it  can  not  therefore  amaze  us  if  we 
observe  neurasthenia  with  especial  frequency  in  business  men,  whose  bold  specu- 
lations are  attended  by  the  excitements  of  hope  and  fear;  in  politicians,  whose 
minds  are  constantly  stirred  by  the  eager  strife  of  parties ;  or  in  those  artists  and 
scholars  whose  never  quiet  ambition  forces  them  into  restless  competition. 
]Sreurasthenia  develops  often  enough,  however,  in  persons  disposed  to  it  from 
the  first  through  a  congenital  defect,  without  any  special  exciting  cause.  We 
can  readily  understand  that  a  disease,  which  plays  its  part  chiefly  in  the  idea- 
tional life  of  those  affected  by  it,  should  be  materially  influenced  by  the  degree 
of  education  of  its  victims ;  that  is,  by  the  richness  and  activity  of  their  ideational 
life ;  but  it  is  incorrect  to  call  neurasthenia  a  disease  chiefly  of  the  "  educated  " 
or  of  the  "  higher  classes."  ISTeurasthenic  conditions  occur  very  frequently  in  the 
uneducated  and  in  the  lower  classes,  although  they  may  manifest  themselves  in  a 
somewhat  different  fashion. 

The  Symptoms  of  Neurasthenia.  1.  The  Mental  Symptoms.— One  of  the 
most  important  changes  in  the  ideational  life  of  the  neurasthenic  is  the  frequent 
and  ready  appearance  of  ideas  of  an  anxious  character.  So  far  as  these  ideas 
refer  to  the  patient's  own  corporeity,  they  have  been  called  from  old  times  hypo- 
chondriacal. Sometimes  they  seem  to  arise  of  themselves,  at  other  times  they 
are  produced  by  readily  recognized  causes  (reading  of  histories  of  patients  or  of 
medical  works,  cases  of  sickness  and  death  in  the  neighborhood,  etc.).  These 
ideas  may  constantly  arise  into  consciousness  often  in  quite  a  fixed  and  definite 
form,  and  then  dominate  more  or  less  all  the  rest  of  the  ideational  life.  A  large 
number  of  neurasthenics  are  dominated  by  the  thought  that  they  are  threatened 
or  already  attacked  by  a  serious  organic  disease.  One  constantly  fears  an  im- 
pending attack  of  apoplexy,  another  heart  disease,  a  third  beginning  consumption, 
a  fourth  believes  he  has  noticed  positive  signs  of  disease  of  the  spinal  cord,  cancer 
of  the  stomach,  etc.  The  anxious  ideas,  however,  may  also  take  other  forms ;  they 
sometimes  refer  to  the  patient's  nearest  relatives  rather  than  to  himself.  Women 
are  sometimes  tormented  by  the  constant  dread  that  their  husbands  or  children 
may  fall  sick.  The  ideas  may  also  relate  to  external  processes,  with  which  the 
anxious  ideas  are  easily  and  incessantly  associated.  The  so-called  agoraphobia 
(anxious  ideas  on  entering  a  large  open  space),  the  dread  of  a  crowd,  of  a  railway 
journey,  of  society,  the  fear  of  sitting  under  the  chandelier  in  a  theatre,  the  fear 
of  fire,  and  many  other  symptoms  of  a  similar  character,  are  often  observed  in 
neurasthenics. 

ISTot  infrequently  such  ideas  of  an  anxious  nature  come  on  suddenly  with  es- 
pecial severity  and  lead  to  actual  attacks  of  anxious  distress  with  pronounced 
physical  symptoms  as  a  consequence.  Such  attacks  may  come  on  at  night  during 
sleep,  drive  the  patient  from  his  bed,  and  put  him  into  a  state  of  the  greatest 
unrest  and  excitement. 

We  can  readily  understand  that  the  ease  with  which  these  ideas  of  an  anxious 
nature  arise  may  keep  the  patient  to  some  degree  in  a  state  of  constant  irritation. 
Hence  such  patients  often  complain :  "  I  am  always  so  restless — every  trifle  vexes 
me — everything,  no  matter  how  small,  irritates  me."  Only  when  their  thoughts 
are  taken  up  by  something  else  do  they  become  quiet  and  behave  in  a  way  that 
seems  perfectly  normal. 

These  anxious  ideas  are  by  far  the  most  frequent,  but  they  are  not  the  only 
form  of  morbid  ideas  which  are  observed  in  neurasthenia.  In  so  far  as  such  ideas 
constantly  arise  in  consciousness  independently  of  external  events  and  constantly 

*  [The  disease  had  previously  (1867)  been  described  under  the  same  name  by  Van  Deusen,  of 
Michigan,  and  the  name  itself  is  found  in  the  first  edition  of  Dunglison's  Dictionary  in  1833. — K.] 


NEURASTHENIA  1195 

take  possession  of  the  patient,  so  to  speak,  we  give  them  the  general  and  fit  name 
of  imperative  ideas.  The  following  are  some  of  the  especially  frequent 
forms  of  imperative  ideas  :  Many  patients  are  distressed  by  the  constant  recur- 
rence of  wholly  superfluous  questions :  Why  is  this  so,  why  is  it  not  so  ?  What 
would  happen  if  this  or  that  should  ensue?  etc.  (Orilhelsucht,  metaphysical  or 
reasoning  insanity,  folie  raisonnante).  Other  patients  distress  themselves  with 
constant  doubts,  with  the  constant  feeling  of  uncertainty  whether  this  or  that 
has  been  done  correctly,  whether  they  have  not  written  something  wrong,  have  not 
forgotten  something,  etc.  (insanity  of  doubt).  [Other  patients  are  impelled  to 
repeat  certain  words,  or  to  perform  acts  a  certain  number  of  times. — K.]  These 
and  other  imperative  ideas,  which  occur  in  a  pronounced  fashion  only  in  the 
severe  forms  of  neurasthenia,  form  the  transition  to  the  special  forms  of  neuras- 
thenic insanity. 

Although  the  morbid  ideational  life  in  most  cases  gives  the  mental  constitu- 
tion of  the  neurasthenic  the  characteristics  of  excitement  and  restlessness,  there 
may  be  also  a  pronounced  inhibition  of  the  rest  of  the  ideational  life  and  conse- 
quently a  depressed,  melancholy  disposition.  The  mental  dispositions  may  some- 
times vary  in  different  forms.  If  there  is  in  general  an  increased  liveliness  of  the 
ideational  life,  the  frequent  and  rapid  transition  from  being  "  exalted  to  the 
clouds "  to  being  "  worried  to  death "  may  be  especially  striking. 

The  worst  result  of  the  disturbed  ideational  life,  however,  is  the  disturbance 
and  inhibition  of  all  other  trains  of  ideas  by  the  constant  intrusion  of  the  morbid 
ideas  into  consciousness.  This  is  the  chief  reason  why  the  neurasthenic  is  so 
often  incapable  of  any  persistent,  methodical  mental  work,  or  at  least  why  he 
can  perform  it  only  with  the  greatest  effort.  Sensations  of  bodily  weakness 
(vide  infra)  are  often  added  to  the  feeling  of  mental  fatigue,  among  them  being 
the  inability  to  read  or  write  continuously,  sometimes  associated  with  unpleasant 
subjective  sensations  of  weakness  or  pressure  in  the  eyes  ("  nervous  asthenopia  ")• 
Of  course  in  these  disturbances  of  the  power  of  mental  work  we  must  always  make 
a  sharp  distinction  between  a  congenital,  primary,  functional  weakness  and  an 
impediment  to  mental  work  due  merely  to  secondary  causes. 

[The  special  morbid  fears  like  agoraphobia  and  the  questionings  and  doubts 
are  rarely  met  with  in  neurasthenia,  and  are  usually  indicative  of  a  pronounced 
neuropathic  taint  of  a  degenerative  type.  They  may  exist  without  neurasthenia. 
Anxiety,  mental  depression,  and  a  tendency  to  worry  are  much  commoner  and  are 
of  less  serious  import.  Many  neurasthenics,  however,  show  hardly  a  trace  of 
these  mental  disturbances,  beyond  a  normal  depression  over  their  inability  to  per- 
form the  ordinary  duties  of  life  or  their  failure  to  regain  their  health.  Their 
chief  symptoms  consist  of  inability  to  make  any  long-continued  physical  or 
mental  effort  and  of  physical  weakness.  As  a  result  of  over-exertion  various 
physical  symptoms — headache,  insomnia,  backache,  anorexia,  indigestion,  etc. — 
ensue,  without  any  marked  mental  symptoms.  Neurasthenia  seems,  therefore,  to 
be  rather  a  condition  of  pathological  fatigue,  upon  which  the  various  mental 
symptoms  above  described  may  develop  secondarily. — K.] 

2.  The  Physical  Symptoms. — Although  the  mental  symptoms  of  neurasthenia 
are  recognized  only  by  the  experienced  physician  as  the  special  center  of  the  dis- 
ease, the  neurasthenic  himself,  as  a  rule,  claims  to  suffer  from  countless  subjec- 
tive symptoms,  which  may  occur  in  almost  every  organ.  By  far  the  largest  part 
of  all  these  countless  subjective  sensations  are  in  our  opinion  merely  the  result 
of  the  primary  disturbance  of  the  ideational  life.  We  admit  merely  to  the  second 
place  the  possibility  that  there  are  independent  functional  nervous  disturbances 
in  other  parts  as  well  as  the  mental  anomaly,  and  that  these  may  lead  to  special 
bodily  symptoms ;  but  it  is  evident  that  most  of  these  subjective  symptoms  have  a 
psychogenic  origin,  since  they  almost  always  conform  absolutely  to  the  character 


1196  DISEASES   OE  THE  NERVOUS   SYSTEM 

of  the  existing  hypochondriacal  ideas,  and  since  they  disappear  entirely  as  soon 
as  we  succeed  in  driving  these  ideas  out  of  consciousness. 

In  order  to  review  the  commonest  neurasthenic  symptoms  we  may  very  well 
classify  them  according  to  the  organs  to  which  the  patient's  fears  generally  refer 
them.  The  idea  of  a  dreaded  org-anic  disease  actually  provokes  the  corresponding 
subjective  sensations.  Thus  the  "  imaginary  "  diseases  develop.  If  the  patient's 
thoughts  are  occupied  chiefly  with  the  dreaded  advent  of  a  spinal  disease,  many 
symptoms  apparently  spinal  ensue,  especially  pain  in  the  back  and  unpleasant 
sensations  along  the  spine,  pain  and  parsesthesite  in  the  legs,  etc.  The  more  the 
patient  knows  about  actual  diseases  by  experience  or  reading,  the  more  manifold 
become  his  symptoms.  Neurasthenic  physicians  are  therefore  the  worst  pa- 
tients.— As  we  speak  of  a  "  spinal  neurasthenia,"  so  we  can  also  speak  of  a 
"  cardiac  neurasthenia,"  a  "  gastric  neurasthenia,"  etc.  The  cardiac  neuras- 
thenics, who  live  in  constant  anxiety  about  heart  disease  and  its  consequences, 
complain  of  palpitation,  pressure,  pain  and  "  fluttering  "  in  the  cardiac  region, 
vertigo,  and  distress  for  breath.  Patients  with  gastric  neurasthenia  ("  nervous 
dyspepsia,"  q.  v.)  have  a  feeling  of  pain  and  pressure  in  the  stomach  after  taking 
any  food,  and  therefore  are  afraid  to  eat  anything  that  is  at  all  indigestible,  sufl'er 
from  unconscious  voluntary  eructations,  etc. 

The  long  series  of  physical  neurasthenic  symptoms  is  by  no  means  exhausted, 
however,  with  such  subjective  symptoms  provoked  by  definite  anxious  ideas  (or 
by  "auto-suggestion,"  as  the  modern  technical  term  is).  In  almost  all  cases  a 
large  number  of  physical  symptoms  are  apparent,  which  we  regard  as  the  necessary 
(that  is,  the  physiological)  result  of  the  general  mental  irritation.  As  in  every 
healthy  man  every  great  psychical  excitement  is  followed  by  a  number  of  physical 
symptoms,  it  is  plain  that  the  abnormal  state  of  excitement  of  the  neurasthenic, 
coming  on  without  sufiicient  external  cause,  may  often  have  somatic  results  even 
in  increased  degree.  Among  these  we  may  reckon  first  a  large  number  of  so- 
called  "  cerebral  symptoms,"  such  as  headache,  vertigo,  and  pressure  and  disturb- 
ance in  the  head,  to  which  may  of  course  be  added  many  cerebral  symptoms  due  to 
auto-suggestion.  Among  these  belongs  also  the  neurasthenic  insomnia,  one  of 
the  commonest  and  most  important  symptoms  and  a  direct  result  of  the  mental 
irritation  itself.  In  many  cases  the  insomnia  forms  the  center  of  the  neuras- 
thenic symptom-complex.  We  may  then  say  that  the  fear  of  insomnia  is  the  chief 
reason  for  the  actual  insomnia.  Many  vaso-motor  symptoms  are  also  a  direct 
result  of  the  general  psychical  irritation — palpitation,  a  rapid  pulse,  redness  or 
pallor  of  the  face  and  hands,  increased  sweating  or  persistent  coldness  of  the 
hands  and  feet,  etc.  We  may  also  add  tremor  and  the  not  infrequent  increase 
of  the  tendon  reflexes.  Finally,  the  loss  of  appetite  which  many  patients  show, 
the  habitual  constipation,  and  in  other  cases  the  tendency  to  diarrhcea,  are  cer- 
tainly often  most  closely  related  to  the  psychical  processes. 

The  liveliness  of  the  motor  innervations  also  depends  in  the  main  upon  the 
general  psychical  state.  While  many  neurasthenics,  impelled  by  constant  rest- 
lessness, exhaust  themselves  in  long  and  useless  walks,  there  is  in  others  a  great 
physical  weakness,  which  is  due  to  inadequate  cerebral  volitional  innervation  of 
the  muscles,  so  far  as  it  is  not  dependent  upon  actual  functional  abnormality  or 
impaired  general  nutrition.  Such  patients  are  soon  tired  on  walking,  they  can 
not  work  persistently,  they  sometimes  feel  so  weak  that  they  will  scarcely  leave 
their  rooms,  and  they  spend  most  of  their  time  in  lying  on  the  bed  or  the  sofa. 

It  is  hard  to  decide  whether  neurasthenia  exerts  a  direct  influence  upon  the 
general  bodily  nutrition.  We  find  neurasthenia  in  both  full-blooded,  corpulent 
persons  and  those  who  are  frail  and  anaemic.  Neurasthenia,  however,  very  often 
exerts  an  indirect  influence  upon  the  patient's  nutrition,  since  loss  of  appetite 
or  fear  of  taking  food  gradually  results  in  marked  emaciation.     We  may  mention 


NEUEASTHEOTA  1197 

that  large  amounts  of  phosphates  are  often  found  in  the  urine,  the  reason  for 
which  is  still  uncertain.  [In  most  cases  of  neurasthenia  there  is  defective 
metabolism.  The  urine  is  scanty,' the  uric  acid  is  increased  relatively  to  the  urea, 
and  in  sexual  neurasthenia  there  may  be  an  excess  of  indican.  Many  neuras- 
thenics, however,  drink  very  little  water. — K.] 

We  must  also  devote  a  few  words  to  a  form  of  neurasthenia  which  is  of  great 
practical  importance — sexual  neurasthenia.  It  usually  develops  in  persons  who 
have  practiced  masturbation  in  their  youth,  and,  by  reading  or  their  own  reflec- 
tion, have  fallen  into  the  most  exaggerated  anxiety  as  to  the  supposed  evil  conse- 
quences of  this  vice.  Such  pitiable  patients  usually  fear  that  they  are  affected 
past  help  with  some  disease  of  the  brain  or  spinal  cord,  and  suffer  accord- 
ingly from  a  host  of  corresponding  subjective  symptoms ;  but  the  very  common 
"  psychical  impotence  "  is  still  more  significant.  This  is  a  sexual  impotence  which 
is  the  result  of  anxious  ideas  which  disturb  the  sexual  act  and  make  it  impossible. 
Other  sexual  disturbances  are  usually  added  to  these,  which  are  at  least  in  part 
a  direct  result  of  the  physiological  hyperexcitation  which  has  occurred  in  youth 
(frequent  pollutions,  urethrorrhosa,  etc.).  In  sexual  neurasthenia,  therefore,  the 
whole  host  of  general  neurasthenic  symptoms  above  described  are  naturally 
grouped  about  this  nucleus. 

As  has  been  indicated  above,  we  are  not  justified  in  regarding  all  the  physical 
symptoms  occurring  in  neurasthenia  as  secondary  psychogenic  symptoms.  Since 
neurasthenia  is  due  to  a  general  constitutional  abnormal  disposition  of  the 
nervous  system,  it  is  not  strange  if  functional  disturbances  in  other  parts  of  the 
nervous  system  should  occur  along  with  the  abnormal  symptoms  in  the  patient's 
ideational  life.  Thus  neurasthenia  may  be  associated  with  true  neuralgia,  or 
with  migraine  or  other  forms  of  headache.  It  is  therefore  an  important  and  often 
a  difficult  task  for  the  physician  to  analyze  the  whole  aspect  of  the  disease  in  the 
individual  case,  to  recognize  the  purely  psychogenous  symptoms  as  such,  and  to 
separate  from  them  any  co-existing  physical  nervous  symptoms.  This  distinction 
is  of  great  importance,  especially  in  regard  to  the  treatment  to  be  advised.  [It 
may  also  be  important  to  determine  how  far  the  neurasthenic  condition  may  be 
the  result  of  some  pre-existing  physical  condition,  which,  by  the  attendant  suffer- 
ing, as  of  habitual  headache,  may  have  led  to  the  general  nervous  exhaus- 
tion.—K.] 

General  Course  and  Prognosis  of  Neurasthenia. — ^The  course  of  neurasthenia 
is  governed  in  the  main  by  the  degree  of  general  nervous  predisposition  that 
exists  and  the  severity  of  the  unfavorable  influences  that  act  upon  the  patient 
from  without.  If  we  are  dealing  with  a  patient  who  was  previously  in  normal 
mental  health  and  in  whom  a  neurasthenic  state  of  irritation  or  exhaustion  has 
come  on  merely  as  an  effect  of  unusual  mental  excitement  or  effort,  such  conditions 
of  "  acute  neurasthenia  "  may  wholly  or  mainly  disappear  under  proper  treatment 
and  the  removal  of  the  injurious  external  influences.  The  condition  is  different 
in  cases  where  the  neurasthenic  tendency  has  appeared  quite  early  in  the  patient's 
whole  mental  nature.  Here  also  we  may  often  notice,  of  course,  great  variations 
in  the  prominence  of  the  morbid  symptoms;  but  an  actual  recovery  is  scarcely 
possible,  since  it  would  be  equivalent  to  a  complete  change  in  the  whole  mental 
individuality ;  but  in  later  life  there  may  sometimes  occur,  even  in  such  cases,  a 
striking  retrogression  in  the  morbid  symptoms.  In  the  milder  cases  there  is 
little  outward  evidence  of  derangement;  the  patient  endeavors  to  hide  his 
troubles,  as  his  indefinite  symptoms  seldom  gain  much  sympathy,  and  are  appar- 
ently contradicted  by  his  well-nourished  and  healthy  appearance.  In  the  severe 
cases,  however,  the  patient's  vigor  is  so  much  impaired  that  the  disease  acquires 
a  grave  aspect  even  for  others  than  the  patient,  and  fills  them,  as  well  as  him, 
with  infinite  anxiety.     The  disease  is  never  actually  dangerous,  and  its  exist- 


1198  DISEASES  OE  THE  NEEYOUS   SYSTEM 

ence  only  exceptionally  prepares  the  way  for  more  severe  secondary  nervous  dis- 
ease. Thus  it  happens  that  many  neurasthenics,  especially  when  external  con- 
ditions are  favorable,  lead  a  comparatively  endurable  life  and  work  hard  and 
profitably  in  their  calling. 

Diagnosis. — Neurasthenia  can  usually  be  detected  without  difficulty,  but  th*^ 
establishment  of  the  diagnosis  requires  the  exclusion  of  organic  lesions  of  the 
nervous  system.  Every  case,  therefore,  must  be  submitted  to  a  thorough  and 
careful  examination.  Grave  cerebral  diseases,  such  as  incipient  tumors  or  gen- 
eral paralysis,  have  been  repeatedly  mistaken  for  neurasthenia.  One  important 
point  in  diagnosis  is  always  the  aetiology,  including  both  the  outward  circum- 
stances and  the  presence  or  absence  of  a  constitutional  predisposition  to  nervous 
diseases. 

"We  can  not  draw  an  absolutely  sharp  boundary,  naturally,  between  neuras- 
thenia, nervousness,  and  hysteria.  In  all  these  three  conditions  we  are  dealing,. 
as  has  been  said,  with  an  abnormal  nervous  constitution,  which  is  congenital  or 
which  has  at  least  developed  from  outward  circumstances  on  the  basis  of  a  con- 
genital predisposition.  This  constitution  is  manifest  in  the  first  place  in  the 
purely  psychical  domain,  and,  in  the  second,  in  the  relations  between  the  mental 
and  the  corporeal  life.  If  the  abnormal  state  shows  itself  merely  in  slight  mental 
irritability,  sensitiveness  with  a  tendency  to  anxious  ideas  and  unfounded  fears, 
and  thus  to  the  development  of  all  sorts  of  subjective  abnormal  sensations  re- 
ferred, however,  to  the  corporeity,  we  call  it  nervousness.  If  there  is  also  asso- 
ciated a  marked  weakening  of  the  capacity  for  mental  effort  and,  in  consequence 
of  the  defective  or  much  inhibited  mental  energy,  for  physical  effort  as  well — 
symptoms  which,  as  a  rule,  are  associated  with  increased  anxiety  and  with  con- 
sequent subjective  sensations — ^we  have  pronounced  neurasthenia.  If,  howeveiv 
the  relation  between  the  mental  processes  and  the  corporeity  has  become  so  vac- 
illating that  there  is  a  complete  loosening  of  these  relations  (paralysis,  anes- 
thesia), or  that  wholly  abnormal  states  of  mental  irritation  (spasms,  attacks)  have 
developed  in  consequence  of  the  loss  of  all  healthy  mental  inhibition,  we  have 
before  us  pronounced  hysteria.  The  basis  of  all  these  three  states  is — figuratively 
expressed — the  lack  of  all  determined  order  and  fixity  in  the  course  of  all  those 
processes  which  we  include  under  the  name  of  psychical  processes  in  the  broadest 
sense  of  the  word. 

Treatment. — As  in  hysteria,  so  also  in  neurasthenia,  psychical  or  moral  treat- 
ment is  of  prime  importance ;  but  here  it  must  be  a  different  kind  from  that  neces- 
sary in  hysterical  cases.  The  neurasthenic  requires  sympathy.  As  soon  as  we 
recognize  by  means  of  a  careful  inquiry  the  hypochondriacal  anxiety  which  is 
usually  present,  this  is  to  be  removed,  as  far  as  possible,  by  soothing  persuasion  on 
the  basis  of  the  thorough  physical  examination  which  has  been  made.  The  neuras- 
thenic must  be  frequently  examined  and  constantly  encouraged  and  soothed. 
Herein,  especially,  is  shown  the  physician's  skill  and  personal  influence.  Every 
examination,  which  ends  with,  the  physician's  assurance  that  he  has  found  nothing 
to  give  occasion  for  any  serious  anxiety,  has  an  extremely  soothing  and  beneficial 
effect  upon  the  patient.  In  so  far  as  hypochondriasis  is  a  prominent  symptom, 
this  moral  influence  may  alone  restore  the  patient  to  health.  We  should  also  pay 
attention  to  the  patient's  mental  life  otherwise.  If  the  patient  has  been  exposed 
to  great  strain  and  much  excitement,  we  should  of  course  procure  a  change.  In 
such  cases  as  these  we  prescribe  mental  rest,  recreation,  and  abstention  from  work 
or  any  strenuous  activity.  Nothing,  however,  would  be  more  improper  than  to  try 
to  make  this  prescription  universal.  On  the  contrary,  it  is  absolutely  necessary 
to  prescribe  resumption  of  regular  and  methodical  work  and  occupation  for  many 
patients  who,  as  a  result  of  their  mental  disposition,  do  nothing  but  give  way  to 
their  hypochondriacal  breedings  the  whole  day  long.    In  this  way  alone  can  the 


NEUKASTHENIA  1199 

thoughts  of  such  patients  be  diverted,  and  the  patients  themselves  be  gradually 
brought  back  to  take  pleasure  in  their  life  and  occupation.  Of  course  we  must 
beware  of  any  over-exertion. 

Besides  the  psychical  or  moral  treatment,  which  must  always  take  the  first 
place,  we  must  consider  all  the  means  at  our  coramand  for  "strengthening"  the 
nervous  system.  In  this  respect  there  can  be  no  doubt  that  the  favorable  results 
from  physical  methods  of  treatment  in  neurasthenia  are  to  be  referred  in  great,  if 
not  the  greatest,  part  to  their  indirect  psychical  ("  suggestive  ")  influences.  All 
methods  of  treatment  must  therefore  be  used  methodically  and  continued  long 
enough  for  the  patient  to  remain  for  some  time  under  the  permanent  personal 
influence  of  the  physician.  In  this  way  alone  can  the  patient  have  that 
mental  schooling  which  he  needs  to  make  him  conquer  his  own  disease.  What 
has  been  said  explains  why  treatment  in  a  sanitarium  is  so  often  desirable  or 
even  necessary  for  a  neurasthenic. 

Certain  prescriptions  as  to  diet  are  of  importance  in  the  physical  treatment 
of  neurasthenics.     These  are  governed  by  the  needs  of  the  individual  case. 

For  a  corpulent  patient  treatment  calculated  to  diminish  obesity  will  some- 
times be  followed  by  decided  improvement  in  the  general  condition  and  in  bodily 
vigor.  In  those  frequent  instances  where  the  patient  is  pale  and  thin,  and  very 
likely  oppressed  by  nervous  dyspepsia  (see  page  463),  we  should,  on  the  other  hand, 
make  vigorous  efforts  to  improve  nutrition.*  Definite  instructions  must  be  given 
in  order  that  the  patient  may  ing'est  a  proper  amount  of  food.  Milk,  butter,  fresh 
meat,  eggs,  simple  pud'dings,  artificial  foods,  etc.,  are  appropriate  articles  of  diet. 
Often  both  the  weight  and  strength  improve  rapidly.  Any  large  amount  of 
alcohol  or  of  tobacco  should  be  forbidden.  Nothing  is  worse  than  to  prescribe 
strong  wine  for  a  neurasthenic  to  "  strengthen  "  him.  We  have  countless  tinges 
won  a  patient's  gratitude  by  releasing  him  from  such  a  prescription,  which  in  his 
own  experience  he  had  found  disagreeable  (causing  heat  in  the  head,  vertigo,  etc.). 
Tea  and  coffee  may  be  taken  in  moderation,  if  the  patient  is  accustomed  to  their 
use.  In  regard  to  bodily  exercise,  we  must  again  be  guided  by  the  condition  of 
the  individual.  We  would  most  earnestly  warn  the  physician  against  the  error, 
frequently  committed,  of  driving  weakly  and  debilitated  persons  to  take  long 
walks.  For  such,  bodily  rest  is  much  more  desirable;  and  fresh  air  may  be  en- 
joyed at  the  same  time,  if  the  patient  sits  or  lies  out  of  doors  or  drives.  The 
sluggish  and  corpulent,  on  the  other  hand,  often  require  persistent  exercise. 
It  is  a  good  plan  in  many  instances  to  employ  the  Swedish  movement  cure,  or 
similar  gymnastic  exercises.  [In  many  cases  the  treatment  must  be  directed 
primarily  toward  increasing  the  nutrition  of  the  patient  and  building  up  the  gen- 
eral strength  in  every  possible  way — forced  feeding,  cod-liver  oil,  tonics,  etc.  To 
this  we  must  add  rest  and  a  change  of  occupation  or  at  least  diversion.  These 
are  often  more  important  than  the  psychical  treatment,  especially  in  the  cases  of 
pathological  fatigue,  where  the  morbid  ideas  are  few  or  absent. — K.] 

Of  other  other  general  remedies  electricity  and  hydropathy  are  at  present  most 
in  use.  Electricity  is  warmly  praised  by  many  patients.  The  galvanic  current  is 
generally  employed,  and  is  applied  either  over  the  sympathetic  nerve  or  along  the 
spinal  cord.  Its  use  demands  great  caution.  The  current  should  not  be  too  strong, 
and  there  should  be  no  abrupt  changes  in  it.  Galvanism  applied  to  the  head  is  sel- 
dom well  borne.     Another  very  valuable  mode  of  treatment  was  first  practiced  by 

*  Playfair,  Weir  Mitchell,  and  certain  other  neurologists,  have  built  up  a  special  "method"  of 
treating  neurasthenia  and  allied  conditions  of  nervous  exhaustion;  this  consists  in  "over-feeding"  the 
patient — that  is,  in  introducing  as  large  an  amount  of  nourishment  as  possible  into  the  system  at  the 
same  time  that  complete  bodily  and  mental  rest  is  secured.  Faradic  electricity  and  massage  are  also 
daily  employed.  This  mode  of  procedure  is  certainly  excellent  in  many  cases,  but  it  must  not  be 
regarded  as  universally  applicable.    There  are  cases  of  neurasthenia  for  which  it  is  not  suitable. 


1200  DISEASES  OF  THE  IsTERVOUS   SYSTEM 

Beard  and  Eockwell,  and  consists  of  general  faradization.  The  patient  is  c^most 
completely  stripped,  and  places  both  feet  upon  a  large,  flat  electrode,  while  the 
various  parts  of  the  body  are  stroked  with  another  large  sponge  electrode;  in 
place  of  this  second  electrode  the  "  electrical  hand  "  of  the  physician  may  be  em- 
ployed. The  physician  takes  the  second  electrode  in  his  left  hand  and  allows  the 
current  to  pass  through  his  own  body.  Various  institutions  have  lately  begun 
to  employ  electrical  baths;  these  also  often  seem  to  produce  good  results.  In 
addition  to  peripheral  galvanization  and  faradization  of  the  nerves  and  muscles, 
it  is  advantageous  to  employ  the  faradic  wire-brush,  particularly  on  the  back 
of  the  neck,  along  the  spinal  column,  and  over  the  shoulders  and  thighs.  It  is 
hard  to  say  whether  all  these  methods  of  electrical  treatment  have  any  specific 
action.  The  greatest  part  of  the  benefit  obtained  is  undoubtedly  of  a  suggestive 
nature ;  but  there  are  few  other  methods  by  which  such  a  suggestive  effect  can  be 
so  easily  produced  as  by  electricity,  and  therefore  it  is  hard  to  dispense  with  it 
in  the  treatment  of  neurasthenics,  in  spite  of  what  has  just  been  said,  since  we 
often  have  to  change  our  methods  of  treatment  in  so  chronic  a  disease. 

The  hydro-therapeutic  treatment  may  be  quite  well  carried  out  at  the  patient's 
home,  but  a  severe  case  will  be  better  off  in  some  well-conducted  institution.  Cold 
sponging,  douches,  hip-baths,  lukewarm  baths  (or  swimming),  are  all  employed. 
Douches  must  not  be  applied  to  the  head.  If  there  is  sexual  disturbance,  hip- 
baths of  cold  water  are  advisable.  They  should  not  be  taken  at  night.  Douching 
of  the  genitals  and  loins  is  also  excellent.  We  can  not  here  give  a  detailed  de- 
scription of  the  different  hydro-therapeutic  methods.  The  efiicacy  of  hydro- 
therapy is  due  in  part  to  its  physical  influence  on  the  patient,  which  is  undoubt- 
edly favorable,  but  also,  of  course,  in  large  part  to  suggestion,  just  as  with  all 
other  forms  of  treatment.  Subsequently  sea-bathing  will  prove  extremely  benefi- 
cial for  many  patients.  We  would  recommend  the  seashore  especially  for  emaci- 
ated and  anaemic  subjects,  who  are  frequently  greatly  benefited  by  the  improved 
appetita  and  rest  thus  obtained.  If  the  patient  be  well  nourished,  on  the  other 
hand,  a  journey  on  foot  through  the  mountains,  if  made  cautiously,  may  be  very 
valuable.  Massage  is  also  much  used  as  a  general  means  of  strengthening  in 
nervous  conditions.  We  can  judge  of  its  value  from  what  has  been  already  said. 
It  is  prescribed  most  advantageously  in  those  forms  of  nervous  trouble  which  are 
associated  with  painful  sensations  in  the  spine,  the  extremities,  etc.  Massage 
displays  an  excellent  direct  effect  when  there  is  habitual  constipation. 

In  neurasthenia,  internal  remedies  should  be  given  only  as  indicated  by  the 
symptoms  or  in  the  way  of  suggestion.  If  there  is  anaemia,  iron,  quinine,  or 
Fowler's  solution  is  prescribed;  if  there  is  dyspepsia,  some  stomachic,  such  as 
dilute  hydrochloric  acid,  pepsin,  or  some  bitter.  The  constipation  (see  page  495) 
should  be  overcome  mainly  by  diet,  and  laxatives  should  be  given  only  in  case  of 
necessity.  When  there  are  vaso-motor  symptoms  (a  feeling  of  heat,  congestion, 
palpitation),  we  often  prescribe  ergotine,  four  to  six  one-grain  (gramme  0.05) 
pills  a  day.  In  all  states  of  nervous  irritation  bromide  preparations  are  much 
used,  a  powder  of  potassic  and  sodic  bromides,  or  bromine  water.  In  nervous 
headaches,  and  also  in  other  nervous  states,  antipyrine  often  has  a  good  effect. 
Antifebrine  and  phenacetine,  and  many  similar  recent  remedies,  act  in  the  same 
way. 

■  The  treatment  of  the  insomnia  which  results  from  neurasthenia  deserves  a 
brief  mention.  It  is  usually  a  difficult  problem.  Since  the  insomnia  is  in  most 
cases  merely  the  result  of  the  mental  excitation,  especially  the  onset  of  anxious 
ideas,  the  suggestive  action  of  all  the  remedies  that  can  be  thought  of  plays  of 
course  the  chief  part,  and  the  physician  should  take  advantage  of  this  circum- 
stance. We  must  utter  an  urgent  warning  against  the  misuse  of  the  stronger 
narcotics  (chloral  and  morphine).     The  attempt  should  always  first  be  made  to 


THE  SO-CALLED  TEAUMATIC  NEUROSES  "1201 

secure  sleep  by  a  rational  general  treatment,  or  by  some  less  injurious  remedies. 
Often  a  warm  bath  for  half  an  hour  at  bedtime  soothes  the  patient  and  brings  him 
sleep ;  and  in  other  cases  a  wet  cloth  laid  upon  the  head  or  back  of  the  neck  pro- 
duces the  same  favorable  result.  Patients  often  report  that  general  faradization 
at  bedtime  is  an  excellent  soporific.  Sometimes  a  moderate  dose  of  alcohol  may 
be  tried  as  a  true  hypnotic.  A  glass  of  beer  at  bedtime  often  has  a  particularly 
good  effect.  If  none  of  these  means  avail,  our  next  resort  should  be  the  bromide  of 
potassium.  Very  likely  small  doses  of  this  have  only  a  subjective  effect,  but  there 
can  be  no  doubt  that  a  large  dose,  about  a  drachm  (grammes  3-5)  in  a  glass 
of  water,  does  have  a  direct  tendency  to  produce  sleep.  We  may  also  mention 
as  the  best  of  the  other  hypnotics,  sulphonal,  twenty  to  thirty  grains  (grammes 
1.5-2)  in  a  large  amount  of  water,  in  soup,  [hot  milk,]  or  tea,  two  or  three  hours 
before  bedtime.  Trional  is  equally  to  be  recommended.  These  and  other  reme- 
dies, however,  seldom  give  great  satisfaction,  and  we  must  therefore  rely  mainly 
on  general  treatment. 


CHAPTEE   XI 
THE  SO-CALLED  TRAUMATIC  NEUROSES    (ACCIDENT  NEUROSES) 

As  an  appendix  to  the  last  two  chapters  on  hysteria  and  neurasthenia,  we  must 
now — more  from  practical  than  from  scientific  reasons — speak  in  particular  of  a 
series  of  morbid  states  which  are  at  any  rate  most  closely  related  to  the  above- 
mentioned  affections,  but  which  yet  show  certain  peculiarities.  The  morbid 
states  in  question  develop  as  the  result  of  various  sorts  of  physical  injuries 
(trauma,  accidents).  They  were  first  noticed  after  railway  accidents  (the  so- 
called  "railway  spine"  and  "  railway  brain "  of  English  and  American  neu- 
rologists), and  it  was  formerly  the  belief  that  the  coarse  material  concussion  of 
the  central  nervous  system  was  to  be  regarded  as  the  cause  of  the  subsequent 
nervous  symptoms.  Later  the  name  of  "  traumatic  neurosis  "  was  often  used  for 
these  morbid  states.  By  this  we  would  imply  that  the  nervous  symptoms  pro- 
duced by  the  trauma  do  not  depend  upon  coarse  material  injuries  of  the  nervous 
system,  but  upon  finer  changes  not  yet  made  out  anatomically.  Soon,  however,  it 
was  shown  that  in  at  least  the  great  majority  of  these  cases  the  material  injury 
itself  plays  no  other  part  than  that  of  the  exciting  cause  of  a  purely  psychical 
change  in  the  person  affected  by  the  injury.  The  material  trauma  is,  as  we  ex- 
press it,  associated  with  a  "  psychical  trauma."  Among  these  we  may  reckon  not 
merely  the  fright  associated  with  the  accident  but  the  whole  series  of  new  ideas 
occasioned  by  the  accident  and  entering  most  vividly  into  the  consciousness  of  the 
injured  person — anxiety  about  the  further  course  of  the  injury,  about  the  restora- 
tion of  the  capacity  to  work  and  earn  a  living,  and  also  about  obtaining  any  proba- 
ble damages,  etc.  Sordid  mental  motives  also  are  sometimes  mixed  with  the 
others  in  consciousness,  the  desire  for  indemnification  in  money,  for  a  better  way 
of  living,  etc.  From  what  has  been  said  in  the  two  previous  chapters  we  can 
easily  understand  that  this  primary  change  in  the  ideational  life  of  the  injured 
person  may  be  followed  by  a  considerable  number  of  apparently  physical  dis- 
turbances. 

The  type  of  disease  thus  arising  is  peculiarly  characteristic.  Sometimes  the 
original  trauma  (fall,  blow,  etc.)  is  so  severe  that  directly  after  it  the  well-known 
symptoms  of  cerebral  or  spinal  concussion  (loss  of  consciousness,  general  motor 
paralysis,  etc.)  may  ensue  with  more  or  less  severity.  In  other  cases,  however, 
the  intensity  of  the  trauma  or  the  special  seat  of  its  action  (fall  on  the  sacrum, 
76 


1202 


DISEASES   OF  TB:E  NEEVOUS   SYSTEM 


back,  or  side,  injury  of  a  limb,  etc.)  is  such  that  there  can  be  no  question  of  a 
material  cerebral  concussion.  ISTot  infrequently  there  may  be  some  organic  in- 
juries at  first  (contusion,  haemorrhage,  fracture),  but  these  of  themselves  are 
capable  of  perfect  recovery. 

The  characteristic  feature  is  that  after  the  severe  or  slight  initial  material 
results  of  the  injury  have  run  their  full  course,  there  is  not  a  complete  cure,  as 
might  have  been  expected.  The  patient  recovers,  tries  to  get  about  again,  and 
the  improvement  goes  on  up  to  a  certain  point;  but,  nevertheless,  a  number  of 
symptoms  remain  which  do  not  disappear,  and  which  diminish  or  wholly  destroy 

the  victim's  capacity  for  work. 
If  we  now  examine  such  patients 
we  find  no  signs  of  material  in- 
jury either  in  the  nervous  sys- 
tem or  in  any  other  internal 
organ.  What  at  once  strikes 
as  is  a  peculiar  psychical  change. 
The  patients  are  dull,  depressed, 
disinclined  to  any  occupation, 
wholly  without  energy,  and  they 
have  no  more  pleasure  in  inter- 
course with  their  families  and 
friends.  They  brood  constantly 
over  their  accident  and  its  re- 
sults. In  very  many  cases  the 
gloomy  and  listless  disposition 
is  mirrored  in  the  patient's 
whole  appearance,  and  especially 
in  his  facial  expression.  A  prac- 
ticed observer  can  often  recog- 
nize the  genuine  "  accident 
case "  at  the  first  glance  (see 
Fig.  185).  The  sleep  is  dis- 
turbed and  often  rendered  un- 
easy by  dreams.  Of  subjective 
symptoms  we  must  mention 
especially  pains  in  the  part 
which  was  hurt ;  these  are  com- 
monest in  the  back,  the  sacral  re- 
gion, the  sides  of  the  chest,  the 
hips,  etc.  Patients  also  com- 
plain of  headache,  vertigo,  dull- 
ness, dim  vision,  tinnitus,  spots 
before  the  eyes,  loss  of  appetite, 
etc.  Objective  examination  often  shows  a  general  motor  weakness.  Many  pa- 
tients can  walk  quite  well  alone,  but  they  are  soon  fatigued;  others  walk  only 
slowly  and  stifily  with  support,  complaining  of  pain  in  the  back  on  walking,  and 
therefore  holding  the  hand  on  the  back,  etc.  The  nutrition  of  the  muscles  is 
usually  good.  The  electrical  excitability  of  nerves  and  muscles  is  completely 
normal.  The  reflexes  are  sometimes  lively  and  sometimes  weak,  but  never  so 
much  changed  as  we  find  them  in  actual  organic  diseases.  Examination  of  the 
sensibility  may  reveal  very  marked  changes,  which  do  not  occur  in  all  cases.  This 
examination  must  always  extend  to  all  the  sensory  organs.  The  skin  over  almost 
the  entire  body  is  often  very  insensitive  to  painful  irritations,  pin-pricks,  the 
electric  current,  etc.     There  is  analgesia.     In  some  places  we  find  complete  anses- 


FiG.  185. — Accident  case,  with  hysterical  paresis  and  tremor 
of  the  right  arm.    (Personal  observation.) 


THE  SO-CALLED   TEAUMATIC  NEUROSES  1203 

thesia,  which  may  affect  an  entire  extremity  or  only  circumscribed  parts  of  the 
extremities  and  the  trunk.  The  boundary  between  the  anaesthetic  and  the  nor- 
mally sensitive  parts  is  indistinct  or  quite  sharply  defined,  and  the  arrangement 
is  often  very  peculiar,  in  a  way  that  can  never  occur  in  organic  nervous  diseases. 
Examination  of  the  eyes  sometimes  shows  loss  of  visual  acuteness,  limitation  of 
the  visual  field,  and  imperfect  color  perception.  Very  often  the  hearing  is  poor 
on  one  or  both  sides.  The  smell  is  often  much  blunted,  and  the  taste  completely 
lost,  so  that  even  quinine,  vinegar,  and  substances  of  equally  strong  taste  no 
longer  excite  any  sensation  of  taste. 

Besides  the  symptoms  of  impairment  of  sensation  and  motion  just  described, 
we  often  find  also  symptoms  of  sensory  and  motor  irritation.  Pain  in  the  head, 
spots  before  the  eyes,  and  tinnitus  have  been  mentioned  above.  Hyperaesthesia  of 
the  skin  is  more  characteristic — tenderness  of  the  vertebral  column,  and  particu- 
larly great  tenderness  of  such  parts  of  the  body  as  were  most  affected  by  the  origi- 
nal injury.  Among  the  symptoms  of  motor  irritation  we  may  mention  muscular 
contraction  and  muscular  rigidity,  again  most  common  in  the  limbs  most  affected 
by  the  injury.     A  marked  tremor  is  also  very  common. 

Almost  always  the  subjective  symptoms  are  referred  definitely  to  the  spot 
which,  was  first  injured.  If  the  injury  has  affected  the  head,  the  chief  com- 
plaint is  there;  if  one  side  of  the  trunk  or  one  limb  has  been  affected,  most 
of  the  symptoms  are  manifested  there;  but  of  course  the  symptoms  often  ex- 
tend beyond  the  part  originally  injured.  If,  for  example,  one  shoulder  receives 
a  blow,  the  whole  side,  including  the  leg,  etc.,  is  often  weak  and  painful.  Gen- 
eral nervous  symptoms,  especially  the  subjective  feelings  of  vertigo  and  pres- 
sure in  the  head,  are  found  in  the  majority  of  cases,  even  after  peripheral  in- 
juries. 

If  we  ask  after  the  cause  and  the  special  nature  of  this  peculiar  affection,  char- 
acterized chiefly  by  psychical  disturbances  and  in  the  second  place  by  subjective 
sensations  of  pain,  sensory  ansesthesia,  and  motor  weakness,  the  purely  material 
effects  of  the  injury  are  in  most  cases  not  to  be  considered,  as  we  have  said.  Al- 
though we  at  present  believe  that  there  are  morbid  states  which  we  must  actually 
regard  as  traumatic  neuroses  in  the  stricter  sense  of  the  word,  and  as  permanent 
functional  disturbances  resulting  from  an  actual  material  cerebral  concussion,  the 
assumption  does  not  hold  for  the  vast  majority  of  all  "  traumatic  neuroses,"'  for 
the  neurosis  is  certainly  produced  by  the  ensemble  of  psychical  effects,  associated 
with  the  trauma  (accident),  which  have  been  described  in  detail  above.  The  per- 
plexity and  frequent  contentions  about  sick  funds,  insurance  societies,  and  claims 
for  damages,  do  their  part  in  keeping  the  patient  disturbed. 

In  laborers,  who  have  accident  insurance,  and  in  whom  the  "  traumatic  neuro- 
ses "  are  far  most  frequently  observed,  we  often  find  a  peculiar  obstinacy  in  their 
claims  and  their  opinions  in  regard  to  a  presumed  right  of  damages  after  every 
accident.  We  may  therefore  assert  that  the  traumatic  neuroses  have  become 
decidedly  more  common  as  a  result  of  the  accident  legislation. 

[In  America  claims  for  "  damages  "  against  corporations  are  much  more  im- 
portant factors  in  the  aetiology  of  the  traumatic  neuroses  than  any  claim  for  insur- 
ance. The  various  psychical  influences  associated  with  the  litigation  consequent 
upon  such  claims  have  given  rise  to  the  term  "  litigation  neuroses."  Although  it 
is  undoubtedly  true  that  litigation  aggravates,  and  sometimes  perhaps  originates, 
nervous  conditions,  it  is  equally  true  that  we  often  see  precisely  similar  condi- 
tions developing  after  an  accident  in  which  there  was  no  possibility  of  making 
any  claim  for  damages  or  insurance,  and  where  the  other  psychical  factors  above 
referred  to  had  only  a  slight  influence.  Furthermore,  on  considering  a  large 
number  of  cases,  there  seems  to  be  some  relation  between  the  severity  of  the 
physical  injury  and  the  severity  of  the  subsequent  nervous  conditions,  even  in 


1204  DISEASES   OF  THE  WEEVOUS   SYSTEM 

the  cases  of  genuine  hysteria,  although  hysteria  may  at  times  develop  after  a  very 
slight  physical  injury.  The  pain  and  other  physical  effects  of  the  injury  may, 
of  course,  if  long  continued,  so  far  aifect  the  general  condition  as  greatly  to  ag- 
gravate the  nervous  sequelae,  but  the  influence  of  the  actual  material  concussion 
is  often  under-estimated,  and  the  "  accident  case  "  often  receives  less  consideration 
than  he  really  deserves. — K.] 

Various  factors  therefore  act  in  producing  a  condition  which  has  the  closest 
points  of  contact  with  general  nervousness,  neurasthenia,  hypochondria,  and  hys- 
teria. It  would  therefore  be  proper,  now  that  our  views  as  to  the  nature  of  the 
traumatic  neuroses — a  term,  by  the  way,  which  we  have  always  used  merely  in 
a  symptomatic  significance,  and  therefore  justifiably — ^have  become  clear,  to  use 
this  term  merely  as  a  symptomatic  appellative  and  replace  it  by  the  terms  "  trau- 
matic neurasthenia,"  "  traumatic  hysteria,"  etc.  On  the  other  hand,  we  must  not 
forget  that  the  neurasthenic  and  hysterical  affections  following  accidents  often 
have  a  certain  peculiar  stamp,  a  common  type  which  we  do  not  often  find  in 
ordinarj'-  hysteria  and  neurasthenia.  The  chief  characteristics  are  the  patient's 
peculiar  psychical  state,  manifestly  conditioned  by  the  special  external  circum- 
stances, his  lack  of  courage  and  energy,  his  depression,  the  tendency  to  complain 
and  be  querulous,  and  also  the  great  obstinacy  with  which  these  conditions  persist 
and  often  resist  any  attempts  at  treatment.  "We  know  many  cases  where  such 
patients,  in  spite  of  the  fulfillment  of  every  desire,  have  lived  for  years  in  a  state 
of  permanent  neurasthenia,  incapable  of  anj^thing,  and  finally  have  fallen  into  a 
state  of  pronounced  mental  dullness.  We  may  therefore  still  use  the  name  "  trau- 
matic neurosis,"  or,  better,  "  accident  neurosis  "  or  "  accident  psychosis,"  for  such 
cases  from  practical  reasons,  if  we  only  associate  the  correct  meaning  with  it. 
In  all  those  cases,  however,  where  there  are  pronounced  objective  symptoms  of  hys- 
teria (anaesthesia,  paralysis,  contractures  at  the  seat  of  the  injury),  we  should 
speak  merely  of  hysteria,  with  the  appropriate  adjective,  "  traumatic  "  hysteria. 

In  the  great  majority  of  cases  it  is  not  at  all  difficult  to  recognize  positively 
the  "  traumatic  neuroses."  The  existence  of  gross  material  injuries  can,  as  a 
rule,  be  easily  excluded.  It  may  be  harder  to  decide  whether  there  is  real  disease 
or  simulation.  In  such  cases  we  can  not  decide  by  single  criteria — as  has  been 
supposed — but  ultimately  only  by  careful  observation  of  the  constitutional  state 
(if  possible,  in  a  hospital)  and  by  consideration  of  the  general  conditions  (the  pa- 
tient's behavior,  previous  life,  external  circumstances,  etc.).  From,  our  own 
experience  we  must  in  general  state  that  conscious  and  intentional  complete 
simulation  is  not  very  common,  although,  of  covirse,  it  occurs  often  enough.  Ex- 
aggeration and  apparent  simulation  are  of  course  very  common,  since  the  pa- 
tients report  symptoms,  which  careful  investigation  shows  to  be  absent  or  at 
least  not  to  be  constant.  Such  a  condition,  however,  is  no  proof  of  conscious 
simulation,  since  we  see  it  every  day  in  all  the  psycho-neuroses  (hysteria,  neu- 
rasthenia). A  hysterical  woman  who  claims  that  she  can  not  leave  her  bed,  and 
then  walks  very  well  when  led  by  the  physician;  another  who  says  she  can  not 
bear  the  slightest  touch  on  her  back,  and  then  hardly  feels  the  strongest  pressure 
when  her  attention  is  diverted;  a  third  who  claims  to  have  pain  in  the  stomach 
after  a  swallow  of  tea,  and  soon  after  eats  a  beefsteak  with  relish — would  not  be 
called  a  "  simulator  "  by  any  physician.  A  similar  thing  occurs  of  course  in  the 
accident  neuroses,  because  they  are  precisely  analogous  conditions.  It  is  of 
course  very  hard  to  decide  the  question,  which  is  often  of  such  practical  im- 
portance, how  far  such  neurasthenic-hypochondriacal  patients  have  a  claim  for 
damages  and  pecuniary  assistance.  In  such  cases  we  are  decidedly  of  the  opinion 
that  the  examining  physician  should  not  be  too  generous,  since  it  is  necessary 
from  a  therapeutic  point  of  view  to  cure  the  patient  of  his  delusion  that  he  has 
a  serious  acquired  disease.     We  should  therefore  always  try  in  the  first  place  to 


THE   SO-CALLED  TEAUMATIC  NEUEOSES  1205 

bring  about  an  amelioration  or  a  recovery  from  the  condition,  and  of  course  the 
chief  stress  is  to  be  laid  upon  the  proper  psychical  influence  to  be  exerted  on  the 
patient;  but  we  must  also  consider  all  the  other  methods  of  treatment  (baths, 
sponging,  electricity,  gymnastics),  with  which  we  have  become  acquainted  in  the 
two  preceding  chapters.  In  this  way  we  sometimes  succeed  undoubtedly  in  bring- 
ing about  improvement  and  even  recovery,  but  the  outlook  for  the  permanent 
success  of  the  treatment  is  not  in  our  experience  very  good.  The  accident 
neuroses  apparently  have  an  especially  unfavorable  prognosis,  although,  as 
we  know,  the  same  is  unfortunately  often  enough  the  case  in  non-traumatic  states 
of  severe  neurasthenia  and  hypochondria.  In  the  accident  eases,  however,  we 
often  notice  from  the  outset  that  they  do  not  wish  to  be  treated  or  cured.  The  in- 
curability of  their  condition  has  become  a  matter  of  conviction  to  them,  and  their 
only  interest  is  to  obtain  as  large  an  accident  annuity  as  possible.  In  most  cases, 
at  least,  we  should  therefore  advise  against  any  continuous  medical  treatment,  un- 
less we  have  the  impression  that  the  patient  will  submit  willingly  and  trustingly 
to  the  physician's  directions.  It  seems  to  us  of  the  greatest  practical  importance  to 
"  strangle  "  the  traumatic  neuroses  "  in  the  embryo,"  if  possible,  on  their  first 
development.  Not  infrequently  we  have  seen  accident  cases  who  began  to  com- 
plain constantly  of  all  possible  nervous  troubles  after  some  slight  external  injury 
was  evidently  wholly  cured.  In  such  cases  we  should  cut  short  such  complaints  as 
completely  as  possible  from  the  outset  and  make  the  patient  understand  that  he 
is  now  actually  and  completely  well.  The  granting  of  a  high  accident  annuity  at 
first  is  therefore  quite  incorrect  in  such  cases  and  makes  recovery  much  harder, 
while  the  immediate  and  complete  refusal  is  of  the  best  influence.  The  patients 
are  forced  to  resume  their  work  and  to  forget  their  imagined  symptoms.  If  a  trau- 
matic neurasthenia  has  continued  for  years,  it  is  usually  very  hard  to  convince  the 
patient  that  his  complaints  have  no  objective  foundation. 

[In  many  cases  the  patient  is  actually  injured  by  resuming  work  too  early. 
It  is  sometimes  of  decided  advantage,  especially  in  the  early  stages  of  the  trouble, 
to  prescribe  a  thorough  "  rest  cure,"  with  isolation,  massage,  forced  feeding,  etc., 
as  prescribed  by  Weir  Mitchell.  The  worries  of  litigation  should  be  eliminated, 
if  possible,  by  an  early  settlement  of  the  case.  It  must  be  borne  in  mind  that  the 
various  therapeutic  procedures,  which  are  often  advisable  in  neurasthenic  and 
hysterical  conditions,  such  as  massage,  electricity,  gymnastics,  good  nursing, 
travel,  etc.,  are  extremely  expensive  and  often  impracticable  for  those  in  poor 
circumstances.  This  is  of  importance  when  the  physician  is  called  upon  to  de- 
termine the  amount  of  the  damages  or  the  accident  annuity. — K.] 


APPENDIX  I 


SUMMARY    OF    THE     SYMPTOMS    AND     TREATMENT    IN    CASES     OF 

POISONING 

1.  Sulphuric  Acid. — Mucous  membrane  of  mouth,  throat,  oesophagus,  and 
stomach  deeply  corroded.  In  the  worst  cases  rapid  death  ushered  in  by  convul- 
sions and  asphyxia,  or  more  rarely  consequent  upon  perforation  of  the  stomach. 
Usually  the  case  is  more  protracted.  The  mouth  and  throat  are  whitened,  or  in 
severe  cases  blackened.  They  are  soon  attacked  by  an  intense  ulcerative  inflam- 
mation. Deglutition  is  extremely  painful,  and  there  are  most  distressing  chok- 
ing and  retching.  The  vomitus  contains  black  lumps.  Profuse  salivation.  Pain 
along  the  oesophagus.  Abdomen  usually  distended  and  very  tender  on  pressure. 
There  may  be  intestinal  discharges  of  a  bloody  character,  resembling  dysentery. 
Urine  is  generally  scanty,  and  often  contains  albumen  and  blood.  Collapse. 
Small  and  rapid  pulse. 

In  mild  cases,  slow  recovery,  the  necrosed  tissues  gradually  sloughing  off. 
Cicatricial  stricture  of  the  oesophagus  frequently  ensues  and  it  may  prove  fatal. 
[N'euralgia,  hyperaesthesia,  and  various  other  nervous  disturbances  may  also  occur 
as  sequelae. 

In  fatal  cases,  the  autopsy  discloses  necrosis,  ulceration,  and  inflammation  in 
the  upper  portion  of  the  digestive  tract.  The  lining  of  the  stomach  is  usually 
coal-black.  Well-marked  parenchymatous  degeneration  of  the  liver  and  kidneys. 
Perhaps  nephritis.    In  later  stages,  extensive  cicatrices. 

Treatment:  If  used  at  all,  the  stomach-pump  must  be  introduced  very  cau- 
tiously, for  fear  of  causing  perforation.  The  best  remedy  to  give  at  once  is  sev- 
eral teaspoonfuls  of  magnesia  in  water,  or  a  few  drops  of  liquor  soda3  in  mucilage. 
Later,  the  symptoms  are  to  be  combated  with  bits  of  ice,  disinfecting  mouth- 
washes and  gargles,  tonics,  and  cautious  feeding  with  milk,  eggs,  etc.  If  stricture 
of  the  oesophagus  develops  afterward,  an  endeavor  should  be  made  to  dilate  it 
with  bougies. 

2.  Hydrochloric  and  Nitric  Acids. — Symptoms  similar  to  those  of  sulphuric 
acid.  The  most  prominent  symptoms  are  the  local  ones,  intense  stomatitis,  phar- 
yngitis, etc.  There  is  usually  albuminuria,  with  casts  and  blood  in  the  urine. 
ISTitric  acid  sometimes  stains  the  corroded  spots,  especially  the  angles  of  the 
mouth,  yellowish;  and  the  vomitus  may  have  the  same  tinge  (xanthoproteic  acid). 
In  poisoning  from  fuming  nitric  acid  the  inhaled  vapors  cause  pulmonary  symp- 
toms.   Prognosis  and  treatment  as  in  case  of  sulphuric  acid. 

3.  Nitrous  and  Sulphurous  Acid  Fumes. — Intense  local  inflammation  of  the 
air-passages.  Violent  dyspnoea,  cough,  abundant  bloody  or  yellowish  expectora- 
tion. There  may  also  be  grave  nervous  disturbance  and  collapse.  Treatment : 
Symptomatic:  sinapisms,  narcotics,  expectorants,  and  inhalations. 

4.  Oxalic  Acid. — Local  corrosive  action  similar  to  that  of  the  other  acids,  only 
less  severe.  In  severe  cases  collapse  from  cardiac  paralysis.  Apt  to  occasion  cer- 
tain nervous  symptoms — formication,  anaesthesia  of  the  flnger-tips,  tonic   and 

1206 


APPEliTDIX  I  1207 

clonic  convulsions,  trismus,  and  tetanus;  later  paresis.  There  is  sometimes 
sug-ar  in  the  urine,  and  nephritis  may  develop.  Anuria  is  frequent,  and  is  due  to 
plugging  of  the  tubules  by  calcic  .oxalate  crystals.  The  treatment  should  be 
symptomatic,  and  should  also  include  the  administration  of  preparations  of  cal- 
cium— liquor  calcis,  calcii  carbonas,  or  even  egg-shells — to  form  insoluble  calcic 
oxalate.    Magnesia  is  also  useful. 

5.  Ammonia. — The  fumes  affect  the  air-passages  chiefly;  the  solution,  the 
upper  part  of  the  digestive  tract.  The  specific  local  effect  is  the  production  of  an 
intense  croupous  inflammation  of  the  mucous  membrane.  Accordingly,  the 
symptoms  are  salivation,  dysphagia,  vomiting  of  strongly  alkaline  matter,  and 
diarrhoea,  or  cough,  dyspnoea,  etc.  In  severe  cases  there  is  collapse,  with  rapid 
pulse,  and  such  nervous  symptoms  as  pain,  parsesthesia,  vertigo,  convulsions,  etc. 
Treatment :  In  fresh  cases  the  stomach-pump.  The  cautious  use  of  acids — for 
instance,  acetic  or  citric.  Also,  symptomatically,  emulsions  of  oil,  bits  of  ice, 
and  narcotics. 

6.  Caustic  Potash  or  Soda. — Symptoms  and  treatment  as  in  case  of  ammonia. 
In  contrast  to  acid  poisoning,  it  is  to  be  noted  that  alkalies  do  not  withdraw  water 
and  precipitate  albumen,  but  dissolve  it.  The  corroded  spots  are  therefore  not 
dry  and  brittle,  but  softened  ("  colliquation  ")• 

7.  Potassic  Nitrate. — Vomiting  and  diarrhoea.  Severe  abdominal  pain.  Col- 
lapse, with  cold  skin  and  rapid,  thready  pulse.  Occasionally  the  pulse  is  slow. 
Nervous  disturbances,  such  as  painful  muscular  contractions,  and,  in  severe  cases, 
convulsions  and  coma.  Treatment :  Symptomatic;  opium  and  other  narcotics, 
stimulants  (camphor,  ether),  and  bits  of  ice. 

8.  Chlorine  Gas. — Violent  convulsive  cough.  Bloody  expectoration.  Spasm 
of  the  glottis.  Dyspnoea.  Darting  pains  through  the  chest.  Sneezing  and  pro- 
fuse flow  of  tears.  In  severe  cases  pneumonia.  Treatment :  Fresh  air.  Inhala- 
tion of  warm  aqueous  vapor,  or  of  ammonia  to  form  ammonic  chloride.  Chloro- 
form may  also  be  tried,  and  narcotics. 

9.  Iodine. — 1.  Acute  iodism,  as  seen,  for  instance,  after  the  injection  of  large 
amounts  of  tincture  of  iodine  into  ovarian  cysts :  collapse,  with  pallor  and  cya- 
nosis, and  small  and  very  rapid  pulse.  Vomiting.  Often  marked  dyspnoea. 
Suppression  of  urine.  Sometimes  heemoglobinuria.  Later,  the  skin  becomes  very 
red.  There  is  albuminuria;  also  sore  throat,  coryza,  conjunctivitis,  severe  frontal 
headache,  and  cutaneous  eruptions.  2.  Chronic  iodism,  caused,  for  example,  by 
long-continued  internal  administration  of  potassic  iodide :  coryza,  conjunctivitis, 
sore  throat.  Gastric  symptoms.  Vertigo,  headache,  and  similar  nervous  phe- 
nomena of  a  mild  character.  Acne  or  erythema,  sometimes  in  the  form  of  ery- 
thema nodosum.  Treatment:  In  acute  cases,  white  of  egg  and  stimulants. 
Other  than  this,  treatment  must  be  symptomatic.  Prophylaxis  demands  caution 
in  the  internal  administration  of  iodine  or  its  compounds.  According  to  Ehrlich, 
the  symptoms  of  iodism  often  disappear  rapidly  after  the  exhibition  of  about  a 
drachm  and  a  half  (grammes  6)  of  sulpho-nitro-salicylic  acid  (sulphanilic  acid). 

10.  Bromine. — 1.  Acute  poisoning  from  the  fumes  of  bromine  excites  the  same 
symptoms  as  does  chlorine  gas.  2.  Bromism,  resulting  from  the  long-continued 
use  of  potassic  bromide,  causes  languor,  debility,  mental  apathy,  and  impaired 
intellectual  vigor.  The  reflexes  are  diminished,  particularly  the  reflex  irritability 
of  the  soft  palate  and  pharynx.  Anorexia.  Diarrhcea.  Impotence.  Almost 
invariably  a  characteristic  acne,  the  onset  of  which  may  be  delayed  by  giving 
arsenic  at  the  same  time. 

11.  Lead. — (a)  Acute  lead  poisoning  produces  severe  gastro-enteritis.  The 
best  antidote  is  sulphate  of  sodium  or  magnesium;  or  phosphates,  white  of  egg, 
and  milk.  In  fresh  cases  the  stomach-pump,  or  emetics  and  purgatives.  Other 
than  this,  s:^Tnptomatic  treatment. 


1208  APPENDIX  I 

(&)  Chronic  lead  poisoning:  Seen  in  type-setters,  type-founders,  painters, 
potters,  and  others.  General  symptoms :  Lead  line  on  the  gums,  lead  anaemia, 
and  lead  cachexia.  Important  groups  of  symptoms  are:  1.  Lead  colic:  Violent 
colicky  pains,  radiating  from  the  umbilicus.  Usually  constipation,  exceptionally 
diarrhoea.  Abdomen  concave  and  hard.  Vomiting.  Hard,  slow  pulse.  Tempera- 
ture usually  normal.  Urine  sometimes  contains  a  trace  of  albumen.  Duration, 
one  or  two  weeks.  Treatment :  If  severe  pain,  opium  and  hot  compresses.  Atro- 
pine may  also  be  tried.  Por  constipation,  enemata  and  gentle  laxatives.  Warm 
baths.  2.  Lead  paralysis  {vide  page  873)  :  Paralysis  of  the  larjoigeal  muscles 
due  to  lead  poisoning  has  been  reported.  3.  Saturnine  encephalopathy :  Sudden 
development  of  grave  cerebral  symptoms ;  convulsions,  coma,  delirium,  great  men- 
tal uneasiness,  and  excraciating  headache.  Saturnine  amaurosis.  In  severe 
cases,  death.  Cerebral  lesions  are  very  rarely  found  post  mortem.  Treatment 
is  symptomatic.  Lukewarm  baths,  with  douching,  narcotics,  and  stimulants. 
Later,  potassic  iodide.  4.  Lead  arthralgia:  Most  frequently  attacks  the  knee. 
Also  seen  in  the  joints  of  the  upper  extremities.  Sometimes  associated  with 
painful  muscular  contractions.  Objective  lesions  are  rarely  seen.  The  treatment 
consists  of  warm  baths  and  the  administration  of  potassic  iodide.  It  should  be 
remembered  that  chronic  lead  poisoning  may  occasion  gout  and  chronic  inter- 
stitial nephritis.  The  reader  is  referred  to  the  chapter  describing  these  dis- 
eases. 

12.  Copper  (Blue  Vitriol,  Yerdigris). — (a)  Acute  copper  poisoning :  Copper 
taste.  Vomiting  of  greenish  matter,  colic,  tenesmus,  and  bloody  stools.  Also 
nervous  symptoms,  headache,  vertigo,  anaesthesia,  paralysis,  delirium.  Collapse. 
Dyspnoea.  Treatment:  White  of  Qgg,  milk,  wood  charcoal.  Magnesia  is  also 
valuable.  Yellow  potassic  ferrocyanide,  milk  sugar.  (J)  Chronic  copper  poison- 
ing is  rare.  It  occasions  gastro-intestinal  disturbance,  colic,  and  a  reddish  or 
greenish  discoloration  of  the  hair. 

13.  Zinc  {Zinc  Sulphate  and  Chloride). — In  acute  poisoning,  symptoms  of 
severe  gastro-enteritis,  especially  vomiting.  Also  albuminuria.  Treatment: 
Albumen,  tannin,  and  alkaline  carbonates.  Chronic  poisoning  (zinc  fumes !)  : 
Pever,  distress,  vertigo,  vomiting,  metallic  taste.  General  ansemia  and  emaci- 
ation. 

14.  Mercury. — (a)  Acute  poisoning  from  corrosive  sublimate:  The  mucous 
membrane  of  the  mouth,  throat,  oesophagus,  stomach,  and  intestines  is  deeply 
corroded.  Metallic  taste.  Vomiting.  Diarrhoea  with  painful  tenesmus.  Ischu- 
ria or  complete  anuria.  Collapse.  Generally  quickly  fatal.  Treatment :  Milk, 
white  of  egg,  rediiced  iron,  narcotics,  (h)  Chronic  mercurial  poisoning :  Seen  in 
the  makers  of  thermometers,  scientific  instruments,  and  mirrors.  Rarely  occa- 
sioned by  the  prolonged  use  of  antisyphilitic  remedies.  The  symptoms  are 
anaemia,  emaciation,  with  great  muscular  weakness,  and  gastro-intestinal  disturb- 
ance. In  the  therapeutic  use  of  mercury,  besides  the  rarer  mercurial  enteritis, 
mercurial  stomatitis  is  the  most  important  toxic  symptom ;  onset  of  foul-smelling 
necrosis  of  mucous  membrane,  with  ulceration  of  mucous  membrane  of  cheeks, 
jaws,  gums,  etc.  Treatment :  Immediate  discontinuance  of  medication;  potassic 
chlorate  as  mouth-wash  and  gargle. 

Mercurial  Tremor. — Tremor  is  common  in  chronic  mercurial  poisoning  and  is 
of  special  interest.  It  is  usually  preceded  by  a  stage  of  pronounced  mental  irri- 
tability ("mercurial  erethism"),  and  often  some  mental  excitement,  fright,  etc., 
is  the  exciting  cause  of  the  tremor.  The  tremor  itself  is  a  pronounced  intention 
tremor — that  is,  it  is  usually  not  present  when  the  body  is  kept  quiet,  but  it  comes 
on  with  all  movements,  like  the  tremor  in  multiple  sclerosis.  The  finer  the 
movements  the  patient  tries  to  make  the  more  marked  is  the  tremor.  Mental 
excitement  usually  increases  the  tremor  considerably.    In  severe  cases  the  tremor 


APPENDIX  I  1209 

is  so  great  that  the  patients  can  not  leave  their  beds.    In  rare  cases  there  is  also 
paralysis. 

Treatment :  Dietetic  and  hygienic.  Iodide  of  potassium,  hyoscine,  and  some- 
times galvanism,  are  also  useful. 

15.  Phosphorus. — (1)  Acute  phosphorus  poisoning,  as  from  matches:  Violent 
epigastric  pain,  vomiting — the  vomitus  smells  of  phosphorus,  and  it  may  be  phos- 
phorescent. After  these  initial  symptoms  usually  comes  a  period  of  comparative 
comfort,  lasting  two  or  three  days.  Then  appear  grave  symptoms:  jaundice, 
severe  pain  in  the  hepatic  region  and  whole  abdomen,  hepatic  enlargement,  fever, 
feeble  and  rapid  pulse,  sometimes  gastric  or  intestinal  haemorrhage,  cutaneous 
ecchymoses,  hsematuria,  epistaxis,  or  metrorrhagia.  The  intellect  usually  re- 
mains clear,  except  that  just  before  death  there  may  be  drowsiness  or  convulsions. 
The  urine  contains  albumen,  blood,  casts,  bile-pigment,  and  sometimes  leucine 
and  tyrosine.  jSTo  urea  is  excreted.  Death  occurs  usually  at  the  end  of  one  or 
two  weeJiS,  but  is  may  be  more  speedy.  In  mild  cases  the  above  symptoms  are  not 
strongly  marked,  and  recovery  may  ensue.  A  very  grave  prognosis  should  be  made 
in  every  case  at  the  start.  Post-mortem  appearances  in  acute  phosphorus  poison- 
ing:  Jaundice.  Dark  blood.  ISTumerous  internal  ecchymoses — for  example,  in 
the  serous  and  mucous  membranes  and  kidneys.  Fatty  degeneration  of  most  of 
the  internal  organs,  including  the  liver,  heart,  muscles,  and  kidneys.  Treatment : 
In  fresh  cases,  washing  out  of  the  stomach.  Laxatives.  As  an  emetic,  sulphate 
of  copper.  The  best  antidote  is  old  oil  of  turpentine  (30-40  drops  in  mucilage). 
Oily  substances  should  be  avoided,  as  phosphorus  is  soluble  in  oil.  Narcotics  and 
other  symptomatic  remedies  may  also  be  indicated.  (2)  Chronic  phosphorus 
poisoning :  Necrosis  of  the  lower  jaw,  less  often  of  the  upper  jaw,  extending 
from  caries  of  the  teeth.  Necrosis  of  the  bone  with  exuberant  growth  of  osteo- 
phytes. 

16.  Arsenic  (Arsenious  Acid,  Schweinfurth  Green,  Scheele's  Green,  Arsen- 
ical Wall-paper). — (1)  Acute  arsenic  poisoning :  Symptoms  of  intense  gastro-en- 
ten'tis,  suggesting  cholera.    Violent  vomiting.    Eice-water  stools.    Severe  abdom- 

\inal  pain.  Nervous  symptoms :  Vertigo,  headache,  faintness,  twitchings.  Car- 
diac weakness.  Cyanosis.  Collapse.  Not  infrequently  a  cutaneous  eruption 
resembling  urticaria  or  eczema.  Sometimes  albumen  and  blood  are  present  in  the 
uriii^.  Severe  cases  are  fatal  in  one  or  two  days.  With  regard  to  arsenical 
paral^'^sis,  vide  page  875.  Treatment :  At  first  the  stomach-pump  or  emetics — for 
example,  sulphate  of  zinc.  The  best  antidotes  are  freshly  prepared  ferric  hydrate 
in  water  two  to  four  tablespoonfuls  every  fifteen  to  thirty  minutes;  ferrum  oxy- 
datum  saccharatum  solubile  (P.  G.),  in  teaspoonful  doses;  magnesia;  and,  best 
of  all,  the  compound  of  magnesia  and  ferric  hydrate  known  as  "  ant ido  turn 
arsenici"  (P.  G.),  of  which  a  tablespoonful  may  be  given  every  fifteen  to  thirty 
minutes.  (2)  Chronic  arsenic  poisoning:  Acquired  in  arsenic  works  and  glass 
factories,  or  from  arsenical  fabrics,  papers,  and  flowers.  Conjunctivitis,  chronic 
gastro-intestinal  catarrh,  eczema,  and  cutaneous  ulcerations.  Anaemia  and  ca- 
chexia, falling  out  of  the  hair,  loss  of  sleep.  Treatment  is  purely  symptomatic, 
except  as  regards  prophylaxis.  In  poisoning  with  arseniuretted  hydrogen,  hsemo- 
globinuria  and  jaundice  occur,  with  severe  nervous  symptoms. 

17.  Alcohol. — (1)  Acute  alcoholic  poisoning:  Unconsciousness;  anaesthesia; 
pupils  either  dilated  or  contracted,  usually  not  reacting  to  light;  pulse  small, 
sometimes  slow;  skin  cold  and  clammy;  vomiting;  stertorous  respiration.  There 
may  be  delirium  and  clonic  convulsions  instead  of  coma.  Such  cases  last  three  or 
four  days.  Death  has  been  repeatedly  observed.  Treatment:  Bathing  and 
douching.    Stimulants. 

(2)  Chronic  alcoholism,  (a)  Physical  and  mental  dehility :  Chronic  catarrh 
of  the  throat,  larynx,  stomach,  and  intestines.     Alcoholic  tremor.     Numerous 


1210  APPENDIX  I 

organic  diseases,  including  cirrhosis  of  the  liver,  contracted  kidney,  heart-disease, 
cerebral  disease,  and  neuritis. 

(&)  Delirium  tremens:  Usually  a  sudden  onset,  as  in  connection  with  some 
acute  disease  or  after  a  surgical  injury.  Disordered  intellect.  Great  restlessness, 
hallucination  (vermin,  etc.),  excitement,  and  loss  of  sleep.  Treatment :  Bathing 
and  douching.  Injections  of  strychnine.  The  use  of  chloral  and  other  narcotics 
should  be  cautious.  Physical  restraint  should  be  avoided  if  possible.  The  patient 
may  often  be  allowed  to  go  about  the  room  as  he  likes,  if  only  he  be  watched. 
Alcohol  should  be  given  if  collapse  be  threatened. 

[(c)  Alcoholic  insanity:  Marked  mental  confusion  with  loss  of  memory  of 
recent  events,  failure  to  appreciate  time  or  place,  occasional  hallucinations.  In 
some  cases  marked  depression  or  excitement,  in  other  cases  more  systematized 
delusions,  of  persecution,  marital  infidelity,  etc.  In  more  severe  cases  pronounced 
mental  failure.  Conditions  of  physical  weakness  often  associated  (neuritis? 
vide  supra,  polyneuritic  psychoses,  page  894).  Treatment :  Abstinence  from  alco- 
hol, strychnine,  forced  feeding,  free  elimination. — ^K.] 

18.  Chloroform. — Unconsciousness.  Loss  of  sensibility  and  reflexes.  Slow 
pulse.  Pupils  dilated.  Failure  of  respiration,  and  finally  of  the  heart.  Danger  of 
heart  failure,  especially  in  persons  with  weak  hearts.  Treatment :  Artificial  res- 
piration.   Injections  of  strychnine.     Stimulants.     Counter-irritation. 

19.  Iodoform. — (Repeatedly  seen  from  the  use  of  iodoform  on  wounds.)  First 
of  all,  nervous  symptoms :  headache,  vertigo,  sleeplessness.  Peculiar  psychoses, 
maniacal  attacks,  delusions  of  persecution,  refusal  of  food.  In  severe  cases  con- 
vulsions, deep  coma.  Very  small,  rapid  pulse.  Treatment:  Symptomatic,  by 
stimulants,  baths,  etc.  Alkalies  and  atropine  are  recommended,  but  their  action 
is  doubtful. 

20.  Carbonic-oxide  Gas  (Illuminating  Gas). — At  first,  vertigo,  headache, 
throbbing  in  the  temples,  ringing  in  the  ears,  and  spots  before  the  eyes.  The 
patient  gradually  becomes  unconscious.  Skin  pale  and  cyanotic.  Respiration  in- 
termittent. Subnormal  temperature.  The  urine  may  contain  albumen  and  sugar. 
The  carbonic  oxide  may  be  demonstrated  in  the  blood  by  means  of  the  spectro- 
scope. Its  color  is  clear  cherry-red  (CO-hsemoglobine).  Subsequently  paralysis, 
disturbances  of  sensation  and  of  speech.  Treatment :  Fresh  air,  artificial  respi- 
ration, stimulants,  transfusion. 

21.  Sulphuretted  Hydrogen. — Headache,  vomiting,  diarrhoea.  In  severe 
cases,  unconsciousness,  dyspnoea,  cyanosis,  convulsions,  and  death.  The  blood  is 
thin,  fluid,  and  black  (sulph-h^moglobine).  Treatment:  Artificial  respiration, 
fresh  air,  and  the  cautious  inhalation  of  chlorine  gas. 

22.  Bisulphide  of  Carbon. — (Workers  in  rubber  factories.)  Vomiting.  Se- 
vere nervous  symptoms.  Incontinence  of  urine,  atrophic  paralyses,  anaesthesia, 
mental  disturbances,  especially  loss  of  memory,  spasmodic  conditions,  etc.  The 
red  blood-corpuscles  are  destroyed;  the  black  blood  contains  many  flakes  of  pig- 
ment.    Treatment:  Symptomatic. 

23.  Hydrocyanic  Acid  (Potassic  Cyanide;  Bitter  Almonds). — Characteristic 
odor  of  bitter  almonds.  In  severe  cases  death  may  occur  in  a  few  minutes.  If 
the  course  be  more  protracted,  convulsive  and  extremely  slow  respiration,  the 
expiratory  act  being  much  prolonged;  the  eyeballs  protrude,  and  the  pupils  are 
somewhat  enlarged  and  do  not  react  to  light.  Cardiac  weakness,  cyanosis,  uncon- 
sciousness. Twitching  of  the  muscles.  Trismus.  Treatment :  Merely  symptom- 
atic. Emetics,  artificial  respiration,  cool  douches,  stimulants.  Atropine  may  be 
tried ;  also,  hydrated  ferric  oxide  and  chlorine  water. 

24.  Nitrobenzine  (Nitrobenzole,  Oil  of  Mirbane). — Strong  odor  of  bitter  al- 
monds. At  first,  dizziness.  The  skin  soon  assumes  a  bluish  hue,  rapidly  increasing 
to  the  deepest  cyanosis.     Increasing  anxiety,  sense  of  suffocation,  and  gradual 


APPENDIX  I  .  1211 

loss  of  consciousness.  In  severe  cases,  death,  ushered  in  by  convulsions.  In 
milder  cases,  gradual  recovery.  Treatment :  Stomach-pump.  Artificial  respira- 
tion. Stimulants.  In  the  Leipsic  clinique,  transfusion  has  worked  admirably  in 
two  cases.  The  symptoms  caused  by  aniline  and  the  aniline  dyes  closely  resemble 
poisoning  from  nitrobenzole. 

25.  Carbolic  Acid,  also  Lysol  and  the  like. — Corrosion  of  mouth,  throat,  and 
stomach.  In  mild  cases,  vertigo,  headache,  and  collapse;  in  severe  cases,  coma, 
preceded  in  rare  instances  by  symptoms  of  cerebral  irritation.  Contracted  pupils. 
Vomiting.  Pulse  slow  at  first,  then  rapid.  The  urine  has  a  dark,  olive-green 
color.  Sometimes  hsemoglobinuria  and  nephritis.  Carbolic  acid  is  very  readily 
absorbed  from  the  rectum,  so  that  great  caution  should  be  employed  in  its  use 
as  an  injection.  Treatment:  Stomach-pump.  Slaked  lime  and  water.  Large 
doses  of  sulphate  of  sodium  are  especially  to  be  recommended.  [Alcohol  is  an 
antidote.  Administer  three  or  four  ounces  of  whisky  at  once,  then  wash  out  the 
stomach  with  water  containing  sulphate  of  sodium.  In  desperate  cases,  vene- 
section followed  by  infusion  of  normal  salt  solution  has  been  successful. — Y.] 

26.  Atropine  {Belladonna). — Dryness  of  the  mouth  and  throat.  Excessive 
thirst.  Dizziness  and  headache.  Peculiar  mental  disturbances :  hallucinations 
are  particularly  frequent.  Pupils  very  widely  dilated.  Cutaneous  erythema 
resembling  that  of  scarlet  fever.  In  severe  cases,  pulse  enormously  accelerated, 
with  violent  pulsation  in  the  arteries.  Convulsions  may  occur.  Nervous  symp- 
toms persist  for  some  time.  Treatment :  The  following  physiological  antidotes 
should  be  tried:  physostigmine  (eserine),  pilocarpine,  and  morphine. 

27.  Digitalis. — Vomiting.  Diarrhcea.  Pulse  very  slow  (forty  beats  per  min- 
ute, or  less).  Dyspnoea.  Symptoms  of  collapse.  Cold  extremities,  muscular 
tremor.  Somnolence.  In  the  worst  cases,  sopor  and  death.  Even  the  milder 
cases  are  protracted.  Treatment :  Emetics,  stomach-pump.  Tannin.  Camphor, 
strong  cafe  noir,  ether,  ammonia.    Counter-irritation. 

28.  Nicotine  (Smoking;  Tobacco  Juice;  Tobacco  Enemata).  —  1.  Acute: 
Pulse  small  and  slow,  syncope,  sense  of  oppression,  salivation,  vomiting.  In  se- 
vere cases,  loss  of  consciousness,  tetanic  spasms,  both  pulse  and  respiration  inter- 
mittent. 2.  Chronic  (from  excessive  use  of  tobacco)  :  Palpitation,  irregular  ac- 
tion of  the  heart,  paroxysms  of  asthma  and  angina  pectoris.  Tremor,  muscular 
weakness.  Loss  of  sleep.  Sometimes  there  are  symptoms  of  ataxia  ("nicotine 
tabes"  seen  in  cigar  makers).  Amblyopia,  scintillating  scotoma.  Gastric  dis- 
turbance, chronic  catarrh  of  the  pharynx  and  larynx.  Treatment :  In  acute  cases, 
stimulants.  Chronic  poisoning  necessitates  the  giving  up  of  tobacco.  Further 
treatment  is  symptomatic. 

29.  Strychnine. — Violent  tetanic  reflex  convulsions.  Exaggeration  of  the  cu- 
taneous and  tendon  reflexes.  Trismus.  Opisthotonos.  Pulse  small  and  very  rapid. 
The  convulsions  come  in  paroxysms,  with  intervals  between  them.  The  intellect 
is  usually  perfectly  clear.  Recovery  occurs  only  in  mild  cases.  Treatment : 
Emetics,  stomach-pump.  Tannin.  Tincture  of  iodine.  Castor-oil.  The  convul- 
sions are  to  be  combated  by  morphine,  chloroform,  chloral,  or  potassic  bromide. 
Curare  has  also  been  tried. 

30.  Coniine  (Hemlock). — In  severe  cases  convulsions,  then  general  paralysis, 
especially  of  the  respiratory  muscles,  loss  of  consciousness,  and  death.  Pupils 
dilated.  In  milder  cases  confusion,  muscular  weakness,  vomiting,  and  diarrhcea. 
Treatment :  Emetics,  tannin,  stimulants. 

31.  Morphine  (Opium). — 1.  Acute:  Begins  with  fatigue,  headache,  darken- 
ing of  the  visual  field,  nausea,  vomiting.  Then  coma  comes  on  with  slow,  ster- 
torous, sometimes  irregular  respiration.  Muscles  completely  lax.  Pupils  usually 
very  small.  Pulse  often  slow,  but  in  other  cases  rapid  and  small.  Toward  the 
end  of  life  Cheyne-Stokes's  respiration.     In  milder  cases  only  vomiting,  stupor, 


1212  APPENDIX  I 

headacHe,  etc.  Treatment:  Sulphate  of  zinc,  or  some  other  emetic;  stomach- 
pump.  [One-per-cent.  solution  of  permanganate  of  potassium. — V.]  Tan- 
nin. Cafe  noir.  Atropine  may  be  tried  as  a  physiological  antidote.  Stimu- 
lants (camphor,  ether)  are  best,  also  cold  baths  with  shower-baths;  arti- 
ficial respiration.  2.  Chronic  (morphine  habit)  :  Emaciation,  ansemia,  headache, 
vertigo,  wakefulness.  Tremor.  Mental  disturbance.  Unconquerable  longing  for 
morphine;  and,  if  this  be  denied,  the  appearance  of  grave  symptoms.  To  break 
up  the  morphine  habit  is  almost  impossible  except  in  hospitals  and  special  asy- 
lums. The  withdrawal  of  the  drug  is  abrupt  according  to  the  practice  of  some, 
and  gradual  according  to  others.     Eor  particulars  consult  monographs. 

32.  Ergot  (Ergotine). — 1.  Acute:  At  first  nausea,  vomiting,  colic,  and  diar- 
rhoea. Then  vertigo,  headache,  and  muscular  weakness.  Pulse  slow.  In  severe 
cases,  sopor,  disturbance  of  respiration,  and  sometimes  death.  Treatment :  Emet- 
ics and  purgatives.  Tannin.  Ether,  camphor,  and  cafe  noir  as  stinaulants.  2, 
Chronic  ergotism:  Gastric  symptoms,  vertigo,  languor,  cardiac  weakness.  The 
nervous  disturbances  are,  however,  of  especial  importance.  Of  these,  parsesthesia 
has  long  been  recognized.  Recently  attention  has  been  attracted  to  the  great 
resemblance  of  the  nervous  symptoms  to  those  of  tabes  dorsalis;  and  there  is, 
moreover,  an  anatomical  change  in  the  posterior  columns  of  the  cord.  Convul- 
sions and  psychical  phenomena  are  also  observed.  A  second  form  of  chronic 
ergotism  is  called  gangrenous  ergotism.  It  results  in  dry  gangrene  of  the  hands 
and  feet.  A  line  of  demarcation  forms  and  the  gangrenous  parts  slough  off. 
The  process  may  be  attended  by  fever  and  pysemia.  The  probable  explanation  is 
that  the  minute  blood-vessels  become  spasmodically  contracted  and  thrombi  form 
under  the  influence  of  the  poison.  The  different  symptoms  are  due  in  part  to  the 
different  constituents  of  the  ergot.  The  best  known  are  sphacelinic  acid,  which  is 
probably  the  cause  of  g-angrenous  ergotism  and  ergotine  tabes;  cornutine,  which 
causes  severe  convulsive  symptoms  (convulsive  ergotism)  and  uterine  contrac- 
tions; and  finally  ergotinic  acid.  The  treatment  of  chronic  ergotism  is  purely 
symptomatic. 

33.  Poisonous  Mushrooms. — 1.  Poisoning  from  morels:  Fresh  morels  ("mor- 
eheln  "  or  "  lorcheln  ")  contain  a  poison  which  is  readily  soluble  in  hot  water,  and 
which  evaporates  completely  if  the  morels  be  dried.  Morels  that  have  been  dried 
or  parboiled  are  therefore  perfectly  harmless,  but  the  fresh  ones  are  poisonous. 
The  symptoms  are  nausea,  vomiting,  diarrhcea,  headache,  coma,  and,  above 
all,  haemoglobingemia  and  hsemoglobinuria  (q.  v.),  associated  with  which  is  a 
hsematogenous  icterus.  In  severe  cases  death  occurs,  ushered  in  by  convulsions. 
Treatment  is  symptomatic,  and  includes  the  administration  of  emetics,  purga- 
tives, and  stimulants.  2.  Poisoning  from  the  red  agaric  (amanita  muscaria). 
This  contains  the  poisonous  alkaloid  muscarine.  Gastric  symptoms  and  diar- 
rhoea. Mental  excitement,  delirium,  tetanic  and  epileptiform  convulsions.  A 
rapid  pulse,  small  pupils,  disturbed  vision  from  spasm  of  accommodation,  sweat- 
ing, salivation,  and  in  most  of  the  severe  cases  sopor  and  death.  Treatment: 
Emetics,  etc.  Atropine,  which  acts  as  a  physiological  antidote  to  muscarine. 
Also  tannin,  and  stimulants.  3.  Poisoning  from  hulhous  mushrooms  (ama- 
nita phalloides),  confused  with  young  button  mushrooms  (champignons).  Di- 
gestive disturbances,  later  jaundice,  somnolence,  coma.  The  autopsy  shows  fatty 
degeneration  of  the  liver,  kidneys,  and  stomach,  as  in  phosphorus  poisoning. 

34.  Poisoning  from  Sausages  (BotuUsmus). — This  sometimes  occurs  as  the 
result  of  eating  partially  decayed  sausages.  The  symptoms  are  pain  in  the  stom- 
ach, nausea,  vomiting,  colic,  and  diarrhoea.  There  are  also  marked  feebleness, 
prsecordial  anxiety,  and  dyspnoea ;  vertigo,  headache,  somnolence ;  and  very  often 
disturbance  of  vision  (amblyopia,  spots  before  the  eyes),  and,  what  is  surprising, 
ptosis.    In  severe  cases,  dysphagia,  as  a  result  of  more  or  less  complete  paralysis- 


APPEI^DIX  I  1213 

of  the  tOBgue  and  the  constrictors  of  the  pharynx.  The  mouth  is  dry.  The  heart 
is  feeble;  this  and  the  general  prostration  and  malnutrition  may  prove  fatal. 
The  cases  are  usually  protracted,  rarely  being  very  acute.  The  active  principles 
(alkaloids  of  putrefaction)  have  lately  become  known  in  part.  In  sausage  and 
also  in  meat  poisoning  the  most  important  substance  is  ptomato-atropine,  a  sub- 
stance which  acts  almost  exactly  like  atropine.  Treatment :  Emetics,  purgatives 
(calomel),  stimulants,  and,  if  indicated,  artificial  feeding. 

35.  Poisoning  from  Meat. — In  repeated  instances  severe  symptoms  have  been 
occasioned  by  eating  tainted  meat,  or  possibly  that  obtained  from  animals  which 
had  been  diseased.  These  symptoms  are  certainly  due  to  the  products  of  putre- 
faction, substances  which  act  partly  like  muscarine,  partly  like  atropine,  neurine, 
methylguanidine,  etc.  The  special  poison  is  not  yet  fully  known.  Probably 
there  are  several  poisons,  either  chemical  or  organic  and  infectious.  The  usual 
symptoms  are  vomiting  and  diarrhoea.  The  case  may  closely  simulate  cholera.  In 
most  instances  certain  nervous  phenomena  are  also  observed — wakefulness,  de- 
lirium, headache,  and  changes  in  the  pupils.  There  may  be  roseola,  wheals  or 
erythema.  Frequently  there  is  a  high  fever,  but  sometimes  the  temperature  is 
subnormal.  The  pulse  is  small  and  slightly  accelerated,  although  it  may  occa- 
sionally be  slower  than  normal.  There  is  a  sense  of  thoracic  oppression.  The 
cases  are  often  protracted.  Tendency  to  relapses.  Death  may  occur.  Post  mor- 
tem, there  is  usually  found  an  intense  and  often  hsemorrhagic  enteritis  with  sec- 
ondary changes  in  the  spleen,  kidneys,  lungs,  and  other  organs.  Treatment: 
Symptomatic :  calomel,  emulsions,  stimulants,  and  baths.  Food  should  be  given 
cautiously. 

36.  Poisoning  from  Fish. — The  eating  of  tainted  fish  has  likewise  caused 
grave  disturbance.  The  symptoms  vary.  Usually  there  are  pain  in  the  stomach, 
praecordial  anxiety,  vertigo,  dryness  of  the  throat,  aphonia,  and  labored  respira- 
tion. There  may  also  be  disturbance  of  vision,  amblyopia,  and  colored  vision,  or 
paralysis  of  the  motores  oculi  and  of  accommodation.  In  severe  cases  there  may 
be  dysphagia  and  general  paresis.  Sometimes  dyspnoea  and  cardiac  weakness  are 
observed.  The  cases  are  frequently  very  tedious.  Here,  too,  there  are  many 
active  poisonous  products  of  putrefaction,  among  them  one  which  acts  like  mus- 
carine.   Treatment  similar  to  that  recommended  in  the  two  preceding  paragraphs. 

37.  Poisoning  from  Mussels  (MytUus  E dulls). — This  is  also  common.  A 
drawing  feeling  in  the  neck,  a  blunt  feeling  in  the  teeth,  crawling  and  burning  in 
the  arms  and  legs,  dullness  in  the  head,  mental  excitability,  feeling  as  if  every- 
thing were  light,  as  if  the  patient  must  fly ;  in  the  later  stages  dilated,  immobile 
pupils,  difficult  speech,  paresis  and  ataxia  of  the  muscles ;  also  nausea,  skin  erup- 
tions (urticaria),  fall  of  temperature.  In  severe  cases  death  may  ensue  in  a  few 
hours.  At  the  autopsy  we  find  severe  enteritis,  enlargement  of  the  spleen,  and 
often  a  peculiar  speckling  of  the  liver.  The  poison  of  mussels  has  been  isolated, 
and  it  is  called  mytilotoxine. 

38.  Poisoning  from  Cheese. — Vomiting,  colicky  pains,  diarrhoea,  vertigo,  sense 
of  thoracic  oppression,  headache,  languor,  and  disturbance  of  vision.  Treatment 
as  in  paragraphs  35  and  36. 


APPENDIX   II 


TABLE    OF    WEIGHTS    AND    MEASTJUES 


Table  of  Relation  of  U.  S.  Fluid  to  Metric  Measure 


Minims 

Cubic 
Centimetres. 

Minims. 

Cubic 
Centimetres. 

Fluid 
Drachms 

Cubic 
Centimetres. 

Fluid 
Ounces. 

Cubic 
Centimetres. 

1 

=               .06 

30 

=              1.85 

4 

=            14.79 

4 

=            118.24 

2 

=               .12 

40 

=              2.46 

6 

=            22.18 

6 

=            177.39 

5 
10 

=               .31 
=               .62 

Fluid 
Drachms. 

Cubic 
Centimetres. 

Fluid 
Ounces. 

Cubic 
Centimetres. 

8 
12 

=           236.53 

=          354.83 

15 

=               .92 

1 

=r              3.70 

1 

=            29.57 

16 

=          473.11 

16i 

=             1.00 

3 

=            7.39 

2 

=           59.10 

20 

=            1.23 

3 

=           11.09 

3 

=           88.67 

Table  of  Relation  of  Troy  Weight  to  Grammes 


Grains. 


Grammes. 

Grains. 

Grammes. 

Drachms. 

Grammes. 

Ounces. 

Grammes. 

.008 

8 

=               .52 

1               = 

3.89 

1 

31.1 

.011 

10 

=              .65 

U 

5.83 

li 

46.6 

.016 

15 

=              .97 

2            = 

7.77 

2 

63.3 

.032 

15.43 

=            1.00 

3            = 

11.66 

3 

93.3 

.065 

20 

=            1.29 

4            = 

15.55 

4 

134.4 

.13 

30 

=            1.94 

6            = 

23.3 

6 

186.6 

.26 

40 

=            2.59 

8 

348.8 

.32 

61.73 

=            4.00 

.39 

Table  of  Comparison  between  Centigrade  and  Fahrenheit  Scales 


Degrees  Centigrade.       Degrees  Fahrenheit. 


Degrees  Centigrade.       Degrees  Fahrenheit. 


25 
36 
37 
28 
29 
30 
31 
32 
33 
34 
35 


77 

78.8 

80.6 

82.4 

84.3 

86 

87.8 

89.6 

91.4 

93.3 

95 


36 
37 

38 
39 
40 
41 
43 
43 
44 
45 


96.8 
98.6 
100.4 
102.2 
104 
105.8 
107.6 
109.4 
111.3 
113 


1214 


APPEKDIX  n  1215 


The  Metric  System  in  Medicine 


Old  Style.  Jletric. 


m  ]  or  gr.  ]  = 

f  3  j  or     3  i  =  4 

f  3  3  or     3  i  =  32 


06  grm. 


The  decimal  Ujie,  instead  of  points,  makes  errors  impossible.  As  .06  (drug)  is 
less  than  a  grain,  while  4.  and  32.  (vehicle)  are  more  than  the  drachm  and  ounce, 
there  is  no  danger  of  giving  too  large  doses  of  strong  drugs. 

C.  c.  (cubic  centimetres),  used  for  grms.  (grammes),  causes  an  error  of  five  per 
cent,  (excess). 

A  teaspoonful  is  usually  five  grammes ;  a  tablespoonful,  twenty  grammes. 


INDEX 


Abasia,  1178,  1189. 

Abdomen,  in  cholera,  8S;  in  peritonitis,  524; 
in  typlioid,  10. 

Abdominal  typhus,  1. 

Abducens  nerve,  paralysis  of,  856. 

Abnormalities  in  size  and  position  of  the 
stomach,  460;  gastroptosis,  462;  idiopathic 
dilatation,  460;  motor  efficiency  in,  461; 
neurasthenic  symptoms,  463;  palpation  in, 
461;  treatment,  461. 

Abortion,  in  acute  yellow  atrophy  of  the  liver, 
568;  in  small-pox,  58;  in  typhoid,  S. 

Abortive  typhoid,  20. 

Abscess,  cerebral,  1106;  from  foetid  bron- 
chitis, 169;  embolic  in  the  lungs,  274,  275; 
gastric,  432;  hepatic,  577  (see  also  Sup- 
purative Hepatitis);  in  acute  peritonitis, 
527,  528;  in  erysipelas,  65;  in  glanders,  126; 
in  glossitis,  388;  in  laryngeal  perichondritis, 
145;  in  pericarditis,  306;  in  peripleuritis, 
295;  in  plague,  109;  in  septic  and  pyaemic 
diseases,  118;  in  small-pox,  58;  in  suppura- 
tive parotitis,  391;  in  typhlitis  and  peri- 
typhlitis, 485;  of  the  brain,  1106;  para- 
nephritic, 641;  peritoneal,  434;  pulmonary, 
from  pneumonia,  221,  222;  renal,  641,  642, 
655;  retropharyngeal,  403;  subphrenic,  438; 
tonsillar  and  peritonsillar,  396;  worm,  516. 

Absorptive  powers  of  the  stomach,  tests  of, 
421. 

Accessory  nerve,  spasm  of,  878. 

Accident  neuroses.    See  Traumatic  Neuroses. 

Acetonsemia.    See  Diabetic  Coma. 

Acetone  test,  754. 

Achillodynia,  821. 

Achlorhydria,  452. 

Acholia,  569. 

Achromatopsia,  hysterical,  1176. 

Achylia  gastrica.  See  Anomalies  of  Secre- 
tion OP  Gastric  Juice. 

Acid  dyspepsia,  455. 

Acid  fumes,  1206. 

Acid  perspiration  in  articular  rheumatism. 
680. 

Acoustic  tract,  1089. 

Acromegaly,  902;  tumor  of  brain  in,  903;  in 
diabetes  mellitu.s,   750. 

Acropareesthesia,  822. 

Actinomycosis  of  the  thoracic  cavity,  302; 
77 


diagnosis  and  treatment,   303;  haemorrhage 
in,  303;  infection.  303. 

Acute  bulbar  myelitis,  1051. 

Acute  febrile  jaundice,   542. 

Acute  yellow  atrophy  of  the  liver,  565;  in 
typhoid,  12. 

Addison's  disease,  650;  aetiology  and  patho- 
logical anatomy  of,  650;  anaemia  in,  652; 
course  and  termination  of,  653:  pigmen- 
tation in,  651;  symptomatology,  652; 
treatment,  653;  tuberculosis  of  adrenals, 
651. 

Adenia.    See  Pseudo-leuk^mia. 

•  Adenitis,  inguinal,  108. 

Adenitis,  in  plague,  109. 

Adenoid  growths  in  pharynx,  401. 

Adiposis  dolorosa,  902. 

JEgophony,  in  pleurisy,  287. 

Agaric,  red.    See  Mushroom  Poisoxixg. 

Agaricine  in  night-sweats,  260. 

Agoraphobia,   1194. 

Agraphia,  1081. 

Akinesia  algera,  1178. 

Albuminuria,  589. 

Albuminuria,  in  croupous  pneumonia,  215; 
in  small-pox,  58;  in  typhoid,  19. 

Alcohol,  in  chronic  gastritis,  425,  430;  in  cir- 
rhosis of  the  liver,  556;  in  nephritis,  606, 
613. 

Alcohol  poisoning,  1209. 

Alcoholic  insanity,  1210;  paralysis,  893;  poly- 
neuritis, 889-893. 

Alcoholic  stimulants,  in  croupous  pneumonia, 
225;  in  interstitial  myocarditis,  344-346:  in 
pulmonary  tuberculosis,  257;  in  yellow  fever. 
106. 

Alcoholism,  chronic,  1209;  effect  of,  in  pri- 
mary weakness  of  myocardium,  352;  in 
arterio-sclerosis,  370;  in  contracted  kidney, 
626;  in  diabetes  mellitus,  750,  751. 

Alexia.  1081. 

Alkaline  carbonates  in  gastric  ulcer,  441. 

Allochiria,   791. 

Allorhythmia,  328. 

Alopecia  in  small-pox,  56. 

Alveolar  ectasis.  See  Pulmon.uiy  Emphy- 
sema. 

Amanita.    See  Mushroom  Poisoning. 

-Vniaurosis.  uraemic,  599. 

1217 


1218 


II^DEX 


Amblyopia  in  ctirouic  nepliritis,  622. 

Amimia,  1080. 

Ammonia  poisoning,  1207. 

Ammonic  urate  crystals,  669. 

Amnesia,  1078;  agraplaic,  1081. 

Amoeba  coli  in  dysentery,  81-84. 

Amphoric  respiration  in  tuberculosis,  243. 

Amusia,  1081. 

Amyl  nitrite,  in  cardiac  neuroses,  356;  in 
epilepsy,  1151,  1152;  in  interstitial  myocar- 
ditis, 345. 

Amyloid  diseases  in  phthisis,  250. 

Amyloid  kidney,  635;  setiology  of,  635;  clini- 
cal history,  637;  degeneration  in  other 
organs  in,  639;  dropsy  in,  638;  pathological 
anatomy,  636;  predisposing  conditions,  636; 
prognosis,  diagnosis,  and  treatment,  639; 
urine  in,  637,  638,  640. 

Amyloid  liver,  580;  diagnosis,  580;  fatty  liver, 
580. 

Amyotrophic  lateral  sclerosis,  986;  setiology 
and  pathological  anatomy  of,  986;  atrophy 
of  muscle  in,  987,  988;  clinical  history,  988; 
diagnosis,  prognosis,  and  treatment,  990; 
gait  in,  989;  respiratory  disturbances,  990; 
tendon  reflexes  in,  989. 

Anaemia,  708;  baths  in,  719;  blood  in,  716; 
cardiac  murmurs  in,  713,  715;  classification 
and  Eetiology  of,  708;  clinical  history  of 
chlorosis,  714;  diagnosis  and  prognosis,  716; 
fatty  degeneration  in,  714;  from  arsenic, 
711;  pernicious  form,  710  (see  also  719); 
pulse  in,  713;  relation  to  iron  supply,  710; 
sj-mptomatology  of,  711;  treatment,  717; 
urine  in,  714. 

Anaemia,  cerebral,  1066;  in  Addison's  disease, 
652;  in  gastric  ulcer,  436;  in  pulmonary 
tuberculosis,  247. 

Anaemia,  progressive  pernicious,  719;  blood 
in,  724;  bone-marrow  in,  721,  723;  definition 
and  aetiology,  719;  diagnosis,  725;  digestive 
organs  in,  723;  fever  in,  725;  general  course, 
duration,  and  prognosis,  725;  haemorrhages 
in,  721;  retinal,  722;  pathology,  720;  re- 
spiratory symptoms,  722;  symptoms,  721; 
treatment,  726. 

Anaesthesia,  cutaneous,  causes  of,  799;  treat- 
ment, 803. 

Anaesthesia,   hysterical,  1175-1177. 

Anaesthesia  of  the  trigeminus,  802  (see  also 
Diseases  op  the  NBRVotrs  System). 

Analgesia,  in  hysteria,  1175;  in  syringomyelia, 
1031. 

Anasarca,  in  scarlet  fever,  43;  in  cirrhosis  of 
the  liver,  559. 

Anchylosis  in  arthritis  deformans,  689. 

Anchylostoma,  720;  duodenale  (see  Intes- 
tinal Paeasites),  518. 

Aneurism,  cardiac,  341;  dissecting,  380;  mil- 
iary, in  cerebral  haemorrhage,  1090. 

Aneurism  of  the  abdominal  aorta,  379. 

Aneurism,  of  thoracic  aorta,  374;  aetiology  and 
pathological  anatomy  of,  374;  auscultation 
in,  376;  cardiac  hypertrophy  in,  376;  clinical 
symptoms,  375;  course  and  termination  of, 
377;  diagnosis  and  treatment,  378;  dyspnoea 
in,  377;  galvano-puncture  in,  379;  haemor- 
rhages in,  377;  physical  signs,  375;  Roentgen 


rays,  use  in,   376;   sequelae,   376;   syphilis  as- 
cause   of,    374;   venous   signs,   377. 

Aneurism,  of  the  trunk  of  innominate,  379;  of 
the  other  vessels,  380. 

Angina  Ludovici,  392. 

Angina  pectoris,  327,  343,  355. 

Angioneurotic  oedema,   900. 

Ankle  clonus,  948,  1099,  1179. 

Anorexia,  in  achylia  gastrica,  etc.,  452,  454;  in 
a^cute  gastric  catarrh,  423;  in  cholera,  87,- 
88;  in  chronic  gastritis,  428,  432;  in  diph- 
theria, 70;  in  erysipelas,  64;  in  relapsing 
fever,  34;  in  small-pox,  55. 

Anosmia  and  hyperosmia,  827. 

Anthracosis  pulmonum,  271. 

Anthrax,  127;  bacillus  anthracis,  127,  128,  130;. 
clinical  history,  129;  convulsions  in,  129; 
fever  in,  129;  infection,  128;  inoculation, 
127-130;  intestinal,  129;  in  animals,  127,  128; 
malignant  pustule,  129;  pathology,  diagno- 
sis, and  treatment,  130;  pulmonary,  130. 

Antipyrine,  in  articular  rheumatism,  686;  in. 
erysipelas,  67;  in  migraine,  907;  in  neu- 
ralgia, 809;  in  scarlet  fever,  47;  in  septic- 
and  pyemic  diseases,  122;  in  small-pox,  62; 
in  tj'phoid,  26. 

Antitoxine,  in  diphtheria,  74;  in  plague.  111. 

Anuria,  in  acute  nephritis,  609;  in  cholera,  89; 
in  jaundice,  542. 

Aorta,  narrowing  of,  380;  rupture  of,  380;  dis- 
secting aneurism,  380;  haemorrhage  in,  380. 

Aortic  stenosis,  320. 

Apex  catarrh,  161. 

Aphasia  and  allied  conditions,  1077;  agraphia, 
alexia,  and  amnesia,  1081;  amimia,  1080; 
amnesic,  1077;  anatomical  changes  occur- 
ring in,  1081;  ataxic,  1078;  Dejerine's  views^ 
on,  1082;  monophasia  and  paraphasia,  1079; 
from  cerebral  embolism,  1105;  in  haemor- 
rhagic  polymeningitis,  1054. 

Aphonia,  hysterical,  152,  1178;  in  laryngeal 
catarrh,  141;  in  paralysis  of  the  laryngeal 
muscles,  151;  in  tuberculosis  of  the  larynx, 
148. 

Aphthae,  Bednar's,  385.  See  also  Aphthous 
Stomatitis. 

Aphthous  stomatitis,  385;  Bednar's  aphthae, 
385;  relation  to  thrush,  385;  treatment, 
385;  ulceration  in,  385,  386. 

Aplasia  of  the  lungs  in  kyphoscoliosis.  See 
Pulmonary   Atelectasis. 

Apoplectic  cyst,  1091. 

Apoplexy,  meningeal,  919;  spinal,  929. 

Appendicitis,  482. 

Arc  de  cercle,  1183. 

Arhythmic  pulse,  314,  328,  342. 

Arsenic,  in  anaemia  and  chlorosis,  711,  719;  in- 
arthritis  deformans,  693;  in  chorea,  1155; 
in  leukaemia,  732;  in  malaria,  101;  in 
pulmonary  tuberculosis,  254;  in  pseudo- 
leuksemia,  735. 

Arsenical  paralysis,  875;  poisoning,  1209;  re- 
semblance to  cholera,  91. 

Arterio-sclerosis,  370;  aetiology  of,  370;  alco- 
holism in,  370;  atheroma,  370;  atheroma- 
tous ulcers,  371;  cardiac  hypertrophy  in,  372, 
373;  cerebral  haemorrhage  in,  373;  clinical 
symptoms,    372;    gangrene   in,    373,    374;    in- 


IXDEX 


1219 


termittent  claudication  in,  373;  pathological 
anatomy  of,  371;  predisposition,  370;  pulse, 
372;  treatment  and  prophj'laxis,  374;  with 
nephritis,  370;  in  myocarditis,  341. 

Arthralgia  in  lead  poisoning,  120S. 

Arthritis  deformans,  688;  in  acute  articular 
rheumatism,  676. 

Arthrogryposis,  881. 

Arthropathy,  in  tabes  dorsalis,  974;  in  syringo- 
myelia, 1031. 

Articular  neuroses,  821. 

Ascaris  lumbricoides.  See  Intestinal  Para- 
sites. 

Ascending  spinal  paralysis,  acute  (so-called), 
1021;  diagnosis  and  prognosis,  1023;  general 
symptomatology,  1022;  pathological  anat- 
omy and  pathogenesis,  1023;  treatment,  1024. 

Ascites,  533;  chylous,  534;  differential  diag- 
nosis, 534;  percussion  in,  533,  534;  respira- 
tion in,  533;  tapping  in,  535;  treatment,  534; 
in  cirrhosis  of  the  liver,  558,  560,  562. 

Asiatic  cholera,  85. 

Asphyxia  stage  of  cholera,  91. 

Aspiration  in  pleurisy,  293. 

Associated  movements,  in  encephalitis  of 
children,  1112;  in  hemiplegia,  1100,  1112;  in 
paralysis,  837. 

Astasia,  1178. 

Asthenia  in  Addison's  disease,  652. 

Asthenic  bulbar  paralysis,   1046. 

Asthenic  pneumonia,  220,  223. 

Asthenopia,  neurasthenic,  1195. 

Asthma,  bronchial,  181;  Curschmann's  spirals 
in,  184;  diagnosis,  185;  definition  and  cause 
of,  181;  dyspnoea  in,  181,  183;  expectoration 
in,  184;  iodide  of  potassium  in,  186;  pro- 
dromata,  183;  reflex,  182;  symptoms  and 
course,  183;  treatment,  186. 

Asthma,  humidum,  164;  hysterical,  185; 
nephritic,  630;  thymic,  see  Spasm  of  the 
Glottis. 

Asthma  crystals,  184;  in  chronic  bronchitis,  163. 

Asthmatic  bronchiolitis,  see  Asthma;  pneu- 
monia, 220,  223. 

Ataxia,  837;  acute,  curable,  see  Multiple 
Neuritis;  alcoholic,  893,  894;  after  small- 
pox, 58;  cerebellar,  1086;  forced  movements 
and  positions  in  cerebellar,  1087;  hereditary 
cerebellar,  984;  hereditary  juvenile,  981; 
locomotor,  see  Tabes  Dorsalis;  in  multiple 
sclerosis,  955;  in  myelitis,  947;  in  poly- 
neuritis, 890,  892. 

Ataxic  aphasia,  1078. 

Ataxic  paraplegia,  1011. 

Atelectasis,  lobular,  233;  pulmonary,  195. 

Atheroma  of  the  vessels.    See  Artbrio-scle- 

EOSIS. 

Athetosis,  836,  1161;  movements  of,  1161; 
symptomatic  and  idiopathic  forms,   1162. 

Athrepsia  in  intestinal  catarrh  of  children, 
479. 

Atony  of  the  stomach,  460. 

Atrophy,  granular,  of  the  kidney,  625;  neu- 
rotic muscular,  996;  of  facial  muscles,  1003; 
of  interossei,  868;  of  lips.  1040:  of  the  liver, 
579:  of  liver  (acute  yellow).  565;  of  mucous 
membranes  in  chronic  bronchitis,  163:  of 
muscles    in    progressive    bulbar    paralysis. 


1040;  of  pancreas,  585;  of  small  muscles  of 
hand,  992:  spinal  progressive  muscular,  990. 

Atropine  for  salivation,  1044;  in  acid  dys- 
pepsia, 459;  in  neuralgia,  809;  in  paralysis 
agitans,  1160;  poisoning,  1211. 

Aura,  epileptic,  1143. 

Babinski  reflex,  839,  940,  989,  1096. 

Bacilli  anthracis,  127,  128,  130;  icteroides,  104; 
of  cholera,  85;  of  glanders,  125;  of  influenza, 
77;  of  tuberculosis,  227,  228,  231,  232,  234, 
240.  489;  pestis  bubonicse,  107,  108;  smegma, 
6.33:  typhoid,  1. 

Bacillus  of  tetanus,  1165. 

Bacteria,  diphtheritic,  68,  69,  71,  73:  in  acute 
catarrh  of  trachea  and  bronchi,  157-159;  in 
catarrhal  pneumonia,  200;  in  cystitis,  668, 
669;  in  endocarditis,  304;  in  foetid  bron- 
chitis, 167;  in  peritonitis,  521;  in  pleurisy, 
281,  290;  in  pulmonary  gangrene,  268:  in 
purulent  nephritis,  640;  in  sore  throat,  394: 
in  suppurative  hepatitis,  553,  554;  in  variola, 
54. 

Bacterium  coli  commune,  544,  548. 

Balanitis  in  diabetes  mellitus,  757. 

Balneo-therapeutics  in  typhoid,  24.  25. 

Barlow's  disease,  743. 

Basilar  artery,  thrombosis  of,  1050. 

Basilar  meningitis.  See  Tubercular  Menin- 
gitis. 

Basedow's  disease.  See  Exophthalmic 
Goitre. 

Baths,  in  acute  nephritis,  615,  617;  in  anaemia 
and  chlorosis,  719;  in  arthritis  deformans, 
693,  694;  in  bronchial  catarrh,  161,  162;  in 
cardiac  hypertrophy,  350;  in  catarrhal  pneu- 
monia, 204:  in  cerebro-spinal  meningitis,  116; 
in  croupous  pneumonia,  224,  226;  in  heart 
disease,  335;  in  muscular  rheumatism,  697; 
in  myelitis,  952;  in  polyneuritis,  892;  in  pul- 
monary atelectasis,  197;  in  scarlet  fever,  47; 
in  small-pox,  61,  62;  in  tabes  dorsalis,  980; 
in  typhoid,  24:  in  typhus,  33;  in  yellow 
fever,  106. 

Bednar's  aphthae,  385. 

Bedsores,  in  cerebral  haemorrhage,  1100;  in 
small-pox,  58:  in  typhoid,  23. 

Belladonna  poisoning,  1211;  in  enuresis,  674. 

Bell's  palsy.    See  Facial  Par.vltsis. 

Benzine  in  trichinosis,  134. 

Beriberi.    See  Endemic  Multiple  Neuritis. 

Bile  ducts,  cancer  of,  572;  diseases  of,  536. 

Bilharzia  haematobia,  646. 

Biliary  calculi,  543;  aetiology  of,  543;  anatomi- 
cal and  clinical  results  of,  545:  bacterium 
coli  commune,  544;  biliary  colic,  546; 
causes  of  colic  in,  547;  changes  in  gall  blad- 
der, 547;  chemical  and  physical  properties 
of,  545;  cholelithiasis,  544;  composition 
of,  543;  diagnosis,  549;  hepatic  calculi, 
545;  narcotics  in,  551,  552;  occurrence.  545; 
predisposition,  544:  prognosis,  550:  sequelae, 
549:  sex.  influence  of,  544:  treatment,  551. 

Biliary  and  hypertrophic  cirrhosis  of  the  liver, 
562. 

Bilious  pneumonia,  210. 

Bisulphide  of  carbon  poisoning,  1210. 

Bitter  almond  poisoning,  1210. 


1220 


IITDEX 


Black  death.    See  Plague. 

Black  small-pox,  59. 

Black  vomit  in  yellow  fever,  105,  106. 

Bladder,  cancer  of,  672;  diseases  of,  654;  irri- 
gation of,  in  cystitis,  671,  672. 

Bladder,  new  growths  in,  672;  cancer  of,  672; 
cystoscopy  in,  672;  papilloma  of,  672. 

Bleeders.    See  Hjsmophilia. 

Blennorrhoea,  bronchial,  164. 

Blepharospasm,  877. 

Blood  and  tissue  metamorphosis,  diseases 
affecting,  708. 

Blood  changes,  in  cholera,  90:  in  typhoid,  IS; 
corpuscles  in  urine,  594;  -fluke,  646;  in 
ansemia  and  chlorosis,  716,  724;  in  gastric 
contents,  422;  in  hsemoglobinsemia,  737;  in 
leukaemia,  729;  in  malarial  diseases,  94;  in 
relapsing  fever,  33;  in  septic  and  pyaemic 
diseases,  120;  in  trichinosis,  133. 

Blue  vitriol  poisoning,  1208. 

Bone-marrow,  in  leukaemia,  728;  in  pernicious 
anaemia,  721. 

Bones,  affection  of,  in  typhoid,  19. 

Borborygmi  in  intestinal  catarrh.  470. 

Bothriocephalus  latus,  511. 

Bottger's  test  for  sugar,  753. 

Botulismus,  1212. 

Bradycardia  from  scarlet  fever,  45. 

Brain,  abscess  of,  1106  (see  also  Bkaix,  In- 
flammation OF). 

Brain,  disturbances  of  circulation  in,  1066; 
anaemia,  1066;  hyperasmia,  1067;  syncope, 
1066. 

Brain,  embolism  and  thrombosis,  1103; 
aetiology  and  pathology,  1103:  aphasia  in, 
1105;  clinical  history,  1104;  diagnosis,  1106. 

Brain,  haemorrhage  of,  1089;  aetiology,  1089: 
acute  malignant  decubitus,  1100:  apoplectic 
cyst,  1091;  associated  movements,  1100; 
clinical  history,  1091;  diagnosis,  1101;  func- 
tional disturbances,  1094,  1095;  hemiplegia 
in;  1095,  1097,  1098,  1100;  miliary  aneurisms 
in,  1090;  muscular  atrophy  in,  1101;  pa- 
thology of,  1091;  prodromata,  1092;  prog- 
nosis and  treatment,  1102;  reflexes  in,  1096; 
symptoms,  1094,  1095;  urine  in,  1094. 

Brain,  haemorrhage  of,  in  arterio-sclerosis, 
373. 

Brain,  hydatids  of,  1124. 

Brain,  hyperaemia  of,  1066. 

Brain,  idiopathic  softening  of,  1110. 

Brain,  inflammation  of,  1106;  aetiology,  1106; 
aphasic  disturbances,  1109;  clinical  history, 
1108;  diagnosis,  1109;  general  and  focal 
symptoms,  1108;  infection,  1106;  pathology 
of,  1107;  treatment.  1110.  (See  also  acute 
and  chronic  encephalitis,  1110;  acute  en- 
cephalitis of  children,  1111:  cerebral  paraly- 
sis of  children,  1111;  curable  form  of  en- 
cephalitis, 1110;  diffuse  cerebral  sclerosis, 
1110;  idiopathic  softening  of  the  brain,  1110.) 

Brain,  lesions  in,  topical  diagnosis  of,  1068. 

Brain,  multiple  sclerosis  of,  954. 

Brain,  sclerosis  of,  diffuse,  1110. 

Brain,  symptoms  in  tabes  dorsalis,  976. 

Brain,  syphilis  of,  1125:  aetiology  of,  1125; 
arteries  in,  1126,  1127:  basal  cerebral  syph- 
ilis.   1127;    clinical   history.    1127:    complica- 


tions, 1128;  diagnosis,  prognosis,  and  treat- 
ment, 1128;  formation  of  syphiloma.  1127; 
pathology  of,  1126;  symptoms,  1127. 

Brain,  tumors  of,  1115;  aetiology.  1115; 
cysticerci  in,  1125;  epileptiform  convul- 
sions, 1118;  general  course  and  diagnosis, 
1122;  general  symptoms,  1117;  glioma, 
1116;  gumma  and  solitary  tubercle,  1116; 
hydatids  of  the  brain,  1124;  location  of 
tumor  and  focal  symptoms,  1119-1122; 
optic  neuritis,  1118;  prognosis,  1123; 
psammoma,  1116;  sarcoma  and  carcinoma, 
1116;  treatment,  1124;  tubercular  growths 
in,  1124;  varieties  of,  1116. 

Brand's  method  in  typhoid,  24. 

Bright's  disease.    See  Nephritis. 

Bromide  of  sodium  in  gastrosynsis,  460. 

Bromides,  in  chorea,  1156;  in  epilepsy,  1149. 

Bromine  poisoning,  1207. 

Bromism,  1207. 

Bronchial  dilatation.  See  Beonchiectasis, 
176. 

Bronchial  rales,  159. 

Bronchial  stenosis,  181. 

Bronchiectasis,  167;  cylindrical,  176:  expecto- 
ration in,  178;  pulmonary  haemorrhages  in, 
179;  rales  in,  177;  relation  to  tuberculosis, 
178,  179;  saccular,  177;  terminal  phalanges 
thickened  in,  179;  treatment,  179. 

Bronchiolitis,  exudative.    See  Asthma. 

Bronchitis,  acute,  156;  aetiology,  156;  bac- 
teria in,  157,  159;  baths,  161;  bronchial 
catarrh,  156;  capillary  bronchitis,  160; 
catarrh  of  the  flner  bronchi,  160;  cough  in, 
158;  diagnosis  and  treatment,  161;  expecto- 
ration of,  158;  fever  in,  159;  infectious 
causes  and  irritating  inhalations,  157; 
milder  forms  of,  159;  pains  in,  158;  physical 
examination  in,  158;  predisposition  to,  157; 
rales  and  rhonci  in,  159;  respiration  in,  160; 
secondary  bronchitis,  157;  severer  febrile 
forms  of,  159;  symptoms,  157;  tracheitis,  157. 

Bronchitis,  chronic,  162;  aetiology  of,  162; 
asthma  humidum,  164:  atrophy  of  mucous 
membranes  in,  163;  bronchial  blennorrhoea 
in,  164;  chronic  bronchial  catarrh,  162; 
course  of  the  disease.  164;  diagnosis,  prog- 
nosis, and  treatment,  165;  dry  chronic 
catarrh  in,  164;  emphysema  of  lungs  in, 
162;  expectoration  of,  163,  164;  in  renal  dis- 
eases, 162;  noxious  inhalations,  effect  of, 
162;  pathological  anatomy  of,  163:  physical 
examination  in,  163;  rales  in,  163;  serous 
brouchorrhoea.  164. 

Bronchitis,  croupous,  170;  aetiology  of.  170 
casts  of  bronchi,  171;  chronic  form  of,  171 
dyspnoea  in,  170,  171;  in  typhoid.  170 
pathological  anatomy  of.  171:  prognosis,  171 
spirals  in  sputum.  171;  symptoms  and 
course,  170;  treatment,  172. 

Bronchitis.  fibrinous.  See  Beonchitis, 
Ceoupous. 

Bronchitis,  foetid,  167:  istiology  of,  167;  ana- 
tomical changes,  symptoms  and  course  of. 
167:  bacteria  of,  167;  bronchiectasis,  167: 
Dittrich's  plugs,  168;  expectoration,  167; 
fatty  acid  crystals,  168;  fever  in,  167;  gan- 
grene in,  168,  169;  inhalations  in,  170:  pueu- 


INDEX 


1221 


monia,  108;  sputum  of,  168;  symptoms,  diag- 
nosis, prognosis,  and  treatment,  169. 

Bronchitis,  in  glanders,  126;  in  erysipelas,  66; 
in  relapsing  fever,  34;  secondary,  157.    " 

Bronchitis,  putrid.    See  Bronchitis. 

Broncho-pneumonia.       See     Pneumonia,     Ca- 

TAKEHAL. 

Bronchophony,  in  catarrhal  pneumonia,  203- 
212;  in  pleurisy,  287. 

Bronchorrhcea,  serous,  164. 

Bronzed  skin.    See  Addison's  Disease. 

Brown  induration  of  the  lungs,  275;  cells  of 
heart  disease,  176;  dyspnoea  in,  276;  sputum 
in,  276. 

Bruit.    See  Murmurs. 

Bubonic  plague.    See  Plague. 

Bulbar  paralysis,  acute  and  apoplectiform, 
1048;  chronic  and  asthenic,   1045. 

Bulbar  paralysis,  progressive,  1039;  aetiology 
and  clinical  history  of,  1039;  diagnosis,  1043; 
muscular  atrophy  in,  1040;  pathology  of, 
1042;  prognosis  and  treatment,  1044;  saliva- 
tion in,  1041. 

Bulbous  pulse,  332. 

Butyl  chloral  in  neuralgia  of  trigeminus,  813. 

Cachexia,  chronic  malarial,  99;  in  dysentery, 
83;  strumipriva,  901,  913. 

Caecum,  inflammation  of.  See  Typhlitis 
and  Perityphlitis. 

Caffeine  in  valvular  heart  disease,  337. 

Caisson  disease,  932. 

Calculi,  biliary,  543;  faecal,  483;  intestinal, 
500;  pancreatic,  587;  renal,  567,  568. 

Calomel,  in  cardiac  dropsy,  338;  in  cholera 
morbus,  477;  in  dysentery,  83:  in  intestinal 
catarrh,  481;  in  relapsing  fever,  38;  in  tuber- 
cular meningitis,  1064;  in  typhoid  fever,  23. 

Camp  fever,  31. 

Camphorated  oil  in  typhoid,  28. 

Cancer,  colloid,  445;  of  the  intestines,  491;  of 
the  small  intestines,  492. 

Cancer  of  the  csecum,  492. 

Cancer,  of  the  colon,  492;  of  the  kidney,  644; 
of  the  larynx,  156. 

Cancer  of  the  liver  and  bile  ducts,  572; 
aetiology  and  pathology  of,  572;  clinical  his- 
tory, 573;  diagnosis,  573,  574;  histological 
structure  of,  573;  jaundice  in,  574;  melanotic 
sarcoma,  574;  palpation  and  percussion  in, 
573;  relation  to  biliary  calculi,  573;  syphilitic 
growths,  574;  tumors  in,  573. 

Cancer  of  the  lungs,  276;  expectoration  of, 
277;  sequelae,  278. 

Cancer  of  the  oesophagus,  412;  aetiology  and 
pathology  of,  412;  clinical  history,  414;  gan- 
grene, pulmonary,  in,  413,  414;  prognosis  and 
treatment,  414;  symptoms  and  complica- 
tions, 413;  termination.  414;  ulceration  of, 
413. 

Cancer  of  the  pancreas,  .586. 

Cancer  of  the  peritoneum,  535;  colloid  cancer 
of,  .535,  5.36;  diagnosis,  536;  inflammation  in, 
536;  miliary  carcinosis,  ,535:  symptoms  and 
treatment.  536. 

Cancer  of  the  pleura,  300. 

Cancer  of  the  stomach,  444;  {etiology  of,  444; 
blood    in,    448;    diagnosis,    440;    gastric    con- 


tents in,  447;  hepatic  growths  in,  448;  palpa- 
tion and  percussion  in,  446;  pathology  of, 
445;  sarcinae  in,  446;  treatment,  451;  ulcera- 
tion in,  445. 

Cancer  of  the  vertebrae,  941. 

Cancrum  oris.     See  Noma. 

Cantharides  as  cause  of  cystitis,  668. 

Capillary  bronchitis,  160;  congestion  in  yellow 
fever,  105,  106. 

Carbolic  acid,  in  erysipelas,  67;  in  foetid  bron- 
chitis. 170;  in  scarlet  fever,  47;  in  typhoid, 
28;  poisoning,  1211. 

Carbolic  mask,  170,  270. 

Carbon  in  the  lungs,  271. 

Carbonates  of  lithia  and  soda  in  nephro- 
lithiasis, 661. 

Carbonic  oxide  gas  poisoning,  1210. 

Cardiac  neuroses,  355;  angina  pectoris,  355, 
3.56;  cardiac  neuralgia,  355;  nervous  palpita- 
tion, 356:  prognosis  and  treatment,  357; 
pulse  in,  355;  stenocardia,  355;  tachycardia, 
357. 

Cardialgia,  in  gastritis,  426;  in  gastric  ulcer, 
435. 

Caries  of  vertebrae,  934. 

Casts  of  the  brouchi  in  croupous  bronchitis, 
171,  210. 

Casts,  urinary,  592,  593. 

Catalepsy,  1170;  anaesthesia  in.  1171;  progno- 
sis and  treatment,  1171;  relation  to  hys- 
teria, 1171. 

Catarrh,  of  bronchi,  156;  gastric,  422;  intes- 
tinal, 468;  laryngeal,  140;  of  trachea.  156; 
vesical,  see  Cystitis. 

Catarrhal   inflammation  of  the  mouth,   383. 

Catarrhal  jaundice,  536. 

Catarrhal  pneumonia,  199. 

Catarrhal  sore  throat,  395.  ' 

Catarrhal  stomatitis,  382. 

Caustic  potash  or  soda  poisoning,  1207. 

Cephalalgia.    See  Habitual  Headache. 

Cephalic  cry  of  children  in  tubercular  menin- 
gitis, 1063. 

Cephalic  tetanus,  1167. 

Cerebellar  ataxia,  hereditary,  984;  and  ver- 
tigo, 1086. 

Cerebellum,  1086;  forced  movements  and  posi- 
tions, 1087. 

Cerebellum,  tumors  of,  1121. 

Cerebral  diseases,  localization  of,  1068. 

Cerebro-spinal  fever.     See  Meningitis,  Cere- 

BRO-SPINAL. 

Cervico-brachial  neuralgia,  814. 

Cestodes.  508. 

Chalicosis  pulmonum,  271. 

Charbon.    See  Malign.\nt  Pustule. 

Charcot's  crystals,  184;  in  leukaemia,  728. 

Cheese,  poisoning  from,  1213. 

Cheyne-Stokes,    breathing    in    heart    disease, 

3.33. 
Chicken-pox.    See  Varicella. 
Cinchonism  in  malarial  diseases,  102. 
Chloral  amide  in  heart  diseases,  338,  356. 
Chloral  hydrate  in  heart  disease,  3.38. 
Chlorate    of    potassium,    in    cystitis.    671;    in 

genito-urinary  tuberculosis,  664. 
Chlorine  gas  poisoning,  1207. 
Chloroform  in  hydrophobia,  124. 


1222 


I^DEX 


Chloroform  poisoning,  1210. 

Chlorosis,   708. 

Choked  disk,  in  cerebral  syphilis,  1127;  in 
chronic  hydrocephalus,  113S;  in  tumor  of 
brain,  1118. 

Cholsemia,  569. 

Cholelithiasis.     See   BiLiAur   Calculi. 

Cholera,  85;  abdomen  in,  88;  absorption  im- 
paired. 93;  anorexia  in,  87,  88;  blood  in,  90; 
catarrhal  inflammation  in,  90,  91,  sicca,  88; 
typhoid,  89;  choleraic  diarrhoea,  87;  choler- 
ine, 87;  circulatory  system  in,  88;  clinical 
history,  87;  comma  bacillus,  85;  complica- 
tions, 91;  dejections  of,  88;  diagnosis,  prog- 
nosis, prophylaxis,  and  treatment,  91;  diet, 
92;  disinfection  in,  91,  92;  history,  85; 
immunity,  87;  in  animals,  86;  infection,  86; 
mortality,  91;  muscular  cramp  in,  89;  nerv- 
ous symptoms,  89;  pathology  and  patho- 
genesis, 90;  Peyer's  patches  in,  90;  predis- 
posing causes,  87;  relation  to  ground  water, 
87;  temperature  in,  88;  urine  in,  87,  89. 

Cholera  infantum.    See  Cholera  Morbus. 

Cholera  morbus,  475;  diagnosis,  476;  fever  in, 
476;  infection,  475;  symptoms,  475;  tem- 
perature in,  476;  treatment,  477. 

Cholera  nostras.    See  Cholera  Morbus. 

Cholera  sicca,  88. 

Cholitis.  chronic,  from  dysentery.  83. 

Chorditis,  tuberosa,  143. 

Chorea,  1152;  aetiology,  1152;  causation,  11-52; 
chronic  hereditary,  1156;  clinical  history, 
11.53;  diagnosis,  prognosis,  and  treatment, 
1154;  electrical,  1156:  hydrotherapeutics  and 
electricity  in,  1156;  motor  disturljances,  1153, 
1154;  nature  of  the  disease.  1155:  tendency 
to  valvular  cardiac  disease,  1154. 

Chorea,  chronic  hereditary,  1156;  Hunting- 
ton's, 1156. 

Chorea,  post-hemiplegic,   1100. 

Chyluria,  646. 

Cicatricial  contraction  of  the  stomach.  434- 
438. 

Cirrhosis,  biliary,  562. 

Cirrhosis  of  the  liver,  555;  aetiology  and 
pathology  of,  555;  ascites  in,  558,  560,  562; 
cerebral  sj^mptoms,  560;  clinical  history,  557; 
diagnosis  and  prognosis,  560;  diet  in,  561; 
hfemorrhage  in,  558;  influence  of  alcohol  in, 
556;  intestinal  symptoms,  5.58;  spleen  in, 
558;  treatment,  561;  venous  stasis  in,  557. 

Clap-threads  in  cystitis.  670. 

Claudication,  intermittent,  in  sclerosis.  373. 

Clownismus,  1184. 

Coagulation  necrosis  in  small-pox.  57. 

Coccygodynia,  820. 

Colchicum  in  gout,  779. 

Cold  in  the  head.    See  Cortza. 

Cold  pack  in  measles,  .52;  in  typhoid.  26. 

Cold-water  treatment  in  epilepsy,  1150. 

Colic,  hepatic,  see  Biliary  Calculi;  in 
dysentery,  82;  mucous,  474. 

Colon,  cancer  of,  492;  clinical  symptoms,  401; 
shape  of  faeces  in.  492;  ulceration  in.  491. 

Coma,  in  cholera,  90;  diabetic.  578.  579; 
urtemic.  597. 

Comma  bacillus,  85. 

Compensated  pyloric  stenosis,  4.39. 


Compression  of  the  lungs.  See  PuLiioxART 
Atelectasis. 

Compression  of  medulla,  1052. 

Compression  of  spinal  cord,  934. 

Condurango  in  chronic  gastritis,  431. 

Coniine  poisoning,  1211. 

Conjunctivitis,  in  scrofula,  787;  from  measles, 
50. 

Constipation,  habitual,  495;  dejections  in,  497; 
injections,  497,  498;  relation  to  neuras- 
thenia. 496;  treatment,  497. 

Constitutional  diseases,  708. 

Consumption,  of  the  larynx,  see  Tubercu- 
losis OF  THE  Larxnx;  pulmonary,  see 
Tuberculosis. 

Contagious  carbuncle.  See  Maligxant  Pus- 
tule. 

Contractures,   hysterical,   1179;  law  of,  844. 

Convulsions,  epileptic  vs.  hysterical,  1188 
epileptiform,  from  cerebral  tumor,  1118 
hysterical  vs.  epileptic,  1188;  infantile,  1151 
in  cholera,  90;  in  hydrophobia,  123,  124;  in 
malarial  diseases,  98;  in  plague,  109. 

Copper  poisoning,  1208. 

Coprolalia  in  hysteria,  1187. 

Corpora  amylacea  in  tabes  dorsalis,  964. 

Corpulence.    See  Obesitt. 

Corrigan's  pulse.  319. 

Corrosive  sublimate  poisoning,  1208. 

Corset  liver,  581. 

Cortex  cerebri,  motor  region  of,  1069. 

Coryza,  135;  dyspnoea  in,  136;  hay  fever,  135; 
headache,  136;  infection,  135;  treatment, 
136;  cause  of  erysipelas,  64;  diphtheritic,  70; 
in  influenza,  78. 

Cough  in  bronchitis,  158;  in  tuberculosis, 
237. 

Cramps,   muscular,   in  cholera,  89,  90. 

Creasote  in  foetid  bronchitis,  170;  in  intes- 
tinal catarrh,  481;  in  tuberculosis  of  lungs. 
254. 

Cretinism,  901. 

Croup.    See  Diphtheri.4.. 

Curare  in  hydrophobia,  124. 

Curschmann's  spirals,  184. 

Cyanosis  in  valvular  heart  disease,  323,  330. 

Cynanche  contagiosa,  see  Diphtheria;  gan- 
grenosa, 392. 

Cysticercus  cellulosae,  509;  in  the  brain,  1225; 
racemosus.  510. 

Cystitis,  667;  aetiology  of,  667;  bacteria  in.  668. 
669;  cantharides  in,  668;  clinical  symptoms. 
668;  infection.  667;  pathological  anatomy. 
668:  treatment  and  prophylaxis,  670:  urine 
in.  669. 

Cystitis  in  typhoid.  19. 

Cystoscopy,  672. 

Cysts,  apoplectic.  1091;  echinococcus,  278; 
echiuococcus  of  the  kidney.  646;  in  larynx, 
155:  pancreatic,  586. 

Dandy  fever.     See  Dexgue. 

Decubitus,   acute  malignant,  1100. 

Degeneration,  fatty,  in  anaemia.  714. 

Degeneration  of  muscles  and  nerves,  anatomi- 
cal changes  in.  849:  reaction  of,  848-850. 

Delirium,  in  cholera.  90:  in  croupous  pneu- 
monia, 215;  in  erysipelas,  65;  in  small-pox. 


INDEX 


1223 


55;  in  tubercular  meningitis,  1061;  tremens, 
1210. 

Delivery  paralyses,  S69. 

Dementia,  paralytic  and  paretic,  1129.     _ 

Dengue,  102;  aetiology  and  pathology  of,  103; 
diagnosis,  prognosis,  and  treatment,  103; 
prodromata,  symptoms  and  course  of,  103. 

Dentition,  anomalies  of,  392;  nervous  disturb- 
ances in,  393. 

Desquamation,  in  measles,  49;  in  scarlet  fever, 
42,  44. 

Diabetes  insipidus,  767;  clinical  history,  768; 
diagnosis,  769;  definition  and  aetiology,  767; 
post-mortem  appearances,  769;  treatment, 
770;  urine  in,  76S. 

Diabetes  mellitus,  748;  abnormal  appetite  in, 
755;  acromegaly  in,  750;  alcoholism,  750; 
circulatory  symptoms  in,  756;  clinical  his- 
tory, 751;  coma  in,  758;  constitutional 
symptoms  in,  755;  cutaneous  affections  in, 
757;  definition  and  aetiology  of,  748:  diag- 
nosis and  treatment,  763;  diet  in,  763; 
digestive  symptoms  in,  755;  exercise  in,  766; 
genito-urinary  symptoms  in,  756;  glycosuria 
in,  749;  hereditary  influence,  750;  kidneys 
and  liver  in,  760;  nature  of,  762;  nervous 
system  in,  757;  organs  of  special  sense  in, 
757;  oxybutyric  acid  in.  754;  pathological 
anatomy  and  histo-chemistry  of,  759;  pruri- 
tus in,  757;  pulse  in,  756;  respiratory  symp- 
toms in,  756;  sources  of  sugar  and  variations 
in.  754;  sugar  tests  in,  752:  urine  in,  752; 
varieties,   course,  and  prognosis  of,  760. 

Diabetes  mellitus,  effect  on  gastric  juice,  453; 
relation  to  pulmonary  gangrene,  267. 

Diaphoresis  in  acute  nephritis,  615. 

Diaphragm,  clouic  spasm  of,  882;  paralysis  of, 
871. 

Diarrhoea,  in  intestinal  catarrh,  469;  in 
intestinal  tuberculosis,  489:  in  pulmonary 
tuberculosis,  249:  in  typhoid,  10,  28;  in 
whooping-cough,   174:   septic.   121. 

Dicrotism  in  typhoid.  17. 

Diet,  in  cancer  of  the  stomach,  451:  in  catar- 
rhal jaundice,  541:  in  cholera,  92;  in  chronic 
gastritis,  429;  in  cirrhosis  of  liver,  561; 
in  croupous  pneumonia,  226;  in  diabetes  mel- 
litus, 763;  in  diphtheria,  75;  in  dysentery, 
83;  in  gastric  ulcer,  441;  in  gout,  778;  in 
interstitial  myocarditis,  344;  in  intestinal 
catarrh,  474;  in  measles.  52;  in  nephro- 
lithiasis, 661;  in  pulmonary  tuberculosis, 
257;  in  scarlet  fever,  46:  in  symptomatic 
achj'lia,  455:  in  typhoid,  23. 

Digitalis,  in  croupous  pneumonia.  225:  in  valv- 
ular heart  disease,  335;  poisoning,  1211. 

Diphtheria,  67;  aetiology  and  general  pa- 
thology of,  67;  cardiac  weakness  in,  72; 
causes  of,  68:  clinical  history,  69:  con- 
tagiousness, 69;  croup,  68:  ascending  croup, 
70;  false  croup,  141:  diagnosis.  73:  diph- 
theritic coryza,  70:  diphtheritic  paralysis, 
72;  in  animals,  69:  incubation,  69:  laryngeal, 
70;  micro-organisms  of,  68;  nephritis  in, 
72;  nervous  sequelae,  72:  of  the  external 
genitals,  72;  pharyngeal,  68;  pneumonia 
(lobular),  72;  prognosis  and  treatment.  74; 
prognosis   of   nervous   sequela?.    73:    prophy- 


laxis, 76;  relation  of  filth  to,  69;  serum  in- 
jection and  treatment,  74;  sopor,  71:  source 
of  infection,  69:  temperature  in,  70:  toxines, 
69,  71,  73;  tracheotomy  in,  69,  74,  76. 

Diphtheritic  ocular  paralysis,  857. 

Diplegia  facialis,  1045. 

Diplegia,  infantile  spastic,  1012. 

Diplococci,  in  cerebro-spinal  meningitis.  111; 
diplococcus  pneumoniae,  205,  206,  208,  210, 
215,  219. 

Diplococci,  in  influenza,  79;  in  pleurisy,  280; 
in  sore  throat,  394;  in  tuberculosis,  234. 

Diplococcus  pneumoniae,  205. 

Disinfection,  in  cholera,  91;  in  plague,  108; 
in  small-pox,  60;  in  typhoid,  28;  in  yellow 
fever,  106;  of  sputum  in  foetid  bronchitis, 
170. 

Dittrich's  plugs  in  foetid  bronchitis,  168. 

Diuretics,  in  acute  nephritis,  616;  in  pleurisy, 
292. 

Drinking  water  as  cause  of  typhoid,  2. 

Dropsy,  in  pulmonary  emphysema,  191;  of 
renal  disease,  594,  610,  617,  622,  638;  tho- 
racic, 299. 

Drunkard's  pneumonia,  218. 

Dubini's  disease,  1157. 

Duodenum,  cancer  of,  493:  perforating  ulcer 
of,  488. 

Dura  mater,  hsematoma  of,  1053:  aetiology  and 
pathology  of,  1053;  aphasia  in,  10.54;  diag- 
nosis and  treatment,   1055;  symptoms,  1054. 

Dust,  diseases  from  inhalation  of,  270. 

Dysentery,  81;  aetiology  of,  81:  amoebae  coli 
in,  81;  bacteria,  82;  clinical  history,  82; 
complications,  diagnosis,  prognosis,  treat- 
ment, and  prophylaxis,  83;  diet,  83;  diph- 
theritic and  catarrhal  forms,  81;  gangrenous 
form,  81;  infection,  81:  in  animals,  81;  sec- 
ondary, 82:  tenesmus  in,  82. 

Dyspepsia,  chronic,  of  children,  see  Intes- 
tinal Catakrh  of;  anaemic,  722;  gouty, 
774:  nervous,  463:  with  hyperacidity,  456; 
with  hypersecretion  of  gastric  juice,  457. 

Dysphagia  in  stenosis  of  the  oesophagus,  409, 
410. 

Dyspnoea,  from  heart  disease,  276;  in  anthrax, 
128:  in  aortic  aneurism,  377:  in  bronchial 
asthma,  181,  183,  185:  in  cancer  of  the  lungs, 
277;  in  chronic  bronchitis,  163:  in  coryza, 
136;  in  croupous  bronchitis,  170;  in  croupous 
pneumonia,  208:  in  diphtheria,  70;  in  hydro- 
thorax,  299;  in  mediastinal  tumors,  301:  in 
miliary  tuberculosis,  262:  oedema  of  the 
glottis,  146:  in  pericarditis,  361:  in  pleurisy, 
283,  293:  in  pulmonary  emphysema,  190; 
in  pulmonary  gangrene,  268;  in  pulmonary 
oedema,  197;  in  pulmonary  tuberculosis.  241; 
in  retropharyngeal  abscess,  403:  in  scar- 
let fever,  41:  in  spasm  of  the  glottis,  154;  in 
tabes  dorsalis,  974:  in  tracheal  stenosis,  ISO; 
in  valvular  heart  disease.  320.  .33.3.  339. 

Dystrophy,  progressive  muscular,  998:  infan- 
tile, 1002:  diagnosis  and  treatment  of.  1005; 
infantile  form  of.  1002:  juvenile  form  of, 
1003. 

Ecchymosis.  cutaneous,  in  malarial  diseases, 
99:  in  purpura.  744:  in  small-pox.  .50:  in  ty- 


1224 


INDEX 


plioid,  18;  in  acute  yellow  atrophy  of  liver, 
567. 

Ecliinococcus  of  the  kidney,  646. 

Echinococcus  of  the  liver,  575;  clinical  symp- 
toms, 576;  complications,  576;  diagnosis  and 
treatment,  577;  hepatic  abscess,  577;  hydatid 
cysts,  575;  infection,  575;  natural  his- 
tory and  pathology,  575;  rupture,  576;  sup- 
puration, 577;  taenia  echinococcus,  575. 

Echinococcus  of  the  lungs,  276;  multilocularis, 
577;   expectoration,   278;   symptoms  of,    278. 

Echolalia  in  hysteria,  1187. 

Eclampsia  infantum,  1151;  in  dentition,  393; 
uraemic,  599. 

Ectasis,  alveolar.  See  Pulmonary  Emphy- 
sema. 

Ehrlich's  reaction  in  typhoid,  19;  test  (foot- 
note), 19. 

Elastic  fibers  in  tuberculosis  expectoration, 
240,  268. 

Electrical  chorea,  1156. 

Electrical  excitability  in  motor  nerves  and 
muscles,  842. 

Electricity,  in  cerebral  haemorrhage,  1102;  in 
cutaneous  anaesthesia,  803;  in  enuresis,  674; 
in  gastroptosis,  463;  in  hysteria,  1190;  in 
hysterical  aphonias,  153;  in  muscular 
rheumatism,  697;  in  myelitis,  952;  in  nerv- 
ous dyspepsia,  467;  in  neuralgia,  808;  in 
neurasthenia,  1199;  in  progressive  bulbar 
paralysis,  1044;  in  sciatica,  819;  in  tetany, 
1165. 

Embolic  infarction  in  the  kidneys,  643. 

Embolic  processes  in  the  lungs,  273;  aetiology 
of,  273;  expectoration  of,  274;  hsemorrhagic 
infarction,  273;  pathological  anatomy  and 
symptoms,  274. 

Embolic  processes  in  valvular  heart  disease, 
331. 

Embolism  and  thrombosis  of  basilar  artery, 
1050;  cerebral,  1103. 

Emphysema,  in  rupture  of  oesophagus,  414;  of 
lungs  in  chronic  bronchitis,  162,  188;  of  lungs 
in  croupous  bronchitis,  171;  pneumonia  in, 
219;  pulmonary,  187;  pulmonary,  after 
whooping-cough,  174,  189;  pulmonary  (vicari- 
ous), 181;  vicarious,   in  pleurisy,  288. 

Empyema  in  septic  and  pyaemic  diseases, 
120. 

Encephalitis,  acute  and  chronic  non-suppu- 
rative,  1110;  acute  haemorrhagie,  1113;  cur- 
able form  of,  1110. 

Encephalitis  of  children,  acute,  1111;  asso- 
ciated movements  in,  1112. 

Encephalitis,  suppurative,  1106. 

Enchondroma  of  lungs,  277. 

Endarteritis  chronica  deformans,  see  Ar- 
TERio-scLBROSis;  sypMlitic,  341. 

Endocarditis,  acute,  304;  abscesses,  306; 
aetiology  of,  304;  bacteria  in,  304;  diag- 
nosis, 307;  diphtheritica,  .305;  embolism, 
305;  fever  in,  307;  hfemorrhages,  306; 
inoculation  and  infection,  304;  malignant, 
non-septic  form,  306;  pathological  anatomy 
of,  305;  prognosis  and  treatment,  308;  pulse, 
306;  recurrent  form  and  septic  ulcerative 
form,  307:  ulcerosa,  305;  verrucosa,  305,  306. 

Endocarditis,  chronic,  see  V.UjVdlar  Disease 


OP  THE  Heart;  septic  ulcerative,  307;  rheu- 
matic, 679;  ulcerosa  and  verrucosa,  see- 
Endocarditis. 

Endothelioma  of  the  lungs,  277. 

Enemata,  in  dysentery,  83;  in  intestinal  ob- 
structions, 507;  in  jaundice,  541;  of  air,  507. 

Enteric  fever.     See  Typhoid. 

Enteritis,  see  Intestinal  Catarrh;  mem- 
branous, 474. 

Enuresis  nocturna,  673. 

Epilepsy,  1141;  aetiology,  1141;  causative  fac- 
tors, 1142;  clinical  history,  1143;  clonic 
spasms  in,  1144;  cortical  origin  of,  1148; 
diagnosis,  1148  (see  also  1188);  eclampsia 
infantum,  1151;  epileptic  aura,  1143;  gen- 
eral course  of,  1145;  hereditary  influence, 
1141;  infantile  convulsions,  1151;  milder  and 
rudimentary  forms,  1144;  pathology  of,  1147; 
petit  mal,  1144;  prodromata,  1143;  prog- 
nosis, 1147;  reflex,  1142;  relation  to  physical 
degeneracy,  1146;  stages  of  the  paroxysm, 
1143;  traumatic  form,  1142;  treatment,  1149; 
treatment  during  paroxysm,  1150;  urine  in, 
1144. 

Epilepsy,  Jacksonian,  partial  or  cortical,  1072. 

Epistaxis,  see  Nosebleed;  in  malarial  dis- 
eases, 99;  in  relapsing  fever,  37;  in  typhoid,  8. 

Erethism,  mercurial,  1208. 

Ergot,  in  caisson  disease,  933;  poisoning,  1212.. 

Ergotine  injections,  in  aortic  aneurisms,  379; 
in  pulmonary  tuberculosis,  260;  in  typhoid, 
23. 

Ergotism,  chronic,  1212. 

Eruptions,  in  small-pox,  55;  in  typhus,  32. 

Erysipelas,  63;  clinical  history  of,  64;  compli- 
cations, 66;  contagiousness,  64;  diagnosis, 
prognosis,  and  treatment,  66;  erysipelas 
migrans,  65;  fever  in,  65;  inoculation,  64; 
in  drunkards,  66;  in  the  newborn,  63;  intes- 
tinal disturbances,  66;  recurrence  of,  64; 
skin  in,  64;  temperature  in,  65. 

Erysipelas  in  small-pox,  58. 

Erythema  of  small-pox,  55. 

Brythromyelalgia,  900. 

Ethyl-chloride  spray  in  intercostal  neuralgia,. 
816. 

Eucalyptus  oil  in  leukaemia,  733. 

Eustrongylus  gigas,  647. 

Exalgiue  in  chorea,  1156. 

Exfoliation  in  scarlet  fever,  39. 

Exophthalmic  goitre,  909;  aetiology  of,  909; 
course  and  diagnosis  of,  913;  pathological 
anatomy  and  pathogenesis,  912;  pulse  in, 
910:  relation  to  mental  excitement,  910; 
symptomatology,  910;  treatment,  914;  tremor 
in,  911. 

Eyes,  disturbances  in  tabes  dorsalis,  972;  dis- 
turbances in  erysipelas,  66;  strain  of,  in  ha- 
bitual headache,  825;  strain  of,  in  migraine, 
905:  S3'mptoms  in  acute  miliary  tuberculosis, 
265:  symptoms  in  tubercular  meningitis, 
1061. 

Face-ache,    Pothergill's.     See   Neuralgia    of- 

Trigeminus. 
Facial  hemiatrophy,  908. 
Facial   muscles   and   muscles   of   mastication,. 

851. 


INDEX 


1225' 


Facial  paralysis,  85S:  fetiology,  858;  diagnosis, 
prognosis,  and  treatment,  862:  symptoms 
and  course  of,  859;  various  forms  of,  861. 

Facial  spasm,  clonic,  876. 

Facial  tic.    See  Clonic  Facial  Spasm. 

Faecal  calculi,  483. 

Ffeces  in  diphtheria.  68. 

Fainting.    See  Ceeebral  Anemia. 

Falling  sickness.    See  Epilepsy. 

Famine  fever,  31. 

Farcy.    See  Glanders. 

Fastigium  in  typhoid,  6,  21. 

Fat  in  urine,  594. 

Fatty  acid  crystals  in  sputum,  168. 

Febrile  jaundice,  acute,  542. 

Febris  recurrens.    See  Relapsing  Fever. 

Fehling's  test  for  sugar,  753. 

Fermentation  test  for  sugar,   753. 

Ferric  hydrate  in  arsenic  poisoning,  1209. 

Fever,  anaemic,  436;  and  ague,  see  Malarial 
Diseases;  break-bone,  102;  intermittent, 
96;  in  acute  articular  rheumatism,  677;  in 
acute  catarrh  of  trachea  and  bronchi,  159; 
in  laryngeal  catarrh,  141;  in  catarrhal  pneu- 
monia, 201,  216;  in  eerebro-spinal  menin- 
gitis, 114;  in  cholera,  88;  in  diphtheria, 
70;  in  endocarditis,  307;  in  erysipelas,  65; 
in  foetid  bronchitis,  167;  in  glanders,  125, 
126:  in  influenza,  78;  in  malignant  pus- 
tule, 129;  in  measles,  50;  in  plague,  108;  in 
pleurisy,  284;  in  pulmonary  tuberculosis, 
246.  253,  260:  in  purulent  meningitis, 
1058;  in  rheumatism,  677;  in  septic  and 
pysemic  diseases,  119;  in  small-pox,  55;  in 
typhlitis  and  perityphlitis,  484;  in  typhoid, 
6,  15,  20,  24:  in  varicella,  62;  splenic,  see 
Malignant  Pustule;  thermic,  see  Insola- 
tion; typho-malarial,  100;  yellow,  104. 

Fibrillary  contractions  in  neurotic  muscular 
atrophy,  997. 

Fibroid  phthisis,  243. 

Fibroma  of  larynx,  155. 

Filaria  sanguinis,  647. 

Filth,  relation  to  diphtheria,  69;  relation  to 
plague,  107. 

Fish,  poisoning  from,  121.3. 

Flajam's  disease.  See  Exophthalmic 
Goitre. 

Fowler's  solution,  in  chorea,  1155;  in  epilepsy, 
1149. 

Friedrich's  disease  (Hereditary  Ataxia"),  981; 
aetiology  and  pathological  anatomy  of,  981; 
clinical  history,  982;  diagnosis  and  treat- 
ment, 984;  pathological  anatomy,  983. 

Furunculosis.  after  influenza,  80;  in  diabetes 
mellitus,  757. 

Gait,  ataxic,  966;  cerebellar,  984,  1086;  in  neu- 
ritis, 890;  of  osteomalacia,  705:  spastic 
paretic,  1008. 

Gall-stones,  543:  in  diphtheria.  68. 

Galvano-puncture  in  aortic  aneurism,  379. 

Gangrene,  pulmonary,  221;  pulmonary,  in 
cancer  of  oesophagus,  413:  self-induced, 
1180:  symmetrical  spontaneous,  900;  in 
arterio-sclerosis,  373:  in  erysipelas,  65;  in 
foetid  bronchitis.  168:  in  plague,  109;  in  pneu- 
mothorax. 295:  in  small-pox.  .58. 


Gangrene  of  the  lungs,  266;  aetiology  of,  266; 
bacteria  in,  268;  clinical  history,  268;  diag- 
nosis and  prognosis,  269;  dyspnoea  in,  268; 
elastic  fibers,  268;  expectoration,  268,  269; 
haemoptysis  in,  268;  pathological  anatomy 
of,  267;  pneumothorax  from,  268;  relation  to 
diabetes  mellitus,  267;  treatment,  270. 

Gangrene  of  the  tonsils  in  scarlet  fever,  40. 
See  also  Noma. 

Garrod's  thread-test  for  uric  acid,  777. 

Gas  in  pneumothorax,   composition  of,   298. 

Gastralgia,  in  gastritis,  426;  in  gastric  ulcer,, 
435. 

Gastric  catarrh,  acute,  422. 

Gastric  contents,  blood  in,  422;  examination 
of,  415;  tests  for,  417. 

Gastric  crisis  in  tabes  dorsalis,  974. 

Gastric  juice,,  anomalies  of  the  secretion  of, 
452;  achylia  gastrica  and  achlorhydria,  452; 
anacidity  of  the  stomach,  452;  diagnosis, 
454;  dyspepsia  in,  454;  hypersecretion  and 
hyperacidity  of,  455  et  seq.;  in  diabetes  mel- 
litus, 453;  treatment,  455. 

Gastric  juice,  constituents  of,  417. 

Gastric  juice,  hypersecretion  and  hyperacidity 
of,  455  (see  also  Anomalies  in  the  Secre- 
tion OF);  dyspepsia  with,  456;  gastric  con- 
tents in,  458;  periodical  hypersecretion,  459;- 
prognosis  and  treatment,  458;  relation  to 
gastric  ulcer,  457;  relation  to  migraine,  459; 
resemblance  to  gastric  crisis,  459. 

Gastric  neurasthenia.  See  Nervous  Dys- 
pepsia. 

Gastric  ulcer,  432;  aetiology  of,  432;  cicatri- 
cial contraction  of  stomach  in,  434:  clinical 
history,  434;  diagnosis,  440;  diet,  443;  fever 
in,  436:  gastralgia  in,  435;  gastric  contents 
in.  437;  haematemesis  in,  436;  haemorrhage 
in,  434;  in  chlorotic  patients,  433;  pathologi- 
cal anatomy  of,  434;  perforation  in,  438; 
prognosis  and  treatment,  441;  pyloric  ste- 
nosis in,  434,  438,  443;  urine  in,  436;  vomiting 
in,  439. 

Gastritis,  acute,  aetiology  and  pathologi- 
cal anatomy  of,  422;  from  alcohol,  423;  in- 
fection and  predisposition,  423;  symptoms, 
423;  toxic  gastritis  in,  423;  treatment,  425; 
urine  in,  424. 

Gastritis,  chronic,  425;  aetiology  of,  425; 
alcohol  In,  425;  chronic  catarrh  of  the 
stomach,  425;  course  of  the  disease,  428; 
diagnosis,  429:  motor  functions  of  stomach 
in.  428;  nervous  disturbances  in,  428:  other 
symptoms.  428:  pathology  of.  426;  predisposi- 
tion, 425;  symptoms  on  part  of  the  stomach, 
426;  treatment,  429:  urine  in,  428. 

Gastritis,  phlegmonous,  432;  abscess  in,  432. 

Gastro-duodenal  catarrh.  See  Catarrhal 
Jaundice. 

Gastroptosis,  462. 

Gastroxynsis,  459. 

General  paresis,  1129. 

General  progressive  paralysis  of  the  insane, 
1129;  aetiology,  1130;  aphasic  disturbances 
in.  1132:  clinical  history,  11.31:  cortical 
changes  in,  11.34;  delusions,  1133;  diagnosis, 
1135:  early  symptoms.  1133;  literal  ataxia 
in,   11.31;   nature  of  the  disease  and   patho- 


1226 


INDEX 


logical  anatomy,  1134;  preliminary  remarks, 
1129;  prognosis  and  treatment,  1136;  pulse 
and  temperature,  1134;  relation  to  syphilis, 
1130;  speech  and  handwriting  in,  1132. 

Genitals,  neuralgia  of,  820. 
-Genito-urinary  apparatus  in  typhoid,  19. 
■Genito-urinary  tuberculosis,  229,  2.50,  662. 

German  measles.     See  Rothelx. 

Gigantism,  903. 

Gin-drinkers'  liver.    See  Cirrhosis  of  Liter. 

Gingivitis,  382-384. 

Glanders,  125;  abscesses  in,  126;  aetiology  of, 
125;  clinical  history  and  diagnosis,  126 
fever  in,  125;  infection,  125;  inoculation,  126 
in  animals,  135;  malleine  in,  127;  treatment, 
127;  ulcers  in,  125. 
■Glioma,  of  brain,  1116;  of  spinal  cord,  1024. 

Gliosis,  central,  1030. 

Globus  hystericus,  415,  1186. 

Glossitis,  acute  parenchymatous,  388;  disse- 
cans, 388. 

Glosso-labio-laryngeal  paralysis.  See  Bulbar 
Pajraltsis,  Progressive. 

Glottis,  spasm  of,  153;  aetiology  of,  153;  rela- 
tion to  rachitis,  153;  symptomatology  and 
treatment,  1.54. 

Gluteal  nerves,  paralyses  of,  872. 

Glycosuria  in  pancreatic  diseases,  586.  See 
also  Diabetes  Mellitus. 

Gmelin's  test,  540. 

Goitre,  exophthalmic,  909. 

Gonococci  in  cystitis,  668. 

Gonorrhoea,  endocarditis  in,  307. 

■Gout,  770;  aetiology  of,  770;  anatomical 
changes  in,  775;  chronic,  773;  clinical 
history,  771;  complications  in,  775;  diag- 
nosis in,  776:  diet  in,  778;  gouty  diseases  of 
various  organs,  773;  gouty  dyspepsia,  774; 
hereditary  influence,  771:  kidneys  in,  775; 
nature  of,  775;  nephritis  in,  776:  prodromata, 
772;  prognosis  and  treatment,  777:  uric  acid 
in,  772. 

•Gout  in  contracted  kidney,  626. 

Granular  kidney.     See  Contracted  Kidnex. 

Graves's  disease.    See  Exophth.^bmic  Goitre. 

Green  sickness.    See  Chborosis. 

Grippe.    See  Influenza. 

Guaiac-turpentine  test  for  blood,  422,  445,  492. 

Guaiacol  in  pulmonary  tuberculosis,  2-54. 

Guarana,  in  headache,  826;  in  migraine,   908. 

Giinzburg's  test,  417. 

Gymnastics  in  cardiac  hypertrophy,  350. 

Haematemesis,  in  gastric  ulcer,  435,  440;  in 
hypertrophic  cirrhosis  of  liver,  564. 

Hsematidrosis,  904. 

Haematoidine  crystals  in  croupous  pneumonia, 
222. 

Haematomyelia,  929. 

Haematothoras,  300. 

Haematuria  in  papilloma  of  the  bladder,  673. 

Haemine  crystals  in  gastric  contents.  422. 

TIsemoglobinaemia  and  heemoglobinuria,  736 
blood  in,  737;  definition  and  aetiology,  7.36 
influence  of  cold  in,  737;  origin  of,  736 
paroxysmal  type.  737:  pathology  and  symp 
toms,  736;  prognosis,  7.38:  urine  in,  737. 

Haemophilia.  746;  clinical  history,  747;  defini 


tion  and  aetiology,  746;  prognosis  and  treat- 
ment, 748. 

Haemoptysis,  hysterical,  1179;  in  pulmonary 
cancer,  277;  in  pulmonary  gangrene,  268;  in 
tuberculosis,  236,  2.59. 

Haemorrhages,  cerebral,  1089;  conjunctival, 
in  whooping-cough,  173;  in  aortic  aneurism, 
877;  in  aortic  rupture,  380;  in  cirrhosis  of 
the  liver,  558;  in  gastric  ulcer,  434;  in 
leukaemia,  731:  in  pernicious  anaemia,  721; 
in  plague,  109;  in  pulmonary  tuberculosis, 
238,  253;  in  septic  and  pyaemic  diseases,  120; 
in  yellow  fever,  105. 

Haemorrhages  into  medulla  oblongata  and 
pons,  1048;  paralysis  in,  1049. 

Haemorrhages,  into  pancreas,  585;  into  spinal 
cord,  929;  into  spinal  meninges,  919;  pul- 
monary, in  bronchiectasis,  179;  pulmonary, 
in  cancer,  277:  renal,  in  endocarditis,  307; 
retinal,  in  septic  and  pyaemic  diseases,  121. 

Haemorrhagic  encephalitis  in  adults,  acute, 
1113. 

Haemorrhagic  pachymeningitis,  1053. 

Haemorrhagic  infarction  of  the  lungs.  See 
Embolic  Processes  in. 

Haemorrhagic  pericarditis,  360. 

Haemorrhoids,  493;  haemorrhage  in,  494,  495; 
mucous,  494;  predisposition,  494;  treatment, 
494. 

Hair,  loss  of,  in  typhoid,  19. 

Handwriting  in  general  paralysis,  1132. 

Hay  fever  (footnote),  135. 

Head,  deformed,  in  rachitis,  702. 

Headache,  habitual,  824;  predisposition  and 
causes,  824:  relation  to  eye-strain,  825; 
treatment,  825. 

Headache,  in  cerebral  tumors,  1117;  in  coryza, 
1.36;  in  erysipelas,  64;  in  gastroxynsis,  459; 
in  plague,  108;  in  purulent  meningitis,  1057: 
in  small-pox,  55;  in  tubercular  meningitis, 
1061;  in  typhoid,  15;  in  yellow  fever,  105. 

Heart,  aneurism  of,  341:  complications  in 
croupous  pneumonia,  214:  disease,  cells  of, 
276;  disease,  compensation  in.  .311,  316,  326, 
334;  diseases  of,  304;  diseases  of,  congenital, 
323:  diseases  of,  valvular,  308;  failure  in 
diphtheria,  71;  failure  in  nephritis.  602. 

Heart,  congenital  lesions  of.  324. 

Heart,  congestion  of  liver,  330:  mental  dis- 
orders in,  332;  musical  murmur,  317,  318; 
oedema  in,  330-338:  pericarditis,   329. 

Heart,  constitutional  symptoms,  332:  fever, 
332. 

Heart,  Corrigan's  pulse,  319:  cyanosis  in,  323- 
330:  diastolic  murmur,  .315.  317,  318:  dilata- 
tion of  left  ventricle,  317:  dyspnoea,  in,  326, 
333,  3.39:  embolic  processes,  331:  fatty  de- 
generation, 329;  general  course  and  prog- 
nosis, 333;  general  pathology,  310. 

Heart,  fatty,  353:  aetiology  and  pathological 
anatomy  of.  353;  clinical  symptoms.  354; 
relation  to  fatty  degeneration.  353;  treat- 
ment, 355. 

Heart,  fatty  degeneration  of,  329;  fibrinous 
degeneration  of  the  myocardium,  see  Myo- 
carditis. Interstitial. 

Heart,  hypertrophy  of.  345:  aetiology  and  gen- 
eral   pathology.    345:    clinical    history,    347; 


IXDEX 


122- 


diagnosis  and  treatment.  348:  effect  of  alco- 
holic stimulants,  346:  influence  of  amount  of 
fluid,  348;  massage,  passive  morements, 
gymnastics,  and  baths,  350;  nephritis  in, 
348;  pulse  in,  347;  strengthening  of  cardiac 
muscle,  349. 

Heart,  hypertrophy  of,  31.5,  317,  320;  origin  of 
murmur,  315;  hypertrophy  of  left  rentricle, 
320. 

Heart,  insufHciency  of  mitral  valve,  311; 
auscultation  in,  313;  inspection,  palpation, 
and  percussion,  313. 

Heart,  insufBcienoy  of  pulmonary  valves,  316; 
insufficiency  of  semilunar  valves,   316. 

Heart,  insufliciency  of  tricuspid  valves,  322; 
hypertrophy  in,  322;  pulse  in,  322;  systolic 
murmur  in,  322. 

Heart,  mechanical  strain  of.  see  Idiopathic 
Hypertrophy;  nervous  palpitation  of,  356; 
neuralgia,  355;  neuroses,  355;  sounds  in  pul- 
monary emphysema,  192. 

Heart,  pulmonary  stenosis,  323;  congenital, 
323. 

Heart,  pulse,  313,  814,  319,  328:  arhythmic, 
314,  315,  328;  curve  of,  319. 

Heart,  relation  to  articular  rheumatism,  308, 
.327. 

Heart,  sequelae  and  complications.  326. 

Heart,  sequelae  in  heart  itself,  327;  allorhyth- 
mic  pulse,  328;  myocarditic  nodules,  329; 
pericarditis,  329;  pulsus  bigeminus,  328. 

Heart,  stenosis  of  aortic  orifice,  320;  ausculta- 
tion, inspection,  palpation,  and  percussion, 
320. 

Heart,  stenosis  of  tricuspid  orifice,  .322:  rheu- 
matism in,  323. 

Heart,  subjective  symptoms,  326;  palpitation, 
327:  tachycardia,  327. 

Heart,  symptoms  in  peripheral  arteries,  318: 
symptoms  of  stasis  in  organs.  .329. 

Heart,  systolic  murmur,  312,  319. 

Heart,  treatment,  3-34:  caffeine  in,  337;  digi- 
talis in,  335:  morphine  in,  3.39:  prophylaxis, 
3.34;  of  ruptured  compensation,  335;  stro- 
phanthus,  338:  symptomatic  treatment.  338. 

Heart,  urine  in.  331. 

Heart,  valvular  disease  of.  308:  aetiology  of, 
308:  affections  of  the  joints  in,  3.32;  angina 
pectoris,  .327;  baths  in,  335;  bulbous  pulse  in, 
322;  Cheyne-Stokes  breathing.  .3.33:  com- 
bined valvular  disease,  325;  comparison  of 
physical  signs  in,  325:  compensated  heart 
disease.  .311.  316,  .326.  .3.34;  complications  on 
part  of  nervous  system,  .3.32. 

Heat  prostation,  see  Ixsolatiox:  test  for 
albumen,  590. 

Helminthiasis.    See  Intestinal  Parasites. 

Hemianaesthesia.   hysterical,   1176. 

Hemianopsia,  1075. 

Hemiatrophy,  facial.  908. 

Hemicrania.    See  Migraine. 

Hemiplegia,  cerebral,  1095,  1097:  associated 
movements  of,  1100. 

Hemiplegia,  in  heart  disease,  .332:  in  tabes 
dorsalis,  976:  in  whooping-cough.  173:  in 
relation  to  cerebral  lesions,  1085:  spastic 
infantile,  1111. 

Hemiplegic  gait,  1099. 


Hemlock  poisoning.    See  Coniine. 

Hepatic  calculi.  545;  colic,  see  Biliary  Cal- 
culi. 

Hepatitis,  diffuse,  interstitial.  See  Liver, 
Cirrhosis  of. 

Hepatitis,  suppurative,  553;  aetiology  of,  553; 
bacteria  in,  533:  clinical  history,  554;  fever 
in,  554;  hepatic  abscesses,  553;  infection, 
553;  pathology,  553;  perforation  in,  554; 
treatment,   555. 

Herniae,  500. 

Heroine  in  tuberculosis,  259. 

Herpes  facialis,  114. 

Herpes,  in  croupous  pneumonia,  208,  216,  219; 
in  erysipelas,  66;  in  malarial  disease,  98;  in 
typhus.  32. 

Herpes  labialis,  114;  in  influenza,  79. 

Hiccough.    See  Clonic  Spasm  of  Diaphragm. 

Hobnailed  liver.    See  Liver,  Cirrhosis  of. 

Hodgkin's  disease.    See  Pseudo-leukemia. 

Hot-air  treatment  in  arthritis  deformans. 
694. 

Huntington's  chorea,  1156. 

Hydatid  cysts  of  the  liver,  575. 

Hydatids  of  the  brain,  1124. 

Hydrocephalus,  chronic,  1137:  aetiology  and 
pathology,  1137;  clinical  history,  1137:  diag- 
nosis and  treatment,  1138;  hydrocephalic 
fluid.  1137;  in  adults,  1138:  motor  disturb- 
ances in,  11-38;  physical  signs,  1137:  predis- 
posing causes,  1137. 

Hydrochloric  acid  poisoning.  1206. 

Hydrocyanic  acid  poisoning,  1210. 

Hydromyelus.  1029. 

Hydronephrosis.  665;  aetiology  of,  665:  clinical 
symptoms,  665;  diagnosis,  666;  pathological 
anatomy,  665;  treatment.  667;  tumor  in,  665; 
urine  in,  666. 

Hydronephrosis  from  movable  kidney.  649. 

Hydroperitoneum.    See  Ascites. 

Hydrophobia.  122:  blood  in.  124;  chloroform 
in,  124:  clinical  history,  123:  convulsions  in, 
123;  curare  in,  124;  diagnosis,  treatment, 
and  prophylaxis.  124:  hysterical  hydro- 
phobia. 124;  immunity,  123:  inoculation.  123; 
inoculation.  Pasteur's,  124:  paralysis  in,  122; 
prodromata.  122:  rabies  in  dogs,  122:  tem- 
perature in,  123. 

Hydrophobic  tetanus,  1167. 

Hydro-pnoumothorax.    See  Pneumothorax. 

Hydrops   articulorum  intermittens.   904. 

Hydrorrhachis.     See  Spina  Bifida. 

Hydrotherapy,  in  neurasthenia.  1200:  in  pul- 
monary tuberculosis.  259;  in  typhoid.  24. 

Hydrothorax,  299;  dyspnoea  of,  209:  lymphat- 
ics in.  299. 

Hydrothorax.  in  acute  nephritis.  614:  in  scar- 
let fever.  44. 

Hyoscine  in  paralysis  agitans,  1160. 

Hyperaemia,  cerebral,  1066:  in  erysipelas.  65; 
of  the  liver,  578. 

Hyperfpsrhesia  in  typhoid.  17. 

Hyperchlorhydria.  456. 

Hyperosmia.  827. 

Hyperostosi.'*  cranii,  904. 

Hyperplasia  from  intestinal  catarrh.  469. 

Hypertrophy,  of  the  heart.  315.  341,  .345:  in 
aortic    aneurism.    376:    in    arterio-sclerosis, 


122S 


IITDEX 


372:    associated    with    congenital    smallness 
of  the  systemic  arteries,  350. 

Hypertrophy  of  the  tonsils,  chronic,  399. 

Hypnotism  in  hysteria,  1185. 

Hypophysis  cerebri  in  acromegaly  and  gigan- 
tism, 903. 

Hypoplasia  of  aorta.    See  350. 

Hysteria,  1172;  abasia  and  astasia,  1178,  1189; 
achromatopsia  in,  1176;  aetiology  and  defini- 
tion, 1172;  aphonia  in,  1178;  arc  de  cercle, 
1183;  attacks,  conditions  of  spasm,  etc., 
1182;  causes,  1173;  clownismiis,  1184; 
contractures,  1179;  coprolalia  and  echo- 
lalia  in,  1187;  diagnosis,  1187;  diagnosis, 
differential,  1188;  general  course  of,  1187; 
globus  hystericus,  1186;  hsemorrhages  in, 
1179;  hereditary  predisposition,  1174; 
hypnotic  symptoms  and  treatment,  1185, 
1191;  hysterical  paralysis,  1178;  hysterical 
vs.  epileptic  convulsions,  1188;  hysteroge- 
nous  zones,  1186  (see  also  1149);  influence  of 
sex,  nationality,  and  race,  1174;  ischuria  and 
polyuria  in,  1180;  in  children,  1174;  mental 
and  bodily  constitution  in,  1181;  metallo- 
therapy,  1192;  muscular  sense  in,  1176; 
psychical  factors,  1173,  1181,  1191;  reflexes 
in,  1175;  respiration  in,  1183;  sensory 
anaesthesia  and  hypersesthesia,  1175;  stig- 
mata, 1173;  suggestion  in.  1184.  1191 
symptoms  and  manifestations  of,  1175 
symptoms  in  the  internal  organs,  1179 
traumatic  influences,  1173;  treatment,  1189 
Taso-motor  and  secretory  disturbances,  1179. 

Hysterical  asthma,  185;  hydrophobia,  124. 

Hysterogenous  zones,  1149,  1186. 

Icterus  catarrhalis.  See  Catarrhal  Jaun- 
dice. 

Icterus  neonatorum,  570. 

Icterus  in  typhus,  33. 

Icteric  casts,  540. 

Ileo-typhus,  1. 

Illuminating  gas  poisoning,  1210. 

Indican  test  (footnote),  504. 

Infantile  convulsions,  1151. 

Infantile  hemiplegia,  spastic,  1111;  spastic 
diplegia,  1012;  spinal  paralysis,  1014. 

Infarction,  embolic,  in  the  kidneys,  643. 

Inflammation  of  the  pericardium,  see  Peei- 
CARDTTis;  of  the  soft  palate  and  tonsils,  see 
Sore  Throat. 

Influenza,  77;  aetiology  of,  77:  bacilli,  77; 
catarrhal  form,  78;  clinical  history  and 
symptoms,  77;  complications  and  sequelae, 
79:  diagnosis,  prognosis,  and  treatment,  80; 
fever,  78;  furunculosis,  80:  herpes  labi- 
alis  in,  79;  in  animals,  77;  nervous  sequelae, 
80;  otitis  media,  79;  pandemics  of,  77;  pneu- 
monia in,  79;  rheumatoid  form.  78. 

Inhalations,  carbolic  mask,  170;  cause  of 
acute  catarrh  of  bronchi  and  trachea,  157; 
in  foetid  bronchitis,  170;  in  pulmonary  gan- 
grene, 270;  in  tuberculosis  of  larynx,  149. 

Inhalations  of  dust,  diseases  from,  270; 
anthracosis  pulmonum,  271;  black  pigment 
and  carbon  in  the  lungs,  271;  chalicosis,  271; 
sequelae.  272. 

Inhalations  of  oxygen  in  croupous  pneumonia. 


225;  of  steam  in  bronchial  catarrh,  161;  of" 
steam  in  laryngitis,  142;  treatment  of 
chronic  bronchitis,  166. 

Inoculation  of  measles,  49. 

Insolation,  1113;  aetiology  and  pathology,  1113; 
diagnosis,  prognosis,  and  treatment,  1114; 
pathological  anatomy,  1113;  symptoms  and 
course,  1114. 

Insufliciency  of  muscular  fiber  of  stomach, 
460;  of  the  pylorus,  439;  valvular,  311.  316,- 
321,  323. 

Intention  tremor,  836;  in  multiple  sclerosis, 
955. 

Intercostal  neuralgia,  815. 

Intermittent  fever.     See  Malarial  Diseases.- 

Intermittent  tetanus.     See  Tetany. 

Intertrigo  in  obesity,  782. 

Intestinal  catarrh,  468:  aetiology  of,  468; 
atrophy  of  mucous  membrane  in,  469;  diar- 
rhoea in,  469;  diet  in,  474:  different  forms 
of,  470:  hypei'plasia  in,  469;  infection,  468; 
pathological  anatomy,  468;  stools,  examina- 
tion of,  470;  symptomatology  of,  469;  treat- 
ment, 473;  ulceration  in,  468. 

Intestinal  catarrh  of  children,  477;  arthrepsia 
in,  479:  complications,  479;  feeding  in,  480; 
pedatrophy,  479:  prophylaxis,  482;  stools 
in,  478,  481;  tenesmus  In,  478;  treatment, 
481. 

Intestinal  constriction,  500. 

Intestinal  ecchymoses  in  septic  and  pyaemic 
diseases,  121. 

Intestinal  mycosis,  129. 

Intestinal  obstruction,  499. 

Intestinal  parasites,  508;  anchylostoma  duo- 
denale,  518:  ascaris  lumbricoides,  515;  blood 
in,  512;  bothriocephalus  latus,  511;  cestodes, 
508;  cysticercus  cellulosae,  509;  cysticercus 
racemosus,  510;  oxyuris  vermicularis,  516; 
round  vrorms,  515;  symptoms  and  diagnosis, 
512;  taenia  cucumerina,  511;  taenia  nana,  511  r 
taenia  solium,  508;  tape- worms,  508;  treat- 
ment, 513;  trichocephalus  dispar,   519. 

Intestinal  puncture,  508. 

Intestines,  cancer  of,  491;  congenital  closure 
of,  499;  invagination  of,  501. 

Intestines,  stricture  and  obstructions  of,  499; 
Eetiology  and  pathological  anatomy  of,  499; 
clinical  history,  502;  compression  from  with- 
out, 501;  congenital  closure,  499;  diagnosis, 
504;  intestinal  constriction,  500;  intestinal 
obstruction,  499:  intussusception,  501:  patho- 
logical changes.  502;  physical  examination, 
502;  puncture,  508:  stercoraceous  vomiting, 
503;  treatment,  .506;  tumors  and  cicatricial 
strictures,  499;  twists  and  knots  of  intes- 
tines, 500:  ulceration  in,  502:  urine  in,  504; 
varieties  of,  504:  volvulus,  500. 

Intestines,  tuberculosis  of,  488;  volvulus,  500. 

Intussusception,  501. 

Inunction  in  glanders,  127:  in  myelitis,  952; 
in  scarlet  fever,  46. 

Iodide  of  potassium  in  arterio-sclerosis,  374; 
in  asthma,  186:  in  cerebral  syphilis.  1129; 
in  interstitial  myocarditis,  345;  in  lead 
paralysis,  874;  in  neuralgia,  808;  in  spinal 
syphilis,  1029:  in  syphilis  of  the  liver,  572. 

Iodine,    in    contracted    kidney,    635;    in    ery- 


INDEX 


1229 


sipelas,  67;  in  parotitis,  391:  in  peritonitis, 
532;  in  small-pox,  61;  poisoning,  1207.     • 

lodism,  chronic,  1207. 

Iodoform  poisoning,  1210. 

Iritis,  from  gout,  775:  from  measles,  50. 

Iron,  in  anaemia  and  chlorosis,  710,  718:  in 
amyloid  kidney,  639. 

Irrigation  of  the  bladder  in  cystitis,  671,  672. 

Ischialgia.    See  Sciatica. 

Ischuria,  hysterical,  1180. 

Jacksonian  epilepsy,  1072. 

-Jaundice,  acute  febrile,  542;  fever  in,  543; 
haemorrhages  in,  543:  muscular  pains  in, 
542;  treatment,  543;  urine  in,  542. 

-Jaundice,  catarrhal,  536;  aetiology  and  patho- 
logical anatomy,  536;  bile  absorption  in,  539; 
diagnosis  and  treatment,  541;  diet,  541; 
epidemics  of,  537;  examination  of  liver  in, 
540;  fseces  in,  539;  infection,  537;  pulse  rate 
in,  538;  symptoms  and  clinical  course,  537; 
tympanites,  539;  urine  in,  539;  xanthelasma, 
538. 

-Jaundice,  infectious,  see  Jaundice,  Acute 
Febrile;  in  acute  yellow  atrophy  of  liver, 
566;  in  croupous  pneumonia,  214;  in  heart 
disease,  330;  in  malarial  diseases,  98;  in 
yellow  fever,  105;  of  the  new-born,  570;  per- 
nicious, 569;  xanthelasma  in,  538. 

Joints  affected,  in  arthritis  deformans,  690; 
in  articular  rheumatism,  678;  in  chronic 
rheumatism,  690-692;  in  glanders,  126;  in 
gout,  773;  in  heart  disease,  332;  in  septic  and 
pysemic  diseases,  120;  in  syringomyelia,  1031; 
in  tabes  dorsalis,  974;  in  typhoid,  19. 

Juvenile  muscular  dystrophy,  1003. 

Kamala,  for  tape-worm,  514. 

Keratitis,  in  anaesthesia  of  the  trigeminus, 
803;  from  gout,  775;  from  influenza,  79; 
from  measles,  50. 

Kidney,  contracted,  625;  alcoholism  in,  626; 
anatomical  complications,  632;  arterio-scle- 
rosis  in,  632;  cardiac  hypertrophy  in,  629; 
clinical  symptoms,  628;  deflnition  and 
aetiology  of,  625;  diagnosis,  633;  dyspnoea  in, 
630;  general  course,  duration,  and  termina- 
tion, 633;  gout,  626;  htemorrhage  in,  632; 
pathological  anatomy,  627;  treatment,  634; 
uric  acid,  627;  urine,  628. 

Kidney  disease,  pathology  and  preliminary 
remarks  on,  588  (see  also  564);  albuminuria. 
589;  blood-corpuscles  in  urine,  594;  cardiac 
hypertrophy  in,  602;  casts  and  other  abnor- 
mal morphological  constituents  of  urine. 
592;  changes  in  circulatory  apparatus,  601; 
dropsy  of  renal  diseases.  594;  fat  In  urine, 
594:  nephritic  oedema,  596;  toxines,  589.  See 
also  Ur.tsmia. 

Kidneys,,  amyloid,  635. 

Kidneys,  calculi  of,  in  diphtheria,  68;  calculus, 
see  Nephrolithiasis. 

Kidneys,  cancer  of,  64;  circulatory  disturb- 
ances in,  643;  congenital  sarcoma  of,  644. 

Kidneys,    dilatation   of   pelvis.     See    Hydho- 

NEPHROSIS. 

Kidneys,  floating,  648;  granular,  625. 
Kidneys,    inflammation    of    pelvis,    654:    ab- 


scesses, 655;  aetiology,  654;  clinical  symp- 
toms, 655;  nervous  symptoms,  656;  patho- 
logical anatomy  of,  654;  treatment,  657; 
urine  in,  655,  656. 

Kidneys  in  diabetes  mellitus,  760. 

Kidneys,  movable,  648;  aetiology,  648;  hydro- 
nephrosis in,  649;  hysteria  and  neurasthenia 
in,  650;  symptoms,  649;  treatment,  650. 

Kidneys,  new  growths  in,  644;  diagnosis, 
prognosis,  and  treatment,  645;  haematuria 
in,  645;  treatment,  645. 

Kidneys,  parasites  of,  646;  chyluria,  647: 
distoma  haematobium,  646;  echinococcus  of, 
646;  echinococcus  cysts.  646;  fllaria  san- 
guinis, 647;  strongylus,  647. 

Kidneys,  tumors  of,  644. 

Kousso  for  tape-worm,  514. 

Kyphoscoliosis  in  croupous  pneumonia,  220. 

Kyphosis,  angular,  in  vertebral  caries,  936; 
in  osteomalacia,  705. 

Labyrinthine  vertigo.  See  Meniere's  Dis- 
ease. 

Laennec's  cirrhosis.    See  Cirrhosis  of  Liver. 

Larjmgeal  catarrh,  acute,  140. 

Laryngeal  crises  in  tabes  dorsalis,  974. 

Laryngeal  perichondritis,  145;  abscesses  in, 
145;  pathological  anatomy  of,  145;  sympto- 
matology and  diagnosis,  145;  treatment,  146. 

Laryngeal  phthisis.  See  Tuberculosis  of 
Lartns. 

Laryngeal  polypi,  155. 

Laryngismus  stridulus.  See  Spasm  of  the 
Glottis. 

Laryngitis,  acute,  140;  aphonia  in,  141;  false 
croup  in,  141;  fever  in,  141;  irritants  as  cause 
of,  140;  symptomatology  of,  140:  treatment, 
142. 

Laryngitis,  chronic,  143;  pachydermia  laryn- 
gis,  143:  symptomatology  of.  143;  treatment, 
144. 

Laryngitis  from  measles,  51. 

Larynx,  new  growths  in,  155. 

Lateral  sclerosis,  primary,  1006. 

Laudanum  in  intestinal  catarrh,  481. 

Lead  arthralgia,  1208;  colic,  1208;  encepha- 
lopathy, 1208. 

Lead  paralysis,  873  (see  also  1208);  prognosis 
and  treatment  of,  874;  urine  in,  874. 

Lead  poisoning,  1207;  chronic,  1208;  in  gout, 
771. 

Lepto-meningitis,  acute,  915:  chronic,  917: 
purulent  cerebral,  1055. 

Leptothrix  fibers  in  sputum,  168. 

Leucine  and  tyrosine  in  liver,  566. 

Leucocythajmia.    See  Leukaemia. 

Leucocytosis,  in  croupous  pneumonia,  214:  in 
erysipelas,  66. 

Leucoplacia.    See  Lingual  Psoriasis. 

Leukaemia,  726;  blood  in,  729;  Charcot's  crys- 
tals, 728;  clinical  history.  731;  deflnition  and 
aetiology,  726;  haemorrhages  in.  731;  lymph 
glands  in.  728:  other  organs  in.  72S:  patho- 
logical anatomy,  727:  priapism  in.  731;  prog- 
nosis, diagnosis,  and  treatment,  732; 
retinitis  in,  730:  spleen  in.  727.  730,  732; 
symptoms  in,  729. 

Lime  in  rachitis.  704. 


1230 


INDEX 


Lime-water  in  croupous  bronchitis,  172. 

Lingual  psoriasis,  388. 

Lingual  spasm,  877. 

Lipoma  of  larynx,  1-5.5. 

Little's  disease.  See  Ixfaxtile  Spastic 
Diplegia. 

Liver,  acute  yellow  atrophy  of,  565;  abortion 
in,  568;  acholia  and  cholsemia,  569;  setiology 
and  pathology  of,  565;  anaemia,  hepatic,  578; 
clinical  history,  566;  cutaneous  ecchymoses, 
567;  diagnosis,  568;  jaundice  in,  566;  leucine 
and  tyrosine  in,  566;  nervous  symptoms, 
566,  569;  pernicious  jaundice,  569;  prodrom- 
ata,  566;  splenic  tumor  in,  566;  in  typhoid, 
12;  urine  in,  566;  vomiting  in,  .568. 

Liver,  amyloid.  580;  anomalies  in  shape  and 
position,  581;  atrophy,  hypertrophy,  and 
degeneration  of,  579;  biliary  and  hyper- 
trophic cirrhosis  of,  562;  cancer  of,  572; 
circulatory  disturbances  in,  578;  cirrhosis  of, 
555;  haemorrhages  in,  564;  primary  hyper- 
trophic cirrhosis,  563;  prognosis,  564;  sec- 
ondary, 562;  splenic  tumor  in,  563. 

Liver,  circulatory  disturbances  in,  578. 

Liver,  congestion  of,  578;  echinococcus  of, 
575-577;  fatty.  580;  hypertrophic  and  biliary 
cirrhosis  of,  562;  in  diabetes  mellitus,  760; 
in  heart  disease,  330;  in  pleurisy,  286. 

Liver,  secondary  cirrhosis  of,  562;  syphilis  of, 
571;  waxy,  580. 

Lobar     pneumonia.      See     Ckoupous     Pneu- 

ilOXIA. 

Lobular  atelectasis,  233. 

Localization  of  cerebral  diseases,  1068; 
anatomical  changes  occurring  in  aphasia, 
1081;  aphasia  and  allied  conditions,  1077; 
central  ganglia  and  optic  thalamus,  1084; 
centers  and  disturbances  of  speech,  1077; 
centrum  ovale,  1083;  cerebellum,  1086;  cor- 
pora quadrigemina  and  crura  cerebri,  1085; 
course  of  conducting  tracts,  1089;  frontal 
convolutions,  1074;  Jactsonian,  partial  or 
cortical  epilepsy,  1072;  motor  region  of 
cortex  cerebri,  1069:  occipital  convolutions, 
1075;  parietal  convolutions,  1075;  soul  blind- 
ness and  deafness,  1076;  temporal  convolu- 
tions, 1076. 

Localization,  spinal,  920;  reflexes  in,  927. 

Lock-jaw.    See  Tetaxus. 

Locomotor  ataxia.    See  Tabes  Does.u^is. 

Lower  extremity,  paralyses  of.  871. 

Ludwig's  angina,  392. 

Lumbago,  696. 

Lumbar  puncture,  in  acute  miliary  tubercu- 
losis, 265;  in  cerebro-spinal  meningitis,  115; 
in  chronic  hydrocephalus,  1138. 

Lumbo-abdominal  neuralgia.  816. 

Lung  fever.    See  Pneumonia,  CROfPOus. 

Lungs,  atelectasis  of,  195;  setiology  of,  195; 
baths  in,  197;  in  kyphoscoliosis,  196;  in 
the  new-born,  195;  symptoms,  196;  treat- 
ment, 197. 

Lungs,  brown  induration  of,  275;  cancer  of, 
276;  echinococcus  of,  276. 

Lungs,  emphysema  of,  187;  alveolar  ectasis, 
190;  complications,  194;  diagnosis,  prog- 
nosis, and  treatment,  194:  dropsy  in.  191: 
dyspnoea    in,    190;    expiratory    pressure    in. 


193;  nature  and  setiology  of,  187;  other  symp- 
toms in  lungs  and  other  organs,  193:  patho- 
logical anatomy,  189;  physical  examination^ 
191;  symptoms  and  course,  190. 

Lungs,  malignant  lymphosarcoma  of,  278. 

Lungs,  oedema  of,  197;  setiology  and  general 
pathology  of,  197;  dyspnoea  in,  198;  from 
paralysis  of  left  ventricle,  198;  rEles  in,  198; 
symptoms  and  treatment,  198. 

Lungs  of  heart  disease,  see  Brown  Indura- 
tion; sarcoma  in,  277;  syphilis  of,  276-279; 
tumors  of,  276. 

Lupus,  tubercular,  229,  251. 

Lymph  glands,  in  scrofula,  787;  swollen,  in 
glossitis,  388;  swollen,  in  pulmonary  cancer, 
278:  swollen,  in  stomatitis,  384;  swollen,  in 
tuberculosis,  230,  236,  250;  tumors  of,  734. 

Lymph,  stasis  of,  in  vertebral  caries,  936. 

Lymphatic  leuksemia,   728. 

Lymphoma       and        lymphosarcoma.  See 

PSEUDO-LEUKiEMIA. 

Lymphosarcoma,  malignant,  of  the  lungs,  278. 
Lyssa.    See  Hydrophobia. 

Maculae  tendinse,   in  pericarditis,   360. 

Magnesium  borocitrate  in  nephrolithiasis,  661. 

Malaria,  93;  setiology  and  pathological 
anatomy  of,  93;  blood  in,  94;  cardiac  disturb- 
ances in,  98;  cinchonism,  102:  chronic- 
malarial  cachexia,  99;  collections  of  pig- 
ment in  viscera,  95;  diagnosis  and  treatment, 
100;  dropsy  in,  99;  epistaxis  in,  99;  geo- 
graphical distribution  of,  93;  intermit- 
tent fever,  96:  in  animals.  95:  jaundice  in. 
98,  99:  manner  of  communication,  95; 
masked  intermittent.  99;  non-contagious,  93; 
periodicity,  98;  pernicious  intermittent 
fever,  98;  Plasmodium  malarise,  94,  95; 
quinine  in,  97,  100:  remittent  forms,  99; 
skin  in,  98;  spleen  in,  95,  98;  temperature- 
curve  of,  96;  time  of  incubation,  96:  typho- 
malarial  fever,   100. 

Male  fern  for  tape-worm,  513,  516. 

Malignant  pustule.   127.     See  Anthrax. 

Malleine  in  glanders,  127. 

Malum  cotunnii.    See  Sciatica. 

Marasmus,   predisposing  to   erysipelas,   64. 

Massage  in  arthritis  deformans,  693;  in  ar- 
ticular rheumatism,  686;  in  cardiac  hyper- 
trophy, 350;  in  muscular  rheumatism,  697; 
in  sciatica,  820;  of  paralyzed  limbs,   1102. 

Mastodynia,  816. 

Measles.  48;  acquired  resistance  to,  48:  black, 
50;  catarrhal  pneumonia  in,  202;  clinical  his- 
tory, 49;  complications  of,  50:  contagious- 
ness of.  48:  diagnosis  and  prognosis  of.  52; 
desquamation  in,  49;  epidemic  nature  of,  48: 
eruption  of.  49;  fever  in,  50:  hsemorrhagie, 
50;  initial  stage,  49;  inoculation  of,  49;  in- 
testinal symptoms,  51;  noma  in,  51;  pe- 
culiarities in  the  course  of,  51;  temperature 
curve  in.  49:  treatment  of.  .52. 

Measles,   German.  53.    See  Rotheln. 

Meat  juice  and  meat  peptones  in  typhoid,  24. 

Meat,   poisoning  from,   1213. 

Median  paralysis,  S68. 

Mediastiuo-pericarditis,  363. 

Mediastinum,  tumors  of,  301;  diagnosis,  prog- 


DTDEX 


1231 


nosis,  and  treatment,  302;  dyspnoea  of,  301; 
vascular  stasis  in,  301. 

Medulla,  compression  of,  1052. 

Megaloblasts  in  blood,  724. 

Megrim.     See  Migeaixe. 

Melanine  in  malarial  diseases,  94. 

Membranous  enteritis,  474;  course  and  treat- 
ment of,  475. 

Meniere's  disease,  1139. 

Meninges,  spinal,  tisemorrliage  into,  919. 

Meningitis,  basal  gummatous,  1127;  basilar, 
see  Tubercular  Meningitis. 

Meningitis,  epidemic  cerebrospinal,  111;  aeti- 
ology of.  111;  cerebral  symptoms,  113;  clini- 
cal history,  112;  contagiousness,  111;  diag- 
nosis, 115;  diplococci  of.  111;  fever  in, 
114;  herpes  labialis  in,  114;  infection, 
111;  in  animals,  112;  lumbar  puncture 
in,  115;  mortality  in,  116;  pathological 
anatomy,  112;  prodromata,  112;  prognosis 
and  treatment,  116;  reflexes,  114;  secondary, 
116;  sequelae,  115;  tinnitus  aurium,  113; 
urine  in,  114. 

Meningitis,  puruleut,  1055;  aetiology,  1055; 
clinical  history,  1057;  diagnosis,  1058;  fever 
in,  1058;  pathology,  1056;  prognosis  and 
treatment,  1059. 

Meningitis,  spinal  chronic  gummatous,  1027; 
secondary,  116. 

Meningitis,  tubercular,  1059;  aetiology  of,  1059; 
delirium  in,  1061;  diagnosis,  1063;  eyes  in, 
1061;  in  children,  1062;  pathology  and  clini- 
cal history,  1060;  prodromata,  1061;  pulse 
and  temperature  in,  1062;  relation  to 
phthisis,  1059;  treatment,  1064. 

Meningocele.    See  Spina  Bifida. 

Menstruation,  in  chlorosis,  715;  in  epilepsy, 
1146;  vicarious,  139. 

Mental  disturbances,  in  anaemia,  712;  in 
athetosis,  1162;  in  articular  rheumatism, 
681;  in  cerebellar  abscess,  1108;  in  cerebral 
embolism,  1105;  in  cerebral  haemorrhage, 
1101;  in  cerebral  syphilis,  1127;  in  cerebro- 
spinal meningitis,  113;  in  cholaemia,  569;  in 
cholera,  88;  in  chorea,  1154;  in  convulsions, 
123,  1120,  1188;  in  epilepsy,  1141,  1145;  in 
general  paralysis  of  insane,  1131;  in  haema- 
toma  of  dura  mater,  1054;  in  heart  disease, 
332;  in  hydrocephalus,  1138;  in  hysteria, 
1181;  in  infantile  paralysis,  1115;  in  neu- 
rasthenia, 1194;  in  neuralgia,  822;  in  peri- 
tonitis, 526;  in  poliomyelitis,  1016;  in  syn- 
cope, 1067;  in  tuberculosis,  263;  in  typhoid, 
15. 

Mercurial  tremor,  836,  1208. 

Mercury,  in  hepatic  syphilis,  572;  in  intestinal 
obstruction,  507;  in  myelitis,  592:  in  general 
paralysis,  1136;  in  peritonitis,  532;  poison- 
ing, 1208;  in  syphilis,  1029,  1129;  in  tuber- 
cular meningitis,  1064. 

Metallic  sound,  in  pericarditis,  360:  in  pneu- 
mothorax, 297. 

Metallotherapy  in  hysteria,  1191. 

Metatarsalgia,  821. 

Methyl-chloride  spray,  in  intercostal  neu- 
ralgia, 816:  in  sciatica,  819. 

Metrorrhagia  in  phosphorus  poisoning,  1209. 

Microcytes  in  the  blood,  448,  724. 


Migraine,  905;  aetiology  of,  905;  diagnosis  and 
treatment,  907;  hereditary  influence,  905; 
prodromata,  906;  relation  to  eye-strain,  905; 
relation  to  gastroxynsis,  459;  symptoma- 
tology of,  906. 

Miliaria  in  typhoid,  18. 

Miliary  tuberculosis,  261. 

Milk-cure  in  acute  nephritis,  615. 

Millar's  asthma.    See  Spasm  of  the  Glottis. 

Mitral  insufficiency,  311;  stenosis,  312. 

Mogigraphia,  882. 

Monophasia,  1079. 

Monoplegia,  831. 

Moore's  test  for  sugar,  753. 

Morbilli.    See  Measles. 

Morbus  maculosus  Werlhofi.    See  Purpura. 

Morbus  sacer.    See  Epilepsy. 

Morel  poisoning.    See  Mushroom  Poisoning. 

Morphine,  in  cerebro-spinal  meningitis,  116; 
in  croupous  pneumonia,  223;  in  heart  dis- 
ease, 339;  in  neuralgia,  809;  poisoning,  1211. 

Morvan's  disease,  1031. 

Mosquitoes,  relation  to  chyluria,  648;  relation 
to  malarial  diseases,  95;  relation  to  yellow 
fever,  104. 

Motility,  disturbances  of,  829. 

Motor  ataxia  in  polyneuritis,  890. 

Motor  disturbances  of  the  stomach,  460;  effi- 
ciency of  the  stomach,  461. 

Motor  region  of  cortex  cerebri,  1069;  diseases 
in,  1072. 

Motor  tabes,  1007. 

Motor  tract,  primary  degeneration  of,  985. 

Mucous  colic,  474;  haemorrhoids,  494. 

Muguet.    See  Thrush. 

Multiple  sclerosis  of  brain  and  spinal  cord, 
954;  aetiology  and  pathology,  954;  ataxia  and 
tremors  in,  955;  clinical  history  of,  955; 
diagnosis,  958;  prognosis  and  treatment,  959; 
pseudo-scleroses,  959;  reflexes  in,  956;  un- 
usual forms  of,  958. 

Mumps.    See  Parotitis. 

Murmurs,  anaemic,  713,  715,  723,  731;  cardiac, 
325,   362. 

Muscle  changes  in  typhoid,  19. 

Muscles  of  head  and  trunk,  851. 

Muscles  of  mastication,  paralysis  of,  858. 

Muscular  atrophy  in  progressive  bulbar 
paralysis,   1040. 

Muscular  atrophy,   neurotic,  99. 

Muscular  atrophy  of  small  muscles  of  hand, 
992. 

Muscular  atrophy,  spinal  progressive,  990; 
aetiology  and  clinical  history,  992;  atrophy 
of  small  muscles  of  the  hand  in,  992;  cu- 
taneous sensibility  in,  995;  diagnosis,  995; 
duration.  994:  electrical  excitability  of 
muscles  in,  994;  hereditary  and  generic  influ- 
ences, 992;  preliminary  remarks  and  patho- 
logical anatomy,  990;  prognosis  and  treat- 
ment, 966;  reflexes  in,  995;  respiratory  dis- 
turbances, 994. 

Muscular  dystrophy,   progressive,  998. 

Muscular  sense,  794,  1176. 

Mushroom  poisoning,   1212. 

Mussels,  poisoning  from,  1212. 

Mutism,  hysterical,  1178. 

Myalgia.    See  Muscular  Rheumatism. 


1232 


INDEX 


Myasthenia,  pseudo-paralytic,  1046. 

Mycosis,  intestinal,  129. 

.Myelitis,  acute  and  chronic,  943;  ataxia  in, 
947;  baths  in,  952;  cervical,  dorsal,  and  lum- 
bar forms  of,  950;  definition  and  aetiology  of, 
943;  diagnosis,  951;  disturbances  of  bladder 
and  rectum,  949;  disturbances  of  sensibility 
in,  987;  individual  symptoms  of,  946;  infec- 
ition,  944;  motor  irritation  in,  946;  motor 
paralysis  in,  946;  pathological  anatomy,  944; 
reflexes  in,  948;  relation  to  syphilis,  943; 
treatment,  952;  trophic  disturbances,  949. 

Myelitis,  acute  bulbar,  1051. 

Myelitis,  diffuse,  943;  syphilitic,  1028;  trans- 
verse, 943. 

Myelocele.    See  Spina  Bifida. 

Myelocytes,  730. 

Myocarditic  nodules,  329. 

:Myocarditis,  interstitial,  340;  aetiology  and 
pathological  anatomy  of,  .340;  angina  pec- 
toris, 343;  apoplectiform  paralysis,  343; 
arterio-sclerosis  in,  341;  cardiac  aneurism, 
:341;  clinical  history,  342;  diagnosis,  prog- 
nosis, and  treatment,  .344;  diet,  344;  hyper- 
trophy of  heart  in,  341;  pulse,  342;  syph- 
ilitic endocarditis,  341. 

Myocardium,  primary  v^eakness  of,  351; 
effect  of  alcoholism  in,  352;  prognosis  and 
treatment,  353;  pulse  in,  352. 

Myoclonia,  1157. 

Myokymia  in  sciatica,  818. 

Myopathic  muscular  atrophy,  998;  diagnosis 
of,  1006. 

Myositis.    See  Muscular  Rheumatism. 

Myositis  in  trichinosis,  132. 

Myotonia,    congenital,   1169. 

Myxoedema,  901. 

Myxedematous  infantilism,  902. 

Myxomata  of  larynx,  155. 

Nails,  curved,  in  heart  disease,  324;  loss  of,  in 
typhoid,  19. 

Narcotics  in  cholelithiasis,  551. 

Nasal  catarrh,  135,  137;  in  measles,  49. 

Nasal  catarrh,   acute,  1.36;  chronic,   137. 

Nephritic  oedema,  596. 

Nephritis,  acute,  603;  aetiology,  603;  alco- 
holic nephritis,  606;  anuria  in,  609;  baths 
in,  615;  casts,  609;  clinical  history,  60S; 
course  and  different  forms  of,  612;  diag- 
nosis, 613;  diuretics  in,  616;  dropsy  in,  611, 
617;  milk  cure,  615;  oedema  in,  610;  patho- 
logical anatomy,  606;  in  pregnancy,  606,  613; 
primary  idiopathic  form,  612;  prognosis,  614; 
prophylaxis,  614;  relation  to  scarlet  fever, 
604;  relation  to  small-pox,  604;  relation  to 
cholera,  604;  relation  to  erysipelas,  605; 
symptoms,  610;  toxic  nephritis,  605;  treat- 
ment, 614;  ui-aemia  in,  617;  urine  in,  608; 
vomiting  in,  611. 

Nephritis,  alcoholic,  606,  613:  choleraic,  89. 

Nephritis,  chronic  and  subchronic,  618;  aeti- 
ology of,  618;  cardiac  hypertrophy,  621; 
clinical  history,  621;  course,  duration,  and 
termination  of,  623:  diagnosis,  622;  different 
forms  of,  622;  dropsy  in,  622;  hsemorrhagic 
form,  619;  inflammatory  fatty  kidney,  620; 
oedema  in,   621;   pathological  anatomy,    619; 


retinitis  in,  622,  632;  secondary  contracted 
kidney,  620;  treatment,  624;  urine  in,  621. 
Nephritis,  chronic  interstitial,  625;  erysipel- 
atous, 66;  in  croupous  pneumonia,  215;  in 
diphtheria,  72;  in  gout,  776;  in  hyper- 
trophy of  the  heart,  348;  in  influenza,  79; 
in  scarlet  fever,  43;  in  septic  and  pysemie 
diseases,  119;  in  typhoid  (nephro-typhoid), 
19;  of  pregnancy,  606,  613;  primary  idio- 
pathic, 612. 
Nephritis  and  perinephritis,  purulent,  640; 
abscesses  in,  641;  aetiology  of,  640;  bac- 
teria in,  640;  clinical  symptoms,  641;  diag- 
nosis and  treatment,  642;  fever  in,  642;  in- 
fection, 640;  pathology,  640. 
Nephritis,    toxic,    605;    tubercular,    250;    with 

arterio-sclerosis,  370. 
Nephrolithiasis,    657;    anatomical   changes   in, 
658;    clinical   symptoms,    659;   colic   in,    659- 
662;  diagnosis,  660;  diet  in,  661;  occurrence, 
chemical  composition,  and  aetiology  of  renal 
concretions,    657;   predisposing   causes,    658; 
sequelae,  659;  treatment,  661;  urine  in,  659. 
Nephrophthisis,  663. 
Nephro-typhoid,  19. 
Nerve-stretching,    in   sciatica,    820;   in   tabes, 

980. 
Nervous  debility.    See  Neurasthenia. 
Nervous  dyspepsia,  463  (see  also  1181);  diag- 
nosis,   465;    nervous    symptoms,    465;    prog- 
nosis,   466;    psychical    influence,    464;   treat- 
ment, 465. 
Nervous  fever,  15. 

Nervous  palpitation  of  the  heart,  356. 
Nervousness.    See  Neurasthenia. 
Neuralgia,    aetiology    of,    804;    articular,    821; 
cardiac,   355;   cervico-brachial,   814;  of  geni- 
tals,   820;    infection,    805;    intercostal,    815; 
ischiatic,    817;    of    lumbar    plexus,    816;    in 
malarial   diseases,    99;    of   mammary   gland, 
816. 
Neuralgia,     occipital,     813;    of    rectum,     820; 
symptomatology,  806;  treatment,  807;  in  ty- 
phoid, 17. 
Neuralgia  of  the  trigeminus,  810;  aetiology  of, 
810;    diagnosis,    prognosis,    and    treatment, 
812;  symptoms  and  course  of,  811. 
Neurasthenia,     1193;    aetiology,    1193;    agora- 
phobia in,  1194;  asthenopia  in,  1195;  concept 
of  the  disease,  1193;  congenital  factors,  1193; 
diagnosis,    1198;    general    course    and    prog- 
nosis, 1197;  insomnia  in,  1200;  mental  symp- 
toms,     1194;      physical      symptoms,      1195; 
psychical    factors    in,    1198;    sexual,    1197; 
treatment,  1198;  urine  in,  1196. 
Neurasthenia,   gastric,   see  Nervous  Dyspep- 
sia; spinal,  933. 
Neuritis,  degenerative,  885;  diabetic,  887;  en- 
demic, 985. 
Neuritis,    multiple,    886    (see    also    Endemic); 
acute  curable  form,  892;  alcoholic  form  of, 
889;  ataxic  form  of,  892;  diabetic,  887:  diag- 
nosis, prognosis,  and  treatment,  892;  distri- 
bution of,  891;  mental  disturbances  in,  894; 
motor  ataxia  in,  890:  pathological  anatomy 
of,   888;  primary,  acute,  and  ^hronic  forms, 
890;    symptoms    and    course   of,    890;    toxic, 
887. 


II^DEX 


1233 


Neuritis,  multiple  bulbar,  1051;  optic,  1118; 
primary,  secondary,  and  simple,  885. 

Neuro-fibromata,  897. 

Neuroma,  multiple,  896. 

Neuroses,  articular,  821;  cardiac,  355. 

Neuroses  of  the  cesophagus,  414;  globus  hys- 
tericus, 415;  paralysis  of  the  oesophagus, 
415;  spasm  of  the  oesophagus,  414;  ulcera- 
tion in,  415. 

Neuroses,  professional,  882;  traumatic,  1201; 
vaso-motor  and  trophic,  898;  without  known 
anatomical  basis,  1141. 

Neurotic  muscular  atrophy,  996;  fibrillary  con- 
tractions in,  997. 

New  growths  in  the  larynx,  155;  benignant, 
155;  carcinoma  of,  155;  fibroma,  155;  laryn- 
geal cysts,  155;  laryngeal  polypi,  155;  lipo- 
mata  of,  155;  malignant,  155;  myxoma  of, 
155;  papilloma,  155;  treatment,  156;  tumors 
of,  155. 

New  growths  in  the  peripheral  nerves,  896. 

New  growths  of  the  pleura,  300;  endothelial 
carcinoma  of,  300;  prognosis,  301. 

New  growths  of  the  spinal  cord,  1024;  patho- 
logical anatomy  of,  1024;  symptoms  and 
course,  1025. 

Nicotine  poisoning,  1211. 

Nicotine  tabes,  978. 

Nitrate  of  silver  in  chronic  gastritis,  431. 

Nitrobenzine  poisoning,  1210. 

Nitroglycerine  in  heart  disease,  356. 

Nitrous  acid  fumes,  1206. 

Nocturnal  incontinence  of  urine.  See  Enure- 
sis   NOCTURNA. 

Nodular  sclerosis.    See  Multiple  Sclerosis. 

Noma,  389;  fever  in,  389;  prognosis  and  treat- 
ment, 390. 

Noma  in  measles,  51. 

Normoblasts  in  blood,   724. 

Nosebleed,  139. 

Nutmeg  liver,  578. 

Obesity,  779;  alcoholic  beverages  in,  781;  baths 
in,  786;  cardiac  disturbance  in,  782;  defini- 
tion and  aetiology,  779;  dyspnoea  in,  782; 
intertrigo  in,  782;  muscular  exercise  in,  786; 
pathology  of,  782;  treatment,  784. 

Obturator  nerve,  paralysis  of,  872. 

Occipital  neuralgia,  813. 

Occupation  paralyses,  870. 

Ocular  muscles,  paralyses  of,  854;  in  cerebral 
lesions,  1085;  in  diphtheria,  72;  in  purulent 
meningitis,  10.57;  in  tabes,  972;  in  tumors  of 
the  brain,   1128. 

Oildema,  in  valvular  heart  disease,  330;  acute 
angioneurotic,  900;  in  plague,  109;  in  trichi- 
nosis, 133;  in  typhoid,  18:  nephritic,  596,  610, 
621. 

(Edema  of  the  glottis,  146. 

03dema,  pulmonary,  197. 

Oilsophagismus,  414. 

CEsophagitis,   corrosive,  405;  purulent,  405. 

(Esophagus,  cancer  of,  412. 

(Esophagus,  dilatation  of,  406;  aetiology  and 
pathology  of,  406;  clinical  history,  407;  dif- 
fuse dilatation,  406;  diverticula,  406;  maras- 
mus in,  408;  symptoms,  406;  treatment,  408; 
ulceration  in,  408. 
78 


(Esophagus,  disease  of,  404. 

(Esophagus,  inflammation  of,  404;  aetiology 
and  pathology  of,  404;  corrosive  and  puru- 
lent oesophagitis,  405;  symptoms  and  treat- 
ment, 405;  ulcers  in,  405. 

(Esophagus,  neuroses  of,  414;  paralysis  of, 
415;  rupture  of,  414;  spasm  of,  414;  stenosis 
of,  409. 

Oleoresina  aspidii  for  intestinal  parasites,  513. 

Oligocythaemia,  512-518. 

Oliguria  in  cholera,  89. 

Omalgia  in  muscular  rheumatism,  695. 

Ophthalmoplegia,  progressive,  1045. 

Opisthotonos  in  tetanus,  1166. 

Opium,  in  acute  peritonitis,  528;  in  diabetes 
mellitus,  766;  in  dysentery,  84;  in  intestinal 
catarrh,  473;  in  intestinal  obstruction,  507; 
in  perityphlitis,  486;  in  tuberculosis  of 
the  intestine,  490;  in  typhoid,  27;  poison- 
ing, see  Morphine. 

Optic  atrophy,  in  chronic  hydrocephalus,  1138; 
in  diabetes,  757;  in  general  paralysis  of  the 
insane,  1133;  in  multiple  sclerosis,  957;  in 
tabes,  972. 

Optic  neuritis,  cerebral  tumors,  1118;  in  puru- 
lent meningitis,  1058. 

Optic  tract,  1089. 

Orchitis,  in  parotitis,  391;  in  typhoid,  20. 

Organo-therapy,  in  acromegaly,  903;  in  Addi- 
son's disease,  653;  in  myxcBdema,  901. 

Orthopnoea  in  pleurisy,  286. 

Osteomalacia,  704;  aetiology  and  pathology, 
704;  clinical  history,  705;  diagnosis  and 
treatment,  707;  ovariotomy  in,  707;  relation 
to  pregnancy  and  menstruation,  705. 

Osteomyelitis  in  septic  and  pyaemic  diseases, 
117-120. 

Otitic  abscess  of  the  brain,  1110. 

Otitis,  in  influenza,  79;  in  measles,  51;  in 
scarlet  fever,  40;  in  typhoid,  13;  in  typhus, 
33. 

Ovaries  in  osteomalacia,  705. 

Oxalic-acid  poisoning,  1206. 

Oxybutyric  acid  in  diabetes  mellitus,  754. 

Oxygen  in  pernicious  anaemia,  726. 

Oxyuris  vermicularis.  See  Intestinal  Para- 
sites. 

Ozaena,  137,  138. 

Pachydermia  laryngis,  143. 

Pachymeningitis  cervicalis  hypertrophica,  918; 
interna  haemorrhagica,  1053;  spinal,  915,  916, 
919. 

Pain,  in  chorea,  1154;  in  hysteria,  1178;  paraly- 
sis agitans,  1159;  rheumatoid,  in  paralysis  of 
the  insane,  1131. 

Pain,  sense  of,  793. 

Pains  of  tabes  dorsalis,  965. 

Palisade-worm,  647. 

Palpitation  in  valvular  heart  disease,  327. 

Pancreas,  diseases  of,  585;  atrophy  of,  585; 
calculi,  587;  cancer,  586;  cysts,  586;  diag- 
nosis, 586;  glycosuria  in,  586;  haemorrhages 
into,  .585;  prognosis,  587;  vomiting  in.  585. 

Pancreatitis,  585. 

Papilloma  of  the  bladder,  672. 

Papilloma  of  larynx,  155. 

Paradoxical  contraction,  842. 


1234 


IKDEX 


Paralj-sis,  829;  aetiology  of,  832;  acute  bulbar 
1048;  of  arm  muscles,  869;  arsenical,  875 
ascending  spinal,  1021;  asthenic  bulbar,  1046 
of  back  and  abdomen,  865;  Bell's,  858 
Brown-S§quard's,  1036;  bulbar,  1049;  cere- 
bral infantile,  1111;  classiflcation  of,  829;  of 
diaphragm,  871;  diphtheritic,  72;  electrical 
reactions  in,  842;  facial,  858;  family  periodic, 
1047;  flaccid,  834;  general,  1127;  gluteal,  872; 
hysterical,  1178;  in  hydrophobia,  122;  Lan- 
dry's, 1021;  lead,  873,  1208;  of  leg  muscles, 
871;  median,  868;  musculo-spiral,  866;  ob- 
stetrical, 869;  obturator,  872;  occupation, 
870;  peripheral,  854;  peroneal,  872;  radial, 
866;  reflex,  833;  sciatic,  872;  of  shoulder,  863; 
spastic,  1007;  spinal  infantile,  1014;  syph- 
ilitic spinal,  1028;  of  tibialis,  873;  toxic,  832; 
trigeminal,  858;  in  typhoid,  17;  ulnar,  868; 
vaso-motor,  898. 

Paralysis  agitans,  1157;  aetiology  and  clinical 
history,  1157;  diagnosis  and  treatment,  1160; 
nature  of  the  disease,  1160;  propulsion  and 
retropulsion  in,  1159;  temperature  in,  1159; 
voice  in,  1159. 

Paralysis,  laryngeal,  150;  of  arytaenoideus, 
152;  of  crico-arytaenoid,  153;  of  dilators  of 
the  glottis,  151;  prognosis,  152;  of  recurrent 
laryngeal,  151;  of  superior  laryngeal,  150;  of 
thyro-arytaenoid,  152;  treatment,  153. 

Paralysis,  ocular,  854;  of  abducens,  856;  aeti- 
ology of,  854;  of  oculo-motor,  856:  recurrent, 
857;  strabismus  in,  855;  trochlear,  856. 

Paralytic  dementia,  1129. 

Paramyoclonus,  1157. 

Paranephritic  abscess,  641. 

Paraphasia,  1079. 

Paraplegia,  831;  in  acute  ascending  spinal 
paralysis,  1022:  ataxic,  1011;  congenital 
spastic,  1012;  in  hydrocephalus,  1138;  in 
myelitis,  946. 

Parasites,  intestinal,  508. 

Paretic  dementia,  1129. 

Parkinson's  disease.    See  Pahalysis  Agitans. 

Parotitis,  390;  clinical  history,  390;  complica- 
tions, 391;  idiopathic,  390;  infection,  390 
secondary  suppurative  form  of,   391. 

Parotitis,  in  scarlet  fever,  42;  in  typhoid,  13 
in  typhus,  33;  in  secondary  suppurative,  391 

Parry's  disease.    See  Exophthalmic  Goitre 

Pedatrophy,  479.  See  also  Intestinal 
Cataerh  of  Children. 

Peliosis.    See   Purpura. 

Pelvis,  deformed,  in  osteomalacia,  706. 

Peptonuria  in  croupous  pneumonia,  215. 

Percussion,  in  acute  peritonitis,  524;  in 
ascites,  533;  in  pulmonary  emphysema,  192; 
in  tuberculosis,  245. 

Pericarditis,  359  (see  also  329);  adhesive  peri- 
carditis, 364;  aetiology  of,  359:  clinical  symp- 
toms, 860;  course,  367;  diagnosis,  366; 
dyspnoea  in,  361;  effusion  of,  360;  explora- 
tory puncture  in,  367;  fever  in,  361;  friction 
in,  362,  366;  haemorrhagic,  360;  maculae 
tendinae,  360;  mediastino-pericarditis,  363; 
obliteration  of  the  pericardial  cavity,  364; 
pathological  anatomy,  360;  percussion  reso- 
nance in,  362;  pericardial  friction  rub,  362, 
366;  pericarditis  externa,  363;  physical  signs, 


361;  pleuro-pericarditis,  363;  prognosis,  367; 
pseudo-cirrhosis  of  liver  in,  365;  pulse,  361; 
pulsus  paradoxus,  363;  relation  to  articular 
rheumatism,  359-367;  relation  to  tubercu- 
losis, 359;  sequelae,  363;  special  forms  of, 
363;  treatment,  367;  tubercular  pericarditis,, 
365. 

Pericarditis,  purulent,  360. 

Pericarditis,  rheumatic,  679. 

Pericardium,  diseases  of,  359. 

Perinephritis,  640. 

Periodic  family  paralysis,  1047. 

Peripheral  nerves,  new  growths  in,  896. 

Peripleuritis,  295. 

Peritoneal  tuberculosis,  249. 

Peritoneum,  cancer  of,  535;  colloid  cancer  of,^ 
536;  miliary  cancer  of,  535. 

Peritonitis,  acute,  .520;  abscesses  in,  527;  aeti- 
ology  of,  520;  bacteria  in,  520;  circum- 
scribed, 526;  clinical  history,  523;  diagnosis, 
527;  infection,  520;  pathology  of,  521;  per- 
cussion in,  524;  pulse  in,  525;  rheumatic,  521; 
symptoms,  523;  treatment,  528:  ulceration, 
.522;  vomiting  in,  525. 

Peritonitis,  chronic  and  tubercular,  529;  aeti- 
ology of,  529;  clinical  history,  530;  defor- 
mans, 530;  diagnosis,  530;  fever  in,  531;  in 
children,  531;  palpation  in,  530;  pathology, 
529;  treatment,  532;  tubercles,  530. 

Peritonitis,  from  gastric  ulcer,  438;  from 
typhlitis  and  perityphlitis,  485;  in  relapsing 
fever,  37;  in  typhoid,  12;  tubercular,  249, 
530, 

Perityphlitis,  482. 

Pernicious  anaemia,  710. 

Pernicious  intermittent  fever.  See  Malarial 
Diseases. 

Peroneal'  paralysis,  872. 

Perturbatio  critica.  32,  217;  in  relapsing  fever, 
35. 

Pertussis,  see  Whooping-cough;  after 
measles,  52. 

Pestis  minor.    See  Plague. 

Petechiae,  in  plague.  110:  in  typhoid,  18;  in 
typhus,  32. 

Petit  mal,  1144. 

Peyer's  patches,  in  cholera,  90;  in  typhoid,  9. 

Phalanges,  terminal,  thickened,  in  bronchi- 
ectasis, 179;  in  heart  disease,  324. 

Pharyngeal  diphtheria,  68. 

Pharyngitis,  chronic,  400:  aetiology  of,  400; 
adenoid  growths  in  pharynx,  401;  anatom- 
ical changes  in,  400;  catarrh  of  the  naso- 
pharynx, 400;  hypertrophic  catarrh  in- 
pharynx,  401;  posterior  nasal  catarrh,  400; 
prognosis  and  treatment,  402;  sicca,  401; 
symptoms  and  variations  of,  400. 

Phenacetine,  in  neuritis.  892:  in  typhoid,  27. 

Phimosis  in  diabetes  mellitus,  757. 

Phlegmon  in  small-pox,  58. 

Phloridzine-glycosuria,  749. 

Phosphorus,  in  osteomalacia.  707;  in  rachitis, 
704. 

Phosphorus  poisoning,  1209;  diagnosis  from- 
acute  yellow  atrophy  of  liver,  568. 

Physostigmine  in  paralysis  agitans,  1160. 

Picro-nitrate  of  potassium  in  chyluria,  648. 

Pigment  in  the  lungs,  271. 


i:^DEX 


1235 


Pilocarpine  hydrochlorate  in  acute  nephritis, 
616. 

Pin-worms.    See  Intestinal  Parasites. 

Piperine  in  leukfemia,  733. 

Plague,  107;  adenitis  in,  109;  antitosine  of, 
111;  bacillus  pestis  bubonicse,  107;  conA'ul- 
sions  in,  109;  course  and  symptoms,  108; 
diagnosis,  prognosis,  and  treatment,  110; 
disinfection,  108;  flltli,  relation  to,  108;  gan- 
grene, 109;  hsemorrliages,  109;  headache 
in,  108;  history  in  distribution,  107;  im- 
munity, 111;  incubation,  108;  infection,  108; 
inguinal  adenitis  in,  108;  inoculation,  108; 
in  animals,  107;  mortality,  110;  in  different 
races,  108;  pestis  minor,  110;  pulse  and  tem- 
perature in,  108;  therapeutic  measures.  111; 
urine,  109. 

Plasmodium  malarise,  94,  95. 

Pleura,  diseases  of,  279;  after  emphysema, 
283;  cicatricial  contractions  of,  282;  new 
growths  of,  300. 

Pleurisy,  279;  absorption  of  effusion,  288; 
adhesions,  285;  aetiology,  279;  aspiration 
in,  293;  auscultation,  285;  complications, 
^288;  cough  and  expectoration,  283;  course  of 
the  disease,  283;  diagnosis,  290;  diplococci 
in,  280;  diuretics  in,  292;  dyspnoea  in,  283, 
293;  emphysema,  290;  exploratory  puncture, 
291;  fever  in,  284,  289;  flbrine  in,  281;  fibri- 
nous, 2S5;  haemorrhages  in,  281;  infection, 
281;  inflammation,  280;  orthopnosa  in,  286; 
pathological  anatomy  of,  281;  percussion, 
285;  pleuritic  contraction,  288;  pleuritic 
effusion,  285;  pneumothorax,  290:  primary 
rheumatic,  288;  prognosis,  291;  purulent,  281, 
284,  290;  resonance,  tympanitic,  etc.,  285; 
sicca,  285;  symptoms,  283;  temperature 
curve,  293;  treatment,  291;  tubercular,  280, 
289;  urine  in,  284;  various  forms  of,  288; 
vocal  fremitus  in,  290. 

Pleurisy  in  influenza,  79;  sanious,  from  pul- 
monary gangrene,  268;  tubercular,  289. 

Pleuritis.     See  Pleurisy. 

Pleuro-pericarditis,   363. 

Pleuropneumonia.  See  Pneumonia,  Croup- 
ous. 

Pneumatic  treatment  of  pulmonary  emphy- 
sema, 195. 

Pneumatosis  pulmonum.  See  Pulmon.\ry 
Emphysema. 

Pneumonia  alba,  279;  asthenic,  220;  bilious, 
210. 

Pneumonia,  catarrhal,  199  (see  also  60);  aeti- 
ology of,  199;  bacteria  in,  200;  in  childhood, 
202;  expectoration,  201;  fever,  201;  in  in- 
fluenza. 79;  origin  of,  199;  pathological 
anatomy,  201;  pulse  in,  202;  relation  to  lobu- 
lar, 200;  respiration,  202;  secondary  catar- 
rhal, 202;  symptoms  of  primary  catarrhal, 
of  adults,  201;  treatment  and  prophylaxis, 
203;  tuberculosis  in,  203. 

Pneumonia,  croupous,  204;  aetiology  of,  205; 
alcohol  in,  225;  asthmatic,  220;  ausculta- 
tory signs,  211;  baths  in,  224;  blood  in, 
213;  cardiac  complications  in,  214,  222, 
224;  casts  of  bronchi  in,  210;  central,  219; 
cholesterine  crystals  in,  222;  circulatory  ap- 
l>ai'atus   in,    213;    course   of   the   fevei-.   216; 


crisis  in,  218;  delayed  resolution  of,  220; 
delirium,  215;  diagnosis,  222;  digestive  appa- 
ratus in.  214:  diplococci  of,  205,  208,  210,  215, 
219,  222;  drunkard's,  218;  dyspnoea  in,  208, 
223;  expectoration,  205,  209,  219,  221;  exu- 
dation of,  207;  fever  in,  209,  216,  221;  gen- 
eral course  of,  208;  hsematoidine  crystals 
in,  222;  in  animals,  205;  in  children  and  the 
aged,  218,  223;  infection,  205,  220;  jaundice 
in,  214;  kidneys  and  urine  in,  215;  lung 
symptoms,  209;  meningitis  in,  215,  216; 
nervous  system  in,  215;  oxygen  inhalation 
in,  225;  pathological  anatomy  of,  207;  pe- 
culiarities and  anomalies,  218:  peptonuria 
in,  215;  physical  examination,  210;  pleural 
symptoms,  213;  pleurisy  in,  208;  pre-exist- 
ing, 219;  pneumo-typhoid,  220;  predisposi- 
tion, 206;  prodromata,  208;  prognosis,  222; 
pulse,  213;  rales  in,  212,  219,  221;  respiration 
in,  211;  rudimentary  and  abortive  forms, 
219;  skin  in,  216;  sputum  septicaemia,  205; 
stages  of,  207;  stitch  in  the  side,  209;  tem- 
perature curve  of,  216;  termination,  221; 
traumatic,  206;  treatment,  223;  typhoid, 
217. 

Pneumonia,  croupous,  in  influenza,  79;  de- 
layed, 220;  diplococci,  205;  drunkard's,  218; 
fibrinous,  see  Pneumonia,  Croupous;  in  the 
aged,  218;  in  children,  218;  in  erysipelas,  66; 
in  foetid  bronchitis,  168;  in  measles,  51;  in 
plague,  110;  in  pre-existing  chronic  diseases, 
219;  in  scarlet  fever,  43. 

Pneumonia,  lobular,  see  Catarrhal  Pneu- 
monia; after  whooping-cough,  174;  in  bron- 
chial stenosis,  181;  in  diphtheria,  72;  in 
influenza,  79;  in  septic  and  pyaemic  diseases, 
120;  in  typhus,  33;  rudimentary  and  abor- 
tive forms,  219. 

Pneumonia,  stripe,  in  catarrhal  pneumonia, 
203;  typhoid,  220;  wandering,  212. 

Pneumonic  pulmonary  tuberculosis,  245. 

Pneumonoconiosis.  See  Diseases  from  In- 
halation of  Dust. 

Pneumothorax,  295;  aetiology,  295;  ausculta- 
tion, 297;  composition  of  gas  in,  298;  diag- 
nosis, 298;  effusion  in,  296;  forms  of,  297; 
from  phthisis,  295;  hydro-pneumothorax, 
296;  inflammation  in,  296;  metallic  rales, 
297;  pathological  anatomy  of,  296;  per- 
cussion note  in,  297;  pleura  in,  296;  pulse  in, 
296;  pyo-pneumothor(ix,  296;  sacculated, 
296;  symptoms  and  course  of.  296;  treat- 
ment, 299. 

Pneumothorax,  in  pleurisy,  290;  from  pul- 
monary gangrene,  268. 

Pneumo-typhoid,  220. 

Podagra.    See  Gout. 

Poikilocytes,  in  anaemia  and  chlorosis,  724:  in 
the  blood,  448,  512,  518. 

Poisoning,  symptoms  and  treatment,  1206. 

Poliomyelitis,  acute  and  chronic,  in  children, 
1014;  aetiology  and  pathological  anatomy  of, 
1014;  clinical  history,  1015;  diagnosis,  1017; 
prognosis  and  treatment,  1018;  reflexes  in, 
1016. 

Poliomyelitis  of  adults,  acute,  1019. 

Poliomyelitis,  subacute  and  chronic,  1020. 

Polyartliritis,  chronic,  688. 


1236 


INDEX 


Polymyositis,  acute,  698;  complications,  698; 
diagnosis  and  treatment,  699;  polyneuritis 
in,  699;  pulse  in,  698;  splenic  tumor.   698. 

Polyneuritic  psychoses,  894. 

Polyneuritis,   888  (see  Multiple  Neuritis). 

Polysarcia  adiposa.    See  Obesity. 

Pomegranate  root  in  tape-worm,  513. 

Portal  vein,  diseases  of,  536;  purulent  inflam- 
mation of,  582. 

Portal  vein,  thrombosis  of,  583;  eetiology  and 
pathology  of,  583;  clinical  history,  584;  col- 
lateral circulation,  584;  diagnosis,  584; 
spleen  in,  584. 

Posterior  nasal  catarrh,  400. 

Post-hemiplegic  chorea,  1100. 

Potassic  bromide  in  epilepsy.  1149. 

Potassic  chlorate  in  stomatitis,  384. 

Potassic  cyanide  poisoning,  1210. 

Potassic  nitrate  poisoning,   1207. 

Potassium  acetate  in  cirrhosis  of  the  liver, 
562. 

Pott's  disease,  934. 

Pressure  paralyses  of  spinal  cord,  934;  aeti- 
ology, 934;  clinical  history  of,  937;  diagnosis, 
941;  in  cancer  of  the  vertebrae,  935;  patho- 
logical anatomy  of,  935;  reflexes  in,  939; 
stasis  of  lymph  in,  936:  treatment,  942; 
tubercular  spondylitis,  935;  vertebral  caries 
in,  934. 

Priapism,  in  leukaemia.  731;  in  traumatic 
lesions  of  spinal  cord,  931. 

Professional  neuroses,  882. 

Prosopalgia.    See  Neuralgia  of  Trigeminus. 

Pruritus  in  diabetes  mellitus,  757. 

Psammoma,  1116. 

Pseudo-cirrhosis  of  the  liver,  .365. 

Pseudo-crises  in  croupous  pneumonia,  217. 

Pseudo-hypertrophy  of  the  muscles,  1000. 

Pseudo-leucocythaemia.  See  Pseudo-leuke- 
mia. 

Pseudo-leukaemia,  733;  lymphatica,  734;  patho- 
logical anatomy,  734;  prognosis,  735;  symp- 
toms, 734;  treatment,  735;  tumors  in,  734. 

Pseudo-membranous  bronchitis.  See  Croup- 
ous Bronchitis. 

Pseudo-sclerosis,  959. 

Pseudo-tabes  (ataxia)  of  alcoholism.  893. 

Psoriasis,  lingual,  388. 

Pulmonary  anthrax.  See  Malignant  Pus- 
tule. 

Pulmonary  consumption.  See  Tuberculosis 
OF  Lungs. 

Pulse,  arhythmic,  314,  328;  bulbous,  322;  curve 
in  aortic  insufiiciency,  319:  curve  in  mitral 
stenosis,  314;  curve  in  stenosis  of  aortic 
orifice,  321;  in  acute  peritonitis,  525;  in 
anaemia  and  chlorosis,  713;  in  arterio-scle- 
rosis,  372;  in  catarrhal  pneumonia,  202;  in 
cholera,  88;  in  croupous  pneumonia.  213;  in 
diphtheria,  69:  in  endocarditis,  306;  in 
plague,  108;  in  pleurisy,  284;  in  pneumo- 
thorax, 296;  in  polymyositis,  698;  in  pul- 
monary tuberculosis,  250;  in  scarlet  fever, 
47:  in  septic  and  pyaemic  diseases,  120;  in 
tabes  dorsalis,  974;  in  tubercular  meningitis, 
1062;  in  typhoid.  17;  in  valvular  disease  of 
the  heart,  313.  319. 

Pulse  rate  in  catarrhal  jaundice.  .5.38. 


Pulsus  bigeminus,  328. 

Pulsus   paradoxus,    363;   in  tracheal   stenosis. 

180. 
Purpura,    744:    cutaneous   ecchymosis   in.    744. 

745;  rheumatica,  745;  treatment,  745. 
Pyaemia.    See  Septic  and  PviBMic  Diseases. 
Pyelitis,  654. 

Pyelitis  calculosa.    See  Nephrolithiasis. 
Pylephlebitis,     chronic    adhesive,     583;    from 

typhlitis  and  perityphlitis,  485. 
Pylephlebitis,   suppurative,  582;  aetiology  and 

clinical  history,   582;   in  the  new-born,   582; 

pathology,     582:     pyaemic     symptoms,     583; 

splenic  enlargement  in,  582. 
Pylethrombosis.    See  Thrombosis  of  Portal 

Vein,  583. 
Pyloric    stenosis,    in   cancer   of   the   stomach, 

447;  from  gastric  ulcer,  434,  438,  443:  vomit- 
ing in,  439. 
Pyo-pneumothorax.    See  Pneumothorax. 

Quincl'iie's  capillary  pulse,  319. 

Quinine,  injection,  101;  in  amyloid  kidney, 
639;  in  malarial  diseases,  96,  100;  in 
Meniere's  disease,  1140;  in  neuralgia,  809;  in 
relapsing  fever.  38:  in  small-pox,  62. 

Quinsy,  396. 

Quotidian  fever,  97. 

Rabies  cauina.    See  Hydrophobia. 

Rachitis,  699;  aetiology,  699;  clinical  history, 
701;  diagnosis  and  treatment,  703;  head  and 
thorax  in,  702;  pathology,  700;  symptoms, 
702. 

Radial  paralysis,  866. 

Ragpickers'  disease.    See  Anthrax. 

Railway  spine.    See  Traumatic  Neuroses. 

Rales,  bronchial,  159;  in  bronchiectasis,  177: 
in  chronic  bronchitis,  163;  in  croupous  pneu- 
monia, 212,  219,  221;  in  pleurisy,  287;  in  pul- 
monary oedema,  198:  in  tuberculosis.  242; 
metallic,  in  pneumothorax.  297. 

Rash,  initial,  of  small-pox,  55;  in  plague,  109; 
in  scarlet  fever,  39. 

Raynaud's  disease,  900. 

Reaction  of  degeneration,  848. 

Rectum,  syphilis  of,  490. 

Recurrent  endocarditis,  307. 

Reflex  asthma,  182. 

Reflex  epilepsy,  1142. 

Reflex  neuralgia,  805. 

Reflex  paralysis,  803. 

Reflexes,  abdominal,  839;  in  amyotrophic 
lateral  sclerosis,  989;  in  cerebral  haemor- 
rhage, 1097;  in  cerebro-spinal  meningitis, 
114;  in  chorea,  1154;  cremaster,  839;  cuta- 
neous, 839;  in  hysteria.  1175;  in  multiple 
sclerosis,  956;  in  myelitis.  948:  in  neu- 
ralgia, 804;  in  neuritis,  890:  in  paralysis. 
834,  1022.  1057:  in  primary  degeneration 
of  motor  tract.  955:  in  polyneuritis,  891; 
in  progressive  bulbar  paralysis,  1041;  in 
sciatica,  818:  in  segmental  diagnosis.  927;  in 
spinal  infantile  paralysis,  1015;  in  spinal 
progressive  muscular  atrophy,  995;  in  tabes, 
965,  971:  tendon,  834:  in  tetanus.  1167;  in 
traumatic  lesions.  931:  in  trigeminal  anaes- 
thesia, 931:  in  vertebral  caries.  939. 


INDEX 


1237 


Regeneration  of  nerves,  850. 

Relapses,  in  scarlet  fever,  46;  in  typhoid, 
20. 

Relapsing  fever,  33;  blood  in,  38;  clinical 
history,  84;  complications  and  varieties,  37; 
contagiousness,  34;  course  of,  35:  epidemics 
of,  in  Germany,  84;  in  America,  34;  epistaxis 
in,  37;  inoculation  of,  34;  number  of  attacks, 
36;  peritonitis  in,  37;  perturbatio  critica,  35; 
prognosis  and  treatment,  87;  stage  of  incu- 
bation and  prodromal  symptoms,  84;  tem- 
perature, 84,  35. 

Relapsing  typhus.    See  Relapsing  Fever. 

Remittent  malarial  fever.  See  Malarial  Dis- 
eases. 

Ren  mobilis,  648. 

Resorcine,  in  acute  gastric  catarrh,  425;  in 
thrush,  387. 

Respiration,  in  acute  peritonitis,  526;  in 
ascites,  533;  in  bronchial  asthma,  184;  in 
capillary  bronchitis,  160;  in  retropharyn- 
geal abscess,  403. 

Respiratory  muscles,  spasms  of.  881. 

Retina,   in  nephritis,   622. 

Retinitis,  albuminuric,  622,  632;  leukaemia, 
730. 

Retropharyngeal  abscess,  408;  deglutition  in, 
403;  dyspnoea  of,  408;  treatment,  404. 

Rheumatic  peritonitis,  521. 

Rheumatism,  acute  articular,  675;  aetiology  of, 
675;  cardiac  symptoms,  679;  course,  682; 
diagnosis,  688;  duration,  682;  fever  in,  677; 
general  symptoms,  682;  hyperpyrexia  in,  681, 
687;  infection,  675;  joints  in,  678;  nervous 
symptoms  in,  683;  peculiarities  of,  678;  pro- 
dromata,  677;  prophylaxis,  688;  prognosis, 
682;  purulent  arthritis  in,  676;  serous  and 
mucous  membranes  in,  680;  skin,  680; 
staphylococci,  676;  symptomatology  of,  677; 
symptoms  referable  to  different  organs,  678; 
temperature  in,  683;  treatment,  684;  viscera, 
682. 

Rheumatism,  acute  and  chronic  muscular,  694; 
baths  in,  697;  clinical  history  of,  695;  defi- 
nition and  aetiology  of,  694;  omalgia,  695; 
treatment,  697. 

Rheumatism,  cerebral,  681. 

Rheumatism,  chronic  articular,  688;  aetiology 
of,  688;  baths  in,  693;  course,  692;  pathology 
of,  689;  prognosis,  693;  spondylitis  defor- 
mans, 691;  symptomatology,  690;  treatment, 
693. 

Rheumatoid  influenza,  78. 

Rhinitis,  chronic,  1.37;  ozsena  simplex,  137; 
relation  to  syphilis,  138;  treatment,  '  1.37, 
138;    turbinated    bones    in,    137.      See    also 

CORYZA. 

Rhonci  in  acute  catarrh  of  trachea  and 
bronchi,  159. 

Rickets.    See  Rachitis. 

Rigor,  in  erysipelas,  64;  in  septic  and  pyaemic 
diseases,  122;  in  small-pox,  55;  in  typhus, 
33. 

Rontgen  rays,  in  aneurism,  376;  in  nephro- 
lithiasis, 660;  in  tumor  of  the  brain,  1121. 

Roseola,  in  cerebro-spinal  meningitis,  114;  in 
influenza,  80;  in  miliary  tuberculosis,  262; 
in  typhoid.  18;  vaccine,  61. 


Rothelu.    53:    period   of  incubation,   53;    prog- 
nosis, 54;  relation  to  measles,  53. 
Round-worms.    See  Intestinal  Paeasites. 

Saccular  bronchiectasis,  177. 

Salicylic  acid,  in  articular  rheumatism,  684; 
in  neuritis,  892;  in  relapsing  fever,  38;  in 
tetanus,  1168. 

Salivation  in  progressive  bulbar  paralysis, 
1041. 

Santonica  in  ascarides,  516. 

Sapo  viridis  in  scrofula,  788. 

Sarcinae  in  cancer  of  the  stomach,  446. 

Sarcoma,  in  brain,  1116;  of  the  kidneys,  con- 
genital, 644;  in  lungs,  277;  mediastinal,  301; 
melanotic,  574;  of  the  nerves,  897. 

Sausages,  poisoning  from,  1212. 

Scarlatina.    See  Scarlet  Fever. 

Scarlatinal  angina,  42;  diphtheria,  39;  erup- 
tions, 39;  nephritis,  89;  synovitis,  44;  tongue, 
42. 

Scarlet  fever,  38;  aetiology  of,  88;  anasarca  in, 
43;  baths  in,  47;  clinical  history,  39;  con- 
tagiousness. 38;  diagnosis,  46;  diet  in,  46; 
diphtheritic  rhinitis  in,  42;  fever  in,  40;  geo- 
graphical distribution  of,  39;  hygienic  treat- 
ment of,  28,  48;  intestinal  symptoms,  45; 
joints  in,  44;  kidneys  in,  48;  miliary,  42; 
otitis  media,  40,  42,  47;  papular,  42;  predis- 
position to,  88;  prodromata,  39;  prognosis, 
46;  rash  in,  39;  relapses,  46;  rudimentary 
forms,  45;  severe  forms  of,  45;  spleen  in,  89; 
streptococci  in,  41;  temperature  in,  39,  43; 
tenacity  of  contagium,  38;  throat  in,  40; 
treatment,  46;  variations  in  course  of,  45. 

Sciatic  nerve,  paralyses  in  region  of,  872; 
paralysis  of  trunk  of,  873. 

Sciatica,  817;  aetiology,  817;  diagnosis  and 
treatment,  819;  myokymia  in,  818;  nerve- 
stretching  in,  820;  sciatic  scoliosis,  818; 
symptoms,  817;  treatment,  819. 

Scleroderma,  902. 

Sclerosis,  amyotrophic  lateral,  986;  arterio-, 
870;  diffuse  cerebral,  1110;  lateral  primary, 
1006;  multiple,  954;  of  the  coronary  arteries, 
see  Interstitial  Myocarditis;  posterior 
spinal,  see  Tabes  Dorsalis;  pseudo-,  959. 

Scoliosis  in  tuberculosis,  244. 

Scorbutus.    See  Scurvy. 

Scrofula,  787;  complications,  787;  definition 
and  symptoms,  787;  lymph  glands  in,  787; 
treatment,  788;  tubercle  bacilli  in,  788. 

Scrofula,  relation  to  tuberculosis,  226,  236. 

Scurvy,  788;  aetiology  of,  739;  clinical  history, 
740;  complications,  742;  contagiousness,  740: 
course  of,  742;  diagnosis,  742;  gums  and 
mucous  membranes  in,  741;  haemorrhages 
in,  739,  742:  prognosis,  742;  treatment,  743; 
ulceration,  741;  varieties  of,  742. 

Seat-worms.    See  Intestinal  Parasites. 

Secretion,  disturbances  of,  904. 

Sensory  conduction  tracts,  796;  localization 
of,  1075. 

Septic  and  pyaemic  diseases,  116;  abdominal 
symptoms,  121;  affections  of  the  joints  in, 
120;  cerebral  symptoms,  120;  circulatory 
disturbances,  120;  clinical  history,  119; 
course  of  the  disease,  121;  course  of  fever  in. 


1238 


INDEX 


119;  cutaneous  symptoms,  119:  diagnosis, 
121;  empyema,  120;  hsemorrliages,  120;  in- 
fection, 118;  ocular  disturbances,  121;  osteo- 
myelitis, 117;  pathological  anatomy,  118 
prognosis,  121;  pulmonary  symptoms,  120 
pyaemic  fever,  119;  renal  clianges,  120 
spleen  in,  121;  streptococci  and  staphy- 
lococci, 117;  treatment,  122. 

Septic  ulcerative  endocarditis.  307. 

Serum  reaction  (Widal's)  in  typhoid,  22. 

Sexual  neurasthenia,  1197. 

Sexual  organs,  relation  to  hysteria,  1174. 

Shaking  palsy.    See  Paealtsis  Agitans. 

Ship   fever.    See  Typhus. 

Sick  headache.    See  Migraine. 

Silver  nitrate  in  cystitis,  672. 

Singultus,  882. 

Sinuses,  cerebral,  thrombosis  of,  1064;  symp- 
toms, 1065. 

Skin,  in  erysipelas,  64;  in  malarial  diseases, 
98;  in  pulmonary  tuberculosis,  247;  in  ty- 
phoid, 18. 

Small-pos,  54;  anomalies  in,  58;  articular 
swelling,  58;  bacteria  in,  54;  circulatory 
system  in,  58;  complications,  58;  contagious- 
ness, 54:  course  of,  55;  course  of  fever,  57; 
diagnosis  and  prognosis,  59;  digestive  system 
in,  58;  eyes  in,  62;  hsemorrhagic,  55,  59,  62; 
in  animals,  55,  60;  incubation  stage,  55; 
initial  stage,  55;  inoculation  of,  55;  mor- 
tality of,  60;  nervous  system  in,  58:  organs 
of  special  sense,  58:  predisposition  to,  54; 
prodromal  symptoms,  55;  prophylaxis,  60; 
respirators'  organs  in,  58;  skin  in,  57:  spinal 
disease  after,  58;  suppurative  fever  in,  57; 
temperature  curve,  57;  tenacity  of  poison 
of,  54;  treatment,  60;  variola  vera,  55:  vario- 
loid, 56. 

Smegma  bacilli  vs.  tubercle  bacilli.  663. 

Smell,  anomalies  in  sense  of,  826. 

Snuffles.     See  Coexza. 

Sodium  salicylate,  in  articular  rheumatism. 
685;  in  migraine,  907. 

Softening  of  the  brain,  from  embolism  or 
thrombosis,  1103;  idiopathic,  1110. 

Soor.    See  Thrush. 

Sopor,  in  acute  yellow  atrophy  of  liver,  566; 
in  cholera,  90;  in  diphtheria,  71. 

Sore  throat,  394;  setiology  of,  394:  bacteria  in, 
394:  catarrhal,  395;  clinical  history,  394; 
diagnosis,  prognosis,  and  treatment,  398: 
fever  in,  395;  infection,  394;  parenchym- 
atous, 396;  phlegmonous,  397:  predispo- 
sition, 394;  quinsy,  396;  various  forms  of, 
395. 

Sore  throat  in  erysipelas,  64. 

Soul-blindness,  1076. 

Soul-deafness,  1076. 

Spasm,  of  accessory  nerve,  878;  of  diaphragm, 
882;  in  epilepsy,  1144;  facial,  876:  of  leg 
miiscles,  880:  lingual,  877;  localized.  875:  in 
neck  muscles,  875;  in  paralysis,  835;  in  pro- 
fessional neuroses,  882;  of  respiratory  mus- 
cles, 881;  saltatory  reflex,  881:  of  shoulder 
and  arm  muscles,  880;  in  writer's  cramp, 
882. 

Spastic  infantile  hemiplegia,  1111. 

Spastic  paraplegia,  congenital.  1012. 


Spastic  spinal  paralysis,  1007;  diagnosis,  1012; 
prognosis,  1012;  treatment,  1012. 

Spastic  spinal  paralysis,  syphilitic,  1028. 

Speech,  centers  of,  and  disturbances  of,  1077. 
See  also  Aphasia. 

Spina  bifida,  1032. 

Spinal  apoplexy,  929. 

Spinal  cord,  diseases  from  variation  of  atmos- 
pheric pressure,  932;  disturbances  of  circu- 
lation in,  928;  in  haemorrhage  into,  929;  in 
multiple  sclerosis  of,  954;  in  new  growths  of, 
1024;  in  pressure  paralyses  of,  934. 

Spinal  cord,  secondary  degeneration  in,  1033; 
after  amputations,  1036;  after  cerebral 
lesions,  1033;  in  affections  of  spinal  cord, 
1034. 

Spinal  cord,  segmentation  of,  927. 

Spinal  cord,  syphilitic  affections  of,  1026. 

Spinal  cord,  traumatic  lesions  of,  930;  reflexes 
in,  931. 

Spinal  cord,  tumors  of,  1024. 

Spinal  cord,  unilateral  lesions  of,  1036. 

Spinal  localization,  920  et  seq.;  reflexes  in, 
927. 

Spinal  meninges,  acute  inflammation  of,  915; 
setiology  and  pathology  of,  915;  lepto-menin- 
gitis,  915;  symptoms,  diagnosis,  prognosis, 
and  treatment,  916. 

Spinal  meninges,  haemorrhage  into,  919. 

Spinal  meningitis,   acute,  915;   chronic,   917. 

Spinal  neurasthenia,  933. 

Spinal  paralysis,  Brown-Sequard's,  1036;  acute 
ascending,  1021;  of  children,  1014. 

Spinal  progressive  muscular  atrophy.  990. 

Spirilli  in  blood,  33-36. 

Spleen,  in  acute  yellow  atrophy  of  liver,  566, 
567;  in  cholera,  90;  in  cirrhosis  of  liver,  558; 
in  leukaemia.  727;  in  malarial  diseases, 
95;  in  plague,  109;  in  relapsing  fever,  34; 
in  septic  and  pyaemic  diseases,  121;  in  small- 
pox, 55;  in  suppurative  pylephlebitis,  582; 
in  thrombosis  of  portal  vein.  584:  in  ty- 
phoid. 12;  amyloid,  250. 

Splenic  fever.    See  Malignant  Pustule. 

Spondylitis.  934;  deformans.  691;  tubercular, 
935. 

Spotted  fever.  30.  See  also  Cerebro-spinal 
Meningitis. 

Sputum  crudum  and  sputum  coctum.  158. 

Sputum  of  bronchiectasis.  178;  of  bronchitis. 
164;  foetid.  168;  of  central  pneumonia.  219. 

Staphylococci,  in  articular  rheumatism,  676- 
679:  in  endocarditis,  304;  in  septic  and 
pyaemic  diseases.  117:  in  sore  throat,  394; 
in  typhoid,  19. 

Staphylococci  and  streptococci  in  septic  and 
pyaemic  diseases.  117,  120. 

Stenocardia,  355. 

Stenosis,  from  cicatrices,  etc.,  507;  mitral, 
312;  of  aortic  orifice,  320;  pulse  curve  in, 
321. 

Stenosis  of  the  intestines.  499. 

Stenosis  of  the  oesophagus,  409:  aetiology  and 
pathology  of,  409;  auscultation  in,  410: 
causes  of.  409:  dysphagia  in.  409;  nutrient 
enema ta  in.  412;  prognosis  and  treatment. 
411:  regurgitation  of  food  in.  410:  symp- 
toms. 410. 


INDEX 


1239 


stenosis  of  pylorus  In  gastric  ulcer,  434,  438, 
443. 

Stenosis  of  the  rectum  in  syphilis,  490. 

Stenosis,  of  trachea  and  bronchi,  180;^  aeti- 
ology and  symptoms  of,  180;  bronchial, 
181;  pneumonia  from,  181;  prognosis  and 
treatment,  181;  pulsus  paradoxus,  180. 

Stenosis,  valvular,  314,  320,  322. 

Stercoraceous  vomiting,  503. 

Stitch  in  the  side,  in  croupous  pneumonia,  209; 
in  pleurisy,  283. 

Stomacaco.    See   Stomatitis,   Ulcerative. 

Stomach,  abnormal  position  of,  462;  abscess, 
432;  anacidity  of,  452;  atony  of,  460;  can- 
cer of,  444;  chronic  catarrh  of,  425;  cicatri- 
cial contraction  of,  434. 

Stomach,  diseases  of,  415;  estimation  of  size 
and  position,  420  (see  also  460);  motor  dis- 
turbances of,  460;  purulent  inflammation  of, 
see  Phlegmonous  Gastritis;  tests  of  ab- 
sorptive power  of,  421. 

Stomach,  motor  activity  of,  419;  in  gastric 
ulcer,  437. 

Stomatitis,  aphthous,  385. 

Stomatitis,  catarrhal,  382;  aetiology,  382;  bac- 
teria in,  382;  clinical  history,  382;  from 
chemical  irritation,  382;  infection,  382;  in 
drunkards,  383;  gingivitis,  382;  in  scarlet 
fever,  41;  superficial  ulcers  in,  383;  treat- 
ment, 383;  in  typhoid,  12. 

Stomatitis,  disseminated  fibrinous.  See 
Stomatitis,  Aphthous. 

Stomatitis,  mercurial,  384. 

Stomatitis,  ulcerative,  383;  aetiology  of,  383; 
fever  in,  384;  gingivitis  in,  384;  infection, 
383;  swollen  lymph  glands  in,  384;  symp- 
toms, prophylaxis,  and  treatment,  384;  ul- 
ceration in,  384. 

Strabismus  in  ocular  paralysis,  855. 

Streptococci,  in  diphtheria,  70;  in  influenza, 
79;  in  septic  and  pyaemic  diseases,  117;  in 
sore  throat,  394;  in  tuberculosis,  234. 

Streptococcus  pyogenes,  in  endocarditis,  304; 
in  erysipelas,  63;  in  pleurisy,  290. 

Stripe-pneumonia  in  catarrhal  pneumonia,  203. 

Strongylus,  647. 

Strophanthus,  in  arterio-sclerosis,  374;  in 
heart  disease,  338. 

Strychnine,  in  alcoholic  neuritis,  895;  in  al- 
cohol poisoning,  1210;  in  muscular  atrophy, 
996;  in  myelitis,  9.53;  poisoning,  1211. 

St.  Anthony's  fire.    See  Erysipelas. 

St.  Vitus's  dance.    See  Chorea. 

Subnitrate  of  bismuth,  in  gastric  ulcer,  441, 
442;  in  intestinal  catarrh,  481. 

Suggestion  in  hysteria,  1184. 

Sulphonal,  in  chorea,  1156;  in  neurasthenia, 
1201. 

Sulphur,  in  cirrhosis,  719;  in  hremorrhoids, 
495. 

Sulphur  baths  in  lead  paralysis,  874. 

Sulphuretted-hydrogen  poisoning,  1210. 

Sulphuric-acid  poisoning.  1206. 

Sulphurous-acid  poisoning,  1206. 

Sunstroke.     See  Insolation. 

Suppuration  in  plague,  109. 

Suppurative  encephalitis.  1106;  hepatitis,  553; 
pylephlebitis.   .582. 


Supra-renal  capsules,  diseases  of,  650;  tuber- 
culosis of,  651. 

Swamp  fever.    See  Malarial  Diseases.  ^ 

Sydenham's  chorea.    See  Chorea. 

Syncope.    See  Cerebral  Anaemia. 

Synovitis  in  articular  rheumatism,  678. 

Syphilis  as  cause  of  aneurism,  374. 

Syphilis,  by  vaccinia,  61;  cerebral,  1125;  in 
myelitis,  943,  1028. 

Syphilis  of  the  liver,  571;  aetiology,  pathology, 
and  clinical  history,  571;  diagnosis  and  treat- 
ment, 572. 

Syphilis  of  the  rectum,  490  (see  also  499); 
stenosis  in,  490;  tenesmus  in,  490;  treatment, 
491;  ulceration  of,  490. 

Syphilis,  pulmonary,  276. 

Syphilis,  relation  to  general  paralysis,  1130; 
relation  to  tabes  dorsalis.  900. 

Syphilitic  affections  of  spinal  cord,  1026. 

Syphilitic  endarteritis,  341;  myelitis,  1028; 
spinal  paralysis,  1028. 

Syphiloma,  cerebral,  1127. 

Syringomyelia,  803,  1029;  central  gliosis,  10.30: 
clinical  symptoms,  1030;  pathological 
anatomy  and  pathogenesis,  1029. 

Tabes  dorsalis,  960;  aetiology  of,  960;  anaes- 
thesia in,  969;  arthropathy  in,  974;  ataxic 
gait  in,  966;  cerebral  symptoms,  976;  clini- 
cal history,  964;  diagnosis,  977;  degenera- 
tion in,  962;  disturbances  of  bladder,  rec- 
tum and  sexual  organs,  973;  disturbances  of 
motility  in,  966;  disturbances  of  special 
sense  organs,  972;  gastric  crisis  in,  973; 
laryngeal  crisis  in,  974;  ocular  disturbances 
in,  972;  patellar  reflex  in,  965;  other  reflexes, 
971;  pathological  anatomy,  962;  pulse  in, 
974;  relation  to  syphilis,  960;  symptoms  in 
internal  organs,  973;  treatment,  978;  trophic 
disturbances,  974. 

Tabes  mesenterica,  532;  motor,  1006. 

Tachycardia,  327,  357;  from  scarlet  fever,  45. 

Tactile  sensibility,  790. 

Taenia  cucumerina,  511;  echinococcus,  575; 
mediocanellata,  510;  nana,  511;  solium,  508. 

Taenicides,  513. 

Talalgia,  821. 

Tannin,  in  intestinal  catarrh,  481:  in  tuber- 
culosis of  the  intestines,  490. 

Tape-worms,  .508. 

Tapping  in  ascites,  535. 

Tarsalgia,  821. 

Taste,  anomalies  of  sense  of,  827. 

Temperature,  sense  of,  792;  variations,  in 
traumatic  lesions  of  the  spinal  cord,  931:  in 
syringomj'elia,  1031. 

Tendon  reflexes,  834,  840,  995,  1022;  in  amyo- 
trophic lateral  sclerosis,  989;  tests  of,  840. 

Tenesmus,  in  children,  478;  in  dysentery,  82; 
in  intestinal  catarrh,  472;  in  syphilis  of  the 
rectum,  490. 

TerTian  intermittent  fever,  97. 

Test  breakfast,  etc.,  use  of,  417,  437,  439,  455. 

Tetanilla.     See  Tetany. 

Tetanus.  1165;  bacilli  of,  1165:  clinical  history 
of,  1166:  diagnosis,  1168:  hydrophobic,  1167; 
opisthotonos  in,  1166;  pulse  and  temperature 
in,  1167;  symptoms  of.  1166;  treatment,  1168. 


1240 


INDEX 


Tetanus  neonatorum,  1166. 

Tetany,  1162;  aetiology,  1162;  clinical  history, 
1163;  diagnosis,  1164;  exciting  causes,  1163; 
prodromata,  1163;  symptoms,  1164;  tempera- 
ture in,  1164;  treatment,  1165. 

Thermic  fever.    See  Insolation. 

Thermo-cautery,  in  noma,  .390;  in  spondylitis, 
943. 

Thomsen's  disease.  See  Congenital  Myo- 
tonia. 

Thorax,  in  emphysema,  187,  219,  414;  in  osteo- 
malacia, 706;  in  rachitis,  702. 

Thrombosis,  in  typhoid,  18;  of  basilar  artery, 
1050. 

Thrombosis  of  the  cerebral  sinuses,  1064;  aeti- 
ology and  pathology  of,  1064;  symptoms, 
1065. 

Thrombosis  of  the  portal  vein,  583. 

Thrush,  386;  aetiology  of,  386;  fungus  of,  386; 
symptoms  and  treatment,  387. 

Thymic  asthma.    See  Spasm  of  the  Glottis. 

Thyroid  extract,  in  myxcedema  and  cretin- 
ism, 901;  in  scleroderma,  902. 

Tibial  nerve,  paralysis  of,  873. 

Tie  convulsif.    See  Spasm,   Clonic  Facial. 

Tic  douloureux.    See  Neuealgia  op  Tkigemi- 

NUS. 

Tinnitus  aurium,  118;  in  cerebral  anaemia, 
1067;  from  salicylic  acid,  685. 

Tobacco-poisoning.    See  Nicotine. 

Tonsillar  and  peritonsillar  abscess,  396. 

Tonsillitis,  follicular,  396;  necrotic,  397. 

Tonsils,   chronic  hypertrophy  of,  399. 

Topical  diagnosis  of  cerebral  lesions,  1068; 
of  spinal  lesions,  920. 

Toxic  paralyses,  832,  873.. 

Trachea,  diseases  of,  156. 

Tracheal  stenosis,  180. 

Tracheitis.    See  Bronchitis,  Acute. 

Tracheotomy  in  diphtheria,  69,  74,  76. 

Tract,  chief  centripetal,  1089;  motor,  1089; 
optic  and  acoustic,  1089. 

Ti^nsfusionof  blood  in  pernicious  anaemia,  726. 

Traumatic  lesions  of  spinal  cord,  930. 

Traumatic  neuroses  (so-called),  1201;  prog- 
nosis and  treatment,  1205;  psychical  factors 
in,  1202;  relation  to  hysteria.  1204. 

Tremor,  in  amyotrophic  lateral  sclerosis,  988; 
in  epilepsy,  1147;  in  exophthalmic  goitre, 
911;  intention,  in  multiple  sclerosis,  955; 
osteomalacia,  706;  in  typhoid,  15. 

Tremor,  hysterical,  1172;  mercurial,  836,  1208. 

Trichina  spiralis,  131. 

Trichinosis,  131;  aetiology  and  clinical  history, 
132;  blood  in,  133;  diagnosis,  133;  fever  in, 
133;  infection,  132;  in  animals,  132;  muscles 
in,  133;  myositis  in,  132;  oedema  in,  133; 
treatment,  134. 

Trichocephalus  dispar.  See  Intestinal  Para- 
sites. 

Trigeminus,  anaesthesia  of,  802.  See  also  Dis- 
eases of  the  Nervous  System. 

Trigeminus,  neuralgia  of,  810. 

Trional  in  neurasthenia,  1201. 

Triple  phosphate  crystals,  669. 

Trommer's  test  for  sugar,  752. 

Trophic  disturbances,  in  arsenical  paralysis, 
875;    in   bones  and   joints,    975:    in   cerebral 


haemorrhage,  1096;  in  facial  hemiatrophy, 
909;  in  myelitis,  949;  in  nails  and  skin,  869, 
974;  in  neuralgia,  807;  in  paralysis,  888;  in 
progressive  muscular  atrophy,  993;  in  tabes, 
974. 

Trophic  influence  of  nerves,  834,  849,  899;  in 
facial  hemiatrophy,  909. 

Tubercle  bacilli,  227,  231,  240.  489;  in  scrofula, 
788. 

Tubercula  dolorosa,  897. 

Tubercular  meningitis,  1059;  pericarditis,  365; 
peritonitis,  249,  530;  pleurisy,  289;  spondy- 
litis, 935. 

Tuberculiue,  252. 

Tuberculosis,  acute  miliary,  261;  aetiology  of, 
261;  caseation  in,  261;  circulatory  apparatus 
in,  264;  clinical  history,  262;  diagnosis,  265; 
digestive  apparatus  in,  264;  dyspnoea  in,  262, 
263;  eyes  in,  265;  fever  in,  263;  lumbar 
puncture  in,  265;  miliary  tubercles,  261; 
nervous  system  in,  265;  pathological 
anatomy  of,  262;  prognosis  and  treatment, 
266;  protracted  intermitting  form,  263;  re- 
spiratory apparatus  in,  264;  single  symp- 
toms, 263;  typhoidal  form,  262;  with  pre- 
dominant cerebral  or  pulmonary  symptoms, 
263. 

Tuberculosis,  after  catarrhal  pneumonia,  203; 
after  measles,  52;  disseminated  pulmonary, 
245;  distinguished  from  bronchiectasis,  178. 

Tuberculosis  of  the  genito-urinary  apparatus, 
662;  aetiology  and  pathological  anatomy  of, 
662;  bacilli  in,  668;  clinical  symptoms,  668; 
diagnosis,  664;  infection,  662;  treatment, 
664;  ulceration  in,  663. 

Tuberculosis  of  the  intestines,  488;  diarrhoea 
in,  489;  infection,  488;  miliary  tubercles  in, 
489;  tubercle  'bacilli,  489;  treatment,  489; 
ulceration  in,  489. 

Tuberculosis  of  the  larynx,  147;  clinical  symp- 
toms, 148;  diagnosis,  148;  pathological 
anatomy,  147;  resemblance  to  syphilis,  148; 
treatment,  149;  tubercle  bacilli,  148;  tuber- 
culiue injection  in,  149;  ulcers  in,  148. 

Tuberculosis    of   lungs,    226;    aetiology    of,    in 
man,    228;   anaemia   in,    247;   bacilli   of,   227, 
231,  284;  caseation,  226,  232,  250;  cicatricial 
formations,    238;    circulatory    organs,    250; 
clinical   history,   234;    contraction  of   lungs. 
248;  cough  in,  237:  diagnosis,  251:  physical, 
242;  of  cavities,  243;  diarrhoea  in,  249;  diet. 
257;    disseminated    pulmonary    tuberculosis, 
245;    dyspnoea    in,    241;    elastic    flbers,    240; 
emaciation  in,  235;   expectoration,  227,  288, 
245;  fever  in,  246;  fibroid  phthisis,  243:  gen- 
eral pathology  and  aetiology  of,  226;  general 
symptoms,  246;  genito-urinary  tuberculosis, 
229,  250;  hsemorrhage,  pulmonary,  238,  253 
haemorrhage,  influence  on  temperature,  239 
health   resorts,   257;   hectic  fever,   246,   260 
hemoptysis  in,  286,  259;  hereditary  influence 
229;  hydrotherapy  in.  259:  in  animals.  226 
individual  predisposition,  229;  in  drunkards 
230;    infection,    226;    influence   of   age,    231 
inoculation,    226;    intestinal    infection,    229 
kidueys.  250:   larynx,  pharynx,  and  trachea 
in,  248:  liver  and  spleen.  249;  lobular  atelec- 
tasis. 233;   lung  symptoms.  237;  lupus,  229: 


INDEX 


1241 


miliary  tubercles,  232.  248;  night-sweats. 
235;  nervous  disturbances,  247;  pathological 
anatomy,  231;  percussion  note,  241;  peri- 
toneum in,  249:  physical  symptoms,  241: 
pleural  complications.  248;  pneumonic  pul- 
monary tuberculosis.  24.5;  prognosis,  253; 
pulse  in,  250;  rales  in,  242;  respiration  in, 
241;  scoliosis  in,  244;  skin  in,  247;  special 
symptoms  and  complications,  237;  stomach 
and  intestinal  canal,  249;  swelling  of  lymph 
glands  in,  230,  236,  250;  temperature  curve, 
246:  treatment  and  prophylaxis,  254;  tuber- 
culine,  252:  ulcers,  232,  248:  urinary  pas- 
sages and  sexual  organs,  250;  after  whoop- 
ing-cough. 174. 

Tuberculosis,  peritoneal.  249. 

Tufnell's  method  in  aneurism,  379. 

Tumors  and  cicatricial  strictures  of  the  intes- 
tines, 499. 

Tumors,  of  the  brain,  1115;  of  the  cerebellum, 
1121;  of  the  kidneys,  644;  of  the  larynx,  1.55. 

Tumors,  of  the  lungs,  276;  expectoration  of. 
277;  sequelee,  278;  of  the  lymph  glands.  7.34; 
mediastinal.  301:  of  the  spinal  cord.  1024. 

Turbinated  bones  in  chronic  rhinitis,  137. 

Turpentine,  oil  of,  in  chronic  bronchitis,  166; 
in  cystitis,  671;  in  genito-urinary  tubercu- 
losis, 664;  in  pulmonary  gangrene.  270. 

Tussis   convulsira.    See  Whoopixg-cocgh. 

Tympanites  in  jaundice,  539. 

Tympanitic  resonance,  in  catarrhal  pneu- 
monia, 203:  pleurisy.  286,  287. 

Typhlitis  and  perityphlitis,  482;  aetiology  and 
pathological  anatomy  of,  482:  colon  bacilli, 
483:  diagnosis.  486;  faecal  calculi,  483:  fever 
in,  484,  485.  487;  perforation  in,  485:  prog- 
nosis. 486;  symptoms  and  clinical  course, 
483:  treatment,  486;  typhlitis  stercoralis, 
482;  ulceration  in,  483. 

Typho-malarial  fever.  See  Malarial  Dis- 
eases. 

Typhoid  fever,  1;  abortion  in,  8:  affections  of 
respiratory  organs  in.  13.  28:  albuminuria 
and  cystitis  in,  19:  antipyrine  in.  26:  arti- 
ficial infection,  2:  bacilli,  1:  bacilli  in  the 
lungs,  14.  22:  bacilli,  culture  of,  1:  baths  in, 
24:  bed-sores,  23;  blood  changes  and  oedema 
in,  18;  bones  and  joints  in,  19;  bronchitis  and 
pleurisy  in,  13;  care  of  mouth.  12.  23; 
changes  in  mouth  and  throat.  12:  circu- 
latory .system  in.  17,  28;  clinical  symptoms, 
10;  cold-pack  in,  26;  contagiousness,  2; 
course  of  fever.  6;  diagnosis  of.  21:  diag- 
no.sis  of,  in  the  aged,  20;  diarrhoea  in,  10.  28; 
diet,  23:  disinfection.  28:  entrance  of 
bacilli  into  human  body.  4:  epidemic  from 
polluted  water  supply.  4:  Ehrlich's  reaction, 
19;  fastigium  in.  6,  25:  febrile  sequelae.  9: 
fumigation,  30;  general  course,  5:  genito- 
urinary apparatus,  19:  hepatic  symptoms, 
12:  hyperaesthesia  in.  17:  influence  of  amount 
of  water  in  the  soil  on  development  of 
bacilli,  3:  intestinal  haemorrhage  and  epi- 
staxis,  8.  11.  27:  immunity.  4:  manner  of  in- 
fection. 2.  23:  miliaria  in.  18:  mortality  in, 
22;  muscle  changes  in,  19;  nephritis  in 
nephro-typhoid.  19.  26:  nervous  symptoms 
in.  16-28:  neuralgia  in.  17:  opium  in.  27,  28; 


orchitis  in,  20:  orchitis,  prognosis  in,  22; 
outcry  of  children  in,  20;  paralysis  in,  17; 
pathognomonic  changes,  9;  peculiarities  in 
the  course  of.  20;  period  of  incubation,  5; 
perforation.  11.  12;  peritonitis,  12,27;  Peyer's 
patches  in.  9:  phenomena  and  complications, 
8;  predisposing  influences.  5;  prodromal 
symptoms,  5;  prophylaxis,  28;  relapses,  20; 
roseola  in,  18;  sewer  gas  not  a  cause  of,  4; 
skin  in,  18,  27;  stomach  changes  in.  12;  swell- 
ing of  lymph  glands  and  spleen,  12;  tempera- 
ture. 6,  25;  thrombosis  in,  18:  treatment,  22; 
tympanites,  10;  typhus  levissimus,  20;  urine 
in.  19:  Widal's  serum  reaction  in,  22. 

Typhoid  measles,  51. 

Typhoid  pneumonia,  217. 

Typhoidal  form  of  miliary  tuberculosis,  262. 

Typhus  fever,  30;  aetiology  of,  31;  complica- 
tions and  varieties  in,  .32;  contagiousness, 
31;  course  and  symptoms  of,  31;  diagnosis, 
33;  distinguished  from  typhoid,  30:  epi- 
demics of,  81;  geographical  distribution  of, 
31:  nervous  symptoms  of,  32;  perturbatio 
critica,  32;  prognosis,  33;  rigor  in,  33;  tem- 
perature in,  32;  treatment,  33;  urine  in,  .32. 

Uffelmann's  test  for  lactic  acid,  419. 

L'lcer,  atheromatous,  371;  cancerous,  445; 
catarrhal,  468;  dysenteric,  83;  gastric,  432; 
in  glanders,  125;  in  intestinal  tubercu- 
losis, 489;  in  perityphlitis  and  typhlitis, 
483;  in  septic  and  pyaemic  diseases.  119; 
in  syphilis  of  the  rectum,  490  (see  also  499); 
in  tuberculosis  of  the  larynx,  148;  of  the 
duodenum,  488;  of  the  oesophagus.  404; 
of  the  stomach,  432;  on  the  tongue  in  whoop- 
ing-cough, 173;  peptic,  433;  scorbutic,  741; 
superficial,  in  stomatitis,  383;  tuberculous, 
232,  248. 

Ulcerative  stomatitis,  383. 

Ulnar  paralysis,  868. 

Unilateral  lesions  of  spinal  cord,  1036. 

Uraemia,  596;  in  acute  nephritis,  617;  amau- 
rosis. 599:  clinical  symptoms,  599;  convul- 
sions. .599:  diarrhoea  in,.  600;  dyspnoea,  601; 
eclampsia,  599;  pulse  in,  600:  sequelae,  599; 
vomiting,  600. 

Urea  elimination,  in  acute  yellow  atrophy  of 
liver.  567:  in  cirrhosis  of  liver,  599;  in  ty- 
phoid, 19. 

Uric  acid,  in  contracted  kidney,  627;  in  gout, 
772. 

Urinary  sediments,  594. 

Urine,  in  acute  gastric  catarrh,  424:  in  acute 
yellow  atrophy  of  liver.  566;  in  amyloid  kid- 
ney, 6.37;  in  aneemia,  714;  in  cancer  of  the 
stomach,  449;  in  cerebro-spinal  meningitis, 
114;  in  cholera,  87:  in  chronic  gastritis, 
428:  in  chyluria,  647;  in  cirrhosis  of  the  liver, 
•5.59:  in  contracted  kidney,  628,  631;  in 
croupous  pneumonia,  215:  in  cystitis,  669;  in 
diabetes  insipidus,  768:  in  diabetes  mellitus, 
752:  in  diphtheria,  74:  in  epilepsy,  1144; 
in  erysipelas.  66;  in  gastric  ulcer,  436; 
in  haemoglobinuria,  737:  in  heart  disease, 
331:  in  hydronephrosis,  666;  in  hydro- 
thorax,  299:  in  interstitial  obstruction, 
504:    in    jaundice,     .5.39:    in    nephritis,    608. 


1242 


INDEX 


621;  in  neurasthenia,  1196:  in  pliospliorous- 
poisoning,  1209;  in  plague,  109;  in  pleurisy, 
284:  in  pulmonary  emphysema,  193;  in  scar- 
let fever,  43;  in  septic  and  pysemic  diseases, 
120;  in  small-pox,  55;  in  typhoid.  19;  in  ty- 
phus, 32;  in  yellow  fever,  105. 

Urotropine,  in  cystitis,  671;  in  genito-urinary 
tuberculosis,  664. 

Urticaria,  in  articular  rheumatism,  680;  in 
goitre,  912;  in  neuralgia,  807. 

Vaccination,  60. 

Vaccinia,  60. 

Valerian,  in  diabetes  insipidus,  770:  in  epi- 
lepsy, 1150;  in  hysteria,  1191. 

Valvular  disease  of  the  heart,  308. 

Valvular  pneumothorax,  297. 

Varicella,  62;  diagnosis,  62;  eruption  of.  62; 
fever  of,  62;  prognosis,  63:  stage  of  incu- 
bation, 62. 

Variola.    See  Small-pox. 

Varioloid.    See  Small-pox. 

Vascular  stasis,  in  cirrhosis  of  the  liver,  557; 
in  mediastinal  tumors,  etc.,  301. 

Vaso-motor  spasm,  899. 

Vaso-motor  and  trophic  neuroses,  898;  paraly- 
sis, 898;  spasm,  899. 

Venesection  in  apoplectic  shock,  1102. 

Verdigris  poisoning,  1208. 

Vertigo,  in  anaemia,  712;  in  cerebellar  disease, 
984,  1086;  in  cerebral  abscess,  1110;  in  cere- 
bral haemorrhage,  1092;  in  cerebral  tumor, 
1118;  in  chlorosis,  712;  in  epilepsy,  1145; 
in  insolation.  1114;  labyrinthine.  see 
Mexieke's  Disease;  in  leukaemia,  731;  in 
multiple  sclerosis,  957;  in  oculo-motor 
paralysis,  856;  in  cerebro-spinal  meningitis. 
113. 

Vesical  catarrh.    See  Cystitis. 

Vesicatory  treatment  of  neuralgia,  SOS. 

Vicarious  menstruation,  139. 

Vitiligo  in  goitre,  912. 

Vocal  fremitus,  in  pleurisy,  290;  in  pneumo- 
thorax, 297. 

Volvulus,  500. 

Vomit,  black,  105,  1206. 

Vomiting,  in  acute  yellow  atrophy  of  liver. 
568;  cerebral,  1118;  in  cholera,  88;  in  chronic 
gastritis,  426—428;  in  croupous  pneumonia. 
214;  in  diphtheria,  70;  in  dysentery,  82;  in 
erysipelas,  64;  in  gastric  ulcer.  435,  442;  in 
influenza,  78:  in  intestinal  anthrax.  129;  in 
migraine,  906;  in  nephritis.  611;  in  ocular 
paralysis,  857;  in  peritonitis.  .525:  in  pyloric 


stenosis,  439;  in  scarlet  fever,  39;  in  typhoid, 
12;  in  uraemia,  600;  in  whooping-cough.  173. 
Vomiting,  stercoraceous,  503. 

Warmth-,  sensation  of,  in  paralysis  agitans, 
1159. 

Water  cancer.     See  Noma. 

Water-cures  for  chronic  laryngitis,  144. 

Waxy  liver,  580. 

Weights  and  measures,  table  of,  1214. 

Weil's  disease.    See  Acute  Febrile  Jauxdice. 

Wernicke's  hemiopic  pupillary  reaction  (see 
footnote),  1076. 

Whip-worm.     See  Ixtestixal  Paeasites. 

Whooping-cough,  172;  aetiology,  symptoms, 
and  course  of,  172;  catarrhal  stage,  173; 
complications  and  sequelae,  174;  contagious- 
ness. 172;  diagnosis,  174;  fever  in,  172; 
haemorrhages  in,  173;  hemiplegia  in,  173; 
prodromal  symptoms,  173;  prognosis,  175; 
pulmonary  emphysema  in,  174.  189;  treat- 
ment, 175;  ulcer  in.  173. 

Widal's  serum  reaction,  22;  in  acute  miliary 
tuberculosis,  265;  in  septic  and  pysemic  dis- 
eases, 121. 

Wintergreen.  oil  of.  in  articular  rheumatism, 
685. 

Word-blindness,  1083. 

Word-deafness,  1080. 

Worms,  seat.     See  Ixtestixal  Parasites. 

Writer's  cramp,  882. 

Xanthelasma  in  jaundice,  538. 
Xanthine,  766:  calculi.  658. 

Yawning,  spasmodic,  712. 

Yellow  fever,  104;  aetiology  of,  104;  bacillus 
icteroides.  104;  baths  in,  106;  black  vomit, 
105;  boxwood  liver,  105;  capillary  con- 
gestion, 105;  contagiousness,  104:  course 
and  symptoms,  105;  diagnosis,  prognosis, 
and  treatment,  106;  disinfection.  106;  haem- 
orrhage, 105:  headache  in,  105:  immunity, 
104;  influence  of  temperature,  104:  jaundice 
in,  105;  negro  susceptibility  to.  104:  patho- 
logical anatomy,  105:  prognosis.  106;  tem- 
perature in.  105;  urine,  105. 

Zinc    oxide,    in    epilepsy.    1150:    in    localized 

spasm,  877. 
Zinc  oxide  and  valerianate  in  chorea.  1156. 
Zinc  poisoning.  1208. 
Zones,  hysterogenous,  1149,  1186. 
Zoster.  805,  815:  in  tabes  dorsalis,  974. 


THE    END 


A  TEXT-BOOK  OF 
OEN^ERAL    SUKGEKT. 

By   dr.   HERMANN   TILLMANNS, 

PKOFESSOK  IK  THE   UNIVERSITY   OF  LEIPSIC. 

VOLUME  I. 

The  Principles  of  Surgery  and  Surgical  Pathology.  General  Rules 
governing  Operations  and  the  Application  of  Dressings.  Translated  from 
the  third  German  edition  by  John  Rogers,  M.  D.,  and  Benjamin  T.  Tilton, 
M.  D.     With  441  Illustrations. 

VOLUME   IL 
Pegional  Surgery.      Translated  fronn  the  fourth  German  edition  by  Benjamin 
T.  Tilton,  M.  D.,  Xew  York.     With  411  Illustrations.     Edited  by  Lewis  A. 
Stimson,  M.  D.,  Professor  of  Surgery  in  the  New  York  University. 

VOLUME   III. 

Regional  Surgery.  Translated  from  the  fourth  German  edition  by  Benjamin 
T.  Tilton,  M.  D..  Xew  York.  With  520  Illustrations.  Edited  by  Lewis  A- 
StixMSON,  M.  D.,  Professor  of  Surgery  in  the  New  York  University. 


Cloth,  ©5.00;   slieep,  SO.OO  per  volume 
SOLD    ONLY  BY  SUBSCRIPTION. 


De.  Hermann  Tilljtanns,  Professor  of  Surcjeiy  in  the  University  of  Leipsic,  possesses  as 
a  teacher  those  rare  qualities  which  enable  him  to  instruct  the  student,  step  by  step,  beginning 
by  the  laying  of  a  tirm,  broad  foundation,  upon  which  is  built  the  solid  surgical  structure.  It 
was  on  account  of  these  exceptional  qualities  of  the  author  that  his  work  was  selected  as  the 
best  for  the  use  of  students,  and  at  the  same  time  well  adapted  to  the  needs  of  the  practitioner. 

SuEGERY,  as  presented  in  the  present  volumes,  is  a  translation  of  his  works  on  General 
Surgery  and  Surgical  Pathology,  and  on  Regional  Surgery.  Of  the  latter  there  are 
two  volumes,  the  second  of  which  will  soon  be  on  press. 

Volume  I,  General  Surgery  and  Surgical  Pathology,  is  largely  devoted  to  the  expo- 
sition of  the  essential  principles  which  uuderUe  a  solid  surgical  structure.  This  apphes  not 
only  to  general  surgical  operations,  but  also  to  all  surcical  conditions.  The  work  covers  the 
entire  field  of  general  surgery  and  of  surgical  diseases,  dealing  not  so  much  with  special 
operations  as  with  the  conditions  which  should  govern  them— general  directions  for  their 
performance,  after-treatment,  and  the  etiology,  pathology,  and  treatment  of  the  various 
surgical  diseases. 

Volume  II,  Regional  Surgery,  is  devoted  to  the  surgery  of  the  head,  neck,  thorax,  and 
spine  and  spinal  cord  ;  including  in  the  Jirst  division  injuries  and  diseases  of  the  scalp,  of  the 
cranial  bones,  of  the  brain  and  its  adnexa,  of  the  face,  of  the  nose  and  nasal  fossse,  of  the 
jaws,  of  the  mouth,  fixuces,  and  pharynx,  of  the  ear,  and  of  the  salivar\^  glands.  The  second 
division  includes  injuries  and  surgical  diseases  of  the  neck,  of  the  larynx  and  trachea,  and 
of  the  oesophagus.  The  third  division  covers  injuries  and  diseases  of  the  thorax  and  of  tlie 
heart;  and  the  fovrih  division  treats  of  the  surgery  of  the  spine  and  spinal  cord,  including 
deformities,  fractures,  gunshot  injuries,  tumors,  etc. 

The  list  of  subjects  is  so  full  that  it  includes  even  the  great  surgical  rarities,_  and  tlie 
descriptions  are  suAciently  complete  to  save  the  reader  from  the  necessity  of  consulting  other 
works  to  obtain  the  knowledge  necessary  to  understand  and  to  treat. 


D.  APPLETON  AND  COMPANY,  NEW  YORK. 


DISEASES  OF  THE  EAR 

A   TEXT-BOOK  FOR  PRACTITIONERS 
AND   STUDENTS   OF   MEDICINE. 

By  Edward  Bradford  Dench,  Ph.  B.,  M.  D., 

Professor  of  Ctology  in  the  Bellevue  Hospital  Medical  College  ;  Aural  Surgeon  to  the 
New  York  Eye  and  Ear  Infirmary,  etc. 

Second  Edition,     ^vo,  655  pages. 
With  8  Colored  Plates  and  152  Illustrations  in  the  Text. 

Cloth,  S5-00;  sheep,  $6.00. 

"  An  examination  of  the  contents  will  prove  that  this  volume  carries  its  raison 
d'etre.  It  embodies  in  a  most  satisfactory  manner  the  known  facts  of  otolog)%  hav- 
ing incorporated  most  successfully,  and  with  little  bias,  the  recent  advancements  that 
have  been  made  in  this  branch.  Recognizing  the  aid  which  comes  from  a  faithful 
reproduction  of  the  anatomical  structures  concerned,  and  from  showing  the  site  of 
operative  procedures,  the  plates  have  been  prepared  with  all  the  care  and  precision  of 
modern  engraving  art  from  the  specimens  themselves.  The  high  class  of  illustrations 
in  the  work  is  worthy  of  special  praise.  The  text  maintains  a  character  that  will  rank 
the  author  as  one  of  our  best  otological  writers.  He  has  paid  marked  attention  to  the 
physiological  basis  of  aural  studies  and  to  the  functional  examination  in  cases  of  ear 
disease.  In  mentioning  treatment  he  has  gone  into  manipulative  details  that  other 
writers  have  omitted,  and  yet  which  are  very  necessary  to  the  student  and  practitioner 
who  may  have  never  had  a  chance  to  study  and  obsen'e  these  matters  in  special  aural 
clinics.  The  author  is  perhaps  more  fond  of  operative  procedures  in  middle-ear  dis- 
ease than  some  of  his  colleagues,  but  he  has  given  us  what  we  have  desired — a  good 
modern  r/sume'  on  the  benefiis  to  be  derived  from  such  operations." — Coluinbiis  Med- 
ical Jou7-nal. 

"  One  has  only  to  read  this  volume  in  order  to  see  its  worth.  Whether  there  was 
need  at  present  for  a  new  text-book  on  otology  must  be  seen  from  the  success  which 
will  be  met  with  by  this  work  of  Dr.  Dench.  However,  we  have  no  hesitancy  in  say- 
ing that  it  is  the  best  work  of  its  kind  by  an  American  author.  Dr.  Dench  is  perhaps 
one  of  the  leading  exponents  of  intra-tympanic  surger}',  and  while  his  views  upon  this 
subject  are  perhaps  more  radical  than  the  ma-ority  of  aural  surgeons,  yet  they  must 
be  thoughtfully  considered,  coining  as  they  do  from  one  who  is  so  well  and  favorably 
known.  It  is  almost  impossible  to  display  any  originality  in  writing  a  work  upon  the 
ear,  yet  in  this  text-book  the  author  has  dealt  in  no  superficial  vagaries,  but  he  speaks 
as  one  with  a  lai'ge  amount  of  clinical  experience,  and  thus  gives  to  the  reader  those 
points  which  are  of  practical  importance." — Atlanta  Medical  and  Surgical  Journal. 

"  In  this  valuable  work  minute  pathology  has  not  been  considered  extensively,  be- 
cause it  has  been  the  aim  of  the  author  to  adapt  it  to  the  needs  of  the  general  prac- 
titioner and  special  surgeon.  Dr.  Dench  has  written  at  length  upon  the  importance 
of  a  thorough  functional  examination,  which  many  works  upon  otolog}'  have  failed  to 
emphasize.  He  has  placed  the  results  of  recent  investigations  at  the  disposal  of  the 
reader  in  such  a  manner  as  to  enable  him  to  use  them  in  diagnosis.  The  author  has 
written  from  his  extensive  personal  experience  in  advocating  operative  procedures 
upon  the  middle  ear.  On  the  whole  the  work  is  an  exceedingly  good  one,  and  admi- 
rably adapted,  as  was  the  author's  aim,  to  the  general  practitioner  and  the  special 
surgeon." — Kansas  City  Medical  Rtxord. 


D.   APPLETON    AND    COMPANY,    NEW   YORK. 


THE  DISEASES  OF  THE 
STOMACH. 

By    Dr.    C.    A.    EWALD, 

EXTBAOEDIXARY    PROFESSOR    OF    ilEDICIJTE    AT   THE    VXIVERSITT    OF    BERLIN. 

Second  American  Edition,  translated  and  edited,  with  numerous  Additions, 
from  the  Tliird  German  Edition, 

By  MORRIS    MANGES,   A.  M.,  M.  D., 

ASSISTANT    VISITING    PHYSICIAN    TO    MOUNT    SINAI    HOSPITAL  :     LECTURER    ON 
GENERAL    iLEDICINE,    NEW    TOEK     POLYCLINIC,    ETC. 

This  work  has  been  thoroughly  revised,  rearranged,  largely  rewritten,  and 
brought  up  to  date  from  the  most  recent  literature  on  the  subject. 

8vo,  602  pages.     Sold  by  subscription.     Cloth,  $5.00  ;  sheep,  $6.00. 

"In  giving  the  medical  profession  this  second  revised  translation  of  Prof. 
Ewald's  treatise  on  the  Diseases  of  the  Stomach,  Dr.  Manges  has  placed  the  profes- 
sion under  even  greater  obligations  than  we  owed  for  the  fii'st.  The  first  transla- 
tion was  then  an  almost  exhaustive  treatise,  and  now,  with  so  much  new  and 
valuable  data  added,  the  work  is  a  sine  qua  non." — Atlanta  Iledical  and  Surgical 
Journal. 

"  This  work  as  it  now  stands  is  the  best  on  the  subject  of  stomach  diseases  in 
the  English  language.  Xo  physician's  library  is  complete  without  it.  It  is  in 
every  way  well  adapted  to  the  requirements  of  the  general  practitioner,  although 
complete  enough  to  meet  also  the  requirements  of  the  specialist." — American 
Medico- Surgical  Bulletin. 

"  The  present  American  edition  is  a  peculiarly  valuable  one,  as  the  editor. 
Dr.  Manges,  has  done  his  work  in  a  thoroughly  creditable  manner.  His  numer- 
ous notes,  additions,  and  new  illustrations  have  made  the  book  a  classic  one. 
Under  these  circumstances  it  should  find  a  place  in  the  library  o[  every  Amer- 
ican physician,  as  their  clientele  is  composed  of  such  a  large  proportion  of  patients 
suffering  from  gastric  complaints  and  more  or  less  improper  medication  which 
most  often  ends  in  failure.  There  is  no  doubt  that  more  properly  directed  efforts 
in  the  proper  direction,  as  outlined  in  Ewald's  book,  would  soon  remove  from 
Americans  the  reputation  of  being  a  nation  of  dyspeptics." — St.  Louis  Medical 
and  Surgical  Journal. 

"  Dr.  Ewald's  book  has  met  with  a  very  cordial  reception  by  the  medical  pi'o- 
fessiou.  Within  a  short  period  three  editions  have  appeared,  and  translations 
published  in  England.  Spain,  France,  Italy,  and  the  United  States.  To  the 
present  edition  the  author  has  not  only  added  considerable  new  matter,  but  he 
has  also  entirely  rewritten  the  work.  The  arrangement  of  the  chapters  has  been 
somewhat  changed,  and  many  new  personal  observations  and  therapeutic  experi- 
ences added.  The  desirability  of  surgical  interference  is  carefully  considered,  and 
the  pros  and  cons  given  so  far  as  would  be  necessary  to  enable  a  physician  to 
determine  whether  the  aid  of  the  surgeon  might  be  required.  The  translator  has 
done  his  work  well,  and  has  incorporated  much  new  matter  into  the  text  and 
footnotes." — North  American  Journal  of  Homoeopathy. 


D.  APPLETON  AND  COMPANY,  NEW  YOPwK. 


INJURIES    OF  THE   BRAIN 

AND  ITS  MEMBRANES. 

WitJi  a  Special  Strtdt/  of  Pistol- Shot  Wounds  of  the  Head  in  their 
Medico-Legal  and  Surgical  Relations. 

By  CHARLES   PHELPS,  M.  D., 

Surgeon   to   Bellevue   and   St.    Vincent's   Hospitals. 

Second  Edition,  Revised  and  Enlarg-ed. 

8vo,  616  pages,    With  49  Illustrations.    Oloth,  $5.00. 

SOLD    BY    SUBSCKIPTION. 

"  This  work  is  a  concise  and  systematic  treatise  on  that  division  of  brain  sur- 
gery arising  from  injuries  of  the  brain  through  extei'nal  violence,  and  has  been 
based  almost  exclusively  on  the  observation  of  five  hundred  consecutive  cases  of 
recent  occurrence.  Although  the  cases  were  so  numerous,  it  seems  they  were  in- 
complete only  in  the  illustration  of  secondary  pyogenic  infection,  which  is  naturally 
a  tribute  to  the  skill  of  the  surgeons  in  charge  of  the  cases,  inasmuch  as  they  were 
kept  from  infection.  This  clinical  deficiency  has  been  supjilied  by  excerpts  from 
Macewen's  work  on  Infiammations  of  the  Membranes  of  the  Brain  and  Spinal  Cord, 
with  the  permission  of  that  gentleman.  We  have  no  hesitation  in  saying  that  it  is 
the  most  complete  work  on  this  division  of  brain  surgery  which  has  yet  appeared 
in  America." — Journal  of  the  American  Medical  Association. 

"  This  book  will  prove  of  great  service  to  both  physician  and  surgeon  ;  and  to 
those  interested  in  medical  jurisprudence  it  will  be  of  incalculable  value.  The 
author  is  not  embarrassed  by  his  great  wealth  of  material  :  he  studies  it  exhaustively, 
and  ari'anges  it  clearly,  concisely,  and  with  great  care  and  discrimination.  The^ 
chapters  on  Pistol-Shot  Injuries  are  particularly  instructive,  and  the  series  of  ex- 
periments on  cadavers  replete  with  interest.  One  of  the  strongest  features  of  the 
book  is  the  large  number  of  photographic  representations  of  cranial  injury." — 
National  Medical  Review. 

"We  have  here  a  new  work  highly  creditable  to  American  authorship  and  add- 
ing a  material  contribution  to  our  present  literature  upon  Brain  Surgery.  The 
first  part  of  the  work  is  devoted  to  the  consideration  of  traumatic  lesions  of  Ihe 
cranium  and  its  contents,  embracing  their  pathology,  symptomatology,  diagnosis, 
prognosis,  and  treatment.  Part  II  is  an  exceedingly  interesting  and  original 
discussion  of  medico-legal  and  surgical  relations  and  treatment  of  pistol-shot 
wounds  of  the  head.  Part  III  contains  a  condensed  history  of  three  hundred 
eases  of  intracranial  traumatism  verified  by  necropsy.  A  most  interesting  feature 
of  the  work  is  the  introduction  of  a  large  number  of  full-page  photographic  illus- 
trations of  the  efiiects  of  pistol-shot  wounds  produced  by  those  of  different  calibers 
and  at  different  distances.  The  work  will  at  once  be  appreciated  as  one  of  original 
investigation,  and  especially  by  those  who  are  particularly  interested  in  brain  sur- 
gery."— North  American  Practitioner. 


D.  APPLETON   AND   COMPANY,  NEW  YORK. 


LECTURES   ON 
THE   MALARIAL  FEVERS. 

By  WILLIAM   SYDNEY   THAYER,   M.  D., 

Associate  Professor  of  Medicine  in  the  Johns  Hopkins  University. 

Small  8to,  326  pages.    With  19  Charts,  and  3  Lithographic  Plates  show- 
ing the  Parasite  of  Tertian,  (Quotidian,  and  Jlstivo-Autumnal 
Fevers.    Cloth,  $3.00. 

Tlds  is  the  only  ivork  in  the  English  language  which  contains  a  full  record  and 
ex^iosition  of  the  subject  of  malaria. 

"  This  work  contains  326  pages,  and  is  probably  one  of  the  most  valuable 
and  readable  books  that  we  have  had  the  pleasure  of  reviewing.  Particularly  to 
the  Southern  physicians  will  it  be  of  special  benefit,  malaria  being  their  most 
prevalent  and  often  difficult  disease  to  manage.  The  work  contains  nine  lectures, 
written  clearly  and  to  the  point.  The  book  is  well  printed  on  good  paper,  and 
makes  a  neat  volume."' — Charlotte  Medical  Journal. 

"  The  work  is  especially  valuable  as  being  the  clearest  and  most  comprehensive 
book  that  has  been  published  on  this  subject.  We  can  not  too  highly  recommend 
it,  and  believe  it  will  find  a  place  in  the  libi-ary  of  every  progressive  physician  who 
has  malarial  fevers  coming  under  his  observation." — Medical  Sentinel. 

"The  work  of  Thayer  in  connection  with  malarial  fever  needs  no  introduction. 
His  name  is  already  closely  identified  with  this  subject  in  America.  He  is  an 
authority  whom  we  all  recognize  and  to  whom  we  all  do  honor.  The  work  under 
consideration  contains  the  results  of  his  labors,  with  the  nature  and  scope  of  which 
we  are  already  familiar  through  the  monograph  previously  written  by  him  in 
collaboration  with  Hewetson.  To  an  exhaustive  knowledge  of  the  literature  of  the 
subject  in  all  languages,  Thayer  adds  the  results  of  a  series  of  original  investigations 
of  inestimable  value.  The  book  represents  the  length  and  breadth  of  our  present 
knowledge  upon  this  topic,  and  excites  the  admiration  of  all  who  take  pride  in 
American  achievement.  The  make-up  of  the  volume  is  excellent ;  the  plates  admi- 
rable in  their  fidelity  and  beauty  of  execution." — National  Medical  Review. 

"This  is  unquestionably  a  strong  and  able  presentation  of  the  advance  thought 
and  teaching  upon  this  important  subject,  covering  the  ground  comprehensively, 
if  not  exhaustively.  It  is  finely  written  in  a  clear,  forceful  manner,  calculated  to 
impress  upon  the  reader  the  salient  ideas.  The  writer,  in  considering  the  condi- 
tions under  which  malaria  prevails,  recognizes  that  we  are  absolutely  ignorant  of 
the  form  in  which  the  malarial  parasite  exists  outside  of  the  human  body,  and 
equally  ignorant  of  the  manner  in  which  it  enters.  An  excellent  study  is  given  of 
its  presence  in  the  body.  The  work  is  one  of  unusual  interest  to  the  advanced 
clinician." — Uahnemannian. 


D.  APPLETON   AND   COMPANY,    NEW  YORK. 


THE  DISEASES  OF 
mUMJ  AND  CHILDHOOD. 

J^&r  the  Use  of  Students  and  Practitioners  of  Medicine. 
By  L.  EMMETT  HOLT,  A.  M.,  M.  D., 

Professor  of  Bimises  of  Children   iii    the  Eew   Tor-lc  Polyclinic ;    Attending  Physician  to 

the  Babies'  Hospital  and  to   the  I^'ursery  and    Child'' s  Eospital,  Sew   York  ; 

Consulting  Physician  to  the  New  York  Infant  Asylum^  and  to  the 

Hospital  for  Ruptured  and   Crippled. 

With  7  full-page  Colored  Plates  and  203  Illustrations.     Cloth,  $6.00  , 
sheep,  $7.00  ;  half  morocco,  $7.50. 

SOLD    O^STL^^    B^^    SXJBSCRIPTIO?^. 


American  Medico-Surgical  Bulletin: 

"  ThLs  work  is  in  every  sense  of  the  word  a  new  book  ;  for,  while  the  best  work  of  other 
authors  in  this  and  other  countries  has  been  di-awn  upon,  especially  that  in  the  form  of 
monographs  and  in  the  tiles  of  psediatrie  Hterature,  the  majority  is  derived  from  the  author's 
own  clinical  observations.  Obsolete  dicta  handed  down  from  te.xt-book  to  text-book  are 
here  con.^picuously  absent,  and  nothing  has  been  accepted  which  has  not  been  earetully 
tested.  ...  It  is  not  venturing'  too  much,  after  a  careful  perusal  of  these  pages,  to  predict 
for  this  volume  a  pre-eminent  and  lasting  position  among  the  treatises  upon  this  subject. 
We  heartily  recommend  that  it  find  a  place  not  only  in  the  library  of  every  physician,  but 
■wide  open  at  the  elbow  of  every  man  Avho  desires  to  deal  iutelhgently  with  the  problems 
which  confront  him  in  the  treatment  of  infants  and  children  intrusted  to  his  care." 

Nash  villa  Jo  urnal  of  Medicine  : 

"  This  magnificent  work  is  one  of  the  most  valuable  recent  contributions  to  medical  liter- 
ature. It  will  rapidly  win  its  way  to  a  front  rank  with  other  standard  works  upon  kindi-ed 
•subjects.     It  is  as  nearly  complete  as  a  treatise  upon  this  subject  can  be." 

Virginia  Medical  Semi-Monthly  : 

"  When  one  recalls  the  teachings  of  a  decade  or  two  ago  and  compares  the  inculcations 
of  to-day,  he  can  scarcely  help  recognizing  that  '  old  things  have  passed  away,  and  all 
things  have  become  new.'  The  volume  before  us  is  practically  the  record  of  information 
obtained  by  the  author  from  eleven  years  of  special  study  and  practice,  so  that  nearly  eveiy 
subject  is  presented  from  the  standpoint  of  personal  observation  and  experience.  The 
information  given  is  therefore  reliable,  for  Dr.  Holt  is  a  close  observer  and  a  careful  student 
of  his  ripe  experience.  ...  In  short,  tliis  book  appears  to  us  to  be  the  best  all-round,  up-to- 
<iate  book  for  practitioners  and  students  of  children's  diseases  that  we  know  of." 

Medical  Progress : 

"  The  work  before  us  is  one  which  reflects  great  credit  upon  the  distinguished  author. 
Dr.  Holt  has  long  been  known  as  a  most  industrious  and  naiustaking  investigator,  and  in 
this  volume  he  sustains  that  reputation.  The  work,  we  may  saj-  in  a  sentence,  is  fully  up 
to  the  requirements  of  the  times,  and  there  is  no  advance  known  to  p»diatrics  which  has 
not  been  fully  dealt  with  according  to  its  merits." 


D.   APPLETON   AND   COMPANY,   NEW   YOEK. 


X  ^ 


RCU6 
St  81 
Strlimpell  1901 

Textbook  of  medicine. 


